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A set of QA-style flashcards covering body fluid compartments, sources and losses of water, regulation mechanisms (thirst, ADH, aldosterone, RAS, SNS), capillary dynamics, and related pathophysiology (DI, SIADH, Addison's, Conn's).
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What are the two main body fluid compartments?
Intracellular and extracellular.
What makes up the extracellular fluid?
Interstitial fluid and plasma (intravascular fluid).
Approximately what percent of total water intake comes from drinking water?
About 60% (roughly 1,400–1,800 mL).
Approximately what percent of water intake comes from food?
About 30% (roughly 700–1,000 mL).
Approximately what percent of water intake comes from oxidation (metabolic water)?
About 10% (the water produced during metabolism).
What is the typical total daily water intake range given in the notes?
Approximately 2,400–3,200 mL.
What is the major route of water output?
Urine (about 60%).
What are other routes of water loss besides urine?
Lungs (respiratory water loss) and skin (sweat), plus stool.
What happens if water intake exceeds output over time?
Fluid overload with potential edema and rising blood pressure.
In fluid regulation, what unit is used for electrolytes and what does concentration refer to?
Milliequivalents per liter (mEq/L); concentration refers to amount per liter (not total quantity).
Name the four mechanisms by which the body maintains fluid regulation.
Thirst, aldosterone, sympathetic nervous system, and antidiuretic hormone (ADH).
What triggers thirst physiologically?
Dehydration causes concentrated blood; osmoreceptors in the hypothalamus trigger thirst.
Which gland produces aldosterone?
Adrenal cortex.
What is the primary effect of aldosterone on the kidneys?
Increases sodium (Na+) reabsorption and water retention; causes loss of potassium (K+) and hydrogen ions (H+).
How does aldosterone affect acid-base balance?
Loss of hydrogen ions (and potassium) can contribute to metabolic alkalosis. Alkalosis can occur with aldosterone activity.
Which organ produces renin in the renin-angiotensin mechanism?
The kidneys (juxtaglomerular cells) release renin.
Which organ produces angiotensinogen?
Liver.
Where does angiotensin-converting enzyme (ACE) convert angiotensin I to II?
Lungs.
What are the main actions of angiotensin II (Ang II)?
Vasoconstriction and stimulation of aldosterone release, increasing blood pressure and blood volume.
What are common adverse effects to monitor with ACE inhibitors?
Hyperkalemia and hyponatremia; potential hypotension.
What is Addison's disease?
Adrenal insufficiency with low aldosterone; hyponatremia, hyperkalemia, hypotension, weight loss.
What is Conn's (primary hyperaldosteronism) syndrome?
Excess aldosterone causing sodium retention, potassium loss, hypertension, edema.
What happens to capillary hydrostatic pressure and water movement in edema formation?
High capillary hydrostatic pressure promotes filtration (water leaving capillaries); edema can result from increased filtration, especially with venous obstruction.
What is nephrotic syndrome and its effect on oncotic pressure?
Loss of protein in urine (hypoalbuminemia) lowers oncotic pressure, leading to edema and ascites.
What is diabetes insipidus (DI)?
Lack of ADH or renal insensitivity to ADH; polyuria and polydipsia with risk of dehydration.
What is SIADH?
Syndrome of inappropriate ADH; excessive ADH leading to water retention and hyponatremia.
What is the role of ADH in fluid balance?
Antidiuretic hormone promotes renal reabsorption of water; produced by the posterior pituitary and released in dehydration to conserve water.
What condition involves low aldosterone leading to hyponatremia and hyperkalemia?
Addison's disease.