Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Block II Pharmacology > Drugs to Know > Flashcards

Drugs to Know Flashcards

1
Q

Botulin Toxin

(most potent natural toxin)

A

Prevents Ca2+ influx; no ACh
release = muscle paralysis

Uses: Botox; paralyzes muscles
of the face for wrinkles

Side Effects: Causes death d/t
paralysis of diaphragm muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Nicotine

A

Binds at 1 or 2 α sites on the
nicotinic receptors, induces a
conformational change to open
the cation channel

Uses: Smoking cessation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Muscarine

A

Effects the muscarinic receptors
(M1-M3) of the CV system, CNS,
and glands (but poisonous)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Bethanechol

A

Orally administered, but not
absorbed by GI tract b/c it is
charged.
Activated M3 receptors in GI

Uses: Post-surgical stimulation of
peristalsis in the GI tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Carbachol

A

Slows hydrolysis by AChE;
Charged d/t quaternary N–
cannot be absorbed;
Constricts eye muscles to drain
aqueous humor and decr.
intraocular pressure

Uses: Short-term treatment of
glaucoma (eye drops)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Curare

A

NMJ blocker: 10C between 2N’s;
Paralyzes the muscle by
preventing effect of ACh

Uses: Surgery–temporary muscle
paralysis
Side Effects: Toxic @ high doses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Hexamethonium
Trimethaphan

A

Ganglionic blocker: 6C between 2N’s; Blocks ANS completely

Uses: Hypertensive crisis (decr. SM contraction)
Side Effects: PNS suppression
(tachycardia, dry mouth, etc.);
orthostatic hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Atropine

A

Blocks muscarinic receptors resulting in anti-cholinergic activity; M3 receptors are not innervated, so they are not affected; Can cross the BBB and cause hallucinogenic effects

**Uses**: Bradycardia; Sarin gas
poisoning treatment (along w/
pralidoxime)

Side Effects: Anti-cholinergic
• Eye dilation (blurred vision) • No secretions (dry mouth) •Bronchodilation • Increased HR • No peristalsis (constipation)
• Urinary retention • No BP effects • Increase temperature (decreased sweating) • No sexual function • Hallucinations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Tolterodine

A

Blocks muscarinic receptors

Uses: Urinary retention

Side Effects: Anti-cholinergic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Homatropine

A

Blocks muscarinic receptors

Uses: Pupil dilation

Side Effects: Blurred vision

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Physostigmine

A

Carbamate group (analogous to acetate) is hydrolyzed slower than acetate group; ACh levels increase while AChE is inhibited

Uses: Glaucoma; Anti-cholinergic poisoning (atropine, etc.)

Side Effects: Cholinergic
syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Neostigmine

A

Carbamate group (analogous to acetate) is hydrolyzed slower than acetate group; ACh levels increase while AChE is inhibited

Uses: Myasthenia gravis; reverse muscle relaxants

Side Effects: Cholinergic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Edrophonium

A

Binds to the negative charges in the binding sits of cholinesterases; short-lasting effects (5-10 min.)

Uses: Reverses curare blockade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Donepezil
Rivastigmine

A

AChE inhibitors. Uncharged, tertiary amines that can cross the blood brain barrier.

Uses: Treatment of neurogenerative disorders like Alzheimer’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Organophosphates (e.g. Sarin)

A

Irreversible inhibitors of AChE; phosphate group forms a covalent bond w/ Ser on AChE resulting in exacerbation of cholinergic effects

“Uses”: Chemical Warfare

Side Effects: Death via
overstimulation of ACh receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Pralidoxime

A

Cleaves bond between organophosphate and Ser on AChE; Return AChE to normal activity

Uses: Sarin gas poisoning treatment (along w/ atropine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Metyrosine

A

Competes with tyrosine; inhibits catecholamine synthesis

Uses: Anti-hypertensive; pts. w/ pheochromocytomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

L-DOPA

A

Crosses BBB and is converted into dopamine

Uses: Parkinson’s disease (insufficient dopamine d/t cell death in basal ganglia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Carbidopa

A

Inhibits conversion of L-DOPA to dopamine; Cannot cross BBB, but used with L-DOPA to incr. amount of dopamine conversion in brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Amphetamines

A

Competes with re-uptake pumps (prolong catechol. in the synapse), inhibits VMAT and MAO (increase NE and Epi in the cytoplasm), so NE and Epi travel down conc. gradient into synapse;

Result: incr. [NE & epi] in
periphery, [NE, 5-HT, DA] in CNS

Uses: ADHD; narcolepsy; general stimulant

Side Effects: High abuse potential; tolerance (d/t receptor desensitization)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Ephedrine (Ephedra)

A

Enters nerve terminal to displace NE from the cytoplasm; causes bronchi relaxation, stimulates heart, and incr. BP

Uses: Asthma; CNS stimulant; appetite suppressant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Pseudoephedrine

A

Enters nerve terminal to displace NE from the cytoplasm; causes bronchi relaxation, stimulates heart, and incr. BP

Uses: Nasal decongestant; OTC cold drugs

Side Effects: Rebound hyperemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Tyramine

A

Enters SNS nerve terminals via reuptake pump; incr. release of NE; found in high conc. In fermented foods; MAO takes care of it, but not when combined with MAOI

Side Effects: Hypertensive crisis if [tyramine] accumulates in periphery (can occur when MAO inhibitor is given)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Cocaine

A

Competitively blocks both peripheral and CNS re-uptake of NE, DA, and serotonin (5-HT); the reward centers in the brain from dopamine are responsible for addiction and abuse of cocaine

Uses: Local anesthetic in ENT

Side Effects: CNS excitation, anorexia, euphoria; high abuse potential; incr. BP & HR, vasoconstriction

Note: If given w/ a β-blocker, patient will go into hypertensive crisis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Desipramine

A

A tricyclic antidepressant that selectively blocks NE re-uptake but not serotonin re-uptake in periphery & CNS

Uses: Anti-depressant

Side Effects: Tolerance, but no risk of abuse (no DA involvement, so no euphoria)

26
Q

Phenelzine

A

Inhibits MAO-A/B causing a buildup of NT is the cytoplasm; reverses uptake pumps, and NT flow down their conc. gradient into the synapse.

Uses: 3rd-line treatment for depression d/t food & drug interactions

Side Effects: Serotonin syndrome can occur when taken with opiates, anti-depressants, decongestants

27
Q

Selegiline

A

Selectively inhibits MAO-B; MAO-A is still functional in the periphery

Uses: Parkinson’s disease treatment

28
Q

Aminophylline (aka theophylline)

A

Potentiates effect of cAMP by increasing [cAMP] causing bronchiole SM relaxation (β2), cardiac stimulation (β1 & β2)

Uses: Asthma; COPD; heart failure

Side Effects: arrhythmias, anxiety, convulsions

29
Q

Sildenafil

A

Increase [cGMP] to relax SM of corpora cavernosa of penis; decr. pulmonary vascular resistance; incr. cerebral blood flow

Uses: ED; pulmonary HTN; acute RDS; altitude sickness

Side Effects: Dangerous drop in BP

30
Q

Epinephrine

A

Gs-PCR causes incr. [cAMP]; β2: SM relaxation (bronchi, vasculature); β1: incr. cardiac contractility, HR, ~incr. BP (from kidney renin) (incr. vasodilation at low dose OR incr. vasoconstriction at high dose)

Uses (Low Dose): Cardiac arrest, asthma

Uses (High Dose): Anaphylactic shock; w/ anesthetic to prolong vasoconstriction

Side Effects: Arrhythmias

31
Q

Norepinephrine

A

Incr. diastolic BP via α1 stimulation, leads to incr. TPR; baroreceptor reflex causes decr. sympathetic tone and incr. vagal output to decr. HR

Result: incr. BP and cardiac force; HR and CO do not change

Uses: Septic shock; hypotensive states (anesthesia); incr. perfusion pressure w/o incr. HR decreases arrhythmia risk

32
Q

Isoproterenol

A
  • *β1**: incr. HR, SV, and CO
  • *β2**: decr. diastolic BP via vasodilation
  • *Result**: MAP decr. slightly, TPR decr.

Uses: Heart failure (but there are better drugs for this, e.g. dobutamine, β-blockers)

Side Effects: Arrhythmias

33
Q

Dopamine

A

D1: Gs-PCR (just like β2) incr. [cAMP] causes dilation of renal, mesenteric, coronary vessels; incr. renal blood flow
β1: cardiac stimulation
α1: maintain vascular tone; may
override renal vasodilation

  • *D1 Use**: Maintain kidney perfusion
  • *D1 & β1 Use**: incr. HR, CO, and flow to kidneys & mesentery
  • *Over-administration (α1)**: vasoconstriction
34
Q

Dobutamine

A

Less β2 vasodilation & modest α1 activation leads to less reflex tachycardia via baroreceptors;
Result: increased contractility compared to rate increase

  • *Uses**: Acute heart failure (incr. CO w/o incr. in TPR = heart beating more efficiently)
  • *Side Effects**: Tachyphylaxis if used chronically
35
Q

Albuterol

A

Gs-PCR causes incr. [cAMP]; β2: SM relaxation (bronchi, vasculature); No β1 activity means fewer heart side effects

Uses: Asthma; bronchospasm

Side Effects: Cardiac stimulation at high/repetitive doses

36
Q

Phenylephrine

A

Gq-protein receptors coupled to phospholipase C; when activated increases IP3 and DAG from PIP2, and IP3 stimulates the release of Ca2+ causing contraction of vascular muscle;
Result: Incr. BP & reflex bradycardia

Uses: OTC nasal decongestant

Side Effects: rebound hyperemia (incr. redness of eye) & ischemia

37
Q

Clonidine

A

High doses via IV cause vasoconstriction; Low oral dose causes activation of α2A receptors at CNS vasomotor center and decreases SNS outflow and lowers BP

Uses: Anti-hypertensive

Side Effects: Hypertensive episode during withdrawal

38
Q

Brimonidine

A

Decreases aqueous humor production so decreases intraocular pressure (unknown mechanism)

Uses: Glaucoma treatment

39
Q

Propranolol

A

Decreases CO (by decr. HR & contractility, and decr. BP from no renin release from kidney); Prevents Epi-mediated bronchodilation (β2); Partially blocks Epi-mediated glycogenolysis in liver (β2)

  • *Uses**: (see clinical uses), also decr. performance anxiety and essential tremors
  • *Side Effects**: Bronchoconstriction in pts. w/ asthma; masks hypoglycemic symptoms in pts. w/ insulin-dependent diabetes
40
Q

Metoprolol

A

Decreases CO (by decr. HR & contractility); no β2 effects, so incr. exercise capacity

Uses: Incr. exercise tolerance for pts. w/ peripheral vascular disease

41
Q

Pindolol

A

“Partial agonist” meaning intrinsic sympathomimetic activity on β receptors.

Result: Reduce HR and CO caused by SNS activity (less likely to cause bradycardia); but not as much as a pure antagonist

  • *Uses**: Incr. exercise tolerance for pts. w/ low HR (e.g. endurance
    athletes) . Note: β-blockers are banned by the NCAA and the IOC
42
Q

Carvedilol

A

Decr. in CO (via β effects– decr. HR, conduction, contractility) and decr. TPR (via α effects); Decr. SNS tone from baroreceptor because β receptors are blocked at the heart; Anti-proliferative & antioxidant properties.

Uses: HTN; decr. mortality & morbidity in pts. w/ moderate heart failure

43
Q

Labetalol

A

Decr. in CO (via β effects– decr. HR, conduction, contractility) and decr. TPR (via α effects); Decr. SNS tone from baroreceptor because β receptors are blocked at the heart

Uses: pts. who are pregnant; hypertensive emergencies

44
Q

Phentolamine

A

Dramatic decr. in BP (α1) with reflex tachycardia from baroreceptor reflex; increase NE release from no neg. feedback on α2 presynaptic receptors.

Uses: Diagnosis & treatment of pre-op. pheochromocytoma surgery (catecholamine-secreting tumor)

Side Effects: Angina from incr. HR (and incr. O2 consumption)

45
Q

Phenoxybenzamine

A

Dramatic decr. in BP (α1) with reflex tachycardia from baroreceptor reflex; increase NE release from no neg. feedback on α2 presynaptic receptors. Same as phentolamine, but longer-lasting. Alkylates a-, serotonin, and histamine receptors), making them irreversibly bound.

Uses: pheochromocytoma long-term management

46
Q

Prazosin

A

No vasoconstriction so decr. in TPR and BP; less reflex tachycardia because α2 neg. feedback receptors aren’t blocked

Uses: pts. w/ HTN

Side Effects: Orthostatic hypotension

47
Q

Tamsulosin

A

Blocks Gq receptors so decr. in Ca2+ causing smooth muscle relaxation of muscles in the prostate

Uses: treatment for BPH (benign prostate hyperplasia)

48
Q

What are the nicotinic and muscarinic agonists?

A

Nicotinic: Nicotine

Muscarinic: Muscarine, methachol, bethanechol, carbachol

49
Q

What are the nicotinic and muscarinic antagonists?

A

Nicotinic: Trimethaphan, Hexamethonium, Curare

Muscarinic: Homatropine, Atropine, Tolterodine

50
Q

What are the ACh potentiators (AChE inhibitors)?

A

Physostigmine, Neostigmine, Rivastigmine, Donepezil, Edrophonium, and organophosphates (VX, Sarin gas, etc.)

51
Q

What reverses the AChE inhibitors?

A

Combination of Atropine and Pralidoxime

52
Q

What drugs affect catecholamine synthesis?

A

Metyrosine (Tyrosine hydroxylase), L-DOPA (DOPA decarboxylase), Carbidopa (DOPA decarboxylase)

53
Q

What drugs affect catecholamine release?

A

Amphetamines (MAO, VMAT, and NE, EPI, 5-HT reuptake transporters) Ephedrine, Pseudoephedrine, Tyramine (pre-synaptic vesicles)

54
Q

What are the NMJ reuptake blockers?

A

Cocaine (reuptake transporters)

Desipramine (NET)

55
Q

What are the MAOIs?

A

Phenelzine (MAO-A/B), Selegiline (MAO-B), Amphetamines (MAOI general)

56
Q

What are the PDE inhibitors?

A

Aminophylline/theophylline (non-selective), Sildenafil (PDE-5)

57
Q

What are the catecholamines?

A

Epinephrine (B2>B1), NE (a1/2, B1), Isoproterenol (B1/2), Dopamine (D1, moderate dose D1 + B1, high dose D1 + B1 + a1)

58
Q

What are the beta agonists?

A

Dobutamine (B1>B2), Albuterol (B2)

59
Q

What are the alpha agonists?

A

Phenylephrine (a1), Clonidine (a2), Brimonidine (a2)

60
Q

What are the beta blockers?

A

A-M are B1, N-Z are non-selective (carve+lab block a1 as well)

Carvedilol (B1/2 + a1)

Labetalol (B1/2 + a1)

Metoprolol (B1)

Pindolol (B1/2 partial)

Propranalol (nonselective)

61
Q

What are the alpha blockers?

A

Phentolamine (nonselective, competitive and reversible)

Phenoxybenzamine (nonselective, noncompetitive and irreversible)

Prazosin (a1 effect >>> a2, competitive antagonist)

Tamsulosin (a1a, mostly prostate SM)

Block II Pharmacology (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions