Section 1: Cellular Processes, Adaptations & Injury (Weeks 1–2) – Questions 1–15Which adaptation involves an increase in cell number through mitosis?
A. Atrophy
B. Hypertrophy
C. Hyperplasia
D. Metaplasia
The most common cause of irreversible cell injury leading to necrosis is:
A. Mild hypoxia
B. Severe ATP depletion
C. Reversible swelling
D. Autophagy activation
Coagulative necrosis is most characteristic of:
A. Brain infarct
B. Myocardial infarction
C. Pancreatic fat necrosis
D. Bacterial abscess
Apoptosis differs from necrosis because it is:
A. Inflammatory
B. Programmed and non-inflammatory
C. Associated with cell swelling
D. Caused by severe ischemia only
Free radical injury is primarily neutralized by:
A. Catalase, superoxide dismutase, glutathione
B. Calcium channels
C. Na+/K+ ATPase
D. Proteases
(SATA) Reversible cellular injury features include:
A. Hydropic swelling
B. Fatty change
C. Nuclear pyknosis
D. Plasma membrane blebbing
In autosomal dominant inheritance, the risk to each offspring is:
A. 25%
B. 50%
C. 75%
D. 100%
An example of X-linked recessive disorder is:
A. Huntington disease
B. Cystic fibrosis
C. Hemophilia A
D. Marfan syndrome
Genomic imprinting is best exemplified by:
A. Prader-Willi vs. Angelman syndrome
B. Sickle cell trait
C. Down syndrome trisomy
D. Klinefelter syndrome
The primary mechanism in multifactorial (polygenic) diseases is:
A. Single gene mutation
B. Cumulative genetic + environmental liability
C. Complete penetrance
D. Mitochondrial transmission
Epigenetic modifications include:
A. DNA sequence changes
B. Histone acetylation and DNA methylation
C. Frameshift mutations
D. Chromosomal translocations
Incomplete penetrance means:
A. Not all individuals with the genotype show the phenotype
B. Variable severity of phenotype
C. Parent-of-origin effect
D. Anticipation across generations
In cancer genetics, tumor suppressor genes require:
A. One hit
B. Two hits (Knudson hypothesis)
C. Gain-of-function only
D. Viral integration
The Philadelphia chromosome is associated with:
A. Chronic myeloid leukemia
B. Breast cancer
C. Colorectal cancer
D. Melanoma
A common environmental modifier of genetic disease risk is:
A. Diet and obesity in type 2 diabetes
B. Purely genetic transmission
C. Mitochondrial DNA only
D. Complete environmental independence
Section 2: Neurological System (Week 3) – Questions 16–25The most common cause of ischemic stroke is:
A. Embolism from atrial fibrillation
B. Hemorrhagic rupture
C. Vasculitis
D. Trauma
In temporal lobe epilepsy, the classic pathologic finding is:
A. Hippocampal sclerosis
B. Lewy bodies
C. Amyloid plaques
D. Neurofibrillary tangles
Central sensitization in chronic pain involves:
A. Peripheral nociceptor activation only
B. Wind-up phenomenon and glial activation in CNS
C. A-delta fiber dominance
D. Gate control theory blockade
Referred pain occurs due to:
A. Convergence of visceral and somatic afferents
B. Direct nerve damage
C. Cortical misinterpretation
D. Descending inhibition failure
In Alzheimer’s disease, early pathology predominantly affects:
A. Substantia nigra
B. Hippocampus and entorhinal cortex
C. Cerebellum
D. Motor cortex
The primary neurotransmitter deficit in Parkinson’s is:
A. Acetylcholine
B. Dopamine
C. GABA
D. Serotonin
Status epilepticus is defined as seizure activity lasting >:
A. 5 minutes
B. 30 minutes
C. 60 minutes
D. 2 hours
Cushing’s triad indicates:
A. Increased intracranial pressure
B. Hypoglycemia
C. Sepsis
D. Hypovolemia
Neuroplasticity is most prominent in recovery from:
A. Acute ischemic stroke
B. End-stage Alzheimer’s
C. Complete spinal cord transection
D. Advanced Parkinson’s
Migraine aura is thought to result from:
A. Cortical spreading depression
B. Dopamine surge
C. GABA inhibition
D. Glutamate excess only
Section 3: Cardiovascular System (Week 4) – Questions 26–40The primary compensatory mechanism in acute heart failure is:
A. RAAS suppression
B. Sympathetic activation (tachycardia, inotropy)
C. Natriuretic peptide decrease
D. Vasodilation
In diastolic heart failure (HFpEF), the main defect is:
A. Reduced ejection fraction
B. Impaired ventricular relaxation/filling
C. Decreased preload
D. Low afterload
Atherosclerotic plaque rupture most commonly triggers:
A. Stable angina
B. Acute myocardial infarction
C. Prinzmetal angina
D. Chronic ischemia
The enzyme most specific for myocardial injury is:
A. CK-MB
B. Troponin I/T
C. LDH
D. AST
Chronic hypertension leads to:
A. Left ventricular dilation initially
B. Concentric hypertrophy
C. Right heart failure first
D. Decreased afterload
In deep vein thrombosis, the major risk of complication is:
A. Arterial embolism
B. Pulmonary embolism
C. Myocardial infarction
D. Stroke
Coarctation of the aorta is a common cause of:
A. Secondary hypertension in children/young adults
B. Primary essential hypertension
C. Orthostatic hypotension
D. Hypotension
Natriuretic peptides (BNP/NT-proBNP) are elevated in:
A. Decompensated heart failure
B. Hypovolemia
C. Hypernatremia
D. Acute asthma
The primary mechanism in essential hypertension is:
A. Increased peripheral resistance
B. Decreased cardiac output
C. Renal artery stenosis
D. Coarctation
Post-MI ventricular remodeling involves:
A. Dilation and wall thinning
B. Immediate contraction
C. Decreased fibrosis
D. Reduced sympathetic tone
Raynaud phenomenon is characterized by:
A. Vasospasm of digital arteries
B. Venous thrombosis
C. Arterial aneurysm
D. Chronic venous insufficiency
In cardiogenic shock, the primary issue is:
A. Pump failure → low cardiac output
B. Vasodilation
C. Hypovolemia
D. Obstruction
The circle of Willis provides:
A. Collateral circulation in stroke
B. Venous drainage
C. Lymphatic return
D. Coronary bypass
Endothelial dysfunction in atherosclerosis involves:
A. Increased nitric oxide
B. Reduced vasodilation and increased adhesion molecules
C. Decreased LDL oxidation
D. Platelet inhibition
(SATA) Risk factors for atherosclerosis include:
A. Hypertension
B. Dyslipidemia
C. Diabetes
D. Smoking
Section 4: Respiratory System (Week 5) – Questions 41–55The primary cell type in asthma late-phase response is:
A. Neutrophil
B. Eosinophil
C. Basophil
D. Macrophage
In COPD, air trapping results from:
A. Loss of elastic recoil (emphysema)
B. Bronchoconstriction only
C. Surfactant increase
D. Alveolar expansion
ARDS is characterized by:
A. Cardiogenic pulmonary edema
B. Diffuse alveolar damage and non-cardiogenic edema
C. Reversible airflow limitation
D. Chronic fibrosis only
Hypoxic pulmonary vasoconstriction is a protective mechanism to:
A. Increase V/Q mismatch
B. Redirect blood to better-ventilated alveoli
C. Cause systemic hypertension
D. Decrease cardiac output
The GOLD classification for COPD severity is based on:
A. FEV1 % predicted post-bronchodilator
B. PaO2 level
C. DLCO
D. 6-minute walk distance
In pulmonary hypertension (Group 1 PAH), the primary defect is:
A. Left heart failure
B. Endothelial dysfunction → vasoconstriction and remodeling
C. Chronic hypoxia only
D. Thromboembolism
Cor pulmonale is right ventricular hypertrophy/failure due to:
A. Primary lung disease
B. Systemic hypertension
C. Valvular disease
D. Cardiomyopathy
Surfactant deficiency contributes to:
A. Atelectasis in ARDS
B. Bronchiectasis
C. Emphysema
D. Asthma
Chronic bronchitis in COPD is defined by:
A. Productive cough ≥3 months for 2 consecutive years
B. FEV1 3.5 g/day, hypoalbuminemia, edema
B. Hematuria only
C. Oliguria
D. Hypertension alone
In sickle cell anemia, vaso-occlusive crisis is triggered by:
A. Deoxygenation → HbS polymerization
B. Iron overload
C. Platelet activation
D. Complement activation
Immune thrombocytopenia (ITP) involves:
A. Autoantibodies to platelets → destruction
B. Bone marrow failure
C. Hemolysis
D. Clotting factor deficiency
Type II hypersensitivity is best exemplified by:
A. Goodpasture syndrome
B. SLE
C. Serum sickness
D. Contact dermatitis
Complement activation in immune complex disease leads to:
A. Type III hypersensitivity
B. Type I anaphylaxis
C. Cell-mediated immunity
D. Delayed hypersensitivity
In chronic kidney disease stage 5, the primary treatment is:
A. Dialysis or transplantation
B. Diuretics only
C. ACE inhibitors
D. Erythropoietin alone
Secondary hyperparathyroidism in CKD results from:
A. Hypocalcemia and hyperphosphatemia
B. Hypercalcemia
C. Low PTH
D. Vitamin D toxicity
The direct Coombs test detects:
A. Antibodies on RBC surface (autoimmune hemolytic anemia)
B. Platelet antibodies
C. Complement only
D. Clotting factors
Leukemoid reaction differs from leukemia by:
A. Being reactive (infection/stress) with left shift
B. Malignant blasts
C. Bone marrow failure
D. Pancytopenia
In multiple myeloma, the hallmark is:
A. Monoclonal protein (M-spike)
B. Polyclonal gammopathy
C. Hypogammaglobulinemia
D. Thrombocytosis
Primary immunodeficiency example:
A. SCID (severe combined)
B. AIDS
C. Drug-induced neutropenia
D. Splenectomy
The primary defect in SLE is:
A. Loss of self-tolerance → autoantibodies
B. Complement deficiency only
C. T-cell suppression
D. B-cell aplasia
(SATA) Features of hemolytic uremic syndrome include:
A. Microangiopathic hemolytic anemia
B. Thrombocytopenia
C. Acute kidney injury
D. Normal ADAMTS13 activity (in typical HUS)
Section 7: Reproductive & Genitourinary (Week 10) – Questions 86–95The most common cause of pelvic inflammatory disease is:
A. Chlamydia trachomatis and Neisseria gonorrhoeae
B. E. coli
C. Candida
D. HSV
Long-term sequela of untreated PID includes:
A. Tubal infertility and ectopic pregnancy
B. Immediate renal failure
C. Bone loss
D. Cardiac failure
Benign prostatic hyperplasia primarily affects:
A. Transition zone → urinary obstruction
B. Peripheral zone
C. Seminal vesicles
D. Urethra only
In polycystic ovary syndrome (PCOS), the key feature is:
A. Hyperandrogenism and anovulation
B. Estrogen excess
C. Thyroid dysfunction
D. Adrenal hyperplasia
The primary mechanism in postmenopausal vaginal atrophy is:
A. Estrogen deficiency
B. Androgen excess
C. Progesterone dominance
D. FSH suppression
Cryptorchidism increases risk of:
A. Testicular cancer
B. Prostate cancer
C. Bladder cancer
D. Renal cell carcinoma
The most common cause of acute bacterial prostatitis is:
A. Ascending gram-negative bacteria (E. coli)
B. Viral
C. Fungal
D. Autoimmune
Endometriosis is defined by:
A. Ectopic endometrial tissue outside uterus
B. Adenomyosis
C. Leiomyoma
D. Cervical dysplasia
The primary treatment for chlamydia cervicitis is:
A. Azithromycin or doxycycline
B. Fluconazole
C. Metronidazole
D. Acyclovir
Infertility due to varicocele results from:
A. Increased scrotal temperature → impaired spermatogenesis
B. Hormonal imbalance
C. Obstruction only
D. Autoimmune attack
Section 8: Cancer Genetics & Oncology + Course Synthesis (Week 11) – Questions 96–100The “two-hit” hypothesis applies to:
A. Tumor suppressor genes
B. Oncogenes
C. DNA repair genes only
D. Viral oncogenes
The most common inherited cancer syndrome gene pair is:
A. BRCA1/BRCA2
B. APC
C. RB1
D. NF1
Angiogenesis in tumors is stimulated by:
A. VEGF overexpression
B. Endostatin
C. Thrombospondin
D. Angiostatin
Paraneoplastic syndrome example:
A. Lambert-Eaton myasthenic syndrome in small cell lung cancer
B. Direct tumor invasion
C. Metastatic compression
D. Chemotherapy toxicity
The most important course takeaway for advanced practice is:
A. Pathophysiology knowledge enables early recognition, precise diagnosis, and targeted interventions across the lifespan
B. Memorization of drug doses
C. Surgical techniques
D. Billing codes
ANSWERS
Section 1: Cellular Processes, Adaptations & Injury (Weeks 1–2)C. Hyperplasia
Hyperplasia is an increase in cell number via mitosis (e.g., endometrial response to estrogen). Atrophy decreases size, hypertrophy increases size, metaplasia changes cell type.
B. Severe ATP depletion
Severe/prolonged ATP depletion leads to irreversible injury (pump failure, membrane rupture, enzyme release). Mild hypoxia or reversible swelling is early/reversible; karyorrhexis is late necrosis.
B. Autosomal recessive inheritance
CFTR mutation in cystic fibrosis requires two defective alleles (one from each parent); carriers are asymptomatic. Not dominant, X-linked, or mitochondrial.
B. Expressivity
Expressivity refers to variable severity/phenotype among individuals with the same genotype (e.g., neurofibromatosis café-au-lait spots vary). Penetrance is presence/absence.
B. Lipid peroxidation of membranes
Free radicals (ROS) cause chain reactions oxidizing membrane lipids, proteins, DNA. ATP depletion, Ca²⁺ influx, and proteases are downstream effects.
A, B, D (SATA)
Reversible features: hydropic swelling (oncosis), fatty change (steatosis), membrane blebbing. Nuclear pyknosis is irreversible (necrosis/apoptosis marker).
B. 50%
Autosomal dominant: one mutated allele transmits disease; each child has 50% chance regardless of sex.
C. Hemophilia A
X-linked recessive (factor VIII deficiency); males express fully, females carriers. Huntington (autosomal dominant), CF (recessive), Marfan (dominant).
A. Prader-Willi vs. Angelman syndrome
Both result from chromosome 15q deletion/imprinting; phenotype depends on parental origin (paternal → Prader-Willi, maternal → Angelman).
B. Cumulative genetic + environmental liability
Multifactorial diseases (e.g., type 2 DM) require liability threshold exceeded by polygenic + environmental factors (obesity, diet).
B. Histone acetylation and DNA methylation
Epigenetics alters gene expression without DNA sequence change (acetylation activates, methylation silences). Mutations change sequence.
A. Not all individuals with the genotype show the phenotype
Incomplete penetrance: genotype present but phenotype absent (e.g., some BRCA carriers never develop cancer).
B. Two hits (Knudson hypothesis)
Tumor suppressors require both alleles inactivated (inherited + somatic or two somatic). Oncogenes need one activating hit.
A. Chronic myeloid leukemia
BCR-ABL fusion (Philadelphia chromosome t(9;22)) drives CML.
A. Diet and obesity in type 2 diabetes
Environmental modifiers (obesity, sedentary lifestyle) interact with genetic predisposition in polygenic diseases.
Section 2: Neurological System (Week 3)A. Embolism from atrial fibrillation
Cardioembolic (AFib) is a leading cause of ischemic stroke (clots from left atrium to MCA). Hemorrhage is separate.
A. Hippocampal sclerosis
Mesial temporal sclerosis (hippocampal neuron loss, gliosis) is classic in drug-resistant temporal lobe epilepsy.
B. Wind-up phenomenon and glial activation in CNS
Central sensitization: repeated C-fiber input → NMDA receptor activation, glial (microglia/astrocyte) release of cytokines → amplified pain.
A. Convergence of visceral and somatic afferents
Visceral and somatic neurons synapse on same spinal cord dorsal horn neurons → referred pain (e.g., cardiac ischemia → left arm).
B. Hippocampus and entorhinal cortex
Earliest/most severe atrophy in AD affects medial temporal lobe (memory formation).
B. Dopamine
Degeneration of substantia nigra dopaminergic neurons → reduced striatal dopamine → bradykinesia, rigidity, tremor.
A. 5 minutes
Status epilepticus: continuous seizure ≥5 min or recurrent without recovery (updated definition).
A. Increased intracranial pressure
Cushing triad: hypertension, bradycardia, irregular respirations — late sign of herniation risk from ↑ ICP.
A. Acute ischemic stroke
Neuroplasticity (synaptic remodeling, axonal sprouting) is most effective in subacute recovery post-stroke.
A. Cortical spreading depression
Migraine aura: wave of neuronal depolarization followed by suppression, causing visual/sensory symptoms.
Section 3: Cardiovascular System (Week 4)B. Sympathetic activation (tachycardia, inotropy)
Acute HF → baroreceptor unloading → catecholamine surge → ↑ HR/contractility (compensatory).
B. Impaired ventricular relaxation/filling
HFpEF: stiff LV → diastolic dysfunction, preserved EF, often from hypertension/hypertrophy.
B. Acute myocardial infarction
Plaque rupture → thrombus → coronary occlusion → transmural necrosis (STEMI).
B. Troponin I/T
Cardiac-specific troponins rise within 3–6 h, peak 24 h, remain elevated days; most sensitive/specific for MI.
B. Concentric hypertrophy
Chronic pressure overload (HTN) → parallel sarcomere addition → thick walls, small cavity.
B. Pulmonary embolism
DVT clot dislodges → travels to pulmonary arteries → infarction/hypoxemia.
A. Secondary hypertension in children/young adults
Coarctation causes upper-body HTN via mechanical obstruction and RAAS activation.
A. Decompensated heart failure
BNP/NT-proBNP released from stretched cardiomyocytes → natriuresis, vasodilation; diagnostic marker.
A. Increased peripheral resistance
Essential HTN: ↑ TPR from vascular remodeling, endothelial dysfunction, sympathetic overactivity.
A. Dilation and wall thinning
Post-MI remodeling: infarct zone thins/dilates → aneurysm risk, reduced EF.
A. Vasospasm of digital arteries
Raynaud: episodic pallor → cyanosis → rubor from cold/emotion-induced vasospasm.
A. Pump failure → low cardiac output
Cardiogenic shock: severe LV dysfunction → ↓ CO despite adequate preload.
A. Collateral circulation in stroke
Circle of Willis connects anterior/posterior circulations → potential bypass in occlusion.
B. Reduced vasodilation and increased adhesion molecules
Endothelial injury → ↓ NO, ↑ VCAM/ICAM → monocyte adhesion, foam cell formation.
A, B, C, D (SATA)
All are major modifiable risk factors for atherosclerosis (Framingham criteria).
Section 4: Respiratory System (Week 5)B. Eosinophil
Late-phase asthma: eosinophil recruitment via IL-5 → major basic protein release → epithelial damage.
A. Loss of elastic recoil (emphysema)
Destruction of alveolar walls → collapse of small airways on expiration → air trapping.
B. Diffuse alveolar damage and non-cardiogenic edema
ARDS: injury → cytokine storm → permeability edema, hyaline membranes, surfactant loss.
B. Redirect blood to better-ventilated alveoli
HPV: low alveolar O₂ → local vasoconstriction → improves V/Q matching.
A. FEV1 % predicted post-bronchodilator
GOLD stages 1–4 based on FEV1 (mild ≥80%, very severe 3.5 g/day, hypoalbuminemia, edema
Nephrotic: massive glomerular permeability → hypoalbuminemia → oncotic edema.
A. Deoxygenation → HbS polymerization
Sickle crisis: deoxy-HbS forms polymers → RBC sickling → vaso-occlusion.
A. Autoantibodies to platelets → destruction
ITP: IgG against GPIIb/IIIa → splenic clearance.
A. Goodpasture syndrome
Type II: antibodies against basement membrane (lung/kidney).
A. Type III hypersensitivity
Immune complexes deposit → complement activation → inflammation (e.g., serum sickness).
A. Dialysis or transplantation
ESRD (stage 5): GFR <15 mL/min → renal replacement therapy.
A. Hypocalcemia and hyperphosphatemia
CKD → ↓ 1,25-(OH)₂D → hypocalcemia → secondary hyperparathyroidism.
A. Antibodies on RBC surface (autoimmune hemolytic anemia)
Direct Coombs: detects IgG/complement on RBCs.
A. Being reactive (infection/stress) with left shift
Leukemoid: extreme neutrophilia mimicking leukemia but polyclonal/reactive.
A. Monoclonal protein (M-spike)
Myeloma: plasma cell neoplasm → paraprotein (IgG most common).
A. SCID (severe combined)
Primary: genetic (e.g., ADA deficiency); secondary acquired (HIV, chemo).
A. Loss of self-tolerance → autoantibodies
SLE: antinuclear antibodies, immune complexes → multi-organ inflammation.
A, B, C (SATA)
Classic triad of HUS; D incorrect (typical HUS has normal ADAMTS13; atypical has low).
Section 7: Reproductive & Genitourinary (Week 10)A. Chlamydia trachomatis and Neisseria gonorrhoeae
Most common pathogens in sexually active young women with PID.
A. Tubal infertility and ectopic pregnancy
Scarring/adhesions from PID → blocked tubes.
A. Transition zone → urinary obstruction
BPH: stromal/epithelial hyperplasia in periurethral transition zone → LUTS.
A. Hyperandrogenism and anovulation
PCOS: insulin resistance → ↑ androgens → oligo/anovulation, cysts.
A. Estrogen deficiency
Menopause → thin, dry vaginal epithelium → atrophy, dyspareunia.
A. Testicular cancer
Cryptorchidism → 4–6× increased risk of germ cell tumors.
A. Ascending gram-negative bacteria (E. coli)
Most acute prostatitis from urinary tract ascent.
A. Ectopic endometrial tissue outside uterus
Endometriosis: cyclic bleeding → inflammation, adhesions, pain.
A. Azithromycin or doxycycline
CDC-recommended for uncomplicated chlamydia.
A. Increased scrotal temperature → impaired spermatogenesis
Varicocele → venous stasis → heat → DNA damage in sperm.
Section 8: Cancer Genetics & Oncology + Course Synthesis (Week 11)A. Tumor suppressor genes
Knudson: both alleles inactivated for loss of function (e.g., RB1 in retinoblastoma).
A. BRCA1/BRCA2
Most common high-penetrance hereditary breast/ovarian cancer genes.
A. VEGF overexpression
Tumors secrete VEGF → new vessel formation for growth/metastasis.
A. Lambert-Eaton myasthenic syndrome in small cell lung cancer
Paraneoplastic: autoantibodies to voltage-gated Ca²⁺ channels.
A. Pathophysiology knowledge enables early recognition, precise diagnosis, and targeted interventions across the lifespan
Core course goal: integrate cellular → systemic understanding for advanced nursing practice.
