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D115 Advanced Pathophysiology
Comprehensive Answer Guide & Study Reference
OA Exam Prep — Units 2 through 7
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? A: Trisomy 21 (three copies of chromosome 21). Features: intellectual disability, flat facial profile, upslanting palpebral fissures, single palmar crease, low-set ears, hypotonia. Risks: congenital heart defects (AV canal), early-onset Alzheimer's, hypothyroidism, leukemia. 1..
D115 Advanced Pathophysiology — OA Answer Guide ⭐ HIGH YIELD: Down syndrome = Trisomy 21. Most common chromosome abnormality. Associated with advanced maternal age. Q: Turner syndrome — chromosomes, features, treatment? A: Monosomy X (45,X). Features: short stature, webbed neck, shield chest, primary amenorrhea, infertility, coarctation of aorta, bicuspid aortic valve. Treatment: growth hormone, estrogen replacement therapy. Q: Klinefelter syndrome — chromosomes, features? A: 47,XXY. Features: tall stature, small testes, gynecomastia, infertility (azoospermia), learning difficulties. Often not diagnosed until puberty or adulthood. Q: Types of genetic testing? A: Carrier screening (identifies carriers of recessive disorders), prenatal testing (amniocentesis, CVS), newborn screening, diagnostic testing, predictive/presymptomatic testing (e.g., BRCA gene testing).
Module 2: Pathological Defense Mechanisms & Immunity
Q: What are the 3 layers of human defense? A: 1st line: Physical/mechanical barriers (skin, mucous membranes, cilia, stomach acid). 2nd line: Innate immunity (inflammation, phagocytes, fever, complement). 3rd line: Adaptive immunity (T cells, B cells, antibodies — specific and memory-forming). ⭐ HIGH YIELD: Know the sequence: Barrier → Innate (non-specific, fast) → Adaptive (specific, slow but memory). Q: How do acute and chronic inflammation differ? A: Acute inflammation: rapid onset (minutes-hours), dominated by neutrophils, vascular changes (redness, heat, swelling, pain, loss of function), usually resolves. Chronic inflammation: weeks-months, dominated by macrophages and lymphocytes, may cause tissue destruction and fibrosis (e.g., rheumatoid arthritis, TB). Q: What are the phases of wound healing? A: 1) Hemostasis (0–24 hrs): vasoconstriction, platelet plug, clot formation. 2) Inflammation (1–3 days): neutrophils then macrophages clean debris. 3) Proliferation (3–21 days): fibroblasts lay collagen, angiogenesis, epithelialization. 4) Remodeling (21 days–2 years): collagen reorganizes, scar matures. Q: Describe the process of adaptive immunity. A: Antigen is presented by APCs (antigen-presenting cells) via MHC molecules. Naïve T cells are activated and differentiate into helper T cells (CD4+) and cytotoxic T cells (CD8+). B cells are activated (with T cell help) → differentiate into plasma cells that produce antibodies. Memory cells are formed for faster future responses. Q: Identify the 4 types of hypersensitivity reactions. A: Type I (Immediate/Anaphylactic): IgE mediated, mast cells/basophils, occurs within minutes. Examples: anaphylaxis, allergic asthma, hay fever. Type II (Cytotoxic): IgG/IgM against cell surface antigens. Examples: hemolytic transfusion reactions, Graves disease. Type III (Immune complex): IgG/IgM complexes deposit in tissues. Examples: SLE, serum sickness, glomerulonephritis. Type IV (Delayed/Cell-mediated): T cell mediated, 48–72 hrs. Examples: contact dermatitis, TB skin test, transplant rejection. ⭐ HIGH YIELD: Type I = IgE. Type IV = T cells (no antibodies). Memorize: 1=IgE/mast cells; 2=cytotoxic; 3=immune complex; 4=T-cell delayed. Q: What causes autoimmune diseases? A: Molecular mimicry (pathogen antigens resemble self-antigens), failure of clonal deletion, loss of regulatory T cell function, exposure of hidden antigens, genetic predisposition (HLA alleles). Q: What are HLA alleles and disease associations? A: HLA = Human Leukocyte Antigen (MHC). Key associations: HLA-DR3/DR4 → Type 1 Diabetes; HLA-B → Ankylosing Spondylitis; HLA-DR4 → Rheumatoid Arthritis; HLA-DR3 → SLE; HLA-DR3 → Graves disease.
D115 Advanced Pathophysiology — OA Answer Guide ⭐ HIGH YIELD: Conductive loss: Weber → affected ear. Sensorineural: Weber → better ear. Rinne normal = AC > BC. Q: Allergic rhinitis vs. rhinitis medicamentosa?
D115 Advanced Pathophysiology — OA Answer Guide Q: 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. 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. ⭐ HIGH YIELD: Bell's Palsy = CN VII. Upper AND lower face paralysis distinguishes it from central (stroke) facial palsy, where forehead is SPARED. 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 =
- 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. ⭐ HIGH YIELD: Myasthenia gravis = anti-AChR antibodies. Fatigable weakness. Gets worse with use. Ptosis = classic early sign. Q: 5 categories of pain?
D115 Advanced Pathophysiology — OA Answer Guide Q: ⭐ HIGH YIELD: Insulin = ANABOLIC hormone. It stores energy. Glucagon = CATABOLIC. It mobilizes energy. Q: Hypothyroid vs. hyperthyroid differences? A: Hypothyroidism (↓T3/T4): cold intolerance, weight gain, fatigue, constipation, bradycardia, dry skin/hair, myxedema. TSH ↑ (primary). Causes: Hashimoto thyroiditis (autoimmune, anti-TPO antibodies). Hyperthyroidism (↑T3/T4): heat intolerance, weight loss, tachycardia, diarrhea, exophthalmos (Graves), anxiety, tremor, warm moist skin. TSH ↓. Causes: Graves disease (TSI antibodies stimulate TSH receptor). ⭐ HIGH YIELD: Hypo = SLOW everything. Hyper = FAST everything. Graves = exophthalmos + goiter + hyperthyroid. Hashimoto's = most common hypothyroid. Q: Types of diabetes? A: Type 1 DM: autoimmune destruction of beta cells → absolute insulin deficiency. Onset in children/young adults, prone to DKA. Type 2 DM: insulin resistance + relative insulin deficiency. Associated with obesity, 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. 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. 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). ⭐ HIGH YIELD: LH surge = ovulation trigger. Progesterone = dominant in luteal phase. Low progesterone → menstruation. 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. ⭐ HIGH YIELD: PCOS = insulin resistance + androgen excess + anovulation. High LH:FSH ratio. High yield! Q: Pathophysiology of primary vs secondary amenorrhea?
D115 Advanced Pathophysiology — OA Answer Guide Q: 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 (highflow): 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: HPV 16/18 = cancer. HPV 6/11 = genital warts. Chlamydia = most common bacterial STI.
D115 Advanced Pathophysiology — OA Answer Guide 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? A: By morphology — Microcytic (MCV<80): iron deficiency (most common), thalassemia, sideroblastic. Normocytic (MCV 80–100): acute blood loss, hemolytic, aplastic, chronic disease. Macrocytic (MCV>100): B12/folate deficiency (megaloblastic), alcohol, hypothyroid. By etiology: decreased production, increased destruction, blood loss. ⭐ HIGH YIELD: Iron deficiency anemia = most common anemia worldwide. Microcytic, hypochromic. Low ferritin, low iron, high TIBC. Q: Pathophysiology of sickle cell anemia? A: Autosomal recessive mutation: glutamate → valine at position 6 of β-globin chain. HbS forms polymers under low O2 → RBCs sickle → vessel occlusion (pain crises, organ damage), hemolysis (chronic anemia). Complications: acute chest syndrome, stroke, splenic sequestration, avascular necrosis, infections (functional asplenia → encapsulated organisms). Trait (HbAS): protective against malaria. Q: Pathophysiology of DIC? A: Disseminated Intravascular Coagulation: systemic activation of coagulation (from sepsis, trauma, obstetric catastrophe, cancer) → widespread fibrin clot formation → consumption of clotting factors and platelets → paradoxical BLEEDING. Lab findings: ↑PT, ↑PTT, ↑D-dimer, ↑fibrin degradation products, ↓fibrinogen, ↓platelets. Treatment: treat underlying cause; supportive (FFP, platelets, cryoprecipitate). ⭐ HIGH YIELD: DIC = 'clot then bleed.' Caused by: sepsis, trauma, obstetric emergencies. D-dimer ↑↑↑ is hallmark. Q: Pathophysiology of acute vs. chronic leukemia? A: Acute leukemia: sudden proliferation of immature blasts that don't differentiate → replace normal marrow → anemia, infections, bleeding. Presents acutely. ALL: most common in children. AML: most common acute leukemia in adults. Chronic leukemia: proliferation of more mature cells, slower progression. CML: Philadelphia chromosome (BCR-ABL t(9;22)). CLL: most common leukemia in adults overall; indolent. ⭐ HIGH YIELD: Philadelphia chromosome (BCR-ABL) = CML. Imatinib (Gleevec) is the treatment. HIGH YIELD.
Module 2: Cardiovascular & Lymphatic System
Q: Pathological process of hypertension? A: Essential HTN (95%): increased peripheral vascular resistance + increased cardiac output. Risk factors: age, obesity, sodium intake, sedentary lifestyle, family history, smoking. Sustained HTN → left ventricular hypertrophy, arterial remodeling, endothelial damage → atherosclerosis, CAD, stroke, renal failure, retinopathy. Stages: Elevated (120–129/<80), Stage 1 (130–139/80–89), Stage 2 (≥140/≥90), Hypertensive crisis (≥180/≥120). Q: Cardiac output and key hemodynamic terms? A: CO = HR × SV (Stroke Volume). Normal CO: 4–8 L/min. Preload: ventricular filling pressure (EDV). Afterload: resistance against which ventricle ejects (SVR). Contractility: intrinsic myocardial strength. Ejection Fraction (EF): SV/EDV × 100; normal ≥55%. Cardiac Index (CI) = CO/BSA; normal 2.5–4 L/min/m². ⭐ HIGH YIELD: CO = HR × SV. EF <40% = systolic dysfunction (HFrEF). Know normal values! Q: Pathophysiology of angina types? A: Stable angina: predictable chest pain with exertion, relieved by rest/nitrates; ≥70% fixed stenosis of coronary arteries. Unstable angina (UA): pain at rest or with minimal exertion; indicates plaque rupture with partial occlusion; medical emergency (part of ACS). Variant/Prinzmetal angina: coronary artery SPASM (not fixed stenosis); often at rest, at night; ST elevation during episode; treated with CCBs/nitrates, NOT betablockers.
D115 Advanced Pathophysiology — OA Answer Guide ⭐ HIGH YIELD: Stable = predictable, exertion-related. Unstable = ACS, rest pain = EMERGENCY. Variant/Prinzmetal = spasm. Q: Pathological process of heart failure? A: HF = heart unable to pump sufficient blood for metabolic needs. HFrEF (systolic, EF<40%): reduced contractility (MI, cardiomyopathy). HFpEF (diastolic, EF≥50%): impaired relaxation/filling (HTN, hypertrophy). Compensatory mechanisms: SNS activation (tachycardia, vasoconstriction), RAAS activation (fluid retention), 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). ⭐ HIGH YIELD: VFib = cardiac arrest = defibrillate NOW. AFib = irregular irregular rhythm. 3rd degree block = pacemaker. 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. 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. ⭐ HIGH YIELD: GFR is the key marker of kidney function. Normal ~125 mL/min. CKD staging is based on GFR. 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.
D115 Advanced Pathophysiology — OA Answer Guide
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? A: Decreased bone mineral density (BMD) → ↑fracture risk. Type I (postmenopausal): ↓estrogen → ↑osteoclast activity > osteoblast activity → trabecular bone loss. Type II (senile): age-related, cortical + trabecular bone loss, ↓Vit D/calcium. Risk factors: female, postmenopausal, Caucasian/Asian, thin, smoking, alcohol, sedentary, corticosteroid use, family history. T-score ≤ -2.5 = osteoporosis; -1 to -2.5 = osteopenia. ⭐ HIGH YIELD: T-score ≤ -2.5 = osteoporosis. Every 1 SD decrease in BMD doubles fracture risk. Q: Osteoarthritis vs. Rheumatoid Arthritis? A: Osteoarthritis (OA): degenerative/wear-and-tear; cartilage erosion → subchondral bone exposure; DIP joints (Heberden's nodes) and PIP joints (Bouchard's nodes), weight-bearing joints; worse with activity, better with rest; NO systemic inflammation; treatment: NSAIDs, PT, joint replacement. Rheumatoid Arthritis (RA): autoimmune (anti-CCP, RF+); symmetric synovitis; PIP, MCP, wrists (NOT DIP); morning stiffness >1 hour; systemic: fatigue, rheumatoid nodules; pannus formation → joint destruction; DMARDs (methotrexate) are cornerstone. ⭐ HIGH YIELD: OA = DIP + weight-bearing. RA = PIP/MCP, symmetric, morning stiffness, RF+, antiCCP+. Q: Pathophysiology of gout? A: Hyperuricemia → monosodium urate crystal deposition in joints → acute inflammatory arthritis. Triggers: alcohol, purine-rich foods (red meat, shellfish), diuretics, renal insufficiency. Classic presentation: sudden severe pain, swelling, erythema of 1st MTP joint (podagra). Dx: joint aspiration showing negatively birefringent needle-shaped crystals. Treatment: colchicine, NSAIDs (acute); allopurinol (chronic, ↓uric acid production). Q: Rhabdomyolysis — causes, diagnosis, treatment? A: Breakdown of skeletal muscle → release of myoglobin, CK, electrolytes into blood → myoglobin obstructs renal tubules → AKI. Causes: crush injury, extreme exercise, medications (statins, antipsychotics), heat stroke, seizures, alcohol/drug toxicity. Dx: ↑↑↑CK (>1000 IU/L), ↑myoglobin, myoglobinuria (dark 'cola' urine), ↑creatinine. Treatment: aggressive IV hydration (prevent AKI), treat underlying cause. ⭐ HIGH YIELD: Rhabdo = dark cola urine + ↑CK. Risk of AKI from myoglobin. Fluids are the cornerstone of treatment. Q: Compartment syndrome? A: Increased pressure within a closed fascial compartment → compromises blood flow → ischemia → tissue necrosis. Causes: fractures (tibial most common), crush injuries, tight casts. 6 P's: Pain (out of proportion, especially with passive stretch — EARLIEST sign), Pressure (tense compartment), Paresthesia, Paralysis, Pallor, Pulselessness (late signs). Emergency: fasciotomy. ⭐ HIGH YIELD: Compartment syndrome = PAIN out of proportion to injury + pain with passive stretch. Surgical emergency — fasciotomy.
Module 2: Integumentary System
Q: Layers of the skin? A: Epidermis (outer): Stratum corneum (keratinized dead cells, barrier), Stratum granulosum, Stratum spinosum, Stratum basale (basal cell layer — regeneration, melanocytes). Dermis: collagen, elastin, blood
D115 Advanced Pathophysiology — OA Answer Guide vessels, nerves, hair follicles, sweat/sebaceous glands. Hypodermis (subcutaneous): adipose tissue, insulation. Q: Types of skin cancer? A: Basal Cell Carcinoma (BCC): most common skin cancer; from stratum basale; pearly papule with rolled borders, telangiectasia; rarely metastasizes; caused by UV exposure. Squamous Cell Carcinoma (SCC): from keratinocytes; scaly plaque/ulcer; can metastasize (especially in immunocompromised); caused by UV, chronic wounds, HPV. Melanoma: from melanocytes; MOST DEADLY; ABCDE criteria: Asymmetry, Border irregular, Color varied, Diameter >6mm, Evolving. Staging: TNM (Breslow depth most important prognostic factor). ⭐ HIGH YIELD: BCC = most common. Melanoma = most deadly. Breslow thickness = most important prognostic factor for melanoma. 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.
