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ACVIM General Exam > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is calcineurin?

A

Calcium/calmodulin dependent PHOSPHATASE

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2
Q

Which proteins/immunoglobulins (when bound to their drug) will inhibit calcineurin?

A

Cyclophilin (Cyclosporin)
FK Binding Protein (Tacrolimus)
Macrophilin (Pimecrolimus)

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3
Q

Actions of cyclosporine

A
  1. Prevents early T cell activation
  2. Prevents synthesis of cytokines (esp. IL-2)
  3. Stimulates secretion of TGF-B
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4
Q

What are unique toxicities of cyclosporine?

A
  1. Hirsutism

2. Gingival hyperplasia

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5
Q

Azathioprine affects which phase of the cell cycle?

A

S phase

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6
Q

Azathioprine mechanism

A

Purine Analog (A, G)

  • Metabolized to ribonucleotide monophosphates (and some di or tri phosphates) → feedback inhibition of enzymes required for purine nucleotides
  • Triphosphates become incorporated into DNA and cause RNA miscoding and faulty transcription
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7
Q

Azathioprine has a greater affect on (humoral/cell mediated) immunity

A

Cell mediated

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8
Q

Side effects of azathioprine?

A
  1. BM suppression
  2. Acute pancreatitis
  3. Hepatotoxicity
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9
Q

Mycophenolate blocks which phase of the cell cycle?

A

S phase

*Non-myelotoxic

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10
Q

Mycophenolate MOA

A

Inhibits monophosphate dehydrogenase → responsible for purine synthesis

  • Inhibits lymphocyte proliferation
  • Reduces IFN-y production and auto-antibody products
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11
Q

Mycophenolate adverse effects

A
  1. GI Hemorrhage
  2. Anorexia
  3. Diarrhea
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12
Q

Leflunomide blocks which phase of the cell cycle?

A

S phase

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13
Q

Leflunomide MOA

A
  1. Inhibits dihydroorotate dehydrogenase → blocks pyrimidine synthesis
    - Inhibits T and B lymphocytes
    - Anti-proliferative effect on smooth muscle cells and fibroblasts
  2. Inhibits tyrosine kinase
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14
Q

What is the metabolite of leflunomide?

A

TMFA

  • GI effects in humans
  • Renal effects in dogs
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15
Q

What is the formula for carbonic anhydrase activity?

A

H + HCO3 -> H2CO3 -> H2O + CO2

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16
Q

What is essential for carbonic anhydrase activity?

A

Zinc

17
Q

What are the clinical uses for carbonic anhydrase inhibitors?

A
  1. Antiglaucoma agents
  2. Diuretics (weak diuretic)
  3. Decrease CSF production
18
Q

What is an important adverse event for tacrolimus?

A

Severe vasculitis

*Others include hepatic failure and intussusception

19
Q

Cyclosporine formulations: Which is better?

Neoral vs Sandimmune?

A

Neoral is better

*Sandimmune requires emulsification by bile salts

20
Q

What toxicities are associated with digoxin?

A
  1. CNS: Depression
  2. GI: Anorexia, vomiting
  3. Myocardium: Prolongation of PR interval and AV block, severe myocardial toxicity
  4. Renal failure
  5. Electrolyte abnormalities: Hyperkalemia, Hyponatremia

*Things that will exacerbate the toxicity: Hypokalemia, Hypercalcemia, Hypothyroidism, and Renal Disease

21
Q

What is a contraindication of digoxin use?

A

Ventricular arrhythmias

22
Q

Demeclocycline

  1. Class
  2. Uses
  3. AE
A
  1. Tetracycline
  2. ADH inhibitor, Used for treatment of SIADH
  3. Nephrotoxic
23
Q

Macrocyclic lactones

1. MOA

A

Irreversible opening of glutamate gated chloride channels leading to neuronal depolarization - parasitic paralysis

24
Q

Class?

1. Ivermectin, mibemycin, selamectin, moxidectan

A
  1. Macrocyclic lactones
25
Q

TMS

  1. Class
  2. Bacteriostatic/Bacteriocidal
  3. Time/Concentration Dependent
  4. MOA
  5. Targets
  6. AE
  7. Resistance
  8. BBB?
A
  1. Sulfa
  2. Bacteriostatic
  3. Time dependent
  4. Inhibition of DNA/RNA synthesis → folic acid inhibitor, purine synthesis inhibitor
  5. Gram + and Gram -, minimal effect on anaerobes
  6. Allergic reactions to sulfonamide component
  7. Resistance due to altered DHFR or DHFR overproduction
  8. Lipid soluble → penetration of BBB
26
Q

Rifampin

  1. MOA
  2. Targets
  3. AE
  4. Resistance
A
  1. Inhibits bacterial RNA polymerase → no mRNA production
  2. Intracellular bacteria (mycobacterium, brucella, bartonella)
  3. Hepatotoxicity → one of the most powerful microsomal hepatic enzyme inducers, Induces p450
  4. Resistance via RNA polymerase point mutation → resistance arises quickly when used with other drugs

ACVIM General Exam (15 decks)

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