Signs, Symptoms, And Pathophysiology - NAPLEX

Predictable exertional chest pressure relieved by rest or nitroglycerin. Stable angina presents with consistent, trigger-related symptoms that resolve quickly, distinguishing it from unstable or acute presentations.

Myocardial ischemia from fixed coronary stenosis and supply–demand mismatch. Occurs when myocardial oxygen demand exceeds supply due to atherosclerotic narrowing, leading to reversible ischemia during exertion.

Dysregulated inflammatory response causing vasodilation, capillary leak, and hypoperfusion. Infection triggers cytokine storm, leading to endothelial dysfunction and distributive shock with multiorgan failure.

Sudden focal neurologic deficit that fully resolves, typically within 24 hours. Transient ischemia causes temporary dysfunction without infarction, resolving as perfusion is restored.

Fever with severe headache and neck stiffness, often with photophobia. Meningeal irritation from infection causes inflammation, leading to classic signs of meningeal involvement.

IgE-mediated mast cell degranulation causing vasodilation and airway edema. Allergen cross-links IgE on mast cells, releasing histamine and leukotrienes that mediate systemic allergic responses.

Reduced hemoglobin lowers oxygen delivery, causing fatigue and exertional dyspnea. Insufficient iron impairs erythropoiesis, reducing oxygen-carrying capacity and triggering compensatory mechanisms.

Cerebral artery occlusion causing focal brain ischemia and infarction. Thrombus or embolus interrupts blood supply, resulting in neuronal death in the affected vascular territory.

Periumbilical pain migrating to right lower quadrant with anorexia and fever. Appendiceal obstruction leads to inflammation and bacterial overgrowth, with pain shifting as peritonitis develops.

Premature pancreatic enzyme activation causing autodigestion and inflammation. Triggers like gallstones or alcohol cause intra-acinar enzyme activation, leading to tissue damage and systemic inflammation.

Postprandial right upper quadrant pain radiating to the back or right shoulder. Gallstones obstruct cystic duct during fatty meal-induced contraction, causing visceral pain referral patterns.

COX inhibition lowers prostaglandins, reducing mucosal protection and bicarbonate. Prostaglandins maintain gastric mucosa; their depletion by NSAIDs increases susceptibility to acid-induced injury.

Heartburn and regurgitation worse after meals or when supine. Lower esophageal sphincter incompetence allows acid reflux, exacerbated by gravity and increased intra-abdominal pressure.

Pulmonary arterial obstruction causing V/Q mismatch and increased dead space. Embolus blocks blood flow, causing ventilation-perfusion imbalance and hypoxic vasoconstriction in unaffected areas.

Acute fever, productive cough, pleuritic chest pain, and focal crackles. Bacterial infection leads to alveolar consolidation, inflammation, and systemic response, differentiating from viral causes.

COPD has largely irreversible airflow limitation from alveolar and airway damage. Long-term smoking causes emphysema and chronic bronchitis, resulting in fixed obstruction not responsive to therapy.

Reversible airway inflammation with bronchoconstriction and mucus hypersecretion. Allergic triggers induce immune-mediated responses that are reversible with bronchodilators, unlike chronic conditions.

Chronic hyperglycemia causing microvascular nerve ischemia and axonal injury. Sustained high glucose levels damage vasa nervorum, leading to nerve dysfunction and sensory loss in extremities.

Diaphoresis, tremor, palpitations, hunger, and confusion. Low blood glucose triggers sympathetic activation and neuroglycopenic effects, manifesting as autonomic and cognitive symptoms.

Absolute insulin deficiency causing ketogenesis and anion-gap metabolic acidosis. Lack of insulin promotes lipolysis and ketone production, leading to acid-base imbalance and systemic effects.

Polyuria, polydipsia, and weight loss with nausea or abdominal pain. Severe hyperglycemia induces osmotic diuresis and dehydration, while ketoacidosis contributes to gastrointestinal symptoms.

Elevated left atrial pressure causing increased pulmonary capillary hydrostatic pressure. Left ventricular dysfunction backs up pressure into pulmonary veins, forcing fluid into alveoli and impairing gas exchange.

Dyspnea, orthopnea, and peripheral edema from fluid retention and congestion. Impaired cardiac output activates compensatory mechanisms like renin-angiotensin system, resulting in sodium and water retention.

HHS has minimal ketones; DKA has significant ketogenesis and acidosis. HHS occurs in type 2 diabetes with residual insulin preventing ketosis, unlike DKA's profound insulinopenia.