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71 Cards in this Set

  • Front
  • Back
pilocarpine(action, degredation, targets)
direct acting PSP, is not hydrolyzed by ChE, is most active on the eye
muscarinic receptors (where they are located, which agonist drugs work on them)
located on postganglionic parasympathetic fibers of SM, heart and glands, both PSPs and ChE inhibitors act on them
nicotinic receptors (where they are located, which agonist drugs work on them)
in autonomic ganglia, skeletal muscle and adrenal gland, only ChE work on these, require 2 molecules to bind
physostigmine
tertiary ChE inhibitor, antidote to centrally acting muscarinic blockers, binds to both sites on ChE, inhibits both forms of ChE
atropine
competitive muscarinic blocker, IA of 0, combines will all types of muscarinic receptors, does not bind nicotinic
ganglionic blockers (include 1 example)
combine with nicotinic receptors in para and symp ganglia and block them, don't affect the nicotinic of skeletal muscle, ex: hexamethonium
sites of action of nicotine (5) and effects
ganglia of para (salivation, peristalsis), ganglia of symp (tachycardia, elevated BP, sweating), muscle end plate (fasciulations), CNS (emesis, convulsions), adrenal gland (releases EPI and NE which increaes BP and HR)
phenylephrine
a1 agonist, nasal decongestant, pressor agent in hypotensive states, mydriatic, causes vasoconstriction which increases BP (but not PP) and this causes reflex bradycardia,
norepi
a1 b1 agonist, causes vasoconstriction which increases BP, also is + ionotrope, so PP increases; HR after injection is combo of NE (b1 agonist) and Ach (vagal response) but Ach is greater, so bradycardia results; if you gace atropine before you gave NE, you would block Ach so you would get tachycardia
epi
a1 b1 b2 agonist, used for bronchial asthma and anaphylactic shock; is ionotropic so it increases PP, in low to moderate doses, b2>a1 so diastolic pressure decreases, because the mean pressure does not change, there is no reflex action of the heart; but the b1 action also increases HR via SA node; at high doses, a1>b2 (if you see an increase in diastolic, think high)
isoproterenol
b1 b2 agonist, used to stimulate HR and dilate bronchioles, diastolic decreases due to vasodilation, PP increases due to + ionotropic, B1 also increases heart rate, because mean pressure has dereased there is also reflex tachycardia, so the combined response causes a large increase in HR; if you gave a ganglionic blocker, you would still get an increase in HR but not as high
tryptophan hydroxylase
converts TRP to 5 hydroxytryptophan, rate limiting step, polymorphisms exist and may be associated with bipolar
tryptophan
required for the synthesis of 5HT, melatonin, levels vary with circadian rhyums
AAADC
decarboxylase, produces 5HT
5-HIAA
breakdown product of 5HT, MAO and aldehyde dehydrogense make it, you can measure these levels to give you an idea of how much 5HT is present in the body
melatonin
created from seratonin (via tryptophan), helps you sleep and supresses ovulation
seratonin receptors
are mostly g-protein associated (- 5HT3), 1b and 1d are autoreceptors, have hallucinogenic effects (LSD)
reserpine
blocks the uptake/storage of 5HT so it gets depleted
ecstasy
mdma is an indirect agonist, causes release of 5HT, can reduce your 5HT stores for long periods of time, can cause paranoia, may be permenent loss of 5HT neurons
histimine (produced where, 2 examples of specific receptors and effects)
only produced in the hypothalamus (in CNS), alters food and water uptake, blocking action on H-1 causes sedation since it is an excitatory receptor; H-1 activation also causes bronchoconstriction; H-3 is autoreceptor
GABA
found in Cerebellar Purkinje and SC, metabolism is linked to the TCA, glial cells also involved, large variety of receptor subtypes
histidine decarboxylase
converts histidine to histamine
GABA-A (include 2 agonists and antagonist)
GABA gated Cl- channel w/ 5 subunits, agonism causes hyperpolarization, benzos and barbituates(agonists), and picrotoxin (antagonist) all have action here
picrotoxin (include clinical use)
noncompetitive inhibtor of GABA and Gly, causes seizures, is a barbituate OD antidote; toxicicity treatment includes depressants and lavagel
alcohol and GABA
low level alcohol increases the activity of some GABA receptors, subunit structure may change after alcohol consumtion suggesting some sort of altered gene expression
GHB
breakdown product of GABA, incudes coma and can cause seizures, respiratory depression and amnesia
glycine
major inhibitor NT, has a Cl- ion channel, used by short interneurons, is also a receptor modulator, is synthesized from serine
strychnine
selective competititve antagonist for gly, strong action in the SC, is a pesticide, is a potent convlusant and tonic extension of the limbs; treat with diazepam to control the seizures, support of respiration, lavage with charcoal
hyperplexia
human startle, due to overexcitability and diminished inhibition
GABA transaminase
converts alpha-ketogluterate to glutamic acid
GAD
converts glutamic acid into GABA via decarboxylation, is the regulatory event
tricyclic antidepresants TCAs (1 example, 3 side effects)
amitriptyline, blocks NT reuptake, can be lethal in OD, side effects include sedation, weight gain, cardiac toxicity, may induce a manic stage in a bipolar patient
SSRIs (1 ex, 5 side effects)
fluoxetine, antidepressant, blocks NT reuptake, first line for juviniles, most commonly prescribed, is a stimulant so it is good for patients who are sleeping a lot and being inactive, side effects: increase suicide initially, insomnia and restlessness, sexual changes, may induce manic stage with bipolar patient
MAOIs
phenelzine, antidepressant, blocks MAO which inactivates tyramine, is also a good anti-anxiety and anti-phobic.
side effects: stimulant so there is an increase in suicide rate and also insomnia dn restlessness. also, tyramine interaction (tyramine levels get so high that they cause NE release)causes hypertensive crisis which is in aged cheeses, wine, pepperoni, avocados,
mirtazapine
antidepressant, SE include sedation and weight gain,
bupropion (include mechanism and NTs involved, uses, side effects)
Wellbutrin, antidepressant and used in smoking cessation, works by blocking DA and NE reuptake, has a risk of seizures
lithium
causes NT stabalization, inhibits excitatory, increases 5HT to provide antidepressant activity and is used in bipolar; has the best relapse prevention, is water soluble so it takes a few weeks to build up in the system, need to keep this in mind when prescribing it, is toxic in OD, must do blood tests to monitor; kidney exretion
valproate (also which NT it works through)
mood stabilizer, facilitates GABA which has calming effects on the brain, used in bipolar,is a FA so only takes a few days to be effective, is less likely to OD than lithium, hepatic elimination, also used as antiseizure and migraine prophylaxis, safer in elderly
treatment for bipolar patients who don't respond to lithium or valproate alone
mood stabalizer + antipsychotic +/- benzo
angina pectoris
chest pain due to ischmia of heart muscle, often precipitated by exercise due to increased symp tone, made better by rest
dose response for a drug plus either a competitive vs non competitive adrenergic blocker
non-competitive limits the max response but no right shift, competitive has the same max/line but it is shifted to the right
alpha 1 adrenergic blockers and BP
block the symp tone to arterioles and cause a decrease in BP, is even worse when standing since normally your symp tone standing would be high (vs in supine when it is low so there are fewer effects)
broad spectrum alpha 1 adrenergic blockers (2 examples)
blocks a1 and a2, produces tachycardia because as the a1 causes a decrease in BP, the heart is stimulated, also, a2 is blocked, so there is no feedback inhibition, so NE and EPI are circulting which increases the HR even more; phentolamine and phenoxybenzamine
propranolol
is a broad spectrum beta blocker, B1=B2, is contraindicated in asthmatic patients because it may precipitate an attack
phentolamine
is a alpha 1 adrendergic blocker (also a2), used for a1 vasoconstriction (large amounts of NE), lower BP in essential hypertension, facilitate voiding in patients with enlarged prostate
atenolol
is a cardio selective beta blocker, B1>B2, less chance of having an asthmatic effect
pindlol
is a broad spectrum beta blocker (B1=B2) with intrinsic activity (partial agonist), if you gave this to a patient having a asthma attack, you would use up the receptors in the lungs with the partial agonist and wouldn't be able to give enough albuterol to overcome it
thereupeutic and unwanted effects of broad specturm beta blockers
b1 blocks reflex tachycardia which is the therapuetic effect but can cause asthma attack (unwanted)
use of beta blockers
useful in the treatment of angina, arrythmias and hypertension; also to block the physical manifestations of anxiety
albuterol
is a b2 selective agonist (B2>B1), used in asthma, may precipitate an angina attack in predisposed patients (B1)
diazepam
benzodiazapine, long acting when given chronically, has a metabolite which can accumulate and is active and contibutes the major therepeutic effects; liver oxidation (not good for pts with liver disease), if given for 1 dose, it will act quickly because its lipophilic but it also leaves quickly
lorazepam
short acting benzo when given chronically, are less lipophilic so they have a longer onset, if given only once it will appear to act for a long time since it takes awhile to exit the brain, is glucuronidated (easier on liver, better choice for pts with liver disease)
precautions of benzos
CNS depression (sedation, ataxia), anterograde amnesia, disinhibition, tolerence, withdrawal, dependence
drug interactions of benzos
need to be careful with other CNS depressants such as EtOH, antacids, cigarettes; want to give lowest dose for shortest amount of time, need to watch for hx of subst abuse, pregnancy and suicidality
buspirone
is a 5HT1a agonist, has only anxiolytic function and possibly some sedation, little abuse potential, lag time to onset
benzo mode of action
GABA system
uptake 1
takes up excess NE in the cleft and returns it to be reused
cocaine (mech, NT it works on, what to do give in OD, eye effects)
blocks the reuptake of NE and causes symp effects, potentiates NE, also DA in the CNS; is a vasoconstrictor (alpha 1) so it can be used to stop nose bleeds in surgery; can use propanolol in cocaine OD to block the effects on the heart, will have mydriasis but still have light reflex
tyramine
indirect acting sympathomimetic with no agonist action so it requires the presence of a post ganglionic nerve, is taken up by Uptake 1 and once inside the presynaptic terminal, it causes release of NE; can inhibit its action by depleting NE (reserpine) or by giving cocaine to block its reuptake into the presynaptic terminal
reserpine
depletes NE in the adrenergic terminal (has no action if there is no NE stored), inhibits both the uptake of NE into vssicles as well as the uptake of DA (precursor to NE)
ephedrine
has both indirect agonist and direct agonist action on the adrenergic terminal, is transported via uptake 1 into the presyn and causes release of NE which acts on the a1 receptors in nasal vasculature and constricts them and inhibits mucosal secretion; also acts directly by binding to b2 and causing bronchdilation; side effects are hypertension (a1) and cardiac arryhtmias (b1)
methyl dopa
used for lowering BP, is a prodrug that becomes methyl-NE in the cell, this acts on a2 autoreceptors to decrease the release of NE and decrease BP, side effects: diarrhea, ejaculation failure, postural hypotension, sedation (crosses BBB)
clonidine
used in lowering BP, is a central a2 agonist, decreases BP by lowering NE output; patient must avoid stopping medication immediately because they will experience rebound hypertension (when on clonidine, you downregulate a2 and upregulate a1, so when you stop taking it abruptly, you get hypertension crisis); can reduce the eleveated NE activity associated with nicotine withdrawal
treatment for clonidine rebound hypertension
give an alpha 1 blocker to decrease the BP (phentolamine); also give a b1 blocker to decrease tachycardia (propanolol)
guanethidine
is good at lowering severe hypertension but has a very sharp dose response curve, so you need to be careful when titrating your patient; has no agonist or antagonist action but works by deleteing NE (is taken into the presyn by uptake 1, fills the vessicles and is released, but doesn't bind to the receptor); can cause severe postural hypotension but doesn't cross the BBB
methyl tyrosine
is a tyrosine hydroxlase inhibitor, inhibits syntehsis of NE and epi; used in patients with pheochromocytomas
p-chlorophenylanin
irreversibly inactivates tryptophan hydroxylase which decreases 5HT
phenoxybenzamine
is an irreversible broad spectrun a1/a2 blocker
prazosin
an a1 specific blocker, no a2 effects
labetalol
broad spectrum b blocker with a1 blocking activity too
main problem and benefit of antihistamines as anxiolytics
take advantage of the sedative effects; are highly anticholinergic (constipation and blurred vision);
almost no abuse potential