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Pharm > Nicole: Renal failure meds in CKD > Flashcards

Nicole: Renal failure meds in CKD Flashcards

1
Q

What are the classes of bone mineral metabolism disorder drugs?

A
  • Phosphate binders
  • Vitamin D analogues
  • Calcimemetics
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2
Q

What are the Diuretics used for Renal Failure?

A

Thiazide

Loop

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3
Q

What is the erythropoesis stimulating agent

A

Epoetin alpha

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4
Q

What are the electrolyte supplements

A

Magnesium

Potassium

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5
Q

Describe the role of phosphate in BMMD

A
  • Widely distributed in the body
  • component of many foods (proteins)
  • Passive GI uptake although Vit D stimulates active transports of phosphate for GI tract
  • approx 2/3 of ingested Phosphorus is absorbed
  • Primarily renally excreted
  • Reabsorption is regulated by PTH
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6
Q

Explain the pathophysiology of PTH in BMMD

A
  • Maintains constant Ca++ concentration in extracellular fluid in response to plasma Ca++ concentration
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7
Q

What is the mechanism for increased secretion of PTH in CKD?

A

Decreased renal phosphorus excretion and decreased Vit D activation causes decreased GI Ca++ absorption. This leads to elevated serum phosphate and decreased serum Ca++ concentration –> to increased secretion of PTH

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8
Q

What are the reasons for the parathyroid gland releasing PTH?

A
  1. Increases Ca++ resorption from bone and in Prox renal tubule
  2. Decreased phosphorus resorption in prox renal tubule
  3. Increased activation of Vit D leads to increased GI absorption of Ca++ and mobilization of Ca++ from the bone (increased serum ca++ levels)
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9
Q

What happens in regards to bone metabolism mineral density when Vitamin D is activated?

A

It increases GI absorption of Ca++ and mobilizes it from the bone, but also leads to increased GI phosphorus absorption and mobilization from bone and decreased PTH secretion. This initial negative feedback loop maintains serum calcium concentration and Ca:Phosphorus ratio.
BUT, when GFR

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10
Q

Treatment of BMMD

A

Reduce serum phosphate levels by:

  1. Reduce dietry phosphorus intake (max 800-1000mg/24h) by decreasing protein
  2. Phosphate binding agents:
    a. Calcium based phosphate binders
    b. Sevelamir
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11
Q

What are the 2 phosphate binding drugs?

A
  1. CaCO3

2. Sevelamer

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12
Q

What are the indications for the use of phosphate binding drugs?

A

Hyperphosphatemia

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13
Q

How do the phosphate binders work?

A

They bind phosphate in the GI tract, promoting excretion

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14
Q

What is a common s/e of CaCo3 and sevelamer?

A

constipation

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15
Q

CaCO3 has drug interactions that include what?

A

Antagonizes verapamil
Thiazides increase serum Ca++
Decreases atenolol absorption

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16
Q

What is important to monitor in CaCO3?

A

hypercalcemia - may cause vascular and soft tissue calcifications

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17
Q

Sevelamer is in what drug class?

A

Phosphate binding agent

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18
Q

What are some important contraindications of sevelamer?

A

Hypophosphatemia
bowel obstruction
dysphagia
bowel disorder

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19
Q

What are some s/e of sevelamer

A 
NVD
Constipation
Rash
May dec Vit D, E, K (fat soluble vitamins)
May dec folate absorption
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20
Q

Drug interactions to remember about sevelamer include what?

A

Decreases absorption of Cirprofloxin
Anti-seizure drugs
anti-arrythmic drugs

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21
Q

Sevelamer has an added benefit that includes what?

A

Also reduces LDL-C up to 30%

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22
Q

What is the vitamin d analogue?

A

calcitriol

23
Q

What are the indications for the use of calcitriol?

A

Reduction of PTH levels, hypocalcemia in ESRD

24
Q

Describe the MoA of calcitriol

A

Up-regulates Vit D receptor on PT gland decreasing gland hyperplasia and PTH synthesis

25
Q

What are the drug interactions of calcitriol?

A

May increase risk of digitalis toxicity

Coadministration with steroids may decrease Ca absorption

26
Q

What are common S/E of calcitriol?

A

Anorexia
constipation
arrhythmias
HTN

27
Q

Contraindications of calcitriol include what?

A

hypercalcemia

vit D toxicity

28
Q

What is another benefit of the use of calcitriol?

A

up-regulates GI Vit D receptors increasing Ca++ and phosphorus absorption

29
Q

Another formulation of calcitriol is what?

A

Paricalcitol - less GI receptor impact which helps to avoid anorexia and constipation

30
Q

Because calcitriol suppresses PTH, what are some things you must consider?

A

Over suppression of PTH levels can induce adynamic bone disease (Low bone turnover)

31
Q

what is the calcimemetic drug?

A

Cinacalcet

32
Q

What are the indications of using cinacalcet?

A

Elevated serum PTH, Ca++ and Ca-P product

33
Q

Explain the MoA of cinacelcet

A

Reduces PTH secretion by sensitizing PT gland Ca++ receptors lowering Ca++ and phosphorus levels

(Mimics the action of Ca++ at the receptor)

34
Q

What is something very important to remember about cinacalcet?

A

You should be cautious when it comes to using in patients with seizure disorders because it has drug interactions with anti-seizure meds

35
Q

Something important to know about cinacalcet and patients who benefit from its use

A

Those who can’t used Vitamin D to normalize serum Ca++ levels

36
Q

Why is it important to use epoetin alfa in CKD?

A

Because the reduction in number of functioning nephrons in CKD reduces renal production of erythropoetin

37
Q

Remember this about a uremic state in regards to RBC life span

A

shortens RBC life span from 120 days to 60 days

38
Q

What are the indications for use of Epo Alfa?

A

Anemia in CKD

39
Q

What is the MoA of Epo Alfa?

A

It stimulates erythroblasts to proliferate and differentiate into normoblasts, then reticulocytes

40
Q

What is a side/effect of the use of Epo Alfa?

A

can increase BP, so be cautious with use in patients who have High BP (>180/100)

41
Q

What is the preferred method of admin for Epo Alfa?

A

Subcutaneous

Also IV administration can be done

42
Q

MgCl is used for what purpose?

A

hypomagnesemia

43
Q

What is the 2nd most abundant intracellular cation?

A

Magnesium

44
Q

Renal failure will do what to serum levels of magnesium?

A

Cause hypermagnesemia (>2.4mg/dL)

45
Q

KCl is used for what purpose?

A

Hypokalemia

46
Q

What is very important to remember about KCl?

A

Tablets can be caustic to mucosa in the esophagus

47
Q

Why is the use of ACEIs and ARBs beneficial in CKD?

A

They preserve renal function

48
Q

Afferent and Efferent arterioles are dilated/constricted by what compounds?

A

Prostaglandin (dilation) and Angtiotensin 2 (constriction)

49
Q

Where are AT2 receptors more sensitive?

A

In the efferent arterioles

50
Q

ACEIs and ARBs exert more impact on what arterioles?

A

Efferent arterioles (which carry blood away from the glomerulus)

51
Q

When should you be cautious with ACEIs and ARBs?

A

Renal Artery Stenosis
Volume Depletion
Severe CHF
Pre-existing renal dysfunction

52
Q

What is the physiology of NSAIDs and their impact on GFR?

A

They inhibit PGE production resulting in unopposed afferent renal arteriole AT2 impact, leading to vasoconstriction.
Interfere with PGE modulated inhibition of na and Cl reabsorption

53
Q

What impact does cyclosporine have on the kidneys?

A

Causes renal vasoconstriction

54
Q

What impact to ionic contrast materials used in imaging studies have on the kidneys?

A
  1. Cause osmotic diuresis
  2. Mechanism of renal injury not well established but thought to cause direct tubular toxicity, renal ischemia, tubular obstruction
  3. Nephrotoxicity is increased in patients with CKD, DM, dehydration, high dose contrast agent
    ++ Avoid if possible in patients with decrease kidney function

Pharm (12 decks)

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