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40 Cards in this Set

  • Front
  • Back
Rapidly raising K+ causes
1) intitially
2) eventually
1) increased myocyte, endocrine cell, and neuron excitability/depolarization
2) blocking of upstroke of action potential
1) How can intense neuromuscular activity cause hyperkalemia
2) How is this defended against by the existence a specific cell type?
3)How do highly active cells protect themselves from this danger? How can this backfire if the mechanism is overused?
1) repolarization causes intense K+ efflux from cells into the surrounding ECF. This accumulated rapidly enought to block excitability if not taken up soon
2) Glia cells mop up extra ECF K+
3) promote local vasodilation to wash out locally released K+. This however can then cause a systemic problem.
What normal daily activity can cause hyperkalemia?
eating meat! K+ must be rapidly excreted or sequetered into intracellular stores.
1) Which organ is in most imminent danger of hypokalemia?
2) electrophysiologically, what gets changed in the heart in the face of MODERATE (4.5-6.5) hyperkalemia?
3) How does this effect electrical activity in the heart?
4) how is this seen on the EKG?
5) what happens to the heart in the fact of grve hyperkaleima (> 7.5)?
6) how will this manifest on the EKG?
1) heart
2) increase the conductance of both inward rectifyer and delayed rectifyer K+ channels
3) Hastens repolarization
4) Peaked T waves
5)severely depolarizes myocardial membranes, inactivates voltage dependant Na+ currents
6) Flattened (lost) P-wave, widened R wave (slower ventriculr contracton) along with peaked T-waves give a SINE wave apearance.
1) Hyperkalemia has what effect on myocardial conduction of an impulse
2) What cardiac problems can this cause
1) slows it downand may cause AV dissociation
2) decreased CO, arrhythmias, Vfib
Depletion of what cation can dispose to SIne wave pattern of EKG
Mg++ (they also said K+ depletion can cause it, but this doesnt make sense.)
1-2) upon ingestion K+ deposition into cellular stores is dependent upon ___1_____ and ___2___ via __3__
4)-5 eventual release of K+ into urine is dependant upon what____4__and ___5___?
3) Na/K ATPAses
4) Aldo
5) catechoamines
3 routes of removal of K+
Name the two steps of extra-renal K+ buffering
1) tissue uptake of K+ load into depot intracellular stores via the Na/K ATPase dependant upon insulin and catecholamines
2) Slow release of K+ through K+ channels also modulated by catecholamines and aldosterone
Name the two major tissue depots of K+
muscle and liver
3 things that can decrease the rate of K+ buffering
insulin deficiency
catecholamine deficiency
Na/K+ ATPAse blockade by cardiac glycoside
These three things/conditions can cause reduce K+ buffering
1) openers of K+ selective channels
2) Serum hypertonicity (draws K+ out)
3) Cell acidification
1)What two min parts of the nephron reabsorb K+?
2)What part secretes K+
1) PCT (70%) and Ascending loop
2) Principle cells of C and MCD
1) How is aldosterone produced in response to increased K+
2) How does Aldo cause increased K+ secretion
3) how does increased fluid flow past the principle cell of the C and MCD cause K+ secretion.
Increased K+ depolarizes aldo secreting cells which activates T-type Ca++ channels (similar to SA node). This allows Ca+ entry which signals aldo production.
2)Aldo diffuses to the C and MCD principle cells where is causes activity if basolateral Na/K ATPase and lumenal ENaC channels. This activation allows Na+ entry into the cell from the lumen, depolarizing the membrane. As usual, depolarization leads to eit of K+ through K+ channels (in this case ROMK1) in to the lumen.
3)Deformation of an apical cilium activates apical non-elective cation channel which allows allow Ca++ influx. This causes activation of apical K+ channel allowing K+ to be secreted.
1) deficiency of what hormone can impair K+ secretion?
2) what 2 drug classes produce a state vary much like this deficiency?
3) How?
1) aldosterone
2) NSAIDs and ACE-inhibitors
3) NSAIDS block prostglandin secretion and reduce renin
ACE-Inhibitors block AII generation
what anticoagulant can block AII secretion and hence cause K+ retention?
Defects in the rate of fluid and NA+ presentation to C and MCD OR injury to the C and MCD can cause?
How can TALH actin diuretics cause K+ wasting?
Promote Na+ presentation to the C and MCD, so much is absorbed there, causing massive depolarization and K+ release.
Causes of Hyperkalemia:
Decreased cellupar uptake of K+ can be caused by? (7)
metabolic acidosis
insulin deficiency, hyperglycemia
Tissue breakdown/hemolysis
severe muscle contraction
Digitalis overdose
Hyperkalemia can be caused by overdose of what common cardiac drug?
If a patients lab values suggest sever hyperkalemia, but looks fine, what should you suspect?
(release of K+ from RBCs in test tube)
4 ways to get hyperkaleima involving reduced urinary excretion
Decreased GFR
Decreased distal presentation of salt (to principle cell of C and MCD)
Decreased effective IVV
how do we prevent the lethal effect of hyperkalemia on the heart? how does it work?
Ca++ infusion tricks the heart into thinking it is less depolarized than it is. (more negative nernst potential)
1) in treating pure hyperkalemia, we want to lower ECF by stimulating what pump?
2) we do this with what two drugs?
3) if major systemic acidosis was promoting hyperkalemia, how would we treat?
1) Na/K ATPase
2) insulin and B2 agonist
We can do three things to remove K+ from the body. One is diuresis, and one is dialysis, what is the third and what two drugs to we use to do it?
Induce gut clearance of K+ with sorbitol (osmotic diarrhea) or Kaexylate, an Na+/K+ exchange resin
How fast is it safe to reduce K+ with dialysis
1.5 meq/L/hr
1)How do we treat CHRONIC hyperkalemia
2) avoid (drug)
3-4) give fludcortisone which is a ___3___ or kaexylate which is a ____4___
1) K+ restriction (<60meq/day).
3) fludcortisone- a long acting mineraocorticoid
4) Na+/K+ exchange resin
Chronic Hypoklemia can be cause by:
1) GI
2) kidney
3) drug side effect
4) skin
1) prolonged vomiting or diarrhea
2) chronic diuretic administration, primary mineralocorticoid excess (causing Na+ retention and hence K+ secretion)
3) Polyene antifungals which create a cation selective channel in apical membrane of tubule cells
4) sweatin
Acute hypokalemia can be caused by:
1) endocrine
2) Adrenergic
3) Hematological
1) increased insulin allowing cellular uptake by stimulating Na/K ATPAse
2) Increased B-adrenergic activity (stress, drugs, asthma treatment)
3) treatment of anemia
Hypokalemia reflects the depletion of ___cellular stores
hypokalemia can cause Enymes to work sum-optimally. what sort of problems an this cause?
muscle weakness (glygoenolysis and glycolysis enzymes)
acid-base disturbanes (ammoniagenesis)
Imparied urinary concentration (relates to impaired ADH induction of cAMP)
why is K+ repletion often not good enough in hypokaleima
it is often caused by inability to conserve K+, so administered dose will just be lost in urine or feces.
1) EKG appearance of Hypokalemia, one new wave, and one modification of an old wave.
2) where does the "new" wave it appear?
3) What is the cause of the old wave modification.
4) What causes the new wave to develop?
1) U wave and flattened T-wave
2) on the end of T
3) Slower repolarization by the delayed rectifier K+ current
4) slowing aaction of Na/K ATPAse causes rise in intracellular Na+. This then reverses the Ca/Na exchanger which is usually used to couple uphill Ca++ exit to downhill Na+ entry. This now allows Ca++ in and puts Na+ out. Ca++ entry causes an after-depolarization sen as the U-wave.
hypokalemia can be life threatening only when an acute drop in K+ occurs on the background ......? (two possible)
1) already reduced bodily total K+ or 2) significant pharmacological blockade of Na+/K+ ATPAse (cardiac glycosides)
Chronic hypokalemia can produce positive feedback making itself worse in 2 ways...
1) in an effort to maintain ECF K+ it lowers insulin and epineprine which sequester K+ intracellularly. This depletes K+ stores even more by leaving K+ in ECF where it can be lost.
2) K+ depleted tubular cells cannot fine tune their reabsorption to conserve K+
Chronic Hypokalemia Renal effects
1) renal tubular injury causing...
2) reduces activation of adenylate cyclase by ADH at the C and MCD causin.....
3) Cause activation of PCT glutamine deaminase causing....
1) increased Na+ presentation to macula densa--> Tubulo-glomerular feedback--> decrease GFR
2)concentrating defect and polyuria
3) ammoniagenesis
Hypokalemia can cause activation of glutamine deaminase in the PCT increasing ammoniagenesis and hence serum NH4. This is a particularly bad thing in the case of ___1___ hwere NH$ is already increased, and can cause___2___.
1. Liver Failure
2) metabolic encephalopathy
K+ repletion of a hypokalemic patient will not work if __1__ is not repleted as well becuse K+ cannot be taken up byt the Na/K ATPase in the absence of _____2_____
1) Mg++
2) Mg-ATP
1) how does the kidney repspond t prolonged hypokalemia?
2) what side effect does this cause?
1) Type A interalated cells express H+/K+ ATPase which pumps out acid and reclaims K+? Also these cells are increased in number.
2) mild alkalosis
Why are C and MCD intercalated cells low in intracellular K+
Low K+ due to apical K+ channel and low levels of basolateral Na+/K+ ATPase