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ECVECC Board Exam > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Define effective dose (ED50).

A

The dose of drug needed to induce the desired effect in 50% of the animals to which it is administered.

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2
Q

Define potency.

A

The concentration of the drug needed to achieve a pharmacological effect equal to 50% of Emax.

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3
Q

Define toxic dose (TD50).

A

The dose of a drug needed to induce toxic effect in 50% of the animals to which it is administered.

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4
Q

Define therapeutic index

A

TD50/ED50

The higher the therapeutic index, the safer the drug is considered to be.

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5
Q

What is the difference between zero order kinetics and first order kinetics?

A

Zero order kinetics: a constant amount of drug is being eliminated per unit time
First order kinetics: a constant proportion of drug is being eliminated per unit time

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6
Q

After you change the dose of a drug, how many half-lives are required for the new steady serum concentration to be achieved?

A

4-5 half-lives

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7
Q

After you stop a drug, how many half-lives are required for the drug to be fully eliminated from the body?

A

4-5 half-lives

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8
Q

What is the formula for loading dose calculation using desired concentration and volume of distribution?

A

Loading dose = Desired concentration x the volume of “central compartment”

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9
Q

Define first pass effect.

A

When the drug is given in different route (e.g. PO), the drug may be metabolized at certain location (most commonly liver) before reaching to the site of action and therefore the concentration of active drug is reduced.

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10
Q

Dose IV route always mean 100% bioavailability?

A

No. If a drug can be eliminated via the lung, the bioavailability may not be 100%.

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11
Q

Which phase of biotransformation does cytochrome P450 mainly involve?

A

Phase I

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12
Q

What is phase II biotransformation also called?

A

Conjugation phase

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13
Q

What are the 4 pathways of acetaminophen metabolism?

A

1) Sulfuric acid conjugation → bile & urine
2) Glucuronidation → bile & urine
3) Transformed and oxidized by cytochrome P450 system to NAPQI (toxic!!!) → react with glutathione to form mercapturic acid → urine
4) deacylation by hepatic microsomal carboxyesterases → para-Aminophenol (PAP) → conjugated with glutathione, sulfation, biotransformation through N-acetylation with N-acetyltransferase (NAT)

  • Cats cannot do 2) because they don’t have glucuronyl transferase
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14
Q

What is isoproterenol?

A

Non-selective 𝜷 agonist

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15
Q

What is the MOA of Dantrolene?

A

Bind to the ryanodine receptor to depress excitation-contraction coupling in skeletal muscle.

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16
Q

Fill out the blank:
The minimum inhibitory concentration (MIC) is defined as “the lowest concentration of an antibiotic that will __________ of a given bacteria.”

A

inhibit the visible growth

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17
Q

Fill out the blank: MDR organism is defined as the microorganism that acquired non-susceptibility to _________.

A

At least one agent in three or more antimicrobial categories

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18
Q

Fill out the blank: Extensively drug-resistance (XDR) organism is defined as the microorganism that acquired non-susceptibility to _________.

A

At least one agent in all but two or fewer antimicrobial categories

19
Q

What is the organism called if it shows non-susceptibility to all agents in all antimicrobial categories?

A

Pandrug-resistant (PDR)

20
Q

For canine skin infection, the CLSI has determined the Staphylococcus pseudointermedius has a breakpoint of ≤ 0.25 mg/L for susceptible and > 0.5 mg/L for resistant, based on oral amoxicillin. If you performed a pyoderma bacterial culture and found the MIC was 1 mg/dL, would you say this patient’s pyoderma is susceptible or resistant to oral amoxicillin?

A

Resistant

Because MIC > resistant breakpoint

21
Q

What is MOA of Nitrofurantoin?

A

Nitrofurantoin is taken up by bacterial intracellular flavoproteins → reduce nitrofurantoin to reactive intermediates → binds to bacterial DNA & RNA and inhibits their synthesis

22
Q

How does glucocorticoids decrease high calcium level?

A

1) Inhibition of osteoclast-activating factor, prostaglandins, and vitamin D
2)Promoting calciuresis

23
Q

What is MOA of Bisphosphonates?

A

promoting osteoclast apoptosis → decrease bone reabsorption

24
Q

What is the relative minerocorticoid and glucocorticoid activity for hydrocortisone, prednisone, methylpredinisolone and dexamethasone?

A

MC:GC (compared to cortisol)
Hydrocortisone = 0.8:1
Prednisone = 1:4
Methylpredinisolone = 0:5
Dexamethasone = 0:30

25
Q

True or False: Dexamethasone’s GC effect is more potent than prednisone.

A

True

26
Q

What is the difference between prednisone and prednisolone?

A

Prednisone is biologically inactive, and need to be converted into prednisolone in the liver to be active.

27
Q

Fill out the blank: cats require ______ times as much prednisone compared to prednisolone to achieve equivalent biologic effects.

A

3-5

28
Q

What is the difference between dexamethasone and dexamethasone SP (sodium phosphate)?

A

Dexamethasone is free alcohol
dexamethasone SP is water-soluble ester

Both can be given as IV or IM, but IV dexamethasone may cause hypotension, hemolysis, collapse, CNS signs or seizure if giving too fast
→ low volume and slow infusion rate!

29
Q

True or False: Glucocorticoid can inhibit the transcription of inducible NO synthase and prevent vasodilatory effect from NO.

A

True

30
Q

What does glucocorticoid do at inflammatory dose and immunosuppression dose?

A

Anti-inflammatory doses:
- inhibit phospholipase A2 (and further inhibit COX & LOX pathway) and the release of proinflammatory cytokines
- stabilize granulocyte cell membranes

Immunosuppressive doses:
- target macrophage function by down regulating Fc receptor expression
- decreasing responsiveness to antibody-sensitized cell and decreasing antigen processing

31
Q

What is mycophenolate mofetil (MMF) converted to?

A

Mycophenolic acid

  • Undergo enterohepatic recirculation; highly protein-bound
32
Q

How does mycophenolate mofetil (MMF) exhibit its immunosuppressive effect?

A

mycophenolate mofetil converts to Mycophenolic acid → reversibly inhibit IMPDH II → inhibit nucleotide guanine (a type of purine) synthesis → inhibit B & T lymphocytes synthesis

33
Q

What is the common side effects for mycophenolate mofetil (MMF)?

A

GI signs (especially diarrhea)
Myelosuppression (uncommon)
Hepatic toxicity (uncommon)

34
Q

What is the MOA of cyclosporin?

A
  • Calcineurin inhibitor
    Cyclosporine binds to cytoplasmic cyclophilin → cyclosporine-cyclophilin complex → this complex binds and blocks the function of calcineurin → inhibit the dephosphorylation of nuclear factor of activated T cells (NFAT) → prevent gene transcription for T cell activation
  • Decreased expression of IL-2, IL-3, IL-4, TNF-𝜶, INF-𝛄
  • Alter the function of granulocytes, macrophages, NK cells, eosinophils and mast cells
35
Q

Which immunosuppressant does not cause myelosuppression?
1) Prednisone
2) Mycophenolate
3) Cyclosporin
4) Azathioprine

A

3) Cyclosporin

36
Q

List 3 side-effects from cyclosporin.

A

1) Gingival hyperplasia
2) GI upset
3) Hepatotoxicity
4) Lymphoproliferative disorders
5) Anaphylaxis
6) Thromboembolic complications

37
Q

True or False: When cyclosporin is used with azole antifungal drug, its metabolism can slow down due to competitive binding of cytochrome P450.

A

True

38
Q

In veterinary medicine, what is the target trough serum concentration of cyclosporin?

A

400-600 ng/mL

39
Q

What is MOA of azathioprine?

A
  • Azathioprine is converted to 6-mercaptopurine (6-MP) → 6-MP generates 6-thioguanine nucleotides (6-TGNs) → 6-TGNs compete with endogenous purines for incorporation into RNA and DNA → create nonfunctional DNA and RNA & disrupt DNA and RNA synthesis and mitosis → inhibit lymphocyte proliferation
  • Also inhibits IMPDH
  • Avoid in cats
40
Q

Name 3 side effects from azathioprine.

A

1) Myelosuppression
2) GI signs
3) Hepatic necrosis
4) Pancreatitis

41
Q

Calculate Vd

A

Vd = total amount of drug in the body (mg) / plasma concentration of the drug (mg/L)

42
Q

Maintenance rate CRI formula

A
43
Q

Define ARC

A

Augmented Renal Clearance
condition seen in a subset of critically ill patients (i.e. septic) in which the renal clearance of certain drugs is significantly increased.
Drugs mostly affected are antibiotics, enoxaparin and levetiracetam.
ARC can be estimated by calculating creatinine clearance overnight: Ucrea x Vurine / Pcrea

44
Q

Pathophysiology of ARC

A
  • Hyperdynamic state
  • Glomerular vasodilation due to increased synthesis of L-arginine and NO
  • Recruitment of renal functional reserve due to systemic stress
  • Catabolic state = increased protein load = further recruitemnt of renal functional reserve
  • Increased tubular secretion (particularly important for antimicrobials (i.e. beta lactams)
  • Aggressive IVFT

ECVECC Board Exam (24 decks)

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