NURS 3123 Test 2 Notes
NURS 3123 Test 2 Notes NURS 3123
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This 142 page Class Notes was uploaded by Hope Gulley on Tuesday October 20, 2015. The Class Notes belongs to NURS 3123 at Auburn University taught by Dr. Ramona Lazenby; Dr. Edward Campbell in Fall 2015. Since its upload, it has received 31 views. For similar materials see Nursing Pathophysiology in Nursing and Health Sciences at Auburn University.
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NURS 3123 Pathophysiology Module 3 Fluid and Electrolytes Edward Campbell MSN RNBC A Look at Balancing Fluids Acids and Bases 1 A Look at Fluid Just about all major organs work together to maintain proper uid balance To maintain that balance the amount of uid gained should equal the amount lost a Fluid Losses may be both sensible and insensible lnsensibe Fluid Losses are those that cannot be seen or measured This includes losses from evaporation of sweat and moister lost during breathing And fever may cause increased sweating and faster breathing tachypnea which can cause uid losses Sensible Fluid Losses are those that can be measured These would include uid lost though defecation urination emesis blood loss and etcetera b Fluid compartments include both intracellular and extracellular Intracellular uid normally consists of approximately 40 of the person s body weight and is found inside of the cells Extracellular uid normally consists of approximately 20 of the person s body weight and is found outside of the cells 1 Interstitial uid is the uid that immediately surrounds cells and accounts for 70 of the extracellular uids 2 lntravascular uid is the uid that makes up the plasma portion of the blood and accounts for 25 of the extracellular uid 3 Transcellular uid is the uid that is found in compartments in the body including the cerebrospinial column plural cavity pericardial sac and etcetera This uid accounts for approximately 5 of the extracellular uid c Fluid Types found in the body consist of both diluted and nondiluted forms An isotonic uid is one that has the same concentration ie osmotic and oncotic pressures as the uid it is being compared to For example normal saline solution is considered isotonic because it has roughly the same concentration of sodium in the blood 09 Sodium Chloride A hypertonic uid is one that as a greater osmotic or oncotic pressure due to more dissolved particles than the one it is being compared to For example 3 Sodium Chloride solution is considered hypertonic to the blood because it has a higher osmotic pressure due to having more NaCl than the blood itself A hypotonic uid is one with less osmotic or oncotic pressure due to fewer dissolved particles than the one it is being compared to For example 045 Sodium Chloride solution is considered hypotonic to the blood because it has a lower osmotic pressure due to having less NaCl than the blood itself d Fluid and particle movement may occur in one of three different ways Passive Diffusion When two uids are separated by a semipermeable membrane that is post any membrane in our body particles will move from an area of high concentration to an area of low concentration This process happens passively with the ionic gradient because particles want to space themselves out as much as possible from each other It will also eventually equalize the osmotic gradient Active diffusion When two uids are separated by a semipermeable membrane the body may use energy in the form of Adenosine Triphosphate ATP to move particles against an ionic gradient For example cells utilize sodium potassium pumps to move sodium out of the cell and potassium into the cell However they must use ATP in the process Osmosis When two uids are separated by a semipermeable membrane especially one that does not allow the exchange of solutes or one that actively changes the ionic gradients water will move across the osmotic gradient toward the compartment with more particles Le a higher osmotic pressure Passive Diffusion Active Diffusion Osmosis Figure 1 Passive diffusion involves moving particles with the ion gradient Active diffusion involves moving particles against it And osmosis involves moving water with the osmotic gradient e Capillary Filtration is the movement of uid into and out of the capillaries which allows for exchange of uids and solutes i Hydrostatic Pressure is the pressure caused by the heart beating that pushes uids out of the capillary bed ii Oncotic Pressure also called the plasma colloid pressure is the pulling pressure that causes uid to be drawn back into the capillaries This pressure is caused by protein particles that act as a solute drawing water back to the capillaries by osmosis 1 While the oncotic pressure remains relatively stable throughout the circulatory system the hydrostatic pressure decreases drastically from the precapillary arterioles to the post capillary venuoles In effect the hydrostatic pressure is greatest in the arterioles causing water to be pushed out But it quickly becomes less than the oncotic pressure causing water to be pulled back in due to the pulling force of proteins Oncotic pressure llilydlrostatic Pressure HZO Exchange Figure 2 The balance between hydrostatic pressure and oncotic pressure allows the body to exchange uid electrolytes and waste products f Maintaining Balance The renal system and related hormones also play a signi cant role in maintaining uid balance If the kidneys do not work properly the body will have a hard time controlling uid balance i Antdiuretic Hormone ADH or vasopressin is a hormone released by the posterior pituitary This signal from the brain causes the kidneys to reabsorb water and results in concentrated urine ii ReninAngi0tensinAdoster0ne System RAAS begins with the juxtaglomerular cells which secrete an enzyme called renin when pressure in the glomerulus stops ie too little blood too little pressure The renin then undergoes several conversions as follows 1 Renin l Angiotensin Liver 2 Angiotensin l Angiotensin II Lungs 3 Angiotensin II stimulates Aldosterone release Adrenal Cortex The result is a rise in blood pressure because Angiotensin II causes vasoconstriction and Aldosterone causes the kidneys to retain more water Side Note To understand blood pressure remember three rules of thumb 1 More water More pressure 2 More constriction More pressure 3 More pumping More pressure Atrial Natriuretic Peptide ANP is stored in the cells of the atria It is released when the cells of atria are stretched by too much water volume andor increased pressure The hormone counteracts the effects of the RAAS by stopping the release of renin Atrial Vasopressin ADH Natriuretic amp Peptide Aidosterone P Urine Output L Blood Pressure L UWine Output F Blood Pressure Figure 3 Hormones acting on the kidneys can help maintain uid balance by increasing or decreasing the urine output This increase and decrease in urine output has the added effect of raising and lowering blood pressure Thus blood pressure is often closely associated with uid balance 2 A Look at Acids and Bases The chemical reactions that sustain life depend on a delicate balance between acids and bases in the body Even a slight imbalance can profoundly affect the essential body functions a Regulating Acids and Bases A person s ability to regulate their acidbase balance depends on two major systems namely the metabolic and the respiratory system The metabolic system is a complex system of chemical buffers including bicarbonate phosphate and protein buffers that bind with acids and bases to neutralize them In a medical sense the most important buffer is bicarbonate lt binds with both strong and weak acids to increase the blood s pH The kidneys assist the buffer system by controlling the production of bicarbonate ii The respiratory system regulates carbon dioxide which is a gas that combines with water to form carbonic acid Thus the more C02 that a person has in their blood the higher the acid level People can control their C02 levels by breathing faster to expel C02 or breathing slower to retain C02 The way that C02 is usually measured is through the partial pressure of the dissolved gas in the blood ie PaCOZ The Big Picture When considering AcidBase balance the most important acid in the body is carbon dioxide C02 The most important base is bicarbonate HCO3 The kidneys regulate bicarbonate and the lungs regulate carbon dioxide b Arterial Blood Gas A86 is the most common way to diagnose an acidbase imbalance They can be obtained by taking a sample of oxygenated blood from the arteries And normal results for acidbase balance should fall between the following ranges ipH 735 to 745 ii PaCOZ 35 to 45 mmHg iii HCO3 22 to 26 mEqL c Interpreting an ABG Most resources will teach a 56 step methodology for assessing ABGs but this can be simpli ed into only three steps see quotInterpreting an ABGquot d AcidBase imbalances may be caused by either the respiratory or the metabolic system They may also result in either a decrease in pH Acidosis or an increase in pH Alkalosis Respiratory Acidosis occurs when there is a buildup of C02 in the blood stream which causes a decrease pH The causes of increased C02 can include Hypoventilation Rebreathing C02 Lack of hypoxic drive Overdose of CNS depressants Obstructive Pulmonary Disease wewwe Some symptoms of respiratory acidosis include 1 Altered level of consciousness 2 Confusion 3 Shallow rapid breathing 4 Signs of increased iCa2 The kidneys will often try to compensate by increasing production of bicarbonate ions to raise the pH level We also tend to treat respiratory acidosis by increasing the ability to expel C02 such as giving medications to increase ventilation Respiratory Akaosis occurs when C02 levels get too low causing an increased pH The causes of decreased C02 can include 1 Hyperventilation 2 Hypoxia 3 Overdose of CNS Stimulant The symptoms of respiratory alkalosis include Confusion Tachycardia Kusmal s Breathing Decreased iCa2 ewNH The kidneys will often try to compensate by decreasing production of bicarbonate ions to raise the pH level We also tend to treat respiratory alkalosis by having someone rebreathe C02 ex paper bag over the mouth Metabolic Acidosis occurs when there is a lack of metabolic buffers primarily bicarbonate which causes the pH to decrease Some of the causes may include 1 Increased production of acids due to metabolism of protein muscle or fat 2 Decreased production of bases due to renal failure 3 Toxic drugs or chemotherapy The symptoms are similar to those in respiratory acidosis And the treatment is to correct the underlying cause while supplementing the body s bicarbonate Metabolic Alkalosis occurs when there is too much metabolic bases primarily bicarbonate which causes the pH to increase Some of the causes may include 1 Loss of acidic GI content 2 Overdose of antacids 3 Metabolic causes The symptoms are similar to those in respiratory alkalosis And the treatment is to correct the underlying cause while supplementing the body s acids with drugs like ammonium chloride INTER PH ETING AN ABG Step 1 Cheek the pH if the pH is lew ie less than 235 the prehlern is tee nineh aeidi Therefereiwe hatre eeidesisi if the pH is high ie less than TASLthe prehlern is tee nineh easequot Therefere we have elkefesisi Step 2 Eheek fer HOME I if the PaGUZ is trending in the eppesite direetien frenn the pH then the cause ef the pureelent is respireteryn I if the BEDS is trending in an eerie direetien as the pH then the eanse ef the prehlenn is metebeiiei A ninenienie fer Step 2 is JEDME Respiraterjris Uppesite Metahelie is Equal Step 3 Eheek fer Eemeensetien I if the BEDS is geing in the same direetien as the PaCUZJ then the bed is eempenseting fer the imbalance That is either the respiraterjr system is eernpensating fer the meta helie system er V153 versai I if the HCUB is net geing in the same direetien as the Pa Ui then the bed is net eempenseting fer the imbalancequot Figure 4 Most resources will teach a 56 step methodology for assessing ABGs but this can be simpli ed into only three steps as shown above 10 Fluids and Electrolyte lmbalances 1 Sodium and Water as a 3060 deal In most cases water will follow sodium due to osmosis And sodium will follow water due to simple diffusion This is true up to the point that the body has to conserve either water or sodium Thus imbalances of sodium are also imbalances of water except in unusual circumstances a Hyponatremia or water toxicity occurs when there is too much water in the vascular system andor too little sodium lt135mEqL Think of this as dilution of CoolAid If you add more water to a cup of CoolAid then your drink will taste weak because there is not enough Cool Aid mix Excess uids tend to cause an increase in blood pressure ie more water more uid And the uid will leak out into extracellular and transcellular spaces General symptoms of hyponatremia may include i Increased Vascular Volume 1 Increased BP 2 Distended veins ii Fluid on lungs 1 Pulmonary Edema 2 Oxygen Hunger 3 Crackles on Auscultation iii Increased Intracranial Fluid 1 Decreased Levels of Consciousness 2 Increased pressure on brain 3 Confusion 4 Seizures iv Increased extracellular Fluid 1 Peripheral EdemaSwelling 2 Weight gain Treatment for hyponatremia is aimed at decreasing vascular volume by giving diuretics and increasing sodium by giving hypertonic uids b Hypernatremia or dehydration occurs when there is not enough water in the body or when there is too much sodium gt145mEqL Think of this as concentration of Cool Aid If you leave an open glass of Cool Aid out on a 11 summer day the water will evaporate and your drink will become stronger and sweeter Decreases in uid volume cause a decrease in blood pressure ie less water less pressure As water decreases in the vascular space it will also decrease in the extracellular and intracellular spaces General signs of hypernatremia tend to include i Thirst ii Decreased BP iii Weak pulses iv Decreased skin turgor v Increased HR and RR vi Loss of tissue perfusion 1 Decreased Level of Consciousness 2 Multiple organ failure 3 Confusion Treatment is generally aimed at replacing lost uids with oral uid replacement and hypotonic IV uids 2 Calcium and Magnesium as Depressants Calcium and magnesium are both cations that affect the transmission of nerve impulses by decreasing the cell s excitability In addition to action potential of nerve cells these ions also function to decrease the excitability of the sacrolemma cell membrane of muscle bers Thus increased levels of either ion will 1 depress the CNS 2 block signals in the PNS and 3 decrease muscle contraction strength a A closer look at calcium Before we can understand calcium balances there are a few basics that we need to know i How to Measure Calcium Levels Because nearly half of all calcium is bound to albumin and citrate serum protein levels can in uence serum calcium levels And thus measurements of calcium can be taken in two different ways 1 Total calcium levels are a measure of all calcium in the serum This includes calcium that is bound to 12 protein as well as calcium that is not 2 lonized calcium level measures all of the calcium that is not bound to protein or citrate This ionized form is the only form that the body has available to use in metabolic processes and is affected by the following a Protein decreases ionized calcium by binding free Ca2 ions b Citrate is a derivative of citric acid that is found in the body which also binds calcium to make calcium citrate c pH changes calcium by changing the af nity that proteins have for calcium ions An increase in pH will increase the af nity for Ca2 causing less available iCa2 And a decrease in pH will cause a decrease in af nity for Ca2 causing more available iCa2 ii How We Regulate Serum Levels The body regulates calcium by hormones of the thyroid and parathyroid 1 Parathyroid Hormone When calcium levels fall the releases parathyroid hormone which stimulates osteoclasts to degrade bone and release calcium into the blood ie PTH quotpullsquot calcium into the blood 2 Calcitonin When calcium levels rise the thyroid gland releases calcitonin to promote the actions of osteoblasts which encourages deposition of calcium into the 13 bones ie Calcitonin keeps calcium in the bone iii How we Regulate Absorption The body also regulates calcium by controlling how much calcium is absorbed through the intestines and how much is resorbed by the kidneys 1 Vitamin D has two active forms namely calcidiol and calcitriol lnitially vitamin D is converted to calcidiol by the liver which then acts on the kidney to decrease excretion of calcium and promote resorption of calcium The kidney then converts calcidiol into calcitriol which promotes absorption of calcium into the serum by the small intestine See gure 5 2 Phosphorus plays a role in serum calcium levels because it has nearly the exact opposite effect as Vitamin D That is to say phosphorus inhibits absorption of calcium by the intestines and causes a decrease in serum calcium Thus there is an inverse relationship between calcium and phosphorus So when calcium is up phosphorus is down and vice versa l Calcitriol 14 Figure 5 Vitamin D has two active forms Calcidiol acts on the kidney to increase resorption of calcium and Calcitriol acts on the intestines to increase absorption of calcium b Hypercalcemia occurs when the calcium levels get too high gt105mgdL total calcium or gt53mgdL ionized calcium Because calcium decreases the excitability of both nerve and muscle bers too much of this ion can be understood to be a problem of too much depressant Too much calcium results in the following general signs and symptoms CNS depression 1 2 Confusion Fatigue 3 Altered mental status Peripheral nervous system depression 1 2 Decreased re exes Lack of coordination ataxia Depression of skeletal cardiac and smooth muscles P P PP N General muscle weakness Slow cardiac rhythms Decreased cardiac contraction Decreased GI motility Constipation Urine retention Other signs of Hypercalcemia are often summarized by the mnemonic quotBones stones groans thrones and psychiatric 0 vertones 1 Bones refers to bonerelated complications which include pathological fractures bone pain and arthritis quotStonesquot refers to kidney stones due to formation of calcium salts in the urine 15 3 quotGroansquot refers to gastrointestinal symptoms of constipation indigestion nausea and vomiting 4 quotThronesquot refers to increased urination because of particle induced diuresis 5 quotPsychiatric Overtonesquot refers to effects on the central nervous system including lethargy fatigue depression memory loss psychosis ataxia delirium and coma Treatment includes increasing uid intake to increase calcium excretion by kidneys administering calcitonin and removing one or more of the parathyroid glands Hypocacemia occurs when calcium levels get too low lt85 mgdL total calcium or 46mgdL ionized calcium Because calcium decreases the excitability of both nerve and muscle bers too little of this ion can be understood to be a problem of too little depressant or a problem of excitability Too little calcium results in the following general signs and symptoms i CNS Excitability 1 Seizures 2 Altered mental status ii Peripheral nervous system excitability 1 Increased re exes 2 Tingling or numbness of the handsfeet iii Excitability of skeletal cardiac and smooth muscles Tetany Muscle spasms Fast cardiac rhythms Increased cardiac contraction Increased GI motility Diarrhea UnneinconUnence P P FWN 16 8 Positive Trousseau s and Chvostek s signs See Figure 6 iv Other signs of hypocalcemia may be summarized by the mnemonic quotCATS go numbquot Convulsion Arrhythmias Tetany Stridor Numbness or tingling wewwe Treatment includes administration of calcium and vitamin D supplements including IV forms like calcium guconate or calcium chloride Figure 6 Trousseau s and Chvostek s signs are symptoms of induced tetany and muscle spasms that can be caused by stimulating the brachial plexus or facial nerves d anermaanesemia is an increase of magnesium ions gt21mgdL that causes depression of the neuromuscular system That is magnesium is a neuromuscular depressant just like calcium Too much magnesium results in similar signs as too much calcium including i CNS depression ii PNS depression iii Depression of muscles Magnesium imbalances can easily be mistaken for Ca2 imbalances or K imbalances However the most signi cant features of the hypermagnesmia are decreased re exes due to 17 depression of PNS and low blood pressure due to smooth muscle dilation in arteries e Hypomagnesemia is a decrease of magnesium ions lt13mgdL that causes excitation of the neuromuscular system Too little magnesium results in similar signs as too little calcium including i CNS excitation ii PNS excitation iii Excitation of muscles Magnesium imbalances can easily be mistaken for Ca2 imbalances or K imbalances However the most signi cant features of the hypomagnesmia is increased re exes due to depression of PNS 3 Potassium and Phosphorus as Stimulants Potassium and phosphorus both affect the transmission of nerve impulses by increasing the cell s excitability And these ions function to increase the excitability of the sacrolemma cell membrane of muscle bers Thus increased levels of either ion will 1 excite the CNS 2 excite the PNS and 3 cause muscle tetanyspasms a vaerkaemia is the condition that results when serum potassium levels get too high gt5mEqL Because potassium increases the excitability of nerve and muscle bers too much potassium is a problem of excitability Too much potassium results in the following general signs and symptoms i CNS Excitability 1 Seizures 2 Altered mental status ii Peripheral nervous system excitability with paradoxical effect 1 NumbnessTingling 2 Decreased re exes 3 Flaccid Paralysis 18 4 Lack of Trousseau s and Chvostek s gtlltgtllt Special note Too much potassium has a paradoxical effect on the PNS because it causes quottoo muchquot electrical activity which shuts down the peripheral nervous system due to the inability of the nerves to repolarize In essence the electrical activity becomes so disorganized that the signal is not moving much like a traf c jam during rush hour traf c This paradoxical effect often helps us distinguish between hyperkalemia too much stimulant and hypocalcemia too little depressant iii Excitability of skeletal cardiac and smooth muscles Tetany Muscle spasmsweakness Increased GI motility Diarrhea Increased cardiac contraction causing Decreased cardiac lling Decreased cardiac output Decreased tissue perfusion Decreased urine output wewwe 1000 iv Other signs of hyperkalemia may be summarized by the mnemonic MURDER 1 Muscle weakness Muscle spasms will often lead to muscle weakness either from spasms or from paradoxical effect of PNS system 2 Urine output may be decreased due to poor cardiac output 3 Respiratory failure may occur because of accid paralysis related to paradoxical effect of PNS system 4 Decreased cardiac output is caused by decreased lling 19 increased excitability of cardiac muscles and paradoxical effect of PNS system 5 EKG Changes are caused by increased excitability of cells and paradoxical effects of the PNS system 6 Re exes are decreased due to paradoxical effect of PNS system Treatment may be aimed at binding potassium with drugs like kaexelate so it can be completely removed from the body Or when given together glucose and insulin can drive potassium back into intracellular uid while decreasing potassium in extracellular uid and serum b Hypoaemia is a condition that occurs when serum potassium gets too low lt35 mEqL causing a problem where there is not enough stimulant for the neuromuscular system Too little potassium has similar effects as too much calcium or too much magnesium including i CNS depression ii PNS depression iii Depression of muscles Other signs of hypokalemia may be summarized by the mnemonic quotSIC WAL quot i Shallow Respirations may occur due to depression of depression of CNS and PNS ii lrritability may occur due to mental confusion iii Confusion may occur due to depressed CNS iv Weakness may occur doe to depression of PNS and muscle sarcolemma 20 Summary of Electrolytes v Arrhythmias irregular rates may occur These generally begin with a slow rate But they progress to a fast rate as the body tries to compensate vi Lethargy occurs due to muscle weakness and depression of the CNS vii Thready pulses occur due to decreased heart rate and contractile force One of the most common causes of hypokalemia is the loss of potassium from gastric contents ie GI suctioning or vomiting Therefore treatment often includes either oral or IV potassium replacement Hyperphosphatemia is a problem that occurs when phosphate becomes too high gt26mEqL However because phosphate has an inverse relationship with calcium hyperphosphatemia is the same as hypocalcemia And we usually diagnose and treat the calcium imbalance Hypophosphatemia is a problem that occurs when phosphate becomes too low lt18mEqL However because phosphate has an inverse relationship with calcium hypophosphatemia is the same as hypercalcemia And we usually diagnose and treat the calcium imbalance ELEIE39T FI HEITY Proteins nfa Water Magnets Albumin 35 55 gde Mal 135 1il5 m quL 332 85 105 mgde Depressa nts MEEEl 13 21 mgfdlL H 35 5 m Eqr39L Stimulants Panes 25 45 mgde Figure 7 The most clinically signi cant electrolytes can be summarized by categorizing their effects on the body 21 Some are important for water balance Others act as stimulants And even others act as depressants 22 NURS 3123 Pathophysiology Module 4 Cardiac System Edward Campbell MSN RNBC Disorders of Blood Flow and Blood Pressure 1 Disorders of Arterial Blood Pressure a Three Rules of Blood Pressure Regulation There are three basic rules that govern how the body regulates blood pressure They are i ii Rule 1 More Water More Pressure Think of two different ows of water On one hand you have a drainage ditch that collects water on the side of the road On the other hand you have the Mississippi River Which one has more pressure You probably guessed that the Mississippi has more pressure based on instinct But the reason that is has more is because it has more water For blood pressure what this means is that larger intravascular volume will cause higher arterial and venous blood pressures Our bodies control intravascular volume by increasing or decreasing urine output See Fluid and Electrolyte notes on hormonal control of uid Rule 2 More Constriction More Pressure Assuming the same uid volume imagine that you attached a re hose and aquarium tubing to a kitchen faucet Which has more pressure Unlike the previous example the answer may not be quite so intuitive In this example the aquarium tubing will have more pressure because we are pushing the same volume of uid through a smaller space So the smaller the opening the more pressure the tubing will create For blood pressure what this means is that constricted blood vessels cause blood pressure to increase Our bodies control vessel constriction with a variety of hormones See Fluid and Electrolyte notes on hormonal control of uid iii Rule 3 More Pumping More Pressure Now imagine that you are pumping water from an aquifer with a hand operated pump The harder and faster you pump the faster you will get water into your bucket The heart works in much the same way If it pumps harder and faster the heart will move more blood ie volume Therefore a higher heart rate and a more forceful contraction will increase blood pressure Moreover our bodies increase heart rate and contraction with the Sympathetic Nervous System and it decrease it with the Parasympathetic System b It s all about quotperfusionquot The word used to describe the degree to which oxygen can move from the blood to the tissues is perfusion In order to perfuse tissues adequately the hydrostatic pressure must be high enough to force uid out of the arterioles in the capillary bed i Wow that s a lot of vocabulary We generally speak of blood pressure in terms of systolic and diastolic pressures However the most important pressure measurement is the mean arterial pressure This is the pressure needed for adequate tissue perfusion and it is generally de ned to be gt65 mmHg Some of the factors that can affect the mean arterial pressure are as follows 1 Systemic Vascular Resistance resistance to ow in blood vessels 2 Cardiac Output amount of blood that leaves the heart in a minute 3 Stroke Volume the amount of blood that leaves the heart with each stroke 4 Heart rate the number of heart beats in a single minute 5 End diastolic volume amount of blood in the ventricle after each lling 6 l nol systolic volume the amount of blood left in the ventricles at the end of each contraction Side Note There are mathematical formulas by which one can calculate the mean arterial pressure You won t be asked to calculate a MAP for pathophysiology but it may help to understand how all of these factors t together SR MAP HR EDV X CO 5V ESV or 2 DBP SBlP MAP c Hypertension occurs when the blood pressure get too high and is de ned by the joint National Committee on the Detection Evaluation anol lieatment of Blood Pressure or quotJNCquot for short as a systolic BP gt140 mmHg or a diastolic BP gt90 mmHg However a prehypertension category is de ned as SBPgt120 mmHg or DBP gt80 mmHg i Patho amp Etiology Elevated pressures cause the blood vessels to stretch more than they normally would This constant stretching causes loss of elasticity and results in weakened andor scarred vessels While this scarring can cause problems with any major organ or tissue it often affects the arterioles or the Bowman s capsule and the glomerulus within the kidney In addition to the damage done to the vessels themselves the increased resistance caused by lack of elasticity in the vessels causes an increase workload for the heart And the ventricles will need to beat harder to overcome the increased resistance to blood ow Causes of increased blood pressure are said to be primary caused by lifestyle factors or secondary caused by an underlying disease For example Cushing Syndrome is a disease related to the excess excretion of endogenous glucocorticoids from the adrenal gland This excess release of glucocorticoids will cause an increase in uid retention and stimulation of the sympathetic nervous system In short it will raise the BP Gestational hypertension is another speci c cause of high blood pressure in pregnancy It results from an increased blood volume and an increase in pregnancy related hormones such as estrogen In some cases this increase in blood pressure can cause renal damage seizures and strokes Signs and Symptoms There are few signs of mild or moderate hypertension However complications may result as organ systems are slowly affected by vessel damage Investigations Blood pressure monitoring is the best and most effective way of diagnosing hypertension Blood pressures gt14080 indicate hypertension However persons with diabetes or renal disease the goal is a blood pressure lt13080 7739eatment The rst step in treating primary hypertension is lifestyle modi cations including diet and exercise However pharmacological treatment may be needed as well These pharmacological treatments are often aimed at the following 1 Decreasing intra vascular volume Ex Diuretics 2 Decreasing arterial constriction Ex Hydralazine 3 Inhibiting the 5N5 Ex Betaadrenergic antagonists d Orthostatic Hypotension refers to an abnormal drop in blood pressure that occurs when a person changes position such as going from a sitting to a standing position Patho and Etiology When a person changes position there is a momentary shift in blood volume When going from a sitting or lying position to a standing position blood is shifted from the upper body to the lower part of the body resulting in a decrease in blood pressure in the upperbody Normally this decrease in BP is met by an increased stimulation of the sympathetic nervous system However patients on blood pressure medication are more susceptible to orthostatic changes because BP medications block the SNS Other risk factors might include decreased blood volume prolonged bed rest and various disorders of the autonomic nervous system ii Signs and Symptoms Decreased BP will result in loss of tissue perfusion even if only momentary And momentary loss of perfusion to the brain will result in dizziness light headedness or syncope fainting iii Investigations Orthostatic blood pressure measurements may help reveal the presence of hypotension The procedure for this includes serial blood pressure measurements 1 starting in a lying position 2 moving to a sitting position 3 then in a standing position In order to get the most accurate measurements serial blood pressures should be taken as close together as possible iv Featment Safety cautions should be taken to prevent injury from falls And treatment should focus on the underlying cause ex medication doses dehydration and etcetera 2 Disorders of Arterial Circulation a Atherosclerosis vs ArteriosCerosis Two terms that are easily confused are atherosclerosis and arteriosclerosis And while they often happen together these are distinctly different disease processes Patho amp Etiology Atherosclerosis can be de ned as the narrowing of arteries due to fatty plaque buildups This narrowing can result in decreased blood ow to tissues distal to the ow of blood However this plaque buildup is usually preceded by Arteriosclerosis or scarring of the arteries This scarring results in hardening due to calcium deposits that cause rough surfaces from which fatty deposits can cling In essence arteriosclerosis scarring and loss of elasticity often leads to atherosclerosis narrowing of the arteries The general cause of arteriosclerosis is in ammation of the endothelial lining which causes damage and scarring And the source of in ammation may include diets high in simple carbohydrates uncontrolled diabetes alcohol drugs and high blood pressure When coupled with a diet high in cholesterol andor saturated fats plaques can develop on newly formed scar tissue Signs and Symptoms Generally there are no signs or symptoms of atherosclerosis or arteriosclerosis until blood ow is suf ciently impeded resulting in other disease Investigations Mediators of in ammation may be found in the blood including homocysteine and C reactive protein These may point to active arteriosclerosis Lipids fats and mediators of lipids may also help with diagnosis Particularly high levels of cholesterol or triglycerides may point an increased risk of atherosclerosis 7739eatment Generally changes in diet and exercise are enough to control arteriosclerosis However some patients will need anticholesterol medications to control atherosclerosis b Coronary Artery Disea5eCAD is the result of arteriosclerosis and atherosclerosis in the vessels that supply blood to the heart Patho amp Etiology As endothelial cells are injured in ammatory WBCs are attracted to the site of injury to help clean up dead cells and debris Lipids collagens other proteins form a plaque that interfere with the ow of blood to the myocardium As the myocardium loses its blood supply it loses its oxygen supply Initially cells switch over to anaerobic metabolism outside of the mitochondria which results in the production of lactic acid However both the low production of ATP from anaerobic metabolism and the accumulation of lactic acid cause cells to die As these cells die they release potassium and lactic acid resulting in further damage to the myocardium Once cell death becomes wide spread the tissue will become necrotic However this does not usually occur until there is a complete blockage of blood ow Le a myocardial infarction Signs and Symptoms There are often few or no symptoms in the early stages of CAD However as arteries continue to narrow blood supply is lost and the following symptoms may occun 1 Chronic Stable Angina Pectoris Chest pain that resolves when the patient is resting 2 Unstable Angina Pectoris Chest pain that does not resolve at rest 3 NonST Segment Elevation Myocardial Infarction Non STEMI a heart attack that does not include a STsegment elevation on EKG tracing see Figure 1 4 ST Segment Elevation Myocardial Infarction STEMI a heart attack that includes a ST segment elevation on EKG Tracing In a STEMI the coronary artery is completely blocked off by the blood clot and as a result virtually all the heart muscle being supplied by the affected artery starts to die 5T Segment Elevation quotFirema rl lla t Figure 1 ST segment elevations indicate cardiac tissue ischemia that is associated with complete blockage of one of the coronary arteries iii Investigations Because CAD is caused by atherosclerosis and arteriosclerosis the investigations for early stages of CAD are the same as the investigations for atherosclerosis and arteriosclerosis including homocysteine CReactive protein and lipid levels If the cardiac tissue has been damaged by a Ml investigations often reveal an elevation in cardiac markers including Troponin Creatinine Kinase lsozyme MB and Myoglobin iv 7739eatment Early stages of CAD are treated the same way as atherosclerosis Diet and exercise are generally enough to manage the disease process in these stages However cholesterol medications may be needed for some patients as well In later stages Coronary Artery Bypass Grafting CABG or Percutaneous Transluminal Coronary Angioplasty PCTA may be needed to correct cardiac ischemia and reperfuse the cardiac tissue c Peripheral Artery Disease PAD is the result of arteriosclerosis and atherosclerosis in the vessels that do not supply blood to the heart i Pathophysioogyamp Etiology The disease process is similar to that found in coronary artery disease It is caused by atherosclerosis and arteriosclerosis See notes for CAD ii Signs and Symptoms Decreased blood supply to the tissues often causes dry skin pain and ischemic ulcer formation Because PAD occurs more commonly in the lower extremities it is most often associated with painful dry wounds on the feet andlegs Other signs of PAD often include the 6 P s of ischemia which include 1 Pulselessness decreased peripheral pulses caused by narrowing of the arteries 2 Pallor pail skin due to decreased blood supply 3 Polar decreased skin temperature due to decreased blood supply 4 Paralysis decreased ability to move an extremity due to nerve damage caused by decreased blood supply 5 Paresthesia numbness or decreased sensation to touch caused be nerve damage due to decreased blood supply 6 Pain painful sensations may be caused by tissue ischemia and cell death Cell death causes the release of lactic acid which builds up during anaerobic metabolism iii Investigations The most common diagnostic method for PAD is Segmental Systolic Blood Pressure SSBP This is accomplished by taking a blood pressure reading in the arm at the brachial arteryand the legs at the femoral popliteal and peroneal artery When there is a large difference between the brachial pressures and the pressures of in the leg this indicates potential arterial disease iv 7739eatment The treatments for PAD are similar to the treatments of CAD They include 1 Percutaneous Transluminal Angioplasty stenting 2 Bypass Grafting and 3 endarterectomy surgical removal of fatty deposits The most common procedure for in ow disease blockage of arteries in the upper legs is a FemoralPopliteal Bypass Graft or a FemPop And the most common procedures for out ow disease blockage of the arteries in the lower legs are endarterectomies and angioplasty Hint Arterial disease often causes dry wounds on the legs But venous disease 3 Disorders of Venous Circulation a Peripheral Venous Disease PVD occurs when valves of the veins are damaged causing decrease blood return to the heart and increased pooling of blood in the veins illsulquotliiiuunv Pathoph ysioog y and Etiology Prolonged hypertension in veins causes damage to venous valves And damaged valves cause blood to ow backward That is there is a decreased blood return to the heart See Figure 2 The decreased blood return causes blood to pool in damaged vessels which in turn causes the blood to clot Also as a result of decreased forward movement of blood uid will leak out of the vessels causing peripheral swelling H20 Figure 2 Damaged valves cause backward ow of blood and a decreased blood return to the heart The resulting pool of blood can cause clotting and swelling Signs and Symptoms Because damage to the venous valves prevent blood from moving forward in circulation the following key characteristics will likely be present during various stages of the disease Blood Stasis Clotting Edema In ammation wNi i 5 Redness 6 Skin Breakdown 7 Ulcer formation Because PVD is most common in the lower extremities these symptoms are most often noted in the legs Hint Arterial disease often causes dry wounds on the legs But venous disease iii Investigations Diagnosis can sometimes be made by assessment alone However other tests might include 1 Venous Duplex Ultrasonography which will allow to visualization of thrombi 2 Presence of brin degradation products in the blood like D Dimer which will be elevated when clots are bring formed iv 7739eatment Rest and elevation are the most common treatments for PVD that does not include the presence of a thrombi Anticoagulant therapy may be helpful in preventing clot formation Thrombolytic therapy and surgery may be needed to remove clots that have already formed A special lter called an inferior vena cave ltration device or umbrella lter can also be placed near the heart to catch thrombi that may break loose b Varicose Veins are a potential cosmetic problem that can occur as a result of peripheral vascular disease In most cases varicose veins are not dangerous But they may be unsightly They are caused by damage to the valves in the surface vessels as opposed to deep veins These veins become dilated because blood is not moving forward in the circulation This causes large twisted veins in the legs They may be prevented with compression stockings and leg exercises that return blood to the heart They are commonly treated with removal or sclerosis of the damaged vessels c Pulmonary Emboism is a potentially fatal complication of PVD The cause is often thrombi that have developed in deep veins also known as Deep Vein Thrombi DVT The complication occurs when a portion of the thrombi breaks loose from the veins and travels 1 through the inferior vena cava 2 through the right side of the heart and 3 into the pulmonary arteries These clots can get lodged in the pulmonary arteries blocking oxygen exchange and blood ow in thelungs 4 In ammatory Disorders a Endocarditis is the in ammation of the innermost lining of the heart that affects the function of heart valves This in ammation is most often caused by an infective agent such as bacteria and viruses However it can be caused by autoimmune diseases as well i Pathophysioogy amp Etiology In ammation of the heart valves associated with microorganisms lnfective endocarditis or with autoimmune disease Nonlnfective Endocarditis can prevent the valves from closing properly Organisms may enter the bloodstream from any site of local infection The most common portals of entry are oral from dental work urinary tract such as from urinary tract infection after catheterization heart from cardiac surgery especially if synthetic material is used valves patches conduits the bloodstream from long term indwelling catheters and intravenous drug usage especially with unclean needles ln infective endocarditis microorganisms grow in the endocardium forming vegetations verruca deposits of brin and platelet thrombi The lesion may invade adjacent tissues such as aortic and mitral valves and may break off and embolize elsewhere especially in the spleen kidney and central nervous system In noninfective endocarditis in ammation still affects the valves but vegetation does not grow and emboli are less common Signs amp Symptoms Vague clinical manifestations are a common occurrence and may include fever malaise and weight loss Other symptoms may include 1 Extracardiac Emboi from vegetative lesions including a Splinter Hemorrhages thin black lines that form in the nail beds b Osler Nodes red painful intradermal nodes found on pads of ngers and toes c Janeway Lesions painful hemorrhagic areas on palms and soles d Roth Spots petechial markings seen on retinal examination 2 Congestive heart failure related to failure to move blood forward in circulation 3 Presence of new murmurs or changes in existing murmurs Investigations Diagnosis is typically made based on the Duke Criteria for infective endocarditis The duke criteria includes both major criteria and minor criteria Duke Criteria 1 Major criteria a Positive blood cultures at least 2 consecutive b Visualization of vegetation c Heart valve regurgitation 2 Minor Criteria a Fever b Predisposing risk factors ex Prosthetic valves c Vascular or immunologic signs ex Osler s node Janeway lesions etc Clinical criteria for infective endocarditis requires 1 two major criteria 2 one major and three minor criteria or 3 ve minor criteria Note These same criteria can be used to diagnose noninfective endocarditis 7739eatment Standard treatment includes antiinfectives ex antibiotics antivirals etc antiin ammatory agents ex aspirin glucocorticoids etc and repair of damaged heart valves b Pericarditis is the in ammation of the membrane surrounding the heart Pathophysioogy amp Etiology Common causes of pericarditis include microorganisms PostMl in ammation and autoimmune disease Pericarditis is an in ammation of the pericardium If you could see and touch it the membrane around the heart would look red and swollen like the skin around a cut that becomes in amed This in ammation causing an increased permeability of the pericardium And Excess uid often develops in the space between the pericardial layers causing a pericardial effusion buildup of excess uid around the heart There are many causes of pericarditis but it is often a complication of a viral infection viral pericarditis usually a gastrointestinal virus or rarely the u virus or AIDS It may also be caused by a bacterial infection bacterial pericarditis fungal infection fungal pericarditis or parasitic infection parasitic pericarditis There are many causes of pericarditis but it is often a complication of a viral infection viral pericarditis usually a gastrointestinal virus or rarely the u virus or AIDS It may also be caused by a bacterial infection bacterial pericarditis fungal infection fungal pericarditis or parasitic infection parasitic pericarditis Certain autoimmune diseases such as lupus rheumatoid arthritis and sceroderma also can cause pericarditis Additional causes of pericarditis include injury to the chest such as after a car accident traumatic pericarditis other health problems such as kidney failure uremic pericarditis tumors genetic diseases such as Familial Mediterranean Fever FMF or rarely medications that suppress the immune system The risk of pericarditis is greater after a heart attack or after heart surgery Dressler s syndrome radiation therapy or a percutaneous treatment such as cardiac catheterization or radiofrequency ablation RFA Pericarditis often becomes recurrent after the initial episode and attacks can last over many years Signs amp Symptoms Chest pain symptoms associated with pericarditis can be described as 1 Sharp and stabbing caused by the heart rubbing against the pericardium 2 May increase with coughing swallowing deep breathing or lying at 3 Can be relieved by sitting up and leaning forward Other symptoms include 1 Pain in the back neck or left shoulder 2 Dif culty breathing when lying down 3 A dry cough 4 Anxiety or fatigue In some people pericarditis can cause swelling of the feet legs or ankles This swelling may be a symptom of constrictive pericarditis a serious type of pericarditis In constrictive pericarditis the patient s pericardium hardens andor thickens preventing the heart muscle from expanding and affecting the function of the heart The heart may be compressed by the constrictive process which may cause blood to back up into the lungs abdomen and legs as well as cause the swelling Investigations Signs and symptoms are often enough to diagnose pericarditis However other problems with similar symptoms should be ruled out Other investigations might include radiological studies elevation of white blood cells and chemical indicators of in ammation Featments often include administration of antibiotics and steroids However in constrictive pericarditis it may be necessary to relieve pressure on the heart in a procedure called a pericardiocentesis This procedure removes uid from the pericardial sac and can prevent the life threating condition cardiac tamponade 5 Disorders Affecting the Pump a Heart Failure is often misunderstood to be a singular disease However it is a set of diseases occurring when the heart cannot meet the output demands of the body That is when the heart is not pumping enough blood Pathophysioogy amp Etiology Essentially HF is an interference with the mechanisms regulating cardiac output This means that the heart is not moving blood forward in the circulatory system And because blood is not moving forward uid begins to build up in the respiratory circulation andor systemic circulation Though this problem with uid is generally true regardless of the classi cation the reason that uid becomes a problem is different depending on the pathogenesis 1 Diastolic Heart Failure occurs when the ventricles become hypertrophied and can no longer adequately ll with blood This failure to ll prevents the heart from moving blood forward in circulation See Figure 3 2Systolic Heart Failure occurs when the ventricles become too weak to eject blood See Figure 3 Diastolic heart failure Systolic heart failure aorta if 39i Thinti quot fir 7 a 3 Wilma irisquot 1 Tilii lta lllill if 7 heart lineall muscle g 3 muscle a quot High Left KIEHEHUEIE 39 yrgnt ji lg Figure 3 Heart failure can be classi ed based on the cardiac cycle that it affects In diastolic failure the heart cannot pump blood because it cannot ll ln systolic failure the heart cannot pump blood because it is too weak 3 RightSided Heart Failure occurs when the right side of the heart is not ef ciently pumping blood to the pulmonary circulation This may happen in addition to leftsided failure or alone The net result is uid accumulation in the systemic circulation More often than not when right sided heart failure occurs by itself it is often due to increased pulmonary artery pressure caused by lung disease or direct tissue damage to the myocardium This can eventually lead to leftsided failure 4 LeftSided Heart Failure occurs when the left side of the heart is not ef ciently pumping blood to the systemic circulation This RIGHT super FNLURE Ear Pulmonals may happen in addition to right sided failure or alone The net result is uid accumulation in the pulmonary circulation More often than not when left sided heart failure occurs by itself it is often due to prolonged high blood pressure or direct tissue damage to the myocardium This can eventually lead to right sided failure LEFfeleD UFAILuRE Figure 4 Heart failure can also be classi ed by which side of the heart is affected Rightsided failure occurs when the right side fails to move blood to the pulmonary circulation and it causes uid to backup in the systemic circulation Leftsided failure occurs when the left side fails to move blood to the systemic circulation and it causes uid to backup in the pulmonary circulation Signs amp Symptoms Because HF is a problem with uid accumulation in either the systemic circulation andor the pulmonary circulation we can simplify the symptoms by noting that they are a result of either uid volume overload or pulmonary edema 1 Fluid Volume Overload will occur with right sided failure and has some of the following characteristics a BSDOFT f Jugular Vein Distension JVD Dependent Edema Hepatosplenomegaly Ascites Fatigue Weight gain 2 Pulmonary Edema will occur with leftsided failure and has some of the following characteristics treeteen Dyspnea Tachypnea Productive cough Crackles on auscultation Blood tinged sputum Cyanogs Tachycardia ResUessness Confusion Elevated Pulmonary Artery Wedge Pressure 3 Another important sign of HF is the presence of extra heart sounds a Ventricular Kick 53 is the sound made when blood oscillates back and forth across dilated walls It is common in systolic heart failure and dilated cardiomyopathy b Atrial Kick 54 is the sound caused by the atria contracting forcefully to overcome a stiff ventricular wall It is common in diastolic heart failure and restrictive cardiomyopathy Investigations In addition to assessment data imaging labs and measurements are important in diagnosis 1 Images including Chest XR CT scan or Echocardiogram can aid in measuring the structural abnormalities 2 Labs including the Atrial and Beta Natriuretic Peptides will aid in identifying excess stretching of the atrium due to uid accumulation 3 Measurements including the Ejection Fraction measure the amount of blood that is pumped from the heart An ejection fraction of lt40 is indicative of heart failure iv ii39eatment The goal of treatment is to reduce the workload on the heart by removing excess uid and aiding in oxygen exchange b Shockis one of three conditions that results in a decrease in tissue perfusion that causes decreased oxygenation of cells Pathophysioogy and Etiology The main characteristic of shock is a decrease in the mean arterial pressure MAP which causes a decrease in tissue perfusion The net result is that cells are not provided with the oxygen needed for aerobic metabolism Momentarily cells will adjust by switching to anaerobic metabolism However anaerobic metabolism involves the conversion of glucose to pyruvic acid If pyruvic acid does not enter the citric acid cycle it will degrade into lactic acid When the cell runs out of energy it will no longer be able to maintain its structural integrity It will lyse and its contents including the lactic acid will be released causing damage to surrounding tissues While decreases in MAP and rises in lactic acid may be common in all types of shock it can also be said that not all types of shock are the same nor should they be treated the same 1 Hypovoemic Shock According to the rst rule of blood pressure decreased intravascular uid volume causes decrease blood pressure ie more water more pressure In hypovolemic shock uid volume decreases causing blood pressure to decrease This is common in dehydration and blood loss When the mean arterial pressure drops below 65mmHg the body can no longer adequately perfuse its tissues This decrease in MAP causes bodily organs to be starved ofoxygen Because the problem is a decrease in intravascular uid volume the treatment for hypovolemic shock is to replace intravascular uid with isotonic uids hypertonic uids volume expanders andor blood products Cardiogenic Shock According to the third rule of blood pressure when the heart pumps harder and faster blood pressure will rise ie More pumping More pressure When the heart fails to pump hard enough or fast enough to create an adequate amount of cardiac output the MAP will drop This is common in both systolic and diastolic heart failure as well as overdoses of certain medications When the mean arterial pressure drops below 65mmHg the body can no longer adequately perfuse its tissues This decrease in MAP causes bodily organs to be starved ofoxygen Because the problem in cardiogenic shock is a decrease pumping power the treatment of cardiogenic shock is to increase the pumping power of the heart by giving positive ionotropic medications to increase contractility Side Note In this case the treatments for hypovolemic shock and distributive shock could make the problem worse Distributive Shock According to the second rule of blood pressure decrease vasoconstriction or increased vasodilation causes decreased blood pressure In distributive shock the problem is that some process in the body is preventing vasoconstriction andor causing vasodilation This could actually include many different problems including a Anaphylactic Shock a massive release of histamines related to a type 1 hypersensitivity that causes systemic vasodilation b Neurogenic Shock a problem with the CNS or PNS that results in the vasodHann c Systemic In ammatory Response Syndrome SIRS an in ammatory response that causes a massive release of histamine d Septic Shock an infection often bacterial that triggers the in ammatory response on a systemic level causing a massive release of histamine Because distributive shock is caused by vasodilation treatment is aimed at causing vasoconstriction AND removing the stimulus that is causing the vasodilation Ex Antibiotics for septic shock Ultimately this decrease in availability of oxygen can cause dysfunction of nearly every organ in the body This failure of multiple organ is called Multiple Organ Dysfunction Syndrome MODS And the most commonly affected systems are the kidneys and liver because the body will shunt blood to the brain heart and lungs Signs amp Symptoms The characteristic signs and symptoms of shock may depend on whether the shock is occurring in early stages compensated or in later stages uncompensated Compensated shock might include Tachycardia Tachypnea Bounding pulses Paleness Confusion Decreased Capillary Re ll Time Normal to Moderately Decreased MAP ie MAP gt 65mmHg 8 Normal serum Lactic Acid NP P PUNE Decompensated shock might include Bradycardia Bradypnea Weak pulses Cyanogs Unresponsiveness Decreased Capillary Re ll Time Moderate to Severely decreased MAP ie MAP lt 65 mmHg 8 Increase in serum Lactic Acid NP P 39gtSquot In vestiga tions N one iv 7739eatment The treatment for any type of shock will depend on the classi cation of the shock see Figure 5 For hypovolemic shock isotonic and isotonic uid can increase intravascular uid volume and correct the decreased uid volume For cardiogenic shock positive ionotropic can increase cardiac contractility and increase cardiac output For distributive shock vasoconstrictors can correct the problem of vasodilation But the underlying cause must also be co rrected H availemic Lgvf o olume cardiogenic Non Vita Faulty pump Distributive Organs lilasoclilation l Figure 5 Shock included three different causes and three different treatments Hypovolemic is caused by low volume cardiogenic is caused be a faulty pump and distributive is caused by vasodilation Module 5 Respiratory This module will focus on the pathogenesis associated with various health alterations of the respiratory system MODULE OBJECTIVES After reviewing this module the student should be able to 1 Describe the normal anatomy and physiology of the respiratory system 2 Discuss the pathogenesis associated with common respiratory alterations 3 Distinguish the most pertinent identifying information related to each alteration 4 Describe clinical manifestations associated with respiratory alterations and relate the ndings back to the pathogenesis 5 Appreciate the impact that respiratory alterations can have on a patient39s lifestyle MODULE CONCEPTS Assessment of the respiratory system Health Alterations o RESPIRATORYTRACTINFECTIONS Rhinosinusitis Otitis media Pharyngitis Tonsillitis Peritonsillar abscess Laryngitis In uenza Pneumonias CAP and HAP Fungal infections 0 CANCER Laryngeal cancer Lung cancer 0 RESPIRATORY ALTERATIONS IN CHILDREN Croup Epiglottitis Bronchiolitis o DISORDERS OF LUNG INFLATION Pleuritis Pleural effusion Pneumothorax o OBSTRUCTIVE AIRWAY ALTERATIONS Sleep apnea Asthma Bronchitis acute and chronic Emphysema Chronic obstructive pulmonary disease COPD Bronchiectasis Module 5 Respiratory Lazenby Page 1 Cystic brosis INTERSTITIAL LUNG DISEASE o PULMONARY CIRCULATION DISORDERS Pulmonary embolism Pulmonary hypertension 0 ACUTE RESPIRATORY DISORDERS Acute respiratory distress syndrome ARDS Respiratory failure 0 OTHER Epistaxis 0 TERMS Alveoli Atelectasis Hypoxia Hypoxemia Cyanosis Bronchiectasis Cough Pneumoconiosis ASSIGNMENTSREADINGS when compl ete Porth Chapter 21 Porth Chapter 22 Porth Chapter 23 View Panopto Part 1 httpsauburnhostedpanoptocomPanoptoPagesVieweraspx idOb8ba812174a4b248146c68a34749aed View Panopto Part 2 httpsauburnhostedpanoptocomPanoptoPagesVieweraspx id2b96c22c6a47487183ee67da08cc7bdb View Panopto Part 3 httpsauburnhostedpanoptocomPanoptoPagesVieweraspx id226d489d17274ea1a23a456ca101ad64ampSignednTrue Assessm respiratory rate ent o respiratory depth symmetrical chest movement Module 5 Respiratory Lazenby Page 2 bilateral breath sounds sputum 0 color consistency odor any changes amount cough 0 protective re ex that clears lower airways o persistent cough presence of disorder 0 acute nonproductive cough bronchitis or viral pneumonia 0 acute dry cough foreign body aspiration or inhalation of fumes 0 chronic dry cough tumor congestion hypersensitive airway retractions nasal aring medications exercise tolerance cyanosis bluish discoloration of nailbeds or mucous membranes 0 caused by increased amounts of desaturated or reduced hgb 0 may be central or peripheral 0 must consider whole scenario cyanosis may or may not be present 0 may be caused by decreased Pa02 righttoleft cardiac shunt decreased CO cold environment anxiety DOE dyspnea on exertion SOB shortness of breath PND paroxysmal nocturnal dyspnea redistribution of body water in recumbent position gt uid in the lungs How many pillows do you sleep with orthopnea dif culty breathing in a reclining position secondary to redistribution of body water gt abdominal contents press on diaphragm gt decreased respiratory muscle ef ciency Dyspnea o subjective sensation of uncomfortable breathing feeling of inability to get air breathlessness air hunger SOB labored breathing preoccupation with breathing usually the result of diffuse and extensive pulmonary problems 0 objective assessment Module 5 Respiratory Lazenby Page 3 nasal aring retractions sinking in with inspirations in any of these areas intercostals subcostal substernal supercostal accessory muscle use hemoptysis o coughing up blood or bloody secretions 0 usually bright red alkaline pH mixed with frothy sputum 0 indicates localized abnormality or in ammation of bronchi or lung parenchyma cancer pulmonary infarction wheezing stridor chest pain 0 originates in pleurae airways chest wall 0 infection in ammation 0 may be accompanied by pleural friction rub o worsened with movement deep breaths coughing laughing clubbing 0 selective bulbous enlargement of distal segment of digits 0 lung cancer bronchiectasis CF pulmonary brosis abscess CHD 0 past medical history childhood infectious diseases immunizations major illnesses and hospitalizations allergies family history 0 habits occupation geographic location 0 environment 0 exercise 0 nutrition chest wall con guration 0 exposure to TB immunocompromised status Developmental changes in the lungs in the pregnant female 0 In the pregnant woman the enlarging uterus elevates the diaphragm 4 cm during pregnancy This decrease is compensated for by an increase in the horizontal diameter The increase in estrogen level relaxes the chest cage ligaments This allows an increase of 2 cm in the transverse diameter of the chest cage and the costal angle widens The total circumference of the chest cage increases by 6 cm Example of a transcultural difference in the thorax Chest volumes vary in size and this in uences pulmonary function In descending order the largest chest volumes are found in whites Module 5 Respiratory Lazenby Page 4 blacks Asians and Native Americans Even when the shorter height of Asians is considered their chest volume remains signi cantly less than that of whites and blacks Age Related Changes In the aging adult the lung is a more rigid structure that is more dif cult to in ate These changes result in an increase in small airway closure yielding a decreased vital capacity and an increased residual volume With aging less surface area is available for gas exchange Also the lung bases become less ventilated owing to closing off of a number of airways This increases the older person39s risk of dyspnea with exertion There is also a greater risk of postop atelectasis because of decreased ability to cough a loss of protective airway re exes and increased secretions Abnormal breathing pattern eupnea rhythmic effortless breathing normal tachypnea increased respiratory rate breathing patterns adjust to minimize the work of the respiratory muscles Kussmaul respirations hyperpnea slightly increased rate large tidal volume and no expiratory pause obstructed airways gt labored breathing slow rate large tidal volume increased effort prolonged inspiration and expiration wheezing stridor stiffening of chest wall or lungs gt decreased lung compliance gt restricted breathing CheyneStokes respirations alternating periods of deep and shallow breathing apnea 1560 seconds followed by increased volume until peak is reached then decreases again to apnea o slowed blood flow to brain stem gt slows impulses sending information to respiratory centers of brain stem Hypoventilationhyperventilation normal PaC02 3545 mm Hg hypoventilation o inadequate alveolar ventilation in relation to metabolic demands 0 caused by altered pulmonary mechanics or altered neurologic control of breathing o hypercapnia results when removal of C02 does not keep up with C02 production may cause somnolence or disorientation hyperventilation o alveolar ventilation exceeding metabolic demands Module 5 Respiratory Lazenby Page 5 o hypocapnia results when C02 removal by lungs is faster than C02 production General Development of Pulmonary System A amp P 0 lower respiratory system develops at approximately the 26th day of gestation Upper Airway includes nasopharynx oropharynx laryngopharynx the ciliated mucosal membrane lining the nasopharynx warms and humidi es air and removes foreign particles Lower Airway includes larynx trachea bronchi bronchopulmonary segments terminal bronchioles acinus alveolar which is the site of gas exchange 0 Why would it be important for the nurse to know that normally the right bronchus is larger than the left and the angle off of the mainstem bronchi is much less on the right side Pulmonary Circulation 0 blood supply is o from bronchial artery system and the pulmonary artery system 0 in uenced by hydrostatic pressure colloid osmotic pressure COP and capillary permeability when capillary hydrostatic pressure gt COP gt uid moves from capillary to interstitium if not stopped it will result in alveolar edema gt impaired gas exchange Mechanics of Breathing lungs have a natural ability to recoil with exhalation passive action 0 during inspiration chest wall muscles contract gt elevation of ribs and downward movement of diaphragm gt negative intrapleural pressure gt lung expansion surfactant decreases surface tension and is necessary to prevent complete closure of the alveoli at the end of expiration during passive inspiration muscular contraction of the diaphragm causes air to move into the lung The mechanisms that drive air movement during passive inspiration are an increase in the size of the thorax and a decrease in intrapleural pressure Airway resistance 0 the result of pressure and ow the smaller the diameter of the airway the greater the pressure and the less the ow other in uencing factors include stress pulmonary conditioning age smooth muscles of bronchioles and terminal bronchioles are innervated by autonomic nervous system stimulation of cholinergic bers gt bronchoconstriction stimulation of beta2adrenergic Module 5 Respiratory Lazenby Page 6 receptors gt bronchodilation Lung Compliance 0 measure of relationship between pressure and volume ex Balloon in uenced by chest wall expandibility and lung expandibility What impact would lqphosis or ARDS have on lung compliance Distribution of Ventilation dependent on position of the client 0 upright ventilation is greatest near the bottom of the lung 0 supine lateral ventilation is greatest in dependent lung 0 rapid shallow breathing ventilation is best in nondependent lung elds Neurologic Control of Ventilation respiratory center in the brain stem obongata and pons nerve impulses travel from brain stem via phrenic nerve to diaphragm gt muscular contraction for inspiration vagus nerve parasympathetic innervates the lung 0 What respiratory ndings would you anticipate in the client with a brain stem injury sensory input to respiratory control center includes 0 central chemoreceptors respond to C02 and pH changes 0 peripheral chemoreceptors located in aortic arch and carotid bodies respond to decrease in arterial 02 and pH and increases in PaC02 o HeringBreuer stretch receptors stretch receptors located in alveolar septa bronchi bronchioles o proprioceptors located in muscles and tendons exercise gt increased respiratory rate and depth to maintain 02 levels 0 pressoreceptors baroreceptors located in aortic arch and carotid bodies that respond to changes in BP environmental sensations cold pin prick stress smoking infection fever Pulmonary Blood Flow 0 Pulmonary vasculature o perfusion blood ow the movement of blood into and out of the capillary beds of the lungs to the body organs and tissues 0 capillary beds surround alveoli to facilitate 02C02 exchange 0 Distribution of Blood Flow 0 affected by body position and exercise VentilationPerfusion Ratios 0 best overall ventilation and perfusion occur in dependent lung elds 0 mismatch of ventilationperfusion results in pulmonary problems Module 5 Respiratory Lazenby Page 7 o a low ventilationperfusion ratio would cause shunting Hypoxic Vasoconstriction o alveolar hypoxia gt vasoconstriction of pulmonary vessels blood is diverted to areas of higher 02 to compensate Diffusion and Transport of Respiratory Gases Barriers to Diffusion o 02 diffuses from alveoli to blood and C02 diffuses from blood to alveoli 02 Transport 0 transported to tissues dissolved in plasma or bound to hemoglobin 0 increased 02 af nity shift to the left gt increased binding of 02 to hgb gt decreased delivery to tissue 0 partial pressure of oxygen at sea level is 21 C02 Transport 0 C02 is a byproduct of cell metabolism 0 C02 combines with H20 in the presence of carbonic anhydrase gt bicarbonate and hydrogen ions hydrogen ions attach to hgb molecule and bicarbonate ions diffuse into plasma and combine with Na this chemical process is reversed when venous blood reaches lungs so that C02 can diffuse across alveolar membrane to be exhaled Acidosis or elevated body temperature would cause a shift to the right of the oxyhemoglobin dissociation curve resulting in more oxygen being released to the cells Diagnosti cs notaH inclusive auscultation pulmonary function testing PFT Bronchial Provocation Tests quanti es airway response after inhalation of methacholine which is a synthetic derivative of acetylcholine may be helpful in evaluating asthma in children pulse oximetry ABGs capnography most reliable indicator that E39IT is in the correct placement ventilationperfusion studies measures ratio of ventilation air reaching the alveoli to the perfusion blood that reaches the alveoli VQ CXR ultrasound uoroscopy CT bronchoscopy Module 5 Respiratory Lazenby Page 8 alveolar lavage thorascopy pulmonary angiography MRI Gallium scan thoracentesis biopsy sputum collection nose and throat cultures peak ow puri ed protein derivative PPD Key Terms 0 Ventilation process of moving air into the lungs Lung VolumesCapacities o The average adult has a total lung capacity of about 6000 mL 0 Vital capacity maximum amount of gas that can be displaced or expired from the lung 0 lnspiratory reserve volume extra air that can be forcefully inspired after a regular inspiration 0 Expiratory reserve volume extra air that can be forcefully expired after a regular expiration 0 Residual volume air that is trapped in the alveoli Dead space nonusable gas this air is not involved in gas exchange a series of alveoli in the lower lobe receive adequate ventilation but do not have adequate perfusion stula abnormal opening usually between esophagus and trachea TEF atresia blind pouch surfactant phospholipid necessary for maintaining alveolar patency it is produced by type II alveolar cells atelectasis incomplete expansion Hypercapnia 0 increased arterial C02 0 caused by hypoventilation 0 causes most are due to a decreased drive to breathe or inadequate ability to respond to ventilatory stimulation some drugs gtgt respiratory depression diseases of medulla infections trauma interruption of spinal conducting pathways SCI polio disease of neuromuscularjunction or of respiratory muscles MD or MG Module 5 Respiratory Lazenby Page 9 thoracic cage abnormality chest trauma congenital deformity large airway obstruction sleep apnea tumor increased work of breathing emphysema 0 clinical manifestations acidosis gt dysrhythmias increased C02 gt cerebral vasodilation gt intracranial pressure changes gt somnolence gt coma alveolar hypoventilation gtgt increased alveolar C02 gt decreased 02 available to blood gt hypoxemia Hypoxemia 0 decreased arterial 02 0 ve causes of hypoxemia 1 decreased 02 content of inspired air ex High altitudes 2 hypoventilation causes increased PaC02 gt less 02 diffused into blood 3 diffusion abnormalities caused by thickened alveolarcapillary membrane andor decreased surface area as in edema or brosis alveoli destruction as in emphysema 4 abnormal ventilationperfusion ratio most common cause as in asthma secondary to bronchoconstriction and pulmonary edema or pneumonia secondary to uid in the alveoli gt VQ mismatch 5 pulmonary righttoleft shunt as in ARDS RDS and atelectasis Hypoxia 0 decrease in tissue oxygenation 0 reduced cellular oxygen may be the result of hypoxemia or other problems such as cardiac Atelectasis o collapse of lung tissue 0 2 types compression caused by external pressure exerted by tumor uid air pleural space abdominal distention gt collapse alveoli absorption results from removal of air from obstructed or hypoventilated alveoli or from inhalation of concentrated 02 or anesthetic agent Health Alteration RHINOSINUSITIS Description o rhinitis in ammation of the nasal mucosa membrane Module 5 Respiratory Lazenby Page 10 o allergic rhinitis is a type I lgE mediated hypersensitivity response to environmental allergens in a genetically susceptible patient sinusitis in ammation with resulting infection of the mucous membranes of one or more of the paranasal sinuses may be acute 1 day 3 weeks subacute 3 weeks to 3 months chronic gt 3 months EtiologyRisk Factors conditions that obstruct narrow ostia that drain the sinuses such as viral URI or allergic rhinitis that obstructs ostiomeatal complex which impairs mucociiary clearance URI viral rhinitis nasal polyps deviated nasal septum tooth abscess prolonged NT or NG intubation abuse of nasal decongestants swimming diving exposure to frequent changes in barometric pressure smoking nasal packing allergies immunocompromised state Pathogenesi s paranasal sinuses are air cells that connect with the nasal cavity and are named for bone in which they are located sinuses are lined with cilia cilia facilitate movement of uids and microorganisms into the nasal cavity for exit from the body viral illness gt in ammation of sinus mucosa gt obstruction of the normal ciliary action gt ideal medium for bacterial growth gt in ammatory response increases swelling and congestion gt further compromise of normal ciliary action gt continued bacterial growth Assessment Clinical Manifestatio ns constant and severe pain over affected area tenderness over affected area pain in teeth headache fever malaise fatigue Module 5 Respiratory Lazenby Page 11 nasalconges on purulent nasal drainage halitosis sore and in amed throat loss of sense of smell andor taste feeling of fullness in the ears postnasal drip hoarseness chronic cough Diagnosis inspection of nose and throat nasal drainage CampS transillumination of sinuses xrays CT scans nasalendoscopy Complicatio ns intracranial and orbital wall complications edema of the eyelid orbital cellulitis subperiosteal abscess formation facial swelling abnormal EOM protrusion of eyeball periorbital edema mental status changes Holistic Implications Health Alteration OTITIS MEDIA Description in ammation andor infection of the middle ear 2 types serous OM and acute OM EtiologyRisk lnfants feeding while lying down Factors 0 exposure Pathogenesi o normally the tympanic membrane TM protects the middle ear 5 from the external auditory canal the eustachian tube connects middle ear with nasopharynx and helps equalize pressure in the middle ear with atmospheric pressure serous OM o obstructed Eustachian tube gt impaired equalization of air pressure in middle ear gt air in middle ear is absorbed continued Eustachian tube obstruction gt prevention of more air from entering gt negative pressure in the middle ear gt serous uid moves into the middle ear gt sterile Module 5 Respiratory Lazenby Page 12 effusion Assessment Clinical Manifestatio ns decreased hearing in affected ear snapping or popping in ear decreased movement of TM retracted or bulging TM uid or air bubbles pain bleeding and or rupture of TMsensory hearing loss vertigo o acute OM entry of pathogen from oropharynx via Eustachian tube gt invasion and colonization by bacteria along with WBC invasion gt pus formation gt increased middle ear pressure gt rupture of TM severe pain in affected ear pulling at ear fever impaired hearing dizziness vertigo redin amed or dull TM bulging TM decreased movement of TM tenderness over mastoid area Diagnosis otoscopic exam CBC CampS of middle ear effusion Complicatio Ruptured tympanic membrane ns Holistic Implications Health Alteration PHARYNGITIS Description an acute in ammation of the pharyngeal walls may also include tonsils palate uvua causes viral bacterial fungal EtiologyRisk sinusitis Factors rhinitis Pathogenesi exposure to organism gt in ammation of the pharynx 5 Assessment pain from mild to extremely severe Manifestatio ns patchy yellow exudates red and edematous pharynx white and irregular patches lymphadenopathy Diagnosis throat CampS rapid antigen test RAT CBC Complicatio Progressive infection ns Holistic Implications Health Alteration TONSILITIS Module 5 Respiratory Lazenby Page 13 Description tonsils are masses of lymphoid tissue located in the pharyngeal cavity which normally lter and protect the respiratory and alimentary tract from pathogenic organisms in ammationinfection of tonsils and lymph tissue contagious air borne EtiologyRisk 0 exposure Factors Pathogenesi o invasion of tonsils by pathogens gt in ammation of the tonsils gt S edema gt obstruction of passage of air or food Assessment sudden onset of mild to severe sore throat Clinical fever Manifestatio muscle aches 5 chills dysphagia odynophagia ear pain anorexia malaise swollen red tonsils with pus possible whiteyellow exudate on tons purulent discharge edematous and in amed uvula tenderenlarged cervical nodes dif culty swallowing dif culty breathing mouth breathing with enlargement of the adenoids gt drying of the mucous membranes and the presence of an offensive mouth odor impaired sense of smell and taste nasal and muf ed voice quality Diagnosis 0 physical exam throat CampS CBC Rapid antigen test Complicatio Peritonsillar abscess ns Holistic Implications Health Alteration PERITONSILLAR ABSCESS Description 0 group A betahemolytic streptococcus is the most common cause EtiologyRisk o tonsillitis Factors Pathogenesi o tonsillitis gt infection spreads to surrounding tissue gt abscess 5 formation Module 5 Respiratory Lazenby Page 14 Assessment Clinical pus behind the tonsil usually onesided swelling and uvua deviation Manifestatio o drooling ns 0 severe throat pain gt earache voice change difficulty swallowing trismus tonic contraction of muscle of chewing difficult breathing bad breath lymphadenopathy Diagnosis 0 intraora or transcutaneous ultrasound Complicatio airway obstruction ns Holistic Implications Health Alteration LARYNGITIS Description a in ammation of the mucus membranes lining the larynx typically caused by a virus EtiologyRisk o irritating inhalants smoke alcohol tobacco chemical fumes Factors 0 voice overuse fume inhalation intubation Pathogenesi o in ammation gt mucosa irritation which may include edema of S larynx Assessment o hoarse raspy or whispering voice Clinical o Manifestatio ns loss of voice aphonia coryza sore throat nasalcongeonn fever 0 HA malaise myalgia Diagnosis inspection with aryngea mirror to assess for polyps edema tumor xray CT scan beroptic aryngosocpic exam Complicatio ns Holistic Implications Module 5 Respiratory Lazenby Page 15 Health Alteration CROUP Description acute viral in ammatory disease of the larynx general term for a symptom complex characterized by hoarseness resonant cough that is quotbarkingquot or quotbrassyquot croupy inspiratory stridor respiratory distress acute laryngotracheobronchitis LTB is the most common type experienced by children it involves mucosal edema and laryngeal secretions occurs more often in boys usually quotsound worse than they look EtiologyRisk o rhinorrhea Factors 0 coryza hoarseness lowgrade fever Pathogenesi infectious agent gt in ammation and edema gt edema formation 5 in subglottic area gt upper airway obstruction gt increased resistance to air ow gt increased intrathoracic negative pressure gt collapse of upper airway gt respiratory failure Assessment 0 history of URI Clinical Manifestatio ns barking cough with stridor rhinorrhea sore throat low grade or absent fever seallike cough retractions stridor agitation tachycardia pallor or cyanosis Diagnosis 0 based on symptoms Complicatio airway obstruction ns Holistic Implications Health Alteration EPIGLOTTITIS Description 0 lifethreatening condition medical emergency do NOT put anything in the patient39s mouth EtiologyRisk Factors upper respiratory in ammation Pathogenesi infecting agent gt localized in supraglottic area gt rapid and Module 5 Respiratory Lazenby Page 16 s potentially fatal in ammation Assessment drooling Clinical Manifestatio fever ns inspiratory stridor child may sit in a quotsniffing dogquot position severe respiratory distress irritability absence of spontaneous cough agitation retractions red and in amed throat large cherry distinctive edematous epiglottis usually quotlook worse than they soundquot acute onset of sore throat and fever pale toxic lethargic sitting with mouth open and chin thrust forward muf ed voice extreme anxiety Diagnosis based on symptoms Complicatio airway obstruction ns death Holistic Implications Health Alteration BRONCHIOLITIS Description in ammatory obstruction of small airways or bronchioles usually RSV in infants occurs more frequently in children occurrence in adults usually accompanies chronic bronchitis infection or toxic gas inhalation EtiologyRisk 224 months of age Factors Exposure to older family member with upper respiratory infection Allele of lL8 Pathogenesi causal agent gt proliferation and necrosis of bronchiolar S epithelium gt obstruction and increased mucus production gt thick tenacious mucus leads to airway obstruction atelectasis hype n a on Assessment rhinorrhea Clinical coughing Manifestatio ns poor feeding Module 5 Respiratory Lazenby Page 17 lethargy fever wheezing crackles diminished breath sounds retractions increased sputum dyspnea severe tachypnea atelectasis distal to in ammation decreased ventilationperfusion ratio gt hypoxemia and increased C02 use of accessory muscles lowgrade fever hyperin ated chest Diagnosis 0 pulse oximetry CXR CBC ABGs culture immuno uorescence analysis of nasal washings to detect RSV Complicatio airway obstruction ns altered gas exchange Holistic Implications Health Alteration INFLUENZA Description a viral infection that can affect upper and lower respiratory tracts account for up to 35000 deaths annually in the US in uenza A B and C EtiologyRisk o age Factors 0 exposure Pathogenesi 0 virus gt kills mucussecreting ciiated and other epithelial cells gt S gaping holes between underlying basal cells gt escape of ECF with spread to lower respiratory tract gt shedding of bronchial and alveolar ces Assessment abrupt onset of symptoms is a distinguishing characteristic Clinical o headache Manifestatio body aches ns chis fever rhinitis Module 5 Respiratory Lazenby Page 18 malaise nonproductive couth sore throat Diagnosis 0 symptoms nasal swab Complicatio o pneumonia ns diffuse pulmonary brosis 0 death Holistic Implications Obstructive vs Restrictive Lung Disease Obstructive 0 Dif culty exhaling all the air 0 Examples asthma COPD bronchiectasis CF Restrictive Inability to fully in ate the lungs with air 0 May be due to stiff lungs stiff chest wall weak muscles nerve damage 0 Examples 0 Interstitial lung disease sarcoidosis obesity scoliosis neuromuscular disease MD ALS Health Alteration PNEUMONIA CAP AND HAP Description 6th leading cause of death in US May be classi ed as typical or atypical approximately 1 of the US population will have pneumonia at some time in their life an acute in ammation of the lung parenchyma in ammatory process of lung parenchyma usually associated with a marked increase in interstitial and alveolar uid in children it occurs more frequently in infancy and early cthhood bacterialgram such as S Pneumonia staph aureus group betahemolytic strepPCN is the drug of choice viralmost common cause in infants and childrendoube mycoplasmamost common communityacquired in young adults fungi protozoa there is also aspiration and nosocomial virus most common type RSV in kidsmycopasmfungus protozoa parasites chemicals aspiration of food uid or vomitus from nasopharynx or oropharynx inhalation of toxic or caustic chemicals smoke dusts gases Module 5 Respiratory Lazenby Page 19 microbes present in air 0 also a common complication related to chronic illnesses and immobility hematogenous spread from primary infection elsewhere in the body 1 CommunityAcquired Pneumonia CAP lower respiratory tract infection of lung parenchyma with onset in community or within 48 hours of hospitalization if the person did not reside in a LTC facility af icts 4 million Americansyear 10 million annual physician visits 500000600000 hospitalizations 45000 deaths cost 23 billionyear 2 HospitalAcquired Pneumonia HAP pneumonia occurring 48 hours or longer after admission and not incubating at the time of hospitalization 510 cases1000 hospital admissions increased in those requiring mechanical ventilation highest morbiditymortality rate of any nosocomial infection 0 usually occurs as a result of aspiration immunosuppressive therapy general debility endotracheal intubaion respiratory equipment that has not been properly cleaned 3 Aspiration Pneumonia also known as necrotizing pneumonia because of pathologic changesinlung most often affects dependent portions of the lung especially superior segments of lower lobes causes altered LOC seizure anesthesia head injury alcohol intake infecting organism is usually one of normal oropharyngeal ora 4 Opportunistic Pneumonia decreased immune system secondary to severe CHONcalorie malnutrition immune de ciencies transplants radiation therapy chemo corticosteroids atered B and T lymphocyte function depressed bone marrow function decreased level of function of neutrophils and macrophages 0 Speci c types of infection 0 Pneumocystis jiroveci pneumonia 0 Pneumocystis carinii Module 5 Respiratory Lazenby Page 20 affects 70 of HIVinfected individuals and is common opportunistic infection in patients with AIDS ss insidious fever tachypnea tachycardia dyspnea nonproductive cough hypoxemia normal breath sounds ss are minimal compared to serious nature treatment with Bactrim and parenteral Nebupent o CMV especially in transplant recipients virus type of herpes virus treat with Cytovene and Foscavir EtiOIOChiRisk a defense mechanisms become incompetent or overwhelmed by Factors virulencequantity of infectious agents anything that interferes with normal defense mechanisms of o ltration and humidi cation o warming of inspired air 0 epiglottis closure over trachea decreased LOC gt aspiration o cough re ex decreased LOC tracheal intubation air pollution cigarette smoking viral URI aging mucociliary escalator tracheal intubation secretion of immunoglobin A malnutrition o alveolar macrophages smoking air pollution altered LOC ie alcoholism head injury seizures anesthesia drug OD E39IT or N39IT URI chronic diseases COPD DM heart disease uremia cancer immunosuppression chemo steroids HIV malnutrition inhalationaspiration noxious substances debilitating illness BRprolonged immobility altered oropharyngeal ora antibiotics leukemia alcoholism diabetes mellitus gt increased frequency of gram bacilli in the oropharynx OO 0 Altered consciousness alcoholism head injury seizure drug OD general anesthesia Immobility Immunosuppression AIDS Malnutrition Dehydration Chronic diseases OOOOOO Module 5 Respiratory Lazenby Page 21 o Debilitating disease 0 Aspiration 0 Close living arrangements Pathogenesi 5 inhalation of infectious agent gt agent penetrates lower airway because of lung39s decreased defenses gt in ammation 4 characteristic stages of disease process 1 Congestion organism reaches alveoli via droplets or saliva gt outpouring of uid in alveoli gt organisms multiply gt infection spreads gt overwhelming growth and interference with lung function 2 Red hepatization massive dilation of capillaries and alveoli lled with organisms neutrophils RBCs and brin lungs look red granular and liverlike 3Gray hepatization blood ow decreases leukocytes and brin consolidate 4Resolution exudate becomes ysed and processed by macrophages Infection from bacteria that multiply extracellular in alveoli gt in ammation and exudation of uid into air lled alveolar spaces gt typical pneumonia Viral or mycopasma infection gt invasion of alveolar septum and interstitium of lung gt atypical pneumonia Assessment Clinical Manifestatio ns complete VS auscultate lungs sounds note perfusion question the client about presence of pain or discomfort determine the nutritional status and uid intake ask about medication or drug allergies signi cant medical history pleuritic chest pain abdominal pain if the lower lobes are affected NampV malaise myalgia weakness tachycardia tachypnea chest splinting dullness to percussion diminished breath sounds over affected area pleural friction rub fever chill Module 5 Respiratory Lazenby Page 22 sweats pleuritic chest pain cough sputum production hemoptysis dyspnea headache fatigue bronchial breath sounds over consolidation crackling sounds RT uid in interstitial and alveolar spaces dulled percussion over affected area may see unequal chest expansion if a large area is involved RT decreased distensibility in affected area Typical Pneumonia has a sudden onset with fever chills purulent productive cough pleuritic chest pain dullness to percussion increased fremitus bronchial breath sounds crackles in elderlydebilitated confusionstridor Atypical Pneumonia has a gradual onset with a dry cough extrapulmonary manifestations such as HA myalgia fatigue sore throat NVampD crackles Viral Pneumonia chills fever dry and nonproductive cough extrapulmonary symptoms Diagnosis history and physical CXR pattern based on cause 0 white opaci cation on CXR RT consolidation sputum gram stain sputum CampS ABGS usually reveal hypoxemia CBC leukocytosis usually gt 15000 with shift to the left blood cultures bronchoscopy and biopsy Complicatio ns usually uncomplicated pleurisy in ammation of pleura pleural effusion usually sterile and reabsorbed in 12 weeks occasionally requires aspiration by thoracentesis atelectasis collapsed airless alveoli usually clear with effective coughing and deep breathing delayed resolution results from persistent infection seen on CXR as residual consolidation usually returns to normal in 24 weeks lung abscess not common emphysema accumulation of purulent exudate in pleural cavity pericarditis result of spread to pericardium Module 5 Respiratory Lazenby Page 23 arthritis result of systemic spread meningitis caused by S pneumoniae endocarditis organisms attack endocardium and heart valves Holistic Implications Health Alteration TUBERCULOSIS Description a chronic infectious disease that is characterized by the formation of tubercles or granulomas in the lungs an infectious disease caused by Mycobacterium tuberculosis usually involves the lungs but may also occur in kidneys bones lymph nodes and meninges can be disseminated throughout the body 10 to 15 million people are infected or harbor the tubercle bacillus a reportable communicable disease caused by Mycobacterium tuberculosis mycobacteria with a waxy cell wall that results in 0 slow growth 0 antigenicity o resistance to detergents disinfectants antibiotics incidence has increased drastically acidfast bacteria that produces niacin airborne transmission droplet nuclei potentially curable and preventable but we are seeing an increase in incidence secondary to o emergence of multidrugresistant strains secondary to inadequate fu failure to monitor compliance treated with meds for which their TB was no longer susceptible epidemic proportion of TB among people with HIV infections it is a grampositive acidfast bacillus EtiologyRisk Factors exposure to those with TB esp in close living quarters correctional facilities dorms homeless shelters long term care facilities homeless residents of inner city neighborhoods those in institutions nursing homes prisons socioeconomically disadvantaged medically undeserved clients with decreased immunity HIV malnutrition cancer Module 5 Respiratory Lazenby Page 24 chemotherapy steroid therapy 0 older clients 0 people dependent on alcohol or other chemicals which typically result in malnutrition and overall poor health racial and ethnic groups such as Native Americans Eskimos blacks immigrants from Southeast Asia Haiti Ethiopia Mexico Latin America 0 clients less than 5 years of age Pathogenesi spread via airborne droplets gt dispersion gt inhalation gt bacilli 5 pass down bronchial system and implant in bronchioles and alveoli gt bacilli multiply with no initial resistance from host gt organisms engulfed by phagocytes and may continue to multiply within the phagocytes inhalation of droplet nuclei containing the TB bacillus gt embedding of TB bacilli in the distal airways or alveoli gt engulfment of TB bacilli by macrophages in which the microbes slowly grow for up to 3 months gt presentation of TB bacilli antigens to T cells as part of a cellmediated response gt lesions known as Ghon foci form from TB bacilli macrophages and T cells gt caseous necrosis of Ghon foci and migration into lymph nodes leads to Ghon complexes 0 a cellular immune response is activated but bacilli can be spread through lymphatic channels to regional lymph nodes and via thoracic duct to circulating blood as the acquired cellular immunity limits multiplication an epithelioid cell granuloma forms the result of the fusion of in ltrating macrophages granuloma is surrounded by lymphocytes takes about 1020 days central portion of the lesion Ghon tubercle undergoes necrosis and has a cheesy appearance thus called caseous necrosis lesion may also undergo liquefactive necrosis in which the liquid sloughs into connecting bronchi and gt cavity tubercular material may enter tracheobronchial system gt airborne transmission healing of primary lesion occurs via resolution brosis and calci cation granulation tissue around the lesion may become brous and form a collagenous scar around the tubercle Ghon complex is formed 0 as the lesion regresses and heals the infection enters a latent period and may produce no symptoms clinical disease may develop if the organisms multiply rapidly or it may remain dormant the potential for reactivation is present organisms like to grow in upper lobes of lungs kidneys epiphyses Module 5 Respiratory Lazenby Page 25 of bone cerebral cortex adrenal glands not highly infectious usually contracted as a result of frequent prolonged and close contact with an infected person Assessment Clinical Manifestatio ns initially asymptomatic fatigue malaise anorexia weight loss persistent longterm lowgrade fever chills amp sweats often at night irregular menses nonresolving bronchopneumonia dyspnea hemoptysis usually associated with more advanced cases persistent progressive and often productive cough cough may be nonproductive and progress to mucoid or mucopurulent sputum reduced lung volumes with pulmonary function tests chest pain pleuritic or dull chest tightness careful history related to previous exposure to TB working and living conditions travel or residency in area with high incidence of TB Diagnosis Sputum culture 0 usually the rst bacteriologic evidence of the presence of tubercle bacilli however at least 10000 bacteria microscopically must be present in order to produce a positive smear 0 culture technique requires only a small amount of bacteria but it may take 68 weeks for mycobacterium to grow Mantoux skin test positive skin reaction occurs 310 weeks post initial infection time taken to mount immune response 0 sensitivity to tuberculin usually persists a lifetime 0 a positive reaction only indicates presence of tuberculous infection does NOT indicate whether the infection is dormant or active CXR cannot differentiate between active or inactive TB the enzymelinked immunosorbent assay ELISA methodology to measure lgG antibody against mycobacterial antigen is a new technique being tested interferon gamma release assays in vitro assays of CD4 Tcell Module 5 Respiratory Lazenby Page 26 interferon gamma release in response to stimulation by speci c M tuberculosis antigens ignores BCG stain so it is superior to PPD Complicatio miiary TB the result of a necrotic Ghon complex eroding into 5 blood vessels and thus allowing large numbers of organisms to invade the bloodstream and spread to all body organs pleural effusion secondary to the release of caseous material into the pleural space gtgt triggers in ammatory process and pleural bacilli of CHONrich uid tuberculous pneumonia result of large amounts of bacilli being discharged into lung or lymph nodes other organ involvement Holistic Implications Health Alteration FUNGAL INFECTIONS most do not produce toxins Description yeasts or molds 2 classi cations o Super cial cutaneous or subcutaneous 0 Skin hair nails 0 Deep or systemic mycoses 0 Pulmonary or systemic infections EtiologyRisk Altered immune responses most people will not be impacted Factors 0 HIV Heavy exposure to fungal source Pathogenesi Molds S 0 Form tubular structures or hyphae o Grow by branching and forming spores May live in soil decaying organic matter Most do not produce toxins Fungi form infectious spores which enter body via respiratory system gt chemical constituents cause a delayed cellmediated hypersensitivity gt antigenspeci c T lymphocytes and cytokineactivated macrophages cause fungicidal properties Macrophage aggregates with organisms form primary pulmonary lesions andor develop in the lymph nodes gt granulomas with giant cells gt central necrosis and calci cation Complicatio May be deadly in those with weakened immune system ns Health Alteration FUNGAL INFECTIONS Histoplasmosis Module 5 Respiratory Lazenby Page 27 Description a Most common mycoses Dimorphic fungus H capsuatum EtiologyRisk a Major river valleys of Midwest Ohio Mississippi Factors 0 Soil enriched with bird andor bat droppings Pathogenesi Source of fungal spores is disturbed gt spores are inhaled gt S exposre to body temp in alveoli gt conversion of spores to parasitic yeast gt distributed to regional lymph nodes gt dissemination throughout the body via bloodstream gt cellular immunity in those with intact immune system Assessment Incubation period 1317 days post exposure Latent asymptomatic Clinical o Healed lesions in lung or hilar lymph nodes ManleStatIO Primary pulmonary histoplasmosis 5 0 Muscle and joint pain 0 Nonproductive dry cough 0 Erythema nodosium or erythema multiforme hivelike lesions 0 Singlemultiple lung in ltrates Chronic histoplasmosis o Resembles reactivation TB 0 In ltration of upper lobes gt cavitation o More common in middleaged male smokers and those with chronic lung disease Productive cough Chest pain Fever Night sweats 0 Weight loss Disseminated histoplasmosis o Follows primary or chronic form 0 More common in very old very young immunocompromised transplant patients patients with hematologic malignancies High fever Generalized lymphadenopathy Hepatosplenomegaly Muscle wasting Anemia Leukopenia Thrombocytopenia Hoarseness Mouthtongue ulcerations N V D abdominal pain OOOO OOOOOOOOOOO Module 5 Respiratory Lazenby Page 28 Diagnosis 0 CXR Cultures sputum blood BM Fungal stains Antigen detection blood urine CSF bronchoalveolar Serologic tests for antibodies Biopsies Complicatio o Meningitis ns Holistic Implications Health Alteration FUNGAL INFECTIONS Coccidioidomycosis Description yeasts or molds quotvalley feverquot C immitis or C posadasi 721 day incubation EtiologyRisk Similar to TB Factors 0 More prevalent in deserts in southwestern U S Pathogenesi Inhalation of spores 5 0 Increased incidence with dust storms digging Assessment 0 Fever Clinical o Cough Manifestatio Pleuritic pain ns Arthralgias or arthritis Erythema nodosum Diagnosis 0 Radiology 0 Bone scans Microscopicserologic evidence of organism Stained biopsy specimen Serologic testing for IgM and IgG antibody detection Complicatio o Disseminated disease lymph nodes meninges spleen liver 5 kidney skin adrenal glands Holistic Implications Health Alteration FUNGAL INFECTIONS Blastomycosis Description a B dermatitidis EtiologyRisk a Most common in southern and north central US Factors 0 Soil with decayed vegetation or decomposed wood Pathogenesi o Inhalation 5 Assessment Suppurative pusforming amp granulomatous lung and skin lesions Clinical o Manifestatio Productive cough Purulent sputum Module 5 Respiratory Lazenby Page 29 ns a Fever Cough Aching joints and muscles 0 Diffuse interalveolar in ltrates Extrapulmonary spread to skin bones prostate which may be the rst evidence of the disease Diagnosis 0 Sputum Tissue biopsy Complicatio a Death if not detected and treated ns Holistic Implications Health Alteration LARYNGEAL CANCER Description 0 cancer of the glottis supraglottis or subglottis causes prolonged use of tobacco and alcohol chronic laryngitis occupational exposure to chemicals and toxins exposed to selected types of HPV genetic predisposition squamous cell carcinoma is the most common type EtiologyRisk irritants such as Factors 0 cigarette smoking 0 alcohol abuse 0 inhalation of other noxious fumes such as pollution 0 chronic laryngitis 0 voice abuse Pathogenesi exposure to irritants gt changes in laryngeal mucosa 5 Assessment precancerous leukoplakia and erythroplakia on laryngeal mucosa Clinical Manifestatio ns lesions may be in any of the three areas lesions of glottis are usually welldifferentiated and slowgrowing hoarseness change in voice dyspnea pain and burning in throat when drinking hot liquids or citrus juices dysphagia foulsmelling breath Diagnosis beroptic laryngoscopy CT scan MRI Biopsy visual examination of the larynx with laryngoscopeook at color of mucous membranes movement of vocal cords presence of Module 5 Respiratory Lazenby Page 30 esionsif client cannot cooperate may use a beroptic endoscope inserted through the nose panendoscopy and biopsy to determine exact location size and extent Complicatio loss of voice ns dis gurement social consequences Holistic Implications Health Alteration LUNG CANCER Description leading cause of death in men and women who have malignant disease in US Since 1987 deaths from lung cancer in women exceeds deaths from all other cancers 5year survival rate is only 14 usually occurs in individuals gt 50 year old with a long history of cigarette smoking found most frequently in persons 4075 years of age peak incidence 5565 years of age types of lung cancer 0 Nonsmall cell adenocarcinoma common in women usually in non smokers usually starts in bronchioles or alveoli less likely to spread so prognosis is better but not as good as squamous cell most common type in North America squamous cell carcinoma commonly found in male smokers less likely to spread so prognosis is better large cell carcinoma highly anaplastic poorly differentiated metastasizes early and has a poor prognosis 0 small cell carcinoma also known as quotoat cellquot spreads early not staged by TNM method may secrete hormonally active products may result in paraneoplastic syndrome manifestations caused by secretion of or immune response to tumor cells Module 5 Respiratory Lazenby Page 31 highly malignant in ltrates widely disseminates early rarely resectable EtiologyRisk a cigarette smoking gt changes in bronchial epithelium Factors epithelium gradually returns to normal after smoking cessation it takes about 15 years for risk for lung cancer of former smoker to return to that of a nonsmoker cigarette smoking is responsible for approximately 8090 of all lung cancers 0 about 1 of 10 heavy smokers eventually develop lung cancer 0 risk related to cigarettes is directly related to 0 total exposure to smoke total of cigarettes smoked in a lifetime 0 depth of inhalation o tar and nicotine content of cigarettes second hand smoke is also a risk factor 0 possible hereditary link genes that potentially determine susceptibility to lung cancer include o protooncogenes and tumor suppressor genes 0 genes eroding enzymes that metabolize procarcinogens o enzymes that detoxify carcinogens cigar and pipe smokers are also at risk inhaled carcinogens asbestos radon nickel iron iron oxides uranium polycyclic aromatic hydrocarbons chromates arsenic air pollution preexisting pulmonary disease TB pulmonary brosis bronchiectasis COPD there is also a correlation with urbanization and population dens y lung cancer may also occur in nonsmokers Pathogenesi 0 most originate from the epithelium of the bronchus gt they grow 5 slowly may take 8 10 years to grow to 1 cm in size gt nonspeci c in ammatory changes gt hypersecretion of mucus desquamation of cells reactive hyperplasia of basal cells and metaplasia of normal respiratory epithelium to strati ed squamous cells prefer upper lobes either nonsmall cell or small cell metastasize via direct extension and via blood circulation and lymph common sites for metastasis are liver bones brain scalene lymph nodes and adrenal glands all types have the potential to cause paraneoplastic syndromes Assessment 0 usually nonspeci c and late in appearing Module 5 Respiratory Lazenby Page 32 Clinical Manifestatio ns pneumonitis with fever chills and cough may be the earliest sign persistent cough may or may not be productive hemoptysis is NOT an early sign chest pain dull intermittent poorly localized retrosternal dyspnea auscultatory wheeze late manifestations anorexia fatigue weight loss NampV hoarseness with laryngeal nerve involvement uniatera diaphragm paralysis dysphagia and SVC obstruction with intrathoracic spread palpable nodes in neck or axia pericardial effusion cardiac tamponade arrhythmias with mediastinal spread elevated levels of ADH and ACTH many bronchogenic carcinomas are so poorly differentiated that they become sites of ectopic production of such hormones high levels of CEA are usually indicative of metastatic disease Diagnosis thorough history and complete physical CXR CT scan andor MRI PET for early detection staging and monitoring cytoogic studies percutaneous needle biopsy de nitive diagnosis via identifying malignant cells early am sputum culture beroptic bronchoscopy allows direct visualization and biopsy mediastinoscopy to determine metastasis into mediastinum and for staging pulmonary angiography and lung scans to assess overa pulmonary status neneedle aspiration if the lesion is near the chest wall this helps prevent a thoracotomy Complicatio superior vena cava syndrome ns pleural effusion paraneoplastic syndrome 0 hypercalcemia from secretion of parathyroidlike peptide 0 Cushing syndrome from ACTH secretion 0 SIADH o Neuromuscular syndromes 0 Hematologic disorders migratory thrombophlebitis nonbacterial endocarditis DIC Holistic Module 5 Respiratory Lazenby Page 33 Implications Health Alteration PLEURITIS or PLEURISY Description 0 in ammation of the parietal pleura EtiologyRisk a viral infections FaCtOFS pneumonia Pathogenesi 0 Respiratory infections extend to the pleura gt irritation S 0 Assessment Unilateral pain with abrupt onset Clinical 0 Pain worse with deep breathing and coughing Manifestatio Decreased tidal volume ns Tachypnea Re ex splinting Diagnosis Distinguishing pain Complicatio Pleural effusion ns Holistic Implications Health Alteration PLEURAL EFFUSION Description abnormal collection of uid or exudate in pleural cavity uid accumulation may be transudate exudate purulent chyle or sanguineous EtiologyRisk o CHF Factors renal failure nephrosis liver failure malignancy Pathogenesi 0 rate of uid accumulation exceeds rate of removal 5 excess uid formation from interstitium of the lung parietal pleura or peritoneal cavity or decreased removal by the lymphatics Assessment 0 decreased lung expansion on affected side Clinical dullness or atness to percussion Manifestatio diminished breath sounds ns hypoxemia due to decreased surface area for diffusion dyspnea due to uid accumulation in pleural cavity compressing the lung gt increased effort or rate of breathing pleuritic pain due to in ammation constant discomfort if the effusion is large Diagnosis CXR chest ultrasonography CT Module 5 Respiratory Lazenby Page 34 Thoracentesis Pleural uid with elevated LDH and protein indicate transudativeexudative effusion Complicatio ns Holistic Implications Health Alteration PNEUMOTHROAX Description presence of air or gas in pleural space EtiologyRisk spontaneous Factors 0 blebs o underlying lung disease traumatic o penetrating or nonpenetrating chest injury 0 fractured or dislocated rib o complication of CPR 0 medical procedures such as transthoracic needle aspiration central line insertion intubation positive pressure ventilation tension 0 intrapeura pressure exceeds atmospheric pressure air enters pleural space but cannot exit gt rapid increase in pressure within the chest gt compression atelectasis of unaffected ung shift in mediastinum to opposite side and compression of vena cava gt decreased venous return to the heart gt decreased cardiac output Pathogenesi opening in the lung gt atmospheric pressure enters the pleural 5 space gt change in the normally negative pressure in the pleural space to a positive pressure gt recoil of the lung to its unexpanded size and remains collapsed gt disruption of cohesion of the parietal and visceral pleura open pneumothorax air pressure in pleural space barametric pressure tension pneumothorax air enters pleural space on inspiration but the pleural rupture site acts as a oneway valve and won39t let air escape with exhalation causes increased pressure gt decreased venous return gt shock bradycardia o hypotension hypoxemia tracheal deviation air pressure in the pleural cavity exceeds barometric pressure in the atmosphere spontaneous pneumothorax occurs when a bleb ruptures 0 causes trauma PEEP etc Assessment unilateral breath sounds Manifestatio Module 5 Respiratory Lazenby Page 35 ns 0 asymmetrical chest movement sudden pleural unilateral chest pain 0 severe hypoxemia dyspnea hypotension tachypnea Diagnosis 0 CXR CT scan ultrasound pulse oximetry ABGs Complicatio respiratory arrest ns Holistic Implications Health Alteration SLEEP APNEA Description 0 partial or complete upper airway obstruction during sleep with disruption of normal ventilation and normal sleep patterns lack of air ow in the upper airways for 3 10 seconds EtiologyRisk adenotonsillar hypertrophy most common in children obesity Factors craniofacial anomalies reduced motor tone of upper airways Pathogenesi 3 different forms 5 obstructive normal pharyngeal muscle tone is lost gt collapse of pharynx during inspiration gt further obstruction when the tongue falls against the posterior pharyngeal wall gt with each attempt to breathe effort shortens until obstructive forces are reduced by movement or position change 0 central respiratory center of the brain is affected and the drive to breathe is inhibited no effort to breathe during period of apnea mixed combination of the above Assessment o snoring Clinical labored breathing during sleep Manifestatio gasping ns frequent repositioning in sleep restless sleep daytime sleepiness Diagnosis 0 sleep studies Complicatio respiratory arrest ns pulmonary hypertension 0 death Holistic Implications Module 5 Respiratory Lazenby Page 36 Health Alteration ASTHMA Description a hyperactive airway reduced expiratory ow rate vagus nerve impulses cause constriction of airways sympathetic stimulation tends to cause airways to dilate histamine causes airways to constrict the incidence of bronchial asthma in the US is increasing 0 about 33 of the 26 million Americans who have bronchial asthma are under 18 years of age asthma caused by inhaled allergens typically begins in younger people with a family history 0 exercise induced asthma is a common form of asthma and is more likely to occur when people exercise in a cold environment asthma is a chronic in ammatory condition 0 the cough associated with asthma is typically worse during the night and early morning 0 the acute or early response typically occurs within 1020 minutes of exposure to an allergen airborne antigens bind to mast cells coated with IgE antibodies lining the airways chemical mediators are then released and cause the 3 hallmark signs of bronchial asthma status asthmaticus refers to a severe chronic form of asthma most asthma deaths have occurred outside the hospital asthma is a common cause for admission to children39s hospital 0 most children who develop asthma have symptoms before they reach school age 0 it is recommended that children be involved in developing their own asthma management plans classi cations 0 mild intermittent 0 mild persistent 0 moderate persistent 0 severe persistent EtiologyRisk 0 potential causes interaction between genetic and FaCtOI39S environmental factors 0 viral respiratory infections medications such as ASA and NSAIDS emotiona upsets hormonal changes inhaed irritants such as tobacco smoke smog occupational fumes gases dusts etc 0000 Module 5 Respiratory Lazenby Page 37 Triggers may include o allergies 0 viral infections 0 autonomic nervous system imbalances that cause increased parasympathetic stimulation 0 medications o psychological triggers Pathogenesi o the in ammatory response is promoted by eosionphils 5 allergen stimulates B lymphocytes which differentiate into plasma cells which produces lgE antibodies which attach to the mast cells and basophils in the bronchial wall which in turn release chemical mediators which cause bronchial smooth muscle contraction which closes the airway These substances also increase vascular permeability which leads to airway edema when airways spasm mucus plugs the airway and traps air distally inhalation of trigger gt abnormal antibodies stimulate mast cells in the lung interstitium gtrelease of histamine and slowreacting substance of anaphylaxis SRSA gt histamine attached to receptor sites in the larger bronchi gt swelling in smooth muscles and slow reacting substance of anaphylaxis attaches to receptor sites in the small bronchi gt swelling of smooth muscle there SRSA also gt fatty acids called prostaglandins that travel via the bloodstream to the lungs where they enhance histamine39s effect gt histamine stimulates the mucous membranes to secrete excessive mucus gt further narrowing of bronchial lumen on inhalation the narrowed bronchial lumen can still expand slightly allowing air to reach the alveoli on exhalation increased intrathoracic pressure closes the bronchial lumen completely mucus lls the lung bases gt inhibits alveolar ventilation gt blood shunted to alveoli in other lungs parts still cannot compensate for diminished ventilation Assessment asthma is now classi ed by severity Clinical o 3 hallmark signs of bronchial asthma Man39fEStat39O o bronchoconstriction 5 o mucosal edema related to increased permeability of mucosal blood vessels 0 increased mucus secretions all three of these lead to a decrease in the diameter of airways nasal aring RT increasing respiratory distress pursed lips RT increased effort to exhale use of accessory muscles RT increased work of breathing Module 5 Respiratory Lazenby Page 38 paradoxic pulse increases RT bronchospasms worsening wheezing cough or dyspnea cyanosislate sign tachycardia anxious decreased FEV lengthened expiration period hyperin ation of lungs as more air is retained in lungs FRC increases wheezing as air is exhaled through narrowed airways decreased forced vital capacity FVC contraction of sternocleidomastoid muscles during ventilation cough due to extra mucus production and irritated mucosa dyspnea and fatigue Diagnosis forced vital capacity FVC lt 40 L forced expiratory volume FEV1 lt 30 L forced expiratory ow FEF is decreased residual volume RV gt 12 L increased up to 400 normal 0 functional residual capacity FRC gt 23 L increased up to 200 CXR pulse oximetry ABGs serum lgE peak expiratory ow rates Complicatio airway obstruction ns altered gas exchange Holistic Implications Health Alteration BRONCHITIS ACUTE AND CHRONIC Description acute infection or in ammation of the airways or bronchi commonly follows a viral illness usually selflimiting a form of COPD in ammation of bronchi caused by irritants or infection hypersecretion of mucus and chronic productive cough last for 3 months of the year and occurs for at least 2 consecutive years distinguishing characteristic is obstruction of air ow caused by mucus cigarette smoking is a major contributing factor EtiologyRisk Factors history of smoking occupational exposures Module 5 Respiratory Lazenby Page 39 air pollution reduced lung function heredity Pathogenesi o inhaled irritants gt in ammation of the tracheobronchial tree gt 5 increased mucus production and a narrowed or blocked airway gt continued in ammation gt changes in cells lining the respiratory tract gt increased resistance in small airways and severe imbalance in VQ ratio gt decreased arterial oxygenation 0 chronic bronchitis gt hypertrophy of airway smooth muscle and hyperplasia of mucus glands increased number of goblet cells ciliary damage squamous metaplasia of columnar epithelium chronic leukocytic and lymphocytic in ltration of bronchial walls hypersecretion of goblets cells blocks free movement of cilia gt impaired defenses gt increased risk for respiratory tract infection narrowing and widespread in ammation within airways in amed and thickened bronchial walls from edema and accumulation of in ammatory cells smooth muscle bronchospasms airways become obstructed and close especially on expiration gt air trapping in distal portions of lung gt hypoventilation gt VQ mismatch gt hypoxemia Assessment fever cough chills malaise nonproductive cough if viral chest Clinical pain from coughing Manifestatio copious gray white or yellow sputum ns dyspnea tachypnea cyanosis use of accessory muscles pedal edema neck vein distention weight gain secondary to edema weight loss secondary to dif culty eating and increased metabolic rate wheezing with prolonged expiratory phase rhonchi pulmonary hypertension Diagnosis sputum analysis CXR PFT ABGs ECG Complicatio o rightsided heart failure ns Holistic Module 5 Respiratory Lazenby Page 40 Implications Health Alteration EMPHYSEMA Description disorder in which the alveolar walls are destroyed which leads to permanent overdistention of the air spaces one of the rst presenting symptoms is dyspnea dif cult expiration RT 0 destruction of septa between alveoli 0 partial airway collapse 0 loss of elastic recoil quotpink puffersquot because of normal arterial 02 levels and dyspnea EtiologyRisk Factors cigarette smoking gt neutrophil activation and retention in lung func onal ssue Pathogenesi 5 air passages obstructed as a result of overdistention changes in the lung are caused by alphalantitrypsin de ciency loss of elastic recoil allows the airways to collapse as alveoli collapse pockets of air form between alveolar spaces blebs and within the lung parenchyma bullae gtgtincreased ventilatory dead space gtgtincreased work of breathing due to decrease in functional lung tissue to exchange 02 and C02 emphysema also causes destruction of pulmonary capillaries gtgtgtfurther decreasing 02 perfusion and ventilation air trapping causes an increased A P diameter 3 types of emphysema 1 centrilobular most commondestruction in bronchioles 2 panlobular destroys air sacs of entire acinus 3 paraseptaldestroys alveoli in lower lobes resulting in isolated blebs along lung periphery believed to be likely cause of pneumothorax Assessment Clinical Manifestatio ns dyspnea weight loss decreased muscle mass increased anteroposterior diameter AP diameter quotbarrel chestquot use of accessory muscles esp sternocleidomastoid and pectoral pursedlip breathing cough with small amount sputum decreased tactile fremitus diffusely hyperresonant sound with percussion decreased or absent breath sounds distant heart sounds wheezes and possibly crackles peripheral cyanosis clubbing of the ngers Module 5 Respiratory Lazenby Page 41 Diagn05i5 decreased cxl antitrypsin AAT level 0 decreased FVC decreased FEV1 decreased FEF increased RV increased FRC CXR CT scan 0 pulse oximetry ABGs CBC ECG Peak expiratory ow rate PEFR Complicatio o Pneumothorax secondary to bleb rupture ns Holistic Implications Health Alteration COPD Description 0 see emphysema and bronchitis group of respiratory disorders characterized by chronic and recurrent obstruction of air ow in pulmonary airways progressive airway obstruction airway hyperreactivity may also be present 0 leading cause of mortality and morbidity worldwide 0 4th leading cause of death in the US projected to become the 3rd leading cause worldwide encompasses emphysema enlargement of air spaces and lung tissue destruction and chronic obstructive bronchitis increased mucus production obstruction of small airways chronic productive cough EtiologyRisk 0 smoking Factors 0 exposure to occupational dusts and chemicals airway infections asthma or airway hyperresponsiveness Pathogenesi o in ammation and brosis of bronchial airway s hypertrophy of submucosal glands hypersecretion of mucus loss of elastic lung bers and alveolar tissue bronchial wall in ammation and brosis excess mucus secretion destruction of elastic bers gt ventilationperfusion mismatch destruction of alveolar tissue gt decreased surface area for gas exchange loss of elastic bers gt impaired expiratory ow rate Module 5 Respiratory Lazenby Page 42 gt increased air trapping gt airway collapse Assessment Manifestatio ns See emphysema and chronic bronchitis Diagnosis See emphysema and chronic bronchitis Complicatio See emphysema and chronic bronchitis ns Holistic Implications Health Alteration BRONCHIECTASIS Description persistent abnormal dilation of bronchi usually occurs in conjunction with other respiratory problems may be the result of mucus plugs atelectasis aspiration of foreign body infection CF TB congenital bronchial wall weakness impaired defense mechanisms EtiologyRisk longstanding pulmonary obstruction of lower airways by tumors Factors chronic infections mucus accumulation such as with cystic brosis exposure to toxins Pathogenesi recurrent in ammation or infections of bronchial walls gt S persistent dilation and destruction of walls in bronchial walls gt loss of ciliated epithelium metaplasia and pus formation gt obstruction of air ow bronchi ll with mucus gt atelectasis abnormal developmental of abnormal connections between the bronchi gt impaired alveoli ventilation Assessment foul smelling sputum Clinical Manifestatio ns purulent sputum chronic and productive cough hemoptysis crackles rhonchi clubbing decreased VC and expiratory ow rates may also have ss associated with bronchitis infection hypoxemia in severe cases Diagnosis xray Complicatio airway destruction ns Holistic Implications Health Alteration CYSTIC FIBROSIS Module 5 Respiratory Lazenby Page 43 Description autosomal recessive inherited disorder involving uid secretion by exocrine glands in epithelial lining of respiratory Gland reproductive tracts chronic respiratory disease pancreatic exocrine de ciency elevation of sodium chloride in sweat EtiologyRisk white population of northern Europe North America FaCtOFS AustraliaNew Zealand Pathogenesi a mutation of single gene in long arm of chromosome 7 that S encodes for CF transmembrane regulator CFTR which functions as chloride channel in epithelial cell membrane gt epithelial membrane relatively impermeable to the chloride ion impaired transport of Cl39 into airway lumen gt increased absorption of Na and H20 from airways into blood gt lowered water content of mucociliary blanket coating respiratory epithelium gt viscid epithelial dehydrated mucous layer gt defective mucociliary function accumulation of viscid secretions gt obstruction of airways gt recurrent pulmonary infections similar patho occurs in pancreatic and biliary ducts and in vas deferens in boys impaired mucociliary clearance lungs infections accumulation of viscid mucus in bronchi Assessment 0 thick viscous respiratory secretions Clinical abnormal pancreatic function Manifestatio ns 0 steatorrhea o diarrhea o abdominal pain meconium ileus Diagnosis a respiratory and GI symptoms typical of CF 0 history of sibling with CF sweat test pilocarpine iontophoresis used to collect sweat which is then analyzed for chloride content 0 analysis of bioelectrical properties of respiratory epithelia in nasal membrane 0 genetic tests for CFRTgene mutation elevated levels of immunoreactive trypsinogen in newborns most likely due to secretory obstruction in pancreas Complicatio o Bronchiectasis ns 0 chronic respiratory infections intestinal obstruction impaired intestinal absorption Holistic o impacts entire family nancial issues lifestyle etc Implications Module 5 Respiratory Lazenby Page 44 Health Alteration INTERSTITIAL LUNG DISEASE Idiopathic Pulmonary Fibrosis and Sarcoidosis Description restrictive lung disorder because of resulting stiff noncompliant lung also referred to as diffuse parenchymal lung disease involves in ammatory and brotic changes in interstitium or interalveolar septa impacts collagen and elastic connective tissue of the alveolar walls variable progression rapid slow static Stiff lungs gt need for increased pressure to in ate lungs gt dif culty breathing Damage to alveolar epithelium and interstitial vasculature gt impaired gas exchange gt hypoxemia EtiologyRisk hypersensitivity FaCtOFS medications such as cancer drugs 0 radiation therapy occupations which include exposure to silica coal dust asbestos immunological conditions such as RA or scleroderma granulomatous diseases Pathogenesi o injury to alveolar epithelium gt in ammatory process involving 5 alveoli and interstitium gt accumulation of in ammatory and immune cells gt continued lung tissue damage with normal tissue being replaced by brous scar tissue alveolar macrophages secrete brogenic factors broblastic growth factor transforming growth factorB plateletderived growth factor gt attraction and proliferation of broblasts destruction of type I alveolar cells with proliferation of type II alveolar cells which secrete chemotactic factors gt attraction of additional macrophages growth factors and cytokines gt brotic changes Assessment dyspnea Clinical tachypnea Manifestatio cyanosis ns hypoxemia decreased tidal volume nonproductive cough insidious onset of breathlessness clubbing of toes and ngers diminished lung compliance decreased vital capacity decreased totally lung capacity Module 5 Respiratory Lazenby Page 45 FEV typically unchanged increased FVC to FEV hypercapnia and respiratory acidosis in the late stages Diagnosis 0 thorough history and physical CXR Biopsy Complicatio Respiratory failure ns 0 Pulmonary hypertension 0 Cor pulmonale Holistic Implications Health Alteration INTERSTITIAL LUNG DISEASE Idiopathic Pulmonary Fibrosis Description 0 Most common type EtiologyRisk 0 Unknown FaCtorS Men 0 Over 60 years of age Cigarette smoking 0 Occupational exposure farmers hairdressers stonecutters metal cutters Genetic predisposition Viral proteins and antibodies to viruses Pathogenesi 0 Diffuse interstitial brosis 5 o Patchy interstitial brosis gt alveolar wall collapse formation of cystic spaces lined by hyperplastic type II alveolar cells or bronchial epithelium lntimal brosis and medial thickening gt secondary HTN Assessment 0 Severe hypoxemia Clinical Cyanosis Manifestatio Gradual insidious onset ns Nonproductive cough 0 Progressive dyspnea Cyanosis Cor pulomale Peripheral edema Diagnosis 0 Surgical biopsy Complicatio ns Holistic 0 Mean survival of 35 years post diagnosis Implications Health Alteration INTERSTITIAL LUNG DISEASE Sarcoidosis Description Multisystem disorder Module 5 Respiratory Lazenby Page 46 Granulomas in many tissues organs esp lungs EtiologyRisk Less than 40 years of age FaCtOFS North American blacks Northern European whites Women Pathogenesi 0 Exposure of genetically predisposed individuals to certain 5 environmental agents Defective HLA genes in major histocompatibility complex Immune response characterized by chronic in ammation monocyte recruitment granuloma formation with multinucleated giant cells Assessment o Unpredictable course Clinical Lungs eyes and skin are most commonly impacted Manifestatio SOB ns Nonproductive cough 0 Chest pain Fever Sweating Anorexia Weight loss Myalgia Fatigue Anterior uveitis Skin papules and plaques Progressive chronicity and remissions Diagnosis 0 Complete history and physical CXR Biopsy Rule out other causes Complicatio ns Holistic Implications Health Alteration PULMONARY EMBOLISM Description 0 not a primary disease but rather a sequelae to other conditions bloodborne substance lodges in branch of pulmonary artery and obstructs blood flow prevention is key be aware of those with EtiologyRisk Factors such as surgery age bedrest etc EtiologyRisk Factors physiologic factors that predispose patients to thrombus formation Virchow39s triad venous stasissluggish blood flow hypercoagulability damage to venous wall Module 5 Respiratory Lazenby Page 47 accidental injection of air mobilization of fat from bone marrow following a fracture amniotic uid from maternal circulation during childbirth oral contraceptive use surgery 0 severe trauma myocardial infarction CHF SCI thrombophilias inherited disorders affecting coagulation which increase the risk for venous thromboemboli Pathogenesi exercise or other mechanism gt dislodging of thrombi gt travel to S pulmonary vascuature gt undissolved detached materials that occlude blood vessels of pulmonary vascuature gt impaired circulation distal to occlusion gt hypoxemia then inhibits production of surfactant gt aveoar coapse Assessment chest pain Manifestatio o dyspnea 5 tachypnea restlessness apprehension nghtfever anxiety tachycardia hypotension distended neck veins cyanosis diaphoresis hemoptysis rapid shallow breathing massive emboi cause sudden collapse crushing substerna chest pain shock and sometimes loss of consciousness Diagnosis clinical manifestations ABGs Ddimer testing measurement of plasma Ddimer a degradation product of coagulation factors activated as a result of thromboembolic event ung perfusion scans ventilationperfusion scan uses radiolabeled albumin injected intravenously an inhaled radiolabeled gas scintillation camera is used to scan various ung segments for blood flow and distribution of radiolabeled gas Module 5 Respiratory Lazenby Page 48 chest CT pulmonary angiography passage of venous catheter through right heart into pulmonary artery under uoroscopy most accurate but invasive Complicatio a pulmonary hypertension ns re ex bronchoconstriction ventilation without perfusion impaired gas exchange 0 loss of alveolar surfactant Holistic Implications Health Alteration PULMONARY HYPERTENSION Description a abnormal elevation of pressure within the pulmonary circulation selfperpetuating introduces secondary structural abnormalities of pulmonary vessels including smooth muscle hypertrophy and proliferation of vessel intima a sustained increase in pulmonary artery pressure secondary pulmonary hypertension is usually the result of chronic pulmonary disease sleep apnea heart failure EtiologyRisk mitral valve disorders FaCtOFS left ventricular diastolic dysfunction COPD heart failure 0 sleep apnea congenital heart disease pulmonary thromboemboli pulmonary vessel hypoxia gt pulmonary vessel constriction in an effort to shunt blood away from the unventilated area interstitial lung disease familial inherited as autosomal dominant trait with variable but low penetrance portal hypertension appetitesuppressant drug that has been removed from the market 0 HIV Pathogenesi exposure to some factor gt pulmonary vessel wall thickening gt S brosis gt greater muscle thickening gt impedence of already compromised pulmonary vasculature gt tissue necrosis and hemorrhage mechanisms responsible for vascular changes may include o diminished levels of nitric oxide which is a potent Module 5 Respiratory Lazenby Page 49 vasodilator o diminished levels of prostacyclin which is a potent vasodilator 0 increased levels of several growth factors including endothelin1 vascular endothelial growth factor and plateletderived growth factor Assessment exerciseintolerance Clinical syncope Manifestatio dyspnea 5 chest pain on exertion fatigue hemoptysis pulmonary edema later cor pulmonale Diagnosis 0 elevated pulmonary artery pressure Complicatio a progressive right heart failure 5 0 low cardiac output 0 death Holistic Implications Health Alteration ACUTE RESPIRATORY DISTRESS SYNDROME ARDS Description sudden progressive pulmonary disorder which develops as a result of an insult condition or noxious event that traumatizes the lung tissue direct or indirect an acute respiratory distress syndrome believed by many to be caused by alveolarcapillary damage and inability to function Severe hypoxemia develops with decreased functional residual capacity intrapulmonary shunting and decreased lung compliance 0 a pulmonary emergency that is a sudden and severe form of respiratory failure ARDS is hallmarked by diffuse acute pulmonary in ltrates associated with dif cult oxygenation in spite of supplemental oxygen therapy with a pulmonary capillary wedge pressure of less than 18 mmHg 0 some event triggers the disruption of the pulmonary capillary endothelium causing interstitial edema decreased lung compliance decreased ventilationperfusion match and hypoxemia As the interstitial edema progresses alveolar collapse and massive atelectasis ensues There is a signi cant decrease of total lung volume lifethreatening hypoxemia and a decreased function residual capacity acute lung injury ALI lesssevere form of the disorder but has Module 5 Respiratory Lazenby Page 50 the potential to evolve into ARDS incidence of ARDSALI in North American is approximately 35 to 60 mortality rate between 35 to 60 morbidity involves physical cognitive emotional EtiologyRisk a any major trauma or insult to the body Factors sepsis secondary to pulmonary or nonpumonary infections aspiration of gastric contents acute pancreatitis hematologic disorders metabolic events reactions to drugs or toxins pneumonia ung contusion fat embolus massive smoke inhalation inhaled toxins prolonged exposure to high concentrations to 02 0 near drowning hemorrhage pulmonary emboli drug overdose fat embolus PathOQEHESi 0 increased permeability of pulmonary endothelium and S alveolar endothelium gt movement of uid into the interstitial and alveolar spaces gt pulmonary edema develops gt decreased ung compliance and 02 transportaveoar cells which produce pulmonary surfactant type II are also damaged gt atelectasis and further impairment in lung distensibility and gas exchange diffuse alveolar cell damage gt accumulation of uid surfactant inactivation formation of brous hyaline membrane that is impervious to gas exchange pulmonary insult direct or indirect gt accumulation of neutrophils in microcirculation gt activation and migration of neutrophils across alveolar epithelial surfaces gt release of proteases cytokines and reactive 02 species gt increased permeability in alveolar epithelial cells and damage to type I and type II alveolar cells gt pulmonary edema hyaline membrane formation and loss of surfactant gt decreased pulmonary compliance gt dif cult air exchange Assessment 0 rapid onset typically within 1218 hours of initiating event Clinical severe dyspnea Module 5 Respiratory Lazenby Page 51 Manifestatio o hypoxemia ns tachypnea marked hypoxemia diffuse bilateral in ltrate Diagn05i5 increased intrapulmonary shunting of blood impaired gas exchange and hypoxemia despite high supplemental 02 therapy Complicatio o DIC ns 0 02 toxicity 0 GI bleeding due to stress ulcers hypoxemia renal failure thrombocytopenia sepsis from invasive lines pulmonary brosis 0 multiple organ failure acute respiratory failure Holistic Implications Health Alteration RESPIRATORY FAILURE Description disturbed gas exchange gt abnormal arterial blood gas inadequate gas exchange Pa02 g 50 and PaC02 3 50 with pH 5 725 with the client on RA EtiologyRisk injury to lungs airway or chest wall FaCtOFS injury to another body system underlying respiratory disease neuromuscular chest problems shock pulmonary emboli pulmonary edema obes y Pathogenesi o hypoxemia secondary to poor matching of ventilation and S perfusion hypercapnia secondary to reduced aveoar ventilation in relation to C02 production Assessment 0 hypoxia Clinical hypercapnia Manifestatio HA 5 confusion restlessness decreased LOC agitation dizziness Module 5 Respiratory Lazenby Page 52 tremors initial HTN then hypotension and tachycardia rapid and shallow breathing increased inspiratory muscle movement cyanosis nasal aring retractions cool and clammy skin decreased capillary re ll Diagnosis arterial P02 less than 60 mm Hg arterial PC02 greater than 45 mm Hg Complicatio o headache due to cerebral vessel dilation ns papilledema increased CSF increased cerebral blood flow due to increased PC02 depressed cardiac contractility Holistic Implications Health Alteration EPISTAXIS Description 0 nosebleed men affected more than women EtiologyRisk Factors medications drying infection trauma cocaine use local infection blood dyscrasias HTN diabetes trauma Pathogenesi s most nosebleeds arise from Kiesselbach s area a rich vascular plexus in the anterior nasal spectrum or from rupture of vessels caused by trauma Assessment Clinical Manifestatio ns bleeding vital signs Diagnosis 0 thorough history and physical Complicatio o aspiration ns Module 5 Respiratory Lazenby Page 53 Holistic Implications Module 5 Respiratory Lazenby Page 54 Module 6 Integumentary This module will focus on alterations of the skin MODULE OBJECTIVES After reviewing this module the student should be able to 1 Describe the normal anatomy and physiology of the integumentary system 2 Discuss the pathogenesis associated with common integumentary alterations 3 Distinguish the most pertinent identifying information related to each alteration 4 Describe clinical manifestations associated with integumentary alterations and relate the ndings back to the pathogenesis 5 Appreciate the impact that integumentary alterations can have on a patient39s lifestyle MODULE CONCEPTS 0 Overview of the integumentary system 0 Health Alterations 0 Infectious processes Fungal infections Tinea of the body or face Tinea of the scalp Tinea of the foot and hand Tinea of the nails Tinea versicolor Candidiasis Bacterial infections Impetigo Cellulitis Viral infections Verrucae Varicella RubeHa Rubeola Roseola Mumps 5th Disease Scarlet fever Herpes simplex Herpes zoster o Pustular disorders Acne vulgaris Acne conglobate Rosacea o Allergic and Hypersensitivity Dermatoses MODULE 6 INTEGUMENTARY LAZENBY 1 Atopic dermatitis Urticaria Contact dermatitis Druginduced skin eruptions Papulosquamous dermatoses Psoriasis Pityriasis rosea Anthropod infestations Scabies Pediculosis Ultraviolet radiation injuries UV radiation skin damage Druginduced photosensitivity Thermal injuries Burn classi cation Complications Treatment Pressure ulcers Nevi Skin cancers Malignant melanoma Basal cell carcinoma Squamous cell carcinoma Agerelated skin conditions Infancy and childhood Birthmarks Common infectious alterations Elderly Normal changes associated with aging Common lesions ASSIGNMENTSREADINGS Porth Chapter 45 Porth Chapter 46 View Panopto httpsauburnhostedpanoptocomPanoptoPagesViewera spxid7f8de719Oa2a4d48 b696 ddc23f694ac2ampSignedlnTrue 1 when complete Assessmen t AampP lntegumentary system includes 0 skin hair nails glands The skin is one of the largest organs of the body composes about 20 of body weight contains sweat glands nerve endings blood vessels MODULE 6 INTEGUMENTARY LAZENBY 2 sebaceous glands pressure sensors heat receptors cold receptors cells Functions of the Skin protection 0 rst line of defense for the body 0 keratin protects the body from excessive uid loss 0 melanin prevents damage from the sun39s UV rays 0 touch and pressure receptors for protection and pleasure temperature regulation 0 works by regulating sweat secretion and regulating blood ow 0 heat is lost as sweat evaporates from the skin 0 if vessels close to the skin have increased blood ow heat is lost via radiation 0 sense organ activity 0 assists with production of Vitamin D Epidermis outermost layer of the skin thin sheet of strati ed squamous epithelium cells are able to regenerate quickly in the deeper layers and as they move to the surface they become specialized cytoplasm is replaced by keratin which provides protection melanocytes brown pigment gives color to the skin 0 cells of the epidermis are tightly packed when there is injury and loosening of the cells blisters occur Dermis and Subcutaneous Tissue Dermis deeper layer which is composed of mostly connective ssue loosely packed cells 0 contains bers that are tough strong stretchable elastic upper region has ridges grooves ngerprinting deeper layer is mostly collagen which gives toughness to the skin specialized network of nerve endings necessary for touch temp pressure pain elastic bers are also present 0 with aging elastin bers decrease in number and amount of subq tissue is reduced gt wrinkles Subcutaneous tissue with fat offers support to the upper 2 layers MODULE 6 INTEGUMENTARY LAZENBY 3 fat insulates against extreme heat and cold 0 fat serves as stored energy source and can be used as food source subq tissue acts as shockabsorber to protect underlying tissue Appendages hair 0 most hair follicles are present at birth 0 lanugo is the soft hair covering the newborn the premature infant has even more 0 cells of epidermal layer grow into dermis and form a hair follicle hair growth begins from hair papilla located in the hair bulb at the base of the follicle root is hidden in the follicle and the shaft is visible 0 new hair will grow as long as the hair follicle remains viable cutting or shaving does not make hair grow faster because the epithelial cells that form the hair embedded in the dermis are not affected 0 alopecia hair loss rapid hair loss in round patches may be the result of metabolic diseases 0 arrector pili this muscle attaches to the base of dermal papilla and the side of a hair follicle with stimulation the pull is in opposite directions gt quothair standing on endquot 0 receptors 0 sensory portion for the skin nails 0 produced by cells in the epidermis skin glands o sweat glands assist in elimination of waste products such as ammonia and uric acid help the body maintain constant body temp o sebaceous glands secrete oil sebum for hair and skin grow where hair grows prevents drying and cracking of the skin if sebum accumulates in the ducts of the sebaceous glands pimples can form and are called blackheads if they darken acne vulgaris is the result of the increase in sebum secretion associated with the adolescent MODULE 6 INTEGUMENTARY LAZENBY 4 period 1019 years of age topical acne meds work by causing drying and peeling of skin which helps remove sebaceous plugs thereby releasing oxygen to inhibit anerobic bacteria on the skin Blood supply and innervation papillary capillaries sympathetic nervous system 0 regulates vasoconstriction and vasodilation via alpha adrenergic receptors lymphatic vessels drain into larger subq trunks Aging and Skin Integrity Cutaneous changes associated with genetic and environmental factors Thinning gt translucent paperthin skin Direr o Wrinkled Change in pigmentation Flattening of dermoepidermal junction Shortened and decreased number of capillary loops Decreased melanocytes gt decreased protection against UV radiation Decreased Langerhans cells gt decreased immune response Decreased vasculature and lymphatic drainage gt loss of barrier protection and atrophy of eccrine apocrine and sebaceous glands gt dry skin Decreased collagen bers Decreased elastin bers Decreased cell proliferation decreased blood supply depressed immune responses gt delayed wound healing Loss of melanocytes from hair bulbs gt graying Decreased number of hair follicles gt thinning and ner hair 0 Increased permeability of stratum corneum Decreased vascularity gt decreased clearance of substances from dermis gt skin irritation Loss of cutaneous vasomotion and subq fat decreased vascularity decreased eccrine sweat production gt altered temperature regulation gt increased risk for hypothermia and heat stroke Decreased pressure and touch receptors and free nerve MODULE 6 INTEGUMENTARY LAZENBY 5 endings gt decreased sensory perception 0 Decrease in protective functions gt increased risk of infection and delayed wound healing PRURITUS Description Most common symptom with skin disorders EtiologyRisk Skin disorder Factors Pathogenesi Involves neuropeptides histamine cytokines serotonin S prostaglandins bradykinin or acetylcholine Stimulation of free nerve endings in the skin gtltch sensation carried by unmyelinated Cnerve bers Assessment Severe itching Clinical Manifestatio ns FUNGAL INFECTIONS Health Alteration Fungal infections Description Fungal infections occur in warm moist areas of skin Tinea pedis athlete39s foot tinea cruris jock itch tinea capitis ringworm of the scalp and tinea unguium nails are generally mild and treated with topical antifungals Fungal infections of the skin and mucous membranes of immunocompromised clients are serious and require oral or parenteral antifungals Super cial or deep EtiologyRisk Moisture Factors Pathogenesi Super cial S o Fungi on dead keratinized cells of epidermis emit enzyme gt digestion of keratin gt super cial skin scaling nail disintegration hair breakage Deep 0 Fungi releases exotoxins gt in ammation Assessment Scaling Clinical Crusting Manifestatio Erythema ns Diagnosis Super cial 0 Microscopic exams of skin scrapings Potassium hydroxide KOH disintegrates human tissue leaving hyphae more evident o Cultures 0 Woods ultraviolent light yellowgreen uorescence MODULE 6 INTEGUMENTARY LAZENBY 6 Complicatio ns Fissures and cracking Holistic Implications Health Alteration FUNGAL INFECTIONS Tinea capitis scalp Description 0 primary 0 nonin ammatory secondary o in ammatory EtiologyRisk 0 children Factors farmers who work with animals 0 sharing of combsbrushes where spores have shed PathOQEHESi 0 caused by a group of fungi that infect and survive on keratin 5 Assessment scaly pruritic scalp with bald areas hair breaks easily Clinical Manifestatio ns nonin ammatory type 0 lesions vary from grayish round hairless patches to balding spots or black dots on head 0 lesions most commonly occur on back of head 0 mild erythema crust or scale 0 may be asymptomatic although prutitus is usually present in ammatory type 0 rapid onset o lesions are usually localized to one area 0 initial lesion consists of pustular scaly round patch with broken hairs o secondary bacterial infection is common and may lead to painful circumscribed boggy and indurated lesion called a kerion Complicatio ns Secondary bacterial infection Health Alteration FUNGAL INFECTIONS Tinea corporis skin Description quotringwormquot caused by a fungus transmission is most commonly from kittens puppies other children with infection EtiologyRisk o children Factors Pathogenesi 0 caused by a group of fungi that infect and survive on keratin 5 Assessment circular clearly circumscribed mildly erythematosus scaly MODULE 6 INTEGUMENTARY LAZENBY 7 Clinical Manifestatio ns patches with a slightly elevated ringlike border some forms are dry and macular other forms are moist and vesicular common on trunk back buttocks less common on foot and groin lesions begin as red papule amp enlarges often with a central clearing patches have raised red borders with vesicles papules or pustules borders are sharply de ned but lesions coalesce lesions are generally circular erythematous wellmarginated with a raised scaly vesicular border lesions are often accompanied by pruritus mild burning sensation and erythema Health Alteration FUNGAL INFECTIONS Tinea cruris groin Description also known as jock itch ringworm of the groin and upper thighs EtiologyRisk heat and high humidity Factors PathOQEHESi 0 caused by a group of fungi that infect and survive on keratin 5 Assessment 0 small erythematosus and scaling vesicular patches with a well Clinical de ned border that spreads over the inner and upper surfaces of Manifestatio ns the thighs lesions are sharply demarcated scaling patches usually extremely pruritic Health Alteration FUNGAL INFECTIONS Tinea pedis foot Description Most common dermatosis also known as athlete39s foot primarily affects spaces between toes soles of feet and sides of feet EtiologyRisk hot weather FaCtOFS exposure to moisture or occlusive shoes PathOQEHESi 0 caused by a group of fungi that infect and survive on keratin 5 Assessment 0 occurs between toes and may spread to soles of the feet nails Clinical skin or toes Manifestatio ns nghtscaHng macerated painful skin occasionally with ssures and vesiculation lesions vary from mildly scaling lesion to painful exudative MODULE 6 INTEGUMENTARY LAZENBY 8 erosive in amed lesion with ssuring lesions may be ne vesiculopustular or scaly areas that are usually itchy lesions may be accompanied by pruritus pain foul odor Health Alteration FUNGAL INFECTIONS Tinea unguium nails Description a Toenails more common than ngernails EtiologyRisk o Injury to the nail Factors Tinea pedis Pathogenesi 5 Assessment 0 Nail is initially opaque white or silver Clinical Next nail becomes yellow or brown Manifestatio ns Eventually nail thickens and cracks Health Alteration Tinea versicolor Description 0 Also known as pityriasis versicolor Common nonin ammatory fungal infection 0 Typically involves upper chest back and sometimes arms EtiologyRisk o More common in teen or young adult Factors Pathogenesi 0 Yeast within stratum corneum and hair follicles in areas with S sebaceous glands Assessment 0 Yellow pink or brown sheet of scaling skin Clinical Multicolored variations of lesion Manifestatio ns Depigmented resilient to tanning 0 Health Alteration CANDIDIASIS Description 0 caused by yeastlike fungus found on mucous membranes GI tract vagina thrush in children with white plaques in the mouth that lead to shallow ulcers EtiologyRisk moist warm environment with maceration or occlusion Factors 0 systemic administration of antibiotics pregnancy 0 DM Cushing disease debilitated states 0 lt 6 months of age immunosuppression MODULE 6 INTEGUMENTARY LAZENBY 9 diseases of blood or monocytemacrophage system Pathogenesi yeastlike fungus releases irritating toxins on the skin 5 Assessment thinwalled pustule with an in ammatory base Clinical Manifestatio ns may burn or itch accumulation of in ammatory cells and scales gt whitish yellow curdlike substance over infected area satellite lesions are a distinguishing characteristic Diagnosis microscopic exam KOH Complicatio Maceration of the skin ns Holistic Implications BACTERIAL INFECTIONS Health Alteration IMPETIGO Description Super cial bacterial infection seen more commonly in children it is lifethreatening if it becomes systemic rare EtiologyRisk caused by staphylococcal or group A betahemolytic streptococci Factors or both midsummer to summer due to hot humid climate living in crowded conditions poor sanitary facilities anemia and malnutrition Pathogenesi break in skin exposure to microorganism gt infection 5 Assessment Thin at honeycolored crust Clinical Manifestatio ns Moist in amed serumweeping base under the crust Pruritus Typically located around mouth and nose Diagnosis Appearance Culture Complicatio Poststreptococcal glomerulonephritis rare ns Holistic Implications Health Alteration CELLULITIS Description Infection of dermis and subq tissue Usually caused by Staphylococcus aureus or group A Bhemolytic streptococci MODULE 6 INTEGUMENTARY LAZENBY 1O EtiologyRisk Diabetes mellitus Factors 0 Edema Peripheral vascular disease Tinea pedis Any portal of entry Pathogenesi a Portal of entry microorganism gt infection 5 Assessment Erythema Clinical o Manifestatio ns Warm swollen painful Red swollen tender plaque with poorly de ned border Diagnosis 0 Culture 0 Elevated WBC Complicatio Dermal brosis ns Lymphedema Septicemia NephnUs Death Holistic Implications VIRAL INFECTIONS Health Alteration VERRUCAE Warts Description 0 type of benign neoplasm caused by papilloma virus nipplelike projections round elevated rough grayish surface contagious via direct transmission removed via freezing drying laser chemical application EtiologyRisk direct contact Factors 0 broken skin autoinoculation Pathogenesi 0 Caused by DNAcontaining human papillomavirus HPV 5 o Irregular thickening of the stratum spinosum and great thickening of the stratum corneum Assessment 0 Appearance varies depending on the type of HPV Clinical Manifestatio ns Common warts or verrucae vulgaris 0 Typically occur on dorsal surface of hand 0 Small grayishwhite to tan at to convex papules Flat warts or verrucae plana 0 Face or dorsal hand surface 0 Slightly elevated at smooth tan papules Verrucae plantaris soles of feet amp verrucae palmaris palms of MODULE 6 INTEGUMENTARY LAZENBY 11 hands 0 Rough scaly up to 12 cm in diameter may coalesce Health Alteration Varicella Description also known as chicken pox highly contagious virus spread by persontoperson contact and by airborne droplets incubation period usually 14 days contagious for at least 1 day before rash development transmission of virus may occur until approximately 56 days after onset of the rst skin lesion consider that a child is contagious for at least 710 days occurs most commonly in late winter and early spring EtiologyRisk exposure to infected person Factors Assessment rst sign is usually itching or the appearance of vesicles usually Clinical on trunk scalp or face Manifestatio ns rash later spreads to extremities lesions such as macules papules and vesicles various stages may include mouth and conjunctiva and pharynx rash is usually profuse on trunk and sparse distally Health Alteration Rubella Description also known as German or 3day measles caused by RNA virus that enters bloodstream via respiratory route mild in most children incubation period 1421 days usually not contagious after rash develops EtiologyRisk exposure to infected person Factors Pathogenesi caused by RNA virus that enter bloodstream via respiratory route 5 virus dissemination to skin gt rash Assessment prodromal CliniCal o enlarged cervical and postauricular lymph nodes Manifestatio ns lowgrade fever headache sore throat runny nose cough 1 to 4 days after onset of initial symptoms 0 faintpink to red coalescing maculopapular rash on face with spread to trunk and extremities OOOOO MODULE 6 INTEGUMENTARY LAZENBY 12 o rash usually subsides in 23 days Complicatio Women of childbearing age should be immunized if their titer is low ns do not get pregnant for at least 3 months after vaccination rubella in the rst trimester may be harmful to the fetus Holistic Implications Health Alteration Rubeola DescriptiOH also known as red measles highly contagious acute viral disease of children transmitted by direct contact with droplets from infected persons caused by RNAcontaining paramyxovirus incubation period 712 days typically lasts 35 days EtiologyRisk exposure to infected person Factors Assessment prod romal CliniCal 0 high fever Manifestatio ns o maaise o enarged lymph nodes 0 runny nose 0 conjunctivitis o quotbarkingquot cough 0 respiratory symptoms within 34 days 0 erythematous maculopapular rash over head and spreads distally over trunk extremities hands feet 0 early lesions blanch with pressure followed by brownish hue that does not blanch as the rash fades o Koplik spots over buccal mucosa pinpoint white spots surrounded by erythematous ring 13 days before rash Health Alteration Roseola Description exanthema subitum presumed viral infection of infants typically between 6 months and 2 years of age incubation period 515 days EtiologyRisk 0 exposure Factors Assessment prodromal Clinical o sudden onset of high fever for 35 days Manifestatio erythematous macular rash that lasts 24 hours primarily over MODULE 6 INTEGUMENTARY LAZENBY 13 ns trunk and neck 0 children typically feel well with few other symptoms Health Alteration Mumps Description 0 also known as parotitis an infection of the parotid glands structurally similar to paramyxoviruses but generally larger transmitted by droplets or direct contact treatment with potassium iodide which increases secretory activity of salivary glands EtiologyRisk vira form of disease FaCtOFS seriously ill people who do not receive adequate oral hygiene and who are unable to take po uids Pathogenesi 0 caused by paramyxovirus 5 Assessment 0 fever Clinical 0 HA Manifestatio Muscle ache 5 0 Fatigue Loss of appetite Swollen and tender salivary glands under the ears on one or both sides parotitis Diagnosis 0 Based on symptoms Complicatio 0 Extremely dangerous in adults especially males ns Holistic Implications Health Alteration Erythema infectiosum Fifth disease Description a transmission is unknown but possibly through respiratory secretions and blood incubation period is typically 414 days but may be as long as 20 days communicability may range from before symptom onset to 1 week after onset of symptoms Pathogenesi 0 caused by human parvovirus 819 HPV 5 Assessment a rash in three stages Clinical o erythema on face esp cheeks quotslapped facequot Manifestatio appearance disappears within 14 days 5 0 approximately 1 day after rash appears on face maculopapular red spots appear symmetrically distributed MODULE 6 INTEGUMENTARY LAZENBY 14 on upper and lower extremities rash progresses from proximal to distal surfaces may last a week or more 0 III rash subsides but reappears with skin irritation or trauma 0 with apastic crisis rash is usually absent and prodromal illness includes fever myalgia lethargy nausea vomiting abdominal paIn Health Alteration Scarlet Fever Description a an acute contagious disease sudden onset usually begins with a sore throat and elevated temperature vomiting followed within 1236 hours by a rash rst on the neck and chest and rapidly extending over the body nally involving the extremities incubation period 0 probably not less than 24 hours may be 13 days EtiologyRisk 0 512 years old Factors Pathogenesi a Group A strep bacteria 5 Assessment 0 sore throat Clinical o strawberry tongue Manifestatio fever ns punctiform scarlet rash sandpaper 0 rapid pulse ushed face rash duration of 23 days Health Alteration HERPES SIMPLEX HSV Description 0 viral infection of skin and mucous membranes 0 HSV type 1 is usually con ned to the oropharynx may sometimes affect the cornea and is spread by direct contact with infected saliva or respiratory droplets o HSV type 2 causes genital herpes and is spread via skinto skin mucous membrane contact during viral shedding Also vertical transmission of mother to neonate HSV 1 may be a primary or recurrent infection 0 after initial infection herpesvirus remains in trigeminal and other dorsal root ganglia in a latent state EtiologyRisk 0 stress Factors 0 sunlight MODULE 6 INTEGUMENTARY LAZENBY 15 menses o injury immunocompromised state Pathogenesi a primary infection gt production of antibodies to the virus gt S recurrent infections are more localized and less severe active lesions shed gt risk of transmission to others Assessment HSV l Clinical 0 Primary ManifestatiO 0 may be asymptomatic 5 0 increased paresthesias sensitivity mild burning prior to lesion development 0 fever sore throat painful vesicles 0 ulcers of tongue palate gingival buccal mucosa lips Recurrent 0 begins with burning or tingling sensation o vesicles and erythema gt pustules ulcers and crusts before healing 0 pain Lesions are most common on lips face or mouth HSV 2 Begins as small vesicles and progress to ulceration with pain itching weeping Diagnosis manifestations Health Alteration HERPES ZOSTER shingles Description also known as shingles acute localized vesicular eruption distributed over a dermatomal segment of the skin caused by the same virus varicellazoster that causes chickenpox incidence increases with age more frequently in people gt 60 years ofage EtiologyRisk 0 age due to decreased cellmediated immunity FaCtOFS HIV infection due to immunocompromised state certain malignancies chronic corticosteroid users 0 people undergoing cancer chemotherapy and radiation therapy Pathogenesi o reactivation of latent varicellazoster virus gt reactivated virus 5 travels from ganglia to the skin of corresponding dermatone Assessment prodrome phase with burning pain tingling sensation extreme Clinical sensitivity of skin to touch pruritus along affected dermatome Manifestatio may be present 13 days prior to appearance of rash ns MODULE 6 INTEGUMENTARY LAZENBY 16 pain and paresthesia along affected dermatome pain may mimic heart disease pleurisy musculoskeletal or GI disorders rash appears as an eruption of vesicles with erythematous base restricted to areas supplied by sensory neurons of a single or associated group of dorsal root ganglia eruptions are usually unilateral in thoracic region trunk face 0 new crops of vesicles erupt for 35 days along nerve pathway vesicles dry form crusts and eventually fall off lesions typically clear in 23 weeks Diagnosis manifestations Complicatio o blindness from eye involvement 5 postherpetic neuralgia Holistic Implications PUSTULAR Health Alteration ACNE VULGARIS Description 0 chronic in ammatory disease of pilosebaceous unit EtiologyRisk 1130 years of age Factors Male Genetic factor Increased sebum production Increased proliferation of keratinizing epidermal cells from sebaceous cells Colonization and proliferation of Proponibacterium acnes In ammation Pathogenesi 0 Increased production of androgen gt increased sebaceous cell 5 activity gt plugging of pilosebaceous ducts Increased sebum gt growth medium for P acnes which contains lipase gt breaks down fatty acids gt in ammation Assessment 0 Open andor closed comedones Clinical In ammatory papules ManifEStatio Erythematous papules and pustules 5 Nodular in amed lesions Diagnosis 0 Based on HampP Complicatio 0 P acnes can form a bio lm that may block antibiotic therapy ns Holistic Implications Health Alteration ACNE CONGLOBATA Description a Chronic form of severe cystic acne MODULE 6 INTEGUMENTARY LAZENBY 17 EtiologyRisk o Later in life Factors Assessment Comedones papules pustules nodules abscesses cysts scars Clinical back buttocks chest Manifestatio ns Comedome or cysts have multiple openings large abscesses interconnecting sinuses In ammatory nodules drainage is odoriferous serous mucoid purulent Diagnosis 0 Symptoms plus 0 Anemia o Leukocytosis esp elevated neutrophil count 0 Elevated ESR Complicatio o Progression to acne fulminans ns Holistic Implications Health Alteration ROSACEA Description a Chronic in ammatory process periods of exacerbation worsened by hot drinks and alcohol secondary to vasodilation which accentuates erythema 4 types EtiologyRisk o gt 30 years age Factors Fairskinned individuals 0 Genetic Environmental Vascular Pathogenesi o immunemediated in ammation typically on the forehead nose 5 cheeks chin in ammatory process vascular instability gt leakage of uid amp in ammatory mediators into dermis Assessment ushing nose checks may extend to forehead and chin Clinical Manifestatio ns persistent central facial erythema in ammation thickening of skin with irregular surface nodularities and enlargement telangiectases rhinophyma irregular bullous hypertrophy of the nose Diagnosis Manifestations Complicatio o Ocular involvement possible resulting in blindness ns Holistic MODULE 6 INTEGUMENTARY LAZENBY 18 Implications ALLERGIC AND HYPERSENSITIVITY Health Alteration ATOPIC DERMATITIS Eczema Description a most common in ammatory condition 0 usually begins in infancy 2530 prevalency rate 0 7580 have a family history of asthma or allergic rhinitis characterized by in ammation accompanied by papules vesicles crusts this is a 55 of some underlying condition not a disease itself worse in fall and winter prone to fungal skin infections secondary to scratching in young children face scalp trunk extensor surfaces of arms andlegs in older childrenadults neck antecubital and popliteal fossae hands feet EtiologyRisk 0 unknown Factors allergies hereditary Pathogenesi 0 may be the result of abnormal function of skin alterations in S sweating peripheral vascular function heat intolerance involves alteration in proteins that bind keratin in the epidermis and reduced stratum corneum lipid levels Assessment 0 itching Clinical o erythema Manifestatio vesides 5 papules weeping oozing crusting scaHng often symmetric clusters of small erythematous or eshcolored papules or minimally scaling patches licheni cation dry thick lesions con uent papules keratosis pilaris MODULE 6 INTEGUMENTARY LAZENBY 19 unaffected skin dry and rough more popular andor follicular lesions in black children other lymphadenopathy increased palmar creases atopic pleats prone to colds pityriasis alba facial pallor quotallergic shinersquot Diagnosis Clinical picture Positive skin tests Complicatio Repeated scratching can result in open skin increasing the risk for 5 infection Holistic Implications Health Alteration URTICARIA Description Also known as hives Cutaneous reaction against systemic allergens EtiologyRisk Factors Hypersensitivity to 0 Food 0 Drugs 0 Systemic disease 0 Physical agent Pathogenesi s Complementmediated Stimulation of lgE gt histamine release bradykinin or kallikrein from mast cells andor basophils gt contraction of endothelial cells of skin blood vessels gt increased permeability Other mediators may include lgG antibodies directed against lgE receptor and other in ammatory mediators serotonin leukotrienes prostaglandins kinins exposure to allergen gt histamine release gt vasodilation leakage of uid from skin39s blood vessels gt raised red lesions called wheals and ares due to blood vessels on wheal edge dilating augmented by SNS response gt itching caused by pruritus common causes include hypersensitivity or allergic reactions physical irritants systemic diseases Assessment Clinical Manifestatio ns ltching Circumscribed area of raised erythema with central pallor in super cial dermis Erythema blanches with pressure ltching Complicatio ns Chronic urticaria may be autoimmune or idiopathic Holistic Implications MODULE 6 INTEGUMENTARY LAZENBY 20 Health Alteration CONTACT DERMATITIS Description in ammatory response con ned to skin initiated by reexposure to an allergen to which a person had previously been exposed EtiologyRisk exposure to irritating substance Factors Pathogenesi a contact with offensive agent gt transdermal transport of antigen gt S presentation to T lymphocytes gt distribution of sensitized lymphocytes throughout the circulation gt localized reaction with subsequent exposure to offensive agent sensitization begins with rst exposure and heightens with each reexposure Assessment erythematous macules papules vesicles Clinical Manifestatio ns swollen warm area with exudation crusting intense pruritus and weeping secondary infection may occur lesions only at the site of contact Diagnosis 0 symptoms Health Alteration DRUGINDUCED SKIN ERUPTIONS Description 0 3 types 0 Erythema multiforme minor 0 StevensJohnson syndrome erythema multiforme major o Toxic epidermal necrolysis TEN most severe EtiologyRisk Hypersensitivity to meds most commonly sulfonamides FaCtOI39S anticonvulsants NSAIDS antimalarials allopurinol Pathogenesi a Full thickness of entire epidermis from dermis 5 Assessment 0 StevensJohnson syndrome erythema multiforme major Clinical 0 Round erythematous papule insect bite appearance Manifestatio ns 0 Lesions may enlarge and merge together 0 May produce small plaques 0 May become concentric zones similar to quottargetsquot outer rings erythematous with opaque white yellow or dusky center 0 Small blisters on purpuric macules Toxic epidermal necrolysis TEN o Prodromal malaise lowgrade temp sore throat o Widespread erythema 0 Large accid bullae gt loss of epidermis gt denudedpainful dermis Diagnosis Dependent on accurate patient history MODULE 6 INTEGUMENTARY LAZENBY 21 For TEN Nikolslq sign separation of surrounding tissue from dermis when pressure is applied Complicatio F amp E imbalances ns 0 Infection 0 Poor temperature control andness Holistic Implications PAPULOSQUAMOUS DERMATITIS Health Alteration PSORIASIS Description 0 chronic in ammatory disorder thought to have a genetic basis characterized by cutaneous in ammation and scaley plaque red patches of skin covered with alql silvercolored scales plaques EtiologyRisk familial predisposition HLA associated inheritance is likely FaCtOFS may be triggered by stress Pathogenesi a genetic immune reaction 5 Tcell mediated autoimmune activated Tcells gt release of in ammatory cytokines excessively rapid turnover of epidermal cells 34 days rather than 2630 gt thickened epidermis and plaque formation scaling or plague is a result of excessive epithelial growth 0 causes an extremely fast skinturnover rate the plaques are shed rapidly and underlying skin is in amed and irritated Assessment 0 usually start at in ammatory lesion Clinical Manifestatio ns welldemarcated thick silvery scaly erythematous plaque surrounded by normal skin remission and exacerbations rst lesions commonly appear in scalp sharply demarcated scaling plaques esp on scalp elbows knees may also involve palms soles ngernails may be intermittent or continuous Health Alteration PITYRIASIS ROSEA Description thought to be caused by a virus benign selflimiting EtiologyRisk Children Factors 0 Young adults Assessment rash may be preceded by headache fatigue sore throat Clinical Manifestatio begins with herald patch which is circular demarcated salmon MODULE 6 INTEGUMENTARY LAZENBY 22 ns pink usually on the trunk and develops along skin lines resembling drooping pine tree PARASITES Arthropod infestations Health Alteration SCABIES DESCI39iD EiOn 0 contagious disease via skintoskin contact caused by itch mite Sarcoptes scabiei transmitted by close personal contact and by infected clothing and bedding EtiologyRisk o overcrowded housing FaCtOFS poor sanitation immunocompromised individuals Pathogenesi female mite tunnels into stratum corneum gt deposits eggs gt 5 creates a burrow gt eggs mature into adult mites over a 3week pedod sensitization to larval stages of parasite gt itching female mites burrow under the skin and lay eggs gt larvae young mites hatch and form tiny red papules hypersensitivity rash erythematous papules may occur after about 1 month intense occur 35 weeks after infestation primary lesions are burrows papules vesicular lesions 0 severe itching that worsens at night 0 Adults lesions may occur in webs of ngers axillae creases of arms and wrists belt line around the nipplesgenitalialower buttocks Infants and young children involvement of palms soles head neck face Assessment 0 small burrow lesions red to reddishbrown Clinical pruritus Manifestatio ns Diagnosis 0 skin scraping presence of mites ova or feces ComplicatiO 0 secondary infections secondary to scratching and eczematous 5 changes itching gt scratching gt excoriation gt secondary bacterial infections Holistic Implications Health Alteration PEDICULOSIS Description head louse MODULE 6 INTEGUMENTARY LAZENBY 23 parasites that survive by sucking blood 0 female louse produces q2weeks produces hundreds of nits body lice pubic lice and head lice EtiologyRisk a close body contact FaCtOFS sharing clothing or headphones Pathogenesi a piercing and sucking mouth of lice attach to the skin gt while 5 piercing the skin gt louse secretes a toxic saliva gt mechanical trauma and toxin gt pruritic dermatitis Assessment 0 itching Clinical pinpoint red macule papule or wheal with a hemorrhagic Manifestatio puncture site 5 0 primary lesion may be masked by excoriations wheals crusts ova or nits are yellowish pinpoint specks that adhere to the hair shaft Diagnosis 0 rmly attached nits or actual lice on the hair shaft louse is gray graybrown or redbrown oval wingless insect Complicatio a skin excoriation from scratching ns Holistic Implications PRESSURE ULCERS Health Alteration PRESSURE ULCERS Description 0 localized area of tissue necrosis 0 most prevalent over bony surfaces esp sacrum heels ischia greater trochanters PREVENTION is the key turn patient at least q2h does NOT require a speci c MD order 0 most common complication is recurrence EtiologyRisk 0 pressure intensity duration especially pressure that disrupts FaCtOI39S blood flow shearing force friction excessive moisture age anemia contractures DM elevated body temp immobility impaired circulation incontinence low diastolic BP mental deterioration neurologic disorders obesity pain prolonged surgery vascular disease poor nutritional status darkly pigmented individuals Pathogenesi o unrelieved pressure gt endothelial cells lining capillaries are S disrupted gt platelet aggregation gt microthrombi gt slowed or obstructed blood flow to an area gt tissue damage or death gt MODULE 6 INTEGUMENTARY LAZENBY 24 lesions gt infection Assessment redness rst indication Clinical progresses to blanching Man39fEStat39o 0 pain fever leukocytosis ns foulodor localized infection which has the potential to become systemic staging based on appearance Classi cation 0 Stage I o Nonblanchable erythema of intact skin 0 Stage II o Partialthickness skin loss epidermis or dermis Stage III 0 Fullthickness skin loss damage or necrosis of subq tissue may extend to fascia Stage IV 0 Fullthickness skin loss amp extensive destruction tissue necrosis or damage to muscle bone supporting structures Complicatio 0 Infection ns Fluid loss 0 Altered temp control Holistic Implications VASCULAR DISORDERS Health Alteration Scleroderma DESCFIPUOH 0 also known as systemic sclerosis chronic autoimmune connective tissue disorder involving skin and other organs organ involvement may include kidney heart Peripheral nervous system GI tract lungs remissions and exacerbations cutaneous lesions typically involve face hands neck upper chest 0 women affected 4x more than men 0 peak incidence is 3550 years of age autoimmune disease of connective tissue characterized by excessive collagen deposition in the skin and internal organs 0 Types 0 Limited or localized Scleroderma MODULE 6 INTEGUMENTARY LAZENBY 25 autoimmune disease affecting blood vessels and connective tissue quothard skinquot begins as area of mild in ammation gt yellow patch of hard skin usually remains localized and mild may progress to systemic form more common in females involves skin on ngers hands face selflimited with good prognosis 0 Systemic Scleroderma involves skin of ngers hands face trunk as well as visceral organs most common visceral organs affected are esophagus intestines lungs heart kidney has the potential to progress rapidly may be lifethreatening depending on extent of organ involvement 0 CREST C calcinosis abnormal deposits of calcium salts on the skin R Raynaud39s syndrome E Esophageal dysfunction S Sclerodactyly scleroderma localized within ngers T Telangiectasis small dilated blood vessels with a brightred enter point and spiderlike branches EtiologyRisk unknown etiology FaCtOFS may be genetic immune or environmental Pathogenesi exposure to toxic substance or autoimmunity gt massive deposits 5 of collagen with brosis accompanied by in ammatory reactions vascular changes in capillary network with a decrease in the number of capillary loops and dilation of remaining capillaries evidence of both humoral and cellular immune system abnormalities overproduction of collagen gt brosis and in ammation gt damage to affected area Assessment skin Clinical o shiny thick skin on ngers hands progressing to arms Manifestatio ns trunk face 0 hard hypopigmented taut shiny tightly connected to underlying tissue gt masklike appearance of face with beak MODULE 6 INTEGUMENTARY LAZENBY 26 appearance of nose pursed lips nonpitting edema of affected areas calcium deposits on the skin teangiectasis hyperpigmentation hands are shiny and sometimes red and edematous ngers become tapered and exed often with depressed scars and loss of ngertips from atrophy vascular Raynaud39s syndrome musculoskeletal poyarthragia and joint stiffness esophageal heartburn and dysphagia intestinal constipation diarrhea malabsorption abdominal distention heart ECG changes 55 of pericarditis lungs SOB on exertion kidneys renal failure OOOOOO Diagnosis ESR elevated UA proteinuria BUN and Creatinine elevated with renal failure ANA elevated skin biopsy results indicate dermal collagen thickening con rms diagnosis PFT abnormal INJURIES Health Alteration UV RADIATION Description damage to the skin is the result of reactive oxygen being generated and damage to melanin genetics certainly play a part in skin cancers but another important variable is the sun39s UV radiation UV radiation damages DNA gt errors in mitosis gt skin cancer Health Alteration DRUGINDUCED Photosensitivity Description caused by drugs that produce an exaggerated response to ultraviolent radiation EtiologyRisk Factors common drug categories include some antiinfective agents antihistamines antipsychotic agents diuretics hypoglycemic agents NSAIDS OOOOOO MODULE 6 INTEGUMENTARY LAZENBY 27 BURNS Types of burns 1 2 3 Thermal most common type thermal contact ame or scald 6080 are the result of scalding or ame depth depends on temperature of burning agent and duration of contact tissue destruction RT coagulation CHON destruction and ionization of cellular content initial systemic effect is burn shock hemodynamic instability due to loss of capillary integrity gt uid shift intravascular to interstitial gt less vascular volume gt CO decreased gt decreased BP gt sympathetic nervous system response gt peripheral resistance gt elevated HR and decreased pulse pressure Electrical Burns result of electrical current conduction and resultant heating of tissue or esh produces a cutaneous injury that is much worse than it looks lowvoltage electricity takes path of least resistance highvoltage takes direct path less resistance to greatest resistance nerve blood muscle skin tendon fat and bone the greater the resistance the more heat is produced as the electricity passes through entry and exist wounds deep tissue destruction entry wound usually charred and has adherent eschar exit wound is larger than entry and may have an explosive appearance cardiac abnormalities usually occur at contact with electrical source C minor dysrhythmia to complete cardiac arrest muscle tetany may cause anoxia vascular damage causes uid leakage delayed hemorrhage may occur in areas of extensive necrosis RBC destruction gtgtgt hematuria for several days muscle damage gtgtgt myoglobin release gtgtgt glomerular and tubular damage stress ulcer EEG changes and occasional unconsciousness rarely spinal cord injuries may have a fracture due to fallsevere muscle contraction watch for cataract formation for up to 3 years Chemical Burns result of contact with substance that is toxic to the skin or the lining of respiratory or alimentary tract chemical agents react with tissue and form thermal energy gtgtgt denatures the CHON MODULE 6 INTEGUMENTARY LAZENBY 28 injury range minor blisters to cell damage and sloughing extent of damage depends on concentration of agent quantity of agent length of exposure mechanism of action and depth of penetration Some chemicals may damage organs even though there is no external evidence of damage CLASSIFICATION OF BURNS based on depth Traditional Terminoloov Anatomic Depth of Involvement 1St degree Epidermis partialthickness 2nCI degree lntradermal super cial partialthickness Deep dermis deep partialthickness 3rCI degree Subdermis full thickness partialthickness rst degree affects super cial dermis 0 skin is pink or red dry painful ex sunburn o no blistering initially may have slight edema 0 affected dermis is shed in about 1 week no scarring super cial partialthickness second degree 0 involves part of the dermis o thinwalled uid lled blisters developing within minutes post injury 0 pain 0 deep partialthickness second degree involves dermis and epidermis prolonged exposure gt10 seconds to intense heat ashes or prolonged contact with hot objects or liquid 0 blistered or wet wound painful red blanches and re lls with pressure waxy white surrounded by super cial partialthickness burns local super cial edema unburned areas may have some edema heals in 23 weeks with little to no scarring unless trauma or infection 0 if deep layer of dermis is affected may need skin graft fullthickness burn destroys dermis and epidermis gt skin cannot regenerate can involve subcutaneous and fat facia tendon and bone 4th degree requires skin grafting o varies in color white to black or charred may have dark network of thrombosed capillaries 0000 0 dry and leathery due to denatured protein covering of eschar o if red does not blanch with pressure 0 dermis elasticity is gone 0 as edema forms distal circulation may be compromised in areas of circumferential burns 0 not painful due to damaged nerves 0 wound edges are painful o escharotomies to release underlying pressure BURN ASSESSMENT First degree burns are not included in total body surface area TBSA MODULE 6 INTEGUMENTARY LAZENBY 29 0 Different assessmentdocumentation tools try to document depth and total area involved 0 Rule of nines Lund Browder chart Fluid resuscitation is based on burn size either in or BSA or in actual burned BSA Severity is also based on age medical history extent and depth of injury body area involved 0 gt20 burned area in an adult is considered to be a major burn EFFECTS ON BODY SYSTEM lntegumentary destroys epidermis gt escape of tissue uids and entry of potential pathogens dermis burned gt epidermal appendages hair follicles sebaceous and sweat glands cannot regenerate clients may have varying degrees of burns depending on duration and source of exposure Cardiovascular burn injury gt outpouring of catecholamines gt peripheral blood vessel constriction but because of injury to the vessels gt vessels more permeable gt leakage of uids and colloids into surrounding tissue gt trapping of uid in interstitial spaces gt edema gt colloids cross into interstitial space gt more uid follows as a result of changes in oncotic pressure gt within several hours gt relative hypovolemia greatest uid leakage occurs in the rst 2436 hours with peak at 12 hours successful uid resuscitation 0 CO returns to normal at the end of the rst 24 hours 0 becomes hypermetabolic during the second 24 hours 0 capilary integrity is restored between 3rd and 5th postburn day and diuresis begins 0 initial vasoconstriction traps RBCs and makes them unavailable to the body 0 uid losses to environment and interstitial space gtgtgt relative hemoconcentration as blood cells are too large to cross the permeable capillary membrane hemoconcentration gt increase in hematocrit and increased blood viscosity gt slowed blood ow gt altered peripheral tissue oxygenation and nutrition and venous stasis gt possible further tissue destruction 0 RBC destruction may begin in the injury itself gt hemolyzed cells die and decompose decreased circulating blood volume gt decreased CO and inadequate tissue perfusion or cellular hypoxia gt shifts cellular metabolism from aerobic to anaerobic gt acidosis from a buildup of lactic acid gt further structural damage and irreversible shock Interference with acidbase homeostasis MODULE 6 INTEGUMENTARY LAZENBY 30 o 1when plasma escapes into the interstitial space bloodborne buffers are removed from the vessels and are not available to achieve acidbase homeostasis o 2smoke inhalation or circumferential eschar may cause increased C02 and hypoventilation o 3decreased CO may impair renal function and cause the excessive elimination of bicarbonate burn injury gt cellular destruction gt intracellular uid released gt K is released gt possible lifethreatening cardiac dysrhythmias once capillary integrity restored the client may excrete large amounts of K via kidneys Pulmonary facial and neck edema may threaten the airway and require intubation uid shifts and uid replacement gt pulmonary edema which should subside when diuresis begins and resolve within a few weeks closure of glottis helps reduce burns of pulmonary parenchyma but can occur esp with steam inhalation very hot air gt damage upper airway burns of oral mucosa palate and pharynx inhalation is the most common type of lung damage inhalation of smoke burning materials etc can cause mucosal sloughing changes in pulmonary capillary permeability in ammation and pulmonary edema re consumes all oxygen and the client inhales carbon monoxide gt asphyxia smoke inhalation gt diminished surfactant atelectasis decreased air exchange uid resuscitation gt edema formation gt deceased tracheal width gt decreased volume of air exchange uid resuscitation gt increased amount of uid accumulation in the lungs presence of foreign substance gt the client is at a great risk for developing bonchopneumonia Renal System hypovolemia gt renal artery constriction gt decreased glomerular ltration rate gt oliguria B this problem is intensi ed by the secretion of ADH from the posterior pituitary as body tries to conserve blood volume RBC gt hematuria but should resolve within 24 hours if not suspect acute glomerular or tubular damage if muscle is involved in burn injury gt myoglobin released from muscle cells gt myoglobin in the urine gt acute tubular necrosis may also experience glycosuria but it should clear with resuscitation clients with preexisting renal problems are at a very high risk watch for decreasing U0 and elevated BUN and creatinine Gastrointestinal Svstem trauma gt catecholamine release gt decreased enteric circulation gt slowcessation of peristalsis gt intestinal gases accumulate gt NampV aspiration MODULE 6 INTEGUIVIENTARY LAZENBY 31 hypovolemia gt gastric dilation and paralytic ileus B may resolve within 2436 hours also at risk for development of Curling s Ulcer gastroduodenal stress ulcer may have black stools may have blood in stools ischemia and irritation gt local capillary engorgement and mucosal sloughing gt gastric bleeding early and duodenal bleeding later Metabolic increased catecholamines in blood and urine increased cortisol glucogan insulin increased gluconeogenesis lipolysis proteolysis Additional Svstem Involvement rapid RBC destruction in the wound gradual hemolysis of damaged cells gt bone marrow releases new erythrocytes burn injury gt release of catecholamines gt increased WBC B but phagocytic function is altered as they become trapped in the intravascular uid initially platelets are destroyed but after about 5 days they increase in number and post a threat of vascular thrombosis hypoxia of hypovolemia or inhalation injury and the psychogenic shock of the brain trauma gt altered mental status mental changes are one of the primary indicators of the adequacy of circulating blood volume or the incidence of carbon monoxide poisoning stress gtof burn stimulation of anterior lobe of pituitary to produce adrenocorticotrophic hormone ACTH gt stimulation of adrenal cortex gt increase in glucose levels ACTH also stimulates epinephrine and norepinephrine that causes ght or ight burn injury gt hyper metabolism increased glucose flow and severe CHON and fat wasting metabolic rates of severely burned clients can be as high as 200 of normal abnormal production and use of glucose B with increased catecholamines the client exhibits a type of insulin resistance B the wound uses a lot of glucose and new glucose is derived from muscle protein in the wound nutrition is of vital importance in the healing process energy needs for maintaining weight nitrogen balance and energy equilibrium may exceed 5000 kcal24 hr to offset massive CHON breakdown INFECTION leading cause of death in those who survive the burn burns destroy the body s rst line of defense inhalation injuries often gt pulmonary infections eschar which is a leathery covering of denatured CHON on a fullthickness burn is excellent medium for bacterial growth severe burns initiate venous stasis microthrombi formation immunosuppression burn injury gt change in blood ow and viscosity gt barrier formation between bacteria and the body s own phagocytes gt interference with the delivery of 02 antibodies and phagocytes to the injured area MODULE 6 INTEGUIVIENTARY LAZENBY 32 neutrophils are altered such that phagocytosis may occur but the bacteria may not die gt gt excellent environment for harboring and multiplying organisms SKIN CANCERS Accounts for about 40 of all cancers Basal cell and squamous cell are the most common Malignant melanoma is the most serious Most important signs of cancer persistent nonhealing ulcer friable bleeding tissue in an ulcer ulcer or nodule of irregular shape and indistinct margins induration of tissue around an ulcer irregularly textured multicolored tissue at bottom of an ulcer indurated skin surrounded by atrophic and keratotic skin typical of sunlight Injury Epithelial Tumors seborrheic keratosis is the most common benign tumor 0 brown solitary or multiple mulberryshaped wartlike attopped corrugatedfurrowed surface 0 loosely attached to skin 0 friable o easily removed basal cell carcinoma 0 usually occurs on upper face 0 less likely to metastasize o malignancy begins in cells at base of epidermis usually begin as papules that erode in the center and form a bleeding crusted crater most common malignant epithelial tumor does not metastasize located on sunexposed skin major risk factor is UV radiation exposure other factors include arsenic and genetic factors 0 slightly elevated nodule with depressed center 0 surface has a pearly appearance and crisscrossed with telangiectatic capillaries o tendency to bleed 0 usually occur above upper lip line 0 treatment includes surgical resection cauterization or radiotherapy with excellent results squamous cell carcinoma 0 slowgrowing malignant tumor of the epidermis most common type of skin cancer lesions are hard raised painless nodules has the potential to metastasize to other organs truly malignant usually occur below lower lip line MODULE 6 INTEGUIVIENTARY LAZENBY 33 00000 0000 00000 sunlight induced lesions risk factors include UV exposure arsenic gamma rays xrays present as at plaque invasive type typically arises from premalignant lesions such as dysplasias scars keratosis etc small persistent ulcer or slightly elevated keratotic plaque may be preceded by actinic keratosis in ltratinglocally invasive early diagnosis is the key biopsy all suspicious ndings Malignant Melanoma Warning Signs of Malignant Melanoma ABCD Rule Asymmet Benign moles are symmetrical their halves are mirror images of each ry other Melanoma lesions are asymmetrical or lopsided Border Benign moles are outlined by a distinct border but malignant melanoma lesions are often irregular or indistinct Color Benign moles may be any shade of brown but are relatively evenly colored Melanoma lesions tend to be unevenly colored exhibiting a mixture of shades or colors Diameter By the time a melanoma lesion exhibits characteristics A B and C it also probably is larger than 6 mm 14 inch fastest increasing cancer in the US 0 most serious form of skin cancer 0 increasing incidence especially in young to middleage adults 0 risk factors genetic predisposition UV exposure steroid hormone activity fair hair light skin 0 O 0 death rate 1 in every 4 cases sometimes develops from a pigmented mole gtgtgt dark spreading lesion early detection and removal are the key to prevent rapidly spreading cancer originates from melanocytes most malignant skin tumor half arise from intact skin and about half arise from freckles or nevi lentigo maligna are at macular lesions super cial spreading melanoma composes approximately 70 most common melanoma irregularly pigmented macules with irregular edges pruritic legs in women and back in men nodular melanoma O O rapidly growing in ltrating variant of malignant melanoma 0 vertical growth with invasion of dermis acrallentiginous melanomas o develops on palms and plantar surfaces or underneath nails 0 most common variant in blacks and Orientals MODULE 6 INTEGUIVIENTARY LAZENBY 34 0 Clinical Features A ssemetry of pigmented lesion intermixed raised and at areas B orders irregular C olor marked color variance Diameter of lesion usually gt 6mm EARLY diagnosis vitally important Dermal Connective Tissue Tumors usually benign and arise from broblasts blood vessels other structures dermato broma is the most common Kaposi s Sarcoma 0 most prevalent malignant lesion in AIDS patients 0 red tumor 0 hemorrhagic nodule 0 multiple and con uent MODULE 6 INTEGUMENTARY LAZENBY 35