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2514 Patho/phys/assess > Week 10 CKD Kidney pharm > Flashcards

Week 10 CKD Kidney pharm Flashcards

1
Q

How does medication slow progression of CKD?

A
  1. reduce damage to the kidney
  2. manage the consequences of reduced GFR
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2
Q

What are the 3 ways we reduce damage to the kidney in CKD?

A

1 Lower BP
2. control atherosclerosis
3. control blood sugar (DM)

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3
Q

What stage is reducing damage to the kidneys in CKD?

A

stage 3

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4
Q

What 3 ways do we manage the physical consequences of reduced GFR?

A
  1. diuretics for fluid overload
  2. rebalance electrolyte imbalances (Na+ K+ Cal phos)
  3. check hormone imbalance (epo) & give endogenous (blood transfusion) epo where needed
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5
Q

What are the CKD meds?

A
  1. Captopril
  2. Candesartan
  3. Atorvastatin (Lipitor)
  4. Furosimide
  5. Hydrochlorothiazide
  6. Spironolactone
  7. Ethropoeitin
  8. Calcium carbonate
  9. Sodium Polystyrene Sulfonate (Kayexalate)
  10. Ferrous Sulfate (Feosol)
  11. Calcitriol (Rocaltrol)
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6
Q

What drug class is captropril and why is it used?

A

ACE inhibitor
to stop angiotensin 1 converting to angiotensin II - RAAS so that Na+ will stop absorbing and stop fluid retention

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7
Q

What alternative is used if the cough from captopril can’t be tolerated?

A

candesartan

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8
Q

What does captopril do for the glomerulus?

A

stops afferent arteriole pressure
dilates efferent arteriole

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9
Q

What is captopril contraindicated in?

A
  1. pregnancy
  2. breastfeeding
  3. renal artery stenosis
  4. angioedema
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10
Q

What are the 3 adverse effects of captopril?

A
  1. first dose hypotension
  2. cough
  3. hyperkalemia
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11
Q

What should nurses monitor with people on captopril?

A
  1. BP - esp first dose and changes
  2. fluid volume/dehydration
  3. blood work - K+, Na+, Urea, creatinine
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12
Q

If blood pressure drops do we have hyperperfusion to the kidneys or hypoperfusion ?

A

hypoperfusion

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13
Q

What is the drug class of candesartan and what does it do?

A

ARB
angiotensin II receptor blocker
blocks angiotensin 2 from reaching the receptor on the adrenal cortex

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14
Q

are the contraindications of candesartan and captopril the same?

A

yes

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15
Q

Do ARBs or ACE inhibitors decrease cardiovascular morbitidy?

A

ACE inhibitors

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16
Q

Which medication causes cough?

A

Captopril

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17
Q

What should we always monitor for patients on atorvastatin?

A

LFTs
CK (creatine kinase - when there is muscle cell damage is releases this enzyme)

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18
Q

How long does it take to see the effects of Atorvastatin?

A

2 weeks

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19
Q

where does Furosemide work?

A

on the ascending limb (the fat part) of the loop of Henle

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20
Q

When GFR is low can we still use a diuretic?

A

yes! this is an advantage!

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21
Q

What is furosemide contraindicated in?

A
  1. someone who has no urine output - anuria <40ml
  2. hepatic coma - a coma from liver issues - can cause cerebra edema
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22
Q

What are the adverse effects of Furosemide?

A
  1. Hyponatremia
  2. Hypocholremia
  3. Dehydration
  4. hypotension
  5. hypokalemia
  6. Ototoxicity
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23
Q

What is a unique side effect to furosemide not seen in other diuretics?

A

ototoxicity - reversed when meds stop

24
Q

what is the MOA of hydrochlorothiazide?

A

Blocks Na and Cl in early segment of the distal convoluted tubule
the top fat part

25
Q

What GFR rate is hydrochlorothiazide ineffective?

A

<15-20ml/min

26
Q

Hydrochlorothiazide and furosomide make all the electrolytes hypo or hyper?

A

Hypo

27
Q

What does Spironolactone work on in the nephron?

A

Blocks the action of aldosterone in the distal nephron
the last straight tube

28
Q

Does spironolactone keep K+ or excrete K+?

A

Keep it so that not too much is lost

29
Q

what is spironolactone contraindicated in?

A
  1. no pee - anuria
  2. Addison’s disease – don’t block what aldosterone they do have b/c blocking it can cause hyponatremia and hyperkalemia
  3. severe renal disease (GFR<30 ml/min)
  4. if they are already hyperkalemic
  5. pregnancy, breastfeeding
30
Q

what GFR rate is spironolactone no longer effective?

A

<30 ml/min

31
Q

what part of the nephron does aldosterone take effect and which diuretic interferes with this?

A

in the late distal convoluted tubule/collecting duct
spironolactone messes with aldosterone here

32
Q

Why does spironolactone have endocrine effects?

A

it’s a steroid derivative so connected to the adrenal gland which is responsible for sex hormone secretion

33
Q

What are the adverse effects of spironolactone?

A
  1. hyperkalemia
  2. endocrine effect
34
Q

What are the 2 endocrine effects of spironolactone on males and the 2 affects on females?

A

male:
impotence
gynecomastia

female:
irregular mestral cycle
hirsutism - facial hair

35
Q

what isErythropoietin (Epogen)?

A

a glycoprotein hormone that stimulates RBC production in bone marrow

36
Q

what do we want to see with Hgb when someone is on EPO?

A

lower Hgb than what is normal due to blood viscosity
100-120g/L

37
Q

What are the adverse effects of EPO?

A

hypertension HTN due to increased blood viscosity
MI and stroke is Hgb is too high

38
Q

when do we not give epo?

A

when someone’s HTN is uncontrolled

39
Q

When does epo start working?

A

2-3 weeks

40
Q

when does epo peak?

A

2-3 months

41
Q

what is the MOA of calcium carbonate?

A

Binds to phosphate in GI tract and is excreted in stool

42
Q

What brand name is calcium carbonate known by?

A

Tums

43
Q

What is the drug class of calcium carbonate?

A

Calcium-Based Phosphate Binder

44
Q

Why do we give calcium carbonate?

A

help reduce too much phosphate in the blood. Calcium binds to phosphate and gets excreted in the stool

45
Q

what is calcium carbonate contraindicated in?

A
  1. hypercalcemia
  2. severe cardiac disease
46
Q

What are the 4 adverse effects of calcium carbonate?

A
  1. constipation
  2. GI irritation
  3. renal calculi (kidney stones)
  4. dig toxicity - check heart
47
Q

how long after a meal should calcium carbonate be given and why?

A

1 hours after meal
to bind with ingested phosphate from food

48
Q

What drug class is Sodium Polystyrene Sulfonate (Kayexalate) ?

A

potassium binding agent to get rid of excess potassium

49
Q

What is the MOA of Sodium polysyrene sulfonate (kayexalate)?

A

a resin removes potassium by exchanging it with sodium in large intestine
The resin gives sodium and takes on potassium to be excreted

50
Q

When is Sodium polysyrene sulfonate (kayexalate) contraindicated?

A

GI obstruction or even suspected obstruction

51
Q

What are the adverse effects of Sodium polysyrene sulfonate (kayexalate)?

A
  • GI issues (N&V, constipation, dehydration)
  • Dig toxicity
52
Q

What is the MOA of Ferrous Sulfate (Feosol)?

A

make more iron
iron is a part of a red blood cell. If lacking iron then RBC can’t be made. If RBC can’t be made then you can’t carry o2 around the body or get rid of Co2.
If you can’t make enough RBC then you have anemia

53
Q

What is the drug class of Calcitriol (Rocaltrol)?

A

activated vitamin D hormone suppliment

54
Q

what is the MOA of Calcitriol (Rocaltrol)

A

helps absorb more calcium in the intestine

55
Q

What disease does Calcitriol (Roclatrol) help prevent?

A

osteodystrophy - when bones don’t develop right because CKD hurts vitamin D production from the kidney so calcium is not properly absorbed for bone formation
hypocalcemia w/ CKD

2514 Patho/phys/assess (27 decks)

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