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Drugs Flashcards

1
Q

SSRI Mechanism

A

Inhibit re-uptake of Serotonin

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2
Q

SNRI Mechanism

A

Inhibit re-uptake of Serotonin and NE

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3
Q

TCA Mechanism

A

Inhibit re-uptake of Serotonin and NE

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4
Q

MAOI Mechanism

A

Inhibit MAO that metabolizes and breaks down Serotonin and NE

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5
Q

SSRI Drugs

A

Fluoxetine, Paroxetine, Sertraline, Citalopram

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6
Q

SNRI Drugs

A

Venlafazine, Duloxetine

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7
Q

TCA Drugs

A

Amitriptyline, Nortriptyline, Imipramine, Desipramine, Clomipramine, Doxepin, Amoxapine

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8
Q

MAOI Drugs

A

Tranylcypromine, Phenelzine, Isocarboxazid, Selegiline

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9
Q

Atypical Anti-Depressants

A

Bupropion - increase NE and Dopamine via unknown mechanism (smoking cessation, add-on to SSRI)
Mirtazapine - Alpha 2 antagonist that increases NE (depression, weight gain)
Trazodone - Blocks 5-HT2 and alpha 1 adrenergic receptors (Insomnia primarily; toxicity causes Priapism)

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10
Q

Selegiline

A

MAO-B inhibitor that is used for Parkinson’s

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11
Q

Priapism is a S/E of this anti-depressant:

A

Trazodone

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12
Q

This anti-depressant lowers seizure threshold:

A

Bupropion

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13
Q

This anti-depressant works well with SSRI and increases REM sleep

A

Trazodone

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14
Q

This anti-depressant is an appetite stimulant that results in weight gain:

A

Mirtazapine (Remeron)

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15
Q

This anti-depressant can be used for smoking cessation:

A

Bupropion (Wellbutrin)

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16
Q

This anti-depressant can be used for bed-wetting in children:

A

Imipramine

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17
Q

TCA overdose symptoms:

A

“Tri-C’s”

Convulsions, Coma, Cardiotoxicity

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18
Q

Serotonin Syndrome symptoms:

A

Hyperthermia; Muscular rigidity, Cardiovascular collapse from autonomic instability

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19
Q

What happens if you ingest Tyramine while on MAOI’s?

A

Hypertensive crisis because you cannot degrade Tyramine and it will be converted to NE that raises BP

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20
Q

Methylphenidate used for…

A

Psychostimulant used for Narcolepsy, ADHD

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21
Q

Modafinil used for…

A

Narcolepsy, Circadian Rhythm Sleep Disorder

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22
Q

Opiate intoxication symptoms

A

Euphoria, respiratory and CNS depression, pupillary constriction (pinpoint pupils), seizures

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23
Q

Opiate withdrawal symptoms

A

Sweating, dilated pupils, piloerection, rhinorrhea, yawning, diarrhea, stomach cramps, nausea,

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24
Q

Treatment for opiate intoxication

A

Naloxone, Naltrexone

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25
Q

Treatment for opiate withdrawal

A

Methadone, Buprenorphine, Suboxone (Buprenorphine + Naloxone)

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26
Q

Measure of alcohol use

A

Serum gamma glutamyltransferase (GGT)

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27
Q

Alcohol withdrawal symptoms

A

Autonomic hyperactivity and DTs

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28
Q

Treatment for alcohol withdrawal

A

Benzodiazepines: Chlordiazepoxide, Lorazepam, Diazepam

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29
Q

Barbiturate intoxication symptoms

A

Respiratory depression

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30
Q

Barbiturate withdrawal symptoms

A

Delirium, life-threatening cardiovascular collapse

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31
Q

BDZ intoxication symptoms

A

Ataxia, minor respiratory depression

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32
Q

Treatment for BDZ intoxication

A

Flumazenil

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33
Q

BDZ withdrawal symptoms

A

Sleep disturbance, depression, rebound anxiety, seizure

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34
Q

Amphetamine intoxication symptoms

A

Euphoria, grandiosity, pupillary dilation, prolonged wakefulness and attention, HTN, tachycardia, anorexia, paranoia, fever
Severe: cardiac arrest, seizure

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35
Q

Amphetamine withdrawal symptoms

A

Anhedonia, increased appetite, hyper somnolence, existential crisis

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36
Q

Cocaine intoxication symptoms

A

Pupillary dilation, hallucinations, paranoid ideations, angina, sudden cardiac death

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37
Q

Treatment for cocaine intoxication

A

BDZs, Haloperidol, alpha blockers

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38
Q

Cocaine withdrawal symptoms

A

Hypersomnolence, malaise, severe psychological craving, depression/suicidality

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39
Q

Treatment for Nicotine withdrawal

A

Bupropion/Varenicline, Nicotine patch

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40
Q

PCP Intoxication symptoms

A

Belligerence, psychomotor agitation, analgesia, vertical and horizontal nystagmus, tachycardia, violence, psychosis, delirium, seizures

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41
Q

Treatment for PCP intoxication

A

BDZs, rapid-acting antipsychotic

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42
Q

PCP Withdrawal symptoms

A

Depression, anxiety, irritability, restlessness, anergia, disturbances of thought and sleep, violence

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43
Q

LSD intoxication symptoms

A

Perceptual distortion (VISUAL), depersonalization, anxiety, paranoid, psychosis, flashbacks

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44
Q

Treatment for LSD intoxication

A

BDZ

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45
Q

Cannabinoid intoxication symptoms

A

Impaired judgement, social withdrawal, euphoria, perception of slowed time, increased appetite, dry mouth, conjunctival injection

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46
Q

What is Methadone?

A

Long-acting oral opiate used for heroin detoxification or long-term maintenance

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47
Q

What is Naloxone + Buprenorphine? Mechanism?

A

Suboxone = antagonist + partial agonist; Naloxone is not orally bioavailable so withdrawal symptoms occur only if injected

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48
Q

What is Naltrexone?

A

Long-acting opioid antagonist used for relapse prevention once detoxified

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49
Q

Alprazolam:

a. Route of administration
b. half life
c. metabolism
d. use

A

a. oral
b. short duration
c. (metabolized by CYP3A4)
d. antipanic, anxiolytic

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50
Q

Diazepam:

a. ROA
b. half life
c. metabolism
d. use

A

a. oral
b. fast onset of action and LONG half life
c. (oxidation and glucuronidation); has active metabolites
d. anxiety states, sleep disorders, muscle relaxant

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51
Q

Lorazepam

a. ROA
b. onset
c. metabolism
d. use

A

a. INTRAMUSCULAR
b. slow onset (less lipophilic)
c. no active metabolites, only glucuronidation
d. anxiety AND sleep

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52
Q

Clonazepam

a. Use

A

a. Acute manic episodes

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53
Q

Chlordiazepoxide

a. Use

A

a. alcohol withdrawal

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54
Q

Benzodiazepines used for insomnia:

A

Flurazepam, Triazolam

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55
Q

Zolpidem mechanism

A

Non-BDZ; binds to BDZ receptor on GABA complex

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56
Q

Zaleplon mechanism

A

Non-BDZ; binds to BDZ receptor on GABA complex

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57
Q

Use of Zaleplon

A

Insomnia; more helpful for falling asleep than staying asleep because it has a short half life and action

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58
Q

Flumazenil

A

Antagonizes effects of BDZ; reduces seizure threshold thought so not used very often

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59
Q

Eszopliclone action and use

A

Interacts with GABA receptor complex; used for insomnia; this is Lunesta

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60
Q

Ramelteon action and use

A

Melatonin MT1 and MT2 receptor agonist; indicated for insomnia characterized by difficulty in falling asleep

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61
Q

Baclofen mechanism

A

GABA-mimetic agent that works at GABA B receptors (only one); causes presynaptic inhibition

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62
Q

Baclofen use

A

Muscle relaxant (as effective as Diazepam and produces less sedation)

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63
Q

Tizanidine mechanism

A

Alpha 2 adrenergic agonist related to Clonidine; may enhance both presynaptic and postsynaptic inhibition

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64
Q

Tizanidine use

A

Muscle relaxant

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65
Q

Atypical anti-psychotics used as adjunct in depression

A

Quetiapine, Olanzapine, Aripiprazole

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66
Q

Anti-psychotics used for Tourette’s syndrome

A

Haloperidol, Pimozide (typical)

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67
Q

Anti-psychotic used for Schizoaffective disorder

A

Paliperidone (metabolite of Risperidone - atypical)

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68
Q

Misoprostol

a. Mechanism
b. Use
c. Toxicity

A

a. PGE1 analog that increases production and secretion of gastric mucous barrier, decreased acid production
b. Prevent NSAID induced peptic ulcers; (NSAIDS block PGE1 production); maintenance of PDA; off-label for induction of labor
c. Diarrhea; C/I in women that are pregnant (abortifacient)

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69
Q

Octreotide

a. Mechanism
b. Use
c. Toxicity

A

a. Long-acting Somatostatin analog; inhibits actions of splanchnic vasoconstriction hormones
b. Acute variceal bleeds, acromegaly, VIPoma, Carcinoid tumors
c. Nausea, cramps, steatorrhea

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70
Q

Antacid meds:

a. Names
b. Mechanism

A

a. Aluminum hydroxide, Calcium carbonate, Magnesium hydroxide
b. Can affect absorption, bioavailability or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying

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71
Q

Aluminum hydroxide toxicity

A

Constipation, hypophosphatemia, proximal muscle weakness, osteodystrophy, seizures

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72
Q

Calcium carbonate toxicity

A

Hypercalcemia that causes rebound acid secretion

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73
Q

Magnesium hydroxide toxicity

A

Diarrhea, hyporeflexia, hypotension, cardiac arrest (because it is a smooth muscle relaxer)

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74
Q

Sulfasalazine

a. Mechanism
b. Use
c. Toxicity

A

a. Combo of Sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory); activated by colonic bacteria
b. Ulcerative colitis, Crohn disease
c. Malaise, nausea, sulfonamide toxicity, reversible oligospermia

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75
Q

Osmotic laxatives

a. Names
b. Mechanism
c. Use
d. Toxicity

A

a. Mg hydroxide, Mg citrate, Polyethylene glycol, lactulose
b. Provide osmotic load to draw water into GI lumen
c. Constipation; Lactulose treats hepatic encephalopathy since it is degraded by gut flora into metabolites that promote nitrogen excretion as NH4+
d. Diarrhea, dehydration, may be abused by bulimics

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76
Q

H2 blockers

a. Names
b. Mechanism
c. Use
d. Toxicity

A

a. Cimetidine, Ranitidine, Famotidine, Nixatidine
b. Reversible blocker of histamine H2 receptors that cause decreased acid secretion by parietal cells
c. Peptic ulcer, gastritis, mild esophageal reflux
d. Cimetidine is inhibitor of CYP450, has anti-androgenic effects; all of them can cause thrombocytopenia

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77
Q

Proton pump inhibitors

a. Names
b. Mechanism
c. Use
d. Toxicity

A

a. Omeprazole, Lansoprazole, Esomeprazole, Pantoprazole, Dexlansoprazole
b. Irreversibly blocks H+/K+ ATPase in stomach parietal cells
c. Peptic ulcer, gastritis, esophageal reflux, ZE
d. Increased risk of C. difficile infection, pneumonia, long term use causes decreased serum Mg

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78
Q

Bismuth

a. Mechanism
b. Use

A

a. Binds to ulcer base to provide physical protection and allows bicarbonate secretion to reestablish pH gradient in mucous layer
b. Increased ulcer healing, travelers diarrhea

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79
Q

Sucralfate

a. Mechanism
b. Use

A

Requires acidic environment to polymerize and binds ulcer base to provide physical protection
b. Increased ulcer healing, travelers diarrhea
(Similar to Bismuth)

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80
Q

Ondansetron

a. Mechanism
b. Use
c. Toxicity

A

a. 5HT3 Serotonin receptor antagonist
b. For post-op nausea, morning sickness or chemotherapy induced nausea
c. Vasodilation –> headache, constipation

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81
Q

Metoclopramide

a. Mechanism
b. Use
c. Toxicity

A

a. D2 receptor antagonist and 5HT4 agonist; increases resting tone, contractility, LES tone and motility
b. Diabetic or post-surgery gastroparesis, anti-emetic
c. Parkinsonian effects, tardive dyskinesia, restlessness, drowsiness, fatigue, depression, diarrhea

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82
Q 
Prokinetic Agents (mechanism)
4 types
A

(Increased Ach, Increased 5-HT, Decreased dopamine)

  1. Cholinergic agonists (Bethanechol)
  2. Acetylcholinesterase inhibitors (Neostigmmine)
  3. Metoclopramide (+ 5HT and - D2)
  4. Macrolides - stimulate smooth muscle motilin receptors
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83
Q

Prodrug of 6-mercaptopurine

A

Azathioprine

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84
Q

Drug that causes phocomelia

A

Thalidomide

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85
Q

Drug that is nephrotoxic in 75% of patients

A

Cyclosporine

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86
Q

S/E’s include: acne, osteoporosis, HTN, hyperglycemia, immunosuppression –> infection

A

Glucocorticoids

87
Q

Inhibits secretion of IL-2 and other cytokines

A

Tacrolimus

88
Q

What is Neostigmine?

A

Indirect cholinergic agonist (anti-cholinesterase) used for neurogenic ileum, post-op reversal of NMJ blockade, treatment for myasthenia gravis

89
Q

What is Pyridostigmine?

A

Indirect cholinergic agonist used for myasthenia gravis

90
Q

What is Edrophonium?

A

Indirect cholinergic agonist used for diagnosis of Myasthenia gravis

91
Q

What is Physostigmine

A

Indirect cholinergic agonist used for atropine overdose

92
Q

What are Donepezil, Rivastigmine, and Galantamine?

A

Indirect cholinergic agonist used for Alzheimer’s

93
Q

a. What is Procainamide?
b. What is it used for?
c. What toxicity can it cause?

A

a. Class IA anti-arrhythmic
b. Wolf Parkinson White syndrome
c. Reversible SLE like syndrome

94
Q

a. What is Quinidine?

b. What are toxic side effects of Quinidine?

A

a. Class IA anti-arrhythmic

b. Cinchonism (headache, dizziness, tinnitus), Thrombocytopenia, Torsades de Pointes

95
Q

a. What is Lidocaine?

b. What is it used for?

A

a. Type IB anti-arrhythmic

b. Acute ventricular tachyarrhythmias, digitalis-induced arrhythmias, tachyarrhythmias post-MI

96
Q

a. What arrhythmias are beta blockers used for?
b. What are the adverse reactions of beta blockers?
c. What is their mechanism?

A

a. SVT, ventricular rate control for atrial fibrillation and atrial flutter
b. Bradycardia, AV block, HF exacerbation, asthma, mask effects of hypoglycemia
c. Decrease SA and AV nodal activity by decreasing cAMP and Ca currents. They suppress abnormal pacemakers by decreasing the slope of phase 4.

97
Q

a. What is the mechanism of K channel blockers? (type III anti-arrhythmics)
b. What are they?
c. What is their use?
d. What are their adverse reactions?

A

a. Work at phase 3 to increase to block K depolarization so that AP duration is increased, ERP is increased and QT interval is increased
b. Amiodarone, Ibutilide, Dofetilide, Sotalol (AIDS)
c. Atrial fibrillaiton, atrial flutter, ventricular tachycardia (Amiodarone used for WPW)
d. Torsades de pointes for all
Amiodarone causes pulmonary fibrosis, hepatotoxicity, hypo/hyper thyroidism, photosensitivity, bradycardia, neurologic effects, constipation

98
Q

What labs should you check when using Amiodarone?

A

PFTs (pulmonary fibrosis)
LFTs (hepatotoxicity)
TFTs (hypo or hyperthyroid - amiodarone is 40% iodine)

99
Q

What drugs cause photosensitivity?

A

Sulfonamides
Amiodarone
Tetracycline

100
Q

a. What is the effect of Calcium channel blocker anti-arrhythmics?
b. What are they used for?
c. What is their toxicity?

A

a. Cause slow rise of action potential that results in decreased conduction velocity, increased ERP, increased PR interval
b. Prevention of nodal arrhythmias, rate control in atrial fibrillation
c. Constipation, flushing, edema, CV effects (heart block, HF)

101
Q

a. What is the drug of choice for supra ventricular tachycardia?
b. How does it work?

A

a. Adenosine
b. Causes increase K efflux that hypoerpolarizes cell and decreases Ca influx. Very SHORT acting - can’t depolarize at all

102
Q

What drugs block the affects of Adenosine?

A

Theophylline (asthma or COPD patients)

Caffeine

103
Q

How is Mg used for arrhythmias?

A

Effective in torsades de points and digoxin toxicity

104
Q

Which anti-arrhythmic has the side effect of Cinchonism? What is Cinchonism?

A

Quinidine; headache and tinnitus

105
Q

What effects will a noncompetitive antagonist have on Vmax and Km?

A

Vmax will be lower and no effect on Km

106
Q

What is the vasopressor of choice for

a. anaphylactic shock?
b. cardiogenic shock?
c. septic shock

A

a. Epinephrine
b. Dobutamine - because it stimulates Beta 1 receptors
c. Norepinephrine because it stimulates alpha 1 without beta 2

107
Q

What are the lengths of the preganglionic and postganglionic sympathetic fibers?

A

Short preganglionic - close to spine, secrete Ach

Long post ganglionic - secrete NE

108
Q

What do alpha 1 receptors cause?

A

Increased peripheral resistance

Increased bladder sphincter tone

109
Q

What do alpha 2 receptors cause?

A

Inhibition of NE release on presynaptic neuron

110
Q

What do beta 1 receptors do?

A

Increase HR and contractility

111
Q

What do beta 2 receptors do?

A

Mild vasodilation

Bronchodilation

112
Q

a. What are nonselective alpha blockers?

b. What are they used for?

A

a. Phenoxybenzamine (irreversible); for Pheochromocytoma

b. Phentolamine (reversible); given to patients on MAO inhibitor who eat foods with tyramine

113
Q

What are side effects of non-selective alpha blockers?

A

Orthostatic hypotension

Reflex tachycardia

114
Q

a. What are selective a1 blockers?

b. What are they used for?

A

a. Prazosin, Terazosin, Doxazosin, Tamsulosin

b. Urinary symptoms of BPH, Prazosin for PTSD, HTN (except not Tamsulosin)

115
Q

What are side effects of Prazosin, Terazosin and Tamsulosin?

A

Orthostatic hypotension
Rebound hypotension when you stop
Dizziness, headache
Reflex tachycardia

116
Q

What is mechanism of Tamsulosin?

A

Selective Alpha 1A,D blocker

117
Q

a. What is mechanism of Mirtazapine?

b. What is it used for?

A

a. Alpha 2 receptor blocker

b. Depression

118
Q

What are the non-selective beta blockers?

A

Nadolol, Propranolol, Timolol

119
Q

What are the B1 selective blockers?

A

Acebutolol, Atenolol, Betaxolol, Esmolol, Metoprolol

120
Q

What are non selective alpha and beta blockers?

A

Carvedilol, Labetalol

121
Q

When would you use Acebutolol or Pindolol over other beta blockers? Why?

A

In patients with HTN and bradycardia; they are weak B1 and B2 agonists (partial agonists) so they don’t have the same effect on HR

122
Q

What are therapeutic uses for beta blockers?

A 
HTN - drug of choice for aortic dissection
MI, angina, SVT, HF
Glaucoma
Hyperthyroidism
Migraine prophylaxis
Anxiety
123
Q

What are adverse effects of beta blockers?

A

Bronchoconstriction - from Beta 2 block
Prevent symptoms of hypoglycemia!
Avoid in cocaine users!! because cocaine causes stimulation of all adrenergic receptors (indirectly from reduced uptake of catecholamines) and blocking beta receptors = unopposed alpha 1 receptors –> increase BP

124
Q

What beta blockers are used for Glaucoma?

A

Timolol, Nadolol

125
Q

a. What is Clonidine mechanism?
b. What is it used for?
c. Toxicity

A

a. alpha 2 agonist –> act centrally to decrease release of NE from presynaptic neuron
b. Malignant HTN (outpatient), ADHD, Tourette syndrome
c. Rebound HTN when stopped, CNS depression, bradycardia, hypotension, respiratory depression, mitosis

126
Q

a. Methyldopa mechanism
b. Use
c. Toxicity

A

a. Alpha 2 agonist; decrease NE from presynaptic terminal
b. HTN in pregnancy
c. SLE like syndrome;

127
Q

In which patients are beta blockers C/I?

A

Diabetics
COPD/Asthma
Cocaine users
Bad/uncontrolled CHF

128
Q

Opioid used in treatment of diarrhea

A

Loperamide, Diphenoxylate

129
Q

Non-addictive weak opioid agonist

A

Tramadol

130
Q

Partial opioid agonist that causes less respiratory depression

A

Butorphanol

131
Q

What does Metyrosine do?

A

Inhibits conversion of Tyrosine to DOPA

132
Q

What does Reserpine do?

A

Inhibits packaging of NE into vesicles

133
Q

What does Hemicholinium do?

A

Inhibits transport of choline into cholinergic nerve terminal

134
Q

What does Vesamicol do?

A

Inhibits storage of Ach into vesicles

135
Q

What drugs can inhibit release of NE from noradrenergic synapse?

A

Bretylium - K channel blocker

Guanethidine

136
Q

What drugs can stimulate release of NE from noradrenergic synapse?

A

Amphetamine
Ephedrine
Tyramine

137
Q

What are other presynaptic receptors that regulate release of NE?

A

M2 receptors - inhibit release of NE (parasympathetic)

De receptors - inhibit release of NE AT2 receptor - stimulate release of NE

138
Q

Which drugs inhibit reuptake of NE?

A

Cocaine

TCA drugs

139
Q

How does COMT metabolize NE?

A

It methylates NE - (it’s Catechol-O-methyl transferase)

140
Q

How does MAO metabolize NE?

A

It oxidizes it

141
Q

What are the actions of these drugs on Ach or NE:

a. Amitriptyline
b. Amphetamine
c. Black widow spider toxin
d. Botulinum toxin
e. Bretylium
f. Cocaine
g. Gunaethidine
h. Hemicholinium
i. Reserpine
j. Vesamicol

A

a. Inhibits NE reuptake
b. Stimulates NE release
c. Stimulates Ach release
d. Inhibits Ach release
e. Inhibits NE release
f. Inhibits NE reuptake
g. Inhibits NE release
h. Inhibits choline transport
i. Inhibits NE packaging
j. Inhibits Ach packaging

142
Q

Which diuretic is used for pseudo tumor cerebri?

A

Acetazolamide

143
Q

What are the two types of cholinergic receptors?

A
  1. Nicotinic - ligand gated ion channels (DON’T use G proteins)
  2. Muscarinic - G protein linked receptors
144
Q

What are the Muscarinic receptors and what are their actions?

A

M1 - enteric nervous system
M2 - decreased HR and contractility of atria (SA node)
M3 - increase bladder contraction, gut peristalsis and lacrimation, miosis, bronchoconstriction

145
Q

What are the adrenergic receptors? And what do they cause?

A

alpha 1 - vasoconstriction, smooth muscle contraction
alpha 2 - presynaptic auto receptors that inhibit NE release
beta 1 - increase HR and myocardial contractility
beta 2 - vasodilation and bronchodilation

146
Q

Besides adrenergic and muscarinic cholinergic (not nicotinic) receptors, which other receptors are G protein linked?

A

Dopamine receptors
Histamine receptors
Vasopressin receptors (ADH)

147
Q

What do D1 receptors cause?

A

Relax renal vascular smooth muscle

148
Q

Where are D2 receptors found?

A

Brain

149
Q

What do H1 receptors cause?

A

Nasal secretions
Bronchial mucus production
Pruritis
Bronchoconstriction

150
Q

What do H2 receptors cause?

A

Increased gastric acid secretion

151
Q

What do V1 receptors do?

A

Increased vascular smooth muscle contraction

152
Q

What do V2 receptors do?

A

Increase reabsorption in collecting tubules of the kidney

153
Q

What do M1 M2 and M3 receptors respond to?

A

Ach

154
Q

What do a1 a2 B1 and B2 receptors respond to?

A

NE, Epi

155
Q

What does Gq do?

A

It activates phospholipase C –> acts on PIP2 and cleaves it into DAG and IP3

  • DAG activates Protein Kinase C
  • IP3 increases intracellular Calcium –> smooth muscle contraction
156
Q

What is the mnemonic for Gq receptors? Which ones are Gq receptors?

A

Cutesies (QC) HAVe 1 M&M
H1, alpha1, V1
M1, M3

157
Q

What does Gs do?

A

Gs –> stimulates adenylyl cyclase –> converts ATP to cAMP –> cAMP activates Protein Kinase A (PKA) –> increase in Ca in heart

158
Q

What does Gi do?

A

Inhibits adenylyl cyclase –> inhibits production of cAMP –> no production of PKA –> no increase in Ca

159
Q

What is mnemonic for Gi?

A

MAD 2s

M2 alpha 2 D2

160
Q

Which G protein does the following:

a. activates PKA
b. less activation of PKA
c. activates PKC
d. activates Phospholipase C
e. increases Calcium
f. increases cAMP
g. decreases cAMP
h. inhibits adenylyl cyclase
i. stimulates adnylyl cyclase
j. PIP2–> IP3 + DAG

A

a. Gs
b. Gi
c. Gq
d. Gq
e. Gs, Gq
f. Gs
g. Gi
h. Gi
i. Gs
j. Gq

161
Q

Clopidogrel

A

ADP receptor inhibitor

162
Q

Prasugrel

A

ADP receptor inhibitor

163
Q

Ticagrelor

A

ADP receptor inhibitor (reversible)

164
Q

Ticlodipine

A

ADP receptor inhibitor (causes Neutropenia)

165
Q

Cilostazol

A

Phosphodiesterase III inhibitor (increases cAMP in platelets resulting in inhibition of platelet aggregation)

166
Q

Dipyridamole

A

Phosphodiesterase III inhibitor (increases cAMP in platelets resulting in inhibition of platelet aggregation)

167
Q

GP IIb/IIIa inhibitors

Mechanism and Use

A

Eptifibatide, Abciximab, Tirofiban
They bind to the GP IIb/IIIa receptor on activated platelets and prevent aggregation
Used for unstable angina, PTCA

168
Q

Nucleotide synthesis inhibitors (drugs and mechanisms)

A
  1. Methotrexate - folic acid analog that inhibits dihydrofolate reductase
  2. 5-FU - pyrimidine analog activated to 5-dUMP that complexes folic acid and inhibits thymidylate synthase
  3. 6-Mercaptopurine (Azathioprine is metabolized to 6-MP); Purine analog that inhibits de novo purine synthesis
  4. Hydroxyurea inhibits ribonucleotide reductase
  5. Cytarabine is a pyrimidine analog that inhibits DNA polymerase
169
Q

What drugs have increased toxicity when taken with Allopurinol or Febuxostat?

A

Azathioprine, 6-MP; they are both metabolized by Xanthine Oxidase

170
Q

What drug treats Hairy Cell Leukemia?

A

Cladribine (purine analog that has multiple mechanisms)

171
Q

Clinical use of 5-FU

A

Basal cell carcinoma

Actinic keratosis

172
Q

What is the rescue agent of 5-FU?

A

Uridine (because 5-FU is a pyrimidine analog that is activated to 5F-dUMP which binds folic acid and inhibits thymidylate synthase –> decreased dTMP –> decreased DNA synthesis)

173
Q

Clinical use of Methotrexate

A

Cancer: Leukemia, Lymphoma, Choriocarcinoma
Ectopic pregnancy, medical abortion
RA, psoriasis, IBD, vasculitis

174
Q

How do you reverse Methotrexate toxicity?

A

Leucovorin

175
Q

Which cancer drugs inhibit the M phase of cell cycle?

A

Paclitaxel
Vinblastine
Vincristine

176
Q

Bleomycin

a. Mechanism
b. Use
c. Toxicity

A

a. Induces free radical formation –> breaks in DNA strands
b. Testicular cancer, Hodgkin lymphoma
c. PULMONARY FIBROSIS, skin hyper pigmentation, mucositis

177
Q

Dactinomycin

a. Mechanism
b. Use
c. Toxicity

A

a. Intercalates in DNA
b. CHILDhood tumors; Wilms tumor, Ewing sarcoma, Rhabdomyosarcoma
c. Myelosuppression

178
Q

Doxorubicin, Daunorubicin

a. Mechanism
b. Use
c. Toxicity

A

a. Generate free radicals, intercalate into DNA and cause DNA breaks
b. Solid tumors, leukemias, lymphomas
c. Cardiotoxicity (dilated cardiomyopathy)

179
Q

Why is the heart susceptible to Doxorubicin?

A

The heart has a deficiency in superoxide dismutase and therefore has greater susceptibility to free radicals

180
Q

What can be given to prevent cardiotoxicity with Doxorubicin or Daunorubicin?

A

Dexrazoxane (iron chelating agent)

181
Q

Busulfan

a. Mechanism
b. Use
c. Toxicity

A

a. Cross-links DNA
b. CML
c. PULMONARY FIBROSIS, hyperpigmentation, myelosuppression

182
Q

Cyclophosphamide

a. Mechanism
b. Use
c. Toxicity

A

a. Cross links DNA at guanine N-7.
b. Solid tumors, leukemia, lymphomas
c. Myelosuppression, HEMORRHAGIC CYSTITIS

183
Q

Nitrosureas

a. Mechanism
b. Use
c. Toxicity

A

a. Require bioactivation (CROSS BLOOD BRAIN BARRIER)
b. Brain tumors
c. CNS toxicity

184
Q

Why are Nitrosureas useful for brain tumors?

A

They cross the blood brain barrier and enter the CNS

185
Q

How do you prevent hemorrhagic cystitis from Cyclophosphamide?

A

Mesna

186
Q

Paclitaxel

a. Mechanism
b. Use
c. Toxicity

A

a. Hyperstabilizes polymerized microtubules in M phase so that mitotic spindle cannot break down
b. Ovarian and breast carcinomas
c. MYELOSUPPRESSION

187
Q

Vincristine, Vinblastine

a. Mechanism
b. Use
c. Toxicity

A

a. Bind Beta tubulin and inhibit it’s polymerization into microtubules –> prevents mitotic spindle formation
b. Solid tumors, Leukemias, Hodgkin (vinB) and non-Hodgkin (vinC) lymphomas
c. Vincristine - PERIPHERAL NEURITIS, Vinblastine - MARROW SUPPRESSION

188
Q

Cisplatin

a. Mechanism
b. Use
c. Toxicity

A

a. Cross link DNA
b. Testicular, bladder, ovary, lung
c. NEPHROTOXICITY, ototoxicity

189
Q

Etoposide, Teniposide

a. Mechanism
b. Use
c. Toxicity

A

a. Etoposide inhibits TOPOisomerase II –> increased DNA degradation
b. Solid tumors
c. Myelosuppression, GI upset, alopecia

190
Q

Irinotecan, Topotecan

a. Mechanism
b. Use
c. Toxicity

A

a. Inhibits topoisomerase I and prevents DNA unwinding/replications
b. Colon cancer (irinotecan), ovarian and small cell lung cancers (topotecan)
c. Severe myelosuppression, diarrhea

191
Q

Hydroxyurea

a. Mechanism
b. Use
c. Toxicity

A

a. Inhibits ribonucleotide reductase
b. Sickle cell, Melanoma, CML
c. Severe myelosuppression, GI upset

192
Q

Bevacizumab mechanism

A

Monoclonal antibody against VEGF

193
Q

Erlotinib mechanism

A

EGFR tyrosine kinase inhibitor (used for non-small cell lung cancer)

194
Q

Imatinib mechanism

A

Tyrosine kinase inhibitor of BCR-ABL (used for CML)

195
Q

Rituximab mechanism

A

Monoclonal Ab against CD20 (used for non-Hodgkin lymphoma, CLL)

196
Q

Tamoxifen, Raloxifene mechanism

A

Estrogen receptor antagonists in breast and agonists in bone

197
Q

What is an increased risk with Tamoxifene? Why?

A

Endometrial cancer; Tamoxifen is partial agonist in endometrium –> causes endometrial hyperplasia

198
Q

Trastuzumab mechanism

A

Monoclonal Ab against HER-2 (tyrosine kinase) –> for HER2 positive breast cancer and gastric cancer

199
Q

Trastuzumab toxicity

A

Cardiotoxicity

200
Q

Mechanism of Protease inhibitors? What do they all end in?

A

They inhibit the cleavage of polypeptide products of HIV mRNA into their functional parts (prevent maturation of new virus) - All end in -NAVIR

201
Q

Which protease inhibitor is known for inhibiting cytochrome P450 and boosting other drug concentrations?

A

Ritonavir

202
Q

What are S/E of Protease inhibitors?

A

GI intolerance, Hyperglycemia, Lipodystrophy
Inhibit CYP450 - Ritonavir
Nephropathy, hematuria - Indinavir

203
Q

What drug is C/I in patients taking protease inhibitors? And why?

A

Rifampin; it can decrease protease inhibitor concentration because it is a CYP/UGT inducer

204
Q

Mechanism of NRTIs

A

COMPETITIVELY inhibits nucleotide binding to reverse transcriptase and terminates the DNA chain - they are nucleoside (Tenofovir is nucleotide) analogs and need to be PHOSPHORYLATED to be active

205
Q

NRTI drug examples?

A

Zidovudine, Tenofovir, Abacavir, Lamivudine, Didanosine, Emtricitabine

206
Q

Which HIV drug is used for prophylaxis during pregnancy to decrease risk of transmission to fetus?

A

Zidovudine (NRTI)

207
Q

S/E of NRTI drugs

A

BM suppression, peripheral neuropathy, lactic acidosis, anemia (Zidovudine), pancreatitis (Didanosine)

208
Q

What are S/E of Zidovudine?

A

Megaloblastic anemia

209
Q

S/E of Didanosine?

A

Pancreatitis (It’s a NRTI)

210
Q

NNRTI mechanism and drugs?

A

Bind to reverse transcriptase; NON competitively inhibits; and do NOT require phosphorylation to be active or compete with nucleotides; Efavirenz, Delavirdine, Nevirapine

211
Q

S/E of NNRTIs

A

Rash, hepatotoxicity
Vivid dreams, CNS symptoms - Efavirenz
C/I in pregnancy - Efavirenz, Delavirdine

212
Q

Mechanism of Raltegravir

A

Inhibits HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase

213
Q

Enfuvirtide mechanism and S/E

A

Binds gp41 and inhibits viral entry

S/E include skin reaction at injection site

214
Q

Maraviroc mechanism

A

Binds CCR-5 on surface of T cells/monocytes and inhibits interaction with gp120

Step 1 AB (29 decks)

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