GALEN COLLEGE OF NURSING
NSG 3280 PATHOPHYSIOLOGY FOR NURSES I
FINAL EXAM
2026
1. A 55-year-old chronic alcoholic presents with hepatomegaly and laboratory results showing elevated liver
enzymes. Liver biopsy reveals cells with accumulated lipids displacing the nucleus to the periphery. This
cellular adaptation is best described as:
A) Hypertrophy B) Hyperplasia C) Metaplasia D) Steatosis
Answer: D Rationale: Steatosis (fatty change) occurs when cells accumulate triglycerides, causing the
characteristic appearance of lipid-filled vacuoles displacing the nucleus. This is reversible cellular injury
commonly seen in alcoholic liver disease, diabetes, obesity, and toxin exposure. Hypertrophy is cell
enlargement; hyperplasia is increased cell number; metaplasia is cell type transformation. Continued injury can
progress from steatosis to steatohepatitis to cirrhosis (irreversible).
2. A patient with severe third-degree burns over 40% of total body surface area develops decreased urine
output, weight gain, and peripheral edema within the first 24 hours. What is the primary pathophysiological
mechanism?
A) Acute kidney injury from hypoperfusion B) Increased capillary permeability causing third-spacing of fluids
C) Syndrome of inappropriate antidiuretic hormone (SIADH) D) Heart failure from fluid overload
Answer: B Rationale: Major burns cause massive inflammatory response with release of histamine,
bradykinin, and other mediators that increase capillary permeability. Plasma proteins and fluids shift from
intravascular space into interstitial space (third-spacing), causing hypovolemia, edema, and decreased organ
perfusion. This occurs in the first 24-48 hours post-burn. Treatment requires aggressive fluid resuscitation
(Parkland formula: 4 mL × kg × %TBSA in first 24 hours). The capillary leak syndrome resolves around 48-72
hours, when mobilization phase begins.
3. A patient's arterial blood gas shows pH 7.28, PaCO₂ 32 mmHg, HCO₃⁻ 14 mEq/L. The anion gap is
calculated at 24 mEq/L (normal 8-12). What is the most likely cause of this acid-base disturbance?
A) Chronic diarrhea B) Diabetic ketoacidosis C) Renal tubular acidosis D) Hyperventilation
Answer: B Rationale: This represents metabolic acidosis (low pH, low HCO₃⁻) with respiratory compensation
(low PaCO₂). The elevated anion gap indicates unmeasured anions (ketoacids, lactate, toxins). High anion gap
metabolic acidosis causes include: MUDPILES (Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol,
Iron/Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates). Normal anion gap (hyperchloremic) acidosis
occurs with diarrhea, RTA, or carbonic anhydrase inhibitors. The respiratory system compensates by increasing
ventilation (Kussmaul breathing) to eliminate CO₂.
,4. A patient develops acute tubular necrosis following prolonged hypotension during surgery. During the
oliguric phase, which electrolyte imbalance poses the greatest immediate threat?
A) Hypernatremia B) Hypokalemia C) Hyperkalemia D) Hypercalcemia
Answer: C Rationale: During the oliguric phase of ATN, the kidneys cannot excrete potassium, leading to
dangerous hyperkalemia. Damaged tubular cells also release intracellular potassium. Hyperkalemia >6.5 mEq/L
causes life-threatening cardiac dysrhythmias (peaked T waves, widened QRS, ventricular fibrillation, asystole).
Other abnormalities include fluid overload, hyperphosphatemia, hypocalcemia, hypermagnesemia, and
metabolic acidosis. Treatment includes calcium gluconate (membrane stabilization), insulin/glucose, sodium
bicarbonate, dialysis if severe. The diuretic phase that follows requires careful electrolyte replacement.
5. A 28-year-old woman with systemic lupus erythematosus develops antibodies against her own nuclear
antigens. This represents which type of hypersensitivity reaction?
A) Type I (IgE-mediated) B) Type II (cytotoxic) C) Type III (immune complex) D) Type IV (cell-mediated)
Answer: C Rationale: SLE is a Type III hypersensitivity reaction where antigen-antibody immune complexes
deposit in tissues (kidneys, joints, skin, blood vessels), activating complement and causing inflammation.
Classic examples include SLE, serum sickness, and post-streptococcal glomerulonephritis. Type I is immediate
allergic (anaphylaxis); Type II involves antibodies against cell surface antigens (transfusion reactions, Graves'
disease); Type IV is delayed cell-mediated (tuberculin test, contact dermatitis). SLE can also have Type II
components (hemolytic anemia, thrombocytopenia).
6. A patient with chronic obstructive pulmonary disease develops increased red blood cell production. What is
the pathophysiological mechanism driving this adaptation?
A) Direct bone marrow stimulation from inflammation B) Increased erythropoietin production in response to
chronic hypoxemia C) Decreased red blood cell destruction D) Vitamin B12 excess
Answer: B Rationale: Chronic hypoxemia stimulates the kidneys to produce erythropoietin (EPO), which
stimulates bone marrow erythropoiesis. This compensatory polycythemia increases oxygen-carrying capacity
but also increases blood viscosity and thrombosis risk. The kidneys sense decreased oxygen delivery via
hypoxia-inducible factor (HIF) pathway. Similar mechanisms occur in high altitude, chronic heart disease, and
sleep apnea. Secondary polycythemia differs from polycythemia vera (primary bone marrow disorder).
Treatment may include phlebotomy if hematocrit becomes dangerously elevated.
7. A patient presents with sudden onset of severe chest pain. Troponin I levels are elevated. What is the
pathophysiological significance of elevated troponin?
A) It indicates reversible myocardial ischemia B) It represents cardiac muscle cell membrane damage and death
C) It shows coronary artery spasm D) It reflects increased cardiac workload
Answer: B Rationale: Troponins (I and T) are structural proteins found exclusively in cardiac myocytes. They
are released only when myocardial cell membranes are damaged, indicating cell death (necrosis). Troponins
begin rising 3-4 hours post-MI, peak at 24-48 hours, and remain elevated for 7-14 days. They are highly
specific and sensitive for myocardial infarction. CK-MB also indicates cardiac damage but is less specific.
Ischemia without infarction doesn't typically elevate troponins. Elevated troponins confirm diagnosis of acute
coronary syndrome and guide treatment decisions.
,8. A patient with sickle cell disease experiences a vaso-occlusive crisis. What is the primary pathophysiological
mechanism?
A) Decreased red blood cell production B) Hemoglobin S polymerization causing RBC sickling and vascular
occlusion C) Excessive red blood cell destruction in the spleen D) Iron deficiency causing abnormal
hemoglobin
Answer: B Rationale: Sickle cell disease results from a point mutation (glutamic acid → valine at position 6 of
β-globin chain), creating hemoglobin S (HbS). When deoxygenated, HbS polymerizes, causing RBCs to assume
rigid sickle shape. Sickled cells occlude microvasculature, causing ischemia, pain, and organ damage. Triggers
include hypoxia, dehydration, infection, cold, and acidosis. Chronic hemolysis occurs but vaso-occlusion causes
acute crises. Complications include acute chest syndrome, stroke, splenic sequestration, priapism, and avascular
necrosis. Treatment includes hydration, oxygen, pain management, and hydroxyurea (increases HbF
production).
9. A patient with left ventricular failure develops pulmonary edema. Explain the sequence of pathophysiological
events:
A) Decreased left ventricular output → increased left atrial pressure → increased pulmonary venous pressure →
fluid transudation into alveoli B) Increased right ventricular output → pulmonary hypertension → capillary
damage C) Decreased oncotic pressure → fluid leak into lungs D) Pulmonary capillary inflammation →
increased permeability
Answer: A Rationale: Left ventricular failure causes backward blood flow: failing LV → increased LV end-
diastolic pressure → increased LA pressure → increased pulmonary venous pressure → increased pulmonary
capillary hydrostatic pressure. When hydrostatic pressure (>25 mmHg) exceeds oncotic pressure (~28 mmHg),
fluid transudes into interstitium then alveoli (pulmonary edema). This is cardiogenic pulmonary edema
(hydrostatic). ARDS causes non-cardiogenic pulmonary edema from increased capillary permeability. Clinical
manifestations include dyspnea, crackles, pink frothy sputum, decreased oxygen saturation. Treatment
addresses the failing heart (diuretics, vasodilators, inotropes).
10. A patient develops disseminated intravascular coagulation (DIC) following sepsis. What is the fundamental
pathophysiological defect?
A) Decreased clotting factor production B) Excessive anticoagulant production C) Widespread activation of
coagulation cascade causing simultaneous thrombosis and hemorrhage D) Isolated platelet destruction
Answer: C Rationale: DIC involves paradoxical simultaneous thrombosis and bleeding. Pathophysiology:
widespread endothelial damage → tissue factor release → massive thrombin generation → widespread
microthrombi formation → consumption of clotting factors and platelets → bleeding. Fibrinolysis generates D-
dimers (markedly elevated). Microthrombi cause organ ischemia/failure. Laboratory findings: prolonged
PT/aPTT, decreased platelets, decreased fibrinogen, elevated D-dimer, schistocytes on peripheral smear. Causes
include sepsis, trauma, malignancy, obstetric complications. Treatment focuses on addressing underlying cause
and supportive care (blood products, platelets).
TRUE/FALSE QUESTIONS
11. Apoptosis is a form of programmed cell death that does NOT trigger an inflammatory response, whereas
necrosis is pathological cell death that DOES cause inflammation.
, Answer: TRUE Rationale: Apoptosis is controlled, energy-dependent cell suicide with cell shrinkage,
chromatin condensation, membrane blebbing, and formation of apoptotic bodies that are phagocytosed without
inflammation. It occurs normally (embryonic development, immune system regulation) and pathologically.
Necrosis is uncontrolled cell death from injury with cell swelling, membrane rupture, and release of
intracellular contents that trigger inflammation. Types of necrosis include coagulative (most common - MI,
kidney infarct), liquefactive (brain infarct, abscess), caseous (TB), fat (pancreatitis), and gangrenous (limb
ischemia).
12. Virchow's triad describes three factors predisposing to thrombosis: endothelial injury, abnormal blood flow
(stasis or turbulence), and hypercoagulability.
Answer: TRUE Rationale: Virchow's triad explains thrombosis pathophysiology. (1) Endothelial injury
exposes subendothelial collagen, activating platelets and coagulation (trauma, atherosclerosis, inflammation,
indwelling catheters). (2) Abnormal flow includes stasis (immobility, atrial fibrillation, heart failure) and
turbulence (aneurysms, bifurcations) preventing dilution of activated factors. (3) Hypercoagulability includes
inherited thrombophilias (Factor V Leiden, prothrombin mutation, protein C/S deficiency) and acquired states
(cancer, pregnancy, oral contraceptives, smoking). Understanding this triad guides prevention strategies
(anticoagulation, compression stockings, early mobilization).
13. Type 1 diabetes mellitus results from autoimmune destruction of pancreatic beta cells, while Type 2
diabetes results from insulin resistance and relative insulin deficiency.
Answer: TRUE Rationale: Type 1 DM (5-10% of cases) involves T-cell mediated destruction of pancreatic β-
cells, causing absolute insulin deficiency. Autoantibodies (GAD, IA-2, insulin) are often present. Onset
typically in childhood/adolescence, requires lifelong insulin. Type 2 DM (90-95% of cases) involves insulin
resistance (decreased cellular glucose uptake despite adequate insulin) plus progressive β-cell dysfunction
causing relative insulin deficiency. Linked to obesity, genetics, sedentary lifestyle. Initially treated with lifestyle
modification and oral agents; may eventually require insulin. Both cause hyperglycemia and chronic
complications (retinopathy, nephropathy, neuropathy, cardiovascular disease).
14. Cor pulmonale refers to right ventricular hypertrophy and failure secondary to pulmonary hypertension
caused by chronic lung disease.
Answer: TRUE Rationale: Cor pulmonale is right heart disease secondary to pulmonary pathology. Chronic
hypoxemia causes pulmonary vasoconstriction and vascular remodeling → pulmonary hypertension →
increased RV afterload → RV hypertrophy → eventual RV failure. Common causes include COPD, interstitial
lung disease, pulmonary embolism, sleep apnea. Clinical manifestations include dyspnea, JVD, hepatomegaly,
peripheral edema, tricuspid regurgitation murmur. ECG shows RVH; echo shows elevated pulmonary artery
pressures. Treatment addresses underlying lung disease, oxygen therapy, and diuretics. Differs from left heart
failure causing pulmonary hypertension.
15. Metastasis can occur through lymphatic spread, hematogenous spread, or direct seeding of body cavities,
with most carcinomas spreading initially through lymphatics and sarcomas through blood.
Answer: TRUE Rationale: Cancer cells detach from primary tumor and invade: (1) Lymphatic spread:
Carcinomas typically spread via lymphatics to regional lymph nodes first (sentinel node concept). (2)
Hematogenous spread: Sarcomas preferentially spread through blood vessels; common sites include lung (from
systemic circulation), liver (from GI tract via portal circulation), bone, brain. (3) Transcoelomic spread: Direct
seeding of peritoneal, pleural, or pericardial cavities (ovarian cancer → peritoneal carcinomatosis). Metastatic
cascade involves invasion, intravasation, survival in circulation, extravasation, and colonization. Understanding
spread patterns guides staging and treatment.
NSG 3280 PATHOPHYSIOLOGY FOR NURSES I
FINAL EXAM
2026
1. A 55-year-old chronic alcoholic presents with hepatomegaly and laboratory results showing elevated liver
enzymes. Liver biopsy reveals cells with accumulated lipids displacing the nucleus to the periphery. This
cellular adaptation is best described as:
A) Hypertrophy B) Hyperplasia C) Metaplasia D) Steatosis
Answer: D Rationale: Steatosis (fatty change) occurs when cells accumulate triglycerides, causing the
characteristic appearance of lipid-filled vacuoles displacing the nucleus. This is reversible cellular injury
commonly seen in alcoholic liver disease, diabetes, obesity, and toxin exposure. Hypertrophy is cell
enlargement; hyperplasia is increased cell number; metaplasia is cell type transformation. Continued injury can
progress from steatosis to steatohepatitis to cirrhosis (irreversible).
2. A patient with severe third-degree burns over 40% of total body surface area develops decreased urine
output, weight gain, and peripheral edema within the first 24 hours. What is the primary pathophysiological
mechanism?
A) Acute kidney injury from hypoperfusion B) Increased capillary permeability causing third-spacing of fluids
C) Syndrome of inappropriate antidiuretic hormone (SIADH) D) Heart failure from fluid overload
Answer: B Rationale: Major burns cause massive inflammatory response with release of histamine,
bradykinin, and other mediators that increase capillary permeability. Plasma proteins and fluids shift from
intravascular space into interstitial space (third-spacing), causing hypovolemia, edema, and decreased organ
perfusion. This occurs in the first 24-48 hours post-burn. Treatment requires aggressive fluid resuscitation
(Parkland formula: 4 mL × kg × %TBSA in first 24 hours). The capillary leak syndrome resolves around 48-72
hours, when mobilization phase begins.
3. A patient's arterial blood gas shows pH 7.28, PaCO₂ 32 mmHg, HCO₃⁻ 14 mEq/L. The anion gap is
calculated at 24 mEq/L (normal 8-12). What is the most likely cause of this acid-base disturbance?
A) Chronic diarrhea B) Diabetic ketoacidosis C) Renal tubular acidosis D) Hyperventilation
Answer: B Rationale: This represents metabolic acidosis (low pH, low HCO₃⁻) with respiratory compensation
(low PaCO₂). The elevated anion gap indicates unmeasured anions (ketoacids, lactate, toxins). High anion gap
metabolic acidosis causes include: MUDPILES (Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol,
Iron/Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates). Normal anion gap (hyperchloremic) acidosis
occurs with diarrhea, RTA, or carbonic anhydrase inhibitors. The respiratory system compensates by increasing
ventilation (Kussmaul breathing) to eliminate CO₂.
,4. A patient develops acute tubular necrosis following prolonged hypotension during surgery. During the
oliguric phase, which electrolyte imbalance poses the greatest immediate threat?
A) Hypernatremia B) Hypokalemia C) Hyperkalemia D) Hypercalcemia
Answer: C Rationale: During the oliguric phase of ATN, the kidneys cannot excrete potassium, leading to
dangerous hyperkalemia. Damaged tubular cells also release intracellular potassium. Hyperkalemia >6.5 mEq/L
causes life-threatening cardiac dysrhythmias (peaked T waves, widened QRS, ventricular fibrillation, asystole).
Other abnormalities include fluid overload, hyperphosphatemia, hypocalcemia, hypermagnesemia, and
metabolic acidosis. Treatment includes calcium gluconate (membrane stabilization), insulin/glucose, sodium
bicarbonate, dialysis if severe. The diuretic phase that follows requires careful electrolyte replacement.
5. A 28-year-old woman with systemic lupus erythematosus develops antibodies against her own nuclear
antigens. This represents which type of hypersensitivity reaction?
A) Type I (IgE-mediated) B) Type II (cytotoxic) C) Type III (immune complex) D) Type IV (cell-mediated)
Answer: C Rationale: SLE is a Type III hypersensitivity reaction where antigen-antibody immune complexes
deposit in tissues (kidneys, joints, skin, blood vessels), activating complement and causing inflammation.
Classic examples include SLE, serum sickness, and post-streptococcal glomerulonephritis. Type I is immediate
allergic (anaphylaxis); Type II involves antibodies against cell surface antigens (transfusion reactions, Graves'
disease); Type IV is delayed cell-mediated (tuberculin test, contact dermatitis). SLE can also have Type II
components (hemolytic anemia, thrombocytopenia).
6. A patient with chronic obstructive pulmonary disease develops increased red blood cell production. What is
the pathophysiological mechanism driving this adaptation?
A) Direct bone marrow stimulation from inflammation B) Increased erythropoietin production in response to
chronic hypoxemia C) Decreased red blood cell destruction D) Vitamin B12 excess
Answer: B Rationale: Chronic hypoxemia stimulates the kidneys to produce erythropoietin (EPO), which
stimulates bone marrow erythropoiesis. This compensatory polycythemia increases oxygen-carrying capacity
but also increases blood viscosity and thrombosis risk. The kidneys sense decreased oxygen delivery via
hypoxia-inducible factor (HIF) pathway. Similar mechanisms occur in high altitude, chronic heart disease, and
sleep apnea. Secondary polycythemia differs from polycythemia vera (primary bone marrow disorder).
Treatment may include phlebotomy if hematocrit becomes dangerously elevated.
7. A patient presents with sudden onset of severe chest pain. Troponin I levels are elevated. What is the
pathophysiological significance of elevated troponin?
A) It indicates reversible myocardial ischemia B) It represents cardiac muscle cell membrane damage and death
C) It shows coronary artery spasm D) It reflects increased cardiac workload
Answer: B Rationale: Troponins (I and T) are structural proteins found exclusively in cardiac myocytes. They
are released only when myocardial cell membranes are damaged, indicating cell death (necrosis). Troponins
begin rising 3-4 hours post-MI, peak at 24-48 hours, and remain elevated for 7-14 days. They are highly
specific and sensitive for myocardial infarction. CK-MB also indicates cardiac damage but is less specific.
Ischemia without infarction doesn't typically elevate troponins. Elevated troponins confirm diagnosis of acute
coronary syndrome and guide treatment decisions.
,8. A patient with sickle cell disease experiences a vaso-occlusive crisis. What is the primary pathophysiological
mechanism?
A) Decreased red blood cell production B) Hemoglobin S polymerization causing RBC sickling and vascular
occlusion C) Excessive red blood cell destruction in the spleen D) Iron deficiency causing abnormal
hemoglobin
Answer: B Rationale: Sickle cell disease results from a point mutation (glutamic acid → valine at position 6 of
β-globin chain), creating hemoglobin S (HbS). When deoxygenated, HbS polymerizes, causing RBCs to assume
rigid sickle shape. Sickled cells occlude microvasculature, causing ischemia, pain, and organ damage. Triggers
include hypoxia, dehydration, infection, cold, and acidosis. Chronic hemolysis occurs but vaso-occlusion causes
acute crises. Complications include acute chest syndrome, stroke, splenic sequestration, priapism, and avascular
necrosis. Treatment includes hydration, oxygen, pain management, and hydroxyurea (increases HbF
production).
9. A patient with left ventricular failure develops pulmonary edema. Explain the sequence of pathophysiological
events:
A) Decreased left ventricular output → increased left atrial pressure → increased pulmonary venous pressure →
fluid transudation into alveoli B) Increased right ventricular output → pulmonary hypertension → capillary
damage C) Decreased oncotic pressure → fluid leak into lungs D) Pulmonary capillary inflammation →
increased permeability
Answer: A Rationale: Left ventricular failure causes backward blood flow: failing LV → increased LV end-
diastolic pressure → increased LA pressure → increased pulmonary venous pressure → increased pulmonary
capillary hydrostatic pressure. When hydrostatic pressure (>25 mmHg) exceeds oncotic pressure (~28 mmHg),
fluid transudes into interstitium then alveoli (pulmonary edema). This is cardiogenic pulmonary edema
(hydrostatic). ARDS causes non-cardiogenic pulmonary edema from increased capillary permeability. Clinical
manifestations include dyspnea, crackles, pink frothy sputum, decreased oxygen saturation. Treatment
addresses the failing heart (diuretics, vasodilators, inotropes).
10. A patient develops disseminated intravascular coagulation (DIC) following sepsis. What is the fundamental
pathophysiological defect?
A) Decreased clotting factor production B) Excessive anticoagulant production C) Widespread activation of
coagulation cascade causing simultaneous thrombosis and hemorrhage D) Isolated platelet destruction
Answer: C Rationale: DIC involves paradoxical simultaneous thrombosis and bleeding. Pathophysiology:
widespread endothelial damage → tissue factor release → massive thrombin generation → widespread
microthrombi formation → consumption of clotting factors and platelets → bleeding. Fibrinolysis generates D-
dimers (markedly elevated). Microthrombi cause organ ischemia/failure. Laboratory findings: prolonged
PT/aPTT, decreased platelets, decreased fibrinogen, elevated D-dimer, schistocytes on peripheral smear. Causes
include sepsis, trauma, malignancy, obstetric complications. Treatment focuses on addressing underlying cause
and supportive care (blood products, platelets).
TRUE/FALSE QUESTIONS
11. Apoptosis is a form of programmed cell death that does NOT trigger an inflammatory response, whereas
necrosis is pathological cell death that DOES cause inflammation.
, Answer: TRUE Rationale: Apoptosis is controlled, energy-dependent cell suicide with cell shrinkage,
chromatin condensation, membrane blebbing, and formation of apoptotic bodies that are phagocytosed without
inflammation. It occurs normally (embryonic development, immune system regulation) and pathologically.
Necrosis is uncontrolled cell death from injury with cell swelling, membrane rupture, and release of
intracellular contents that trigger inflammation. Types of necrosis include coagulative (most common - MI,
kidney infarct), liquefactive (brain infarct, abscess), caseous (TB), fat (pancreatitis), and gangrenous (limb
ischemia).
12. Virchow's triad describes three factors predisposing to thrombosis: endothelial injury, abnormal blood flow
(stasis or turbulence), and hypercoagulability.
Answer: TRUE Rationale: Virchow's triad explains thrombosis pathophysiology. (1) Endothelial injury
exposes subendothelial collagen, activating platelets and coagulation (trauma, atherosclerosis, inflammation,
indwelling catheters). (2) Abnormal flow includes stasis (immobility, atrial fibrillation, heart failure) and
turbulence (aneurysms, bifurcations) preventing dilution of activated factors. (3) Hypercoagulability includes
inherited thrombophilias (Factor V Leiden, prothrombin mutation, protein C/S deficiency) and acquired states
(cancer, pregnancy, oral contraceptives, smoking). Understanding this triad guides prevention strategies
(anticoagulation, compression stockings, early mobilization).
13. Type 1 diabetes mellitus results from autoimmune destruction of pancreatic beta cells, while Type 2
diabetes results from insulin resistance and relative insulin deficiency.
Answer: TRUE Rationale: Type 1 DM (5-10% of cases) involves T-cell mediated destruction of pancreatic β-
cells, causing absolute insulin deficiency. Autoantibodies (GAD, IA-2, insulin) are often present. Onset
typically in childhood/adolescence, requires lifelong insulin. Type 2 DM (90-95% of cases) involves insulin
resistance (decreased cellular glucose uptake despite adequate insulin) plus progressive β-cell dysfunction
causing relative insulin deficiency. Linked to obesity, genetics, sedentary lifestyle. Initially treated with lifestyle
modification and oral agents; may eventually require insulin. Both cause hyperglycemia and chronic
complications (retinopathy, nephropathy, neuropathy, cardiovascular disease).
14. Cor pulmonale refers to right ventricular hypertrophy and failure secondary to pulmonary hypertension
caused by chronic lung disease.
Answer: TRUE Rationale: Cor pulmonale is right heart disease secondary to pulmonary pathology. Chronic
hypoxemia causes pulmonary vasoconstriction and vascular remodeling → pulmonary hypertension →
increased RV afterload → RV hypertrophy → eventual RV failure. Common causes include COPD, interstitial
lung disease, pulmonary embolism, sleep apnea. Clinical manifestations include dyspnea, JVD, hepatomegaly,
peripheral edema, tricuspid regurgitation murmur. ECG shows RVH; echo shows elevated pulmonary artery
pressures. Treatment addresses underlying lung disease, oxygen therapy, and diuretics. Differs from left heart
failure causing pulmonary hypertension.
15. Metastasis can occur through lymphatic spread, hematogenous spread, or direct seeding of body cavities,
with most carcinomas spreading initially through lymphatics and sarcomas through blood.
Answer: TRUE Rationale: Cancer cells detach from primary tumor and invade: (1) Lymphatic spread:
Carcinomas typically spread via lymphatics to regional lymph nodes first (sentinel node concept). (2)
Hematogenous spread: Sarcomas preferentially spread through blood vessels; common sites include lung (from
systemic circulation), liver (from GI tract via portal circulation), bone, brain. (3) Transcoelomic spread: Direct
seeding of peritoneal, pleural, or pericardial cavities (ovarian cancer → peritoneal carcinomatosis). Metastatic
cascade involves invasion, intravasation, survival in circulation, extravasation, and colonization. Understanding
spread patterns guides staging and treatment.
