Hematology, Acid-Base & Temperature MCQ

Hematology and acid-base close the dental physiology loop. PT/INR reads the extrinsic warfarin pathway; PTT reads the intrinsic heparin pathway; aspirin's antiplatelet effect lasts the lifespan of the platelet (7-10 days). Acid-base disturbances shape vital signs and decision-making; respiratory acidosis from oversedation is the dental emergency to recognize. Temperature regulation runs through the hypothalamus; malignant hyperthermia after succinylcholine or volatile agent is treated with dantrolene, and serotonin syndrome from tramadol plus SSRI is the analogous drug-driven hyperthermia. Basic immune cell biology rounds out the chair-side picture.

Blood Composition and Erythropoiesis

• Blood is about 45 percent cellular (hematocrit) and 55 percent plasma. Red cells (about 5 million/uL) carry oxygen via hemoglobin; white cells (about 5,000-10,000/uL) defend against infection; platelets (about 150,000-450,000/uL) drive primary hemostasis.
• RED CELLS have no nucleus and no mitochondria; they use glycolysis for ATP and last about 120 days before splenic and hepatic removal. Erythropoiesis occurs in the red marrow under control of EPO from the kidney (peritubular fibroblasts).
• ANEMIA can be microcytic (iron deficiency, thalassemia), normocytic (acute blood loss, CKD via EPO deficiency, chronic disease), or macrocytic (B12 or folate deficiency, alcoholism, hypothyroidism); chronic kidney disease anemia is treated with exogenous erythropoietin or analogs.
• White cells split into granulocytes (neutrophils, eosinophils, basophils) and agranulocytes (lymphocytes T, B, NK; monocytes/macrophages); neutrophils are the first-responder phagocyte; lymphocytes drive adaptive immunity.

Hemostasis: Primary, Secondary, PT vs PTT

• PRIMARY hemostasis: vessel injury → platelets adhere via von Willebrand factor (vWF) bridging to subendothelial collagen → platelet activation → aggregation via GP IIb/IIIa receptors binding fibrinogen → temporary platelet plug.
• SECONDARY hemostasis (coagulation cascade) produces fibrin to stabilize the plug; the EXTRINSIC pathway (tissue factor + factor VII; rapid initiation in vivo) is tested by PT/INR; the INTRINSIC pathway (factors XII, XI, IX, VIII; activated by contact in vitro) is tested by PTT; the COMMON pathway (X, V, II/thrombin, I/fibrinogen) is tested by both.
• Vitamin K-dependent factors are II, VII, IX, X (plus proteins C and S); WARFARIN inhibits vitamin K epoxide reductase and lowers all of them, prolonging PT/INR (factor VII has the shortest half-life and falls first).
• Heparin (and LMWH) activates antithrombin III; unfractionated heparin prolongs PTT; LMWH (enoxaparin) primarily inhibits factor Xa with less PTT effect. PROTAMINE reverses heparin; vitamin K (and PCC/FFP) reverses warfarin.

Antiplatelets, DOACs, and Dental Bleeding

• ASPIRIN irreversibly acetylates platelet COX-1, preventing thromboxane A2 synthesis and aggregation; because platelets cannot regenerate the enzyme, the effect lasts the platelet lifespan (7-10 days).
• Clopidogrel and prasugrel are P2Y12 ADP-receptor antagonists; clopidogrel is a CYP2C19 prodrug (polymorphism reduces efficacy). Ticagrelor is a reversible P2Y12 antagonist.
• DOACs (direct oral anticoagulants) include apixaban and rivaroxaban (direct factor Xa inhibitors) and dabigatran (direct thrombin inhibitor); they have rapid on/off and do not require routine INR monitoring. Reversal: andexanet alfa for Xa inhibitors; idarucizumab for dabigatran.
• For simple dental extractions, warfarin (INR in range) and the usual antiplatelets are typically continued with local hemostasis (pressure, oxidized cellulose, sutures, tranexamic acid rinse where appropriate); stopping risks thromboembolism that usually outweighs controllable bleeding.

ABO and Rh Blood Groups

• ABO antigens are inherited co-dominantly; A has A antigen + anti-B antibody, B has B antigen + anti-A antibody, AB has both antigens + no antibodies (universal recipient), O has no antigens + both antibodies (universal donor for RBCs).
• Rh blood group: Rh+ has the D antigen; Rh- lacks it. Hemolytic disease of the newborn (HDN) occurs when an Rh- mother is sensitized to an Rh+ fetus's RBCs; RhoGAM (anti-D immune globulin) prevents sensitization at delivery and during pregnancy.
• Transfusion reactions include ACUTE HEMOLYTIC (ABO incompatibility), febrile non-hemolytic (cytokines), allergic/urticarial, transfusion-related acute lung injury (TRALI), and delayed hemolytic.
• Cross-matching tests recipient serum against donor RBCs to detect alloantibodies before transfusion.

Acid-Base Physiology

• Normal arterial pH is 7.35-7.45; HCO3- is 22-26 mEq/L; pCO2 is 35-45 mmHg. The HENDERSON-HASSELBALCH relationship pH = 6.1 + log(HCO3-/0.03 × pCO2) ties bicarbonate (renal) to CO2 (respiratory).
• RESPIRATORY acidosis: hypoventilation raises pCO2 (lowers pH); causes include oversedation (opioid + benzodiazepine), airway obstruction, COPD, neuromuscular disease. RESPIRATORY alkalosis: hyperventilation lowers pCO2 (raises pH); causes include anxiety, sepsis, pulmonary embolism, salicylate (early phase).
• METABOLIC acidosis: low HCO3-; ANION-GAP causes (MUDPILES: methanol, uremia, DKA, propylene glycol, isoniazid/iron, lactic acidosis, ethylene glycol, salicylates) vs NON-anion-gap (diarrhea, renal tubular acidosis). METABOLIC alkalosis: high HCO3-; vomiting, diuretics, contraction.
• COMPENSATION is partial, not complete: respiratory disturbances are compensated by the kidney over hours to days (HCO3- retention or excretion); metabolic disturbances are compensated by the lungs within minutes (hyperventilation or hypoventilation).

Temperature Regulation and Drug-Induced Hyperthermia

• Body temperature is regulated by the hypothalamic preoptic area, which adjusts heat production (shivering, brown fat thermogenesis) and heat loss (sweating, vasodilation, behavior); the normal set point is about 37 °C (98.6 °F).
• FEVER is a regulated rise in the hypothalamic set point driven by pyrogens (interleukin-1, interleukin-6, TNF-alpha, prostaglandin E2 from arachidonic acid); NSAIDs lower fever by blocking COX-mediated PGE2 synthesis.
• MALIGNANT HYPERTHERMIA is a non-regulated hyperthermia triggered by succinylcholine or volatile anesthetics in patients with RYR1 mutations; uncontrolled SR Ca2+ release produces severe muscle rigidity, hyperthermia, acidosis, and hyperkalemia. Dantrolene (blocks SR Ca2+ release) is the antidote, with cooling and supportive care.
• SEROTONIN SYNDROME is drug-induced hyperthermia from excess serotonergic activity (tramadol + SSRI, MAO inhibitor + SSRI, etc.); the triad is mental status change, autonomic instability, and neuromuscular hyperactivity (clonus, hyperreflexia, tremor). Stop the offending drugs, supportive care, benzodiazepines for agitation/tremor, cyproheptadine in severe cases.