Nursing Pathophysiology Exam - Questions and Answers - Respiratory & Oxygenation Pathophysiology
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 nephrotic syndrome presents with proteinuria >3.5 g/day, hypoalbuminemia, edema, hyperlipidemia. What is pathophysiology?
A. Only nephritic
B. No proteinuria
C. 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
D. Nephritic hematuria HTN
Answer: C
Rationale: Nephrotic increased glomerular permeability podocyte injury proteinuria >3.5 g hypoalbuminemia decreased oncotic edema hyperlipidemia liver
lipoprotein synthesis loss antithrombin III hypercoagulable.
2. A patient with osteoarthritis knee pain worse activity morning <30 min crepitus no systemic. Pathophysiology?
A. No OA
B. Only RA
C. OA degenerative wear tear cartilage loss decreased proteoglycan chondrocyte dysfunction osteophyte formation, non-inflammatory pain worse activity
morning <30 min crepitus no systemic
D. RA
Answer: C
Rationale: OA degenerative cartilage loss decreased proteoglycan chondrocyte dysfunction osteophyte non-inflammatory pain worse activity morning <30 min
crepitus.
3. A patient with hyperthyroidism presents with weight loss, heat intolerance, tremor, palpitations, exophthalmos, low TSH high free T4. What is
pathophysiology?
A. Hyperthyroidism Graves autoimmune TSI stimulates TSH receptor increased T4 T3 increased basal metabolic rate heat intolerance weight loss tremor
palpitations increased beta adrenergic, exophthalmos glycosaminoglycan deposition retroorbital
B. Hypothyroidism
C. Only hypothyroid
D. No hyperthyroid
Answer: A
Rationale: Hyperthyroidism Graves TSI stimulates TSH receptor increased T4 T3 increased BMR heat intolerance weight loss tremor palpitations beta
adrenergic exophthalmos glycosaminoglycan deposition.
4. A patient with hyperthyroidism presents with weight loss, heat intolerance, tremor, palpitations, exophthalmos, low TSH high free T4. What is
pathophysiology?
A. Only hypothyroid
B. Hyperthyroidism Graves autoimmune TSI stimulates TSH receptor increased T4 T3 increased basal metabolic rate heat intolerance weight loss tremor
palpitations increased beta adrenergic, exophthalmos glycosaminoglycan deposition retroorbital
C. Hypothyroidism
D. No hyperthyroid
Answer: B
Rationale: Hyperthyroidism Graves TSI stimulates TSH receptor increased T4 T3 increased BMR heat intolerance weight loss tremor palpitations beta
adrenergic exophthalmos glycosaminoglycan deposition.
5. A 70-year-old with sudden unilateral weakness, facial droop, aphasia, CT shows ischemic stroke. What is pathophysiology?
A. Only hemorrhage
B. No stroke
C. 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
D. Hemorrhage only
Answer: C
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.
6. A patient with acute pancreatitis presents with severe epigastric pain radiating back, nausea vomiting, elevated lipase 3x normal, alcohol use.
What is pathophysiology?
A. Only gastritis
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 autodigestion
D. No pancreatitis
Answer: B
Rationale: Acute pancreatitis premature activation trypsin autodigestion inflammation edema hemorrhage alcohol gallstones duct obstruction SIRS lipase
amylase elevated hypocalcemia fat necrosis.
7. 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. Sympathetic activation RAAS activation vasoconstriction sodium water retention increased preload afterload, ventricular remodeling hypertrophy dilation,
initially compensatory eventually maladaptive increased myocardial oxygen demand
B. No compensation
,C. No RAAS
D. Only decreased RAAS
Answer: A
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.
8. A patient with nephritic syndrome presents with hematuria, proteinuria <3.5 g, hypertension, oliguria, RBC casts. What is pathophysiology?
A. Nephritic - glomerular inflammation immune complex deposition decreased GFR sodium water retention HTN oliguria, RBC casts hematuria, proteinuria <3.5
g, example post-strep GN IgA nephropathy
B. Only nephrotic
C. No hematuria
D. Nephrotic only
Answer: A
Rationale: Nephritic glomerular inflammation immune complex decreased GFR Na water retention HTN oliguria RBC casts hematuria proteinuria <3.5 g
post-strep IgA.
9. A patient with DKA presents with polyuria, polydipsia, nausea vomiting, abdominal pain, Kussmaul breathing, glucose 450 mg/dL, pH 7.1,
bicarbonate 8, ketones positive. Pathophysiology?
A. No acidosis
B. DKA absolute insulin deficiency increased glucagon increased lipolysis ketogenesis beta-hydroxybutyrate acetoacetate metabolic acidosis pH low
bicarbonate low Kussmaul compensation hyperglycemia osmotic diuresis polyuria polydipsia dehydration
C. HHNKS
D. Only HHNKS
Answer: B
Rationale: DKA absolute insulin deficiency increased glucagon lipolysis ketogenesis beta-hydroxybutyrate acetoacetate metabolic acidosis low pH low
bicarbonate Kussmaul compensation hyperglycemia osmotic diuresis polyuria polydipsia dehydration.
10. A patient with peptic ulcer disease epigastric pain, H. pylori positive, NSAID use. Pathophysiology?
A. Only stress
B. PUD imbalance aggressive factors acid pepsin H. pylori NSAID decreased protective mucus bicarbonate prostaglandin, H. pylori urease ammonia
inflammation
C. No ulcer
D. No H. pylori
Answer: B
Rationale: PUD imbalance aggressive acid pepsin H. pylori NSAID decreased protective mucus bicarbonate prostaglandin H. pylori urease ammonia
inflammation.
11. 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. No diabetes
C. Type 1 autoimmune beta cell destruction
D. Type 2 insulin resistance peripheral tissues decreased glucose uptake liver increased gluconeogenesis beta cell dysfunction relative insulin deficiency
glucotoxicity lipotoxicity obesity inflammation
Answer: D
Rationale: Type 2 diabetes insulin resistance peripheral decreased glucose uptake liver increased gluconeogenesis beta cell dysfunction relative insulin
deficiency glucotoxicity lipotoxicity obesity inflammation.
12. A patient with shock presents with hypotension tachycardia. What are types of shock pathophysiology?
A. Only hypovolemic
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. No shock types
D. Only one type
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.
13. 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. No compensation
B. Only decreased RAAS
C. Sympathetic activation RAAS activation vasoconstriction sodium water retention increased preload afterload, ventricular remodeling hypertrophy dilation,
initially compensatory eventually maladaptive increased myocardial oxygen demand
D. No RAAS
Answer: C
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.
14. 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 pancreatitis
, 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. Only gastritis
D. No autodigestion
Answer: B
Rationale: Acute pancreatitis premature activation trypsin autodigestion inflammation edema hemorrhage alcohol gallstones duct obstruction SIRS lipase
amylase elevated hypocalcemia fat necrosis.
15. 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. Only hyper
C. No thyroid
D. 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
Answer: D
Rationale: Hypothyroidism Hashimoto autoimmune lymphocytic infiltration decreased T4 T3 decreased BMR fatigue weight gain cold intolerance constipation
dry skin elevated TSH low free T4.
16. A patient with osteoarthritis knee pain worse activity morning <30 min crepitus no systemic. Pathophysiology?
A. Only 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. No OA
D. RA
Answer: B
Rationale: OA degenerative cartilage loss decreased proteoglycan chondrocyte dysfunction osteophyte non-inflammatory pain worse activity morning <30 min
crepitus.
17. 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 pancreatitis
B. No autodigestion
C. 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
D. Only gastritis
Answer: C
Rationale: Acute pancreatitis premature activation trypsin autodigestion inflammation edema hemorrhage alcohol gallstones duct obstruction SIRS lipase
amylase elevated hypocalcemia fat necrosis.
18. A patient with ARDS presents with severe hypoxemia PaO2/FiO2 <300, bilateral infiltrates, no cardiac failure, after sepsis. Pathophysiology?
A. Only cardiogenic
B. Cardiogenic edema
C. No ARDS
D. 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
Answer: D
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.
19. A patient with osteoarthritis knee pain worse activity morning <30 min crepitus no systemic. Pathophysiology?
A. No OA
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. RA
D. Only RA
Answer: B
Rationale: OA degenerative cartilage loss decreased proteoglycan chondrocyte dysfunction osteophyte non-inflammatory pain worse activity morning <30 min
crepitus.
20. 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. No compensation
B. Only decreased RAAS
C. Sympathetic activation RAAS activation vasoconstriction sodium water retention increased preload afterload, ventricular remodeling hypertrophy dilation,
initially compensatory eventually maladaptive increased myocardial oxygen demand
D. No RAAS
Answer: C
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.
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 nephrotic syndrome presents with proteinuria >3.5 g/day, hypoalbuminemia, edema, hyperlipidemia. What is pathophysiology?
A. Only nephritic
B. No proteinuria
C. 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
D. Nephritic hematuria HTN
Answer: C
Rationale: Nephrotic increased glomerular permeability podocyte injury proteinuria >3.5 g hypoalbuminemia decreased oncotic edema hyperlipidemia liver
lipoprotein synthesis loss antithrombin III hypercoagulable.
2. A patient with osteoarthritis knee pain worse activity morning <30 min crepitus no systemic. Pathophysiology?
A. No OA
B. Only RA
C. OA degenerative wear tear cartilage loss decreased proteoglycan chondrocyte dysfunction osteophyte formation, non-inflammatory pain worse activity
morning <30 min crepitus no systemic
D. RA
Answer: C
Rationale: OA degenerative cartilage loss decreased proteoglycan chondrocyte dysfunction osteophyte non-inflammatory pain worse activity morning <30 min
crepitus.
3. A patient with hyperthyroidism presents with weight loss, heat intolerance, tremor, palpitations, exophthalmos, low TSH high free T4. What is
pathophysiology?
A. Hyperthyroidism Graves autoimmune TSI stimulates TSH receptor increased T4 T3 increased basal metabolic rate heat intolerance weight loss tremor
palpitations increased beta adrenergic, exophthalmos glycosaminoglycan deposition retroorbital
B. Hypothyroidism
C. Only hypothyroid
D. No hyperthyroid
Answer: A
Rationale: Hyperthyroidism Graves TSI stimulates TSH receptor increased T4 T3 increased BMR heat intolerance weight loss tremor palpitations beta
adrenergic exophthalmos glycosaminoglycan deposition.
4. A patient with hyperthyroidism presents with weight loss, heat intolerance, tremor, palpitations, exophthalmos, low TSH high free T4. What is
pathophysiology?
A. Only hypothyroid
B. Hyperthyroidism Graves autoimmune TSI stimulates TSH receptor increased T4 T3 increased basal metabolic rate heat intolerance weight loss tremor
palpitations increased beta adrenergic, exophthalmos glycosaminoglycan deposition retroorbital
C. Hypothyroidism
D. No hyperthyroid
Answer: B
Rationale: Hyperthyroidism Graves TSI stimulates TSH receptor increased T4 T3 increased BMR heat intolerance weight loss tremor palpitations beta
adrenergic exophthalmos glycosaminoglycan deposition.
5. A 70-year-old with sudden unilateral weakness, facial droop, aphasia, CT shows ischemic stroke. What is pathophysiology?
A. Only hemorrhage
B. No stroke
C. 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
D. Hemorrhage only
Answer: C
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.
6. A patient with acute pancreatitis presents with severe epigastric pain radiating back, nausea vomiting, elevated lipase 3x normal, alcohol use.
What is pathophysiology?
A. Only gastritis
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 autodigestion
D. No pancreatitis
Answer: B
Rationale: Acute pancreatitis premature activation trypsin autodigestion inflammation edema hemorrhage alcohol gallstones duct obstruction SIRS lipase
amylase elevated hypocalcemia fat necrosis.
7. 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. Sympathetic activation RAAS activation vasoconstriction sodium water retention increased preload afterload, ventricular remodeling hypertrophy dilation,
initially compensatory eventually maladaptive increased myocardial oxygen demand
B. No compensation
,C. No RAAS
D. Only decreased RAAS
Answer: A
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.
8. A patient with nephritic syndrome presents with hematuria, proteinuria <3.5 g, hypertension, oliguria, RBC casts. What is pathophysiology?
A. Nephritic - glomerular inflammation immune complex deposition decreased GFR sodium water retention HTN oliguria, RBC casts hematuria, proteinuria <3.5
g, example post-strep GN IgA nephropathy
B. Only nephrotic
C. No hematuria
D. Nephrotic only
Answer: A
Rationale: Nephritic glomerular inflammation immune complex decreased GFR Na water retention HTN oliguria RBC casts hematuria proteinuria <3.5 g
post-strep IgA.
9. A patient with DKA presents with polyuria, polydipsia, nausea vomiting, abdominal pain, Kussmaul breathing, glucose 450 mg/dL, pH 7.1,
bicarbonate 8, ketones positive. Pathophysiology?
A. No acidosis
B. DKA absolute insulin deficiency increased glucagon increased lipolysis ketogenesis beta-hydroxybutyrate acetoacetate metabolic acidosis pH low
bicarbonate low Kussmaul compensation hyperglycemia osmotic diuresis polyuria polydipsia dehydration
C. HHNKS
D. Only HHNKS
Answer: B
Rationale: DKA absolute insulin deficiency increased glucagon lipolysis ketogenesis beta-hydroxybutyrate acetoacetate metabolic acidosis low pH low
bicarbonate Kussmaul compensation hyperglycemia osmotic diuresis polyuria polydipsia dehydration.
10. A patient with peptic ulcer disease epigastric pain, H. pylori positive, NSAID use. Pathophysiology?
A. Only stress
B. PUD imbalance aggressive factors acid pepsin H. pylori NSAID decreased protective mucus bicarbonate prostaglandin, H. pylori urease ammonia
inflammation
C. No ulcer
D. No H. pylori
Answer: B
Rationale: PUD imbalance aggressive acid pepsin H. pylori NSAID decreased protective mucus bicarbonate prostaglandin H. pylori urease ammonia
inflammation.
11. 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. No diabetes
C. Type 1 autoimmune beta cell destruction
D. Type 2 insulin resistance peripheral tissues decreased glucose uptake liver increased gluconeogenesis beta cell dysfunction relative insulin deficiency
glucotoxicity lipotoxicity obesity inflammation
Answer: D
Rationale: Type 2 diabetes insulin resistance peripheral decreased glucose uptake liver increased gluconeogenesis beta cell dysfunction relative insulin
deficiency glucotoxicity lipotoxicity obesity inflammation.
12. A patient with shock presents with hypotension tachycardia. What are types of shock pathophysiology?
A. Only hypovolemic
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. No shock types
D. Only one type
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.
13. 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. No compensation
B. Only decreased RAAS
C. Sympathetic activation RAAS activation vasoconstriction sodium water retention increased preload afterload, ventricular remodeling hypertrophy dilation,
initially compensatory eventually maladaptive increased myocardial oxygen demand
D. No RAAS
Answer: C
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.
14. 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 pancreatitis
, 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. Only gastritis
D. No autodigestion
Answer: B
Rationale: Acute pancreatitis premature activation trypsin autodigestion inflammation edema hemorrhage alcohol gallstones duct obstruction SIRS lipase
amylase elevated hypocalcemia fat necrosis.
15. 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. Only hyper
C. No thyroid
D. 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
Answer: D
Rationale: Hypothyroidism Hashimoto autoimmune lymphocytic infiltration decreased T4 T3 decreased BMR fatigue weight gain cold intolerance constipation
dry skin elevated TSH low free T4.
16. A patient with osteoarthritis knee pain worse activity morning <30 min crepitus no systemic. Pathophysiology?
A. Only 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. No OA
D. RA
Answer: B
Rationale: OA degenerative cartilage loss decreased proteoglycan chondrocyte dysfunction osteophyte non-inflammatory pain worse activity morning <30 min
crepitus.
17. 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 pancreatitis
B. No autodigestion
C. 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
D. Only gastritis
Answer: C
Rationale: Acute pancreatitis premature activation trypsin autodigestion inflammation edema hemorrhage alcohol gallstones duct obstruction SIRS lipase
amylase elevated hypocalcemia fat necrosis.
18. A patient with ARDS presents with severe hypoxemia PaO2/FiO2 <300, bilateral infiltrates, no cardiac failure, after sepsis. Pathophysiology?
A. Only cardiogenic
B. Cardiogenic edema
C. No ARDS
D. 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
Answer: D
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.
19. A patient with osteoarthritis knee pain worse activity morning <30 min crepitus no systemic. Pathophysiology?
A. No OA
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. RA
D. Only RA
Answer: B
Rationale: OA degenerative cartilage loss decreased proteoglycan chondrocyte dysfunction osteophyte non-inflammatory pain worse activity morning <30 min
crepitus.
20. 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. No compensation
B. Only decreased RAAS
C. Sympathetic activation RAAS activation vasoconstriction sodium water retention increased preload afterload, ventricular remodeling hypertrophy dilation,
initially compensatory eventually maladaptive increased myocardial oxygen demand
D. No RAAS
Answer: C
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.
