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Pathophysiology- Neurological System

by: Shelby Stephens

Pathophysiology- Neurological System NUR 305

Shelby Stephens
GPA 3.5

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This 31 page Study Guide was uploaded by Shelby Stephens on Wednesday December 9, 2015. The Study Guide belongs to NUR 305 at University of Alabama - Tuscaloosa taught by Owings in Fall 2015. Since its upload, it has received 35 views. For similar materials see Pathophysiology in Nursing and Health Sciences at University of Alabama - Tuscaloosa.

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Date Created: 12/09/15
Endocrine System Three general functions:  Growth and development  Reproductions  Maintenance—homeostasis Uses of negative and positive feedback systems to regulate hormone release  Negative feedback= thyroid system  Positive feedback= childbirth  Hormones exert action by interacting with target cells on glands and tissues and causes some kind of change/ activity within those cells  Liver metabolizes hormones  Kidneys secrete hormones Hypothalamus:  Regulates the pituitary gland  Connects the nervous and endocrine system  These receptors stimulate the hypothalamus to secrete releasing and inhibiting hormones  The brain controls the posterior pituitary gland Pituitary gland:  Size of a pea  Divided into the anterior and posterior parts  Anterior pituitary hormones: o Luteinizing hormone (LH) o Follicle Stimulating hormone (FSH) o Thyroid stimulating hormone (TSH) o Prolactin (PRL) o Growth hormone (GH) o Adrenocorticotrophic hormone (ACTH)  Adrenal cortex hormones: cortisol, aldosterone, androgens  Posterior pituitary hormones: o Antidiuretic hormone (ADH) o Oxytocin (OT) What is the final target of each hormone?  FSH and LH= reproductive system  TSH= thyroid  T4= all the tissues and cells of the body  GH= all the tissues and cells of the body  ACTH= adrenal glands  ADH= kidneys  OT= uterus for uterine contractions  PRL= breasts Anterior Pituitary Mnemonic Posterior Pituitary FLAT PiG There are 2 hormones and 2 P’s in Posterior Pituitary Follicle stimulating ADH and Oxytocin Luteinizing Adrenocorticotrophic Thyroid stimulating Prolactin ignore Growth Pancreas:  Lies underneath the stomach between kidneys and the retro peritoneum  Exocrine functions= secrete a sodium bicarbonate solution and digestive enzymes into the duodenum of the GI tract o Glands are released through ducts  Endocrine functions= release of insulin and glucagon  Contain ~1 million islets  Each islet of Langerhans contains o Alpha cells= secrete glucagon o Beta cells= secrete insulin and amylin o Delta cells= secrete somatostatin o F cells= secrete a pancreatic polypeptide o Epsilon cells= secrete ghrelin Thyroid Gland:  Located at the base of the neck below larynx  Two lobes on either side of the trachea  Vascular gland that produces: o Thyroxine (T4) o Triiodothyronine (T3) o Thryro-calcitonin (calcitonin)  The hypothalamus stimulates the pituitary gland to produce the thyroid-stimulating hormone (TSH), which stimulates T and 3 4  T 3nd T (45% of circulating thyroid hormones) regulate cellular metabolism as well as growth and development  Iodine is required to synthesize thyroid hormones  Calcitonin is secreted when serum calcium levels are high—calcium is stored (in the bones).  If calcium levels are high in the blood stream the body senses it. The thyroid gland has C cells that secrete calcium, to tell it to get back into the bones  If calcium levels are low, the parathyroid glands release PTH to make calcium be released from the bones to be put into the blood stream Parathyroid Glands: • Usually four located on the posterior surface of the thyroid • Secretes the parathyroid hormone (PTH) • PTH is secreted when serum calcium levels drop. Mechanism? o Increase osteoclast activity— how calcium is released from bone. o Absorption of calcium increases in GI tract & the kidneys. Adrenal Glands: • Located on top of each kidney • Have an inner and outer region • The Medulla and the Cortex • Medulla = inner portion that produces epinephrine and norepinephrine Adrenal Cortex: • Adrenocorticotrophic Hormone released from anterior pituitary---travels to the adrenal cortex--- • Secretes the following hormones: – Glucocorticoids (Cortisol) – Mineralocorticoids (Aldosterone) – Adrenal androgens and estrogens (male & female hormones). Anterior Pituitary Gland TSH ACTH GH thyroid adrenocorticotrophi growth stimulating c hormone hormone Posterior hormone Adrenal Pituitary Thyroid Acromegaly/ Antidiureti Gland Cortex Parathyroidsm – Cortisol, Toomuch! c T3 and Aldosterone, Gland Hormone T4 Androgens Parathyroi [ADH] Toodlittle! Syndrome of Hyperthyroidis Cushing’s – Inappropriate m – Too much! Hormone Antidiuretic Too much! [PTH] Hormone Hyperparathyroidi [SIADH] – Too Hypothyroidis Addison’s – sm much! m – Too little! Too little! - Too much! Diabetes Hypoparathyroidis Insipidus [DI] – m HYPOPITUITARISM: • Rare, complex condition. • The pituitary gland does not produce sufficient amounts of some or all of its hormones •    Causes: o Congenital defects o Cerebral or pituitary trauma (very common) o Autoimmune conditions o Pituitary tumors o Hypothalamic dysfunction  POSTERIOR PITUITARY: o Diabetes Insipidus (DI)  ANTERIOR PITUITARY: o Hypothyroidism o Addison’s Disease o Dwarfism Diagnosis: o Physical exam o Lab tests—hormones in the blood stream Treatment: o Lifelong hormone replacement o Resolve underlying cause o Infertility treatment, counseling POSTERIOR PITUITARY Diabetes Insipidus:  Deficiency of Anti-Diuretic Hormone (ADH) • Results in the excretion of large amounts of dilute urine. • Distal kidney tubules & collecting ducts require ADH to reabsorb water polyuria and dehydration • Signs & symptoms of dehydration and hypovolemia •    Manifestations: • Hypotension, Tachycardia • Increased urine output • Dry mucous membranes • Poor skin turgor, lethargy • Hyperthermia • Diluted urine and concentrated blood!!! ANTERIOR PITUITARY Hypothyroidism: • When the ANTERIOR PITUITARY IS THE CAUSE= hypo-metabolic state caused by decreased thyroid hormones (T3 & T4) from decreased TSH •    Causes: o Decreased TSH from the anterior pituitary o Decreased T3 & T4 from the thyroid itself • Relatively common-- 1 out of 500 Americans has the condition • May be a result of hypothalamus, pituitary, or thyroid dysfunction o Risk factors: advancing age o Causes: autoimmune thyroiditis (also called Hashimoto’s thyroiditis), increased age, and iatrogenic (don’t know the cause) Manifestations: **Slows everything down**  Fatigue and sluggishness, depression  Increased sensitivity to cold  Constipation  Weight gain and muscle weakness  Heavy periods  Hair loss and thinning  Bradycardia and hypotension  Goiter Diagnosis: o Medical history o Current history of illness o Physical assessment o Lab work (T , 3 ,4TSH) Labs: o T3, 4 are decreased o TSH level is high Treatment:  Thyroid hormone replacement, weight management, constipation measures, and avoidance of cold temperatures What can happen? Goiter: • Visible enlargement of the thyroid gland • Can occur in hyperthyroidism, hypothyroidism, and normal thyroid states • Causes: o Iodine deficiency---outside of US o Over or under production of thyroid---in the US Myxedema Coma:  Rare, serious complication of untreated/ poorly treated hypothyroidism  LIFE THREATENING—high mortality rate Manifestations: o Severe hypotension o Respiratory depression—low shallow breathing o Hypothermia o Lethargy o Coma  Heart muscles become flabby and weak  Heart chamber dilate  Results in decreased cardiac output and tissue perfusion—brain and vital organs  Hypoxia ischemia necrosis Addison’s Disease: Causes: o Anterior pituitary problem= less ACTH means there will be less cortisol and aldosterone released from the adrenal cortex o Adrenal cortex problem= due to autoimmune disease, results in less cortisol and aldosterone o Infections o Hemorrhage o Tumors Manifestations: o Hypotension and changes in heart rate o Hypoglycemia, hyperkalemia, hypotremia o Anorexia, weight loss o Weakness, fatigue, slow movement, mood changes, depression o Chronic diarrhea  Patient cannot respond to stressors when needed—cortisol is the stress hormone Treatment: o Lifelong hormone replacement o Wear a medical alert bracelet o Carry extra medication Dwarfism: • Decrease in bone size caused by decreased (slow or delayed) GH levels. • Because GH produced by the anterior pituitary DIRECTLY stimulates tissues, irregularities in GH are always a direct cause of anterior pituitary disease. •    Manifestations: o Average trunk size with very short limbs o Short fingers o Limited mobility at joints o Normal intellectual functioning HYPERPITUITARISM: • The pituitary gland (anterior & posterior) secretes excessive amounts of one or all of the pituitary hormones • Most commonly caused by tumors that secrete hormone or hormone- like substances • Progressive disorder that can occur suddenly but usually develops slowly • POSTERIOR PITUITARY: o Syndrome of inappropriate ADH • ANTERIOR PITUITARY: o Hyperthyroidism o Cushing’s Disease o Acromegaly/ Gigantism •    Diagnosis: o History o Physical exam o Labs Treatment: o Tumors—surgery, radiation, chemo o Hormone analogues to inhibit hormone production POSTERIOR PITUITARY Syndrome of Inappropriate ADH (SIADH): • Increased renal water retention caused by EXCESSIVE ADH. • As a result of excess levels of ADH, the body retains TOO MUCH fluid The kidneys reabsorb too much water back into the body •    Manifestations: o Focus around over-hydration and fluid overload. o Hypertension, bounding pulses, mental status changes, headaches, edema (generalized) o Weight gain o Diluted blood o Hyponatremia (changes in sodium affect the neuro system) o Decreased urine output o Concentrated urine •    Treatment: o Treat underlying cause (head trauma, drugs, malignant tumors) o Restrict fluids to 800-1000ml/day o In some situations may use diuretics is Na+ > 125mEq/dL o Hypotonic solution= 3% NaCl is only used in severe hyponatremia (can cause dangerous fluid shifts, risky) ANTERIOR PITUITARY Hyperthyroidism: • A condition of excessive levels of thyroid hormones, resulting in a hyper metabolic state •    Causes: o Excessive iodine o Graves’ disease- autoimmune disorder; produce too much T3 and T4 o Nonmalignant thyroid tumors- produce T3 and T4 o Thyroid inflammation o Taking large amounts of thyroid hormones Manifestations: o Wide-eyed, startled look” o Restlessness, Irritability, Fatigue o Size & symmetry of thyroid gland o Muscle tremors & weakness (esp. noted in the hands) o Hair and skin (fine, silky hair, and smooth, warm, moist skin) o Visual changes- (exophthalmoses: bulged eyes, blurred vision, diplopia: double vision) *May be the earliest sign o Unexplained weight loss o Increased appetite o Increase in frequency of bowel movements o Heat intolerance, Diaphoresis (sweating) o Palpitations (feel your heart beating fast & strong), Chest pain (cardiovascular effects), Dyspnea o Decreased menses/amenorrhea Diagnosis: o History, physical examination, o Labs: serum thyroid hormone levels (T , T 3, 4erum TSH o Diagnostic tests: radioactive iodine uptake test and thyroid scan Treatments: o Medications: radioactive iodine, anti-thyroid agents, medications to slow the heart rate (beta blockers) o Surgery: if nothing else works o Manage symptoms: cool compresses, wearing sunglasses, eye lubricants, and elevating the head of the bed). o Increase caloric and calcium intake. What can happen? Thyroid Storm:  A life-threatening event that occurs in patients with uncontrolled hyperthyroidism  A sudden worsening of hyperthyroidism symptoms that may occur with infection or stress  Excess thyroid hormone release-à dramatic increase in metabolic rate Manifestations: o Fever o Tachycardia o Hypertension (systolic: top number is going to be high) risk for heart attack and stroke Cushing’s Disease:  Excessive glucocorticoids (cortisol) are released due to increased ACTH levels from the anterior pituitary.  Cortisol is the body’s STRESS hormone  Can also exist from increased ACTH levels from the anterior pituitary OR from increased cortisol from the adrenal cortex itself Causes: o Iatrogenic from indigestion of glucocorticoid medications o Adrenal tumors that secrete glucocorticoids o Pituitary tumors that secrete ACTH and cortisol Manifestations: o Obesity (especially around the trunk) o “Moon” face, “buffalo hump” o Insulin resistance, hypertension, edema o Acne, purple striae, thin skin that bruises easily o Hirsutism o Mood changes and psychosis o Muscle weakness, osteoporosis o Delayed growth and development  Treatment: o Syndrome—gradual tapering of any glucocorticoids o Disease caused by tumor—radiation and surgery Gigantism:  Caused by excess production of growth hormone  Occurs in children and adolescents o Can reach very tall heights until the epiphyseal growth plates close  Tall statue, long bones  Increased tissue in the body puts a strain on the cardiovascular system can lead to heart failure Mechanism: o GH is released by the anterior pituitary o Travels to the liver where it is converted to its active form o Travels to all of the cells/ tissues Acromegaly:  Excess GH in adulthood  Occurs in adults after the epiphyseal plates close  Facial features get heavy and course appearing  Bones thicken  Feet and hands get large  Increased tissue puts a strain on the cardiovascular system to perfuse the extra tissues heart failure Diabetes Mellitus: • A group of conditions characterized by hyperglycemia resulting from defects in insulin production, insulin action, or both • Approximately 24 million Americans have diabetes • An estimated 220 million people worldwide have diabetes • Most common in people over 60 years of age, American Indians, African Americans, Hispanics, and those living in the Southeast region of the United Sates • A significant contributor to mortality and health care cost •    Manifestations: **Three P’s** ** Hot and dry, sugar high** o Polyuria- pee a lot o Polydipsia- drink a lot o Polyphagia- hungry a lot o Hyperglycemia o Glucosuria- glucose in urine o Weight loss- glucose cant get into cells, cells are still hungry for energy but there is none o Blurred vision Diagnosis: o History o Physical examination Labs: o Random blood glucose test o Fasting blood glucose test o Hemoglobin a1c- one of the standard blood tests o Urinalysis o Cholesterol panel o Oral glucose tolerance test (used more in pregnant ladies) Type 1= insulin dependent and juvenile onset  Develops when the body’s immune system destroys pancreatic beta cells  Must have insulin—without it, glucose builds up and levels get higher o Can go into diabetic ketoacidosis  Risk factors: o Those with tissue types HLA-DR or HLA- DQ o Having a parent with it  Autoimmune: o Beta cell destruction leads to absence of insulin, may be autoimmune or due to pancreatic disorder. Certain viral infections (mumps, congenital rubella, and coxsackievirus infection). o Autoantibodies are found in the first 2-3 months after initial diagnosis Type 2= non-insulin dependent and adult onset  90-95% of all newly diagnosed cases  Begins as insulin resistant then the pancreas gradually loses its ability to produce insulin  Decrease in insulin receptors on the cells are not working properly or obesity  Hyperglycemia results from 3 general causes: o Excessive liver glucose production o Reduced glucose uptake in the cells o Increased rate of gastric emptying = more glucose dumped into the circulation quickly.  As food travels into the GI tract and glucose is being absorbed; if GI tract is fast… Glucose is being absorbed faster Onset: o More insidious, sometimes they present with infections (yeast, fungal, wounds) o Have the same symptoms as Type I except there is no ketone in the blood and urine o Slower onset of the symptoms. o In times of great stress or illness are at risk for Hyperglycemic Hyperosmotic State (sometimes called hyperglycemic hyperosmotic non-ketonic syndrome or HHNKS) Treatment: o Blood glucose monitoring o Oral anti- diabetic medication o Insulin for type 2 DM not controlled by oral medication. o Lifestyle modifications include: diet, exercise, stress reduction o Control-minimize hyperglycemia and hypoglycemia o Normal range of blood glucose is 70-110mg/dL. o Their blood glucose goal-depends (preferably in the normal range and above 70mg/dL HbA1c levels < 7% Gestational Diabetes: • A form of glucose intolerance diagnosed during pregnancy • Treatment usually includes lifestyle changes and insulin • 5–10% of women will be diagnosed with diabetes, usually type 2, immediately following pregnancy • Women who have had gestational diabetes have a 40–60% chance of developing diabetes within 5–10 years Type 1 Type 2 1. Abrupt onset 1. Slow onset 2. Weight loss 2. No to little weight loss 3. Acidosis 3. No acidosis 4. Kussmaul’s respiration—breath 4. No Kussmaul’s or faster and deeper hyperventilation 5. Hyperventilation The 3 emergencies of Diabetes 1. Diabetic Ketoacidosis 2. Hyperglycemic-Hyperosmolar state (HHS) 3. Hypoglycemia ** All three problems require emergency treatment and can be fatal if treatment is delayed or incorrect** 1. Diabetic Ketoacidosis • Occurs as the initial presentation of type 1 Diabetes Mellitus o Illness or infection puts them at risk for DKA o The body needs more glucose and insulin in times of stress • Polyuria • Polydipsia • Polyphagia • Weight loss (20 lbs. or more over 2-3 months) • Extreme fatigue & irritability • Abdominal pain, nausea, vomiting 2. Hyperglycemic- Hyperosmolar State (HHS)  More likely to occur in noncompliant Type 2 Diabetes Mellutis or in times of illness or infection.  Any of the type 1 symptoms  Blurred vision  Cuts/bruises that are slow to heal, frequent infections  Tingling/numbness in the hands/feet  Recurring skin, gum, or bladder infections 3. Hypoglycemia  Glucose is used up and not replenished or patient receives too much insulin.  Glucose is essential for brain function-the only fuel it uses  “Cold and clammy, need some candy” (sugar) Glucose Regulation: • The healthy pancreas balances insulin and glucagon secretion according to the needs of the body. o High glucose levels  Insulin causes uptake of glucose by the cells  After we eat meals o Low glucose levels  Glucagon causes breakdown of glycogen by the liver into glucose o Other hormones that increase glucose levels:  Epinephrine, norepinephrine, growth hormone, and cortisol Hypoparathyroidism: • Maintain calcium and phosphate balance. • Condition in which the parathyroid gland does not produce sufficient amounts of PTH •    Causes: o Congenital defects (a lack of one or more of the four parathyroid glands) and damage (e.g., surgery, radiation, or autoimmune conditions) • Complications: o Hypocalcemia, hyperphosphatemia, hypomagnesemia, and metabolic alkalosis •    Manifestations: o Paresthesias of fingertips, toes, and lips o Muscle twitching or spasms o Fatigue, weakness o Abd cramping o Patchy hair loss o Dysrhythmias o Anxiety, nervousness, depression, or mood swings o Headaches, memory loss Hyperparathyroidism: • Condition of excessive PTH production by the parathyroid glands • Causes: o Tumors o Hyperplasia o Chronic hypocalcemia (renal failure) • Complications: hypercalcemia, hypophosphatemia, hypermagnesemia, and metabolic acidosis •    Manifestations: o Osteoporosis o Renal calculi o Polyuria o Abdominal pain o Constipation o Fatigue, weakness o Flaccid muscles o Dysrhythmias, hypertension o Depression, forgetfulness, o Bone and joint pain o Nausea, vomiting, and anorexia Pheochromocytoma: • Rare tumor of the adrenal medulla that excretes epinephrine and norepinephrine • Results in excessive SNS stimulation • Can be life threatening • Rarely malignant •    Manifestations: o Hypertension o Tachycardia o Forceful heartbeat o Profound diaphoresis o Abdominal pain o Sudden onset of severe headaches, anxiety, feeling of extreme fright, pallor, and weight loss •    Complications: o Hypertensive crisis o Stroke o Renal failure o Psychosis, Seizures • Treatment: o Surgery and Antihypertensive medications Cardiovascular Functions:  Delivers vital oxygen and nutrients to cells   Removes waste products  Transports hormones Branches:     Systemic ­ Carries blood throughout the body to meet the body’s needs and remove waste products ­ Includes arteries, veins, and capillaries ­ Works with the lymphatic system     Pulmonary ­ Carries blood to and from the lungs for gas exchange Heart:  Pericardium ­ Surrounds the heart to provide protection and support     Myocardium ­ Cardiac muscle      Endocardi m ­ Inner structures, including the valves     Four Chambers ­ Two Atria – receiving chambers ­ Two Ventricles – pumping chambers Blood flow through the Heart—Systemic:   Blood from the systemic circulation enters from the superior vena cava and the inferior vena cava   Blood empties directly into the right atrium  From the right atrium, blood travels through the tricuspid valve to the right ventricle  The right ventricle pumps blood through the pulmonic valve to the pulmonary arteries  The pulmonary arteries carries blood to the lungs for gas exchange   Blood flow through the Heart—Pulmonary:  Blood from the pulmonary circulation enters from the pulmonary veins  Blood empties directly into the left atrium  Blood leaves the left atrium through the mitral valve to the left ventricle  The left ventricle then pumps blood through the aortic valve to the aorta  From the aorta the blood is carried the rest of the body Conduction System:  Organizes electrical impulses in the cardiac cells  Involves ­ Excitability – ability of the cells to respond to electrical impulses ­ Conductivity – ability cells to conduct electrical impulses ­ Automaticity – ability to generate an impulse to contract with no external  nerve stimulus *** Mechanical contractility FOLLOWS electrical conduction. One cannot exist without the other!!!*** Conduction Pathway:  Impulses originate in the sinoatrial (SA) node (PACEMAKER) high in the right  atrium at a rate of 60­100 bpm  Impulses travel through the right and left atrium (internodal pathways), causing atrial contraction  Impulses then travels to the  atrioventricular (AV) node, in the right atrium adjacent to the septum  Impulses are delayed in the AV node to allow for complete ventricular filling   Impulses then move rapidly through the bundle of His, right and left  bundle branches, and Purkinje network of fibers, causing ventricular contraction  The AV node can initiate impulses if the SA node fails 40–60 bpm  The ventricles can initiate impulses if the SA and AV nodes fail 20­40 bpm,   which may be inadequate Electrical Activity:     Depolarization  ­ Increase in electrical charge ­ Accomplished through cellular ion exchange ­ Generates cardiac contraction     Repolarization ­ Cellular recovery ­ Ions returning to the cell membrane in preparation for depolarization  Can be read by an electrocardiogram ­ P wave – atria depolarization ­ QRS complex – ventricular depolarization ­ T wave – ventricular repolarization      Sinus rhythm  ­ Electrical activity when impulses originate in the SA node     Dysrhythmias  ­ Abnormal electrical activity ­ Can result from issues such as myocardial infarctions and electrolyte  imbalances Conduction Control:  Electrolyte signals ­ Sodium, potassium, and calcium  Medulla monitoring ­ Autonomic nervous system, endocrine system, chemoreceptors, and  baroreceptors  Effects  ­ Chronotropic – rate of electrical conduction  ­ Dromotropic – rate of contraction ­ Inotropic – strength of contraction  Blood Pressure vs. The Cardiac Cycle: Blood Pressure  Force that blood exerts on the walls of blood vessels  Reflects the how hard the heart is working  Represented as a fraction  ­ Systolic – top number; cardiac work phase  ­ Diastolic – bottom number; cardiac rest phase  ­ Example:  132/82  Pulse pressure (~40)­difference between the two numbers ­ Reflects force of each contraction The Cardiac Cycle  Influences on Blood Pressure:  BP = CO x PVR  Cardiac output (CO)   Peripheral vascular resistance (PVR) ­ Sympathetic nervous system ­ Parasympathetic nervous system ­ Arterial elasticity Cardiac Output (CO): CO= SV x HR  CO = THE VOLUME OF BLOOD EXPELLED FROM THE LEFT  VENTRICLE OVER A MINUTE.  The cardiac output is the gold standard  measure of the heart’s effectiveness.  The heart is a PUMP.  A normal CO is 5­6  L per minute.  What determines the CO? ­ Stroke volume (SV)  ­ The volume of blood expelled with each left ventricular contraction ­ Heart rate (HR) – How many times the left ventricle contracts in a minute What factors influence cardiac output?  Preload= the volume of blood in the left ventricle prior to contraction  Afterload= the resistance the left ventricle has to pump against to push blood into  circulation  Contractility= the force of the left ventricular contraction  Frank Starling’s Law:  A phenomenon that occurs when the heart muscle works HARD over a period of  TIME Blood Vessels:  Arteries – carry blood away  Veins – carry blood back  Capillaries – site of exchange  Three layers Lymphatic System:  Works to return excess interstitial fluid (lymph) to the circulation  Plays a role in immunity  Includes lymph nodes, the spleen, the thymus, and the tonsils Pericarditis:  Inflammation (“itis”) of the pericardium  Fluid accumulates ­ pericardial effusion  Swollen tissue creates friction  Cardiac tamponade  Cardiac compression from excessive fluid accumulation  Life­threatening    Manifestations: o Pericardial FRICTION RUB (grating sound heard when breath is held) o Sharp, sudden, severe chest pain (angina) that increases with deep inspiration  and decreases when sitting up and leaning forward o Muffled heart sounds o Dyspnea (difficulty breathing) o Tachycardia o Edema (swelling) o Flulike symptoms o Complications: heart failure, shock, and death Infective Endocarditis:  Commonly caused by Streptococcus and Staphylococcus infections  Vegetation forms on internal structures and creates small clots (thrombi)  Microemboli occur as they the vegetation is dislodged, resulting in  microhemorrhages     Risk factors: o Intravenous drug use o Valvular disorders (mitral valve prolapse) o Prosthetic heart valves o Rheumatic heart disease Myocarditis:  Inflammation of the myocardium  Uncommon  Organisms, blood cells, toxins, and immune substances invade and damage the  muscle    Complications:  o Heart failure o Cardiomyopathy o Dysrhythmias o Thrombus formation Valvular Disorders:  Brainstorm – What is the purpose of a heart valve?  Disrupt blood flow through the heart  Stenosis – narrowing  ­ Less blood can flow through the valve ­ Causes decreased cardiac output, increased cardiac workload, and hypertrophy  Regurgitation – insufficient closure ­ Blood flows in both directions through the valve ­ Causes decreased cardiac output, increased cardiac workload, hypertrophy,  and dilation   Causes: o Congenital defects o Infective endocarditis o Rheumatic fever o Myocardial infarction o Cardiomyopathy o Heart failure  Cardiomyopathy:  Conditions that weaken and enlarge the myocardium  Classified into three groups—dilated, hypertrophic, and restrictive  Dilated Cardiomyopathy­  Most common type  Risk higher with advancing age and African American men  Cardiomegaly and ventricular dilation damages myocardium muscle fibers, resulting in decreased cardiac output and blood stagnation    Causes:  o Cocaine abuse o Pregnancy   o Infections o Hyperthyroidism o Diabetes mellitus  o Hypertension o Coronary artery disease (CAD)    Manifestations: o Appear as compensatory mechanisms fail o Dyspnea (difficulty breathing) o Dysrhythmias o Angina (chest pain) o Dizziness o Activity intolerance o Blood pressure changes o Tachycardia (fast heart rate) o Tachypnea (fast respiratory rate) o Edema (swelling) o Weak pedal (foot) pulses o Cool and pale extremities o Jugular vein distension (JVD) Hypertrophic (enlarged muscle) Cardiomyopathy­  More common in men and those who are sedentary  Risk higher with hypertension, valvular disease, and thyroid disease   Ventricle wall becomes stiff and unable to relax Restrictive Cardiomyopathy­  Common in South and Central America, India, Asia, and Africa    Causes:  o Radiation exposure to the chest o Connective tissue diseases o Myocardial infarction o Sarcoidosis o Cardiac neoplasms (cancers) Aneurysms:  Weakening of an artery  Can occur in an artery ­ Common in the abdominal aorta, thoracic aorta, and the cerebral, femoral, and popliteal arteries  Can rupture – exsanguination     Risk factors:  o Congenital defect o Atherosclerosis o Hypertension o Dyslipidemia o Diabetes mellitus o Tobacco o Advanced age o Trauma o Infection   True aneurysms – affect all three vessel layers  ­ Saccular aneurysm – bulge on the side  ­ Fusiform aneurysm – occurs the entire circumference   False aneurysm – does not affect all three layers of the vessel ­ Dissecting aneurysms ­ occurs in the inner layers Dyslipidemia:  High levels of lipids (fats) in the blood  Increases risk for many chronic diseases  Lipids come for dietary sources and liver production  Dietary sources ­ Cholesterol – animal products ­ Triglycerides – saturated fats Atherosclerosis:  Leads to vessel obstruction, platelet aggregation, and vasoconstriction    Complications:  ­ Peripheral vascular disease (PVD) ­ Coronary artery disease (CAD) leading to myocardial infarction (MI) ­ Thrombi ­ Hypertension ­ Stroke ** Can occur in any artery in the body**  Peripheral Vascular Disease (PVD):  Narrowing of the peripheral vessels     Causes:  o Atherosclerosis o Thrombus o Inflammation o Vasospasms  Raynaud’s disease – vasospasms of arteries, usually in the hands, because of sympathetic stimulation ­ Raynaud’s phenomenon     Manifestations: o Pain  o Intermittent claudication (intermittent pain) o Numbness o Burning o Non­healing wounds o Skin color changes o Hair loss o Impotency Coronary Artery Disease (CAD): Stages of CAD  Atherosclerotic changes of the coronary arteries  Impairs myocardial tissue perfusion  #1 cause is ATHEROSCLEROSIS  Angina – intermittent chest pain resulting from myocardium ischemia ­ Stable – goes away with demand reduction ­ Unstable – increased intensity or frequency, does not go away with demand  reduction, or occurs at rest   Infarction – permanent necrotic damage to the myocardium – DEATH of heart  tissue!    Complications: o Myocardial infarction o Heart failure o Dysrhythmias o Sudden death    Manifestations: o Angina o Indigestion like sensation o Nausea o Diaphoresis o Fatigue  Thrombus:  Stationary blood clot  Virchow’s Triad – endothelial injury, sluggish blood flow, and increased   Emboli – traveling body ­ May be a thrombus, air, fat, tissue, bacteria, amniotic fluid, tumor cells, and  foreign substances ­ Can become lodged in places like the lungs, brain, and heart Varicose Veins:  Engorged veins resulting from valve incompetency  Most common in the legs  May also occur as esophageal varices and hemorrhoids    Risk factors:  o Genetic predisposition o Pregnancy o Obesity o Prolonged sitting or standing o Alcohol abuse and liver disorders (esophageal varices) o Constipation (hemorrhoids) Lymphedema:  Swelling due to a lymph obstruction  Primary lymphedema  ­ Rare, usually congenital  Secondary lymphedema         Causes:  o Surgery o Radiation o Cancer o Infection/ injury Hypertension:  Prolonged elevation in blood pressure  Excessive cardiac workload due to increased afterload and vasoconstriction     Risk factors:  o Advancing age o Ethnicity/ family history o Being overweight or obese o Physical inactive/ poor diet o Tobacco use and high­sodium diet  Primary hypertension o Most common form o Develops gradually over time  Secondary hypertension o Tends to be more sudden and severe      Causes:   Renal disease, Adrenal gland tumors, Certain congenital heart  defects     Manifestations: o “Silent killer” o Include: fatigue, headache, malaise, and dizziness    Complications:  o Atherosclerosis o Aneurysms o Heart failure o Stroke o Renal damage o Vision loss o Memory problems    Diagnosis:  o History, physical examination,  o Multiple blood pressure (usually three) readings at varying times of the  day o Laboratory tests to determine the presence of complications Myocardial Infarction:  DEATH of the myocardium  Coronary artery blood flow is blocked due to atherosclerosis (Coronary Artery  Disease [CAD]), thrombus, or vasospasms  Risk factors are the same as those for atherosclerosis    Complications:  o Heart failure o Dysrhythmias o Cardiac shock o Thrombosis o Death    Manifestations: o Some are asymptomatic – “Silent” MI o Includes: angina, fatigue, nausea, shortness of breath, diaphoresis, and  indigestion Heart Failure:  Inadequate pumping  Leads to decreased cardiac output, increased preload, and increased afterload  Compensatory mechanisms activated ­ Activation of the sympathetic nervous system ­ Activation of the renin­angiotensin­aldosterone system ­ Ventricular hypertrophy  May be acute or chronic     Manifestations: o Depend on type o Fluctuates in severity o Appear as compensatory mechanisms fail o Includes: indications of systemic and pulmonary fluid congestion Left Sided Failure­  Cardiac output falls  Blood backs up to the pulmonary circulation    Causes:  o Left ventricular infarction o Hypertension o Aortic and mitral valve stenosis    Manifestations:  o Pulmonary congestion o Dyspnea o Activity intolerance  Right Sided Failure­  Blood backs up to the systemic circulation    Causes:  o Pulmonary disease o Left­sided failure o Pulmonic and tricuspid valve stenosis    Manifestations:  o Peripheral edema and weight gain  Cor Pulmonale= ­ Right­sided heart failure that occurs secondary to a PULMONARY conditions and long­tem high blood pressure in the lungs. ­ Causes include COPD and other CHRONIC lung conditions. MAP­ Mean Arterial Pressure:  MAP is determined by Cardiac Output (CO), systemic vascular resistance (SVR),  and central venous pressure (CVP).  MAP= [ (2 X Diastolic) + systolic] / 3  Diastole counts for twice as much because 2/3 of the cardiac cycle is spent in  diastole.  MAP normal range= 70­110


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