Renal - Dyskalemias

Front 1

Rapidly raising K+ causes
1) intitially
2) eventually

Back 1

1) increased myocyte, endocrine cell, and neuron excitability/depolarization
2) blocking of upstroke of action potential

Front 2

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?

Back 2

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.

Front 3

What normal daily activity can cause hyperkalemia?

Back 3

eating meat! K+ must be rapidly excreted or sequetered into intracellular stores.

Front 4

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?

Back 4

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.

Front 5

1) Hyperkalemia has what effect on myocardial conduction of an impulse
2) What cardiac problems can this cause

Back 5

1) slows it downand may cause AV dissociation
2) decreased CO, arrhythmias, Vfib

Front 6

Depletion of what cation can dispose to SIne wave pattern of EKG

Back 6

Mg++ (they also said K+ depletion can cause it, but this doesnt make sense.)

Front 7

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___?

Back 7

1)insulin
2)catecholamines
3) Na/K ATPAses
4) Aldo
5) catechoamines

Front 8

3 routes of removal of K+

Back 8

urine
sweat
feces

Front 9

Name the two steps of extra-renal K+ buffering

Back 9

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

Front 10

Name the two major tissue depots of K+

Back 10

muscle and liver

Front 11

3 things that can decrease the rate of K+ buffering

Back 11

insulin deficiency
catecholamine deficiency
Na/K+ ATPAse blockade by cardiac glycoside

Front 12

These three things/conditions can cause reduce K+ buffering

Back 12

1) openers of K+ selective channels
2) Serum hypertonicity (draws K+ out)
3) Cell acidification

Front 13

1)What two min parts of the nephron reabsorb K+?
2)What part secretes K+

Back 13

1) PCT (70%) and Ascending loop
2) Principle cells of C and MCD

Front 14

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.

Back 14

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.

Front 15

1) deficiency of what hormone can impair K+ secretion?
2) what 2 drug classes produce a state vary much like this deficiency?
3) How?

Back 15

1) aldosterone
2) NSAIDs and ACE-inhibitors
3) NSAIDS block prostglandin secretion and reduce renin
ACE-Inhibitors block AII generation

Front 16

what anticoagulant can block AII secretion and hence cause K+ retention?

Back 16

heparin

Front 17

Defects in the rate of fluid and NA+ presentation to C and MCD OR injury to the C and MCD can cause?

Back 17

hyperkalemia

Front 18

How can TALH actin diuretics cause K+ wasting?

Back 18

Promote Na+ presentation to the C and MCD, so much is absorbed there, causing massive depolarization and K+ release.

Front 19

Causes of Hyperkalemia:
Decreased cellupar uptake of K+ can be caused by? (7)

Back 19

metabolic acidosis
insulin deficiency, hyperglycemia
B-blockde
Tissue breakdown/hemolysis
severe muscle contraction
Digitalis overdose

Front 20

Hyperkalemia can be caused by overdose of what common cardiac drug?

Back 20

Digitalis

Front 21

If a patients lab values suggest sever hyperkalemia, but looks fine, what should you suspect?

Back 21

Pseudonhyperkalemia
(release of K+ from RBCs in test tube)

Front 22

4 ways to get hyperkaleima involving reduced urinary excretion

Back 22

Decreased GFR
Decreased distal presentation of salt (to principle cell of C and MCD)
Decreased effective IVV
Hypoaldosteronism

Front 23

how do we prevent the lethal effect of hyperkalemia on the heart? how does it work?

Back 23

Ca++ infusion tricks the heart into thinking it is less depolarized than it is. (more negative nernst potential)

Front 24

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?

Back 24

1) Na/K ATPase
2) insulin and B2 agonist
3)Bicarb

Front 25

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?

Back 25

Induce gut clearance of K+ with sorbitol (osmotic diarrhea) or Kaexylate, an Na+/K+ exchange resin

Front 26

How fast is it safe to reduce K+ with dialysis

Back 26

1.5 meq/L/hr

Front 27

1)How do we treat CHRONIC hyperkalemia
2) avoid (drug)
3-4) give fludcortisone which is a ___3___ or kaexylate which is a ____4___

Back 27

1) K+ restriction (<60meq/day).
2) NSAID
3) fludcortisone- a long acting mineraocorticoid
4) Na+/K+ exchange resin

Front 28

Chronic Hypoklemia can be cause by:
1) GI
2) kidney
3) drug side effect
4) skin

Back 28

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

Front 29

Acute hypokalemia can be caused by:
1) endocrine
2) Adrenergic
3) Hematological

Back 29

1) increased insulin allowing cellular uptake by stimulating Na/K ATPAse
2) Increased B-adrenergic activity (stress, drugs, asthma treatment)
3) treatment of anemia

Front 30

Hypokalemia reflects the depletion of ___cellular stores

Back 30

intracellular

Front 31

hypokalemia can cause Enymes to work sum-optimally. what sort of problems an this cause?

Back 31

muscle weakness (glygoenolysis and glycolysis enzymes)
acid-base disturbanes (ammoniagenesis)
Imparied urinary concentration (relates to impaired ADH induction of cAMP)

Front 32

why is K+ repletion often not good enough in hypokaleima

Back 32

it is often caused by inability to conserve K+, so administered dose will just be lost in urine or feces.

Front 33

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?

Back 33

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.

Front 34

hypokalemia can be life threatening only when an acute drop in K+ occurs on the background ......? (two possible)

Back 34

1) already reduced bodily total K+ or 2) significant pharmacological blockade of Na+/K+ ATPAse (cardiac glycosides)

Front 35

Chronic hypokalemia can produce positive feedback making itself worse in 2 ways...

Back 35

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+

Front 36

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....

Back 36

1) increased Na+ presentation to macula densa--> Tubulo-glomerular feedback--> decrease GFR
2)concentrating defect and polyuria
3) ammoniagenesis

Front 37

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___.

Back 37

1. Liver Failure
2) metabolic encephalopathy

Front 38

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_____

Back 38

1) Mg++
2) Mg-ATP

Front 39

1) how does the kidney repspond t prolonged hypokalemia?
2) what side effect does this cause?

Back 39

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

Front 40

Why are C and MCD intercalated cells low in intracellular K+

Back 40

Low K+ due to apical K+ channel and low levels of basolateral Na+/K+ ATPase