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STEP 2 Cardio + Renal > fluid/acid-base HYPER K > Flashcards

fluid/acid-base HYPER K Flashcards

1
Q

UW table. medications.
ACEI mechanism?

A

Inhibit angiotensin II formation, leading to decreased aldosterone secretion

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2
Q

UW table. medications. ARB mechanism?

A

Inhibit AT 1 receptor, leading to decreased aldosterone secretion

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3
Q

UW table. medications. K sparing diuretics mechanism?

A

Inhibit ENaC or aldosterone receptor

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4
Q

UW table. medications. nonselective BAB mechanism?

A

Inhibit beta-2- mediated intracellular potassium uptake

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5
Q

UW table. medications. NSAIDS mechanism?

A

Inhibit local prostagland in synthesis, leading to decreased renin & aldosterone secretion

Decreases renal perfusion resulting in decreased K+delivery to the collecting ducts

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6
Q

UW table. medications. cardiac glycosides mechanism?

A

Inhibit the Na+/K+-ATPase pump (eg, digoxin)

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7
Q

UW table. medications. succinylcholine mechanism?

A

Causes extracellular leakage of potassium through acetylcholine receptors

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8
Q

UW table. medications. trimetoprim mechanism?

A

Inhibits ENaC

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9
Q

UW table. medications. cyclosporine mechanism?

A

Blocks aldosterone activity (IL-2 transcription inhibitor – psoriasis, RA)

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10
Q

UW table. medications. heparin mechanism?

A

Blocks aldosterone production

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11
Q

FA. causes. 4 groups?

A

spurious
cellular shift
decr. excretion
incr. intake

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12
Q

FA. causes.
1. spurious causes?

A

hemolysis of blood samples, fist clenching during blood draws, delays in sample analysis, extreme leukocytosis or thrombocytosis

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13
Q

FA. causes.
2. cellular shift/increased potassium release from cells?

A

Cell lysis, tissue injury (rhabdomyolysis), tumor lysis syndrome, insulin deficiency, uncontroled hyperglycemia, hyperosmolality,
acidosis, drugs (from table), exercise

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14
Q

FA. causes. uptd
2. cellular shift/increased potassium release from cells. insulin effect?

A

Insulin promotes potassium entry into the cell.

In normal conditions – ingestion of glucose –> release of insulin –> promoted potassium entry to the cell.

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15
Q

FA. causes. uptd
2. cellular shift/increased potassium release from cells. Uncontroled DM mechanism?

A

The combination of insulin deficiency (either impaired secretion or insulin resistance) and hyperosmolality induced by hyperglycemia frequently leads to hyperkalemia even though there may be marked potassium depletion due to urinary losses caused by the osmotic diuresis.

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16
Q

FA. causes. uptd
2. cellular shift/increased potassium release from cells. Uncontroled DM. 2 mechanisms of K movement?

A
  1. The loss of cell water raises the cell potassium concentration, thereby creating a favorable gradient for passive potassium exit through potassium channels in the cell membrane.
    2.The friction forces between solvent (water) and solute can result in potassium being carried along with water through the water pores in the cell membrane. This phenomenon of solvent drag is independent of the electrochemical gradient for potassium diffusion.
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17
Q

FA. causes. uptd
2. cellular shift/increased potassium release from cells. what other than DM can inc. osmol/decr insulin?

A

somatostatin –> decr. insulin

Fasting is associated with an appropriate reduction in insulin levels that can lead to an increase in plasma potassium. This may be a particular problem in patients on dialysis OR prior SURGERY.

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18
Q

how to avoid hyperK in preop fasting?

A

The risk of hyperkalemia during preoperative fasting can be minimized by the administration of insulin and glucose in patients with diabetes, or glucose alone in patients without diabetes.

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19
Q

FA. causes. uptd
2. cellular shift/increased potassium release from cells.

incr. tissue catabolism?

A

tissue trauma or tissue lysis syndrome –> breakdown –> intracellular K is released into the ECF.

Trauma (including noncrushing), rhabdomyolysis, the administration of cytotoxic or radiation therapy to patients with lymphoma or leukemia (the tumor lysis syndrome), and severe accidental hypothermia.

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20
Q

FA. causes. uptd
2. cellular shift/increased potassium release from cells.
BAB mechanism?

A

Increased beta-2-adrenergic activity drives potassium into the cells and lowers the serum K.

BAB –> decr. K uptake by cells.

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21
Q

FA. causes. uptd
2. cellular shift/increased potassium release from cells.
BAB what incr K?

A

Incr. with nonselective - propranolol, labetolol

Cardioselective has less effect

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22
Q

FA. causes. uptd
2. cellular shift/increased potassium release from cells.

Hypercalemic periodic paralysis – AD disorder, presents as weakness episodes.

A

.

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22
Q

FA. causes. uptd
2. cellular shift/increased potassium release from cells.
Exercise?

A

K is normally released from muscle cells during exercise. The increase in plasma potassium is rarely important clinically.

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23
Q

FA. causes. uptd
2. cellular shift/increased potassium release from cells. Digitalis?

A

dose-dependent inhibition of the Na-K-ATPase pump.

structurally related digitalis glycosides may be due to ingestion of plants: oleander or yellow oleander.

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24
Q

FA. causes. uptd
2. cellular shift/increased potassium release from cells. RBC tranfusion?

A

leakage of potassium out of the red cells during storage

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25
Q

FA. causes. uptd
2. cellular shift/increased potassium release from cells. acetylcholine?

A

Acetylcholine receptors are normally concentrated within the neuromuscular junction, and the efflux of intracellular potassium caused by depolarization of these receptors is confined to this space.

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26
Q

FA. causes. uptd
2. cellular shift/increased potassium release from cells. drug aminocaproic acid?

A

The entry of cationic arginine into the cells presumably obligates potassium exit to maintain electroneutrality. Same mechanism for aminocaproic, since it is structural analogs

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27
Q

FA. causes. uptd
2. cellular shift/increased potassium release from cells.
Activators of ATP-dependent potassium channels (calcineurin inhibitors, diazoxide, minoxidil, some volatile anesthetics) - Use of drugs that activate ATP-dependent potassium channels in cell membranes, such as calcineurin inhibitors (eg, cyclosporine and tacrolimus), nicorandil, and isoflurane.

A

.

28
Q

FA. causes.
3. reduced urinary K secretion. causes?

A

Renal insufficiency, drugs (AKFI, TMP, NSAIDS, K sparing, nonselective bab)
hypoaldosteronism, RTA type IV, calcineurin inhibitors

29
Q

Causes. UPTD groups
3. reduced urinary K secretion. causes?

A

decr. aldosterone secretion
decr. response to aldosterone (eg K sparing)

Other: selective impairment in potassium secretion, Gordon’s syndrome, ureterojejunostomy.

30
Q

FA. causes. uptd
3. reduced urinary K secretion. TMP mechansim of hyperK?

A

blocking the epithelial sodium channel in the collecting tubule, similar to the action of potassium-sparing diuretic amiloride

31
Q

FA. causes. uptd
3. reduced urinary K secretion.

TMP on creatinine?

A

Trimethoprim also competitively inhibits renal tubular creatinine secretion and may cause an artificial increase in serum creatinine; however, GFR is unchanged.

32
Q

FA. causes. uptd
3. reduced urinary K secretion. DUE TO reduced response to aldosterone. what causes?

A

K sparing
TMP
RTA
Pseudohypoaldosteronism type 1
Duced distal sodium and water delivery – effective blood volume depletion (HF - dec. CO, cirrhosis - vasodilation)

Acute or chronic kidney disease - reduced distal sodium and water delivery

Bendrai – disorders that impair renin-angiotensin axis

33
Q

FA. causes.
3. incr. intake. causes?

A

food
iatrogenic
absorption of blood (from hematomas, GI bleeding)

34
Q

Uptd. Symtoms - groups? 4

FA - nausea, vomiting, intestinal colic, areflexia, paresthesias

A

Muscle, ECG, arrhythmias, laidumo sutrikimai

35
Q

Uptd. muscle symptoms?

A

Ascending muscle weakness with flaccid paralysis (can be in hypo/hyperK, hypoMg, hyper/hypoCa)
prasideda kojose ir kyla i virsu

36
Q

Uptd.
ECG changes? in order of presentation

A

Tall peaked T waves with shortened QT interval

PR prolongation and QRS widening

Disappearance of P wave

Conduction blocks, ectopy, or sine wave pattern=severely widened QRS

37
Q

Uptd. symptoms.
Laidumo sutrikimai

A

I, II, III AV blokados
kairės arba dešinės kojyčių blokados

38
Q

Uptd. symptoms.
aritmijos?

A

Sinusinė bradikardija
idioventrikulinis ritmas
skilveline tachikardija
asistolija
skilveliu virpejimas

39
Q

nedidele hyperK?

A

K 5,5-5,9 mmol/l

40
Q

vidutine hyperK?

A

K 6,0-6,5 mmol/l

41
Q

severe hyperK?

A

K > 6,5 mmol/l

42
Q

FA. Diagnosis.
first thing to do when get lab hyperK?

A

repeat blood draw for suspected spurious results.
In the setting of extreme leukocytosis or thrombocytosis - check K because it can be increased due to release from cells

43
Q

FA. Diagnosis.
2nd thing to do when get lab hyperK?

A

Evaluate ECG

44
Q

uptd. Treatment algo.

what hyperkalemic emergency? 3 groups

A

a) Clinical symptoms OR ECG changes

b) >6,5

c) > 5,5 mmol/l + significant renal impairment, ongoing tissue breakdown/absorption of K eg. from GI bleeding, metabolic or respiratory acidosis.

45
Q

uptd. Treatment algo.
Initial emergency treatment?

A

calcium gluconate 1000 mg (10 mL of 10% solution)
or calcium chloride 500 to 1000 mg
over 2-3 min to stabilize cardiac membranes.

Repeat after 30-60min if hyperK persists
If ECG changes persists - repeat after 5 min.

46
Q

uptd. Treatment algo.
Initial emergency treatment. (ECG, > 6,5)

Ca gluc kur i/v duoti?

A

Calcium gluconate – less irritating, can give into peripheral vein.

Dont give calcium with bicarbonate containing solutions –> can precipitate

47
Q

uptd. Treatment algo.
For ALL hypercalemic?

A

Insulin and glucose to shift K+ intracellularly.

Bolus injection of 10 units of regular insulin, followed immediately by 50 mL of 50% dextrose (25 g of glucose) over 5 minutes.
it lowers K by 1 mmol/l.

48
Q

uptd. Treatment algo.

insulin and glucose. mechanism?

A

Insulin enhances the activity of the Na-K-ATPase pump in skeletal muscle –> drives K into cells.
Glucose needed to prevent hypoglycemia.

Give only insulin if serum glucose is >250 mg/dL [13.9 mmol/L]).

Measure glucose every 6h to detect hypoglycemia.

49
Q

uptd. Treatment algo.

insulin and glucose.

when give only insulin?

A

Give only insulin if serum glucose is >250 mg/dL [13.9 mmol/L])

50
Q

keep in mind - insulin effect is prolonged in kidney impairment –> hypoglycemia risk

A

.

51
Q

uptd. Treatment algo.

insulin and glucose.
After initial dose what?

A

To avoid hypoglycemia, we subsequently infuse 10% dextrose at 50 to 75 mL/hour and closely monitor blood glucose levels every hour for five to six hours.

52
Q

Hlab. insulin and glucose gydymas

A

10 VV insulino + 10 % 500 ml gliukozės tirpalo į veną per 60 min.

5 VV insulino + 5 % 500 ml gliukozės tirpalo

10 VV insulino + 25 g gliukozės boliusą

Kas 1 val. (6 val.) stebėk gliukozės kiekį kraujyje dėl hipoglikemijos pavojaus

53
Q

uptd. Treatment algo.
After insulin and glucose.
Then need to remove K from body.
What methods?

A

Diuretics
Dialysis
GI cation exchanger

54
Q

uptd. Treatment algo.
Remove K from body.
Diuretics in normal kidney function?

A

Jeigu nėra galutinio inkstų nepakankamumo, tai furozemidas 1 mg/kg (40-80 mg).

Saline infusion with IV loop diuretics can be administered (eg, 40 mg of furosemide every 12 hours) to nonoliguric patients without severe kidney function impairment.

55
Q

uptd. Treatment algo.
Remove K from body.
Diuretics. Hypervolemic with normal kidney?

A

40 mg of intravenous furosemide every 12 hours or a continuous furosemide infusion

56
Q

uptd. Treatment algo.
Remove K from body.
Diuretics.
Euvolemic/hypovolemicwith normal kidney?

A

Isotonic saline at a rate that is appropriate to replete hypovolemia and maintain euvolemia, followed by 40 mg of intravenous furosemide every 12 hours or a continuous furosemide infusion.

57
Q

uptd. Treatment algo.
Remove K from body.
Diuretics.
If kidney function is not preserved?

A

Intravenous isotonic bicarbonate or isotonic saline infusion plus intravenous furosemide at doses that are appropriate for the patient’s kidney function.

Kai nepakankamumas (HF, cirrhosis, nephrotic kidney), reikia didesnių efektyvių dozių

In chronic kidney disease, the upward dose adjustment varies inversely with the estimated GFR.

58
Q

uptd. Treatment algo.
Remove K from body.
Hemodilaysis.
absoliucios skubios indikacijos?

A

ŪIP: > 6,5 mmol/l ar mažesnei hiperkalemijai su būdingais EKG pakitimais

LIN: >7 mmol/l ar mažesnei hiperkalemijai su būdingais EKG pakitimais

59
Q

uptd. Treatment algo.
Remove K from body.
GI exchangers.
what are 3?

A

Patiromer: 8.4 g, repeated daily as needed

Sodium zirconium cyclosilicate (SZC): 10 g three times daily for 48 hours

Sodium polystyrene sulfonate (sorbisteritas):
Duok išgerti 20-30 g. Uptd: 50 mixed with 150ml tap water.

60
Q

UW sorbisterite mechanism?

In FA called Kayexalate

A
  1. It is a potassium-binding resin that decreases total body potassium content
  2. Mechanism:
    a. It exchanges sodium for potassium in the gut (sodium in, potassium out)

b. It takes at least 1-2 hours to work

61
Q

uptd. Treatment algo.
other therapies. Beta2 agonists? dose

A

10-20 mg Salbutamolio nebulaizeriu
Arba
100-200 mcg (1-2 įpurškimai) Salbutamolio inhaliuoti per inhaliatorių

62
Q

uptd. Treatment algo.
other therapies. sodium bicarbonate. dose?

A

In metabolic acidosis - give.
But does not effectively decr. K in hyperK even metabolic acidosis is present. Therefore it cannot be the only therapy.

4,2 proc. 100-250 ml Arba 8,4 proc. 50 ml greitos infuzijos būdu

63
Q

Need of bicarbonate. formula?

A

4,2 proc. NaHCO3 (ml) = 0,6 x kg x BE mmol/l.

8,4 proc NaHCO3 (ml) = 0,3 x kg x BE mmol/l.

64
Q

uptd. HyperK, but non emergency.

When need to lower promptly? 2

A

K > 5,5 + patient has severe kidney function impairment

K > 5,5 + NO severe kidney function impairment + NEED to prepare patient for surgery

65
Q

uptd. HyperK. Promplty lowering. time, methods

A

within 6-12h
Not require insulin +glucose

These patients usually have ESKD or oliguria, and are treated with dialysis +/- GI exchangers

If normal kidney - diuretics, saline, stop drugs, correct hypovolemia

66
Q

uptd. HyperK, but non emergency.

lower slowly. what patients pagal algo?

A

> 5,5 + no renal imparment + no surgery

or
< 5,5

67
Q

uptd. HyperK, but non emergency.

lower slowly? time, methods

A

over matter days or weeks.

Due to chronic elevation in CKD or medications

Methods: diet, diuretics in HTN or hypervolemia, cessation of drugs

68
Q

UW sorbisterite
In FA called Kayexalate.

Contraindications.

A

Use when renal function impaired.

Contr. ileus, bowel obstruction, ischemic gut, pancreatic transplants (can c ause bowel necrosis)

STEP 2 Cardio + Renal (35 decks)

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