Pyrogens (IL-1, IL-6, TNF-α, prostaglandin E2) raise the hypothalamic set-point, triggering heat conservation and production. Metabolic rate rises ~10–13% per °C, increasing CO₂ output, so the respiratory centre raises minute ventilation — roughly 2–3 extra breaths/min per degree.

Sustained high arterial pressure damages the glomerular endothelium and basement membrane, increasing permeability. Albumin leaks into filtrate (albuminuria), lowering surface tension and producing persistent foam — an early marker of hypertensive nephropathy.

Melena is black, tarry, foul stool from digested blood, indicating an upper-GI source (above the ligament of Treitz). Hematochezia is bright red blood, typically a lower-GI / colorectal source. Pencil-thin stool suggests a luminal narrowing such as a colorectal mass.

H. pylori uses urease to neutralize gastric acid locally, colonizes the mucus layer, and triggers chronic inflammation with cytotoxins (CagA, VacA). This impairs mucosal defence and increases acid in duodenal disease, leading to ulceration. Eradication uses combination antibiotics plus a PPI.

High-temperature cooking of meat forms heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs). After metabolic activation these form DNA adducts, causing mutations in proto-oncogenes and tumor-suppressor genes — a stepwise contribution to carcinogenesis.

They block conversion of angiotensin I to II, reducing vasoconstriction and aldosterone-driven sodium retention. Preferential dilation of the efferent glomerular arteriole lowers intraglomerular pressure, reducing proteinuria and slowing nephropathy progression.

It is a thermal/energetic classification (Ayurveda, TCM) describing a food's physiological effect — warming foods promote circulation and diaphoresis; cooling foods reduce inflammation and mucosal irritation. While not a Western biochemical model, many overlaps exist (e.g. anti-inflammatory 'cooling' foods).

Ejection fraction (EF) quantifies the percentage of blood ejected per beat. HFrEF (EF ≤40%) reflects systolic dysfunction; HFmrEF (41–49%) is mid-range; HFpEF (≥50%) reflects diastolic dysfunction. EF guides therapy choice — e.g., beta-blockers and ACE inhibitors are core in HFrEF.