Systems Physiology BMED 3100
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Date Created: 11/02/15
BMED 3100 Systems Physiology HW7 Due Thursday April 21 2011 1 If 15 L of a hypertonic 3 NaCl solution is infused into the extracellular uid compartment of a 70 kg patient whose initial plasma osmolarity is 290 mOsM what would be the intracellular and extracellular uid volumes and osmolarities after osmotic equilibrium Step 1 calculate the initial conditions volume concentration total milliosmoles in each compartment ECF volume is 20 and ICF volume is 40 28 290 8120 42 290 12180 Calculate the total mOsmoles added to the ECF in 2 L of 3 NaCl 3 solution of NaCl 30 g100mL MW ofNaCl 58 gmol gt 0517 mol L For 15 L 3 07755 molNaC131551 mosmoles added to the ECF Step 2 calculate instantaneous of adding 1551 mosmoles Total of 5611 mosmoles in 155 L yields 362 mOsmL 435 No 13731 Step 3 calculate the volumes and concentrations that would occur within a few minutes after the system reaches osmotic equilibrium by dividing the total mosmoles by the total volume The concentrations in the ICF and ECF would be equal gt 3157 mOsmL Assume that no solute or water has been lost from the body and that there is no movement of NaCl into or out of the cells Therefore divide the total osmoles by the concentration to calculate the final volumes L T BMED 3100 Systems Physiology HW7 Due Thursday April 21 2011 2 Mr Taber is a 68yearold retiree who was just diagnosed with oat cell carcinoma of the lung Oat cell carcinomas sometime secrete excess ADH which is not feedback regulated like normal ADH secretion While he was always a very active and energetic person recently he has no energy His wife noticed he is sometimes confused and lethargic One night Mr Taber had a grand mal seizure and was rushed to the hospital His blood pressure was normal both supine and upright Some lab tests indicated that his plasma Nal was 112 mEq L normal 140 mEq L his plasma osmolarity was 230 mOsM normal 290 mOsM and his urine osmolarity was 950 mOsM His is given an infusion of hypertonic 3 saline and released from the hospital a few days later when he stabilized He was told to limit his water intake at home a What is the major effect of high ADH on the kidney How does this explain his urine osmolarity b Why was Mr Taber s plasma sodium concentration so low Why was his plasma osmolarity so low c Why did Mr Taber have a grand mal seizure d Was Mr Taber s total body water increased decreased or normal Why was his blood pressure normal e Hypertonic NaCl at 3 is equal to a NaCl concentration of 517 mEq L How did the infusion of hypertonic saline help to correct Mr Taber s low plasma Na concentration f Why does Mr Taber have to restrict his water intake What would happen if he did not limit his water intake a What is the major effect of high ADH on the kidney How does this explain his urine osmolarity High water retention If a great amount of water is reabsorbed then the urine becomes more concentrated b Why was Mr Taber s plasma sodium concentration so low Why was his plasma osmolarity so low Increased amount of water from enhanced water retention dilutes the plasma sodium concentration and decreases plasma osmolarity c Why did Mr Taber have a grand mal seizure Low concentration of sodium causes water to enter the cell leading to swelling and thus a grand mal seizure d Was Mr Taber s total body water increased decreased or normal Why was his blood pressure normal Increased Initially blood pressure is increased due the increase in blood volume Because plasma osmolarity is lower than normal the kidneys are going to excrete more water leading to a decrease in blood pressure e Hypertonic NaCl at 3 is equal to a NaCl concentration of 517 mEq L How did the infusion of hypertonic saline help to correct Mr Taber s low plasma Na concentration The infusion of hypertonic saline increases plasma Na concentration f Why does Mr Taber have to restrict his water intake What would happen if he did not limit his water intake The excess amount of ADH leads to increased water retention consumption of more water will lead to more reabsorption of water in the kidneys Therefore he must regulate the amount of water he intakes BMED 3100 Systems Physiology HW7 Due Thursday April 21 2011 3 4 Calculate the volume of a uid compartment after adding 20 mmol of a perfect solute one that is not absorbed metabolized or excreted The equilibrium concentration is 10 mmoll Amount injected 20mmol 2 Concentration a er equilibrium lOmmol l c Plasmapheresis is a procedure used to replace the uid portion of the blood It involves injection of large volumes of a solution of 5 human albumin dissolved in physiological saline 09 NaCl Is this solution isotonic hypertonic or hypotonic to human plasma isotonic b Ifa 5 solution is unavailable pharmacists may substitute a proper dilution of a 25 albumin solution What is the correct dilution factor to obtain a 5 solution 1 part 25 albumin solution to 4 parts isotonic saline If the diluent used is sterile water is the resulting solution isotonic hypertonic or hypotonic to human plasma hypotonic or hypoosmotic What will happen to the blood cells if water is used instead of saline The cells will swell s V 33 5 How are dietary carbohydrates digested in the gastrointestinal tract Include enzymes intermediate stages and products Dietary carbohydrates include starch disaccharides monosaccharides and cellulose which isi indigestible Of these only monosaccharides glucose galactose and fructose are absorbable Thus to be absorbed starches and disaccharides must first be digested to glucose galactose or fructose Starch is digested to disaccharides ocdeXtrins maltose and maltotriose by ocamylase in saliva and pancreatic secretions Other disaccharides present in the diet include trehalose lactose and sucrose Disaccharides are either produced from the digestion of starch or are ingested in food These disaccharides are then digested to monosaccharides by enzymes located in the brush border of intestinal mucosal cells ocdextrins maltose and maltotriose are digested to glucose by ocdextrinase maltase and sucrose respectively Trehalose is digested to glucose by trehelase Lactose is digested to glucose and galactose by lactase Sucrose is digested to glucose and fructose by sucrose The three monosaccharide products are glucose cralactose and fructose CARBOHYDRATE DIGESTIDN Slarch l ILamylasn rlvDDxmnS Mallnsn Malmllmso T rehnluse Laclosa Sucmsa 4 l 39 o mallase 63 lrehalasa lacrase sucrase t i 69 1 t 9o x so r i Glucose Glucose Glucose Galaclose Glucose Fructose Coslanm Physmlogv 4m Edmnn Cupvrlgm us 2010 by Saunders an Impllnl or Elsevler Inc All nghls reserved PATHOPHYSIOLOGY Health and Disease Disease deviation from normal physical mental and social Homeostasis stable internal environment BP temp uids electrolytes values are represented in ranges that can be adjusted for additional factors like age and activity level Terms used in Pathophysiology Pathophysiology study of functional or physiological changes in the body resulting from disease process both gross changes and cellular changes Pathology lab study of cell and tissue changes associated with disease Biopsy surgical specimens Autopsy exam after death Diagnosis identi cation of a disease through the evaluation of signs and symptoms lab tests and other tools Etiology the causative factors of a disease congenital genetic microorganisms metabolic dysfunction burns nutritional deficiency Idiopathic cause unknown Iatrogenic caused by an error in treatment or procedure bladder infections after cath insertion bone marrow damage from prescription drug Predisposing factorstendencies that promote development of a disease in an individual indicates high risk not certain development age gender diet occupational exposure genetic Prevention vaccine dietary and lifestyle modifications stop smoking Terms used to describe the characteristics of a particular disease Pathogenesis development of a disease or sequence of events involved in tissue changes related to a disease process Acute sudden short term illness with marked signs Chronic milder condition but persists for a long time Sub clinical pathological change occurs but no obvious manifestations are exhibited by the patient Latent silen no clinical signs avoidant incubation period Prodromal the time in early development of the disease where the patient is aware of some changes but the signs are nonspecific fatigue loss of appetite Manifestation clinical evidence or effects of a disease Local found at the site of the problem like swelling Systemic a general indicator of illness like fever Signs objective indications of diseases like fever or rash Symptoms subjective feelings like pain or nausea Lesion specific local tissue change can be either microscopic changes or things like blisters Syndrome a collection of signs and symptoms that occur together in response to a certain condition Diagnostic tests lab tests that assist in diagnosing a disease Remission manifestations of disease subside Exacerbations manifestations of a disease increase Precipitating factor something that triggers an acute episode Complication additional problems that arise after the original disease begins Therapytherapeutic interventions measures that promote recovery or slow disease progress surgery drugs behavioral Sequelae potential unwanted outcomes of condition Convalescence period of recovery and return to normal state Prognosis probability for recovery Morbidity disease rates within a group Mortality relative number of deaths resulting from a particular disease Epidemiology the science of tracking pattern and occurrence of diseases infectious diseases u vaccine Epidemics many cases of infectious diseases within a given area Pandemic high number of cases over several areas often worldwide Incidence of new cases within a given stated time period Communicable disease infections that can be spread from one person to another NotifiableReportable diseases must be reported to authorities intended to protect public health measles AIDS Autopsy an exam of the body by a pathologist gross and microscopic exam of the tissues organs and uids Terms used for some of the common changes in cells Atrophy decrease in size of cells which leads to a decrease in tissue mass muscles in a cast Hypertrophy increase in the size of cells which leads to an increase in tissue mass exercise Hyperplasic increase in the number of cells leading to an increase in Tissue mass hormonal changes Metaplasia one mature cell type is replaced by another mature cell type smokers lungs Dysphasia tissue in which cells vary in shape and size Chronic irritation infection precancerous Anaplasia cells that are undifferentiated and have variable nuclei and cell structure and numerous mitotic figures malignancy cancer basis for grading a tumor Neoplasm new growth tumor Benign don t spread not life threatening Malignant cancer Cell damage and Necrosis Cell Damage 2 stages 1 Initial alteration in the metabolic reaction leading to loss of function leads to morphological structural changes that lead to cell death by rupture 2Lysis dissolution releasing lysosomal enzymes which leads to in ammation which leads to the damaging of nearby cells Necrosis dead cells liquefy under the presence of certain cell enzymes Infarction an area of dead cells resulting from lack of oxygen Gangrene an area of necrotic tissue that has been invaded by bacterial In ammation and Healin Review of Normal Defenses in the body Nonspeci c 1 Mechanical ba1rier skin mucus first line of defense 2Associated Enzymes saliva tears destroy foreign material 3 Phagocytes neutrophils and macrophages randomly engulf and destroy bacteria cell debris and foreign agents 4 Interferon nonspecific agents that protect against viruses Speci c Immune system In ammation Repair Cell damage gt sequence of responses in surrounding tissue ie acute in ammation initial nonspecific response attempts to neutralize injurious agent and restore tissue function injured area ooded with neutrophils amp plasma extravasate due to local vascular response namely dilatation gt Tblood ow hyperemia Tpermeability gt plasma protein leakage neutrophil migration from blood gt tissue Acute in ammation gt either resolution organization amp repair g chronic in ammation The latter occurs if the injurious agent cannot be eliminated and results in ongoing damage to surrounding tissue In ammation intended to localize and remove the injurious agent Def1nition the body s response to injury disorders named using the ending ITIS to indicate in ammation Causes direct damage cuts and sprains chemicals acids Ischemia and cell necrosis or infarction allergic reactions physical agents burns radiation foreign bodies splinters or dirt and infection BMED 3100 Systems Physiology HW6 Due Thursday April 7 2011 l 2 What is in ammation Include a de nition and the stages De nition Initial nonspeci c response attempts to neutralize injurious agent and restore tissue function injured area ooded with neutrophils and plasma extravasate Stages Tissue injury gt cell damage gt Mast cells and platelets release chemical mediators histamines serotonin prostaglandin s and leukotrinines into intestinal uid and blood gt affect nerves and blood vessels in the area local vasodilatation gthyperemia increased blood ow to the area gt capillary membrane permeability increases a increase of interstitial uid a dilutes toxic materialaglobulins serve as antibodies and brinogens form a mesh to localize the infection vascular response Cellular response leukocytes are attracted by chemo taxis to the area of in ammation by chemicals released by damaged cells gtneutrophils monocytes and macrophages collect along the capillary wall and move through it into the interstitial area gtdestroy and remove foreign material when phagocytic cells die at site lysosomal enzymes are released damage other cells and prolong in ammation What is the difference between necrosis and apoptosis Necrosis and apoptosis are both forms of cell death Necrosis is passive and apoptosis is active ie programmed Necrosis Cells swell membranes bleb increased membrane permeability Organelles swell ribosomes become detached cytoskeleton becomes degraded Mass degradation occurs due to enzymatic destruction There is usually decreased ATP 9increased glycolysis leading to low pH 9decreased activity of NaK pumps increased cytosolic calcium which activates enzymes free radical formation Nuclei lyse chromosomes fragment Cells burst and release contents into surrounding space exacerbating the cell death Progammed Cell DeathApoptosis Either a natural process of morphostasis mitosis programmed cell death morphostasis in development of an abnormal form of programmed cell death ie back door apoptosis 7 the program is started at any point and results in cell death There is activation of a genetic program Neither neutrophils nor lymphocytes are recruited Cells shrink organelles shrink nuclei shrink and chromosomes fragment into regularly spaced fragments corresponds to nucleotide separation distance therefore it is likely to be enzymatic rather than structural nonspeci c breakdown Cells do no spill contents into surrounding extracellular space 9 it is protective to the tissue Note There are genes that favor and genes that prevent cell death Although the genes activated at the initial stages seem to be highly speci c the genes activated at the temiinal stages seem to be common genes for all forms of cell death BMED 3100 Systems Physiology HW6 Due Thursday April 7 2011 3 What are the stages of healing The Heah no Process 1 Thrombosis Blood Clot 7seal area 3 In ammation 34 days foreign material and cell debris removed Neutrophils macrophages 4 Granulation Tissue grows into gap from nearby connective tissue highly vascular appears moist and pink fragile and easily broken Epithelial cells undergo mitosis and cover wound Fibroblasts enter area and produce collagen scar tissue provides strength Cross linking and shortening of collagen fibers form a tight strong scar Capillaries decrease and color goes from red to white 9 89 4 a What is the partial pressure of oxygen in atmospheric air Explain how you got this answer 760 mmHgl atm 021 160 mm b What happens to this value at 100 humidi ed air Why It is reduced 76047 mian 021 150 mnng vapor pressure is higher 7 moisture in air takes space gas is more soluble in air than liquid 7 liquid vapor pressure displaces oxygen 5 The following measurements were made on anormal individual P Earterial Which of the following breathing patterns will change the subject s P302 Explain your answers Pattern l tidal volume of 400 mL and a f of 30 breathsmin Pattern 2 tidal volume 500 mL and afof 30 breathsmin Pattern 3 tidal volume of 800 mL and afof 10 Pattern 4 tidal volume of 800 mL and afof 75 In a normal person arterial P02 is determined by and is essentially equal to alveolar P02 Hence any pattern of breathing that leaves the alveolar ventilation rate unchanged would not affect the subj ect s P302 or P A02 PA Ealveolar partial pressure As above the alveolar ventilation rate is VA VT 7 VD x f VE VT xf therefore the original VT is 600 mL and the VD 200 mL VA is 6 Lmin Breathing pattern 13 give the same V A whereas breathing pattern 2 4 gives 9 Lmin and 45Lmin respectively