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Renal > 15 - Renal Pharm > Flashcards

15 - Renal Pharm Flashcards

1
Q

There’s a high incidence of acute kidney injury in patients recieving which drugs?

A

Antibiotics (aminoglycosides), chemotherapy, or radiocontrast dyes.

It’s also a complication of thoracic surgury.

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2
Q

What drugs can be used to treat acute kidney injury?

A

There are currently no drugs on the market to treat acute kidney injury.

Some are in clinical trials - primarily for thoracic surgery and radiocontrast dye AKI.

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3
Q

What are the main causes of chronic kidney disease?

A
  • Diabetic nephropathy
  • HTN
  • Glomerulonephritis
  • Reflex nephropathy in kids
  • Polycystic kidney disease
  • Infections and obstructions
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4
Q

What is the main treatment for CKD?

A

Renin-angiotensin system inhibitors (ACE-I’s and ARBs):

  • decrease progression of albumineria
  • decrease progression of GFR decline
  • decrease risk of ESRD

Benefit in part due to BP reduction.

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5
Q

What medication damages the kidneys further and may interact with ACE inhibitors and angiotensin receptor antagonists?

A

NSAIDs

They inhibit the dilation of the afferent arteriole by inhibiting prostaglandins.

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6
Q

How should diabetic nephropathy be treated?

A

Manage the primary disorder via good glycemic control (HbA1c <7%)

Blood pressure control (<140-90)

Minimize proteinuria with ACEI and ARB

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7
Q

Why do people with chronic kidney disease (specifically in the later stages (3-5) develop anemia?

A

Erythropoietin is a hormone produced primarily in the kidney

  • Regulates RBC production by reducing apoptosis and stimulates differentiation/proliferation of erythroid progenitors

When the kidneys don’t work you can’t make erythropoietin

Decificncy in ESRD.

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8
Q

What are symptoms of anemia in CKD? What is the cause?

A

Fatigue and decreased cognition due to the decreased production in RBCs.

This is because erythropoietin cannot be released in response to hypoxia in endothelial cells of the peritubular capillaries due to kidney damage.

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9
Q

How can you treat anemia in CKD? How is this med given? How long does it last?

A

Epoetin

IV or subQ - more rapid with IV but greater response with subQ

Half life 4-6 hours; given 2-3 times/week

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10
Q

What are the unwanted side effects of Epoetin?

A
  • n/v/d
  • Headache
  • Influenza-like symptoms
  • HTN - dose dependent (can be severe and lead to encepalopathy/seizures)
  • Thrombosis of AV shunts
  • Pure red cell aplasia with subQ admin in renal failure: associated with antibodies to epoetin (must stop treatment)
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11
Q

How does CKD impact calcium and phosphate levels?

A

CKD causes reduced renal phosphorous clearance causing hyperphosphatemia and increases FBF-23.

These lead to reduced 1,25 (OH)2 vitD which causes hypocalcemia and this secondary hyperparathyroidism.

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12
Q

What are the CV consequences of hyperphosphetemia nad elevated FGF-23 seen in CKD?

A

High FGF-23 leads to LVH and congestive heart failure.

Hyperphosphotemia causes endothelial dysfunction and atherosclerosis/valvular disease.

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13
Q

What is the physiological important of calcium?

A
  • Excitability of nerves and muscles and regulates permeabiltiy of cell membranes
  • Essential for excitation and couples of all types of muscles
  • Endocrine and exocrine release of nts from nerve endings
  • Intracellular messenger for hormones, autocoids, and transmitters
  • Coagulation of blood
  • Structural funciton in bone and teeth
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14
Q

Plasma calcium is regulated by what three hormones? What is a normal plasma level of calcium and what forms is it found in?

A

Parathyroid hormone, calcitonin, and calcitrol (active VitD).

Normal plasma level: 9-11 mg/dl

40% bound to albumin

10% citract, carbonate and phosphate

50% is free ionized form (active form)

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15
Q

Acidosis and alkalosis favor what in terms of calcium?

A

Acidosis favors ionization of calcium (free active form)

Alkalosis disfavors ionization - hyperventilation precipitates tetany (muscle spasms) and laryngospasm in calcium deficiency

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16
Q

What effect does kidney failure have on calcium and phosphate balance?

A
  • Decreased production of Vit D3 (calcitriol)
  • Decreased serum calcium
  • Increased serum phosphorous

This leads to secondary hyperparathyroidism

  • Can lead to metabolic bone disease, soft tissue calcifications
17
Q

What is the mechanism of calcitriol and vitamin D analogs?

A
  1. Enhance the absorption of Ca and PO4 from the intestines by increaseing the synthesis of calcium channels and a carrier CaBP.
  2. Activates VitD receptor (VDR) to promote endocytotic capture of calcium and transport across the duodenal mucosa.
  3. Also enhances recruitment and differentiation of osteoclast precursors for remodeling to increase resorption of Ca and PPO4 from bone.
18
Q

What is the negative side of calcitriol?

A

It increases intestinal absorption of calcium and phosphate and increases calcium and phosphate mobilization from bone.

Calcitriol can thus result in hypercalcemia and hyperphosphatemia.

2nd and 3rd generation VitD analops have more affinity to the kidney and lower incidence of hypercalcemia and hyperphophatemia and better PTH control.

19
Q

What are the 1st, 2nd, and 3rd generation vitamin d analogs?

A

1st gen: calcitriol (synthetic form of endogenous VitD)

2nd gen: alfacidol, doxercalciferol, maxicalcitol

3rd gen: paricalcitol

20
Q

What vitamin D analog requires 1-a-hydroxylation in the kidney to be active? Which don’t require activation and can be used in kidney disease?

A

Requires hydroxylation to be activated: ergocalciferol

Don’t need to be activated and can be used in kidney disease: alfacalcidol or calcitriol - these also have a short half life (3hrs)

21
Q

Which vitamin D analog requires IV injections? What are the unwanted effects of vitamin D analogs and calcitriol?

A

Paricalcitol: needs IV injection

Unwanted effect: excessive dosing leads to hypercalcemia

22
Q

What are signs of 1,25 hydroxyvitamin D (calcitriol) deficiency in CKD? How would you treat this?

A

Fractures (esp in elderly) and hyperparathyroidism (secondary)

Treat with calcitriol and paricalcitol.

23
Q

What drugs are phosphate binders? How do they work?

A
  • Calcium carbonate
  • Calcium acetate
  • Lanthanum carbonate
  • Sevelamer -calcium and aluminum free structure

React with phosphate and form an insoluble compound so phophsate doesn’t get absorbed from the GI tract.

24
Q

What are side effects of phosphate binders?

A

GI effects and hypercalcemia.

25
Q

Why can prolonged kidney disease be associated with hypercalcemia?

A

Renal transplant pts can have parathyroid hyperplasia and once they get a transplant, their renal function is restored and calcitriol production can lead to hypercalcemia.

Ie the hyperplasia remains when you have your new kidney, so you’re making WAY too much PTH and thus you absorb a ton of calcium causing hypercalcemia.

26
Q

What drugs can treat hypercalcemia specifically? Name the first and third generation meds? Which are more potent?

A

Bisphosphonates treat hypercalemia

First gen: Etidronate (less potent)

Third gen: Zoledronate (much more potent)

27
Q

What is the function of bisphosphonates? How long do they last?

A

Bind hydroxyapatite crystals in mone to inhibit bone resorption (ie they hold calcium in bones)

Short-lived and given weekly (except Zoledronate can work up to 1 year after single dose)

Excreted by kidneys.

28
Q

What are adverse effects of bisphosphonates?

A

GI disturbances

Osteonecrosis of jaw

29
Q

What makes calcitonin and when is it made? How long does it last when given?

A

Parafollicular or C cells of thyroid gland.

Secreted when plasma calcium levels rise to lower plasma calcium by limiting bone resorption and increasing phosphate excretion in urine.

IM or subQ: 1/2 life ~20 min

30
Q

What are unwanted side effects of calcitonin?

A
  • Facial flushing
  • Headaches/dizziness
  • N/V/D
  • Taste disturbanes
31
Q

How do the kidneys hangle uric acid?

A

Kidneys eliminate uric acid from plasma; 8-12% of uric acid filtered load is excreted.

32
Q

What gout medication works by inhibiting mts? How often is it given and what are adverse effects?

A

Colchicine - oral

  • Reduces inflammation
  • Given every 6-12 hrs to relieve symptoms (pain relief begins at 18hrs and is maximal by 48 hours)
  • Side effects: GI toxicity and rash
33
Q

What xanthine oxidase competitive inhibitors can be used to treat gout? What is their half life and adverse effects?

A

Allopurinol (purine) and feboxustate (non-purine)

Half life 1-15 hours with renal excretion.

Side effects: GI upset, risk of acute gout (release of uric acid from tissue deposits), hypersensitivity to allopurinol, drug interactions (inhibits metabolism of azathioprine).

34
Q

What is the function of Rasburicase?

A

IV recombinant enzuyme of urate oxidase - metabolizerd by peptide hydrolysis in plasma.

Used as prophylaxis during chemo to prevent gout.

35
Q

What are the side effects of Rasburicase?

A
  • Fever
  • N/V/D
  • Hypersensitivity
  • Hemolysis due to hydrogen peroxide production as byproduct of allantoin
36
Q

What are the causes of death after kidney transplantation?

A

CVD, infection, malignancy (skin cancer), other.

37
Q

What are three causes of kidney transplant rejection?

A
  • Ischemia-reperfusion injury
  • T cell mediated rejection (most common)
  • Antibody-mediated rejection
38
Q
A

Renal (19 decks)

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