Module 9 Comprehensive Exam Review Notes

Anemias – General Framework

  • Definition
    • Condition in which total number or quality of circulating RBCs and/or Hb is insufficient to transport O2 to tissues
    • Hall-mark lab signals → ↓ Hb, ↓ Hct, often ↓ RBC count
  • Global compensatory themes
    • Tissue hypoxia → fatigue + pallor
    • ↓ O2 delivery → tachycardia/↑ CO, dyspnea
    • Renal sensing of hypoxia → ↑ erythropoietin (EPO) → marrow stimulation

Universal Signs/Symptoms (high-yield test triggers)

  • Fatigue & exercise intolerance
  • Tachycardia/palpitations; possible systolic flow murmur
  • Pallor / cyanotic-tinged mucosa ("low pallor")
  • Lab red flags: \text{Hb}<12\;\text{g/dL (F)};\; <13\;\text{g/dL (M)}, \text{Hct}<36\%

1. Iron-Deficiency Anemia (IDA)

  • Epidemiology → most common world-wide
  • Key labs
    • ↓ Hb / Hct
    • ↓ ferritin (storage form; think "ferric")
    • ↓ serum Fe, ↑ TIBC
  • Etiologies / scenarios
    • Inadequate intake (vegans, malnutrition, developing nations)
    • Chronic blood loss → GI ulcer, heavy menses, chronic NSAID use (occult GI bleed)
    • Pregnancy → fetal iron siphoning
  • Prototype vignette
    • Fatigued female, heavy periods, takes daily ibuprofen → low ferritin, microcytosis

2. Sickle Cell Anemia

  • Genetics → autosomal recessive (carriers asymptomatic; FHx may appear “clean”)
  • Pathophys
    • HbS polymerizes when deoxygenated → RBCs become rigid, sickle-shaped → vaso-occlusion
  • High-yield manifestations
    • Severe pain crisis (ischemia)
    • Dactylitis in kids, stroke, acute chest, splenic sequestration
  • Precipitants → infection, dehydration, hypoxia, acidosis, stress

3. Aplastic Anemia

  • Core defect → pancytopenia from bone-marrow failure
  • Triggers → radiation, chemo, autoimmune, methotrexate, viral hepatitis
  • Clinical clues
    • Anemia (fatigue)
    • Leukopenia → recurrent infections
    • Thrombocytopenia → bleeding, petechiae

4. Vitamin B12 (Pernicious) Anemia

  • Fundamental sign → neuropathy! (numbness, tingling, ataxia, confusion, dementia)
  • Etiology → autoimmune destruction of parietal cells → ↓ intrinsic factor → malabsorption despite adequate diet
  • Labs → macrocytosis, hypersegmented neutrophils, ↓ serum B12, ↑ MMA
  • Test pearl → any anemia + neuropathy ⇒ circle B12 deficiency

Blood Product Reactions & DIC

Acute Hemolytic Transfusion Reaction (AHTR)

  • Cause → ABO incompatible units (e.g.
    giving type A blood to type B pt)
  • Triad → flank pain, hypotension, dark urine (hemoglobinuria)
  • Pathophys → complement-mediated intravascular hemolysis → free Hb → acute renal failure; risk of DIC

Febrile Non-Hemolytic Reaction

  • Donor leukocyte cytokines → fever/chills; not life-threatening, no hypotension/hemoglobinuria

Disseminated Intravascular Coagulation

  • Run-away coagulation consumes platelets & factors → simultaneous micro-clotting & bleeding

Polycythemia Vera (PV)

  • “Opposite of anemia” – neoplastic over-production of all myeloid lines (↑ RBC, WBC, PLT)
  • Blood becomes hyper-viscous → sluggish flow, thrombosis
  • Classic clues
    • Aquagenic pruritus (itching after warm shower)
    • Ruddy (flushed) face, splenomegaly, headache, blurred vision
  • Danger → DVT, stroke, MI

Thalassemias

  • Genetic defective globin chain synthesis (α or β) → malformed RBCs
  • Inheritance → autosomal recessive (need two alleles)
  • Populations → Mediterranean, Middle-East, South-Asian
  • Key findings
    • Microcytic anemia + jaundice, dark urine (hemolysis)
    • Bone deformities / frontal bossing (marrow hyper-activity)
    • Splenomegaly

von Willebrand Disease (vWD)

  • Autosomal dominant platelet function defect → ↓ vWF → platelets "less sticky"
  • Platelet COUNT normal; bleeding time ↑
  • Symptoms → nosebleeds, heavy menses, prolonged bleeding after dental work
  • Distinguish from hemophilia (A/B) (X-linked) by genetics & lab panel

Systemic Compensations for Hypotension / Blood Loss

1. Sympathetic Nervous System (SNS)

  • Catecholamines (epi / norepi) → ↑ HR (tachycardia), ↑ contractility, systemic vasoconstriction → ↑ BP, ↑ CO

2. Antidiuretic Hormone (ADH)

  • Posterior pituitary release → kidneys reabsorb H₂O → ↑ plasma volume

3. Renin–Angiotensin–Aldosterone System (RAAS)

  • ReninAngIACEAngII\text{Renin}\rightarrow \text{AngI}\xrightarrow{ACE} \text{AngII}
    • Ang II → potent vasoconstrictor
    • Ang II → ↑ aldosterone → Na⁺ reabsorption → H₂O follows → ↑ preload/volume

Hemostasis Cascade ("Please Don’t Die")

  1. Vascular injury
  2. Platelet adhesion/aggregation → temporary platelet plug
  3. Local vasoconstriction
  4. Coagulation cascade → fibrin mesh (stable clot)
  5. Reticulocyte count rises within days → marrow pumping out new immature RBCs to replace losses

ANP & BNP – Natural Diuretics

  • Released from over-stretched atria (ANP) or ventricles (BNP)
  • Effects
    • Vasodilation
    • GFR\uparrow GFR → natriuresis + diuresis (Na⁺ & H₂O loss)
    • ↓ renin/AngII/aldosterone → ↓ preload & BP
  • Clinical: BNP >500 pg/mL strongly suggests CHF

Atrial Fibrillation (AFib)

  • "Irregularly irregular" rhythm; no P waves; atrial rate 300–350 bpm
  • Ventricles pick random impulses → irregular pulses
  • Risks → age, CAD, HF, post-cardiac surgery
  • Major danger → embolic stroke (blood pools in quivering atria) → often anticoagulated

Core Hemodynamics

  • Preload = ventricular stretch at end-diastole (↑ with fluids; ↓ with hemorrhage)
  • Afterload = resistance LV must overcome (↑ with HTN, atherosclerosis)
  • Contractility = intrinsic squeeze (measured by EF: EF=SVEDV×100%EF = \frac{SV}{EDV}\times100\%)

Vascular Disorders

Peripheral Artery Disease (PAD)

  • Same atherosclerotic mechanism as CAD
  • Signature → intermittent claudication (leg pain w/ exertion, relieved by rest), ↓/absent distal pulses, cool pallid skin

Essential Hypertension

  • “Silent killer” → long-term vessel & end-organ damage (CAD/MI, LVH, CKD, retinopathy, stroke)

Raynaud’s Phenomenon

  • Paroxysmal arteriolar vasospasm → color sequence White → Blue → Red in fingers/toes, precipitated by cold/stress

Chronic Venous Insufficiency

  • Damaged leg vein valves → pooling
  • Manifestations → edema, stasis dermatitis (brown skin), venous ulcers, varicose veins, aching improved by elevation/compression

Ischemic Heart Spectrum

EntityTroponinST-segmentPredictability
Stable anginanormalexertional, relieved by rest/NTG
Unstable angina± ST ↓/T inversion (never ↑)unpredictable pain at rest
NSTEMI+ST normal/↓partial-thickness infarct
STEMI+ST ↑full-thickness infarct
  • Progression risk ladder → Stable < Unstable < NSTEMI < STEMI

Sudden Cardiac Death vs MI

  • Cardiac arrest = electrical failure (VF/VT) → no pulse, treat w/ CPR + AED
  • MI (NSTEMI/STEMI) = ischemic cell death; can secondarily precipitate arrest

Heart Failure Master Map

Left-Sided HF ("L for Lung")

  • Causes → CAD/MI, HTN, valve disease
  • Sx → pulmonary edema, crackles, orthopnea, PND, ↓ EF (systolic)

Right-Sided HF ("R for Rest of body")

  • Causes → L-HF, COPD (cor pulmonale), pulmonic valve dz
  • Sx → JVD, peripheral edema, ascites, hepatosplenomegaly, weight gain

Systolic vs Diastolic

  • Systolic = weak pump (floppy) → ↓ EF (<40 %)
  • Diastolic = stiff ventricle (hypertrophied) → normal/high EF but ↓ filling volume

Congenital Shunts

  • Remember Left (oxygenated) → Right (deoxygenated) yields acyanotic
    • ASD, VSD, Patent Ductus Arteriosus (PDA)
  • Right → Left yields cyanotic (blue) because deoxygenated blood enters systemic flow
    • Tetralogy of Fallot (TOF)

Tetralogy of Fallot – "PROVe"

  1. Pulmonary stenosis
  2. Right ventricular hypertrophy
  3. Overriding aorta (straddles both ventricles)
  4. Ventricular septal defect
  • "Tet spells" – cyanosis during crying/feeding; child squats to ↑ SVR ↓ shunt

Valve & Endocardial Disorders

Rheumatic Heart Disease (post-GAS)

  • Autoimmune (molecular mimicry) after strep pharyngitis/scarlet fever
  • Antibodies attack valves (esp. mitral) → stenosis / regurg, murmurs, vegetations

Infective Endocarditis

  • Bacterial colonization of valves (often tricuspid in IV-drug users)
  • Sx → fever, night sweats, new murmur, splinter hemorrhages, Osler nodes (painful), Janeway lesions (painless), Roth spots
  • Embolic phenomena → stroke, renal infarct, PE

Myocardial & Pericardial Inflammations

  • Myocarditis – viral (Coxsackie B, COVID-19), arrhythmias, sudden death in young adults
  • Pericarditis – sharp pleuritic pain, pericardial friction rub, relieved by leaning forward; may progress to …
    • Pericardial effusion – fluid accumulation
    • Cardiac tamponade – emergency; Beck’s triad: muffled heart sounds, JVD, hypotension (plus pulsus paradoxus)

Valvular Mechanics – Mitral Focus

DisorderTimingHemodynamicsBuzzwords
Mitral stenosisDiastole (filling)Narrowed orifice; ↑ LA pressure → pulm edemaPost-rheumatic fever; opening snap
Mitral regurgitationSystole (ejection)Incomplete closure; back-flow into LA → volume overloadHolosystolic murmur radiating to axilla
  • Quick test cue: "Obstruction DURING diastole?" ⇒ Mitral stenosis. "Back-flow DURING systole?" ⇒ Mitral regurg.

Rapid-Fire Clinical Case Triggers

  • Fatigue + daily NSAIDs + ↓ ferritin ⇒ IDA
  • 10-y/o severe abdominal pain + known sickle trait ⇒ vaso-occlusive crisis
  • Anemia + neuropathy + vegan diet ⇒ B12 deficiency
  • Blood transfusion → flank pain + dark urine + hypotension ⇒ Acute hemolytic reaction
  • Mild fever during transfusion, vitals stable ⇒ Febrile non-hemolytic
  • Flushed face; itching post-hot shower ⇒ Polycythemia Vera
  • Finger blanch → blue → red in cold office ⇒ Raynaud
  • Chest pain at rest, no troponin, ST depression ⇒ Unstable angina
  • Crushing chest pain, ST elevation in II, III, aVF ⇒ STEMI (inferior wall)
  • A‐fib on ECG, HR irregular 130, no P waves → start anticoag
  • Post-strep teen with new murmur & arthritis ⇒ Rheumatic carditis
  • IV drug user, fever, tricuspid murmur, Osler nodes ⇒ Infective endocarditis
  • Trauma patient, distant heart sounds, BP 80/50, distended neck veins ⇒ Cardiac tamponade