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Diuretics increase urinary sodium loss and can raise FeNa even when kidney perfusion is low. Interpret the result alongside medications, kidney function, urine sediment and volume status.

Both support DNA synthesis and can cause megaloblastic anemia. B12 deficiency can also affect the nervous system, even without anemia. Folate alone does not correct that neurological injury.

In iron deficiency, the stores are depleted. In inflammation, iron is retained and less available. Ferritin can rise with inflammation and mask coexisting iron deficiency.

Transaminases signal cell injury, rather than measuring liver capacity on their own. Albumin and INR help assess synthesis, but nutrition, losses, vitamin K and medications also influence them.

Sodium is a concentration: it can be low because there is relatively too much water. Assess tonicity first; urine osmolality, urine sodium, medications and volume status help explain the mechanism.

Colonization means microorganisms are present without infectious disease at that site. A positive culture alone does not prove infection or determine treatment: symptoms, signs and clinical context matter.

ACE inhibitors reduce the conversion of angiotensin I to angiotensin II and reduce bradykinin breakdown. ARBs block angiotensin II at the AT1 receptor. Think conversion checkpoint versus receptor checkpoint—not two identical mechanisms.

Insulin stimulates potassium movement into cells. This lowers its concentration in blood without removing it from the body. The effect is temporary: potassium can rebound, and blood glucose needs monitoring. The doorway is a metaphor, not a literal insulin-operated potassium channel.