Pathophysiology — High-Yield Review

Highest-Yield Facts by Unit

Unit 1 — Foundations

• Pathophysiology = study of how disease changes normal function; physiology = normal function.
• Homeostasis = steady internal state; allostasis = achieving stability through change (adaptation).
• Etiology = cause; pathogenesis = how the disease develops; idiopathic = unknown cause; iatrogenic = caused by treatment; nosocomial = healthcare-associated.
• Sign = objective finding; symptom = subjective report; syndrome = cluster of signs/symptoms.
• Morbidity = illness/impact; mortality = death. Acute = sudden; chronic = long-lasting.
• Cells adapt via atrophy (shrink), hypertrophy (grow), hyperplasia (more cells), metaplasia (change type), dysplasia (disordered growth — precancerous).
• Hypoxia = low oxygen in tissue; ischemia = low blood flow (worse, also limits nutrient/waste transport).
• Necrosis = messy, inflammatory cell death; apoptosis = programmed, tidy cell death; autophagy = self-eating/recycling.

Unit 2 — Inflammation, Immunity, Infection, Healing

• Acute inflammation: vasodilation (redness, heat) → increased permeability (swelling) → leukocyte recruitment (chemotaxis → phagocytosis). Mediators: histamine, prostaglandins, cytokines.
• Fever = hypothalamic set-point reset by pyrogens; acute-phase proteins (e.g., C-reactive protein) rise.
• Wound healing phases: hemostasis → inflammatory → proliferative (granulation, angiogenesis, epithelialization) → remodeling (collagen reorganization).
• Healing intentions: primary (clean edges closed), secondary (left open, granulation), tertiary (delayed closure).
• Hypersensitivity: Type I (IgE, immediate/allergy), Type II (antibody vs cell), Type III (immune complexes), Type IV (T-cell, delayed).
• Sepsis = dysregulated host response to infection → organ dysfunction; septic shock adds perfusion failure.

Unit 3 — Fluids, Electrolytes, Acid-Base

• ICF = ~2/3 body water (inside cells); ECF = ~1/3 (interstitial + intravascular).
• Hydrostatic pressure pushes fluid out of capillaries; oncotic pressure (albumin) pulls it in.
• Edema = excess interstitial fluid (↑hydrostatic, ↓oncotic, ↑permeability, or ↓lymphatic drainage).
• Third spacing = fluid trapped in a space where it can't contribute to circulation.
• Hyponatremia = low sodium → water shifts into cells → cerebral swelling risk. Hypernatremia = high sodium → cellular dehydration.
• Potassium dominates resting membrane potential; hypokalemia → weakness, ECG changes; hyperkalemia → life-threatening cardiac conduction risk.
• Calcium stabilizes sodium channels (membrane excitability); low Ca → tetany/excitability; high Ca → stones/bones/groans/psychiatric overtones.
• Acidosis = ↓pH; alkalosis = ↑pH. Respiratory = lung-driven (CO₂); metabolic = bicarbonate-driven. Compensation ≠ correction.
• Anion gap helps distinguish causes of metabolic acidosis.

Unit 4 — Hematology and Oncology

• Anemia = low RBC mass; classified by cell size: microcytic (iron deficiency), normocytic (bleeding/chronic disease), macrocytic (B12/folate).
• Hemostasis: vascular spasm → platelet plug → coagulation cascade → fibrin mesh → fibrinolysis.
• DIC = widespread clotting + consumption of platelets/clotting factors → bleeding + thrombosis.
• Cancer hallmarks: sustained proliferation, apoptosis evasion, angiogenesis, invasion, metastasis. Grading = differentiation; staging = spread (TNM).

Unit 5 — Cardiovascular

• Atherosclerosis: endothelial injury → LDL uptake → foam cells → plaque; rupture → thrombosis.
• Hypertension promotes vascular remodeling and end-organ damage (heart, brain, kidneys, eyes).
• Ischemia (reversible) vs infarction (necrosis). Plaque rupture + thrombus → ACS.
• Heart failure: HFrEF = weak squeeze; HFpEF = stiff, poor filling. Left HF → pulmonary congestion; right HF → systemic congestion.
• Neurohormonal compensation: RAAS + SNS activation → vasoconstriction + fluid retention (helps early, harms long-term).
• Shock: hypovolemic (↓volume), cardiogenic (pump failure), distributive (vasodilation — septic/anaphylactic), obstructive (blocked flow).

Unit 6 — Respiratory

• V/Q mismatch, shunt (perfusion without ventilation), dead space (ventilation without perfusion).
• Obstructive (asthma/COPD) = difficulty exhaling, air trapping; restrictive (fibrosis) = difficulty inflating, reduced compliance.
• Type 1 respiratory failure = hypoxemic; Type 2 = hypoxemic + hypercapnic (ventilatory failure).
• ARDS = diffuse alveolar damage → noncardiogenic pulmonary edema.
• Pulmonary embolism = V/Q mismatch + dead space → hypoxemia.

Unit 7 — Renal

• GFR = filtration rate; AKI classified prerenal (↓blood flow), intrinsic (tubular/glomerular damage), postrenal (obstruction).
• Azotemia = elevated nitrogen wastes; uremia = the symptomatic syndrome of advanced kidney failure.
• CKD = progressive nephron loss; complications: anemia (↓erythropoietin), mineral-bone disorder, hyperkalemia, acidosis.
• Nephrotic = heavy protein loss (edema, hypoalbuminemia); nephritic = inflammation with hematuria, hypertension.

Unit 8 — Endocrine

• Negative feedback = the dominant hormone-control mechanism (e.g., thyroid, cortisol, glucose).
• Hypothyroidism = slow metabolism; hyperthyroidism = fast metabolism.
• Type 1 DM = autoimmune beta-cell loss (insulin absent); Type 2 DM = insulin resistance + relative deficiency.
• DKA (type 1) vs HHS (type 2) — both severe hyperglycemic emergencies.
• Cushing = cortisol excess; adrenal insufficiency = cortisol deficiency (primary = Addison).

Unit 9 — Neurologic

• ICP rises when intracranial volume exceeds compensation (Monro-Kellie); ↑ICP → ↓cerebral perfusion → herniation risk.
• Ischemic stroke = blocked vessel; hemorrhagic stroke = bleeding. TIA = transient ischemia without infarction.
• Seizure = abnormal synchronous neuronal discharge; epilepsy = recurrent unprovoked seizures; status epilepticus = prolonged.
• Delirium = acute, fluctuating confusion (medical emergency); dementia = chronic, progressive cognitive decline.

Unit 10 — GI, Hepatic, Pancreatic

• Peptic ulcer = acid/pepsin injury to mucosa (H. pylori, NSAIDs).
• Cirrhosis = diffuse fibrosis + nodular regeneration → portal hypertension → ascites, varices, encephalopathy.
• Jaundice = bilirubin accumulation (pre-hepatic, hepatic, or post-hepatic/obstructive).
• Acute pancreatitis = premature enzyme activation → autodigestion.

Unit 11 — MSK, Integumentary, Reproductive

• Osteoporosis = ↓bone mass (osteoclast activity > osteoblast); osteoarthritis = cartilage degeneration; rheumatoid arthritis = autoimmune synovitis.
• Pressure injury = ischemia from unrelieved pressure over bony prominences.
• Burns: depth (superficial → full-thickness), extent (TBSA), fluid shift + infection risk.
• Pregnancy adaptations: ↑blood volume, ↑cardiac output, hypercoagulability; hypertensive disorders and gestational diabetes are key concepts.

Comparison Tables

Frequently Confused Concepts

Fluid, Electrolyte, and Acid-Base

Shock Types

Respiratory Disorders

Renal Disorders

Diabetes and Endocrine

Disease-Process Mapping Template

For any disease: Normal function → Cause/risk factor → Mechanism → Compensation → Decompensation → Manifestations → Complications.

Cumulative Self-Check (20 questions)

1. What is the difference between etiology and pathogenesis?
2. What is the difference between atrophy and hypertrophy?
3. What is the difference between hypoxia and ischemia?
4. What is the difference between necrosis and apoptosis?
5. Name the four cardinal features of acute inflammation and their causes.
6. What are the three phases of wound healing after hemostasis?
7. Which hypersensitivity type is antibody-mediated against cells/tissues (not IgE)?
8. What is the difference between sepsis and septic shock?
9. Where is most of the body's water located — intracellular or extracellular?
10. What two pressures determine fluid movement across capillaries?
11. Why is hyponatremia dangerous for the brain?
12. Which electrolyte abnormality is most immediately life-threatening for the heart?
13. How do respiratory and metabolic acidosis differ?
14. What does the anion gap help distinguish?
15. How are microcytic, normocytic, and macrocytic anemias distinguished?
16. What are two hallmarks of cancer cells beyond uncontrolled proliferation?
17. What is the difference between HFrEF and HFpEF?
18. Name the four shock categories and one example of each.
19. What is the difference between a shunt and dead space?
20. How do prerenal, intrinsic, and postrenal AKI differ?

Answers and Rationales

1. Etiology is the cause; pathogenesis is the mechanism by which the disease develops. (Cause vs mechanism.)
2. Atrophy = decrease in cell size; hypertrophy = increase in cell size. (Smaller vs larger cells.)
3. Hypoxia = low tissue oxygen; ischemia = inadequate blood flow (which also impairs nutrient/waste exchange). (O₂ vs blood supply.)
4. Necrosis = uncontrolled, inflammatory cell death; apoptosis = programmed, tidy cell death. (Messy vs tidy.)
5. Vasodilation (heat/redness), increased permeability (edema), leukocyte recruitment (chemotaxis/phagocytosis), and pain (mediators/sensitization).
6. Inflammatory → proliferative (granulation, angiogenesis, epithelialization) → remodeling (collagen maturation).
7. Type II (IgG/IgM against cell-surface or matrix antigens). Type I is IgE-mediated; III is immune complexes; IV is T-cell–mediated.
8. Sepsis = dysregulated host response causing organ dysfunction; septic shock = sepsis plus persistent hypoperfusion/vasodilation despite fluid resuscitation.
9. Intracellular (~two-thirds).
10. Hydrostatic (pushes out) and oncotic/colloid (pulls in, mainly albumin).
11. Low sodium lowers osmolality, so water shifts into cells, risking cerebral edema.
12. Hyperkalemia — it disrupts cardiac conduction and can cause fatal dysrhythmias.
13. Respiratory is driven by CO₂ (lungs); metabolic is driven by bicarbonate (kidneys/acid load).
14. Metabolic acidosis with a high vs normal anion gap (unmeasured anions vs bicarbonate loss).
15. By red-cell size (MCV): small, normal, or large.
16. Angiogenesis, invasion/metastasis, and apoptosis evasion (any two).
17. HFrEF = reduced ejection fraction (weak squeeze); HFpEF = preserved ejection fraction (stiff ventricle, poor filling).
18. Hypovolemic (hemorrhage), cardiogenic (MI), distributive (sepsis), obstructive (pulmonary embolism).
19. Shunt = perfused but not ventilated; dead space = ventilated but not perfused.
20. Prerenal = reduced renal blood flow; intrinsic = damage to kidney tissue; postrenal = urinary obstruction.

Last-Minute Review

Core mechanisms to remember:

• Inflammation = vasodilation → permeability → leukocytes.
• Atherosclerosis = endothelial injury → plaque → rupture/thrombosis.
• Heart failure = pump dysfunction + RAAS/SNS compensation → congestion.
• Shock = inadequate tissue perfusion from volume, pump, tone, or obstruction.
• Cancer = proliferation + invasion + metastasis + angiogenesis.
• AKI = prerenal / intrinsic / postrenal.

Compensatory patterns:

• Respiratory compensation for metabolic acid-base changes is fast (minutes); renal compensation for respiratory changes is slow (hours–days).
• RAAS + SNS compensate for low perfusion but can worsen heart failure long-term.
• Lungs and kidneys are the two acid-base regulators.

High-yield distinctions:

• Obstructive vs restrictive lung disease.
• HFrEF vs HFpEF.
• Nephrotic vs nephritic.
• Type 1 vs Type 2 diabetes; DKA vs HHS.
• Ischemia vs infarction; sign vs symptom; compensation vs correction.

Urgent escalation principles:

• Sudden chest pain, severe dyspnea, altered consciousness, signs of shock, stroke-like symptoms, or severe electrolyte/ECG changes require immediate evaluation through local emergency services or a qualified clinician.

Related

• Subject overview
• Course catalog
• Unit 1 — Foundations