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Renal > 15b - Renal Pharm 2 > Flashcards

15b - Renal Pharm 2 Flashcards

1
Q

What are three types of immunosuppresives?

A
  1. Calcineurin inhibitors
  2. Interleukin blockade
  3. Cell cycle regulation of T cells
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2
Q

What are two calcineurin inhibitors and how does each work?

A

Cyclosporine: binds cytosolic receptor cyclophilin in order to block activation of calcineurin

Tacrolimus: binds cytosolic receptor FKBP12 to block activation of calcineurin

Both work to inhibit transcription of cytokines such as IL-2 that are essentual for T cell activation and proliferation

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3
Q

How is cyclosporine given? What is it metabolized by? What is its half life?

A

Oral or IV

Concentrates in tissues such as the liver, kidneys, spleen, and bone marrow.

Metabolized extensively by CYP3A4 in the liver.

Long half life (27 hours)

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4
Q

What are the side effects of cyclosporine?

A
  • Nephrotoxicity
  • HTN
  • Tremor, headache, fatigue
  • Hypertrichosis
  • Gum hypertrophy (common)
  • Hyperlipidemia, hypomagnesia, hypokalemia.
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5
Q

What drug interactions does cyclosporin have?

A

Interacts with nephrotoxic drugs such as NSAIDs, aminoglycosides, and antimicrobials.

Drugs that induce CYP3A4 - phenytoin, carbamazepine (cuts down half life)

Drugs that inhibit CYPP450 - erythromycin, ketoconazole (extends half life)

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6
Q

How is tacrolimus given? How is it metabolized? What are unwanted side effects?

A

Oral or IV.

Metabolized by the liver; highly variable half life (4-41 hours) and must monitor through blood concentration.

Side effects: pleural and pericardial effisions; mardiomyopathy in kids

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7
Q

What are side effects of calcineurin inhibitors?

A
  • Hepatotoxicity
  • CV: HTN and hypercholesterolemia
  • Glucose intolerance
  • Neurotoxicity (more with tacro)
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8
Q

What are drug interactions with calcineurin inhibitors?

A
  • Nephrotoxic agents: NSAIDs, vanco, ganciclovir, aminoglycosides
  • K-sparking diuretics
  • Antacids
  • Statins
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9
Q

What is the mechanism of action of Sirolimus?

A

Binds FKBP12 and the complex binds mTOR, elading to the inhibition of IL-2 induced cell cycle progression from G1 to S phase.

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10
Q

What is the metabolism of sirolimus? How is it given? What is the half life?

A

Oral

Gut absorption by P-glycoproteins

Metabolized by intestinal and liver CYP450.

Very long half life (60 hrs)

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11
Q

What are the side effects of sirolimus?

A

Edema, ascities, tachym, HTN

GI

Lyperlipidemia, hypokalemia, hypophosphatemia

Lymphocele - collection of lymph fluid

Rash

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12
Q

What drug interactions does sirolimus have?

A

Drugs that induce CYP3A4: rifampin

Drugs that inhibit CYP450: itraconazole and ketoconazole

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13
Q

What are the benefits of using sirolimus?

A

Potent prophylaxis against acute cellular rejection.

Less vasocontriction

Not associated with acute or chronic renal insufficiency: less interstitial fibrosis (down reulation of TGF-B and PDGF), sustained GFR

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14
Q

What is the mechanism of action of mycophenolate mofetil?

A

Competitive, reversible inhibitor of IMPDH, a rate-limiting enzyme in de novo purine synthesis

Lymphocytes depend on de novo synthesis (vs other cells that can use salvage)

Inhibits proliferation of B and T lymphocytes

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15
Q

How is mycophenolate mofetil given? How is it metabolized and what’s the half life?

A

Oral or IV

Metabolized in the liver

Long half life (18 hours)

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16
Q

What are the side effects of mycophenolte mofetil?

A
  • HTN, edema, tachy
  • Dyspnea, cough
  • Dizziness, insomnia, tremor, seizures
  • Leucopenia, thrombocytopenia, anemia
  • Opportunistic infections: CMV, macterial UTI
  • lymphoproliferative disease, skin cancer
17
Q

What drugs does mycophenolate mofetil interact with?

A

Antacids, cholestyramine, sevelamer: decrease levels of mycophenolate

Rifampin, phenytoin, phenobarbital: decrease mycophenolate levels

Corticosteroids, cyclosporine: decrease levels

Tacrolimus, sirolimus: no change in MPA levels

18
Q

What is the MOA of a azothioprine?

How do its effects compare to mycophenolate mofetil?

A

Activated in the liver to 6MP then to thiosine monophosphate (TIMP)

TMP decreases synthesis of DNA precursors and incorporates into DNA; more non-specific effects than myophenolate mofetil (effects not limited to lymphoid cells).

Blocks CD28 co-stimulation of T cells.

19
Q

How is azothioprine given? what isthe half life? What are side effects?

A

Oral, short half life (3-5 hrs)

Side effects:

  • BM supression, leucopenia, thrombocytopenia
  • dizziness, GI, fever, rash, hypotension
  • opportunistic infections
  • alopecia
  • lymphomas
20
Q

What drugs interact with azathioprine?

A

Allopurinol decreases 6MP metabolism - need to reduce azathioprine dose by 75% if used together

21
Q

How do azathioprine and MMF differ in their side ffects? What are the clinical implications?

A

Azathioprine: can cause hepatitis, cholestasis, and pancreatitis

  • CBC should be performed regularly to monitor for hematologic side effects

MMF: can cause D/N/V, esophagitis, and gastritis

  • CBC regularly for hematologic side effects
  • GI side effects more common when dose exceeds 1g bid and respond to dose reduction or more frequent admin of smaller dose
22
Q

Define mouse, chimeric, humanized, and human monocloncal Abs? What is their suffix?

A

Mouse: momab: 100% moes

Chimeric: ximab: 75% human, 25% murine

Humanized: zumab: 95% human, 5% murine

Human: 100% human

23
Q

What are three IL-2 receptor antibodies?

A

Basiliximab: anti CD25 chimeric antibody

Daclizumab: anti-CD25 humanized antibody

Alemtuzumab: Anti-CD52 humanized antibody

24
Q

How is basiliximab given? What is the half life?

A

IV

very long half life (1 week)

Given immediately prior to surgery and 4 days following

25
Q

What is the MOA of belatacept? How is it given and what’s the half life?

A

Brings CD80 and CD86 to block co-stimulatory action with CD28 on T cell activation.

Used for renal transplant for pts seropotitive for Ebstein-Barr virus.

Very long half life: 8-10 days

26
Q

What are side effects of belatacept?

A

Lymphoproliferative disorder in those with no prior exposure to Ebstein-Barr virus.

27
Q

What is the MOA of prednisolone?

A

Inhibitors pro-ionflamm transcription factors such as NFkB.

Activates anti-inflamm genes by histone acetylatoin in promotors region.

Reduces T lymphocyte prolif and increases T cell apoptosis.

Reduces T cell activation and B lymphocyte proliferation.

Onset greater than 8 hours due to transcription and protein synthesis.

28
Q

What are the side effects of prednisolone? What are the clinical implications?

A

Acne, cushingoid face, hirsuitism, mood disorder, HTN, glucose intolerace, cataracts, osteoporosis, growth retardation in children.

May potentiate adverse events of calcineurin inhibitors.

29
Q

What are induction agents?

A

Monoclonal or polyclonal Abs given IV at time of surgery

Immunosuppresion to combat kidney transplant rejection

30
Q

What are maintenance agents?

A

Prednisolone, CNIs, and anti-proliferative agents

31
Q

What are 5 induction agents that are used to combat kidney transplant rejection?

A
  1. Muromonab: anti-CD3
  2. Anti-thymocyte globulin: depletes circulating lymphocytes
  3. Basiliximab: anti CD25
  4. Daclizumab: anti CD25
  5. Alemtuzumab: anti CD52
32
Q

What are the most commonly used induction agents used to combat kidney transplant rejection?

A

IL-2 receptor antibodies and T cell depleting drugs

33
Q

What is the most common therapeutic combination for immunsuppresion to combat kidney transplant rejection?

A

Tacrolimus and mycophenolate mofetil

34
Q

How do you treat IgA nephropathy, nephrotic syndome, membranous nephropathy, and focal segmental glomerulosclerosis?

A

IgA nephropathy: ACE-I

Nephrotic syndrome: ACE-I or ARB

Membranous nephropathy: ACE-I or ARB

Focal segmental: ACE-I

35
Q

In what kidney diseases can you use immunosuppressants and/or corticosteroids to treat?

A

IgA nephropathy: corticosteroids or immunosuppressants

Anti-GBM/Goodpastures: corticosteroids

Focal segmental glomerulosclerosis: corticosteroids or immunosuppressants

Lupus nephritis class V: corticosteroids (just maintains kidney function, doesn’t stop the disease)

36
Q

What is the MOA of Rituximab? What is the half life and how is it given?

A

Anti CD20 antibody for B cell targeted therapy - causes B cell depletion.

Given IV, half life ~22 days.

Resistance can occur through CD20 down-regulation.

Can treat nephrotic syndrome.

37
Q

What are the adverse effects of Rituximab?

A

Infusion site rxn: chills, fever, throat itching, urticaria, mild hypotension.

Toxicites alleviated by decreased infusion rates or antihistmines.

38
Q

What drug can treat polycystic kidney disease? What is the MOA?

A

Tolvaptan: vasopressin 2 receptor antagonist for hyponatremia in CHF and cirrhosis.

  • Lets water out but keeps sodium in, sodium levels will increase in plasma

Problem - they have to drink lots of water to suppress the progression of polycistic disease and when they get this drug they ALWAYS have to pee, and don’t sleep well because they always have to get up.

But this is VERY good for hyponatremia.

Renal (19 decks)

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