GNUR 293 – PATHOPHYSIOLOGY
8/13
STUDY Guide: Mechanisms of and Cellular Responses to Injury
1. What are the differences and similarities among the following: hypoxemia, hypoxia, anoxia, and
ischemia?
2. Explain what happens to cells that are not adequately oxygenated in regard to cell metabolism, cell
membrane permeability, ATP production, cell pH, electrolyte and water movement across the cell
membrane.
3. What is oxidative stress and what are the characteristics of reactive oxygen species (ROS)?
How do reactive oxygen species cause damage to cell lipids, proteins, and DNA?
Under what normal physiological and pathophysiological conditions are reactive oxygen species
produced?
4. Explain the general mechanisms by which antioxidant enzymes, vitamins, and minerals protect against
oxidative stress.
5. Compare cell death by necrosis and apoptosis in regard to what causes these two forms of cell death,
cellular changes involved, and whether or not they cause an inflammatory response. Differentiate
physiologic apoptosis from pathologic apoptosis.
6. Define dry gangrene, wet gangrene, and gas gangrene.
7. Explain the causes and consequences of water, fat, and calcium accumulation in cells.
8. What changes occur in cells when they undergo the following alterations?
Explain examples of factors that can cause cells to undergo the following alterations.
a. atrophy
b. hypertrophy
c. hyperplasia
d. metaplasia
e. dysplasia
1
GNUR 293 – PATHOPHYSIOLOGY
8/13
STUDY Guide: Innate Immunity: The Inflammatory Response
1. Describe the physical, mechanical, and biochemical barriers in the body that function as the first line
of defense against infections. Provide examples.
2. Explain the functions of the following cell types in the inflammatory response.
a. mast cells
b. neutrophils
c. monocytes/macrophages
d. eosinophils
e. endothelial cells
3. Describe the functions of the following chemical mediators involved in inflammation:
a. histamine
b. cytokines (interleukins, TNF- alpha, interferon)
c. leukotrienes
d. prostaglandins
4. Explain the general functions of the following plasma protein systems that are part of the acute phase
response involved in inflammation:
a. the complement system
b. the coagulation system
c. the kinin system
5. What activates the inflammatory response and what are the normal functions of the inflammatory
response?
6. Explain the causes and effects of the following events that occur during the inflammatory response:
a. Vasodilation/Increased vascular permeability
b. Emigration of leukocytes
c. Phagocytosis
7. How do phagocytic cells, such as neutrophils and macrophages, destroy microorganisms?
8. Explain the physiological basis for the following manifestations of inflammation: erythema, warmth,
edema, pain, loss of function.
9. Explain the systemic manifestations that would be suggestive of the presence of cell injury
somewhere in the body.
10. What is the erythrocyte sedimentation rate and why does it increase in the presence of inflammation?
11. How is chronic inflammation different from acute inflammation?
2
GNUR 293 – PATHOPHYSIOLOGY
Dr. Klein, edited by Dr. Chin
8/13
STUDY Guide: Fluid and Electrolyte Imbalances
1. Explain the risks for dehydration in the groups listed below, in terms of body water content and
renal function and any other related factors, if their fluid intake were significantly reduced.
a. neonates and infants
b. elderly individuals
c. obese individuals
2. If a person has an acute weight gain or weight loss of 1 kg, how much fluid have they likely
gained or lost? How can fluid balance be monitored in patients?
3. Explain how the serum sodium, urine volume, urine specific gravity, and hematocrit would
change in states of fluid deficit. Explain how these parameters would change in states of fluid
excess.
4. Explain the effects of infusion of an isotonic, hypotonic, and hypertonic intravenous solution on
cell volume. Give an example of each type of solution and provide a clinical situation for which
each of these 3 types of solutions would be used.
5. Explain how conditions that alter the Starling forces [capillary hydrostatic pressure, capillary
oncotic (colloid osmotic) pressure, and capillary permeability] lead to edema formation. Why
does obstruction of lymphatic drainage result in edema? What are the adverse effects of edema
formation?
6. How do antidiuretic hormone (ADH), the rennin-angiotensin-aldosterone system (RAAS), and
natriuretic hormones (natriuretic peptides) function in the regulation of fluid and electrolyte
balance?
7. Explain common causes and clinical manifestations of fluid deficit and fluid excess states.
8. Explain the causes of and pathophysiological alterations that occur in the syndrome of
inappropriate antidiuretic hormone (SIADH) and diabetes insipidus (DI).
9. What is the normal serum concentration of the following electrolytes?
a. sodium
b. potassium
c. magnesium
d. calcium (total and ionized)
e. phosphate
10. What are common causes of hyponatremia? Explain the effects of hyponatremia on cell volume
and central nervous system function. How is hyponatremia treated?
11. What are common causes of hypernatremia? Explain the effects of hypernatremia on cell volume
and central nervous system function. How is hypernatremia treated?
3
12. Explain the causes of hypokalemia and its effects on cardiac and neuromuscular function. How is
hypokalemia treated?
13. Explain the causes of hyperkalemia and its effects on cardiac and neuromuscular function. How
is hyperkalemia treated?
14. Explain how alterations in parathyroid hormone, vitamin D, and calcitonin affect calcium
balance.
15. What are common causes of calcium imbalances? Explain how hypocalcemia and hypercalcemia
alter neuromuscular function. How are hypocalcemia and hypercalcemia treated?
16. What are common causes of magnesium imbalances? How do hypomagnesemia and
hypermagnesemia affect neuromuscular function? Why should deep tendon reflexes and blood
pressure be monitored when a person is receiving intravenous magnesium?
4
GNUR 293 – PATHOPHYSIOLOGY
9/13
STUDY Guide: Acid-Base Imbalances
1. What are the sources of volatile and non-volatile acids in the body?
How are volatile and non-volatile acids eliminated from the body?
2. Although acids are ingested in the diet and produced as by-products of metabolism, why do people not
usually become acidotic? Hint: explain the chemical, renal, and respiratory buffering
mechanisms in the body.
3. Describe the limitations in regard to renal and respiratory buffering in cases of acid-base imbalance.
4. Explain why hypokalemia can lead to metabolic alkalosis and hyperkalemia can lead to metabolic
acidosis. Why does the serum potassium level increase in acidosis and decrease in alkalosis?
5. What is the difference between compensation for and correction of an acid-base imbalance?
6. Explain the following arterial blood gas (ABG) parameters:
a. pH
b. PaCO2
c. HCO3d. PaO2
f. SaO2
(NOTE: you should know the normal ranges for the ABGs listed on the lab sheet posted in the course
menu in Sakai.)
7. How does the anion gap help in the differential diagnosis of acid-base imbalances? Why do renal
failure, diabetic ketoacidosis, and conditions of severe hypoxia increase the anion gap?
8. Compare and contrast metabolic acidosis and respiratory acidosis in regard to their causes, clinical
manifestations, blood gas values in uncompensated states, partially compensated, and fully
compensated states, and treatment.
9. Compare and contrast metabolic alkalosis and respiratory alkalosis in regard to their causes, clinical
manifestations, blood gas values in uncompensated, partially compensated, and fully
compensated states, and treatment.
(It may be helpful to make a chart for items #8 and 9 to view the similarities and differences.)
10. Be able to interpret arterial blood gas results when presented with pH, PaCO2, and HCO3-. Also, if
presented with a clinical condition (e.g. prolonged vomiting or hyperventilation), be able to anticipate
how these values might be affected.
5
GNUR293 – PATHOPHYSIOLOGY
Study Guide: Alterations in Immune Function
1. What are the differences between humoral and cell-mediated immunity? Which cells are
the major participants in each?
2. Through which mechanisms do antibodies and T cytotoxic cells protect the body against
an invader?
3. Describe the differences between active and passive immunity and give examples of
each. Why is passive immunity short-lived? Explain how these systems work together to
create a robust immune response.
4. Differentiate between a primary and secondary immune response. Why is the body able
to mount a faster response during a secondary antigen exposure?
5. What are the differences between the four types of hypersensitivity reactions? What role
does inflammation and/or complement play in each? Which involve a humoral immune
response and which are cell-mediated? Give an example for each reaction.
6. Describe how an individual becomes sensitized to an allergen in type I hypersensitivity
reactions. Describe the common clinical manifestations of allergy reactions and
anaphylaxis.
7. Describe the similarities and differences in the five mechanisms of type II
hypersensitivity.
8. Describe the stimuli of the three hypersensitivity reactions: allergy, autoimmunity, and
alloimmunity. Discuss the significance of human leukocyte antigen (HLA, also known as
major histocompatibility complex) in autoimmune and alloimmune reactions.
9. Discuss the different types of blood group antigens and the issues concerning blood type
compatibility for blood transfusions. What implications do ABO and Rh antigens have
for women of childbearing age?
10. Discuss the difference between primary (congenital) and secondary (acquired) immune
deficiencies. What clinical presentation should you expect for each? Give an example of
each deficiency.
11. What are the implications of having a deficiency of B lymphocytes, T lymphocytes, and
of both? What therapies are appropriate for these disorders?
12. From an epidemiological perspective, who is most at risk for becoming infected with
HIV? What are some primary and secondary interventions that could decrease
transmission?
13. Discuss the pathogenesis of acquired immune deficiency syndrome (AIDS).
14. What is the testing process for HIV exposure/infection and what do the results mean?
15. Describe clinical symptoms that indicate potential HIV infection and its progression to
AIDS.
16. Describe the treatment for HIV/AIDS.
6
GNUR293 – PATHOPHYSIOLOGY
Study Guide: Diabetes Mellitus Part I & II
1. Identify the hormones secreted by the alpha, beta, and delta cells of the pancreas and discuss
their major functions in normal metabolism.
2. Define glucose, glycogen, glucagon.
3. Explain the relationship between the GLUT transporters and insulin. Why are cells with
GLUT 1-3 transporters more susceptible to damage from hyperglycemia?
4. Discuss the similarities and differences in the pathophysiology and clinical manifestations of
type 1 and type 2 diabetes mellitus.
5. Discuss the pathophysiology of gestational diabetes. Explain why women with this condition
are at risk for developing type 2 DM.
6. Discuss the different types of diagnostic tests for DM. What are the
advantages/disadvantages of each?
7. Compare and contrast the acute diabetic complications DKA and HHNS.
8. What are the clinical manifestations of hypoglycemia?
9. List the chronic complications of diabetes mellitus and discuss how maintaining blood
glucose levels within normal limits the cellular degeneration in each instance.
10. What is metabolic syndrome? Discuss the connection between this condition and diabetes
mellitus.
7
GNUR293 – PATHOPHYSIOLOGY
Study Guide: Alterations in Flow (Atherosclerosis and Thromboembolic Disorders)
1. In general, how do pressure, resistance, velocity, turbulence, compliance, and
microcirculation dynamics (Starling forces) impact blood flow? Which contribute to
increased or decreased flow?
2. Describe how alterations in vascular flow result in blood vessel obstructions (i.e. thrombi).
How do the other risk factors in Virchow's triad contribute to spontaneous clot formation?
3. Compare/contrast the expected clinical manifestations for an arterial vs. venous occlusion.
4. Describe the differences between a thrombus and an embolus. What is the relationship
between a DVT and PE?
5. Explain the stepwise progression of atherosclerosis.
6. Identify the risk factors for atherosclerosis. How does diabetes mellitus contribute to
atherosclerosis?
7. Compare and contrast varicose veins and chronic venous insufficiency.
8. How does a blockage in lymphatic nodes cause an alteration in flow? What clinical
manifestations are expected?
8
GNUR293 – PATHOPHYSIOLOGY
Study Guide: Hypertension and Stroke
9. What cardiac event does the systolic pressure represent? Diastolic?
10. What are the pros and cons of direct/indirect blood pressure measurements? How do you
most accurately take a blood pressure?
11. Discuss how factors (autonomic control, neural receptors) regulate blood pressure. How do
hormones (ADH, RAAS, NPs) influence cardiac output/peripheral resistance (and thus affect
blood pressure)? What other clinical events can affect cardiac output and/or peripheral
resistance?
12. Discuss the differences between primary and secondary hypertension. Who is most at risk for
each?
13. Why is hypertension considered a “silent” condition? How can HTN contribute to end-organ
damage?
14. What are the principles of treatment for hypertension?
15. Who is at risk for orthostatic hypotension? How would we treat this condition?
16. How do the two types of stroke (ischemic and hemorrhagic) differ in regards to risk factors,
prevention strategies, and acute management?
17. Describe some of the clinical manifestations of stroke? How are these sequelae managed?
18. How is a TIA different than a stroke?
9
GNUR293 – PATHOPHYSIOLOGY
Study Guide: Coronary Heart Disease and Acute Coronary Syndromes
19. How does atherosclerosis contribute to coronary artery disease and acute coronary
syndromes? What atherosclerotic events are responsible for the progression of disease?
20. Ischemia results from an imbalance of coronary perfusion and/or myocardial workload.
Discuss some examples of each.
21. Compare and contrast the 3 different types of angina. What is the pathophysiological process
behind each? Which impact coronary perfusion (i.e. supply) and which impact cardiac
workload (i.e. demand)?
22. Discuss the clinical presentation of myocardial ischemia and myocardial infarction.
23. Discuss the diagnostic evaluation modalities for myocardial ischemia and myocardial
infarction. Describe basic changes that might be observed on ECG and their implications
(e.g. ST depression, T wave inversion, ST elevation).
24. Compare and contrast the acute coronary syndromes (unstable angina vs. NSTEMI vs.
STEMI). Where do cardiac biomarkers originate from and how do they contribute to a
diagnosis in ACS?
25. What are the goals of treatment for myocardial ischemia and myocardial infarction? Which
treatments can improve the coronary perfusion? Which decrease cardiac workload? Be able
to explain the mechanisms through which these effects occur.
26. How does valvular disease (i.e. stenosis or regurgitation) impact cardiac workload?
10
GNUR293 – PATHOPHYSIOLOGY
Study Guide: Heart Failure
27. Discuss how factors influencing cardiac output reflect cardiac performance. (Include stroke
volume, contractility, preload, afterload, heart rate, and ejection fraction.)
28. Compare and contrast systolic and diastolic heart failure similar.
29. Compare and contrast left and right heart failure, including etiology, clinical manifestations,
treatment, and complications. What is meant by forward and backward effects of heart
failure?
30. Discuss the compensatory mechanisms of sympathetic nervous system activation, increasing
preload, and myocardial hypertrophy/remodeling. How are these processes helpful? How do
these processes eventually contribute to worsening heart failure?
11
GNUR293 – PATHOPHYSIOLOGY
Study Guide: Alterations in Kidney Function Study Guide
1. Explain the relationship between renal blood flow and glomerular filtration rate. What factors
influence glomerular filtration rate?
2. Discuss the clinical significance of blood urea nitrogen and creatinine measurements. What
clinical data can a urinalysis provide regarding renal function?
3. Discuss the etiology of urinary tract infections (acute cystitis). Describe the development of
acute and chronic pyelonephritis independent of cystitis and as a complication of cystitis.
How is pyelonephritis similar to/different from cystitis in terms of severity, clinical
manifestations, and treatment?
4. Describe the pathophysiology of kidney stone formation. How does this obstruction cause the
clinical manifestations observed with this condition?
5. Identify the causes of glomerulonephritis and the resulting changes in glomerular structure
and function. How does the pathology of this condition contribute to the clinical
manifestations? Compare and contrast nephrotic syndrome and nephritic syndrome.
6. Discuss the pathology and staging of severity in acute kidney injury. How does the pathology
contribute to the clinical manifestations observed with this condition (specifically oliguria
and increased serum nitrogenous wastes)? Differentiate between prerenal, intrarenal, and
postrenal causes of acute renal failure.
7. Discuss the pathology and staging of severity in chronic kidney disease. How does the
pathology contribute to the systemic manifestations of chronic renal failure? Explain what is
meant by the term uremia.
12
GNUR293 – PATHOPHYSIOLOGY
Study Guide: Alterations in Gas Exchange and Obstructive Pulmonary Disorders
1. Explain how the lung volumes and capacities measure ventilation.
2. Compare and contrast the different kinds of Ventilation/Perfusion imbalances. Give clinical
examples for each. How do imbalances in ventilation contribute to hypoxemia and hypoxia?
3. What is the pathophysiology of pulmonary hypertension and how does it progress to cor
pulmonale? How is cor pulmonale different from other R heart failure causes?
4. Compare and contrast pulmonary edema and embolus. How does each contribute to a
dysfunction in ventilation, diffusion, and/or perfusion?
5. What etiologies and clinical signs/symptoms are common to all obstructive pulmonary
orders?
6. Discuss the importance of pulmonary function testing in diagnosing and maintaining
obstructive pulmonary disorders. What information do the FEV1 and FVC values provide?
What trends would you expect in these values for obstructive pulmonary disorders?
7. Discuss the role of IgE, mast cells, and inflammation in asthma as it contributes to immediate
and delayed (secondary) bronchial hyper-responsiveness and airway obstruction. How does
tissue remodeling contribute to airway impairment with this condition? Discuss how
environmental controls, preventive strategies, and medications target different etiologies
when treating asthma.
8. Discuss the similarities and differences in the clinical manifestations, underlying
mechanisms, and consequences of obstructive pulmonary diseases like chronic bronchitis and
emphysema. Explain the descriptors “blue bloater” and “pink puffer”. Discuss the treatment
for COPD.
9. How does the pathology of cystic fibrosis contribute to airway obstruction? Discuss the
treatment for this condition. Why are these effective strategies?
13
GNUR293 – PATHOPHYSIOLOGY
Study Guide: Restrictive Pulmonary Disorders
1. What etiologies and clinical signs/symptoms are common to all restrictive pulmonary orders?
2. Discuss the importance of pulmonary function testing in diagnosing and maintaining
restrictive pulmonary disorders. What information do the FEV1 and FVC values provide?
What trends would you expect in these values for restrictive pulmonary disorders?
3. How do inhaled pollutants alter lung function?
4. How do the pathological processes of acute respiratory distress syndrome contribute to acute
respiratory failure? Explain the processes responsible for the clinical manifestations of
ARDS. Why is positive end-expiratory pressure (PEEP) an effective treatment for ARDS?
5. Compare and contrast pneumothorax and pleural effusion in terms of pathology, clinical
presentation, and treatment. How do these conditions restrict pulmonary function?
6. Discuss the clinical symptoms and underlying mechanisms of pneumonia. How do these
mechanisms determine which patients are at-risk for developing pneumonia?
7. Define acute respiratory failure. How would this condition present clinically? What would be
appropriate therapies?
14
GNUR293 – PATHOPHYSIOLOGY
Study Guide: Oxygen Transport Pathophysiology and Anemia
8. Discuss the unique structure and function of hemoglobin in the human body. What role does
it play in O2 and CO2 transport? What role does iron play in the production of hemoglobin?
9. Detail the lifespan of an erythrocyte. What triggers this process and what is the role of
erythropoietin? Identify the role of the mononuclear phagocyte system (macrophages) in the
normal life cycle of an erythrocyte.
10. Discuss the importance of the oxyhemoglobin dissociation curve for evaluating effective gas
exchange. Which clinical conditions cause the curve to shift to the right or left? What does
the P50 value represent? How does hemoglobin’s affinity for oxygen alter this P50 value?
11. Define anemia and discuss the various methods of classifying the anemias.
12. Describe the clinical manifestations of anemia and discuss the pathophysiology that
generates them.
13. Compare and contrast the decreased RBC production anemias (aplastic, pernicious, irondeficiency).
14. Compare and contrast the inherited and extrinsic hemolytic anemias (thalassemia and sickle
cell, and hemolytic disease of the newborn). What factors precipitate a crisis in sickle cell
patients?
15. How is polycythemia different than anemias? What clinical manifestations would be
expected?
15
GNUR293 – PATHOPHYSIOLOGY
Study Guide: Gastrointestinal Disorders Study Guide
1. Discuss the contributing factors to gastroesophageal reflux disease (GERD). How does the
pathophysiology of this condition contribute to the clinical manifestations? Why are the
treatments effective at managing these manifestations?
2. Describe the causes, manifestations, treatments of gastritis. How does this condition
contribute to peptic ulcer disease? Compare and contrast duodenal and gastric ulcers.
3. Discuss the roles of NSAIDs and H. Pylori in contributing to peptic ulcer disease
4. Compare and contrast ulcerative colitis and Chron’s disease. How does the pathology of each
condition result in the symptoms experienced? What treatments are effective for these
conditions?
16
GNUR293 – PATHOPHYSIOLOGY
Study Guide: Liver Disease Study Guide
1. Identify the manifestations of liver disease that are due to hepatocellular failure and which
are due to portal hypertension. Explain the pathophysiology of jaundice.
2. Explain how the different types of viral hepatitis vary with regard to mode of transmission
and severity of symptoms.
3. Describe the clinical and laboratory findings that would lead to a diagnosis of liver cirrhosis.
4. Identify the treatment modalities are available to patients with liver disease.
17
GNUR293 – PATHOPHYSIOLOGY
Study Guide: Shock
31. Explain how impaired oxygen use contributes to cellular impairment/damage in shock.
32. Identify and describe the four different types of shock. In what ways are the pathologic
processes similar? Different? Discuss the clinical presentation and common treatment
modalities for managing shock symptoms.
33. Describe the progression from infection through sepis/septic shock and ultimately to
multisystem organ dysfunction syndrome. How do these pathologic processes result in
decreased perfusion and impaired cellular metabolism?
34. What is the etiology of the shock complications ARDS, DIC, and acute renal failure?
18
GNUR 293 Pathophysiology
Combined Study Guide
To help study for the cumulative final, please revisit your study guides from previous chapters. Focus
your attention on the following points. You are also responsible for the normal ranges for the lab tests you
have learned throughout the semester.
Study Guide: Mechanisms of and Cellular Responses to Injury
1. What are the differences and similarities among the following: hypoxemia, hypoxia, anoxia, and
ischemia?
2. Explain what happens to cells that are not adequately oxygenated in regard to cell metabolism, cell
membrane permeability, ATP production, cell pH, electrolyte and water movement across the cell
membrane.
3. What is oxidative stress and what are the characteristics of reactive oxygen species (ROS)?
How do reactive oxygen species cause damage to cell lipids, proteins, and DNA?
Under what normal physiological and pathophysiological conditions are reactive oxygen species
produced?
8. What changes occur in cells when they undergo the following alterations?
Explain examples of factors that can cause cells to undergo the following alterations.
f. atrophy
g. hypertrophy
h. hyperplasia
i. metaplasia
j. dysplasia
Study Guide: Innate Immunity: The Inflammatory Response
2. Explain the functions of the following cell types in the inflammatory response.
a. mast cells
b. neutrophils
c. monocytes/macrophages
d. eosinophils
e. endothelial cells
3. Describe the functions of the following chemical mediators involved in inflammation:
a. histamine
b. cytokines (interleukins, TNF- alpha, interferon)
c. leukotrienes
d. prostaglandins
4. Explain the general functions of the following plasma protein systems that are part of the acute phase
response involved in inflammation:
a. the complement system
b. the coagulation system
c. the kinin system
5. What activates the inflammatory response and what are the normal functions of the inflammatory
response?
19
6. Explain the causes and effects of the following events that occur during the inflammatory response:
d. Vasodilation/Increased vascular permeability
e. Emigration of leukocytes
f. Phagocytosis
8. Explain the physiological basis for the following manifestations of inflammation: erythema, warmth,
edema, pain, loss of function.
Study Guide: Fluid and Electrolyte Imbalances
3. Explain how the serum sodium, urine volume, urine specific gravity, and hematocrit would change in
states of fluid deficit. Explain how these parameters would change in states of fluid excess.
4. Explain the effects of infusion of an isotonic, hypotonic, and hypertonic intravenous solution on cell
volume. Give an example of each type of solution and provide a clinical situation for which each of these
3 types of solutions would be used.
5. Explain how conditions that alter the Starling forces [capillary hydrostatic pressure, capillary oncotic
(colloid osmotic) pressure, and capillary permeability] lead to edema formation. Why does obstruction of
lymphatic drainage result in edema? What are the adverse effects of edema formation?
6. How do antidiuretic hormone (ADH), the rennin-angiotensin-aldosterone system (RAAS), and
natriuretic hormones (natriuretic peptides) function in the regulation of fluid and electrolyte balance?
7. Explain common causes and clinical manifestations of fluid deficit and fluid excess states.
10. What are common causes of hyponatremia? Explain the effects of hyponatremia on cell volume and
central nervous system function. How is hyponatremia treated?
11. What are common causes of hypernatremia? Explain the effects of hypernatremia on cell volume and
central nervous system function. How is hypernatremia treated?
12. Explain the causes of hypokalemia and its effects on cardiac and neuromuscular function. How is
hypokalemia treated?
13. Explain the causes of hyperkalemia and its effects on cardiac and neuromuscular function. How is
hyperkalemia treated?
Study Guide: Acid-Base Imbalances
2. Although acids are ingested in the diet and produced as by-products of metabolism, why do people not
usually become acidotic? Hint: explain the chemical, renal, and respiratory buffering mechanisms.
3. Describe the limitations in regard to renal and respiratory buffering in cases of acid-base imbalance.
4. Explain why hypokalemia can lead to metabolic alkalosis and hyperkalemia can lead to metabolic
acidosis. Why does the serum potassium level increase in acidosis and decrease in alkalosis?
8. Compare and contrast metabolic acidosis and respiratory acidosis in regard to their causes, clinical
manifestations, blood gas values in uncompensated states, partially compensated, and fully compensated
states, and treatment.
20
9. Compare and contrast metabolic alkalosis and respiratory alkalosis in regard to their causes, clinical
manifestations, blood gas values in uncompensated, partially compensated, and fully compensated states,
and treatment. (It may be helpful to make a chart for items #8 and 9 to view the similarities and
differences.)
10. Be able to interpret arterial blood gas results when presented with pH, PaCO2, and HCO3-. Also, if
presented with a clinical condition (e.g. prolonged vomiting or hyperventilation), be able to anticipate
how these values might be affected.
Study Guide: Alterations in Immune Function
Cell and Chemical Mediators Involved in Immune Disorders
1. What are the differences between humoral and cell-mediated immunity? Which cells are the major
participants in each?
2. Through which mechanisms do antibodies and T cytotoxic cells protect the body against an invader?
3. Describe the differences between active and passive immunity and give examples of each. Why is
passive immunity short-lived? Explain how these systems work together to create a robust immune
response.
4. Differentiate between a primary and secondary immune response. Why is the body able to mount a
faster response during a secondary antigen exposure?
5. What are the differences between the four types of hypersensitivity reactions? What role does
inflammation and/or complement play in each? Which involve a humoral immune response and which are
cell-mediated? Give an example for each reaction.
6. Describe how an individual becomes sensitized to an allergen in type I hypersensitivity reactions.
Describe the common clinical manifestations of allergy reactions and anaphylaxis.
8. Describe the stimuli of the three hypersensitivity reactions: allergy, autoimmunity, and alloimmunity.
Discuss the significance of human leukocyte antigen (HLA, also known as major histocompatibility
complex) in autoimmune and alloimmune reactions.
11. What are the implications of having a deficiency of B lymphocytes, T lymphocytes, and of both?
What therapies are appropriate for these disorders?
13. Discuss the pathogenesis of acquired immune deficiency syndrome (AIDS).
15. Describe clinical symptoms that indicate potential HIV infection and its progression to AIDS.
Study Guide: Diabetes Mellitus Part I & II
4. Discuss the similarities and differences in the pathophysiology and clinical manifestations of type 1 and
type 2 diabetes mellitus.
6. Discuss the different types of diagnostic tests for DM. What are the advantages/disadvantages of each?
7. Compare and contrast the acute diabetic complications DKA and HHNS.
21
8. What are the clinical manifestations of hypoglycemia?
9. List the chronic complications of diabetes mellitus and discuss how maintaining blood glucose levels
within normal limits the cellular degeneration in each instance.
Study Guide: Alterations in Flow (Atherosclerosis and Thromboembolic Disorders)
2. Describe how alterations in vascular flow result in blood vessel obstructions (i.e. thrombi). How do the
other risk factors in Virchow's triad contribute to spontaneous clot formation?
3. Compare/contrast the expected clinical manifestations for an arterial vs. venous occlusion.
5. Explain the stepwise progression of atherosclerosis.
6. Identify the risk factors for atherosclerosis. How does diabetes mellitus contribute to atherosclerosis?
Study Guide: Hypertension and Stroke
3. Discuss how factors (autonomic control, neural receptors) regulate blood pressure. How do hormones
(ADH, RAAS, NPs) influence cardiac output/peripheral resistance (and thus affect blood pressure)? What
other clinical events can affect cardiac output and/or peripheral resistance?
6. What are the principles of treatment for hypertension?
8. How do the two types of stroke (ischemic and hemorrhagic) differ in regards to risk factors, prevention
strategies, and acute management?
Study Guide: Coronary Heart Disease and Acute Coronary Syndromes
1. How does atherosclerosis contribute to coronary artery disease and acute coronary syndromes? What
atherosclerotic events are responsible for the progression of disease?
3. Compare and contrast the 3 different types of angina. What is the pathophysiological process behind
each? Which impact coronary perfusion (i.e. supply) and which impact cardiac workload (i.e. demand)?
6. Compare and contrast the acute coronary syndromes (unstable angina vs. NSTEMI vs. STEMI). Where
do cardiac biomarkers originate from and how do they contribute to a diagnosis in ACS?
7. What are the goals of treatment for myocardial ischemia and myocardial infarction? Which treatments
can improve the coronary perfusion? Which decrease cardiac workload? Be able to explain the
mechanisms through which these effects occur.
Study Guide: Heart Failure
1. Discuss how factors influencing cardiac output reflect cardiac performance. (Include stroke volume,
contractility, preload, afterload, heart rate, and ejection fraction.)
3. Compare and contrast left and right heart failure, including etiology, clinical manifestations, treatment,
and complications. What is meant by forward and backward effects of heart failure?
4. Discuss the compensatory mechanisms of sympathetic nervous system activation, increasing preload,
and myocardial hypertrophy/remodeling. How are these processes helpful? How do these processes
eventually contribute to worsening heart failure?
22
Study Guide: Alterations in Kidney Function
3. Discuss the etiology of urinary tract infections (acute cystitis). Describe the development of acute and
chronic pyelonephritis independent of cystitis and as a complication of cystitis. How is pyelonephritis
similar to/different from cystitis in terms of severity, clinical manifestations, and treatment?
5. Identify the causes of glomerulonephritis and the resulting changes in glomerular structure and
function. How does the pathology of this condition contribute to the clinical manifestations? Compare and
contrast nephrotic syndrome and nephritic syndrome.
6. Discuss the pathology and staging of severity in acute kidney injury. How does the pathology
contribute to the clinical manifestations observed with this condition (specifically oliguria and increased
serum nitrogenous wastes)? Differentiate between prerenal, intrarenal, and postrenal causes of acute renal
failure.
7. Discuss the pathology and staging of severity in chronic kidney disease. How does the pathology
contribute to the systemic manifestations of chronic renal failure? Explain what is meant by the term
uremia.
Study Guide: Alterations in Gas Exchange and Obstructive Pulmonary Disorders
2. Compare and contrast the different kinds of Ventilation/Perfusion imbalances. Give clinical examples
for each.
3. What is the pathophysiology of pulmonary hypertension and how does it progress to cor pulmonale?
How is cor pulmonale different from other R heart failure causes?
4. Compare and contrast pulmonary edema and embolus. How does each contribute to a dysfunction in
ventilation, diffusion, and/or perfusion?
5. What etiologies and clinical signs/symptoms are common to all obstructive pulmonary orders?
6. Discuss the importance of pulmonary function testing in diagnosing and maintaining obstructive
pulmonary disorders. What information do the FEV1 and FVC values provide? What trends would you
expect in these values for obstructive [and restrictive] pulmonary disorders?
7. Discuss the role of IgE, mast cells, and inflammation in asthma as it contributes to immediate and
delayed (secondary) bronchial hyper-responsiveness and airway obstruction. How does tissue remodeling
contribute to airway impairment with this condition? Discuss how environmental controls, preventive
strategies, and medications target different etiologies when treating asthma.
8. Discuss the similarities and differences in the clinical manifestations, underlying mechanisms, and
consequences of obstructive pulmonary diseases like chronic bronchitis and emphysema. Explain the
descriptors “blue bloater” and “pink puffer”. Discuss the treatment for COPD.
Study Guide: Restrictive Pulmonary Disorders
1. What etiologies and clinical signs/symptoms are common to all restrictive pulmonary orders?
4. How do the pathological processes of acute respiratory distress syndrome contribute to acute
respiratory failure? Explain the processes responsible for the clinical manifestations of ARDS. Why is
positive end-expiratory pressure (PEEP) an effective treatment for ARDS?
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6. Discuss the clinical symptoms and underlying mechanisms of pneumonia. How do these mechanisms
determine which patients are at-risk for developing pneumonia?
7. Define acute respiratory failure. How would this condition present clinically? What would be
appropriate therapies?
Study Guide: Oxygen Transport Pathophysiology and Anemia
1. Discuss the unique structure and function of hemoglobin in the human body. What role does it play in
O2 and CO2 transport? What role does iron play in the production of hemoglobin?
4. Define anemia and discuss the various methods of classifying the anemias.
5. Describe the clinical manifestations of anemia and discuss the pathophysiology that generates them.
6. Compare and contrast the decreased RBC production anemias (aplastic, pernicious, iron-deficiency).
7. Compare and contrast the inherited and extrinsic hemolytic anemias (thalassemia and sickle cell, and
hemolytic disease of the newborn). What factors precipitate a crisis in sickle cell patients?
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