Nursing Pathophysiology Exam - Questions and Answers - Endocrine & Metabolic Dysfunctions
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 acute pancreatitis presents with severe epigastric pain radiating back, nausea vomiting, elevated lipase 3x normal, alcohol use.
What is pathophysiology?
A. No autodigestion
B. No pancreatitis
C. Only gastritis
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.
2. A patient with nephritic syndrome presents with hematuria, proteinuria <3.5 g, hypertension, oliguria, RBC casts. What is pathophysiology?
A. Nephrotic only
B. Only nephrotic
C. 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
D. No hematuria
Answer: C
Rationale: Nephritic glomerular inflammation immune complex decreased GFR Na water retention HTN oliguria RBC casts hematuria proteinuria <3.5 g
post-strep IgA.
3. 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. Type 2 insulin resistance peripheral tissues decreased glucose uptake liver increased gluconeogenesis beta cell dysfunction relative insulin deficiency
glucotoxicity lipotoxicity obesity inflammation
B. No diabetes
C. Type 1 autoimmune beta cell destruction
D. Only type 1
Answer: A
Rationale: Type 2 diabetes insulin resistance peripheral decreased glucose uptake liver increased gluconeogenesis beta cell dysfunction relative insulin
deficiency glucotoxicity lipotoxicity obesity inflammation.
4. 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. Type 2 insulin resistance peripheral tissues decreased glucose uptake liver increased gluconeogenesis beta cell dysfunction relative insulin deficiency
glucotoxicity lipotoxicity obesity inflammation
B. Type 1 autoimmune beta cell destruction
C. Only type 1
D. No diabetes
Answer: A
Rationale: Type 2 diabetes insulin resistance peripheral decreased glucose uptake liver increased gluconeogenesis beta cell dysfunction relative insulin
deficiency glucotoxicity lipotoxicity obesity inflammation.
5. 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. Type 2 insulin resistance peripheral tissues decreased glucose uptake liver increased gluconeogenesis beta cell dysfunction relative insulin deficiency
glucotoxicity lipotoxicity obesity inflammation
B. Only type 1
C. No diabetes
D. Type 1 autoimmune beta cell destruction
Answer: A
Rationale: Type 2 diabetes insulin resistance peripheral decreased glucose uptake liver increased gluconeogenesis beta cell dysfunction relative insulin
deficiency glucotoxicity lipotoxicity obesity inflammation.
6. 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.
7. A patient with rheumatoid arthritis symmetric small joint pain morning stiffness >30 min positive RF anti-CCP. Pathophysiology?
A. No RA
,B. RA autoimmune chronic synovitis pannus formation inflammatory cytokines TNF IL-1 IL-6 joint destruction, RF anti-CCP positive symmetric small joints
morning stiffness >30 min systemic
C. Only OA
D. OA
Answer: B
Rationale: RA autoimmune chronic synovitis pannus TNF IL-1 IL-6 joint destruction RF anti-CCP symmetric small joints morning >30 min systemic.
8. A patient with rheumatoid arthritis symmetric small joint pain morning stiffness >30 min positive RF anti-CCP. Pathophysiology?
A. OA
B. No RA
C. RA autoimmune chronic synovitis pannus formation inflammatory cytokines TNF IL-1 IL-6 joint destruction, RF anti-CCP positive symmetric small joints
morning stiffness >30 min systemic
D. Only OA
Answer: C
Rationale: RA autoimmune chronic synovitis pannus TNF IL-1 IL-6 joint destruction RF anti-CCP symmetric small joints morning >30 min systemic.
9. A patient with ARDS presents with severe hypoxemia PaO2/FiO2 <300, bilateral infiltrates, no cardiac failure, after sepsis. Pathophysiology?
A. Cardiogenic edema
B. 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
C. No ARDS
D. Only cardiogenic
Answer: B
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.
10. A patient with hypothyroidism presents with fatigue, weight gain, cold intolerance, constipation, dry skin, elevated TSH low free T4. What is
pathophysiology?
A. 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
B. Only hyper
C. Hyperthyroid
D. No thyroid
Answer: A
Rationale: Hypothyroidism Hashimoto autoimmune lymphocytic infiltration decreased T4 T3 decreased BMR fatigue weight gain cold intolerance constipation
dry skin elevated TSH low free T4.
11. A patient with anemia fatigue pallor low Hb Hct. What are types pathophysiology?
A. Only one type
B. Only blood loss
C. Anemia decreased RBC production iron deficiency B12 folate deficiency decreased erythropoietin, increased destruction hemolysis, blood loss hemorrhage
D. No anemia types
Answer: C
Rationale: Anemia decreased production iron B12 folate erythropoietin increased destruction hemolysis blood loss.
12. 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.
13. 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. Cardiogenic edema
C. No ARDS
D. Only cardiogenic
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.
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. No diabetes
, D. Type 1 autoimmune beta cell destruction
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 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. Type 1 autoimmune beta cell destruction
B. Type 2 insulin resistance peripheral tissues decreased glucose uptake liver increased gluconeogenesis beta cell dysfunction relative insulin deficiency
glucotoxicity lipotoxicity obesity inflammation
C. Only type 1
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.
16. 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 pancreatitis
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.
17. A patient with nephrotic syndrome presents with proteinuria >3.5 g/day, hypoalbuminemia, edema, hyperlipidemia. What is pathophysiology?
A. No proteinuria
B. 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
C. Only nephritic
D. Nephritic hematuria HTN
Answer: B
Rationale: Nephrotic increased glomerular permeability podocyte injury proteinuria >3.5 g hypoalbuminemia decreased oncotic edema hyperlipidemia liver
lipoprotein synthesis loss antithrombin III hypercoagulable.
18. A 70-year-old with sudden unilateral weakness, facial droop, aphasia, CT shows ischemic stroke. What is pathophysiology?
A. Only hemorrhage
B. Hemorrhage only
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. No stroke
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.
19. 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. Only HHNKS
C. 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
D. HHNKS
Answer: C
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.
20. A patient with ARDS presents with severe hypoxemia PaO2/FiO2 <300, bilateral infiltrates, no cardiac failure, after sepsis. Pathophysiology?
A. No ARDS
B. Cardiogenic edema
C. Only cardiogenic
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.
21. 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. Hypothyroidism
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 acute pancreatitis presents with severe epigastric pain radiating back, nausea vomiting, elevated lipase 3x normal, alcohol use.
What is pathophysiology?
A. No autodigestion
B. No pancreatitis
C. Only gastritis
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.
2. A patient with nephritic syndrome presents with hematuria, proteinuria <3.5 g, hypertension, oliguria, RBC casts. What is pathophysiology?
A. Nephrotic only
B. Only nephrotic
C. 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
D. No hematuria
Answer: C
Rationale: Nephritic glomerular inflammation immune complex decreased GFR Na water retention HTN oliguria RBC casts hematuria proteinuria <3.5 g
post-strep IgA.
3. 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. Type 2 insulin resistance peripheral tissues decreased glucose uptake liver increased gluconeogenesis beta cell dysfunction relative insulin deficiency
glucotoxicity lipotoxicity obesity inflammation
B. No diabetes
C. Type 1 autoimmune beta cell destruction
D. Only type 1
Answer: A
Rationale: Type 2 diabetes insulin resistance peripheral decreased glucose uptake liver increased gluconeogenesis beta cell dysfunction relative insulin
deficiency glucotoxicity lipotoxicity obesity inflammation.
4. 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. Type 2 insulin resistance peripheral tissues decreased glucose uptake liver increased gluconeogenesis beta cell dysfunction relative insulin deficiency
glucotoxicity lipotoxicity obesity inflammation
B. Type 1 autoimmune beta cell destruction
C. Only type 1
D. No diabetes
Answer: A
Rationale: Type 2 diabetes insulin resistance peripheral decreased glucose uptake liver increased gluconeogenesis beta cell dysfunction relative insulin
deficiency glucotoxicity lipotoxicity obesity inflammation.
5. 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. Type 2 insulin resistance peripheral tissues decreased glucose uptake liver increased gluconeogenesis beta cell dysfunction relative insulin deficiency
glucotoxicity lipotoxicity obesity inflammation
B. Only type 1
C. No diabetes
D. Type 1 autoimmune beta cell destruction
Answer: A
Rationale: Type 2 diabetes insulin resistance peripheral decreased glucose uptake liver increased gluconeogenesis beta cell dysfunction relative insulin
deficiency glucotoxicity lipotoxicity obesity inflammation.
6. 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.
7. A patient with rheumatoid arthritis symmetric small joint pain morning stiffness >30 min positive RF anti-CCP. Pathophysiology?
A. No RA
,B. RA autoimmune chronic synovitis pannus formation inflammatory cytokines TNF IL-1 IL-6 joint destruction, RF anti-CCP positive symmetric small joints
morning stiffness >30 min systemic
C. Only OA
D. OA
Answer: B
Rationale: RA autoimmune chronic synovitis pannus TNF IL-1 IL-6 joint destruction RF anti-CCP symmetric small joints morning >30 min systemic.
8. A patient with rheumatoid arthritis symmetric small joint pain morning stiffness >30 min positive RF anti-CCP. Pathophysiology?
A. OA
B. No RA
C. RA autoimmune chronic synovitis pannus formation inflammatory cytokines TNF IL-1 IL-6 joint destruction, RF anti-CCP positive symmetric small joints
morning stiffness >30 min systemic
D. Only OA
Answer: C
Rationale: RA autoimmune chronic synovitis pannus TNF IL-1 IL-6 joint destruction RF anti-CCP symmetric small joints morning >30 min systemic.
9. A patient with ARDS presents with severe hypoxemia PaO2/FiO2 <300, bilateral infiltrates, no cardiac failure, after sepsis. Pathophysiology?
A. Cardiogenic edema
B. 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
C. No ARDS
D. Only cardiogenic
Answer: B
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.
10. A patient with hypothyroidism presents with fatigue, weight gain, cold intolerance, constipation, dry skin, elevated TSH low free T4. What is
pathophysiology?
A. 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
B. Only hyper
C. Hyperthyroid
D. No thyroid
Answer: A
Rationale: Hypothyroidism Hashimoto autoimmune lymphocytic infiltration decreased T4 T3 decreased BMR fatigue weight gain cold intolerance constipation
dry skin elevated TSH low free T4.
11. A patient with anemia fatigue pallor low Hb Hct. What are types pathophysiology?
A. Only one type
B. Only blood loss
C. Anemia decreased RBC production iron deficiency B12 folate deficiency decreased erythropoietin, increased destruction hemolysis, blood loss hemorrhage
D. No anemia types
Answer: C
Rationale: Anemia decreased production iron B12 folate erythropoietin increased destruction hemolysis blood loss.
12. 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.
13. 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. Cardiogenic edema
C. No ARDS
D. Only cardiogenic
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.
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. No diabetes
, D. Type 1 autoimmune beta cell destruction
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 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. Type 1 autoimmune beta cell destruction
B. Type 2 insulin resistance peripheral tissues decreased glucose uptake liver increased gluconeogenesis beta cell dysfunction relative insulin deficiency
glucotoxicity lipotoxicity obesity inflammation
C. Only type 1
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.
16. 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 pancreatitis
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.
17. A patient with nephrotic syndrome presents with proteinuria >3.5 g/day, hypoalbuminemia, edema, hyperlipidemia. What is pathophysiology?
A. No proteinuria
B. 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
C. Only nephritic
D. Nephritic hematuria HTN
Answer: B
Rationale: Nephrotic increased glomerular permeability podocyte injury proteinuria >3.5 g hypoalbuminemia decreased oncotic edema hyperlipidemia liver
lipoprotein synthesis loss antithrombin III hypercoagulable.
18. A 70-year-old with sudden unilateral weakness, facial droop, aphasia, CT shows ischemic stroke. What is pathophysiology?
A. Only hemorrhage
B. Hemorrhage only
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. No stroke
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.
19. 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. Only HHNKS
C. 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
D. HHNKS
Answer: C
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.
20. A patient with ARDS presents with severe hypoxemia PaO2/FiO2 <300, bilateral infiltrates, no cardiac failure, after sepsis. Pathophysiology?
A. No ARDS
B. Cardiogenic edema
C. Only cardiogenic
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.
21. 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. Hypothyroidism
