N620 Na, Cl, K Kidney
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1. How many mgs of Na, K, and Cl are needed/day?
2. What are they important for? (4)
3. How is NaCl used in foods? (5)
4. Where are these electrolytes absorbed?
- 1. >100 mgs
- 2. Maintaining membrane potential, regulating fluid balance, transmitting nerve impulses, and maintaining acid/base balance
- 3. Enhance flavor, cut costs, prevent it from going bad, hide bitterness, food safety, increasing consumer acceptance
- 4. ileum and large intestine
1. What is major determinant of resting membrane potential?
2. What is the above crucial for? (3)
3. What is the most common electrolyte abnormality?
- 1. K+
- 2. Cell growth, cell division, and excitability of nerves
- 3. K+
1. How are electrolytes generally lost? (3)
2. What is bioavailability of K+?
3. Is toxicity from K+ possible?
4. What causes deficiencies of electrolytes? (4)
5. What causes excess of electrolytes? (4)
6. Risk factors for hyperkalemia? 2
- 1. Poop, pee, sweat
- 2. ~90%
- 3. Yes, from supplements
- 4. Poor intake, increased urinary excretion, increased GI losses and increased sweating.
- 5. Excessive intake, decreased urinary excretion, decreased GI losses, decreased sweating.
- 6. Chronic renal insufficiency or diabetes
1. What causes hyponatremia?: What happens to salt (4) and water (5) to cause it?
3. Is there toxicity of Na+?
4. Who is more at risk for high salt? Why? (4)
5. What is the Na:K ratio important for?
1. Excess excretion of salt - poor sodium intake, increased urinary excretion, increased GI loss, sweating.
Water: excessive intake, high oxidative phosphorylation, decreased urinary output, decreased GI loss, decreased sweating.
- 3. No
- 4. African Americans - more salt-sensitive, obesity, diabetes, higher K+ intake?
- 5. Hypertension - increased Na+ --> increased blood pressure.
1. What are functions of water? (4)
2. Describe pathway of filtrate (5)
1. Fluid homeostasis, transport, removal, excretion
Glomerulus --> Bowman's Capsule --> PCT --> Loop of Henle --> (descending, ascending) --> DCT ---> collecting duct.
1. What happens in glomerulus? (4) - where does it receive blood from? Where does it go?
What is special about this?
What stays in capillaries and what does this create?
- 1. Receives blood from afferent arteriole and drains into efferent arteriole
- 2. High pressure - ultafiltration forces fluids and soluble materials (especially excess salts and urea) out of capillaries into Bowman's capsule
- 3. Large proteins --> hypertonic soln
1. Bowman's capsule --> PCT. What is reabsorbed here? (3)
2, What happens in descending limb of Loop of Henle?
3. Hairpin loop?
4. Ascending thin loop?
5. Ascending thick loop?
1. Na --> osmotic gradient water, and Ca2+ (PTH) using active pumps on basolateral membrane of epithelial
- 2. Reabsorption of water
- 3. Isotonic
- 4. Passive diffusion (resorption) of Na, Cl, impermeable to H2O
- 5. Na and Cl are actively pumped out of filtrate.
These things are all reabsorbed by network of capillaries around Loop of Henle
1. What happens in distal tubule and collecting duct?
2. What controls this?
3. What is a podocyte?
- 1. Electrolytes and water reabsorbed
- 2. Hormone regulation
- 3. Cells in Bowman's capsule that wrap around capillaries of glomerulus
1. What does collecting duct connect? What is it regulated by? (2)
2. What is juxtaglomerular cells?
3. What is ADH?
4. What is aldosterone? 4
5. What is renin?
6. What is ANP?
- 1. Kidney to ureter; ADH and aldosterone
- 2. Kidney cells that create renin
- 3. ADH - increases water resorption from CD and DCT
- 4. Aldosterone -conserves Na, secretes K, increases water retention and increases BP in CD and DCT
- 5. Renin is secreted by juxtaglomerular cells to increase blood pressure by acting on angiotensin
- 6. ANP - atrial natiuretic peptide = acts against RAS system in response to high BP. Reduces H2O and Na+ from plasma.
1. What is measured to determine glomerular filtration rate?
2. What causes secretion fo ADH?
3. What is the rxn to heat and sweating?
4. What happens when blood is lost?
- 1. Creatinine
- 2. Increased osmolarity is sensed in osmoreceptors in hypothalamus that stimulate secretion from ADH producing neurons AND by stretch receptors in heart and large arteries.
- 3. Heat --> Sweat --> water loss --> increased osmolarity --> ADH is released --> water resorbed --> urine is concentrated.
- 4. Huge ADH secretion
1. How does aldosterone compete with cortisol for mineralocorticoid receptor?
2. Functions? (2) Results? (3)
3. What stimulates aldosterone secretion? (3)
4. What is it inhibited by? (3)
1. Aldosterone responsive cells ahve 11BHSD that convert cortisol to cortisone, less binding affinity for receptor, allowing aldosterone to work. (Cortisol >> aldosterone).
2. Increases Na/K ATPase proteins in DCT and CD & stimulates expression of Na+ channel
Results in increased resorption of Na+, increased excretion of K+ and increased water retention.
- 3. Angiotensin II, Low Na+, high K+ (remember ratio's role in hypertension)
- 4. ANP, High Na+, low K+
What causes apparent mineralocorticoid excess? (2)
- 1. Genetic mutation = loss of 11BHSD function
- 2. Licorice consumption
Hypertension, hypokalemia, metabolic alkalosis
1. Describe mechanism of renin (3)
2. Draw progression of rxn
- 1. Renin is released by juxtaglomerular cells of kidney
- 2. Renin cleaves angiotensiongen into angiotensin I (active form)
- 3. Angiotensin converting enzyme (ACE) from lung converts angiotensin I --> angiotensin II.
Renin --> Angiotensinogen --> Angiotensin I --> Angiotensin II
1. What causes release of renin? (3)
2. How does juxtaglomerular cell sense this?
3. What else senses need for renin?
- 1. Low BP, trauma, blood loss
- 2. Decreased perfusion of juxtaglomerular cells
- 3. Stretch receptors in heart and arteries
1. What does angiotensin II do? (3)
Describe low BP all the way to high BP (5)
- 1. Vasoconstrictor - constricts glomerular arterioles, increasing BP and decreasing blood flow
- 2. Increases aldosterone release
- 3. Increases ADH release
Low BP --> renin release --> activation of angiotensin II --> increase in blood volume --> incrase in BP
1. What is ANP system?
2. What does it do specifically in RAS? (3)
3. What stimulates its release? (3)
4. Wht does it do overall?
- 1. Counter-regulatory system to RAS system
- 2. Decreases angiotensin II, ADH activity, and renin release
- 3. Stimulated by atrial distension, angiotensin II, endothelin and sympathetic stimulation (to decrease BP and increase urine output)
1. What occurs in renal failure?
2. Is acute renal failure reversible? Is chronic? Why or why not?
3. Describe prerenal, renal, and postrenal failure
- 1. Uremia - retention of N waste in blood
- 2. Acute is reversible, chronic isn't b/c it usually isnt' discovered until only 25% of kidney function is left
- 3. Pre-renal - problems with blood flow to kidney, renal = problems with kindey, post renal = blockage of urine flow out of kidney
How do you diagnose renal failure? (2)
Treatment of renal failure? (2)
- 1. Glomerular filtration rate (blood sample or 24 hour urine collection) - creatinine
- 2. BUN
Deal with underlying causes - high calorie, low protein, low Na+ and K+ (esp K+) and fluid restrictions
Which organs are responsible for regulating blood pH? What is optimal pH?
2. What is kidney responsible for? (2) What enzyme does it use? (1)
Draw pathway of acid-base homeostasis in kidney
- 1. Lungs & kidney (~7.4)
- 2. Resorption of bicarbonate and secretion of H+
- 1. In tubules, H2O + CO2 --> H2CO3.
- 2. H2CO3 immediately dissociates to yield H+ and HCO3-
- 3. HCO3 - moves across basolateral membrane --> blood
- 4. H+ is secreted into tubular lumen by H+/ATPase or Na+/H+ pump.
- 5. H+ isn't secreted - instead combines with filtered HCO3 - to form H2CO3 --> H2O + CO2 --> tubular cell to start another cycle.
Basically, allows a way to resorb bicarbonate
2. How does pH relate to hyperkalemia?
What happens if all bicarbonate has been reabsorbed?
1. For each 0.1 unit fall in pH, serum K+ increases by 0.7 mmol. For each 0.1 unit rise, K+ drops by 0.3 mmol.
Extra H+ combines in lumen with buffer (HPO42-) leading to addition to plasma of new bicarbonate --> raises bicarbonate concentration of plasma and alkalinizes it.
What happens if you ahve pH above 7.45? Symptoms?
Hypokalemia --> disturbed function of skeletal muscles and smooth muscles
Hypocalcemia --> tetany - intermittent muscular spasms caused by malfunction of PTH and consequent deficiency of calcium.
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