WGU D115 Exam D115 Advanced Pathophysiology Comprehensive Answer Guide & Study, Exams of Pathophysiology

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WGU D115 Exam D115 Advanced Pathophysiology

Comprehensive Answer Guide & Study Reference OA Exam

Prep Units 2 through 7 ( 2026 - 2027 )

D115 Advanced Pathophysiology

Comprehensive Answer Guide & Study Reference

OA Exam Prep — Units 2 through 7

UNIT 2: Foundations of Pathophysiology — Genes, Lifestyle &

Immunity

Module 1: Genetic Influence on Patient Outcomes

Q: What are genes composed of and where are they located? A: Genes are composed of DNA (deoxyribonucleic acid) — segments of DNA that encode proteins. They are located on chromosomes inside the nucleus of cells. Q: What are the four nitrogenous bases that make up DNA? A: Adenine (A), Thymine (T), Guanine (G), and Cytosine (C). A pairs with T; G pairs with C. In RNA, Uracil (U) replaces Thymine. HIGH YIELD: A-T and G-C base pairing is a common exam question. Remember: in RNA, T → U. Q: How are new strands of DNA formed? A: Through DNA replication: the double helix unwinds, and each strand serves as a template. DNA polymerase adds complementary nucleotides (A→T, G→C) forming two identical daughter strands. Q: How is transcription regulated? A: Transcription (DNA→mRNA) is regulated by promoter regions, transcription factors, enhancers/silencers, and epigenetic modifications (methylation, histone modification) that control whether a gene is expressed or silenced. Q: How many pairs of chromosomes do humans have? A: Humans have 46 chromosomes total — 23 pairs. 22 pairs are autosomes; 1 pair are sex chromosomes (XX = female, XY = male). Q: Most common chromosome abnormalities? A: Trisomy 21 (Down syndrome), Monosomy X (Turner syndrome — 45,X), Trisomy XXY (Klinefelter syndrome — 47,XXY), deletions, duplications, and translocations. Q: How is gender determined genetically? A: The SRY gene on the Y chromosome triggers male development. XX = female; XY = male. Individuals with no Y chromosome develop as female by default. Q: What are multifactorial diseases? Name examples. A: Diseases caused by the interaction of multiple genes AND environmental factors. Examples: type 2 diabetes, hypertension, coronary artery disease, cleft palate, neural tube defects, schizophrenia. Q: How do monozygotic and dizygotic twins differ genetically? A: Monozygotic (identical) twins share 100% of DNA — from one fertilized egg. Dizygotic (fraternal) twins share ~50% of DNA — from two separate eggs fertilized by two sperm. Q: Which chromosome is affected in Down syndrome? Clinical features?

HIGH YIELD: Acute angle-closure glaucoma = sudden, painful vision loss + headache + nausea. Emergency! HIGH YIELD: Conductive loss: Weber → affected ear. Sensorineural: Weber → better ear. Rinne normal = AC > BC. Q: SLE — clinical manifestations, labs, why hard to diagnose? A: SLE is a systemic autoimmune disease affecting multiple organs. Manifestations: butterfly (malar) rash, photosensitivity, oral ulcers, arthritis, serositis (pleuritis/pericarditis), renal disease (lupus nephritis), neurologic symptoms, hematologic (anemia, leukopenia, thrombocytopenia). Labs: ANA (most sensitive, not specific), anti-dsDNA (specific), anti-Smith (most specific), complement low (C3/C4), CBC abnormalities. Hard to diagnose because symptoms are varied, mimic other diseases, and wax/wane. Q: What are the 4 phases of infectious disease? A: 1) Incubation: pathogen enters, replicates, no symptoms. 2) Prodromal: early nonspecific symptoms (fatigue, malaise). 3) Illness: full clinical symptoms. 4) Decline/Convalescence: symptoms resolve, recovery. Q: HIV — characteristics, transmission, treatment? A: HIV (Human Immunodeficiency Virus) targets CD4+ T cells, macrophages, dendritic cells. Transmitted via sexual contact, blood, breast milk, vertical (mother→child). Destroys CD4+ cells → AIDS when CD4 < 200 cells/μL. Treatment: antiretroviral therapy (ART) — HAART (Highly Active Antiretroviral Therapy). Not curable but manageable. Q: How do vaccinations work? A: Vaccines introduce antigens (live-attenuated, inactivated, subunit, mRNA) that stimulate the adaptive immune response WITHOUT causing disease. B cells produce antibodies; memory B and T cells form. On re- exposure, memory cells mount a rapid, strong secondary response. Safer than natural infection because controlled antigen dose, no virulence, no risk of complications. Q: Incidence vs. Prevalence? A: Incidence: number of NEW cases in a population over a defined time period. Prevalence: total number of EXISTING cases (new + old) in a population at a given point in time. Prevalence = Incidence × Duration of disease. UNIT 3: HEENT, Neurologic, Psychiatric & Endocrine Systems

Module 1: HEENT Alterations

Q: What test checks for color blindness? A: Ishihara color plates — patient identifies numbers/patterns hidden within dots. Red-green color blindness is most common (X-linked recessive, more common in males). Q: Eye conditions considered medical emergencies? A: Acute angle-closure glaucoma (sudden increased IOP — severe eye pain, headache, halos, nausea), central retinal artery occlusion (sudden painless vision loss — 'cherry red spot'), retinal detachment (floaters, flashes, curtain over vision), chemical eye injuries, penetrating trauma. Q: Difference between hyperopia and myopia? A: Myopia (nearsightedness): eyeball too long, light focuses in front of retina; can see near, not far. Corrected with concave (diverging) lens. Hyperopia (farsightedness): eyeball too short, light focuses behind retina; can see far, difficulty near. Corrected with convex (converging) lens. Q: Weber and Rinne tests? A: Weber test: tuning fork placed on top of skull. Sound lateralizes to AFFECTED ear in conductive loss; to UNAFFECTED ear in sensorineural loss. Rinne test: compare air conduction (AC) vs bone conduction (BC). Normally AC > BC. In conductive loss: BC ≥ AC. In sensorineural loss: AC > BC (both reduced). Q: Allergic rhinitis vs. rhinitis medicamentosa? HIGH YIELD: HLA-B27 = Ankylosing Spondylitis (axial spondyloarthropathy). HLA-DR3/DR4 = Type 1 DM. Very high yield.

HIGH YIELD: Bell's Palsy = CN VII. Upper AND lower face paralysis distinguishes it from central (stroke) facial palsy, where forehead is SPARED. HIGH YIELD: Myasthenia gravis = anti-AChR antibodies. Fatigable weakness. Gets worse with use. Ptosis = classic early sign. A: Allergic rhinitis: IgE-mediated inflammatory response to allergens (pollen, dust, pet dander). Symptoms: sneezing, watery rhinorrhea, nasal congestion, itching. Rhinitis medicamentosa: rebound congestion from OVERUSE of topical decongestants (oxymetazoline). Causes nasal mucosal inflammation and dependence. Q: Criteria for diagnosing strep throat? A: Centor/McIsaac criteria: 1) Tonsillar exudates, 2) Tender anterior cervical lymphadenopathy, 3) Absence of cough, 4) Fever. 3–4 criteria = treat empirically or confirm with rapid strep test/throat culture. Caused by Group A Streptococcus (GAS).

Module 2: Neurologic System

Q: Functions of the nervous system divisions? A: CNS (brain + spinal cord): processes information, generates responses. PNS (cranial + spinal nerves): transmits signals to/from CNS. Autonomic NS: involuntary — sympathetic (fight/flight: ↑HR, ↑BP, dilates pupils, bronchodilation) vs. parasympathetic (rest/digest: ↓HR, ↑GI motility, constricts pupils). Somatic NS: voluntary motor control. Q: Which cranial nerve is affected in Bell's Palsy? A: CN VII (Facial nerve). Causes ipsilateral facial paralysis (upper AND lower face), inability to close eye, loss of taste (anterior 2/3 of tongue), hyperacusis. Most cases idiopathic or viral (HSV-1). Treatment: corticosteroids (prednisone) within 72 hours, eye protection. Q: Glasgow Coma Scale — stages and brain area evaluated? A: GCS evaluates: Eye opening (1–4), Verbal response (1–5), Motor response (1–6). Total: 3 – 15. Normal =

1. Severe TBI ≤ 8. Evaluates brainstem (arousal) and cortical function. Used to assess level of consciousness and brain injury severity. Q: Describe different neurotransmitters and what they regulate. A: Acetylcholine (ACh): muscle contraction, memory, parasympathetic NS. Dopamine: reward, movement, mood (↓ in Parkinson's; dysregulated in schizophrenia). Serotonin: mood, sleep, appetite (↓ in depression). Norepinephrine: alertness, sympathetic NS. GABA: main inhibitory NT (↓ in anxiety). Glutamate: main excitatory NT. Q: Functions of different brain divisions? A: Frontal lobe: executive function, personality, voluntary movement (motor cortex). Parietal lobe: sensory processing, spatial awareness. Temporal lobe: hearing, memory (hippocampus), language (Wernicke's). Occipital lobe: vision. Cerebellum: coordination, balance. Brainstem (midbrain/pons/medulla): vital functions — breathing, heart rate, consciousness. Hypothalamus: temperature, hunger, thirst, hormones. Q: Pathophysiology of myasthenia gravis? A: Autoimmune disease: antibodies against acetylcholine receptors (AChR) at the neuromuscular junction → blocks ACh binding → muscle weakness. Hallmark: fatigable weakness that worsens with activity and improves with rest. Ptosis and diplopia are classic early symptoms. Diagnosis: serum anti-AChR antibodies, edrophonium (Tensilon) test. Treatment: acetylcholinesterase inhibitors (pyridostigmine), immunosuppression, thymectomy. Q: 5 categories of pain? A: 1) Nociceptive (somatic): sharp, localized from tissue injury. 2) Nociceptive (visceral): dull, crampy, poorly localized from organ injury. 3) Neuropathic: burning, shooting, from nerve damage (e.g., diabetic neuropathy, PHN). 4) Psychogenic: pain influenced by psychological factors. 5) Referred: pain felt at a site distant from its source (e.g., cardiac pain → left arm/jaw). Q: Different levels of altered consciousness?

HIGH YIELD: LH surge = ovulation trigger. Progesterone = dominant in luteal phase. Low progesterone → menstruation. HIGH YIELD: PCOS = insulin resistance + androgen excess + anovulation. High LH:FSH ratio. High yield! HIGH YIELD: HPV 16/18 = cancer. HPV 6/11 = genital warts. Chlamydia = most common bacterial STI. metabolic syndrome. Gestational DM: hyperglycemia during pregnancy; risk of macrosomia, neonatal hypoglycemia. LADA (Latent Autoimmune Diabetes in Adults): autoimmune like T1, but slower onset in adults. Q: Metabolic syndrome — pathophysiology and manifestations? A: Cluster of conditions increasing risk of CVD and T2DM. Criteria (3 of 5): abdominal obesity (waist >35 in women/>40 in men), elevated TG (≥150), low HDL, elevated BP (≥130/85), elevated fasting glucose (≥100). Pathophysiology: insulin resistance → compensatory hyperinsulinemia → promotes dyslipidemia, HTN, inflammation. UNIT 4: Reproductive & Pulmonary Systems

Module 1: Reproductive System

Q: Effects of estrogen? A: Reproductive: develops female secondary sex characteristics, maintains menstrual cycle, thickens endometrium, promotes fertility. Non-reproductive: maintains bone density (prevents osteoporosis), cardioprotective (↑HDL, ↓LDL), improves insulin sensitivity, mood regulation, skin collagen maintenance. Q: Phases of the menstrual/ovarian cycle? A: Ovarian cycle: Follicular phase (days 1 – 13): FSH stimulates follicle development, estrogen rises. Ovulation (day 14): LH surge triggers egg release. Luteal phase (days 15–28): corpus luteum produces progesterone + estrogen; if no pregnancy, corpus luteum degenerates → menstruation. Uterine cycle: Menstruation (1–5), Proliferative (6–14, estrogen-driven), Secretory (15–28, progesterone-driven). Q: Pathophysiology of PCOS? A: Polycystic Ovarian Syndrome: insulin resistance → hyperinsulinemia → stimulates ovarian androgen production → elevated androgens → anovulation, irregular menses, hirsutism, acne. High LH:FSH ratio. Multiple small ovarian cysts (arrested follicles). Comorbidities: T2DM, metabolic syndrome, endometrial cancer, CVD. Q: Pathophysiology of primary vs secondary amenorrhea? A: Primary amenorrhea: no menarche by age 15 (with secondary sex characteristics) or 13 (without). Causes: Turner syndrome, androgen insensitivity, congenital anomalies. Secondary amenorrhea: cessation of menses >3 cycles or 6 months. Causes: pregnancy (first rule out!), hypothalamic amenorrhea (stress, weight loss, exercise), hyperprolactinemia, thyroid disorders, PCOS. Q: Priapism — manifestations and pathophysiology? A: Prolonged, painful erection unrelated to sexual stimulation lasting >4 hours. Types: Ischemic (low-flow, most dangerous): blood trapped → hypoxia → fibrosis → permanent ED if untreated. Non-ischemic (high- flow): from arterial fistula. Causes: sickle cell disease, medications (antipsychotics, phosphodiesterase inhibitors), spinal cord injury. Emergency treatment: aspiration, intracavernosal phenylephrine. Q: Long-term risks of STIs? A: Chlamydia/Gonorrhea → PID → infertility, ectopic pregnancy, chronic pelvic pain. HPV → cervical cancer (strains 16, 18), genital warts (6, 11). Syphilis → neurosyphilis, cardiovascular syphilis, congenital syphilis. Herpes (HSV-2) → neonatal herpes (if primary infection near delivery). HIV → AIDS.

HIGH YIELD: Remember: CO2 = respiratory; HCO3 = metabolic. Acidosis = pH < 7.35. Alkalosis = pH > 7.45. Very high yield! HIGH YIELD: COPD = irreversible obstruction. Asthma = reversible. 'Blue Bloater' = chronic bronchitis. 'Pink Puffer' = emphysema.

Module 2: Pulmonary System

Q: Types of abnormal lung sounds and associated diseases? A: Crackles (rales): fluid in alveoli/small airways — pneumonia, pulmonary edema, HF. Wheezes: narrowed airways (expiratory) — asthma, COPD. Rhonchi: secretions in large airways — bronchitis, COPD. Stridor: upper airway obstruction (inspiratory) — croup, epiglottitis. Pleural friction rub: inflamed pleural surfaces — pleuritis. Q: ABG normal values? A: pH: 7.35–7.45. PaO2: 80 – 100 mmHg. PaCO2: 35 – 45 mmHg. HCO3: 22 – 26 mEq/L. SaO2: ≥95%. Respiratory acidosis: pH↓, PaCO2↑. Respiratory alkalosis: pH↑, PaCO2↓. Metabolic acidosis: pH↓, HCO3↓. Metabolic alkalosis: pH↑, HCO3↑. Q: Pathophysiology of asthma? A: Chronic inflammatory airway disease with bronchial hyperresponsiveness. Trigger (allergen, cold air, exercise) → mast cell degranulation → release of histamine, leukotrienes, prostaglandins → bronchospasm, mucosal edema, increased mucus → airflow obstruction. Reversible (distinguishes from COPD). Long-term: airway remodeling (irreversible structural changes). Q: Pathophysiology of COPD? A: Chronic Obstructive Pulmonary Disease = Chronic bronchitis + Emphysema. Chronic bronchitis: chronic productive cough ≥3 months/year for ≥2 years; hypersecretion, mucus plugging, airflow obstruction → 'Blue Bloater.' Emphysema: destruction of alveolar walls → loss of elastic recoil → air trapping → barrel chest → 'Pink Puffer.' Caused by: smoking (#1), air pollution, α1-antitrypsin deficiency. Q: Kussmaul vs. Cheyne-Stokes respirations? A: Kussmaul respirations: deep, rapid, labored breathing — compensatory response to metabolic acidosis (DKA, renal failure) — blowing off CO2 to raise pH. Cheyne-Stokes: cycles of crescendo-decrescendo breathing alternating with apnea — caused by brainstem damage, HF, altitude, uremia — due to delayed feedback to respiratory center. Q: Pulmonary embolism — pathophysiology and manifestations? A: Thrombus (usually from DVT in leg) → travels to pulmonary artery → occludes blood flow → V/Q mismatch, hypoxemia, pulmonary infarction, right heart strain. Clinical: sudden dyspnea, pleuritic chest pain, tachycardia, hemoptysis. Massive PE: hypotension, syncope, right heart failure. Dx: CT pulmonary angiography (gold standard), D-dimer. Q: Cystic Fibrosis — pathological process? A: Autosomal recessive mutation in CFTR gene (chloride channel). Defective chloride transport → thick, viscous secretions in lungs, pancreas, GI tract, reproductive system. Lungs: chronic infections (Pseudomonas, Staph), bronchiectasis, respiratory failure. Pancreas: exocrine insufficiency → malabsorption, fat-soluble vitamin deficiency (A, D, E, K), CF-related diabetes. UNIT 5: Hematologic, Cardiovascular & Lymphatic Systems

Module 1: Hematologic System

Q: Composition of blood and hemostasis? A: Plasma (55%): water, proteins (albumin, globulins, fibrinogen), electrolytes, nutrients. Formed elements (45%): RBCs (erythrocytes — O2 transport), WBCs (leukocytes — immunity), Platelets (thrombocytes — clotting). Hemostasis: 1) Vascular spasm, 2) Primary hemostasis: platelet plug formation, 3) Secondary hemostasis: coagulation cascade → fibrin clot, 4) Fibrinolysis: clot dissolution. Q: Classifications of anemia?

HIGH YIELD: VFib = cardiac arrest = defibrillate NOW. AFib = irregular irregular rhythm. 3rd degree block = pacemaker. HIGH YIELD: GFR is the key marker of kidney function. Normal ~125 mL/min. CKD staging is based on GFR. HIGH YIELD: Know GFR cutoffs for CKD stages! ESRD = GFR <15. Uremia = accumulation of nitrogenous wastes. ventricular hypertrophy/remodeling → eventually worsen failure. Left HF: pulmonary congestion (dyspnea, orthopnea, crackles, PND). Right HF: systemic congestion (peripheral edema, JVD, hepatomegaly). Q: Common cardiac dysrhythmias? A: AFib: chaotic atrial activity, irregular rhythm; risk of stroke from atrial thrombus. AFl: regular 'sawtooth' atrial flutter. SVT: sudden rapid regular tachycardia; treated with vagal maneuvers/adenosine. VTach: ventricular tachycardia — can degenerate to VFib. VFib: chaotic ventricular activity → no cardiac output → cardiac arrest → immediate defibrillation. Heart blocks: 1st (PR prolonged), 2nd Mobitz I (Wenckebach), 2nd Mobitz II (dangerous — may need pacer), 3rd degree (complete block — pacer required). Q: Cardiogenic shock — pathophysiology? A: Pump failure → markedly reduced CO → inadequate organ perfusion. Most common cause: massive MI with >40% LV damage. Hallmarks: hypotension (SBP <90), cold/clammy extremities, tachycardia, pulmonary edema, oliguria, altered mental status. Hemodynamics: ↓CO, ↓CI, ↑SVR, ↑PCWP. Treatment: revascularization (PCI/CABG), vasopressors/inotropes, IABP or LVAD. UNIT 6: Renal, Urologic & GI Systems

Module 1: Renal & Urologic System

Q: Glomerular filtration, tubular reabsorption vs. tubular secretion? A: Glomerular filtration: blood filtered at glomerulus under pressure → forms filtrate (water, electrolytes, glucose, small molecules). Normal GFR: ~125 mL/min. Tubular reabsorption: useful substances (glucose, amino acids, Na+, water) reclaimed from filtrate back into blood. Tubular secretion: additional waste products (H+, K+, drugs) moved from blood INTO tubule for excretion. Net excretion = filtration - reabsorption + secretion. Q: Renin-Angiotensin-Aldosterone System (RAAS)? A: ↓ renal perfusion/BP → juxtaglomerular cells release RENIN → converts angiotensinogen → Angiotensin I → ACE (in lungs) converts to Angiotensin II → 1) Vasoconstriction (↑BP), 2) Stimulates aldosterone release (adrenal cortex) → ↑Na+ and water reabsorption (↑blood volume), 3) ADH release (↑water reabsorption). Net effect: ↑BP and ↑blood volume. Q: Pathophysiology and manifestations of acute kidney injury (AKI)? A: AKI = abrupt decline in kidney function. Categories: Prerenal (60–70%, hypoperfusion — dehydration, HF, sepsis), Intrinsic (ATN from ischemia/nephrotoxins, glomerulonephritis), Postrenal (obstruction — BPH, stones, tumor). Labs: ↑creatinine, ↑BUN, hyperkalemia, metabolic acidosis, oliguria. Potentially reversible if treated early. Q: Stages of chronic kidney disease (CKD)? A: Staged by GFR: Stage 1: GFR ≥90 (normal, with markers of damage). Stage 2: GFR 60 – 89. Stage 3a: 45 – 59, 3b: 30–44. Stage 4: 15–29. Stage 5: <15 (End-stage renal disease — ESRD, requires dialysis or transplant). Systemic effects: anemia (↓EPO), hypertension, metabolic acidosis, renal osteodystrophy (↓Vit D, ↑PTH), hyperkalemia, pericarditis, uremia. Q: Nephrotic syndrome vs. nephritic syndrome? A: Nephrotic syndrome: massive proteinuria (>3.5g/day), hypoalbuminemia, edema, hyperlipidemia, lipiduria. Causes: minimal change disease (kids), focal segmental glomerulosclerosis, membranous nephropathy, diabetic nephropathy. Nephritic syndrome: hematuria (RBC casts), proteinuria (mild-moderate), hypertension, oliguria, azotemia. Causes: post-streptococcal GN, IgA nephropathy, RPGN.

HIGH YIELD: Barrett's esophagus = GERD complication → pre-malignant. Surveillance endoscopy required. HIGH YIELD: UC = continuous, colon only, bloody diarrhea, curable with surgery. Crohn = skip lesions, transmural, anywhere, fistulas.

Module 2: GI System

Q: Pathophysiology of GERD? A: Gastroesophageal reflux disease: incompetent/transient relaxation of lower esophageal sphincter (LES) → gastric acid refluxes into esophagus → esophageal mucosal damage. Risk factors: obesity, hiatal hernia, pregnancy, certain foods (fat, caffeine, alcohol, chocolate), medications (CCBs, nitrates). Complications: esophagitis, Barrett's esophagus (metaplasia → columnar epithelium → ↑risk of esophageal adenocarcinoma), esophageal stricture. Q: Duodenal vs. gastric ulcers? A: Duodenal ulcers (more common): pain relieved by eating (food buffers acid), occur in first part of duodenum, associated with H. pylori + high acid secretion, rarely malignant. Gastric ulcers: pain worsened by eating, occur along lesser curvature, associated with H. pylori + NSAIDs (↓prostaglandin → ↓mucosal protection), can be malignant (biopsy required). Both: H. pylori infection is major cause; treat with triple therapy (PPI + clarithromycin + amoxicillin). Q: Ulcerative Colitis vs. Crohn's disease? A: Ulcerative Colitis: continuous inflammation of colon and rectum ONLY; mucosa and submucosa; bloody diarrhea, urgency; pseudopolyps; crypt abscesses; ↑colon cancer risk; surgical cure possible (colectomy). Crohn's Disease: any part of GI tract (mouth to anus), skip lesions, transmural inflammation → fistulas, strictures, abscesses; cobblestone mucosa; no cure with surgery; involves terminal ileum most commonly → B12 deficiency. Q: Pathophysiology of irritable bowel syndrome (IBS)? A: Functional disorder — no structural abnormality. Involves: visceral hypersensitivity (↑pain perception), altered gut motility, gut-brain axis dysregulation, altered intestinal microbiome, psychosocial factors. Symptoms: abdominal pain relieved by defecation, alternating diarrhea/constipation. Diagnosis: Rome IV criteria (clinical diagnosis of exclusion). Q: Celiac disease — pathophysiology? A: Autoimmune response to gluten (gliadin component) in genetically susceptible individuals (HLA-DQ2/DQ8). Gliadin → activates T cells → villous atrophy and crypt hyperplasia in small intestine → malabsorption of nutrients (iron, B12, folate, fat-soluble vitamins, calcium). Symptoms: diarrhea, bloating, failure to thrive, dermatitis herpetiformis. Dx: anti-tTG antibodies (IgA); confirmed by biopsy. Treatment: strict gluten-free diet. UNIT 7: Musculoskeletal & Integumentary Systems

Module 1: Musculoskeletal System

Q: Types of fractures? A: Closed (simple): bone broken, skin intact. Open (compound): bone penetrates skin. Comminuted: bone shattered into fragments. Greenstick: incomplete, one cortex broken (common in children). Stress: repetitive microtrauma. Pathologic: through diseased bone (osteoporosis, cancer). Compression: vertebral body compressed (osteoporosis). Spiral: twisting force (suspect abuse in kids). Classification: Gustilo-Anderson for open fractures. Q: Pathophysiology and risk factors of osteoporosis? HIGH YIELD: Nephrotic = protein loss. Nephritic = blood in urine (RBC casts). Nephrotic = massive edema.

Q: Pressure injuries — characteristics? A: Localized tissue damage from prolonged pressure (± shear/friction), usually over bony prominences (sacrum, heel, hip). Stages: Stage 1: non-blanchable erythema, skin intact. Stage 2: partial-thickness loss (open blister/shallow ulcer). Stage 3: full-thickness tissue loss (subcutaneous visible). Stage 4: full-thickness, bone/tendon/muscle exposed. Unstageable: obscured by eschar. Deep Tissue: purple/maroon intact skin. Q: Atopic dermatitis (eczema) — manifestations and pathophysiology? A: Chronic, relapsing inflammatory skin condition. Pathophysiology: filaggrin gene mutation → impaired skin barrier → allergen penetration → Th2-mediated immune response → IgE production, eosinophilia. Features: pruritus (hallmark), eczematous patches (flexural areas — antecubital, popliteal), xerosis (dry skin), associated with asthma and allergic rhinitis ('atopic triad'). Treatment: emollients, topical corticosteroids, topical calcineurin inhibitors, dupilumab (biologic). Q: Herpes zoster (shingles) — manifestations and diagnosis? A: Reactivation of latent VZV (Varicella-Zoster Virus) from dorsal root ganglia → dermatomal vesicular rash with severe burning/shooting pain. Unilateral, does NOT cross midline. Complications: postherpetic neuralgia (most common), Ramsay Hunt syndrome (CN VII — facial paralysis, ear vesicles), herpes zoster ophthalmicus (CN V1 — corneal involvement). Treatment: antivirals (acyclovir, valacyclovir) within 72 hours. Prevention: Shingrix vaccine. Q: ABCDE criteria and TNM staging for melanoma? A: ABCDE: Asymmetry, Border (irregular/notched), Color (multiple colors — brown, black, red, white), Diameter >6mm, Evolving (changing). TNM staging: T = tumor thickness (Breslow depth — most important), N = lymph node involvement, M = distant metastasis. Breslow depth <1mm = excellent prognosis; >4mm = poor. Sentinel lymph node biopsy done for T ≥1mm.