Heart Failure and Ischemic Heart Disease MCQs

Explanation: Triphenyl tetrazolium chloride (TTC) is a histochemical stain frequently used in autopsies to detect myocardial infarction (MI) . Within the first 4 hours of MI, gross examination may not reveal any visible infarct. However, when tissue slices are immersed in TTC solution, the stain differentiates viable from necrotic myocardium: viable myocardial tissue with intact lactate dehydrogenase activity stains brick-red , while infarcted areas remain pale due to leakage of dehydrogenases from damaged cell membranes.

Explanation: Myocardial infarcts that are less than 12 hours old are typically not grossly visible. However, those older than 3 hours (Option A ruled out) can be identified using vital stains like triphenyl tetrazolium chloride (TTC), which is a substrate for lactate dehydrogenase. Infarcts can be grossly visualised as red-blue areas due to trapped blood by 12 to 24 hours (Option C and D ruled out) .

The laboratory evaluation of MI is based on measuring the blood levels of proteins that leak out of irreversibly damaged myocytes; previously, this involved measurement of the MB fraction of creatine kinase (CK- MB). Currently, the most clinically useful biomarkers of myocardial damage are cardiac-specific troponins T and I (cTnT and cTnI), proteins that normally regulate calcium- mediated contraction of cardiac muscle. Reference : Robbins 10th Ed pg 550

Cut surfaces of hyperemic or congested tissues feel wet and typically ooze blood. On microscopic examination, acute pulmonary congestion is marked by blood-engorged alveolar capillaries and variable degrees of alveolar septal edema and intraalveolar hemorrhage. In chronic pulmonary congestion, the septa become thickened and fibrotic, and the alveolar spaces contain numerous macrophages laden with hemosiderin (“heart failure cells”) derived from phagocytosed red cells. Reference: Robbins and Cotran Pathologic Basis of Diseases, 10ᵗʰ ed Pg:97

In chronic pulmonary congestion, the septa become thickened and fibrotic, and the alveolar spaces contain numerous macrophages laden with hemosiderin (“heart failure cells”) derived from phagocytosed red cells. Reference: Robbins and Cotran Pathologic Basis of Diseases, 10ᵗʰ ed Pg:97

Ranolazine inhibits the late sodium current in myocardial cells. It is contraindicated in patients with liver dysfunction and QTc prolongation. Ivabradine helps control the heart rate by inhibiting the funny current (If) in the SA node cells. Reference: Harrison's Principles of Internal Medicine 21 st edition

Side effects of thiazide diuretics: Hypokalaemia(Blocking NaCl channels) Hyponatremia Hypercalcaemia Hyperglycemia hyperuricemia Hyperkalemia is caused by ACE inhibitors and potassium sparing diuretics Loop diuretics can also cause hyperuricemia and gout. Gynaecomastia is caused by spironolactone. Reference: Harrison's Principles of Internal Medicine, 21 st ed, Ch: 277, Pg:20.