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60 Cards in this Set

  • Front
  • Back
choline acetyltransferase (CHaT)inhibitor
interacts with synaptobrevin to prevent ACh release and is used in blepharospasm, strabismus.hyperhydrosis, dystonia, and cosmetics
botulinum toxin
reversible AChE inhibitors (3)
"reversible achy PEN"
irreversible AChE inhibitors (3)
EMP irreversibly screws up electricle circuits

txt for ileus and urinary retention
bethanechol (muscarininc agonist)
diagnoses bronchial hyperreactivity
txt for glaucoma when applied topically.
txt for xerostomia (dry mouth)
used to differentiate myasthenia from cholinergic crisis
reversible acetylcholinesterase inhibitor used to txt glaucoma.
-it is a tertiary amine that can enter the CNS
-It is an antidote in atropine overdose.
Acetylcholinesterase inhibitors that are lipid-soluble
-capable of entering the CNS
-Txt for Alzheimer disease
Donepezil and Tacrine
irreversible acetylcholinesterase inhibitors that are lipid soluble.
txt for glaucoma
Echothiophate is a txt for glaucoma
Organosphasphates are used as insecticides (malathione and parathione) and as nerve gas (sarin)
AChE poisoning"
Excitation (Muscle and CNS)
organophosphate (malathione and parathione) toxixcity side effects

muscarinic effects (dumbbelss"
-CNS stimulation

Nicotininc effects:
-skeletal muscle excitation followed by paralysis
-CNS stimulation

-give atropine to counteract the muscarinic stimulation
-give pralidoxime (2-PAM) for the regeneration of AChE.
***It is important that pralidoxime is given as soon as possible because there is time dependent aging of the phosphorylated organophosphate-AChE cmoplex. after aging, the complex is no longer reversible by pralidoxime!!!
-Muscarinic receptor antagonists
-A tertiary amine
-The drug enters the CNS

-Effecs of the drug in order of increasing dose:
1-decreased secretions (salivary, bronchiolar, sweat)
2-mydriasis (dilation of pupils) and cycloplegia (paralysis of ciliary muscle resulting in inability to accomodate lens)
3-hyperthermia (with resulting vasodilation)
4- tachycardia
5- sedation
6- urinary retention and constipation
7-behavioral excitation and hallucinations
"Dry as a bone, Blind as a bat, red as a beet, mad a a hatter"
Muscarinic antagonist that is used as:
-management of AChE inhibitor overdose
-in ophthamology
muscarininc antagonist used as a topical in opthamology
Muscarinic antagonist used in the txt of asthma and COPD (inhaltional).
Drug has no CNS entry and no change in mucus viscosity
Muscarinic antagonist used in motion sickness.
The drug causes sedation and short-term memory block.
Muscarinic antagonist
-is lipid-soluble (CNS entry)
-used in parkinsonism and in acute extapyramidal symptoms induced by antipsychotics
Benztropine and Trihexyphenidyl
The Nn antagonists are ganglionic blockers (2 drugs?). Thus they affect both the Sympathetic and Parasympathetics.
what are the effects?
Hexamethonium and Mecamylamine

For effector tissues with dual innervation, Parasympathetic is dominant- these include the SA and AV nodes, the pupil, GI and GU muscles, and sphincters. Sympathetics are only dominant in terms of vascular tone and thermoregulatory sweat glands.

effects of blocking sympathetic ganglia:
-arterioles vasodilation, hypotension
-veins: dilation, decreased venous return, decreased cardiac output
-sweat glands: anhydrosis

effects of ganglionic blocking agents in tems of parasympathetic ganglia:
heart: tachycardia
iris: mydriasis
ciliary muscle: cycloplegia
GI tract: decreased tone and motility (constipation)
bladder: urinary retention
salivary glands: xerostomia

** Ganglion blocking drugs prevent reflex changes in heart rate elicited by vasoconstriction (alpha1) and vasodilation (beta2). However, ganglionic blocking drugs do not prevent changes in HR elicited directly by the drug (beta1 or M2 agonists).
alpha1 adrenergic effects
-contraction of radial (dilator) muscle (mydriasis)
-constriction of the arterioles of the skin and viscera (increased TPR and afterload)
-constriction of the veins (increased venous return and pretload)
-bladder and trigone actions (urinary retention)
-vas deferns (ejaculation)
-liver: increased glycogenolysiis
-kidney: decreased renin release
alpha2 adrenergic actions
-prejunctional nerve terminals: decreased transmitter release and NE synthesis
-platelet aggregation
-pancreas: decreased insulin secretion
beta1 adrenergic actions
SA node: increased HR (positive chronotropy)
-AV node: increased conduction velocity (positive dromotropy)
-Atrial and ventricular muscle: increased force of contraction (positive inotropy), conduction velocity, CO and O2 consumption
His-Purkinje: increased automaticity and conduciton velocity
Kidney: increasaed renin release
beta2 adrenergic actions
all blood vessels: vasodilation (decreased TPR, decreased diastolic pressure., and decreased afterload)
-uterus: relaxation
-bronchioles: dilation
-skeletal muscle: increased glycogenolysis (contractility and tremor)
-liver: increased glycogenolysis
-pancreas: increased insulin secretion
actions of D1 in periphery (renal, mesenteric, coronary vasculature)
vasodilation-in kidney (increased renal blood flow, increased GFR, increased Na secretion)
Beta receptors are usually more sensitive to activators than alpha receptors. With drugs that exert both efects, the beta responses are dominant at low doses. At higher doses, the alpha responses will predominate.
As you increase the doses of dopamine to treat shock what receptors will be activated?
first D1
then beta1
finally, alpha1
G-proteins corresponding to adrenergic receptors?
alpha1: Gq coupled (increased phospholipase C=> IP3, DAG, Ca2+)

alpha2: Gi coupled (decreased adenyl cyclase)

all others (beta1, beta2, and D1): are Gs coupled (increased adenyl cyclase)
alpha1 adrenergic agonists (2 drugs and their uses)
phenylephrine: nasal decongestant and opthalmologic use (mydriasis without cycloplegia)

methoxamine: paraxysmal atrial tachycardia (PAT) through vagal reflex.
alpha1 adrenergic agonist

Txt: paraxysmal atrial tachycardia (PAT) through vagal reflex.
alpha1 agonist that is used as a nsal decongestant and used in ophthamology (mydriasis without cycloplegia)
what ate alpha2 agonists used for and what are the two drugs?
clonidine and methyldopa (used to treat mild to moderate HTN).
Beta agonist (beta1=beta2)
-Used for bronchospasm, heart block, and bradyarrythmias.
-Side effects: flushing, angina, and arrythmias
beta agonist (beta1>beta2)
-Txt for congestive heart failure
Selective beta2 agonists

what are the drugs and their uses?
"SAT": Salbuterol, albuterol, and terbutaline are used in asthma

Ritodrine is used in premature labor
Effects of norepinephrine and the recpetors it acts on?
agonist for alpha1, alpha2, and beta1

alpha1: increases TPR and BP
beta1: increases HR, SV, CO, and pulse pressure

** there is a potential reflex bradycardia
*** NE has no effect on beta2 receptors
Effects of epinephrine and the receptors it acts on?
agonist for alpha1, alpha2, and beta1, and beta2

at low doses of Epinephrine:
beta1: increased HR, SV, CO, and pulse pressure
beta2: decreased TPR and BP

at medium doses:
beta1: increased HR, SV, CO, and pulse pressure
beta2: decreased TPR and BP
alpha1: increases TPR and BP!!

At high doses:
beta1: increased HR, SV, CO, and pulse pressure
beta2: decreased TPR and BP
alpha1: increases TPR and BP!!
AND there is potential reflex bradycardia!!!
Other drugs classes that have antimuscarinic effects:
-tricyclinc antidepressants
How do you treat an overdose of muscarinic antagonist (ie atropine)?
physostimine, which is a cholinesterase inhibitor.
In which 2 diseases are antimuscarinics strongly contraindicated?
2- glaucoma
What are the primary used of ganglion blocking agents?
Hexamethonium and Mecamylamine

They prevent baroreceptor reflex changes in HR!!!
Name 2 reuptake inhibitors
2-tricyclic antidepressant (in part)
What drugs should a pt being prescribed MAO inhibitors avoid in order to prevent hypertensive crisis?
The releaser drugs:
1-tyramine (found in red wine and cheese)***
2-amphetamines (clinically used as methyl phenidate in narcolepsy and ADHD) (note that amphetimine is a psychostimulant because of the central release of DA, NE, and 5HT)

3- ephedrine (cold medication)
what are the locations of MAO's
MAO type A: mainly in the liver but AAnywhere (metabolizes NE, 5HT, and tyramine)

MAO type B: mainly in Brain (metabolizes DA)
what drug will you give a pt with BPH (benign prostatic hyperplasia)
a selective alpha1 blocker, which will release the bladder sphincters and allow full voiding whenever going to the bathroom.
what drug is used for male-pattern baldness?
what are the uses of alpha receptor antagonists?
alpha receptor antagonists decrease TPR and decrease BP.

Used for:
2-pheochromocytoma (nonselective alpha blocker)
3-benign prostatic hyperplasia (use alpha1 blocker)
what are the 4 selective alpha1 blockers?
"-azosin" drugs:
what are the 2 selective alpha2 blockers?
1-yohimbine used in postural hypotension and impotence

2-mirtazipine sued as an antidepressant
In what 3 diseases should beta2 blockers be avoided?
beta2 blockers must be avoided in:
1-asthmatics because may precipitate bronchospasm
2-vasospasm disorders (Raynauds's and Prinzmetal Angina)
3-diabetics because block glycogenolysis and gluconeogenesis
what beta blocker drugs shoudl be avoided in diabetics?
All beta blockers should be avoided in diabetics!!
what beta blocker has no CNS depressant (sedative) effect because it is the only one that is very water soluble and thus has no CNS entry?

what beta blocker has the greatest CNS depressant (sedative) effect?
what beta blocker has no CNS depressant (sedative) effect?

what beta blocker has the greatest CNS depressant (sedative) effect?
Pt drinks lots of alcohol, what beta blocker must be avoided?
Propranolol is the beta-blocker with the greatest CNS depressant (sedative) effect
beta-blockers cause hyperlipidemia
what 2 beta blockers are not associated with hyperlipidemia and may actually decrease blood lipids?
The Intrinsic Sympathetmimetic Activity beta-blockers which act as partial antagonists.
Thus they have less bradycardia (beta1) and minimal change in plasma lipids (beta2)

Uses of beta-blockers:
-angina, HTN, post-MI
-migraine, thyrotoxicosis, performance anxiety, essential tremor
Uses of beta-blockers:
-angina, HTN, post-MI (all beta-blockers)
-antiarrythmics (class II: propanolol, acebutolol, esmolol)
-glaucoma (timolol)
-migraine, thyrotoxicosis, performance anxiety, essential tremor (propanolol)
combined alpa1 and beta blocking activity
-used in txt of CHF
K+-channel blocakade and beta-blocking activity
-used as an antiarrythmic (class III)
what 2 drugs are contraindicated in open-angle glaucoma?
1-antimuscarininc drugs
2- alpha1 agonists
What are the three most commonly used drugs used in txt of glaucoma?
Pilocarpine and Echothiophate: activation of Muscarininc receptors causes contraction of ciliary muscle, which increases flow through the canal of Schlemm; echothiophate is an organophosphate (AChE inhiitor leads to increased outflow of aqueous humor)

Timolol: is a beta blocker that blocks the actions of NE at ciliary epithelium and thus decreases aqueous humor production