quick facts for electrolyte analysis

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1. CA inhibitor MOA Eclampsia Urinary excretion decreased acetazolamide - in PCT inhibits H+ HCO3- ->H2CO3- >CO2+H20 in lumen can't reabsorb HCO3 (as CO2) can't reabsorb Na (counter transports w/ H) 2. Thiazide diuretics MOA hydrochlorothiazide.. inhibits Na/Cl co transporter in DCT 3. K sparing MOA spironolactone aldosterone receptor antagonist; decreases Na reabsorption by closing Na channels 4. Loop diuretic MOA furosemide/Lasix inhibit Na/K/Cl channel in loop (thick ascending) by binding to Cl binding site on transporter 5. Diuretics and Calcemia HYPOCAL w/ Loop HYPERCAL w/ Thiazide 6. Diuretics and HYPONATREMIA Thiazide & Loop 7. Diuretics & pH Alkalosis - Loop & Thiazides (w/ K loss, hypokal) Acidosis - CA inhib & K sparing 8. PTH causes high Ca & D low PO4 & HCO3 9. Aldosterone conserves Na excretes K, Mg inhibits vitamin D 10. MOA acidosis w/ CA inhib prevents HCO3 reclaim 11. MOA acidosis w/ K sparing aldosterone blockade prevents H secr blocked w/ K 12. Drugs causing HYPONATREMIA NSAIDS; ACE inhibitors AMIODarone (K channel blocker, also Na, Ca) thiazides HEParin (suppresses aldosterone) 13. Drugs causing HYPERNATREMIA CORTical/anabolicsteroids; (aldost Na conserve) SSRI 14. Drugs causing HYPERKALEMIA K-sparing (spironolactone, mannitol) amphotericin b( methicillin, tetracycline) -renal tox NSAIDS/ace inhibits/beta blockers (red GFR/renal excretion) HEPARIN (aldost antag) antineoplastics, INH/lithium 15. Drugs causing HYPOKALEMIA K-wasting diuretics (acetazolamide, thiazide, loop/furosemide) INSULIN, glucose infusions Amino & acetyl salicylic acid AMPHOtericin B cisplatin phenothaizines 16. Diuretics cause K- wasting HYPOKALEMIA volume depletion triggers ALDOSTERONE secretes K 17. HYPERKALEMIC with METABOLIC ACIDOSIS 18. HYPOKALEMIC with METABOLIC ALKALOSIS 19. HYPERKALEMIA S&S irrit/NV/colic/diarrhea; cardiac .... peaked T waves > 6 arrest > 8 oliguria 20. HYPOKALEMIA S&S INCREASED SENSITIVITY TO DIGOXIN decreased contractility... flattened T waves, prominent U waves weakness, paralysis, hyporeflexia ileus - N/V, constipation polyuria; nocturia 21. Na/C pump in cardiac tissue 3 Na IN for 1 Ca OUT (opposite the 3Na/2K pump) 22. digoxin - inhibits Na/K/ATPase pump (sodium builds up intracellularly) reverses Na/C counter transporter; increases intracell Ca level and build- up in SR slows HR NET; causes incr contr FORCE of the heart w/o incr net energy expenditure 23. Digoxin causes what to K ECF levels can cause HYPERKAL -Na/K pump not working -also binds competitively at K site on pump 24. Digoxin TOXICITY and K levels Toxicity with HYPOKAL; low K inhibits Na/K pump on its own, additive 25. Insulin & potassium K & glucose cotransport; insulin administered for hypergly causes hypokal 26. Glucose & potassium glucose administered; insulin responds K & glucose cotransported into cell (hypokal) 27. INSULIN causes HYPOKALEMIA HYPOMAGNESEMIA HYPOPHOSPHATEMIA 28. licorice is like aldosterone Adjuncts Quiz 2 - Electrolytes Study online at quizlet.com/_21x78o

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Page 1: quick facts for electrolyte analysis

1. CA inhibitor MOAEclampsiaUrinary excretiondecreased

acetazolamide - in PCTinhibits H+ HCO3- ->H2CO3->CO2+H20 in lumencan't reabsorb HCO3 (as CO2)can't reabsorb Na (counter transportsw/ H)

2. Thiazide diureticsMOA

hydrochlorothiazide..inhibits Na/Cl co transporter in DCT

3. K sparing MOA spironolactonealdosterone receptor antagonist;decreases Na reabsorption by closingNa channels

4. Loop diuretic MOA furosemide/Lasixinhibit Na/K/Cl channel in loop (thickascending)by binding to Cl binding site ontransporter

5. Diuretics andCalcemia

HYPOCAL w/ LoopHYPERCAL w/ Thiazide

6. Diuretics andHYPONATREMIA

Thiazide & Loop

7. Diuretics & pH Alkalosis - Loop & Thiazides (w/ K loss,hypokal)Acidosis - CA inhib & K sparing

8. PTH causes high Ca & Dlow PO4 & HCO3

9. Aldosterone conserves Naexcretes K, Mginhibits vitamin D

10. MOA acidosis w/ CAinhib

prevents HCO3 reclaim

11. MOA acidosis w/ Ksparing

aldosterone blockade prevents H secrblocked w/ K

12. Drugs causingHYPONATREMIA

NSAIDS; ACE inhibitorsAMIODarone (K channel blocker, alsoNa, Ca)thiazidesHEParin (suppresses aldosterone)

13. Drugs causingHYPERNATREMIA

CORTical/anabolicsteroids; (aldost Naconserve)SSRI

14. Drugs causingHYPERKALEMIA

K-sparing (spironolactone, mannitol)amphotericin b( methicillin,tetracycline) -renal toxNSAIDS/ace inhibits/beta blockers (redGFR/renal excretion)HEPARIN (aldost antag)antineoplastics, INH/lithium

15. Drugs causingHYPOKALEMIA

K-wasting diuretics (acetazolamide,thiazide, loop/furosemide)INSULIN, glucose infusionsAmino & acetyl salicylic acidAMPHOtericin Bcisplatinphenothaizines

16. Diuretics cause K-wastingHYPOKALEMIA

volume depletion triggersALDOSTERONEsecretes K

17. HYPERKALEMIC with METABOLIC ACIDOSIS

18. HYPOKALEMIC with METABOLIC ALKALOSIS

19. HYPERKALEMIA S&S irrit/NV/colic/diarrhea; cardiac....peaked T waves > 6arrest > 8oliguria

20. HYPOKALEMIA S&S INCREASED SENSITIVITY TO DIGOXINdecreased contractility...flattened T waves, prominent U wavesweakness, paralysis, hyporeflexiaileus - N/V, constipationpolyuria; nocturia

21. Na/C pump incardiac tissue

3 Na IN for 1 Ca OUT(opposite the 3Na/2K pump)

22. digoxin - inhibitsNa/K/ATPase pump(sodium builds upintracellularly)

reverses Na/C counter transporter;increases intracell Ca level and build-up in SRslows HRNET; causes incr contr FORCE of theheart w/o incr net energy expenditure

23. Digoxin causeswhat to K ECF levels

can cause HYPERKAL-Na/K pump not working-also binds competitively at K site onpump

24. Digoxin TOXICITYand K levels

Toxicity with HYPOKAL; low K inhibitsNa/K pump on its own, additive

25. Insulin &potassium

K & glucose cotransport;insulin administered for hyperglycauses hypokal

26. Glucose &potassium

glucose administered; insulin respondsK & glucose cotransported into cell(hypokal)

27. INSULIN causes HYPOKALEMIAHYPOMAGNESEMIAHYPOPHOSPHATEMIA

28. licorice is like aldosterone

Adjuncts Quiz 2 - ElectrolytesStudy online at quizlet.com/_21x78o

Page 2: quick facts for electrolyte analysis

29. body response totrauma, injury, burns -late

ALDOSTERONE (so Na conserved,K excreted)

30. ascites, ileus, bowelobstruction generally

traps fluid w/ electrolytes in 3rdspaceLOWERS blood levels

31. Drugs causingHYPERCHLOREMIA

(cortison aldosteronecan do either??)booknot helpful

acetazolamide & chlorothiazidediureticsNSAIDS; reduce GFRCORTisone (aldost; Na conserve)methylDOPA(estrogen/androgen)

32. DRUGS causingHYPOCHLOREMIA(cortison aldosteronecan do either??)book not helpful

diuretics - (all lose Na Cl w/)corticosteroids, aldosterone - fluidretains -> dilutesbicarbonate (adding HC03, needto lose Cl)

33. Drugs causingHYPERMAGNESEMIA

Thyroid meds (inc ATP)Antacids**, both typesAminoglycoside abx (mycins)Loop diurecticsLithium

34. Drugs causingHYPOMAGNESIA

Laxatives (reduce GI absorption)Diuretics (not loop)INSULIN - (uses ATP shifting K in)ALDOSTERONE (secretes Mg like K)

35. Cushing's causes(hypersecretion ofcortisol)

HYPO kalemia & calcemia (&magnesia)ALKalosisHYPER glycemia & tension

36. Addison's causes(hyposecretion ofcortisol)

HYPER kalemia & calcemia (&magnesia)ACIDosisHYPO glycemia & tension

37. Cortisol impacts(keeps glucose levelshigh protect CNS)

HYPERGLY; prevents uptake bycells (peripheral)catabolic; to muscles/bones/fat(lipolysis; TG up)(components for gluconeogenesis)bones; stims clasts, inhibits blasts -but reduces free Ca (inhibitsabsorption & vit D)

38. Intracellular Ions(HYPER in lysis/crush,etc)

KMgPO4Protein

39. Burns LATE cause early HYPERNATREMIA - fluid losslate HYPONATREMIA - loss inburned tissue (ECF)HYPERKALEMIA - acidosis & shiftout of ICF, vasc perm incr

40. Mechanism ofHYPERKALEMIA inburns

1) Damaged cells spill ICF, incr capperm (inflam) allows K+ to shift intovessels 2) burn releases cell contents uricacid, myoglobin, etc, causesmetabolic acidosis

41. nerve excitability Hypokal - peaked T waves(arrhythmia then block)Hypocal/Hypomag - tetany;Hypochlor

42. sepsis causes respiratory ALKALOSIS(excessive ventilation reduces CO2)

43. ALKALOSIS with HYPOKALEMIAHYPOCHLOREMIAHYPOPHOSPHATEMIA (goes back tobone)

44. ACIDOSIS with HYPERKALEMIAHYPERCHLOREMIAHYPERPHOSPHATEMIA (buffers w/bone)

45. MC cause ofHYPERKALEMIA

renal failure

46. MC cause ofHYPOKALEMIA

diuretics

47. MC cause ofHYPERNATREMIA

excessive water loss; dehydration

48. MC cause ofHYPONATREMIA

CHF/edemadiarrhearenal disease (not reabsorbing)

49. MC cause ofHYPERCHLOREMIA

bicarb loss (diarrhea or renal)-metabolic acidosishyperparathyroid

50. MC cause ofHYPOCHLOREMIA

rarely alone; w/ hyponat (diuretics)or elevated HCO3or vomiting (lose HCL)

51. MC cause ofHYPERMAGNESEMIA

kidney failure when givenmagnesium salts/antacids/laxatives

52. MC cause ofHYPOMAGNESEMIA

malnourished, alcoholicsdiarrhea

53. MC cause of HYPERCAL hyperparathyroidmalig - degrade or secrete PTH

54. MC cause of HYPOCAL parathyroid; thyroid surgeryhypomagnesemia MC in hospitalsRENAL failure; causes PO4 inc & VitD decreaseRickets, stones

55. MC cause ofHYPERPHOSPHATEMIA

usually 2ndary; chronic kidney diseasehypoparathyroidbuffering acidosis

Page 3: quick facts for electrolyte analysis

56. MC cause of HYPOPHOSPHATEMIA hyperparathyroid

57. Anion Gap Equation Cats - AnionsNa + K - HCO3 + Cl

58. Anion Gap Normal < 11 ; else is METABOLIC ACIDOSIScompensated by ion other than 4(lactic acid or ketoacidosis)

59. High Anion Gap acidosis loss of HCO3 - METABOLIC ACIDOSISLAosis, DKAuremia; UA build up - kidneys not workingASA toxicityalcoholism, methanol

60. Low Anion Gap loss of gastric juice w/ HCO3 increasealkali ingesionaldosteronism (alkalosis)