Nursing Pathophysiology Exam - Questions and Answers - Cardiovascular & Hemodynamic Disorders
Nursing Pathophysiology | Cellular Injury Inflammation | Systemic Disorders | High Yield
TABLE OF CONTENTS
1. I. Cellular Injury - Reversible vs Irreversible, Necrosis vs Apoptosis, Oxidative Stress Free Radicals
2. II. Inflammation - Acute Inflammation Vascular Permeability Neutrophils, Chronic Inflammation Macrophages Lymphocytes Granuloma,
Inflammatory Mediators Histamine Prostaglandins Leukotrienes Cytokines
3. III. Cardiovascular - Heart Failure Compensatory Sympathetic RAAS Vasoconstriction Sodium Water Retention Preload Afterload Ventricular
Remodeling Hypertrophy Dilation Maladaptive BNP, Ischemic Heart Disease, Shock Types Hypovolemic Cardiogenic Distributive Obstructive
4. IV. Respiratory - COPD Chronic Bronchitis Emphysema Chronic Inflammation Goblet Hyperplasia Mucus Hypersecretion Loss Alveolar Septa
Elastic Recoil Air Trapping Barrel Chest FEV1/FVC <0.70, Asthma Chronic Inflammation Th2 Eosinophils IgE Mast Cell Histamine
Bronchoconstriction Reversible, ARDS Diffuse Alveolar Damage Increased Permeability Protein-Rich Edema Hyaline Membrane V/Q Mismatch
Shunt Hypoxemia Refractory
5. V. Endocrine - Type 2 Diabetes Insulin Resistance Decreased Glucose Uptake Liver Increased Gluconeogenesis Beta Cell Dysfunction Relative
Deficiency Glucotoxicity Lipotoxicity, Type 1 Autoimmune Beta Cell Destruction Absolute Deficiency, DKA Absolute Deficiency Lipolysis
Ketogenesis Beta-Hydroxybutyrate Acidosis pH <7.3 Bicarbonate <18 Kussmaul Polyuria, HHNKS Relative Deficiency No Ketosis Osm >320
Glucose >600 Dehydration Altered Mental, Hyperthyroidism Graves TSI TSH Receptor Increased T4 T3 BMR Tremor Palpitations Exophthalmos,
Hypothyroidism Hashimoto Lymphocytic Infiltration Decreased T4 T3 BMR Fatigue Weight Gain Cold Intolerance
6. VI. Renal - Nephrotic Increased Glomerular Permeability Podocyte Injury Proteinuria >3.5 g/day Hypoalbuminemia Decreased Oncotic Edema
Hyperlipidemia Loss Antithrombin Hypercoagulable, Nephritic Glomerular Inflammation Immune Complex Decreased GFR Sodium Water
Retention HTN Oliguria RBC Casts Hematuria Proteinuria <3.5 g Post-Strep IgA, AKI vs CKD
7. VII. Gastrointestinal & Hepatic - Cirrhosis Chronic Injury Fibrosis Nodules Portal Hypertension Increased Resistance Decreased Synthetic
Albumin Clotting Factors PT/INR Up Impaired Bilirubin Jaundice Ascites Varices Splenomegaly Estrogen Spider Angiomas Palmar Erythema,
Acute Pancreatitis Premature Trypsin Activation Autodigestion Inflammation Edema Hemorrhage Alcohol Gallstones SIRS Lipase Amylase
Hypocalcemia, PUD Imbalance Aggressive Acid Pepsin H. pylori NSAID Decreased Protective Mucus Bicarbonate Prostaglandin Urease
Ammonia
8. VIII. Neurological - Ischemic Stroke Thrombotic Embolic Occlusion Decreased Cerebral Blood Flow <20 mL/100g/min Ischemia Penumbra
Salvageable Excitotoxicity Glutamate Calcium Cytotoxic Edema Infarction, Normal Pressure Hydrocephalus Triad Wet Wobbly Wacky Confusion
Incontinence Gait Disturbance Enlarged Ventricles VP Shunt
9. IX. Immune - SLE Autoimmune Type III Hypersensitivity Immune Complex ANA dsDNA Low C3 C4 Butterfly Rash Photosensitivity Joint Pain
Nephritis, RA Autoimmune Chronic Synovitis Pannus TNF IL-1 IL-6 Joint Destruction RF Anti-CCP Symmetric Small Joints Morning >30 min
Systemic, OA Degenerative Cartilage Loss Decreased Proteoglycan Chondrocyte Dysfunction Osteophyte Non-Inflammatory Pain Worse Activity
Morning <30 min Crepitus
10. X. Hematologic - Anemia Decreased Production Iron B12 Folate Erythropoietin Increased Destruction Hemolysis Blood Loss Hemorrhage
11. XI. Practice Questions - Each Asked Like Real Nursing Pathophysiology Exam
12. XII. Answer Key with Detailed Rationales
,NURSING PATHOPHYSIOLOGY EXAM - PRACTICE QUESTIONS - EACH QUESTION ASKED LIKE REAL EXAM
Based on Nursing Pathophysiology Blueprint - Cellular Injury Inflammation Cardiovascular Respiratory Endocrine Renal GI Hepatic Neuro Immune Hematologic. High Yield.
1. A patient with heart failure presents with dyspnea on exertion, orthopnea, PND, crackles, peripheral edema, weight gain, elevated BNP, EF 30%.
What compensatory mechanisms are activated?
A. Only decreased RAAS
B. Sympathetic activation RAAS activation vasoconstriction sodium water retention increased preload afterload, ventricular remodeling hypertrophy dilation,
initially compensatory eventually maladaptive increased myocardial oxygen demand
C. No compensation
D. No RAAS
Answer: B
Rationale: HF compensatory sympathetic RAAS vasoconstriction Na water retention increased preload afterload ventricular remodeling hypertrophy dilation
initially compensatory eventually maladaptive increased O2 demand BNP released stretch.
2. A patient with asthma presents with episodic wheezing, dyspnea, cough, reversible obstruction, eosinophils, IgE elevated. Pathophysiology?
A. Only COPD
B. Asthma chronic airway inflammation Th2 eosinophils IgE mast cell histamine leukotrienes bronchoconstriction mucus hypersecretion airway
hyperresponsiveness reversible obstruction
C. COPD fixed
D. No asthma
Answer: B
Rationale: Asthma chronic inflammation Th2 eosinophils IgE mast cell histamine leukotrienes bronchoconstriction mucus hyperresponsiveness reversible.
3. A patient with acute pancreatitis presents with severe epigastric pain radiating back, nausea vomiting, elevated lipase 3x normal, alcohol use.
What is pathophysiology?
A. No autodigestion
B. Only gastritis
C. No pancreatitis
D. Acute pancreatitis premature activation trypsin within pancreas autodigestion inflammation edema hemorrhage, alcohol gallstones cause duct obstruction,
systemic inflammatory response SIRS, lipase amylase elevated, risk hypocalcemia
Answer: D
Rationale: Acute pancreatitis premature activation trypsin autodigestion inflammation edema hemorrhage alcohol gallstones duct obstruction SIRS lipase
amylase elevated hypocalcemia fat necrosis.
4. A 60-year-old male with long history smoking, chronic cough, increased sputum, barrel chest, prolonged expiration, wheezing, FEV1/FVC <0.70,
FEV1 55% predicted. What is pathophysiology?
A. Asthma reversible
B. COPD - chronic bronchitis and emphysema - chronic inflammation, goblet cell hyperplasia mucus hypersecretion, loss alveolar septa decreased elastic recoil
air trapping barrel chest, obstruction FEV1/FVC <0.70, chronic hypoxia hypercapnia
C. No COPD
D. Only infection
Answer: B
Rationale: COPD pathophysiology chronic inflammation smoking goblet hyperplasia mucus hypersecretion emphysema loss alveolar septa decreased elastic
recoil air trapping barrel chest obstruction FEV1/FVC <0.70.
5. A patient with asthma presents with episodic wheezing, dyspnea, cough, reversible obstruction, eosinophils, IgE elevated. Pathophysiology?
A. No asthma
B. Only COPD
C. COPD fixed
D. Asthma chronic airway inflammation Th2 eosinophils IgE mast cell histamine leukotrienes bronchoconstriction mucus hypersecretion airway
hyperresponsiveness reversible obstruction
Answer: D
Rationale: Asthma chronic inflammation Th2 eosinophils IgE mast cell histamine leukotrienes bronchoconstriction mucus hyperresponsiveness reversible.
6. A patient with peptic ulcer disease epigastric pain, H. pylori positive, NSAID use. Pathophysiology?
A. No H. pylori
B. PUD imbalance aggressive factors acid pepsin H. pylori NSAID decreased protective mucus bicarbonate prostaglandin, H. pylori urease ammonia
inflammation
C. No ulcer
D. Only stress
Answer: B
Rationale: PUD imbalance aggressive acid pepsin H. pylori NSAID decreased protective mucus bicarbonate prostaglandin H. pylori urease ammonia
inflammation.
7. What is difference between DKA and HHNKS?
A. Same
B. DKA type 2
C. No difference
D. DKA type 1 absolute insulin deficiency ketosis metabolic acidosis pH <7.3 bicarbonate <18 ketones positive glucose 250-600, HHNKS type 2 relative
deficiency no ketosis pH >7.3 bicarbonate >18 osm >320 glucose >600 severe dehydration altered mental status
,Answer: D
Rationale: DKA type 1 absolute insulin deficiency ketosis acidosis pH <7.3 bicarbonate <18 ketones positive glucose 250-600, HHNKS type 2 relative
deficiency no ketosis pH >7.3 bicarbonate >18 osm >320 glucose >600 severe dehydration altered mental.
8. A patient with shock presents with hypotension tachycardia. What are types of shock pathophysiology?
A. Only hypovolemic
B. Only one type
C. No shock types
D. Types: hypovolemic decreased preload hemorrhage fluid loss, cardiogenic decreased contractility MI pump failure, distributive vasodilation sepsis
anaphylaxis neurogenic decreased SVR, obstructive decreased preload PE tamponade tension pneumothorax
Answer: D
Rationale: Shock types hypovolemic decreased preload hemorrhage fluid loss cardiogenic decreased contractility MI distributive vasodilation sepsis
anaphylaxis neurogenic decreased SVR obstructive decreased preload PE tamponade tension pneumothorax.
9. A patient with acute pancreatitis presents with severe epigastric pain radiating back, nausea vomiting, elevated lipase 3x normal, alcohol use.
What is pathophysiology?
A. No autodigestion
B. Acute pancreatitis premature activation trypsin within pancreas autodigestion inflammation edema hemorrhage, alcohol gallstones cause duct obstruction,
systemic inflammatory response SIRS, lipase amylase elevated, risk hypocalcemia
C. No pancreatitis
D. Only gastritis
Answer: B
Rationale: Acute pancreatitis premature activation trypsin autodigestion inflammation edema hemorrhage alcohol gallstones duct obstruction SIRS lipase
amylase elevated hypocalcemia fat necrosis.
10. A 70-year-old with sudden unilateral weakness, facial droop, aphasia, CT shows ischemic stroke. What is pathophysiology?
A. Ischemic stroke thrombotic or embolic occlusion cerebral artery decreased cerebral blood flow <20 mL/100g/min ischemia, penumbra salvageable,
excitotoxicity glutamate calcium influx, cytotoxic edema, if >10 min infarction
B. Hemorrhage only
C. No stroke
D. Only hemorrhage
Answer: A
Rationale: Ischemic stroke thrombotic embolic occlusion decreased cerebral blood flow <20 mL/100g/min ischemia penumbra salvageable excitotoxicity
glutamate calcium influx cytotoxic edema infarction if >10 min.
11. A patient with peptic ulcer disease epigastric pain, H. pylori positive, NSAID use. Pathophysiology?
A. No H. pylori
B. No ulcer
C. PUD imbalance aggressive factors acid pepsin H. pylori NSAID decreased protective mucus bicarbonate prostaglandin, H. pylori urease ammonia
inflammation
D. Only stress
Answer: C
Rationale: PUD imbalance aggressive acid pepsin H. pylori NSAID decreased protective mucus bicarbonate prostaglandin H. pylori urease ammonia
inflammation.
12. A patient with osteoarthritis knee pain worse activity morning <30 min crepitus no systemic. Pathophysiology?
A. RA
B. OA degenerative wear tear cartilage loss decreased proteoglycan chondrocyte dysfunction osteophyte formation, non-inflammatory pain worse activity
morning <30 min crepitus no systemic
C. Only RA
D. No OA
Answer: B
Rationale: OA degenerative cartilage loss decreased proteoglycan chondrocyte dysfunction osteophyte non-inflammatory pain worse activity morning <30 min
crepitus.
13. A patient with shock presents with hypotension tachycardia. What are types of shock pathophysiology?
A. No shock types
B. Types: hypovolemic decreased preload hemorrhage fluid loss, cardiogenic decreased contractility MI pump failure, distributive vasodilation sepsis
anaphylaxis neurogenic decreased SVR, obstructive decreased preload PE tamponade tension pneumothorax
C. Only one type
D. Only hypovolemic
Answer: B
Rationale: Shock types hypovolemic decreased preload hemorrhage fluid loss cardiogenic decreased contractility MI distributive vasodilation sepsis
anaphylaxis neurogenic decreased SVR obstructive decreased preload PE tamponade tension pneumothorax.
14. A 45-year-old with polyuria, polydipsia, polyphagia, fasting glucose 210 mg/dL, HbA1c 9.2%, obesity, insulin resistance. What is pathophysiology
of type 2 diabetes?
A. Only type 1
B. Type 2 insulin resistance peripheral tissues decreased glucose uptake liver increased gluconeogenesis beta cell dysfunction relative insulin deficiency
glucotoxicity lipotoxicity obesity inflammation
C. Type 1 autoimmune beta cell destruction
, D. No diabetes
Answer: B
Rationale: Type 2 diabetes insulin resistance peripheral decreased glucose uptake liver increased gluconeogenesis beta cell dysfunction relative insulin
deficiency glucotoxicity lipotoxicity obesity inflammation.
15. A patient with anemia fatigue pallor low Hb Hct. What are types pathophysiology?
A. No anemia types
B. Anemia decreased RBC production iron deficiency B12 folate deficiency decreased erythropoietin, increased destruction hemolysis, blood loss hemorrhage
C. Only blood loss
D. Only one type
Answer: B
Rationale: Anemia decreased production iron B12 folate erythropoietin increased destruction hemolysis blood loss.
16. A patient with nephrotic syndrome presents with proteinuria >3.5 g/day, hypoalbuminemia, edema, hyperlipidemia. What is pathophysiology?
A. Only nephritic
B. Nephritic hematuria HTN
C. No proteinuria
D. Nephrotic - increased glomerular permeability loss negative charge podocyte injury proteinuria >3.5 g/day hypoalbuminemia decreased oncotic pressure
edema liver increased lipoprotein synthesis hyperlipidemia loss antithrombin III hypercoagulable
Answer: D
Rationale: Nephrotic increased glomerular permeability podocyte injury proteinuria >3.5 g hypoalbuminemia decreased oncotic edema hyperlipidemia liver
lipoprotein synthesis loss antithrombin III hypercoagulable.
17. A patient with shock presents with hypotension tachycardia. What are types of shock pathophysiology?
A. Types: hypovolemic decreased preload hemorrhage fluid loss, cardiogenic decreased contractility MI pump failure, distributive vasodilation sepsis
anaphylaxis neurogenic decreased SVR, obstructive decreased preload PE tamponade tension pneumothorax
B. Only hypovolemic
C. No shock types
D. Only one type
Answer: A
Rationale: Shock types hypovolemic decreased preload hemorrhage fluid loss cardiogenic decreased contractility MI distributive vasodilation sepsis
anaphylaxis neurogenic decreased SVR obstructive decreased preload PE tamponade tension pneumothorax.
18. What is difference between DKA and HHNKS?
A. DKA type 1 absolute insulin deficiency ketosis metabolic acidosis pH <7.3 bicarbonate <18 ketones positive glucose 250-600, HHNKS type 2 relative
deficiency no ketosis pH >7.3 bicarbonate >18 osm >320 glucose >600 severe dehydration altered mental status
B. Same
C. No difference
D. DKA type 2
Answer: A
Rationale: DKA type 1 absolute insulin deficiency ketosis acidosis pH <7.3 bicarbonate <18 ketones positive glucose 250-600, HHNKS type 2 relative
deficiency no ketosis pH >7.3 bicarbonate >18 osm >320 glucose >600 severe dehydration altered mental.
19. A patient with ARDS presents with severe hypoxemia PaO2/FiO2 <300, bilateral infiltrates, no cardiac failure, after sepsis. Pathophysiology?
A. ARDS diffuse alveolar damage increased alveolar-capillary permeability protein-rich edema, hyaline membrane formation, decreased compliance, V/Q
mismatch shunt severe hypoxemia refractory to O2, due to sepsis pneumonia aspiration
B. No ARDS
C. Only cardiogenic
D. Cardiogenic edema
Answer: A
Rationale: ARDS diffuse alveolar damage increased permeability protein-rich edema hyaline membrane decreased compliance V/Q mismatch shunt severe
hypoxemia refractory O2 sepsis pneumonia aspiration.
20. A patient with hypothyroidism presents with fatigue, weight gain, cold intolerance, constipation, dry skin, elevated TSH low free T4. What is
pathophysiology?
A. Hyperthyroid
B. Hypothyroidism Hashimoto autoimmune thyroiditis lymphocytic infiltration decreased T4 T3 decreased BMR fatigue weight gain cold intolerance constipation
dry skin elevated TSH feedback low free T4
C. Only hyper
D. No thyroid
Answer: B
Rationale: Hypothyroidism Hashimoto autoimmune lymphocytic infiltration decreased T4 T3 decreased BMR fatigue weight gain cold intolerance constipation
dry skin elevated TSH low free T4.
21. A patient with acute pancreatitis presents with severe epigastric pain radiating back, nausea vomiting, elevated lipase 3x normal, alcohol use.
What is pathophysiology?
A. Acute pancreatitis premature activation trypsin within pancreas autodigestion inflammation edema hemorrhage, alcohol gallstones cause duct obstruction,
systemic inflammatory response SIRS, lipase amylase elevated, risk hypocalcemia
B. No autodigestion
C. No pancreatitis
D. Only gastritis
Nursing Pathophysiology | Cellular Injury Inflammation | Systemic Disorders | High Yield
TABLE OF CONTENTS
1. I. Cellular Injury - Reversible vs Irreversible, Necrosis vs Apoptosis, Oxidative Stress Free Radicals
2. II. Inflammation - Acute Inflammation Vascular Permeability Neutrophils, Chronic Inflammation Macrophages Lymphocytes Granuloma,
Inflammatory Mediators Histamine Prostaglandins Leukotrienes Cytokines
3. III. Cardiovascular - Heart Failure Compensatory Sympathetic RAAS Vasoconstriction Sodium Water Retention Preload Afterload Ventricular
Remodeling Hypertrophy Dilation Maladaptive BNP, Ischemic Heart Disease, Shock Types Hypovolemic Cardiogenic Distributive Obstructive
4. IV. Respiratory - COPD Chronic Bronchitis Emphysema Chronic Inflammation Goblet Hyperplasia Mucus Hypersecretion Loss Alveolar Septa
Elastic Recoil Air Trapping Barrel Chest FEV1/FVC <0.70, Asthma Chronic Inflammation Th2 Eosinophils IgE Mast Cell Histamine
Bronchoconstriction Reversible, ARDS Diffuse Alveolar Damage Increased Permeability Protein-Rich Edema Hyaline Membrane V/Q Mismatch
Shunt Hypoxemia Refractory
5. V. Endocrine - Type 2 Diabetes Insulin Resistance Decreased Glucose Uptake Liver Increased Gluconeogenesis Beta Cell Dysfunction Relative
Deficiency Glucotoxicity Lipotoxicity, Type 1 Autoimmune Beta Cell Destruction Absolute Deficiency, DKA Absolute Deficiency Lipolysis
Ketogenesis Beta-Hydroxybutyrate Acidosis pH <7.3 Bicarbonate <18 Kussmaul Polyuria, HHNKS Relative Deficiency No Ketosis Osm >320
Glucose >600 Dehydration Altered Mental, Hyperthyroidism Graves TSI TSH Receptor Increased T4 T3 BMR Tremor Palpitations Exophthalmos,
Hypothyroidism Hashimoto Lymphocytic Infiltration Decreased T4 T3 BMR Fatigue Weight Gain Cold Intolerance
6. VI. Renal - Nephrotic Increased Glomerular Permeability Podocyte Injury Proteinuria >3.5 g/day Hypoalbuminemia Decreased Oncotic Edema
Hyperlipidemia Loss Antithrombin Hypercoagulable, Nephritic Glomerular Inflammation Immune Complex Decreased GFR Sodium Water
Retention HTN Oliguria RBC Casts Hematuria Proteinuria <3.5 g Post-Strep IgA, AKI vs CKD
7. VII. Gastrointestinal & Hepatic - Cirrhosis Chronic Injury Fibrosis Nodules Portal Hypertension Increased Resistance Decreased Synthetic
Albumin Clotting Factors PT/INR Up Impaired Bilirubin Jaundice Ascites Varices Splenomegaly Estrogen Spider Angiomas Palmar Erythema,
Acute Pancreatitis Premature Trypsin Activation Autodigestion Inflammation Edema Hemorrhage Alcohol Gallstones SIRS Lipase Amylase
Hypocalcemia, PUD Imbalance Aggressive Acid Pepsin H. pylori NSAID Decreased Protective Mucus Bicarbonate Prostaglandin Urease
Ammonia
8. VIII. Neurological - Ischemic Stroke Thrombotic Embolic Occlusion Decreased Cerebral Blood Flow <20 mL/100g/min Ischemia Penumbra
Salvageable Excitotoxicity Glutamate Calcium Cytotoxic Edema Infarction, Normal Pressure Hydrocephalus Triad Wet Wobbly Wacky Confusion
Incontinence Gait Disturbance Enlarged Ventricles VP Shunt
9. IX. Immune - SLE Autoimmune Type III Hypersensitivity Immune Complex ANA dsDNA Low C3 C4 Butterfly Rash Photosensitivity Joint Pain
Nephritis, RA Autoimmune Chronic Synovitis Pannus TNF IL-1 IL-6 Joint Destruction RF Anti-CCP Symmetric Small Joints Morning >30 min
Systemic, OA Degenerative Cartilage Loss Decreased Proteoglycan Chondrocyte Dysfunction Osteophyte Non-Inflammatory Pain Worse Activity
Morning <30 min Crepitus
10. X. Hematologic - Anemia Decreased Production Iron B12 Folate Erythropoietin Increased Destruction Hemolysis Blood Loss Hemorrhage
11. XI. Practice Questions - Each Asked Like Real Nursing Pathophysiology Exam
12. XII. Answer Key with Detailed Rationales
,NURSING PATHOPHYSIOLOGY EXAM - PRACTICE QUESTIONS - EACH QUESTION ASKED LIKE REAL EXAM
Based on Nursing Pathophysiology Blueprint - Cellular Injury Inflammation Cardiovascular Respiratory Endocrine Renal GI Hepatic Neuro Immune Hematologic. High Yield.
1. A patient with heart failure presents with dyspnea on exertion, orthopnea, PND, crackles, peripheral edema, weight gain, elevated BNP, EF 30%.
What compensatory mechanisms are activated?
A. Only decreased RAAS
B. Sympathetic activation RAAS activation vasoconstriction sodium water retention increased preload afterload, ventricular remodeling hypertrophy dilation,
initially compensatory eventually maladaptive increased myocardial oxygen demand
C. No compensation
D. No RAAS
Answer: B
Rationale: HF compensatory sympathetic RAAS vasoconstriction Na water retention increased preload afterload ventricular remodeling hypertrophy dilation
initially compensatory eventually maladaptive increased O2 demand BNP released stretch.
2. A patient with asthma presents with episodic wheezing, dyspnea, cough, reversible obstruction, eosinophils, IgE elevated. Pathophysiology?
A. Only COPD
B. Asthma chronic airway inflammation Th2 eosinophils IgE mast cell histamine leukotrienes bronchoconstriction mucus hypersecretion airway
hyperresponsiveness reversible obstruction
C. COPD fixed
D. No asthma
Answer: B
Rationale: Asthma chronic inflammation Th2 eosinophils IgE mast cell histamine leukotrienes bronchoconstriction mucus hyperresponsiveness reversible.
3. A patient with acute pancreatitis presents with severe epigastric pain radiating back, nausea vomiting, elevated lipase 3x normal, alcohol use.
What is pathophysiology?
A. No autodigestion
B. Only gastritis
C. No pancreatitis
D. Acute pancreatitis premature activation trypsin within pancreas autodigestion inflammation edema hemorrhage, alcohol gallstones cause duct obstruction,
systemic inflammatory response SIRS, lipase amylase elevated, risk hypocalcemia
Answer: D
Rationale: Acute pancreatitis premature activation trypsin autodigestion inflammation edema hemorrhage alcohol gallstones duct obstruction SIRS lipase
amylase elevated hypocalcemia fat necrosis.
4. A 60-year-old male with long history smoking, chronic cough, increased sputum, barrel chest, prolonged expiration, wheezing, FEV1/FVC <0.70,
FEV1 55% predicted. What is pathophysiology?
A. Asthma reversible
B. COPD - chronic bronchitis and emphysema - chronic inflammation, goblet cell hyperplasia mucus hypersecretion, loss alveolar septa decreased elastic recoil
air trapping barrel chest, obstruction FEV1/FVC <0.70, chronic hypoxia hypercapnia
C. No COPD
D. Only infection
Answer: B
Rationale: COPD pathophysiology chronic inflammation smoking goblet hyperplasia mucus hypersecretion emphysema loss alveolar septa decreased elastic
recoil air trapping barrel chest obstruction FEV1/FVC <0.70.
5. A patient with asthma presents with episodic wheezing, dyspnea, cough, reversible obstruction, eosinophils, IgE elevated. Pathophysiology?
A. No asthma
B. Only COPD
C. COPD fixed
D. Asthma chronic airway inflammation Th2 eosinophils IgE mast cell histamine leukotrienes bronchoconstriction mucus hypersecretion airway
hyperresponsiveness reversible obstruction
Answer: D
Rationale: Asthma chronic inflammation Th2 eosinophils IgE mast cell histamine leukotrienes bronchoconstriction mucus hyperresponsiveness reversible.
6. A patient with peptic ulcer disease epigastric pain, H. pylori positive, NSAID use. Pathophysiology?
A. No H. pylori
B. PUD imbalance aggressive factors acid pepsin H. pylori NSAID decreased protective mucus bicarbonate prostaglandin, H. pylori urease ammonia
inflammation
C. No ulcer
D. Only stress
Answer: B
Rationale: PUD imbalance aggressive acid pepsin H. pylori NSAID decreased protective mucus bicarbonate prostaglandin H. pylori urease ammonia
inflammation.
7. What is difference between DKA and HHNKS?
A. Same
B. DKA type 2
C. No difference
D. DKA type 1 absolute insulin deficiency ketosis metabolic acidosis pH <7.3 bicarbonate <18 ketones positive glucose 250-600, HHNKS type 2 relative
deficiency no ketosis pH >7.3 bicarbonate >18 osm >320 glucose >600 severe dehydration altered mental status
,Answer: D
Rationale: DKA type 1 absolute insulin deficiency ketosis acidosis pH <7.3 bicarbonate <18 ketones positive glucose 250-600, HHNKS type 2 relative
deficiency no ketosis pH >7.3 bicarbonate >18 osm >320 glucose >600 severe dehydration altered mental.
8. A patient with shock presents with hypotension tachycardia. What are types of shock pathophysiology?
A. Only hypovolemic
B. Only one type
C. No shock types
D. Types: hypovolemic decreased preload hemorrhage fluid loss, cardiogenic decreased contractility MI pump failure, distributive vasodilation sepsis
anaphylaxis neurogenic decreased SVR, obstructive decreased preload PE tamponade tension pneumothorax
Answer: D
Rationale: Shock types hypovolemic decreased preload hemorrhage fluid loss cardiogenic decreased contractility MI distributive vasodilation sepsis
anaphylaxis neurogenic decreased SVR obstructive decreased preload PE tamponade tension pneumothorax.
9. A patient with acute pancreatitis presents with severe epigastric pain radiating back, nausea vomiting, elevated lipase 3x normal, alcohol use.
What is pathophysiology?
A. No autodigestion
B. Acute pancreatitis premature activation trypsin within pancreas autodigestion inflammation edema hemorrhage, alcohol gallstones cause duct obstruction,
systemic inflammatory response SIRS, lipase amylase elevated, risk hypocalcemia
C. No pancreatitis
D. Only gastritis
Answer: B
Rationale: Acute pancreatitis premature activation trypsin autodigestion inflammation edema hemorrhage alcohol gallstones duct obstruction SIRS lipase
amylase elevated hypocalcemia fat necrosis.
10. A 70-year-old with sudden unilateral weakness, facial droop, aphasia, CT shows ischemic stroke. What is pathophysiology?
A. Ischemic stroke thrombotic or embolic occlusion cerebral artery decreased cerebral blood flow <20 mL/100g/min ischemia, penumbra salvageable,
excitotoxicity glutamate calcium influx, cytotoxic edema, if >10 min infarction
B. Hemorrhage only
C. No stroke
D. Only hemorrhage
Answer: A
Rationale: Ischemic stroke thrombotic embolic occlusion decreased cerebral blood flow <20 mL/100g/min ischemia penumbra salvageable excitotoxicity
glutamate calcium influx cytotoxic edema infarction if >10 min.
11. A patient with peptic ulcer disease epigastric pain, H. pylori positive, NSAID use. Pathophysiology?
A. No H. pylori
B. No ulcer
C. PUD imbalance aggressive factors acid pepsin H. pylori NSAID decreased protective mucus bicarbonate prostaglandin, H. pylori urease ammonia
inflammation
D. Only stress
Answer: C
Rationale: PUD imbalance aggressive acid pepsin H. pylori NSAID decreased protective mucus bicarbonate prostaglandin H. pylori urease ammonia
inflammation.
12. A patient with osteoarthritis knee pain worse activity morning <30 min crepitus no systemic. Pathophysiology?
A. RA
B. OA degenerative wear tear cartilage loss decreased proteoglycan chondrocyte dysfunction osteophyte formation, non-inflammatory pain worse activity
morning <30 min crepitus no systemic
C. Only RA
D. No OA
Answer: B
Rationale: OA degenerative cartilage loss decreased proteoglycan chondrocyte dysfunction osteophyte non-inflammatory pain worse activity morning <30 min
crepitus.
13. A patient with shock presents with hypotension tachycardia. What are types of shock pathophysiology?
A. No shock types
B. Types: hypovolemic decreased preload hemorrhage fluid loss, cardiogenic decreased contractility MI pump failure, distributive vasodilation sepsis
anaphylaxis neurogenic decreased SVR, obstructive decreased preload PE tamponade tension pneumothorax
C. Only one type
D. Only hypovolemic
Answer: B
Rationale: Shock types hypovolemic decreased preload hemorrhage fluid loss cardiogenic decreased contractility MI distributive vasodilation sepsis
anaphylaxis neurogenic decreased SVR obstructive decreased preload PE tamponade tension pneumothorax.
14. A 45-year-old with polyuria, polydipsia, polyphagia, fasting glucose 210 mg/dL, HbA1c 9.2%, obesity, insulin resistance. What is pathophysiology
of type 2 diabetes?
A. Only type 1
B. Type 2 insulin resistance peripheral tissues decreased glucose uptake liver increased gluconeogenesis beta cell dysfunction relative insulin deficiency
glucotoxicity lipotoxicity obesity inflammation
C. Type 1 autoimmune beta cell destruction
, D. No diabetes
Answer: B
Rationale: Type 2 diabetes insulin resistance peripheral decreased glucose uptake liver increased gluconeogenesis beta cell dysfunction relative insulin
deficiency glucotoxicity lipotoxicity obesity inflammation.
15. A patient with anemia fatigue pallor low Hb Hct. What are types pathophysiology?
A. No anemia types
B. Anemia decreased RBC production iron deficiency B12 folate deficiency decreased erythropoietin, increased destruction hemolysis, blood loss hemorrhage
C. Only blood loss
D. Only one type
Answer: B
Rationale: Anemia decreased production iron B12 folate erythropoietin increased destruction hemolysis blood loss.
16. A patient with nephrotic syndrome presents with proteinuria >3.5 g/day, hypoalbuminemia, edema, hyperlipidemia. What is pathophysiology?
A. Only nephritic
B. Nephritic hematuria HTN
C. No proteinuria
D. Nephrotic - increased glomerular permeability loss negative charge podocyte injury proteinuria >3.5 g/day hypoalbuminemia decreased oncotic pressure
edema liver increased lipoprotein synthesis hyperlipidemia loss antithrombin III hypercoagulable
Answer: D
Rationale: Nephrotic increased glomerular permeability podocyte injury proteinuria >3.5 g hypoalbuminemia decreased oncotic edema hyperlipidemia liver
lipoprotein synthesis loss antithrombin III hypercoagulable.
17. A patient with shock presents with hypotension tachycardia. What are types of shock pathophysiology?
A. Types: hypovolemic decreased preload hemorrhage fluid loss, cardiogenic decreased contractility MI pump failure, distributive vasodilation sepsis
anaphylaxis neurogenic decreased SVR, obstructive decreased preload PE tamponade tension pneumothorax
B. Only hypovolemic
C. No shock types
D. Only one type
Answer: A
Rationale: Shock types hypovolemic decreased preload hemorrhage fluid loss cardiogenic decreased contractility MI distributive vasodilation sepsis
anaphylaxis neurogenic decreased SVR obstructive decreased preload PE tamponade tension pneumothorax.
18. What is difference between DKA and HHNKS?
A. DKA type 1 absolute insulin deficiency ketosis metabolic acidosis pH <7.3 bicarbonate <18 ketones positive glucose 250-600, HHNKS type 2 relative
deficiency no ketosis pH >7.3 bicarbonate >18 osm >320 glucose >600 severe dehydration altered mental status
B. Same
C. No difference
D. DKA type 2
Answer: A
Rationale: DKA type 1 absolute insulin deficiency ketosis acidosis pH <7.3 bicarbonate <18 ketones positive glucose 250-600, HHNKS type 2 relative
deficiency no ketosis pH >7.3 bicarbonate >18 osm >320 glucose >600 severe dehydration altered mental.
19. A patient with ARDS presents with severe hypoxemia PaO2/FiO2 <300, bilateral infiltrates, no cardiac failure, after sepsis. Pathophysiology?
A. ARDS diffuse alveolar damage increased alveolar-capillary permeability protein-rich edema, hyaline membrane formation, decreased compliance, V/Q
mismatch shunt severe hypoxemia refractory to O2, due to sepsis pneumonia aspiration
B. No ARDS
C. Only cardiogenic
D. Cardiogenic edema
Answer: A
Rationale: ARDS diffuse alveolar damage increased permeability protein-rich edema hyaline membrane decreased compliance V/Q mismatch shunt severe
hypoxemia refractory O2 sepsis pneumonia aspiration.
20. A patient with hypothyroidism presents with fatigue, weight gain, cold intolerance, constipation, dry skin, elevated TSH low free T4. What is
pathophysiology?
A. Hyperthyroid
B. Hypothyroidism Hashimoto autoimmune thyroiditis lymphocytic infiltration decreased T4 T3 decreased BMR fatigue weight gain cold intolerance constipation
dry skin elevated TSH feedback low free T4
C. Only hyper
D. No thyroid
Answer: B
Rationale: Hypothyroidism Hashimoto autoimmune lymphocytic infiltration decreased T4 T3 decreased BMR fatigue weight gain cold intolerance constipation
dry skin elevated TSH low free T4.
21. A patient with acute pancreatitis presents with severe epigastric pain radiating back, nausea vomiting, elevated lipase 3x normal, alcohol use.
What is pathophysiology?
A. Acute pancreatitis premature activation trypsin within pancreas autodigestion inflammation edema hemorrhage, alcohol gallstones cause duct obstruction,
systemic inflammatory response SIRS, lipase amylase elevated, risk hypocalcemia
B. No autodigestion
C. No pancreatitis
D. Only gastritis
