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Pharm Exam 3 > Drugs (ALL) > Flashcards

Drugs (ALL) Flashcards

1
Q

Disulfiram

A

used for substance abuse with alcohol
causes unpleasant run if alcohol is consumed
but no s/s if no alcohol is not consumed

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2
Q

Naltrexone

A

used in substance abuse with alcohol
used as a opiod antagonist = blocks euphoria!
in both cases = blocks the measurable effects of the substances

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3
Q

Acamprosate

A

pharm for maintaining abstinence with alcohol

reduces some of the unpleasant feelings with abstinence

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4
Q

Nicotine replacement therapy

A

we want to substitute cigarettes with a pharmaceutical source nd then you gradually withdraw the nicotine

similar to how methadone used for heoin addicts

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5
Q

bupropion

A

dealing with smoking abstinence
atypical antidepressants and is structurally different to amphetamine
helps by reducing cravings

DO NOT USE with MAOI

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6
Q

Varenicline

A

smoking abstinence
partial nicotine agonist
most effective aid in smoking cessation
promotes the release of DA so it is pleasurable

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7
Q

Methadone

A

opioid agonist
opioid abuse treatment/ abstinence
longer 1/2 life with less euphoria

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8
Q

Buprenorphine

A

opioid agonist/ antagonist
partial mu agonist ad kappa antagonist which helps alleviate the cravings
can be used for abstinence treatment

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9
Q

Flumazenil

A

this is the antidote for Benzos
dealing with benzo. and the pharm of abstinence maintenance
you taper off the drug slowly over. few months

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10
Q

FGA

A

first generation conventional antipsychotics
these are cheaper
more extrapyramidal side effects (tar dive dyskensias) = Parkinson like symptoms (because think about how the mechanism of this drug is to block dopamine)

NO to Parkinson’s patients on these drugs

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11
Q

neuroleptics

A

AKA FGA

a type of first generation anti psychotic

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12
Q

SGA

A

second generation antipsychotic (atypical)
more expensive
more metabolic effects seen –> weight gain etc.
risk for CV events and premature death

NO to alziemers patients taking

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13
Q

Chlorpromazine

A

first generation antipsychotic that is low potency

AE = sedation, orthostatic hypotension, anticholinergic side effects
Occasionally causes photosensitivity reactions & neuroendocrine effects
Prolongs QT interval

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14
Q

Haloperidol

A

H = HIGH
high potency FGA

**** Generally preferred for initial therapy
EPS symptoms earlier in txn 
Lower frequency of all other AE
Prolongs QT interval
Cheaper
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15
Q

Selective serotonin reuptake inhibitors (SSRIs)

A

MOA = blocks the reuptake of 5 - HT and thus increases the concentration in the synapses

since only blocks 5 - HT there less side effects

AE:
Nausea
Agitation/insomnia
Sexual dysfunction
Weight gain
Decreased platelet aggregation (still low risk)
Serotonin syndrome (usually in 1st 3 days of tx)
Withdrawal syndrome w/ abrupt d/c (taper)
In late pregnancy: withdrawal & pHTN in the newborn

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16
Q

Fluoxetine

A

a type of SSRI that is the prototype

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17
Q

Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs)

A

similar mechanism as SSRI

not as safe as SSRI
MAIN AE = dose related hypertension

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18
Q

venlafaxine

A

SNRI prototype

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19
Q

Tricyclic Antidepressants (TCAs)

A

both a 5-HT and NE reuptake inhibitor

Not very selective!
Also can impact histamine/H receptors, ACh/M receptors, and various others

AE (d/t H & M receptors): 
Orthostatic hypotensio
Anticholinergic effects
Sedation
**cardiac toxicity**
Seizure risk
Suicide risk
Toxicity = dysrhythmias, heart block
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20
Q

Amitriptyline

A

TCA

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21
Q

Monoamine Oxidase Inhibitors (MAOIs)

A

Mechanism: inhibition of MAO (liver/intestine)

  • -> Decreased breakdown of NE, 5-HT, DA
  • -> MAO also breaks down tyramine
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22
Q

Nonselective MAOI

A

deals with both MAOI - A and MAOI - B

leads to =
Increase in 5-HT, NE, DA
Breaks down tyramine

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23
Q

MAOI B (selective MAOI)

A

leads to an increase in DA

  • -> Selegiline
  • -> Rasagiline

Parkinson treatment as well

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24
Q

Bupropion

A

atypical antidepressant

Mechanism unclear, may be d/t DA/NE reuptake block
-No effect on ACh, 5-HT, or H

Adverse:

  • Agitation, tremor, insomnia; seizures in high doses
  • Weight loss
  • Agitation
  • GI upset, constipation

**No weight gain or sexual dysfunction issues! ***

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25
Q

Lithium

A

mood stabilizer connected to bipolar disorder

MOA: unclear
PK: PO. Short ½ life (rapid renal excretion)
Must be administered multiple times per day
Caution in renal disease
Renal excretion is affected by [Na+]

VERY LOW THERAPEUTIC INDEX!!!!
MUST MONITOR DRUG LEVELS
Goal range = 0.4-1mEq/L
ideally 0.6-0.8mEq/L).

no treatment for overdose!

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26
Q

Valproate (bipolar considerations:)

A

traditional antiseizure medication

undersand can be used to help with modo stabilizing as well

Valproate has largely replaced lithium as drug of choice
Faster onset & greater margin of safety
Lithium is better at reducing suicide risk & relapses

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27
Q

carbamazepine (bipolar considerations)

A

a traditional antiseizure medication

can also be used as a mood stabilizer for bipolar

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28
Q

Benzodiazepines

A

Mechanism: potentiation of GABA (ceiling effect exists)

PK: highly lipid soluble (easy BBB crossing)
Hepatic metabolism w/ active metabolites (most)

Adverse: 
CNS depression 
Anterograde amnesia
Can have paradoxical effects
PO dosing: minimal resp depression, minimal CV effects
Teratogenic (avoid in pregnancy)

can be used for INSOMNIA!!!!

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29
Q

Zolpidem

A

Benzo like drugs –>
All act as agonists at GABA receptor
All are schedule IV

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30
Q

Ramelteon

A

melatonin agonist
The only sleep aid that isn’t a controlled substance!!!

Rapid onset, short DOA = helpful for falling asleep, not staying asleep
15x more potent at melatonin receptor than melatonin itself
Melatonin usually secreted along w/ circadian rhythm (darkness/environmental light)

AE: no notable. No physical dependence/abuse

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31
Q

Suvorexant

A

Orexin antagonist –>
Orexin = promotes wakefulness

Used for sleep onset & sleep maintenance issues

AE: 
somnolence, dizziness
HA
Dry mouth, cough
Physical dependence/tolerance (schedule IV)

Caution with OSA/COPD

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32
Q

Barbiturates

A

Mechanism: agonize GABA receptor directly
NO CEILING EFFECT TO SEDATION/RESP DEPRESSION

AE: 
Respiratory depression  death
Sedation  general anesthesia
Minimal CV effects at hypnotic doses
CYP450 induction 
Tolerance & physical dependence (schedule III)
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33
Q

buspirone

A

anxiety treatment
Mechanism: not well established
Binds 5-HT receptors, less so to DA receptors
No GABA effects

As effective as benzos, but no abuse potential/CNS depressant interactions
Anxiolysis develops slowly (weeks)

PK: PO, hepatic metabolism (CYP450), renal elimination
Caution w/ CYP450 inducers/inhibitors (+grapefruit juice)

AE: minimal even in large doses. Dizziness, nausea, HA

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34
Q

CNS Stimulation

A

Different from antidepressants in that they cannot elevate mood w/ CNS excitation
At high enough doses, all can cause seizures

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35
Q

Amphetamines

A

CNS stimulation for ADHD
think this is adder all

Cause release of NE & DA, partially inhibit their reuptake
-Actions CNS & PNS
Adverse:
-CNS: insomnia, restlessness, euphoria, talkativeness, appetite suppression
-CV: tachycardia, increased contractility, vasoconstriction à dysrhythmias, HTN
-Psychosis w/ excessive use

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36
Q

Methylxanthines

A

CNS stimulation for ADHD

think this is caffeine

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37
Q

Modafinil

A

CNS stimulant for ADHD

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38
Q

MMR vaccine

A

Live virus

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39
Q

L- Dopa

A

thinking about Parkinson’s and the want to increase dopamine

  • directly activates DA receptors
  • SO this is a prodrug that needs to be converted to DA in the CNS BUT in order to do this we need to avoid three things (see below)
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40
Q

carbidopa

A

Decarboxylase inhibitors needed to go with the L- Dopa

needed in order for L dopa to directly activates DA receptors

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41
Q

entacapone

A

COMT inhibitors

need in order to allow L dopa to work

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42
Q

MAO-B inhibitors

A

in normal states = MAO B will break down dopamine
so in those with Parkinson’s who want to inhibit MAO B in order to have more circulating dopamine
we use this drug in mild to moderate cases

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43
Q

Selegiline

A

MAO B inhibitor

44
Q

rasagiline

A

MAO B inhibitor

45
Q

Amantadine

A

Parkinsons and dopamine agonist

*promotes DA release and inhibits reuptake

46
Q

Dopamine agonists

A

*NON ergot alkaloid = SELECTIVE DA receptor
Act like dopamine
Less effective then L-Dopa BUT less risk of dyskinesia

47
Q

Pramipexole

A

dopamine agonist

less effective then L Dopa but less risk of tarditive dyskinesia

48
Q

Ropinirole

A

dopamine agonist

less effective then L Dopa but less risk of tarditive dyskinesia

49
Q

Rotigotine

A

dopamine agonist

less effective then L Dopa but less risk of tarditive dyskinesia

50
Q

apomorphine

A

dopamine agonist

less effective then L Dopa but less risk of tarditive dyskinesia

51
Q

benzotropine

A

anticholinergic drug for Parkinson’s
Second line drug for tremor
Less effective than L-dopa or DA agonists
Better tolerated

AE
CNS (sedation, confusion, hallucinations)
Peripheral (anticholinergic effects)

52
Q

Cholinesterase inhibitors (AChE inhibitors)

A

in alziemers patients, ACH is 90% less then in normal patients so want to inhibit the break down

  • Donepezil
  • Galantamine
  • rivastigmine
53
Q

Donepezil

A

AChE inhibitor

a reversible drug that is highly protein bound and CNS selective

54
Q

Galantamine

A

AChE inhibitor

a reversible drug

55
Q

Rivastigmine

A

used for AChE in alziembers

this drug is irreversible and has PNS effects

56
Q

memantine

A

NMDA antagonist
Can slow cognitive decline due to allowing for normal signaling
We tolerated and minimal AE

57
Q

Immunomodulators: interferon beta

A

MS

  • preferred choice when looking at these two options to stop the progression of the autoimmune
  • can stimulate antibody production against drug itself
  • special handling
58
Q

Immunosuppressants: mitoxantrone

A

MS
*inhibits DNA synthesis and repair
*decreased immune cell proliferation
Decreased myelin sheath destructions

59
Q

dalfampridine

A

Treat distressing or harmful symptoms

helps with the gait issues in a patient with MS

60
Q

Phenytoin

A 
traditional seizure medication 
prototype 
Na+ selective blocker 
high toxicity risk
due to metabolizing the liver quickly can become maxed out and leads to high toxicity issue
61
Q

Carbamazepine

A 
a traditional anti-seizure medication 
CNS depression 
Bone marrow suppression 
Increase in ADH suppression 
Derm rashes/ hypersensitive
62
Q

Valoprate

A

traditional seizure medication
Enhances GABA transmission and blocks Na+ like phenytoin
do not use in pregnant women

63
Q

Ethosuximide

A

Suppression of Ca++ channel in the thalamus
Absence of seizure usage
minimum AE

64
Q

Phenobarbital

A

Traditional Anti seizure medication

Potentiates effects of GABA used in anesthesia!!

65
Q

Albuterol

A

short acting B2 agonist that is used as a bronchodilator
inhaled so less risk of adverse effects!
Immediate onset, peak 30mins, DOA 3-5hrs
Taken PRN to abort acute attacks
If need to take >2x/week, additional drug should be added

66
Q

salmeterol

A

inhaled long acting bronchodilator = LABAS
Fixed dosing schedule (not PRN)
** Preferred in COPD
When used as sole therapy in asthma → increased incidence of asthma-associated death (use with a glucocorticoid)

67
Q

formoterol

A

inhaled long acting bronchodilator = LABAS
Fixed dosing schedule (not PRN)
** Preferred in COPD
When used as sole therapy in asthma → increased incidence of asthma-associated death (use with a glucocorticoid)

68
Q

terbutaline

A

bronchodilator = PO beta 2 agonist
PO B2 agonists: only for long term control, not first line
-Dosing is 3-4x/day

69
Q

theophylline

A

Methylxanthines
broncho dilators
MOA: Block adenosine receptors → relaxation of bronchial smooth m (probably)

Index = 10 -20 (minter blood levels!!!).
20-25 = N/V, diarrhea, restlessness, insomnia
>30 = risk for death d/t cardioresp collapse due to cardio decline
CYP450 inducers → subtherapeutic theophylline levels
CYP450 inhibitors → supratherapeutic (even toxic) theophylline levels

70
Q

ipratropium

A 
short acting anticholinergic 
MOA: 
Block muscarinic (M) receptors in bronchi = decreased bronchoconstriction
USAGE: 
Approved for COPD
Also used as alternative therapy for asthma
Inhalation administration to avoid AE
AE: 
nhaled drugs really minimal effect 
Nasopharyngitis
URIs
71
Q

tiotropium

A 
long  acting anticholinergic 
MOA: 
Block muscarinic (M) receptors in bronchi = decreased bronchoconstriction
USAGE: 
Approved for COPD
Also used as alternative therapy for asthma
Inhalation administration to avoid AE
AE: 
nhaled drugs really minimal effect 
Nasopharyngitis
URIs
72
Q

Beclomethasone

A

inhaled glucocorticoid

minimal AE when in haled and can prevent by thrush by washing mouth out

73
Q

Budesonide

A

inhaled glucocorticoid

minimal AE when in haled and can prevent by thrush by washing mouth out

74
Q

Fluticasone

A

inhaled glucocorticoid

minimal AE when in haled and can prevent by thrush by washing mouth out

75
Q

Leukotriene receptor antagonists

A

Mechanism: suppression of leukotriene effects

Leukotrienes effects to understand :
Smooth m constriction
Increased blood vessel permeability
Increased inflammatory responses (directly & through recruitment of eosinophils)

Used for maintenance and second line if the person cannot tolerate glucocorticoids

76
Q

Montelukast

A

Leukotriene receptor antagonists
Rapid absorption
-Peak 3-4hrs
-Highly PB (99%)

Liver metabolism
Biliary excretion
AE: 
-minimal!
-Rare neuropsych effects
-No CYP450 inhibition or liver injury
77
Q

Zileuton

A

Blocks leukotriene SYNTHESIS

Rapid absorption
-Peak 2-3hrs
Liver metabolism
Renal excretion

AE:

  • Liver injury (monitor LFTs)
  • Neuropsych effects
  • CYP450 inhibition
78
Q

Cromolyn

A

Mechanism: stabilizes membrane of mast cells = decreased histamine/mediator release  decreased inflammation
Does not cause bronchodilation

SAFEST of all the anti-asthma drugs (very rare AE).
Also used for exercise induced asthma (neb) & allergic rhinitis (intranasal)

79
Q

omalizumab

A

IgE Antibody Antagonist

Mechanism: forms complex w/ IgE that prevents it’s binding with receptors on mast cells
Decreased inflammatory mediator release

AE: viral infections, injection site rxns  hypersensitivity reactions

PK: peak 7-8 days, liver metabolism, ½ life 26 days. Takes approx. 1yr for IgE to return to pre-tx levels

80
Q

IL-5 receptor antagonists

A

monoclonal antibododies –> antiinflammation goal

Mechanism: inhibit IL-5
IL-5 = differentiation/maturation eosinophils
IL-5 inhibition = decreased eosinophils

AE: HA, pharyngitis, fatigue, hypersensitivity rxns
Resilzumab has black box warning d/t anaphylaxis events (0.3%)

81
Q

IL-4 receptor alpha antagonist

A

monoclonal antibodies used for reducing inflammation

Mechanism: inhibit IL-4
IL-4 = inflammatory cytokine expressed on many immune cell types
Inhibition = decreased cytokine-induced inflammation

AE: injection site rxn, oral herpes, conjunctivitis, antibody development against the drug

82
Q

roflumilast

A

PDE4 inhibitor = used for reducing inflammation

Used for severe bronchitis primary COPD (not first line)

Mechanism: inhibits PDE4 (enzyme that breaks down cAMP)
PK: PO, peak 1hr, ½ life 17hrs d/t high PB. CYP450 metabolism, urinary excretion

AE: diarrhea, anorexia, HA, back pain, insomnia.
Avoid in pregnancy
Psych rxns can occur that can be as severe as SI

83
Q

Symbicort

A

glucocorticoid + LABA

84
Q

Advair

A

glucocorticoid + LABA

85
Q

Combivent

A

anticholinergic + SABA

86
Q

Phenylephrine

A

drug for allergic rhinitis
Sympathomimetics
ONLY to relieve congestion
a1 agonism = vasoconstriction, decreased vascular permeability

87
Q

pseudoephedrine

A

drug for allergic rhinitis
Sympathomimetics
ONLY to relieve congestion
a1 agonism = vasoconstriction, decreased vascular permeability

88
Q

Antitussives

A 
drugs for cough 
some act in CNS, some peripherally
Helpful for chronic nonproductive cough
Codeine, hydrocodone
Both act in CNS to elevate cough threshold
89
Q

timolol

A

drugs used to treat glaucoma

beta blockers

90
Q

latanoprost

A

Increases outflow of AH by relaxing ciliary muscle​
​AE: ocular hyperemia (engorged vessels)

prostaglandin analogues

91
Q

brimonidine

A

a2 agonist
Decrease production of AH​
AE: dry mouth, ocular hyperemia​

92
Q

dorzolamide

A

Decrease production of AH​
Less effective, used as adjunct
Carbonic anhydrase inhibitors

93
Q

azelastine

A

H1 receptor blocker

Drugs for allergic conjunctivitis

94
Q

phenylephrine

A

Drugs for allergic conjunctivitis
Ocular decongestants

can also be used for allergic rhinitis because it is a sympathomimetic and is used to help with congestion only

95
Q

bevicizumab

A

Macular Degeneration
Blurring of central vision d/t macular injury
Painless, gradual
Leading cause of blindness in older adults
Tx: angiogenesis inhibitors (VEGf inhibitors)

96
Q

salicylic acid

A

Keratolytic: used for overgrowth/thickening; dandruff, psoriasis, warts, corns
AE: rarely, toxicity with long-term, high-dose use

97
Q

cortisone creams

A

Glucocorticoids: used for rash/itching
Vary in potency
AE: local reactions, thinning of skin with long-term use (increased with higher potency, dressing, large area)

98
Q

benzo peroxide

A

acne
First-line tx
AE: peeling, drying

99
Q

azelaic acid

A

acne treatment
Keratolytic
Suppresses P. acnes
AE: itching, burning, pigment reduction

100
Q

tretenoin

A

acne txn = retinoid
Vitamin A derivatives
Hyperproliferation of epithelial cells
AE: peeling, drying

101
Q

tacrolimus

A

topical immunosuppresents for eczema
AE: erythema, pruritis
No systemic absorption
Possible increase in skin cancer risk; avoid direct sunlight

102
Q

psoriasis treatment

A

Chronic autoimmune disorder
Main sx: plaque formation
Treatment goal: control/minimize symptoms
Topical: glucocorticoids, salicylic acid, coal tar: suppress DNA synthesis, inhibits keratinocytes
Systemic: methotrexate, biologics, TNF agonists

103
Q

Topical minoxidil

A

Androgenetic alopecia (male pattern baldness)
Other types of alopecia=typically different treatments
MOA: direct vasodilator, MOA unknown, possibly d/t increased blood flow
AE: local allergic reactions

104
Q

acetic acid

A

outer ear infection

105
Q

amoxicillin

A

Otitis media: infection, fluid, inflammation of middle ear; outward bulging of TM
Often develops after URI
Observation for 48-72 hours with supportive tx
Abx: high-dose amoxicillin for infants <6m, 6m-2y with confirmed dx, >2y with dx and severe sx

Pharm Exam 3 (5 decks)

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