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PMCOL 200 Final > ALL DRUGS > Flashcards

ALL DRUGS Flashcards

1
Q

Acyclovir

  1. used to treat what?
  2. structure
  3. mechanism of action
A
  1. herpes
  2. nucleoside analog lacking an OH
  3. incorporated into newly synthesized DNA by thymidine kinase during replication
    DNA CHAIN TERMINATION
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2
Q

HAART

  1. what does it stand for?
  2. what does it do?
  3. what does it treat
A
  1. highly active antiretroviral therapy
  2. drug combinations that slow or reverse viral RNA load
  3. HIV
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3
Q

Maraviroc

  1. Belongs to which “class” of medications
  2. Acts on which receptor (and what other receptor neighbours it)
  3. which cell is this receptor located on?
  4. used to treat what?
  5. what does it do?
  6. what is the normal ligand for these receptors
A
  1. entry inhibitors
  2. CCR5 receptors
  3. CD4 +T cells
  4. HIV
  5. prevent HIV from binding with T-cell
  6. gp120
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4
Q

NRTI

  1. what does it stand for
  2. what is the structure
  3. mechanism of action
  4. used to treat what
A
  1. nucleoside reverse transcriptase inhibitors
  2. nucleosides lacking 3’OH
  3. chain termination
  4. HIV
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5
Q

Raltegravir

  1. what class of drugs?
  2. what does it treat?
  3. what does it do?
A
  1. integrase strand transfer inhibitors
  2. HIV
  3. block integrase from integrating HIV DNA into host DNA
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6
Q

Protease inhibitors

  1. what do they do?
  2. what do they treat?
  3. what enzyme do they affect
  4. what are they often used in combination with
A
  1. prevent maturation of HIV
  2. HIV
  3. aspartate protease
  4. reverse transcriptase inhibitors
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7
Q

Amantadine

  1. what does it treat?
  2. what does it act on?
  3. what does it prevent from being activated
  4. how long after contact should it be administered
  5. what strain is resistant to it
A
  1. influenza A ONLY
  2. acts on MH2 enzyme
  3. prevents activation of RNA transcriptase
  4. 48 hours
  5. H3N2
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8
Q

Zanamivir

  1. what does it treat
  2. what does it act on
  3. what is the normal function of the target
  4. what does it impede
A
  1. influenza A or B
  2. neuraminidases
  3. normally neuraminidases cleave sialic acid residues
  4. impedes viral spread (release)
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9
Q

5-FU

  1. class of drugs it belongs to
  2. enzyme that it effects
  3. active form
  4. what does it treat
A
  1. pyrimidine analogues
  2. thymidylate synthase
  3. FdUMP
  4. cancer
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10
Q

6-mercaptopurine

  1. mechanism
  2. class of drug
  3. what does it treat
A
  1. inhibits PRPP
  2. purine analogue
  3. cancer
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11
Q

cisplatin

  1. what does it treat
  2. what does it do?
  3. what class of drugs does it belong to
  4. during what phase of the cell cycle is it most effective
A
  1. cancer
  2. inter-strand cross-links inhibiting DNA synthesis and function
  3. alkylating agents
  4. G1 and S
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12
Q

methotrexate

  1. what does it treat?
  2. what class of drugs does it belong to?
  3. what enzyme does it effect
  4. what stage of the cell cycle is it most effective
  5. what is the usual action of this enzyme (prior to treatment with methotrexate
A
  1. cancer
  2. anti-folates
  3. dihydrofolate reductase
  4. S phase
  5. converts folic acid to FH4 cofactors requires for DNA/RNA repl.
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13
Q

Vinca Alkaloids

  1. where do they come from
  2. what do they treat
  3. mechanism of action
  4. what part of the cell cycle do they act during
A
  1. periwinkle plant
  2. cancer
  3. inhibit tubulin polymerization
  4. M
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14
Q

Paclitaxel

  1. what does it treat
  2. where does it come from
  3. what class of drug does it belong to
  4. mechanism
  5. what time in the cell cycle do they act in
A
  1. cancer
  2. pacific yew tree
  3. taxanes
  4. promote microtubule assembly
  5. M
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15
Q

camptothecin

  1. act on what
  2. what do they treat
  3. mechanism
  4. what stage of cell cycle
A
  1. topoisomerases
  2. cancer
  3. bind to topoisomerases and prevent relinkage resulting in single-stranded breaks
  4. S phase
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16
Q

Anthracyclines or DOXORUBICIN

  1. class of drug
  2. used to treat what
  3. mechanisms of action
A
  1. antibiotic
  2. cancer
  3. inhibit topoisomerases, make free radicals, bind to DNA, alter fluidity and ion transport
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17
Q

imantinib

  1. what does it treat BE SPECIFIC
  2. mechanism of action
  3. which class of drug
A
  1. cancer (leukemia)
  2. inhibits the tyrosine kinase domain of BCR-ABL
  3. tyrosine kinase inhibitors
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18
Q

cetuximab

  1. what does it treat
  2. mechanism of action
  3. which class of drug
A
  1. cancer
  2. monoclonal antibody directed against EGFR
  3. epidermal growth factor inhibitor
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19
Q

tamoxifen

  1. what does it treat
  2. mechanism
  3. class
A
  1. cancer
  2. blocks binding of estrogen to estrogen-sensitive cells in breast tissue
  3. selective estrogen receptor antagonist
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20
Q

Prednisone

  1. mechanism of action
  2. what receptor does it act on
  3. how administered
A
  1. metabolized to prenisolone (prodrug)
  2. glucocorticosteroid receptor
  3. oral/ injection
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21
Q

prednisolone

  1. receptor
  2. mechanism
A

the active form of prednisone

glucocorticosteroid receptor

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22
Q

cortisol

  1. effects on body
  2. target tissues
  3. what is it’s form prior to activation
  4. what it is activated by
A
  1. immunosuppression and catabolism
  2. adipose, muscle, liver
  3. cortisone
  4. 11beta-hydroxysteroid dehydrogenase type I in target tissues
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23
Q

hydrocortisone

  1. treatment for
  2. what is it
A
  1. addison’s disease

GC/MC supplementation

24
Q

cyclosporine

  1. type/ class of drug
  2. what function is it involved in
  3. binds to _____ in order to ____
  4. most important target effect
A
  1. calcineurin inhibitor
  2. immunosuppression
  3. binds to cyclophilin in order to inhibit NFAT mediated gene transcription
    cyclophillin/cyclosporin complex inhibits formation of calcineurin
  4. IL-2 inhibition !1!
25
Q

tacrolimus

  1. type/class of drug
  2. what physiological/pharmalogical function
  3. binds to what?
  4. binding of this does what
  5. MOST IMPORTANT effect
A
  1. calcineurin inhibiTor
  2. immunosuppression
  3. binds to FKBP
  4. inhibits calcineurin, prevents NFAT gene transcription
  5. no IL-2 produced
26
Q

rapamycin

  1. type/ class of drug
  2. physiological/ pharmalogical effect
  3. binds to what?
  4. inhibits what protein complex?
  5. effect?
A
  1. proliferation signal inhibitor
  2. immunosuppression
  3. binds to FKBP
  4. inhibits mTOR
  5. suppress cellular responses to IL2

SAME DRUG AS SIROLIMUS

27
Q

sirolimus

  1. type/ class of drug
  2. physiological/ pharmalogical effect
  3. binds to what?
  4. inhibits what protein complex?
  5. effect?
A
  1. proliferation signal inhibitor
  2. immunosuppression
  3. binds to FKBP
  4. inhibits mTOR
  5. suppress cellular responses to IL2

SAME DRUG AS RAPAMYCIN

28
Q 
cyclophospamide
1. type of drug 
2. action
3, result
4. most effective where
5. physiological function
A
  1. cytotoxic agent
  2. alkylating agent
  3. cross linking between bases, interfere with DNA rep
  4. rapidly dividing cells
  5. immunosuppression/ cancer
29
Q

azathioprine

  1. type/ class
  2. physiological function
  3. metabolized into ____
  4. mechanism
A
  1. cytotoxic agent
  2. immunosuppression/cancer
  3. 6-mercaptopurine
  4. fraudulent nucleotide, inhibiting synthesis of nucleotides
30
Q

alemtuzumab

  1. recognizes what
  2. what kind of protein + don’t forget type
  3. result
  4. physiological use
A
  1. CD52
  2. IgG1 humanized
  3. cell death of B and T cells
  4. immunosuppression
31
Q

basiliximab

  1. type of protein
  2. binds to what
  3. action
  4. physiological importance
A
  1. igG1 chimeric mouse-human
  2. CD25 on IL-2 receptor alpha chain
  3. block IL-2 from binding to activated lymphocytes
  4. immunosuppression
32
Q

levothyroxine

  1. treatment for _____
  2. synthetic version of what
A
  1. hypothyroidism

2. T4

33
Q

methimazole

  1. class of drug
  2. used to treat_____
  3. mechanism
A

thioamides
hyperthyroidism
prevent iodination and coupling steps that are mediated by thyroperoxidase

34
Q

radioactive iodine treatment

  1. function
  2. treatment of
  3. drawbacks
A
  1. radiation to destroy thyroid
  2. hyperthyroidism
  3. should not be used in pregnant women
35
Q

calcitriol

  1. treatment for
  2. how does it work
A

treatment for vitamin D deficiency

active vitamin D metabolite

36
Q

raloxifene

  1. treatment for
  2. type of drug
A
  1. osteoporosis

2. estrogen mimics

37
Q

SERM

  1. stands for what???
  2. function?
A
  1. selective estrogen receptor modulators

2. osteoperosis

38
Q

teriparatide

  1. treatment for???
  2. what is it
  3. mechanism
  4. what specific caution must be taken
A
  1. osteoperosis
  2. fully active PTH fragment
  3. acts on osteoblasts to tip the balance to osteoblastic activity
  4. proper timing and dosage
39
Q

biphosphonates

  1. mechanism
  2. treatment for
  3. effect of combining with teraperatide
  4. STRUCTUre
A
  1. inhibition of osteoclast resorption of bone
  2. osteoperosis
  3. INCONCLUSIVE
  4. 2 phosphonate groups
40
Q

alendroate

  1. mechanism
  2. treatment
A
  1. inhibiton of osteoclast resorption of bone

2. osteoperosis

41
Q

osteoprotegrin

  1. mechanism
  2. treatment
  3. how is it made/found
A
  1. RANKL scavenger, competes with RANK
  2. osteoporosis
  3. naturally occuring
42
Q

denosumab

  1. mechanism
  2. function
A
  1. monoclonal antibody againt RANKL

2. osteoperosis

43
Q

benzodiazepines

A

GABA PAM

44
Q

warfarin

  1. purpose
  2. treatment for
  3. interaction with vitamin K, why?
  4. interaction with CYP3A4
A
  1. anticoagulant
  2. treatment for blood clots , embolism, thrombosis etc
  3. antagonistic because it inhibits vit k epoxide reductase. vit k competes with it
  4. CYP3A4 breaks it down
45
Q

barbiturates

  1. what is it
  2. drug interaction significance
A

GABA PAM

synergism

46
Q

alcohol

1. drug interaction signifiance

A

GABA PAM

synergism

47
Q

zolpidem / ambien

1. drug interaction significance1

A

GABA PAM

synergism

48
Q

monoamine oxidase inhibitors

  1. action
  2. result
  3. drug interaction signicance
A
  1. block breakdown of 5HT by MAO
  2. increase in 5HT
  3. indrect, serotonin syndrome
49
Q

TRICYCLIC antidepressants, selective seratonin inhibitors, serotonin norepinephrine
1. drug interaction significance?1

A

prevent reuptake of 5HT in synaptic cleft

indrect, serotonin syndrome

50
Q

opioids

1. drug interaction signficiance

A

increase 5HT

indirect, serotonin syndrome

51
Q

MDMA , methamphetamine

1. drug interaction signifiance

A

promote serotonin release by reverse pumps

1. indirect, serotonin syndome

52
Q

St John wort

1. drug interaction significance

A

serotonin reuptake inhibitor

1. indirect serotonin syndrome

53
Q

5HTP or L-TRYPTOPHAN

1. drug interaction significance

A

antidepressants

1. indirect serotonin syndrome

54
Q

rifampicin

  1. pharmacokinetic interaction
  2. type of drug
A
  1. CYP3A4 inducer

2. antibiotic

55
Q

phenytoin, carbamazepine

  1. pharmacokinetic interaction
  2. type of drug
A
  1. CYP3A4 inducer

2. anti-convulsant

56
Q

glucocorticoid

1. effect on CYP3A4

A

inducer

57
Q

erythromycin

1. affect on CYP3A4

A

inhibitor

PMCOL 200 Final (11 decks)

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