8- Physiology V - Potassium

omarys's version from 2017-05-29 01:33

Section 1

Question Answer
Insulin secretion requires calcium influx, and Ca channels open upon ____.depolarization
One way to depolarize a b-cell is thrublocking K channels (achieved by decreasing ADP, which would otherwise open the channel)
What happens when glucose enters a b-cell?Metabolism >> ATP/ADP ratio increases
In PHHI there are increased levels of ____, leading to decreased levels of blood ______.insulin ; sugar (HH = HYPERinsulinemic, hypoglycemia)
Cause of PHHI (why is there persistent insulin secretion)?Because persistent depolarization, because K channel is inhibited due to mutation
What protein becomes highly active as a RESPONSE TO acidosis?The K/H exchanger (to take up those H's from plasma)
High potassium citrate (as in vegetables/fruit) is converted in the body intobicarbonate (so said diet lowers acidity)
potassium citrate is analkaline salt (used to tx urinary calculi, regulates acidity)
Normal [K]in120-140 mmol/L
[K]out is approx.4-5.5 mmol/L (so even small changes in this can be dramatic- that's why K imbalances are dangerous)
The K/H exchanger is notelectrogenic

Section 2

Question Answer
Immediate K regulation is thru ___ ____ and late regulation is by _____ _____.cell influx/efflux ; renal secretion
Na/K ATPase activity is increased by (3)insulin, b-adrenergic activity, hyperkalemia
Causes of hyperkalemia (3)Crush injury, acidosis (only if anion can't enter cell w/ proton, e.g. in HCl), solvent drag (e.g. when mannitol causes water efflux by osmosis and the water drags K's w/ it)
Acidosis will only trigger hyperkalemia (thru K/H exchanger) if the anion part of the acid can't enter cell (lactic acidosis and ketoacidosis DON'T cause hyperkalemia)
K ions can mediate _______ _______ in _____ cells, so hypokalemia could cause _______.local vasodilation ; muscle ; rhabdomyolysis
Hypokalemia (<_________ mmol/L) causes _____ _____ (due to increased ______)4 ;
Although hypokalemia causes _______ of the membrane potential, it's actually associated with _______ excitability of the cell.hyperpolarization ; increased
depolarized resting potential, but decreased excitability occurs inHYPERkalemia
Hypokalemia & ECG (3)long QT, flat T waves, U waves
HYPERkalemia & ECG (3)short QT, tall/peaked T waves, long PR
Due to the hyperexcitability in hypokalemia, there are ____ ____ which then _____ further muscle contraction and lead to ____ ______. longer ERP's ; prevent/delay ; muscle weakness (e.g. Ogilvie synd./pseudo-obstruction of GIT)
The muscle weakness in hyperkalemia is due to ______ _______.decreased excitability

Section 3

Question Answer
Normal ECF averages ____ L17 (in which there are around 70 mmol of K = [K]out of 4 mmol/L)
How does bicarbonate help lower extracellular K?It attracts H, which effluxes from the cell via K/H exchanger = K enters cell
It's preferable to normalize extracellular K viadiet (e.g. glucose to trigger insulin > induction of Na/K ATPase)
Insulin is extremely _____ for normalizing hyperkalemiaimportant (think glucose level importance)
Amount of K in urine is determined by amount of K _____ in the _____ ____secreted ; (cortical) collecting duct
T or F- K is secreted actively thru pumps found in the principal cells of the CCD.False. It passively flows down its concentration gradient, from the inside of the P cell to either the interstitium or lumen. Channels are required for said flow.
Aldosterone increases K secretion by _____ ______.multiple mechanisms (affects ENaC, Na/K ATPase, luminal K channels)
T or F- K secretion from the CCD is mediated by chemical gradient only.False. There's also the electrical gradient: when Na's enter the P cell via ENaC the lumen is more negative >> K+ more likely to flow out towards lumen
The higher the distal sodium delivery (to lumen of CCD)-the more effective K secretion becomes
Who secretes H into the lumen/urine?Intercalated cells

Section 4

Question Answer
"P cell ; K secretion ; CCD" is analogous to"intercalated cell ; K absorption ; MEDULLARY CD"
K absorption in the CCD is ____ ____ lumen ____.dependent on ; acidity
The K/H ATPase is found on the _____ surface of _____ cells and is responsible for exchanging K (_____ into ___) for H, which is ____ to the ____.luminal ; intercalated ; absorbed ; cell ; secreted ; urine
In dRTA there is impaired ____ secretion (defect in _________), which might lead to _____.H ; K/H ATPase ; hypokalemia

Section 5

Question Answer
Aldosterone release from adrenal is triggered bylow ECV (>> low Cl delivered to MD >> renin secretion from JG cells >> rest of cascade)
Can there be a trigger to aldosterone in HYPERvolemia?Yes- the trigger depends on renal perfusion specifically (= ECV in the AA) rather than the entire volemic state; e.g. in CHF there'll be hypervolemia (edema etc.) but low ECV >>> aldosterone release
Aldosterone release in euovolemic state?Very possible, if e.g. renal artery stenosis. It all depends on the ECV the AA feels.
Other than low ECV/RAAS activation, _______ may trigger aldosterone release.hyperkalemia
ROMKJust that luminal K channel in P cells. Inhibited by Mg, so hypomagnesemia = overly active ROMK = possible hypok.
What other molecule creates the effect of negativelumenpullingKtowardsit?bicarbonate (i.e. alkaline lumen facilitates K secretion)
I'm so fucking sick and tired ofthe photoshop
Increased distal delivery of Na to lumen of CCD (to help K secretion) needsless Na absorption proximally
Distal flow rate (=more washout of K), which helps K secretion cuz maintenance of chemical gradient for K to efflux, is achieved by (3)acidosis, diuretics, volume expansion

Section 6

Question Answer
Hypervolemia / ^^^ ECF volume _______ ______ ______ but ______ _______ release, so the total effect on ____ _____ is negligible (balance mechanism).increases distal delivery (by ^^ GFR and vv sodium reabs. in PCT) ; decreases aldosterone ; K secretion
Primary HYPERaldosteronism raises both aldosterone levels and _____ _____ (by causing hypervolemia), so its effect is ______.hypokalemia
Hypoaldosteronism causes hyperkalemia by 2 mechanisms:1- it causes hypovolemia (>> low GFR + higher Na abs. in PCT >> low distal delivery) and 2- not enough ENaC
HF patient will have ____ aldosterone lvls and ____ distal delivery.increased (in response to low ECV) ; decreased
HF patients ON FUSID will have _____ aldosterone lvls still, but their distal delivery will actually be ______ since the drug prevents _____ _____ and keeps more of it in the ____.high ; high ; Na abs. (in TAL) ; lumen
HF patients on furosemide are at increased risk ofhypokalemia
Acidosis and hypokalemia go hand in hand indRTA

Section 7: Gettin real tired

Question Answer
muscle cramps and fasciculations characterizehypokalemia
5 broad categories for hypokalemiaRenal losses, GIT losses, skin losses, intracellular shifts, drugs
Renal losses of potassium includeHyperaldosteronism, Liddle synd. (excess ENaC), Bartter and Gitelman synd.'s (damage to K abs.), renal tubular disease (damaged abs.)
4 categories of drugs and their mechanism of causing hypok.Thiazide, loop diuretics, osmotic diuretics (all damage K abs.), penicillin (damages secretion by making lumen negative)
In intracellular shifts of K, the reasons could beinsulin overdose, excess catecholamines (stimulation of Na/K ATPase), alkalosis (H out, K in; trivial effect), barium toxicity (no K efflux from cells), anabolic states, hypokalemic periodic paralysis
Trigger of hypokalemic periodic paralysis?high-carbohydrate meals, strenuous exercise (insulin & epinephrine effect)
States where there's suddenly increased anabolism (that cause K intracellular shift)Tx of pernicious anemia, TPN, leukemias and lymphomas that grow rapidly
HPP has two formsautosomal dominant (manifests early, mutation in Ca channels) and thyrotoxicosis (manifests later, in Asians)
How is K lost in vomiting?Thru the KIDNEYS (not w/ the vomit)
Most common cause of extrarenal K loss?Diarrhea
Dx of renal K loss?[K] in urine is > 20 mEq/DAY plus no history of diarrhea (in extrarenal K loss urinary [K] is less than 20 mEq/day)

Section 7.5: Hypok. kont.

Question Answer
Pseudohypok. occurs inacute myeloid leukemia - crazy WBC's continue to be active in sample so they take up K. No real hypok. here.
Vomiting causes (relative) bicarbonate lvls to rise in serum (later in urine) as well as fluid loss, which means1- more K secretion (bicarbonate pulls + K's to lumen) and 2- more K secretion due to aldos. effect on ENaC and ROMK and shit. FUCK the kidneys, just fucking fuck them.
Hypovolemia and alkalosis (bicarbonate in urine) together, as occurs in vomiting, are characterized byHIGH distal sodium delivery - cuz the bicarbonate hinders sodium abs. in the PCT (which is what normally occurs in hypovolemia alone = low distal delivery) + aldos. as per usual
In vomiting, where there's hypovolemia AND alkalosis, the high levels of bicarbonate in urine areneutralized by high Na in lumen (= distal delivery in alkalosis is high, despite hypovolemia)

Section 7.75: Renal losses of K

Question Answer
3 categories/causes of renal lossPr. hyperreninism ; pr. hyperaldosteronism ; pr. increase in non-aldos. mineralocorticoids
causes of pr. hyperreninism (3 + physiologic increase due to hypovolemia)renal artery stenosis (worse hypokalemia if unilateral cuz healthy kidney would secrete K BOTH due to aldos. AND due to HIGH distal delivery - since it's not retaining Na, since its ECV isn't low) ; malignant hypertension (higher proportion of hypok. but condition itself is less common than RAS) ; neuroendocrine tumor that secretes renin (rare)
In all cases leading to pr. hyperreninism, the kidneys senselow ECV
In general, renal hpyok. develops (mechanisms?)either by primary increase in aldos./cortisol or thru a primary increase in distal delivery of Na (worse hypok. if both)
The renin increase in pr. hyperreninism isnot due to hypovolemia
causes of pr. hyperaldosteronism (relatively low renin)Conn's (adenoma that secretes aldos.) ; bilateral adrenal cortical hyperp. ; glucocorticoid-suppressible hyperaldos. (AD where gene for aldos. synthase is regulated by promotor for ACTH - tx is steroids)
Differentiate bwn different causes of pr. hyperaldos. byCT (then aldos. levels test)
causes of pr. non-aldos. mineralocorticoid increaseCAH (11-b hydrox. def. = virilism ; 17-a hydrox. def. = decreased sex hormones) ; Cushing's (can't turn all that cortisol to cortisone) ; "syndrome of apparent mineralocorticoid excess" (liquorice thing; suppression of 11-b-OH dehyd.)
Liddle's synd.too much ENaC - besides hypok. there will also be Na retention and high BP
Tx of hypok. is usuallyPO - KCl or just K in diet
Tx of hypok in life-threatening situations isIV KCl admin. (but careful not to give too much/not to give w/ sugar in anorexics/not to put Na in saline if patient has pr. hyperaldos.)


Sniff, bark, bork. Brork. Borf, heck. BJORK

Section 8: Hyperkillmea

Question Answer
CLL isChronic lymphocytic leukemia
Pseudohyperk. occurs due to what conditions that affect the cells in the blood sample?hemolysis ; clot formation ; CLL (if a lot of time has passed; early on it's more likely there'll be pseudoHYPOk.)
What may cause extracellular shifts of K?B-blockers ; insulin def. (esp. after meal) ; METABOLIC (not lactic or keto-) acidosis ; anything that causes cell destruction/rupture e.g. catabolism generally or rhabdomyolysis
What renal/adrenal pathologies can cause hyperk.?Addison's (vvv aldos.) ; CRD (cuz low GFR and no filtration of K in the 1st place) and dialyzed patients
Recall that K secretion is a side-kick of the body's mechanism of raising BP (in response to low ECV). Naturally, then, preventing this mechanism of raising BP (e.g. hindering the ____) will also prevent K secretion, leading to hyperk.RAAS (i.e. antihypertensives might cause hyperk.)
Drugs that interfere w/ RAAS (diuretics/tx of hypertension)ACEi ; ARB ; spironolactone (anti-MR) ; B-blockers, NSAIDs & aliskerin (renin inhibitors)
Other than drugs that interfere w/ RAAS, what drugs might cause hyperk.?Blockers of ENaC: amiloride, triamterene
Use of K-sparing diuretics?Combo w/ loop diuretics- recall how fusid blocks NKCC = no K abs. (can cause hypok.). Use of of K-sparing d's (like triamterene) prevents K secretion, balancing the hindered abs. of loop diuretics.
Drugs possibly causing hyperk. that don't specifically target kidneys?Digoxin (blocks Na/K ATPase)
Hyperk. on ECG manifests asFlattened P's, very tall peaked T's, ST depression (latter two plus the QRS complex create a sine wave look)
Hyperk. effect on musclesflaccid paralysis/muscle weakness

Section 9: Tx of hyperk.

Question Answer
3 phases of tx in decreasing order of urgencyprevent lethal CV events (still no rectification of K levels at this point) >>> induce intracellular shift >>> induce K excretion in urine or thru GIT
To prevent arrhythmias/stabilize membrane potentials, givecalcium carbonate/gluconate
To cause an intracellular shift, giveinsulin (w/ glucose to prevent hypoglycemia) ; albuterol (b-agonist)
To promote K excretion in urine, giveloop diuretics (w/ saline to prevent volume depletion)
To promote K excretion in feces, giveK-exalate (inhibits K abs. in GIT)
If all tx are contraindicated, tx hyperk. bydialysis

Section 10: Ricksty factors

Question Answer
Eating a lot of glucosehypok.
Acute MI patient in ERhypok. (b-adrenergic activation bc of stress and things; myocyte death not enough to cause hyperk.)
Diabetic patient who forgot to take insulinhyperk. and by 2 mechanisms: solvent drag (high sugar levels cause water efflux and w/ it come the K's) + no insulin = less b-adrenergic activ.
Mannitol (hyperosmotic) admin.hyperk. (solvent drag)
Acidosis (not organic)hyperk.
B12 tx for anemic patienthypok. (sudden & significant anabolic state)
Digoxin admin.hyperk.
Penicillin admin.hypok. (negative lumen)
Pr. hyperaldos.hypok.
Furosemide admin.hypok. (loss of K in urine due to NKCC block; cuz no abs. in LOH, cuz ^^^ secretion in CCD due to ^^^ distal delivery of Na, and cuz loss of Na induces hypov. which induces aldos. which promotes even more K secretion. Bjork.)
Thiazide admin.hypok. (block of NaCl in CCD >> loss of Na and hypovolemia >> aldos.)
Aldactone admin.hyperk. (anti-MR)
Metabolic alkalosishypok. (cuz bicarbonate in urine and -ive lumen >> K secretion)(effect of bicarbonate on cell shift is minor but it does induce K influx as it pulls out those H's)
Normal saline infusion (0.9%)hypok. (more fluid to be excreted/a mini volume expansion >> less Na abs. & more distal delivery >> more K secretion)(occurs only in susceptible patients)

Section 11: urine electrolytes

Question Answer
Vomitinghigh [K], high [HCO3], low [Cl], HIGH [Na] (the latter- despite hypovolemia)