Pharmacology: Final Review

Front 1

Which drug blokcs the choline uptake into the nerve terminal to make ACh

Back 1

Hemicholinium

Front 2

Which drug blocks ach uptake vesicles in the making of ACh

Back 2

vesamicol

Front 3

Which drug inhibits the actions of tyrosine hydroxylase in making catecholamines?

Back 3

metyrosine

Front 4

Reserpine

Back 4

inhibits the catecholamine carrier of Dopamine which results in catacholamines not being sythesized

Front 5

;NE release is blocked by which 2 drugs that block the fusion event at adrenergic terminals?

Back 5

bretylium and guanethidine

Front 6

How is termination at adrenergic terminals different that termination at cholinergic terminals

Back 6

A: reuptake of neurotransmitter into the nerve terminals
C: enzymatic degredation of acH

Front 7

What type of postreceptors are on M1 and M3

Back 7

G q/11... increase IP3 and DAG

Front 8

How do you get parasymphathetic activation of blood vessels

Back 8

circulating muscarinic agonists will cause vasodilation cuz of M3 receptors on endothelial cells stimulate production of nitric oxide

Front 9

Which choline agonist is the only one given systemically

Back 9

bethanechol

Front 10

when would you NOT use pilocarpine

Back 10

if IOP is highter than 45mmhg

Front 11

Which drug do you give to personell at risk for exposure to nerve gas

Back 11

pyridostigmine: because it is reversible and can block the binding of the irreversible nerve agents to the cholinesterase (therefore if they r exposed they will have more time to get atropine or 2-PAM)

Front 12

Predominant tone of:
1. arterioles
2. veins
3. heart
4. iris
5. ciliary musc
6. GI tract
7.urinary bladder
8. salivary glands
9. sweat glands
10. genital tract

Back 12

1. arterioles: symp (adrenergic)
2. veins: Symp (adrenergic)
3. heart: para
4. iris: para
5. ciliary musc: para (contracted)
6. GI tract: para
7.urinary bladder: para
8. salivary glands: para
9. sweat glands: symp (CHOLInergic)
10. genital tract: both

Front 13

What are the effects of atropine on the heart in:
1. low doses
2. high doses

Back 13

atropine blocks both pre (autoreceptors) and post synaptic receptors. The autoreceptors, when activated, send out more ach.

1. bind to both pre and post synaptic autoreceptors. Result: bradycardia

2. bind to both pre and post synaptic autoreceptors, but so many post are blocked. Result: tachycardia

OVERALL: antimuscarinic effects on heart are not dramatic and usually consist of tachycardia w/ little to no change in BP

Front 14

What is most beneficial for patients with respiratory diseases like COPD or asthma

Back 14

BEST: B adrenergic agonists
ex: Albuterol (b2)

but also cholinergic antagonists like ipratropium

Front 15

what is best to use if mydriasis is the only goal

Back 15

alpha adrenoceptor agonists (short acting and sufficient for exam)


(the antimuscarinic drugs cause cycloplegia and mydriasis (cycloplegia aids in measurement of refractive error)... longest duration antimusc drugs for this causeis atropine, shortest is tropicamide

Front 16

1.what do you use to treat rapid onset poisening?
2. what do you use to treat delayed onset poisening?

Back 16

1. atropine... and make sure you give repeatedly in high doses since the effects of anticholinesterases last longer than atropine

if severe enough, cholinesterase inhibition w/ physostigmine may be necessary
2. NOT atropine

Front 17

Who is contraindicated for antimuscarinics

Back 17

pt w/ glaucoma or Prostatic hyperplasia (precipitates urinary retention)

Front 18

What does ganglionic blockade (mecamylamine) do to blood vessels?

Back 18

vasodilates them

it blocks the dominant divisions effects... so blood vessels usually under sympathetic tone.

Front 19

how do adrenergic receptors work on the eye?

Back 19

alpha 1: mydriasis
alpha 2: decreases aqueous humor production
Beta: increases aqueous humor production, but increases aqueous flow

** epinephrine (mixed adrenergic agonist): decreases IOP by decreasing a. production and inc. flow

Front 20

Uterus contraction?
2. uterus relaxation?

Back 20

1. alpha 1
2. beta 2

Front 21

how does epinephrine effect insulin secretion?

Back 21

INHIBITION of insulin secretion (alpha 2) predominates over B2 receptor stimulation of insulin secretion

Front 22

CNS effects of adrenergic activation

Back 22

1. Catecholamines are exccluded and only enter in high rates of infusion
alpha2 receptors in the brain stem though, decrease sympahtetic outflow and cause hypotension

2. non catecholamines (amphetamine, methylphenidate) readily enter CNS and have range of effects... likely due to increased dopamine activity rather than alpha or beta stimulation

Front 23

Rapid IV infusion of epinephrine

Back 23

Alpha receptors mainly respond: vasoconstriction of skin and viscera
Beta 1 receptors: increased systolic Pressure
beta 2 receptors: slight increase in diastolic p

heart rate: increases due to b1,but at its peak reflex kicks in and it could decrease (also because the unmasking effect of b2 as ep is eliminated and concentration falls)

Front 24

Slow IV infusion of epinephrine

Back 24

Beta dominates; B2 is more sensitive in low conc than alpha 1 so decrease in diastolic BP

Front 25

Slow IV infusion

Back 25

Beta dominates
- B1 : increased rate and force of contraction
- B2: decrease in diastolic P. Also, some vasodilation, but not enough to initiate the baroreceptor reflex

* so heart rate, force of contraction, cardiac output and stroke volume all increase. No real increase or decrease in BP.

Front 26

Norepinephrine

Back 26

effects Alpha and Beta 1.

- because no significant effect on Beta 2, the increased peripheral Resistance due to alpha 1 will cause reflex which will reduce HR. (but *BP and force of contraction still increase)

Front 27

what can isoproterenol be useful for

Back 27

bronchodilator: B2 agonist

increase HR/stroke vol/co: B1 agonist

*the more selective agonists are usually chosen over isoproterenol

Front 28

How does dopamine work?
1. low doses
2. high doses

Back 28

1. VASODILATOR, acts more on Beta
- dilation of renal, coronary, and mesenteric a's (b2)
- increases Force and rate of contraction (b1)

2. VASOPRESSOR, alpha
- vasoconstriction of peripheral

** D2 are also found on presynaptic terminals and they can inhibit and stimulate the release of NE

** cannot cross bbb (so cannot use for parkinsons)

Front 29

what heart condition is phenylephrine used for

Back 29

Paroxysmal ventricular tachycardia
- it is a vasopressor (alpha 1 agonist) so it causes a reflex reduction in HR

** it also has advantages of treating shock states associated with tachycardia

- also used as decongestant and mydriatic.

Front 30

which drug causes increased BP thru stiulating arterial and venous contraction

Back 30

midodrine (alpha 1 selective agonist)

* used for postural HTN

Front 31

what is the primary mechanism underlying the effects of clonidine

Back 31

activates alpha 2 receptors in brain stem which depress symp outflow

Front 32

which drugs are used to reduce intraocular pressure thru reduction in the preoduction of aqueous humor thru a presynaptic autoreceptor mechanism?

Back 32

apraclonidine and brimonidine

Front 33

Which drugs have a long duration and act as bronchodilators/b2 agonists?

Back 33

salmeterol and formoterol

formoterol has a more rapid onset of action tho

Front 34

Which indirect acting sympathomimetic does not have peripheral cardiovascular effects

Back 34

methylphenidate (ritalin): so it is used to treat adhd (CNS) w/o effecting heart

Front 35

Which drugs should specifically NOT be given w/ MAOIs

Back 35

-Tyramine
-amphetamine, methamphetamine, mehylphenidate, pemoline

Front 36

adverse effects of sympathomimetics

Back 36

- IV infusions can increase BP and Cardiac work, bad for cardiac ischemic pt's and cardiac failure
- b agonists can cause sinus tach and provoke ventricular arrhythmias... be careful w/ elderly or those w/ ht or CAD
-CNS toxicity in amphetamines etc.

Front 37

what is the irreversible alpha antagonist.. what does it do to dose response curve?

Back 37

phenoxybenzamine
- shifts it to the right and reduces max effect (increaseing concentrations of phenoxybenzamine reduces the max response attainable by increasing concentrations of norephinephrine)

Front 38

1. What would happen if you gave an alpha antagonist (phentolamine) in the presence of epinephrine?

2. in the presence of NE? **

Back 38

epinephrine reversal

- blocks alpha peripheral vasoconstriction, so the only thing acting on the periphery is the B2 which causes vasodilatiion....result: decrease in BP

** be careful when u exercise if you are on alpha antagonists

2. NE has little to no B2 activity so you would simply BLOCK the increase in BP (no change in BP would result)

Front 39

Mechanism of phentolamine

Back 39

alpha antagonist
result: vasodilation, increase CO, inc rate

- drop in peripheral resistance cuz alpha 1 blocked so you get a reflex which leads to tachycardia. Tachycardia is also due to the fact that alpha 2 on presynaptic terminals are blocked so more NE is being released and is acting on B receptors.

** it is thougth to have little effect on BP of pt's with essential HTN.. it is used to manage hypertensive crisis, especially when excessive catecholamine release assoc w/ pheochromocytoma surgery

Front 40

What is phenoxybenazamine primarily used for

Back 40

htn due to pheochromocytoma
- irreversibility makes it ideally suited for the large amounts of catecholamines released

Front 41

do selective or non-selective beta blockers initially cause a more modest decrease in (diastolic) pressure?

Back 41

non-selective
ex: propranalol:
when you activate B2 receptors you DECREASE diastolic P. since these are not activated there is less of a decrease in diastolic p.

Front 42

How does propranolol decrease BP?

Back 42

B antagonist
- B1: decreases CO, so decrease BP
- B2: no vasodilation

the reduction in CO leads to a decreased BP... triggers a reflex peripheral vasoconstriction (a1) that results in reduced blood flow to the periphery).
** yet there is still reduction of both systolic and diastolic BPs

** no postural HTN cuz does not act on alpha 1



- with chronic use of beta blockers the peripheral resistant returns to initial values or is decreased (when person has HTN)... it is the DELAYED FALL IN PERIPHERAL RESISTANCE AND PERSISTANT REDUCTION OF CARDIAC OUTPUT THAT ACCOUNTS FOR the antihypertensive actions

Front 43

Which block alpha 1 and Beta receptors?

Back 43

labetalol and carvedilol

Front 44

do normotensive pts who take beta antagonists get hypotension?

Back 44

no

Front 45

what treats supraventricular arrhythmias and ventricular arrhythmias?... also angina and heart failure

Back 45

beta blockers

Front 46

What is the longest acting, nonselective Beta antagonist?

Back 46

nadolol (14-24 hrs)

Front 47

What is the shortest acting B1 selective antagonist?

Back 47

esmolol (10min) used in critically ill pts that may be sensitive to bradycardia, controlling ventricular arrhythmias, arrhythmias assoc w/ thyroid stom, and tachycardia during perioperative prd

Front 48

Which drug can reduce performance anxiety

Back 48

propranolol (B nonselective antagonist)

Front 49

should beta blockers be withdrawn abruptly?

Back 49

no because there is an upregulation of b receptors when antagonists are used.. do it gradually instead

Front 50

what causes vasodilation of corpora carvernosa (erection)

Back 50

b2

Front 51

how does reserpine work

Back 51

indirect adrenergic receptor antagonist that blocks uptake of catecholamines from cytoplasm to vesicles... they then get degraded by monoamine oxidase ... leading to a decrease in NE release and a drop in BP and cardiac rate