Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
97 Cards in this Set
- Front
- Back
|
ganglion blockers (2)
|
hexamethonium
mecamylamine lower BP |
|
|
hexamethonium
|
ganglion blocker
lower BP |
|
|
mecamylamine
|
ganglion blocker
lower BP |
|
|
AChE I (2)
|
neostigmine (myasthenia gravis)
physostigmine (atropine poisoning) |
|
|
neostigmine
|
AChE I
myasthenia gravis |
|
|
physostigmine
|
AChE I
gets into CNS atropine poisoning |
|
|
anti-muscarinics (4)
|
Atropine
Scopolamine Diphenhydramine Imipramine |
|
|
scopolamine
|
anti-muscarinic
gets into CNS motion sickness sedation pre-anesthetic (sedation + less bronchial secretions) |
|
|
atropine
|
anti-muscarinic
AChE I poisoning lots of uses |
|
|
diphenhydramine
|
anti-muscarinic
gets into CNS antihistamine motion sickness sedation |
|
|
imipramine
|
anti-muscarinic
gets into CNS tricyclic antidepressant |
|
|
muscarinics (2)
|
bethanechol
pilocarpine |
|
|
bethanechol
|
muscarinic
post-surgical atony post-surgical urinary retention xerostomia (dry mouth) |
|
|
pilocarpine
|
muscarinic
open angle glaucoma (drains aq humor) |
|
|
Nm antagonist (1)
|
curare
muscle relaxation |
|
|
curare
|
Nm antagonist
muscle relaxation |
|
|
Nm + Nn agonist
|
nicotine
|
|
|
nicotine
|
Nm + Nn agonist
gets into CNS |
|
|
blocks ACh vesicle release
|
botulinum toxin
|
|
|
botulinum toxin
|
blocks ACh vesicle release (degrades synaptobrevin, a SNARE)
muscle paralysis |
|
|
side effects of ganglion blockers
|
orthostatic hypotension
palpitations, tachycardia photophobia (from mydriasis) blurred vision (from cycloplegia) constipation urinary retention xerostomia (dry mouth) anhidrosis (dry skin) impotence exercise intolerance |
|
|
use of anti-muscarinics
|
Peripheral:
rhinitis asthma/COPD eye exams bradyarrhythmia reduce gastric secretions urinary incontinence AChE I poisoning myasthenia gravis (+ AChE I) CNS: anti-tremor in parkinson's motion sickness sedation anthistamine antidepressant atypical antipsychotics |
|
|
symptoms of atropine poisoning
|
"dry as a bone, red as a beak, crazy as a loon"
peripheral signs: tachycardia, urinary retention, constipation, blurred vision, dry mouth, less sweating CNS: ataxia, hallucinations peripheral + CNS: hyperthermia |
|
|
treating myasthenia gravis
|
AChE I (increase ACh at NMJ) +
anti-muscarinic (block ACh at para neuroeffector junction) |
|
|
side effects of muscarinics
|
diarrhea, urinary urgency, less HR, etc.
|
|
|
sensitivity to atropine (most-->least)
|
1. salivation, sweating
2. dilation of eye, heart 3. GI, bladder 4. gastric secretion |
|
|
8 ways drugs can act
|
1. limit/modify biosynthesis
2. prevent sequestration of NT into vesicles 3. prevent vesicle release 4. induce vesicle release 5. modify inactivation mechanism 6. agonist/antagonist at receptor 7. block repolarization 8. metabolize into false transmitter |
|
|
a1 response
|
constrict BV mostly veins (skin, mucous membranes, kidneys)
piloerection pupil dilation (constrict radial muscle) constrict bladder neck relax GI CNS effects |
|
|
b2 response
|
all about relaxation:
relax BV (coronary, skeletal muscle) relax GI relax uterus relax bladder bronchodilation |
|
|
b1 response
|
heart (+chrono/ino/dromotropy)
renin release |
|
|
nonselective drugs for adrenergic (5)
|
epi (a, b ag. stronger on b than a)
NE (a, b1 ag) phentolamine (a antag) isoproterenol (b ag) propanolol (b antag) |
|
|
a1 agonist
|
phenylephrine
|
|
|
a antagonist
|
phentolamine
|
|
|
phenylephrine
|
a1 agonist
eye exam (mydriasis) nose spray (reduce congestion by local vasoconstriction) |
|
|
phentolamine
|
a antagonist
antihypertensive side-effect: tachycardia since: baroreceptor reflex block a2 in heart --> more NE release |
|
|
epi
|
alpha + beta agonist
stronger on beta cardiac arrest anaphylactic shock: a1 - constrict BVs --> less secretions + more BP b1 - more CO b2 - bronchodilation b - inhibit mast cell release |
|
|
NE
|
alpha + beta 1 agonist
septic shock increase BP |
|
|
isoproterenol
|
b agonist
acute coronary insufficiency asthma/COPD palpitations, arrythmia, drop in BP |
|
|
propranolol
|
b antagonist
arrythmia all things b-blockers do side effect: bronchoconstriction |
|
|
dobutamine
|
b1 agonist - heart
some a agonist - peripheral vasoconstriction shock (acute coronary insufficiency) |
|
|
b1 agonist
|
dobutamine (part a agonist too)
|
|
|
b1 antagonist
|
atenolol
|
|
|
atenolol
|
b1 antagonist
arrythmia |
|
|
b2 antagonist
|
butoxamine
|
|
|
butoxamine
|
b2 antagonist
no clinical utility |
|
|
b2 agonist (3)
|
terbutaline
ritodrine ephedrine (mixed symp) |
|
|
terbutaline
|
b2 agonist
asthma/COPD at high doses can get b1 effects, since all are selective not specific (dog example) |
|
|
ritodrine
|
b2 agonist
delay parturition |
|
|
ephedrine
|
mixed sympathomimetic
direct: b2 agonist (bronchodilation) indirect: NE release at BVs (less congestion) side effect: increase BP |
|
|
mixed sympathomimetic
|
ephedrine
|
|
|
NT that causes most b2 activation
|
Epi
|
|
|
NT that causes most b1 activation
|
NE
|
|
|
a2 response
|
auto/hetero receptor
gut relaxation (hetero) |
|
|
autoreceptor
|
a2
NE inhibits its own release |
|
|
heteroreceptor
|
a2
NE inhibits ACh release from parasymp nerve terminals |
|
|
how do sympathetics inhibit gut contraction?
|
a1 - direct relaxation
b2 - direct relaxation a2 - relaxation (heteroreceptor of NE for ACh) |
|
|
prazocin
|
a1 antagonist
anti-hypertensive BPH (ease urinary outflow) |
|
|
a1 antagonist
|
prazocin
|
|
|
clinical use of a1 agonist
|
tachyarrythmias (slow heart via baroreceptor)
orthostatic hypotension reduce congestion (local vasoconstriction) eye exam not shock (does more harm than good) |
|
|
clinical use of a2 agonist
|
antihypertensive
|
|
|
a2 agonist (2)
|
a-methyl-DOPA (via a-methyl-NE)
clonidine |
|
|
clonidine
|
a2 agonist
antihypertensive (CNS --> reduce symp outflow) |
|
|
clinical use of a2 agonist
|
antihypertensive (CNS --> reduce symp outflow)
|
|
|
clinical use of a1 antagonist
|
antihypertensive
BPH - ease urinary outflow side effects: orthostatic hypotension |
|
|
gene products of a receptor
gene products of M receptor |
a1A - a1C, a2A - a2C
M1-M5 |
|
|
clinical use of b2 agonist
|
asthma & COPD
delay parturition |
|
|
clinical use of b1 agonist
|
cardiac decompensation
|
|
|
clinical use of b antagonist
|
arrythmia
cardioprotection after MI antihypertensive angina migraine panic attacks glaucoma congestive heart failure (slow titration) |
|
|
side effects of b-antagonist
|
acute CHF
bronchospasm bradyarrhtymia worsen peripheral vascular disease withdrawal syndrome (hypersympathetic) |
|
|
mechanism of beta-blocker for treating hypertension
|
lower CO (b1)
increase TPR initially later lower TPR (unknown mech, possibly by lowering renin) |
|
|
treating angina
|
NG + beta blocker
nitroglycerin (venous dilation --> reduce preload) beta blocker (block baroreceptor reflex caused by NG) |
|
|
how can a beta blocker cause acute CHF
|
b1 effects: lower CO --> cannot adequately perfuse tissue --> acute CHF
|
|
|
Steps in synthesis of NE/Epi
|
Tyr (extracell) --> Tyr (intracell) --> DOPA (via Tyr hydrox) --> DA (via DDC) --> enters vesicle --> NE (via DA b-hydrox)
To get Epi, NE leaves vesicle --> NE in cytoplasm --> Epi (via PMNT) DDC = dopa decarboxylase PMNT = phenylethanolamine-N-methylteransferase |
|
|
what NE can do after release
|
1. diffuse away
2. reuptake (active transport). Primary method of ending NE action. After 2: a. recycle (go to vesicle) b. go to mitochondria --> inactivate by MAO |
|
|
rate liming steps in degradation of NE and Epi
|
MAO and COMT
|
|
|
DDC inhibitor
|
carbidopa
Parkinson's |
|
|
carbidopa
|
DDC inhibitor
Parkinson's - reduce side effects of giving DOPA (reduces DA production in periphery) |
|
|
indirect sympathomimetc
|
tyramine
|
|
|
tyramine
|
indirect sympathomimetc
displace NE in vesicle --> NE diffuse into synapse |
|
|
reserpine
|
inhibit vesicular transporter for NE, DA, 5-HT
tranquilizer side effect: depression |
|
|
vesicular transporter inhibitor
|
reserpine
|
|
|
reuptake inhibitor
|
cocaine
|
|
|
cocaine
|
DA reuptake inhibitor
|
|
|
false neurotransmitter
|
a-methyl-DOPA
|
|
|
a-methyl-DOPA
|
false neurotransmitter
antihypertensive enters brain --> DDC converts to a-CH3-DA --> DBH converts to a-CH3-NE --> released in terminals --> selective a2 agonist --> reduce sympathetic outflow from CNS --> lower BP |
|
|
COMT I
|
tolcapone
|
|
|
tolcapone
|
COMT I
Parkinson's (increase levels of DOPA, which is metabolized by COMT) |
|
|
MAOI
|
trianylcypramine
|
|
|
trianylcypramine
|
non-selective, irreversible MAOI
antidepressant side effects: hypertensive crisis (tyramine and other biogenic amines are not degraded) avoid beer, wine, cheese, pickled fish |
|
|
COMT
|
catechol-O-methyl transferase
soluble enzyme, with high levels in liver and kidney metabolizes NE (no role at synapse), Epi, DOPA |
|
|
treating Parkinson's
|
DOPA
COMTI (tolcapone) - extend half life DDCI (carbidopa) - reduce side effects MAO-B I - slow DA metabolism |
|
|
MAO
|
mitochondrial enzyme found in all tissue
converts 1o and 2o amines --> aldehydes and ketones two forms: MAO-A (NE, 5-HT, a little DA) MAO-B (DA) |
|
|
b3 resopnse
|
lipolysis in fat cells
not targeted by any drugs |
|
|
ACh synthesis
|
Choline (extracellular) --> uptake --> add to Ac-CoA (CAT) --> ACh packaged in vesicles
|
|
|
How does cholinergic transmission end
|
Primary method:
AChE in synapse cleaves ACh --> Choline + acetate --> choline uptake by presynaptic neuron |
|
|
metyrosine
|
TOH (tyr hydrox) inhibitor
loss of DA, NE, and Epi |
|
|
TOH (tyr hydrox) inhibiotr
|
metyrosine
|
