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Renal > Renal Pharmacology > Flashcards

Renal Pharmacology Flashcards

1
Q

What are four medical treatments associated with acute kidney injury?

A

Antibiotics, chemotherapy and radiocontrast dyes, thoracic surgery

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2
Q

Chronic kidney diseases develops in __ - __% of acute kidney injury survivers?

A

20-30%

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3
Q

What are some drugs on the market for treating acute kidney injury (AKI)?

A

there are none

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4
Q

What can cause renal ischemia-reperfusion in AKI?

A

Arterial occlusion

Hypotension

Shock

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5
Q

In AKI, renal iscemia-reperfusion can lead to…?

A
  • Microvascular dysfunction
  • Excess vasoconstriction
  • Inflammation, oxidative stress
  • Endothelial injury
  • Endothelial-leukocyte interactions
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6
Q

Acute Kidney Injury - emerging pharmacological agents

Anti apoptotic:

Anti-inflammatory:

Anti-Sepsis:

Growth factor:

Vasodilator:

A

Anti apoptotic: capsase inhibitors, minocycline

Anti-inflammatory: adenosine A2A agonist

Anti-Sepsis: Insulin

Growth factor: Recombinant erythropoietin

Vasodilator: Fenoldopam, ANP

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7
Q

What are the two most common causes of CKD?

A

Diabetic Nephropathy and Hypertension

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8
Q

What GFR is associated with each stage of CKD?

Stage 1:

Stage 2:

Stage 3:

Stage 4:

Stage 5:

A

Stage 1: ≥ 90

Stage 2: 60 - 89

Stage 3: 30-59

Stage 4: 15-29

Stage 5: <15

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9
Q

What is the goal of treatment for CKD?

A

Inhibit the renin angiotensin system

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10
Q

What function to ACEi and ARBs serve in CKD?

A
  • Decrease progression of albuminuria
  • Decrease progression of GFR decline
  • Decrease risk of ESRD
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11
Q

Why don’t you take NSAIDs with CKD?

A

Damage kidneys further

May interact with ACEi or ARB

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12
Q

In CKD are ACEi and ARBs more effective together or separately?

A

Combination therapy tends to work better, but is still controversial

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13
Q

What are the three management goals in diabetic nephropathy?

A

Good glycemic control (HbA1c < 7%)

Blood pressure control (< 140/90 mmHg)

Medications to minimize proteinuria (ACEi and ARB)

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14
Q

What are two upcoming treatments to combat CKD?

A

Bardoxolone - halted due to safety concerns

EET analogs - pending approval

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15
Q

Anema is most prevalent in which stages of CKD?

A

4-5

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16
Q

What are the symptoms and causes of anemia in CKD?

A

Symptoms: fatigue and decreased cognition

Causes: decrease in release of erythropoietin

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17
Q
  1. What is Epoetin?
  2. How is it administered?
  3. What is it’s half life?
A
  1. A human recombinant synthesized form of erythropoietin
  2. IV (more rapid response) and SubQ (greater response)
  3. 4-6 hour half life
18
Q

What are the unwanted side effects of Epoetin?

A
  • Nausea, vomiting, diarrhea
  • Headache
  • Flu-like symptoms
  • HTN
  • Thrombosis of arteriovenous shunts (Increased RBCs)
19
Q

What are the physiological roles of calcium?

A
  • Nerve conduction and regulation of cell membrane permeability
  • Excitation and coupling of all types of muscles
  • Secretion of endocrine and exocrine glands and release of neurotransmitters
  • Intracellular messenger
  • Impulse generation in the heart
  • Coagulation of blood
  • Bones and teeth
20
Q

What 3 hormones regulate plasma calcium?

A

Parathyroid hormone

Calcitonin

Calcitriol

21
Q

Of the calcium in the plasma, what percentage is bound to albumin?

Does hypoalbuminemia cause a decrease in calcium concentration?

A

40% (50% is free ionized and important form)

no decrease

22
Q

What form of plasma calcium is favored in acidosis?

A

Free ionized form

23
Q

How does Kidney failure affect calcium levels?

A

In kidney failure there is decreased renal excretion of phosphate and diminished production of calcitrol leading to decrease in plasma calcium

24
Q

How does Kidney failure lead to metabolic bone disease and soft tissue calcifications?

A

Increased phorphate and reduced calcium feeeback can lead to Secondary Hyperparathyroidism which leads to metabolic bone disease and soft tissue calcifications

25
Q

What are the major factors leading to an increase in PTH and secondary hyperparathyroidism?

A

Decreased production of Vitamin D3 (calcitriol)

Decreased serum calcium

Increased serum phosphorous

26
Q

What modifications are made in each generation of Vitamin D analogs?

A

1st gen: Synthetic form of endogenous Vitamin D

2nd gen: Side chain modifications

3rd gen: A-ring modifications (paricalcitol)

27
Q

What is the MOA of Vitamin D analogs?

A
  • Enhancement of absorption of calcium and phosphate from intestine
  • Enhances recruitment and differentiation of osteoclast precursor for remodeling-resorption of calcium and phosphate from bone
  • Enhances renal tubular reabsorption of calcium
28
Q

Which Vitamin D analog requires kidney 1-α hydroxylation?

A

Ergocalciferol

29
Q

What Vitamin D analogs are used in kidney disease?

What is their half life?

A

Hydroxylated active forms of alfacalcidol or calcitrol (short half lives - 3 hours)

30
Q

Which vitamin D analog requires IV injections?

A

Paricalcitol

31
Q

What are the signs of vitamin D deficiency?

At what stages of CKD are vitamin D analogs indicated?

A
  • Fractures
  • Hyperparathyroidism

Indicated at stage 3 if Ca < 9.5 and P <4.6

Always indicated at stage 4

32
Q

What are the phosphate binders and how do they work?

A

Calcium carbonate, calcium acetate, lanthanum carbonate

Decrease phosphate absorption by reacting with phosphate to form an insoluble compound

33
Q

What are side effects of phosphate binders?

A

GI side effects

hypercalcemia

34
Q

How can renal transplant cause hypercalcemia?

A

Patients already have high levels of PTH due to previous renal failure so addition of functioning kidney leads to extremely high plasma calcium levels

35
Q

What is the function of bisphosphonates in hypercalcemia?

Which is the most long lasting?

A

Pyrophosphate analogs that bind to hydroxyapatite crystals in bone matrix to inhibit bone resorption

Zoledondrate can suppress bone resorption for up to a year after a single dose

36
Q

What are the three generations of Bisphosphonates?

A
  • First gen:
    • Etidronate
    • Tiludronate
  • 2nd gen:
    • Pamidronate
    • Aledronate
    • Ibadronate
  • 3rd gen:
    • Risedronate
    • Zoledronate
37
Q

What is the function of calcitonin?

A

Produced by parafollicular cells of thyroid gland

Secreted when plasma calcium rises

Lowers plasma calcium by limiting bone resorption and increasing phosphate excretion in the urine

38
Q

What are some unwanted side effects of calcitonin?

A

Facial flushing

Headache

GI

Taste disturbance

39
Q

How do you treat hyperuricemia and gout in kidney disease?

A

Colchicine

Allopurinol

Febuxostat

Rasburicase

40
Q

Colchicine:

onset of action?

Side effects?

A

Onset: pain relief begins at about 18 hours and is maximal by 48 hours

SE: GI, Rash

41
Q

What are the SE of the Xanthine Oxidase Inhibitors (Allopurinol and Febuxostat)?

A
  • GI Upset
  • Risk of acute gout
  • Hypersensitivity (Allopurinol)
  • Drug interactions
42
Q

How does rasburicase work?

What are its SE?

A
  • Recombinant version of enzyme urate oxidase
    • Promotes uric acid conversion to allantoin
  • Metabolized by peptide hydrolysis in plasma
  • Used primarily as prophylaxis during chemotherapy

SE: Fever, nausea, vomiting, hypersensitivity, hemolysis

Renal (17 decks)

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