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This deck focuses on Signs Symptoms And Pathophysiology, giving you a quick way to review the definitions, rules, and examples that matter most for NAPLEX.
Study Signs Symptoms And Pathophysiology in NAPLEX with focused flashcards that help you recognize the idea, recall the key rule, and apply it in practice-style prompts.
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What is the key pathophysiologic difference between DKA and hyperosmolar hyperglycemic state (HHS)?
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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.
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This deck focuses on Signs Symptoms And Pathophysiology, giving you a quick way to review the definitions, rules, and examples that matter most for NAPLEX.
Work through these flashcards in short sessions. Try to answer each prompt before flipping the card, then revisit any cards you miss until the explanation feels automatic.
Answer: 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.
Answer: 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.
Answer: Sudden focal neurologic deficit that fully resolves, typically within 24 hours. Transient ischemia causes temporary dysfunction without infarction, resolving as perfusion is restored.
Answer: Polyuria, polydipsia, and weight loss with nausea or abdominal pain. Severe hyperglycemia induces osmotic diuresis and dehydration, while ketoacidosis contributes to gastrointestinal symptoms.
Answer: 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.
Answer: COX inhibition lowers prostaglandins, reducing mucosal protection and bicarbonate. Prostaglandins maintain gastric mucosa; their depletion by NSAIDs increases susceptibility to acid-induced injury.
Answer: 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.
Answer: 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.
Answer: Reduced hemoglobin lowers oxygen delivery, causing fatigue and exertional dyspnea. Insufficient iron impairs erythropoiesis, reducing oxygen-carrying capacity and triggering compensatory mechanisms.
Answer: 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.
Answer: Fever with severe headache and neck stiffness, often with photophobia. Meningeal irritation from infection causes inflammation, leading to classic signs of meningeal involvement.
Answer: 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.
Answer: Heartburn and regurgitation worse after meals or when supine. Lower esophageal sphincter incompetence allows acid reflux, exacerbated by gravity and increased intra-abdominal pressure.
Answer: Diaphoresis, tremor, palpitations, hunger, and confusion. Low blood glucose triggers sympathetic activation and neuroglycopenic effects, manifesting as autonomic and cognitive symptoms.
Answer: 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.
Answer: 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.
Answer: Cerebral artery occlusion causing focal brain ischemia and infarction. Thrombus or embolus interrupts blood supply, resulting in neuronal death in the affected vascular territory.
Answer: Dysregulated inflammatory response causing vasodilation, capillary leak, and hypoperfusion. Infection triggers cytokine storm, leading to endothelial dysfunction and distributive shock with multiorgan failure.
Answer: 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.
Answer: 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.
Answer: Acute fever, productive cough, pleuritic chest pain, and focal crackles. Bacterial infection leads to alveolar consolidation, inflammation, and systemic response, differentiating from viral causes.
Answer: 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.
Answer: Atherosclerotic plaque rupture with thrombus causing acute coronary occlusion. Unstable plaque leads to thrombus formation, abruptly blocking coronary flow and causing myocardial necrosis.
Answer: 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.
Answer: Reversible airway inflammation with bronchoconstriction and mucus hypersecretion. Allergic triggers induce immune-mediated responses that are reversible with bronchodilators, unlike chronic conditions.