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Cardio-Renal I FINAL > Therapeutics - Cassagnol CKD > Flashcards

Therapeutics - Cassagnol CKD Flashcards

1
Q

in CKD classification, eGFR less than ____ is considered stage 5

what does stage 5 mean

A

less than 15mL/min

KIDNEY FAILURE

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2
Q

explain the general prevention strategies against CKD

A

manage the disorders that can cause or accelerate CKD – ie: hypertension, dyslipidemia, diabetes

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3
Q

which blood pressure agents are preferred in diabetic patients and why

A

ACE inhibitors or ARBs – preferred in diabetes with HTN or albuminuria

bc can slow the progression of CKD

ACE and ARB may even be considered if the pt is NORMOTENSIVE

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4
Q

2 drugs that can induce chronic kidney disease

A

LONG TERM use of NSAIDS, tylenol, codeine, caffeine (only very large amt)

lithium!

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5
Q

pt is taking lithium

what is concern and how often should they be monitored

A

lithium causes LOT of kidney issues and can cause CKD

need to check the SCr every few months for 6 months and then yearly —- need to do risk-benefit analysis if worth continuing

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6
Q

true or false

the complications of CKD become more prominent as the kidney function worsens

A

true

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7
Q

name some complications of CKD

A

fluid and electrolyte abnormalities

anemia

CV disease

mineral and bone issues

malnutrition

drug dose adjustments

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8
Q

lab findings in CKD – state whether elevated or below normal

BUN
phosphate
calcium
potassium

A

high BUN
high phosphate
low calcium
high potassium

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9
Q

CKD can cause the complication of metabolic _____ (alkalosis or acidosis)

A

acidosis

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10
Q

true or false

CKD can cause anemia

A

true

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11
Q

consequence of low calcium from CKD

A

hyperparathyroidism

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12
Q

____ deficiency is a complication of CKD

A

erythropoietin

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13
Q

CLINICAL signs of CKD (not lab)

A

hypertension
uremia (urea accumulation – symptoms are nausea and anorexia)

bleeding, muscle pain, anxiety, depression, pericarditis, itching, fluid retenion, muscle pain, etc

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14
Q

treatment for FLUID OVERLOAD (complication of CKD)

A

diuretics (specifically loops) and sodium restriction (based on extent of overload)

loops usually used, but can add a thiazide (metazolone) if resistant to loops alone (rebound reabsorption in DCT - thiazides will prevent)

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15
Q

thiazide monotherapy is usually not used for fluid overload from CKD, but ESPECIALLY not used if the eGFR is….

A

less than 30 – it’s ineffective at this point

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16
Q

hyperkalemia is a complication of CKD

this can usually be avoided once…

A

routine dialysis is established

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17
Q

WHY does CKD often lead to anemia

A

because there is decreased production of erythropoietin by the kidney – and also a decreased response to erythropoietin and heme production

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18
Q

in order to give exogenous erythropoietin (/erythropoietin stimulating agents) to anemic patients with CKD, what MUST be done first?

A

correct the iron deficiency FIRST - otherwise EPO will not work

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19
Q

we can consider initiating erythropoietin stimulating agents when the hemoglobin is….

A

less than 10g/dL - also consider the symptoms

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20
Q

explain when to reduce/interrupt the dose of ESA’s in dialysis vs non dialysis patients

A

non dialysis - when the hemoglobin is over 10g/dL

dialysis - when over 11g/dL

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21
Q

goal of giving ESA to anemic patients from CKD

A

reduce the need for RBC transfusion!

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22
Q

!!!VERY important consideration when giving erythropoietin stimulating agents

A

***DO NOT TARGET NORMAL HOMOGLOBIN CONCENTRATION!!!!!

13 and over g/dL of hemoglobin changes the viscosity of the blood - prone to clots and CV events like heart attack and stroke!!!!

23
Q

____ is the main cause of ESA unresponsiveness

therefore….

A

iron deficiency

need to check the transferrin saturation (iron ready for production) and ferritin (iron stores)

24
Q

true or false

just correcting the iron deficiency may resolve the anemia, without even having to use ESA

A

TRUE - and this is preferred

25
Q

when correcting the iron deficiency, what formulations are tried 1st and what if they fail

state an issue with the initial route

A

give PO first – but these have low bioavailability and poor adherence

use IF formulations if oral fail

26
Q

COUNSELING POINT for PO iron

A

needs acidic environment to absorb, so take on EMPTY STOMACH with ascorbic acid (orange juice)

27
Q

bone and mineral disorders are a complication of CKD

what are the goals

A

to manage the serum levels of phosphate and calcium, AND to manage the secondary hyperparathyroidism that occurs bc of the low calcium

28
Q

a complication of CKD is elevated phosphate

explain the stepwise approach to correcting this

A

1st - diet restriction on phosphate - less than 1000mg/day

if fails - use phosphate binding agent (calcium containing first)

BUT if the patient is hypercalcemic OR has signs of calciphylaxis OR if calcium x phosphorus 55 or more – SWITCH TO NON CALCIUM CONTAINING BINDER

29
Q

true or false

phosphate is NOT adequately removed by dialysis, so we put a dietary restriction to 1000mg a day

A

true

30
Q

foods to avoid when trying to limit phophate intake

A

preservatives and added salts, and dark carbonated beverages

31
Q

important counseling point for phosphate binding agents

A

GIVE WITH FOOD! to bind the dietary phosphorus

32
Q

issue with giving a calcium containing binder for hyperphosphatemia

A

can fix the hypocalcemia BUT can cause hypercalcemia

33
Q

name 2 non-calcium containing binders

A

sevelamar
lanthanum

34
Q

what 2 salts is sevelamar available as and which should be avoided in cases of metabolic acidosis

A

HCl and carbonate

avoid HCl if metabolic acidosis

35
Q

__ and __ containing binders and products should be avoided to treat hyperphosphatemia

A

aluminum and magnesium containing

36
Q

what is the name of the calcium-containing binder for hyperphosphatemia

A

calcium acetate (phos-low)

37
Q

true or false

Vitamin D elevation is a complication of CKD

A

FALSE - deficiency bc the final conversion to calcitriol (vitamin D) is done by the kidney

38
Q

2 precursors to vitamin D that can be used to treat deficiency

A

ergocalciferol and cholecalciferol

39
Q

*when should ACTIVE vitamin D (calcitriol) and NOT its precursors be used

A

when PTH is high!!!!

40
Q

concern with giving vitamin D

A

can elevate calcium and phosphorus!!!! need to check every month

41
Q

name a calcimimetic

A

cinacalcet (sensipar)

42
Q

only thing that cinacalcet is approved for

what does it do?

high risk of what?

A

ESRD and on dialysis

lower PTH either as an alternative or in addition to vitamin D analogs

high risk of hypocalcemia!!!! - START LOW DOSE - 30mg/day

43
Q

the goal for cinacalcet is to decrease and titrate the PTH

how often to check?

how often to check calcium and phosphorus?

A

every 2-4 weeks

check calcium and phoshorus within ONE WEEK for safety (may cause hypocalcemia)

44
Q

true or false

CKD patients – ALL MEDICATION dependent on the kidneys for elimination need to be assessed for dose reduction

A

true

45
Q

which type of dialysis is more often done at home

A

peritoneal dialysis

46
Q

concern with dialysis

A

removes FOLATE and not vitamin A

need to supplement vitamins (inc folate) – nephrocaps

47
Q

when giving ESAs, need to check hemoglobin how often??
what to do if….

increase over 1 g/dL (or target exceeded)

increased less than 1g/dL after 4 weeks

A

2 weeks after initiation, or 2 weeks after a dose change

over 1g/dL - decrease dose by 25%

less – increase the dose (50% epoeitin and 25% darbepoetin)

48
Q

differentiate between paricalcitol and doxercalciferol

A

paricalcitiol - decreases PTH and does NOT increase calcium or phosphorus (GOOD)

doxercalciferol - decreases PTH but INCREASES CALCIUM AND PHOSPHORUS

49
Q

doxercalciferol is only used in CKD if…

how is it dosed

A

patient is on dialysis

TIW

50
Q

calcitriol is started at what dose and why

A

LOWEST DOSE - to avoid hypercalcemia

51
Q

1mcg calcitriol = ____mcg paricalcitiol

A

4

52
Q

true or false

cancer is an adverse even of ESAs

A

true

53
Q

most common adverse event from ESA

A

hypertension

54
Q
A

Cardio-Renal I FINAL (13 decks)

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