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Too much ADH (SIADH) effect or too little (DI)? Antidiuretic hormone (ADH, aka. vasopressin) = peptide hormone produced by hypothalamus and stored and secreted by posterior pituitary gland; NL ADH Function: Reduce (anti) urine output (diuresis); Path = DI & SIADH

Aortic stenosis - s/s triad = exertional dyspnea, angina, & syncope (especially in elderly patients); Stenotic aortic valve = fixed cardiac output (no increase during exertion --> syncope + dyspnea; Murmur: crescendo-decrescendo systolic, best at right USB plus carotid radiation

Clinical Thinking - The broad categories of "causes" for all allopathic disease presentations (Modified from VINDICATE) --> VITAMINS ABCDEK

Onset, peak and duration of different insulin preparations

Where do diuretics work in the kidney mechanism? 4 areas in the cortex (proximal convoluted, ascending loop, distal convoluted and proximal collecting) and 2 areas in the medulla (distal collecting tubule & Loop of Henle)

Thyroid hormone (T3/T4) affects multiple systems

Small, Medium, Large and Variable vessel Vasculitis

List the salient features of the major Leukemias: ALL, AML, CLL and CML

Unruptured intracranial aneurysms - s/s asymptomatic, often diagnosed incidentally; If symptomatic (compression or thromboembolism): cranial nerve palsies, seizures, facial pain, hemiparesis, ischemia, visual disturbances;  90% saccular at arterial bifurcations

Is a Patent Foramen Ovale the same as an Atrial Septal Defect? No, a patent foramen ovale (PFO) is NOT considered a true atrial septal defect

Immunoglobulin A deficiency = serum IgA level <7 mg/dL in individuals > 4 y/o, w/ NL serum IgG and IgM; s/s: recurrent resp or GI infections, allergic disorders, autoimmune dzs; Path: Defect in differentiation of B lymphocytes into IgA-secreting plasma cells

Diminished left atrial appendage (LAA) velocities = <40 cm/s, reduced blood flow speeds within left atrial appendage, typically detected during transesophageal echocardiography (TEE) --> indicates blood stasis & increased risk of thrombus formation; Dx: Atrial fib (MC)

Secondary hypertension (HTN) = ↑BP (≥130/80 mmHg) caused by an identifiable underlying condition, as opposed to primary (essential) HTN, which has no single clear cause. Causes of Secondary HTN (Renal overall MC):

Pneumonia - classified as "typical" or "atypical based" on causative pathogens, clinical presentation, and lab/imaging findings.

Somatic symptom disorder - excessive thoughts, focus, feelings, behaviors related to somatic s/s; History vague, highly sensitive to meds, seek care from multiple providers. Symptoms > 6 mos. 1 or more somatic s/s are distressing w/ persistent thoughts, anxiety, time devoted

Defining hypertension

What's the difference? HYPERTENSIVE EMERGENCY vs URGENCY - The CRITICAL Distinction: It's NOT about the blood pressure number --> it's about END-ORGAN DAMAGE / "E = Emergency = End organ damage"

"Red flag" evidence of end organ damage in hypertensive emergency:

Candidal Esophagitis: opportunistic C. albicans (MC) infection; s/s: mucosal inflammation, ulceration, white plaques, odynophagia, dysphagia, retrosternal discomfort, low-grade fever; Risk: CD4 <200 (AIDS-defining illness), DM, chemo, steroids, transplant, PPIs, chronic antibx

After bilirubin is conjugated in the liver, how is it eliminated from the body?