Nursing Pathophysiology Exam - Questions and Answers - Musculoskeletal & Integumentary 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 shock presents with hypotension tachycardia. What are types of shock pathophysiology?
A. No shock types
B. Only hypovolemic
C. 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
D. Only one type
Answer: C
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.
2. A 25-year-old female with butterfly rash, joint pain, fatigue, positive ANA dsDNA, low C3 C4, proteinuria. What disease pathophysiology?
A. Systemic lupus erythematosus - autoimmune type III hypersensitivity immune complex deposition ANA dsDNA positive complement consumption low C3 C4,
inflammation multiple organs butterfly rash photosensitivity joint pain nephritis
B. No autoimmune
C. RA
D. Only osteoarthritis
Answer: A
Rationale: SLE autoimmune type III hypersensitivity immune complex deposition ANA dsDNA positive low C3 C4 inflammation butterfly rash photosensitivity
joint pain nephritis.
3. 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. 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. Only 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.
4. 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. 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
B. Only HHNKS
C. No acidosis
D. HHNKS
Answer: A
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.
5. 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.
6. 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. No hyperthyroid
C. 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
D. Hypothyroidism
Answer: C
Rationale: Hyperthyroidism Graves TSI stimulates TSH receptor increased T4 T3 increased BMR heat intolerance weight loss tremor palpitations beta
adrenergic exophthalmos glycosaminoglycan deposition.
7. A patient with cirrhosis presents with ascites, jaundice, spider angiomas, palmar erythema, low albumin, elevated PT/INR, portal hypertension,
esophageal varices. What is pathophysiology?
A. No cirrhosis
,B. Cirrhosis chronic liver injury fibrosis nodule formation portal hypertension increased resistance, decreased synthetic function albumin clotting factors low,
impaired bilirubin conjugation jaundice, portal hypertension ascites varices splenomegaly, estrogen not metabolized spider angiomas palmar erythema
C. No portal HTN
D. Only acute
Answer: B
Rationale: Cirrhosis chronic injury fibrosis nodules portal hypertension increased resistance decreased synthetic albumin clotting factors low PT/INR up
impaired bilirubin conjugation jaundice portal HTN ascites varices splenomegaly estrogen not metabolized spider palmar erythema.
8. 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. No COPD
C. Only infection
D. 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
Answer: D
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.
9. A 25-year-old female with butterfly rash, joint pain, fatigue, positive ANA dsDNA, low C3 C4, proteinuria. What disease pathophysiology?
A. RA
B. No autoimmune
C. Only osteoarthritis
D. Systemic lupus erythematosus - autoimmune type III hypersensitivity immune complex deposition ANA dsDNA positive complement consumption low C3 C4,
inflammation multiple organs butterfly rash photosensitivity joint pain nephritis
Answer: D
Rationale: SLE autoimmune type III hypersensitivity immune complex deposition ANA dsDNA positive low C3 C4 inflammation butterfly rash photosensitivity
joint pain nephritis.
10. 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.
11. A patient with peptic ulcer disease epigastric pain, H. pylori positive, NSAID use. Pathophysiology?
A. No ulcer
B. No H. pylori
C. Only stress
D. PUD imbalance aggressive factors acid pepsin H. pylori NSAID decreased protective mucus bicarbonate prostaglandin, H. pylori urease ammonia
inflammation
Answer: D
Rationale: PUD imbalance aggressive acid pepsin H. pylori NSAID decreased protective mucus bicarbonate prostaglandin H. pylori urease ammonia
inflammation.
12. 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. 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
B. No COPD
C. Only infection
D. Asthma reversible
Answer: A
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.
13. 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. DKA type 2
C. No difference
D. Same
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.
14. A patient with shock presents with hypotension tachycardia. What are types of shock pathophysiology?
, A. Only one type
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 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.
15. A patient with hypothyroidism presents with fatigue, weight gain, cold intolerance, constipation, dry skin, elevated TSH low free T4. What is
pathophysiology?
A. No thyroid
B. Only hyper
C. Hyperthyroid
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 nephritic syndrome presents with hematuria, proteinuria <3.5 g, hypertension, oliguria, RBC casts. What is pathophysiology?
A. Only nephrotic
B. 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
C. Nephrotic only
D. No hematuria
Answer: B
Rationale: Nephritic glomerular inflammation immune complex decreased GFR Na water retention HTN oliguria RBC casts hematuria proteinuria <3.5 g
post-strep IgA.
17. A patient with peptic ulcer disease epigastric pain, H. pylori positive, NSAID use. Pathophysiology?
A. PUD imbalance aggressive factors acid pepsin H. pylori NSAID decreased protective mucus bicarbonate prostaglandin, H. pylori urease ammonia
inflammation
B. No H. pylori
C. No ulcer
D. Only stress
Answer: A
Rationale: PUD imbalance aggressive acid pepsin H. pylori NSAID decreased protective mucus bicarbonate prostaglandin H. pylori urease ammonia
inflammation.
18. 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.
19. 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. No thyroid
C. Hyperthyroid
D. Only hyper
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.
20. A patient with peptic ulcer disease epigastric pain, H. pylori positive, NSAID use. Pathophysiology?
A. PUD imbalance aggressive factors acid pepsin H. pylori NSAID decreased protective mucus bicarbonate prostaglandin, H. pylori urease ammonia
inflammation
B. No H. pylori
C. No ulcer
D. Only stress
Answer: A
Rationale: PUD imbalance aggressive acid pepsin H. pylori NSAID decreased protective mucus bicarbonate prostaglandin H. pylori urease ammonia
inflammation.
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 shock presents with hypotension tachycardia. What are types of shock pathophysiology?
A. No shock types
B. Only hypovolemic
C. 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
D. Only one type
Answer: C
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.
2. A 25-year-old female with butterfly rash, joint pain, fatigue, positive ANA dsDNA, low C3 C4, proteinuria. What disease pathophysiology?
A. Systemic lupus erythematosus - autoimmune type III hypersensitivity immune complex deposition ANA dsDNA positive complement consumption low C3 C4,
inflammation multiple organs butterfly rash photosensitivity joint pain nephritis
B. No autoimmune
C. RA
D. Only osteoarthritis
Answer: A
Rationale: SLE autoimmune type III hypersensitivity immune complex deposition ANA dsDNA positive low C3 C4 inflammation butterfly rash photosensitivity
joint pain nephritis.
3. 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. 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. Only 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.
4. 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. 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
B. Only HHNKS
C. No acidosis
D. HHNKS
Answer: A
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.
5. 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.
6. 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. No hyperthyroid
C. 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
D. Hypothyroidism
Answer: C
Rationale: Hyperthyroidism Graves TSI stimulates TSH receptor increased T4 T3 increased BMR heat intolerance weight loss tremor palpitations beta
adrenergic exophthalmos glycosaminoglycan deposition.
7. A patient with cirrhosis presents with ascites, jaundice, spider angiomas, palmar erythema, low albumin, elevated PT/INR, portal hypertension,
esophageal varices. What is pathophysiology?
A. No cirrhosis
,B. Cirrhosis chronic liver injury fibrosis nodule formation portal hypertension increased resistance, decreased synthetic function albumin clotting factors low,
impaired bilirubin conjugation jaundice, portal hypertension ascites varices splenomegaly, estrogen not metabolized spider angiomas palmar erythema
C. No portal HTN
D. Only acute
Answer: B
Rationale: Cirrhosis chronic injury fibrosis nodules portal hypertension increased resistance decreased synthetic albumin clotting factors low PT/INR up
impaired bilirubin conjugation jaundice portal HTN ascites varices splenomegaly estrogen not metabolized spider palmar erythema.
8. 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. No COPD
C. Only infection
D. 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
Answer: D
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.
9. A 25-year-old female with butterfly rash, joint pain, fatigue, positive ANA dsDNA, low C3 C4, proteinuria. What disease pathophysiology?
A. RA
B. No autoimmune
C. Only osteoarthritis
D. Systemic lupus erythematosus - autoimmune type III hypersensitivity immune complex deposition ANA dsDNA positive complement consumption low C3 C4,
inflammation multiple organs butterfly rash photosensitivity joint pain nephritis
Answer: D
Rationale: SLE autoimmune type III hypersensitivity immune complex deposition ANA dsDNA positive low C3 C4 inflammation butterfly rash photosensitivity
joint pain nephritis.
10. 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.
11. A patient with peptic ulcer disease epigastric pain, H. pylori positive, NSAID use. Pathophysiology?
A. No ulcer
B. No H. pylori
C. Only stress
D. PUD imbalance aggressive factors acid pepsin H. pylori NSAID decreased protective mucus bicarbonate prostaglandin, H. pylori urease ammonia
inflammation
Answer: D
Rationale: PUD imbalance aggressive acid pepsin H. pylori NSAID decreased protective mucus bicarbonate prostaglandin H. pylori urease ammonia
inflammation.
12. 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. 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
B. No COPD
C. Only infection
D. Asthma reversible
Answer: A
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.
13. 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. DKA type 2
C. No difference
D. Same
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.
14. A patient with shock presents with hypotension tachycardia. What are types of shock pathophysiology?
, A. Only one type
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 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.
15. A patient with hypothyroidism presents with fatigue, weight gain, cold intolerance, constipation, dry skin, elevated TSH low free T4. What is
pathophysiology?
A. No thyroid
B. Only hyper
C. Hyperthyroid
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 nephritic syndrome presents with hematuria, proteinuria <3.5 g, hypertension, oliguria, RBC casts. What is pathophysiology?
A. Only nephrotic
B. 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
C. Nephrotic only
D. No hematuria
Answer: B
Rationale: Nephritic glomerular inflammation immune complex decreased GFR Na water retention HTN oliguria RBC casts hematuria proteinuria <3.5 g
post-strep IgA.
17. A patient with peptic ulcer disease epigastric pain, H. pylori positive, NSAID use. Pathophysiology?
A. PUD imbalance aggressive factors acid pepsin H. pylori NSAID decreased protective mucus bicarbonate prostaglandin, H. pylori urease ammonia
inflammation
B. No H. pylori
C. No ulcer
D. Only stress
Answer: A
Rationale: PUD imbalance aggressive acid pepsin H. pylori NSAID decreased protective mucus bicarbonate prostaglandin H. pylori urease ammonia
inflammation.
18. 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.
19. 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. No thyroid
C. Hyperthyroid
D. Only hyper
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.
20. A patient with peptic ulcer disease epigastric pain, H. pylori positive, NSAID use. Pathophysiology?
A. PUD imbalance aggressive factors acid pepsin H. pylori NSAID decreased protective mucus bicarbonate prostaglandin, H. pylori urease ammonia
inflammation
B. No H. pylori
C. No ulcer
D. Only stress
Answer: A
Rationale: PUD imbalance aggressive acid pepsin H. pylori NSAID decreased protective mucus bicarbonate prostaglandin H. pylori urease ammonia
inflammation.
