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76 Cards in this Set

  • Front
  • Back
which adrenergic blocker binds to alpha 2 receptors?
what is reserpine used for?
hypertension --> decline in BP and HR
what is guanethidine used for?
used to be used for hypertension
AEs: excessive sympathetoplegia interferes with male sexual function, orthostatic hypotension
what is pargyline used for?
parkinsons & depression
what is entacapone used for?
which transporters does cocaine block?
DA, and NE
what are cocaine's effects?
stimulates CNS and cardiovascular system
- euphoria, addiction, tolerance
- HTM, coronary vasospasm --> MI
what is imipramine used for?
same mech as cocaine
- one of the first TCA
which receptor types can epi activate?
what is epi used for?
bronchospasm, anaphylaxis, anesthetics, glaucoma
which receptor types can NE activate?
all, but weak B2 effect
what is NE used for?
sometimes as a pressor for shock, although DA is better
which receptor types can DA activate?
primary actions in basal ganglia and kidney
where do you find the cell bodies of sympathetic neurons?
intermediolateral column of spinal cord, from T1 to L3
where do you find the cell bodies of parasympathetic neurons?
nuclei of cranial nerves (II, VII, IX, X) and S2-4 nerve rootes
draw the sympathetic and parasymathetic schema with NTs
sympathetic: ACh --> ganglia far from end point --> adrenergic NT
parasympathetic: ACh --> ganglia close to end point --> mACh
where are nACh receptors found?
motor end plate
autonomic ganglia
what does bugarotoxin do?
antagonizes the nAChR at the motor end plate
explain ganglionic transmission
there are many factors affecting trasnmission
- initial nicotinic effect leads to an increase in Na conductance and fast EPSP.
- this is modulated by M1 (slow EPSP) and M2/adrenergic (IPSP)
give the relative potencies of adrenergic agonists
a: E > NE > phenylephrine>> isoproterenol

B: isoproterenol> E> NE > phenylephrine
define: tachyphylaxis
certain drugs (e.g ephedrine) release stores of NE. After repeated dosing, the NT may be exhausted
define: receptor down regulation
decrease in number of available receptors or decrease in ligand affinity for the receptor.
e.g. decrease in B1 receptors in myocardium of patients with CHF
define: desensitization
reversible uncoupling of receptor occupancy and cellular response by receptor phosphorylation, then internalization by enodcytosis
(e.g. B adrenergic receptor)
where are M1 receptors found?
ganglia, depolarize
where are M2 receptors found?
Heart, hyperpolarize
where are M3 receptors found?
smooth muscle, depolarize
what is the relative NT potency at B receptors?
iso > Epi > NE
what is uptake1?
the transporter for NE (aka NET)
how do you decrease adrenergic transmission?
attack uptake 1
how do you decrease cholinergic transmission?
attack acetylcholinesterase
where does DA act at high concentrations?
alpha receptors
where does DA act at low concentrations?
beta receptors
what happens with DA binds D1 and D2 receptors?
vasodilation of renal and mesenteric vasculature
why do you use DA for shock?
raises BP by B1 stimulation and aviods kidney shutdown by D1,D2 activation
a1> a2.
direct a agonist
nasal decongestant (from vasoconstriction), raises BP
overcome hypotension brought on by anesthetics
also used in supraventricular Tach
lowers BP in essential HTN by acting at CNS
b1, b2
rarely used as a bronchodilator for asthma
increase CO in CHF.
DOES NOT INCREASE HR significantly- minimal impact on O2 demand
used in asthma as bronchodilator.
reduce uterine contractions in premature labor (ritodrine more commonly used now)
why should you not use B2 agonists during shock?
decrease BP!
a1, a2 antagonist (covalent)
pheochromocytoma treatment
a1, a2 antagonist (competitive)
diagnosis of pheochromocytoma
a1 antagonist (competitive)
decrease BP
increase urinary sphincter relaxiation in patients with BPH
B1, B2
HTN, glaucoma, hyperthyroidism, angina, protective against MI
AD: bronchoconstriction, arrhthia, increased risk of hypoglycemia (makss tachycardia and other signs of insulin reaction)
partial agonist at B1 and B2
HTN who have bradycardia - doesn't lower heart rate that much more
b1 blocker
HTN with impaired pulmonary function, diabetic HTN recieving hypoglycemics
causes release of vesicles from presynaptic terminal, and reversal of DAT, NET, 5HTT
used in depression, narcolepsy, appetite controle
1. release of presynaptic vesicles
2. direct action on a and b receptors
Uses: asthma, BP elevation, nasal decongestant
list 3 MAOIs
what is the danger of tyramine?
when there's too much in a patient given MAOIs for depression, you can cause a hypertensive crisis
tell me more about MAOIs and hypertension
can cause a false transmitter octopamine. diminishes the vascular and cardiac responses
blocks uptake of choline
blocks vesicular uptake of acetylcholine
black widow toxin: oligomerizes to form membrane pores and stimulates large release of NT
what is a nicotinic antagonist?
used as a FAST onset muscle relaxnat during surgery
caveat: pseudocholinesterase deficiency
non-depolarizing musle relaxant binds to nAChR without activating --> paralysis
used as muscle relaxant in surgery
avoids fasciuclations (can cause soreness) of succinylcholine, but doesn't work as fast
non-depolarizing muscle relaxant
can cause histamine release
same as pancuronium
nondepolarizing nicotinic blocker. found in snake venom
blocks nAChR at autonomic ganglia
used for initial control of BP with acute dissectin aortic aneurysm
reduces BP and prevents sympathetic reflexes, reducing the pressure rise near the tear
same as hexamethonium
found in mushrooms. activate mAChR
analog of ACH. less susceptible to AChE
analog of Ach
resistant to AChE
used to reduce intraocular pressure in eye (causes pupillary contraction
analog of Ah
stable against AChE
used in emergency reduction of IOP in both kinds of glaucoma
competitive inhibitor at mAChR
antidote for cholinergic agonists as well as AChE inhibitors
antisecretory drug to prevent pulmonary secretions
similar to atropine but enters CNS more readily
used in motion sickness
when AChE tries to hydorlyze this alkaloid, it's trapped at an intermediate with a long half life
prolongs the effects of ACh
used for potentiating parasympathetic effects: increases intestinal and bladder motility
used in glaucoma to cause miosis--> relieves pressure
same mechanims oas physostigmine, but is more polar so it doesn't cross the BBB
used to treat myasthenia gravis
found in insecticides
traps AChE in phosphorylated form
are toxic!
found in insecticides
traps AChE in phosphorylated form
are toxic!
nerve gas
more potent organophosphate than parathion and malathion
antidotes exist: atropine, pralidoxime
less potent organophoslate used clinically
prolonged relieve of pressure in glaucoma
pralidoxime (2-PAM)
regenerates AChE after phosphorylation
organophsophate poisoning antidote
counters muscarinic side effect but doesn't revers teh skeletal musc fasiculations/paralysis