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124 Cards in this Set

  • Front
  • Back
a patient has been overdosed with an irreversible AChE? how do you help them
1. maintain vital signs
2. remove patient from exposure
3. atropine
4. 2-PAM

you can prolong the time to get help by giving a reversible AChE to block the binding site so the irreversible AChE wont bind
in terms of ganglia, what is the difference between somatic and autonomic systems?
autonomic:
1. preganglionic nerves: all cholinergic
2. postganglionic nerves: cholinergic and adrenergic
3. plexuses: complex network of synapses

somatic:
1. NO GANGLIA: peripheral synapses occur on skeletal muscle...NMJ
a patient has a hard trauma with consequent damage to their parasympathetic sacral nerve? what drugs can you use to substitute?
cholinergic agonist
example: bethanechol
in terms of regulation, what are the differences between the autonomic and somatic nervous systems?

where do they synapse
autonomic:
1. Heart
2. Visceral organs
3. Glands
4. Smooth muscle
-spinal efferents form synapses in peripheral ganglia

somatic:
1. Movement
2. Respiration
3. Posture
-synapse within cerebrospinal axis result in spinal efferent nerves
what is the mechanism for succinylcholine
neuromuscular blocking agent
1. depolarizing the NMJ
2. desensitize the nAChR because AChE can't break it down
what allows for a full and rapid ACTIVATION of the sympathetic system
1. interconnectivitiy
2. preganglionic axons are SHORT
when compared to rocuronium, tubocurarine...
preganglionic fibers release...
postganglionic fibers release...
1. preganglionic fibers release...ACh

2. postganglionic fibers release...NE and ACh
what can be used to dephosphorylate AChE
PRALIDOXIME (2-PAM)
where do most of the fibers of the preganglionic parasympathetic system terminate
1. most terminate on ganglion cells distributed diffusely or in networks within the walls of the innervated organs
2. designed so that individual target organs can be activated independently

pre (all) and post (majority) ganglionic parasympathetic fibers release ACh
what is the mechanism for pilocarpine
activate parasympathetic organs secondary to stimulating ganglionic receptors
what are the neurotransmitters of the somatic nervous system
1. presynaptic neurons are cholinergic
2. secrete ACh on postsynaptic muscle cells expressing nicotinic acetylcholine receptors (nAChR)
3. ACh binds to and activates the postsynaptic nAChRs which stimulate muscle contractions
anticholinergic (atropine) should NOT be used for a gastric ulcer because
it is not selective for decreasing stomach acid production and it inhibits gastric acid being emptied from the stomach
what is a reflex arc
the bodies way of detecting a stimulus and responding to the situation.

1. stimulus comes into effector tissue
2. the efferent neuron synapses in the spinal chord either directly with the efferent motor neuron or an interneuron
3. then stimulates the appropriate response from the effected tissue
reserpine acts by...
depleting the reservoirs of norepinephrine from the nerve terminal
where are the cholinergic neurons
1. all preganglionic neurons (para and sympathetic)
2. all skeletal muscle @ NMJ (somatic)
3. postganglionic parasympathetic fibers (not all some use NO or peptides)
4. postganglionic sympathetic fibers innervating the sweat glands
cholinergic agents will have effects that overlap with
anticholinesterase drugs
most sympathetic post ganglionic neurons are...
adrenergic
propranolol is CONTRAINDICATED in patients with
NON SELECTIVE BETA BLOCKER
1. hyperthyroidism
2. congestive heart failure
3. asthma
4. diabetes
what are the steps in CHOLINERGIC TRANSMISSION
1. choline uptake (choline transported into the neuron and acetyl CoA is made by the mitochondria intracellularly)
2. ACh uptake vesicle
3. vesicle fusion (neuron is depolarized, opening Ca++ channels, rise in calcium concentration causes a fusion of vesicle with synaptic membrane)
4. bind to Ach receptors
5. degradation (terminated by acetylcholinesterase, split ACh into acetate and choline)
mechanism by which phenylephrine treats paroxysmal atrial tachycardia is...
phenylphrine will increase blood pressure through stimulation of alpha 1 receptors, which leads to a reflex bradycardia
what are the steps in adrenergic transmission
1. tyrosine uptake
2. tyrosine hydroxylase (rate limiting step, hydroxylation of tyrosine to dopa by tyrosine hydroxylase)
3. dopamine synthesis (dopa decarboxylated to dopamine)
4. dopamine transport
5. NE synthesis (dopa to NE by dopamine-B-hydroxylase)
6. NE release
7. adrenergic receptors
8. termination of transmission (REUPTAKE in nerve terminal)
9. NE degradation (NOT primary mechanism for termination)
muscarine stimulates what receptor sites?
parasympathetic organs and tissues
in respects to activation, what is the difference between sympathetic and parasympathetic
sympathetic:
1. in toto
2. not absolutely required for sustaining life

parasympathetic:
1. predominate tone at resting
2. REQUIRED to maintain life
3. in toto activation is LETHAL (organophosphate poisoning)!!
what alpha antagonist binds IRREVERSIBLY to alpha 1 receptors
PHENOXYBENZAMINE
what is considered the principle loci of autonomic integration
higher level than spinal cord:
1. medulla oblongata
2. hypothalamus

these reflex arcs are extremely important compensatory mechanisms
what is an anticipated effect of a beta 1 blocker (atenolol)
basically beta blocker effects

1. decreased heart rate
2. decreased renin release
3. decreased blood pressure
4. decreased contractility
what is the NET EFFECT of an infusion of NE...in respects to the HEART
1. vasoconstriction
2. increase peripheral resistance
3. increase mean arterial pressure (MAP)
4. decrease sympathetic output to heart
5. increase parasympathetic output to heart
beta receptors would be expected to down regulate with the chronic administration of what
BETA AGONIST like albuterol
what are the two types of cholinergic synapses
1. nicotinic
2. muscarinic
what are the beta 1 blockers
A.N.A.M.E

1. acebutolol
2. nebivolol
3. atenolol
4. metoprolol
5. esmolol
cholinergic antagonists are sometimes called...
parasympatholytic

since they block the actions of the parasympathetic system on effector tissue
what are the non selective beta blockers
1. propranolol
2. penbutolol
3. pindolol
4. carvedilol
5. labetalol
6. nadolol
7. timolol
what is the structure for a muscarinic antagonists...examples
tertiary-amine: ATROPINE (well absorbed in gut and conjunctival membrane, scopolamine even absorbs in skin)

quarternary-amine: IPRATROPIUM (not charge, not absorbed in CNS, used for peripherals)
what is a CONTRAINDICATION of albuterol?

what other drugs have the same contraindications
1. hypertension
2. coronary artery disease
3. congestive heart failure
4. diabetes

TRAM:
terbutaline, ritodrine, albuterol, metaproterenol
what is the mechanism of action for muscarinic antagonist
COMPETITIVE ANTAGONIST

atropine in NON-SELECTIVE (binds equally to M1-M5)
what is a beta 1 agonist
dobutamine
at what site is sympathetic tone dominate
1. arterioles (adrenergic)
2. veins (adrenergic)
3. sweat glands (cholinergic)
4. genital tract
what class of drug is isoproterenol
non selective beta agonist
at what site is parasympathetic (cholinergic) tone dominate
1. heart
2. iris
3. ciliary
4. GI
5. urinary bladder
6. salivary glands
7. genital tract
the primary variable in the cardiovascular system that is controlled by the ANS is...
mean arterial pressure
what happens with antimuscarinic in the EYE
1. pupillary constrictor has parasympathetic tone
2. blocking muscarinic will cause dilation (mydriasis, due to sympathetic dominance)
what is norepinephrine selective for
alpha agonist
beta 1 agonist
what are the cautious situations that must be taken into account when using antimuscarinics with the EYE
1. antimuscarinic can precipitate acute glaucoma in a patient with a narrow anterior chamber angle
2. anticholinergic can block the contraction of the ciliary muscle (CYCLOPLEGIA) and LACRIMINATION

CONTRAINDICATION:
1. dry eye
2. high IOP (glaucoma)
3. small/closed angle
what is an alpha 1 agonist that can be administered systemically as a pressor agent
phenylephrine
what is the result of moderate to HIGH DOSAGE of antimuscarinic (atropine) on the cardiovascular system
blockade of the vagal activity in the SA node of the HEART

TACHYCARDIA (no change in BP)!!!
what are the indirect acting sympathomimetics
1. amphetamine
2. methamphetamine
3. methylphenidate
4. pemoline
what is the result of moderate to LOW DOSAGE of antimuscarinic (atropine) on the cardiovascular system?

why?
BRADYCARDIA!!!

1. presynaptic muscarine receptors (aka autoreceptors) are blocked
2. presynaptic muscarine receptors reduce the release of ACh...blocking these receptors will cause an INCREASE in ACh
what is the mechanism for phenylpropanolamine
induces catecholamine release
what is the effect of antimuscarinic (atropine) on peripheral vasculature
SLIGHT VASOCONSTRICTION

1. no parasympathetic innervation in vasculature
2. muscarinic activity NO release causing vasodilation
what are the cholinergic agonist?
esters:
1. acetylcholine
2. methacholine
3. carbachol
4. bethanechol

alkaloids
1. muscarine
2. pilocarpine
3. nicotine
what is the effect of antimuscarinic on the respiratory system
1. BRONCHODILATION
2. DECREASE SECRETION
3. primarily use during inhalation anesthesia to reduce secretion and laryngospasm

parasympathetic inn. through the vagus of the bronchiole smooth muscle causes constriction and an increase in secretion
what is the selectivity for phenylephrine and methoxamine
alpha 1 selective agonist
what is the effect of antimuscarinic on GI and sweat glands
1. suppress sweating by blocking sympathetics (increase body temp)
2. reduce GI motility
3. reduce secretion of acids, pepsin, mucin and salivation
what is the selectivity for clonidine
alpha 2 selective agonist
what is used for clinical management of Parkinson's Disease
antimuscarinics:
1. Benztropine
2. Biperiden

reduce tremors but little effect on bradykinesia

*usually treated with levodopa
what is the selectivity for norephinephrine
non selective alpha agonist
beta 1 selective agonist
what is cholinergic poisoning?
how is it treated?
caused by anti-cholinesterase insecticide and eating wild mushrooms

1. treated with HIGH DOSE of atropine (1g everyday for up to a month)
2. atropine is only used for RAPID ONSET mushroom poisoning(15-30min)
3. not effective against DELAYED ONSET
what is the selectivity for epinephrine
non selective alpha agonist
non selective beta agonist
what is the mneumonic for anticholinergic toxicity
dry as a bone (sicca)
red as a beet (flushing)
mad as a hatter (confusion)
hot as a hare (hyperthermia)
can't see (mydriasis)
cant pee (urinary retention)
what is the selectivity for dobutamine
beta 1 selective agonist
what is ganglionic blockade
1. agents that block the actions of ACh on nicotinic receptors at BOTH parasympathetic and sympathetic ganglia
2. prevent REFLEX ACTIVITY (all autonomic outflow is blocked)

so whatever the prodominant tone of that site it, during ganglionic blockade the OPPOSITE will happen

DRUG:
Mecamylamine
what is the selectivity for isoproterenol
non selective beta agonist
what do ACh bind to?
Muscarinic receptors:
1. mimic the effects of parasympathetic nerve discharge
2. DOES NOT activate autonomic ganglia

Nicotinic receptors
1. ACTIVATE autonomic ganglia and skeletal muscle fibers
what is TRAM?
beta 2 selective agonist

terbutaline
metaproterenol
albuterol
ritodine
which muscarinic recepters are stimulatory? inhibitory?
stimulatory: M1 and M3

inhibitory: M2
what is phenotolamine
non selective alpha antagonist
what is the mechanism of action for M1? M2? M3?
M1 and M3: stimulatory
1. increase calcium
2. activate PKC

M2: inhibitory
1. decrease cAMP
2. decrease calcium
3. INCREASE potassium
what is phenoxybenzamine
alpha 1 antagonist
where is the location of M1 receptors?

physiological reaction?
Nerves
Glands

1. ganglionic potentiation
2. slow EPSP (excitatory postsynaptic potential)
3. increased gland secretion
what drugs are alpha 1 selective antagonist
1. tamsulosin
2. prazosin
3. terazosin
4. doxazosin

phenoxybenzamine not as selective as above
where is the location of M2 receptors

physiological reaction?
Nerves terminals
Heart
Smooth Muscle

1. slows heart rate and force of contraction
2. slight decrease in contractile force of ventricle
where is the location of M3 receptors

physiological reaction?
Glands
Smooth Muscle
Endothelium

1. increase secretion and contraction of smooth muscle
2. relax sphincter in GI/bladder
3. release NO in vasculature
what is the difference in structure between muscarinic and nicotinic receptors
muscarinic: stimulatory (M1 and M3) and inhibitory (M2) G PROTEINS!!

nicotinic: pentameric ion channels
what are the TWO types of nicotinic receptors
Nm:
1. neuromuscular junction

Nn:
1. CNS membrane of POSTSYNAPTIC neurons in the GANGLIA of the ANS
2. CHROMAFFIN cells of the adrenal medulla
in terms of receptor mediation, what will you use to treat glaucoma?? why?
muscarinic agonist (Pilocarpine)

constrict pupils
accomodation
TM is opened at base of ciliary
DECREASE IOP
what is the effect of muscarinic agonist in the cardiovascular system?

what happens with reflex arc?
HIGH DOSE
1. off set the reflex arc and cause BRADYCARDIA!!
2. slow firing rate within SA node
3. decrease conduction velocity of AV node

LOW DOSE:
1. vasodilation, decrease BP
2. carotid sinus since the drop in BP
3. sends via reflex arc signal to heart to start pumping
4. TACHYCARDIA
what happens during muscarinic over activation (mnemonic)
D.U.M.B.E.L.S

1. diarrhea
2. urination
3. miosis
4. bradycardia and bronchoconstriction
5. emesis
6. lacrimation
7. salivation and sweating
what happens during nicotinic over activation (mnemonic)
M.A.T.C.H.

1. muscle weakness or fasciculation
2. adrenal medulla (increase)
3. tachycardia
4. cramping of skeletal muscle
5. hypertension
what are the type cholinergic DIRECT acting agents
Esters:
1. ACh (sensitive to cholinesterase)
2. Methacholine (longer lasting than ACh)
3. Carbachol (EYE DROPS ONLY)
4. Bethanechol (ONLY ONE given systemically and ONLY acts on MUSCARINIC)

Alkaloids:
1. Muscarine (no clinical use)
2. Pilocarpine (cross BBB and glaucoma treatment)
3. Nicotine (acts on autonomic ganglia, CNS, and skeletal muscle. ACTIVATE and INHIBIT nACh receptors)
4. Varenecline (Chantix, partial agonist)
what are the three class of indirect cholinergic agents?
what are the period of action?
1. simple alcohol (5-15min)
2. carbamic acid esters (30min-6hrs)
3. organophosphates (+100hrs)
why is the period of action for organophosphates so long?
how can it be treated?
1. COVALENTLY bonds to AChE
2. further stabilization through AGING, permanently leaves AChE inactive

treatment:
pralidoxime (PAM) can REGENERATE AChE if it is used BEFORE the aging process
what are the effects of AChE inhibitors on the CNS
low dose:
1. increase activity on EEG
2. increase alertness

high dose:
1. generalized convulsions
2. coma
3. respiratory failure
what is the effect of AChE on the cardiovascular system
bradycardia (or tachycardia)
hypotension
reduce heart rate and CO output
what do you use to test for MG?
what are the results?
1. edrophonium to test for myasthenia gravis
2. (+) transient increase in muscle strength

if increase in muscle weakness indication of onset of a cholinergic crisis (overactivation of all cholinergic system, treat w/ atropine)
what are the reversible anticholinesterase
1. edrophonium
2. physostigmine salicylate
3. neostigmine
4. donepezil
5. tacrine
6. galantamine
7. pyridostigmine
8. ambenonium
9. demecarium
10. carbaryl
what are the IRreversible anticholinesterase
1. echothiophate
2. malathion and parathion
3. nerve gas (sarin, soman, tabun, VX)
which of the anticholinesterase can be used to treat glaucoma?

which are reversible and which are irreversible
reversible:
1. physostigmine salicyclate
2. neostigmine*
3. demecarium*
*quaternary ammoniums

irreversible:
1. echothiophate (low lipid solubility, no systemic absorption)
what is the difference between malathion and parathion
BOTH:
1. thiophosphates insecticides
2. prodrug

malathion:
1. rapidly metabolized into NONTOXIC metabolites in birds and mammals

parathion:
1. not readily metabolized in safer metabolites, TOXIC TO HUMANS
how can we protect ourselves against nerve gases
administering PYRIDOSTIGMINE as a prophylactic

it binds reversibly and cab block the binding of the IRreversible nerve agent to the AChE
direct acting nicotinic stimulant OVERDOSE?? what is a toxic dose? cigarette ingestion??
1. toxic dose: 40mg
2. nicotine makes you vomit (emesis) if you eat it.
3. nicotine is REALLY lipophilic, can cross membrane very easily (absorb through skin)

treatment:
treat symptoms
atropine
diazepam for convulsions
what are the two types of neuromuscular blocking drugs
NONDEPOLARIZING:
1. nicotinic receptor antagonists

DEPOLARIZING:
1. activate nicotinic receptors
what are the two classes of NON-DEPOLARIZING BLOCKADE agents?
how are they administered?
1. isoquinoline
2. steriod derivatives
-given only IM or IV (inactive if given orally)
what is the difference in excretion route for non-depolarizing blockade agents.
RENAL excretion:
1. longer duration of action

LIVER excretion:
1. shorter duration of action
what is the mechanism of action for succinylcholine
1. depolarizing phase, succinylcholine is not metabolized by AChE, so it stays at the nAChR for a longer time. result, a lot of contractions followed by flaccid paralysis

2. desensitizing phase, as it stays longer on the nAChR depolarization decreases. but succinylcholine is still on the nAChR. thus desensitization.
what does beta 1 agonist do?
ONE BEATING HEART

1. increase Ca++ influx
2. increase rate of contraction
3. increase AV node velocity
4. increase cardiac output
5. decrease refractory period
6. cardiac systole is shorter and more powerful
7. increase renin (RAA axis)

this will change with reflex arc...think about it!!
what are the three alpha agonist drugs?? what are they selective for?
1. phenylephrine and methoxamine (alpha 1)

2. clonidine (alpha 2)
what are the two mixed alpha and beta agonist? what are they selective for?
1. Norepinephrine (non selective alpha, beta 1)

2. Epinephrine (NON SELECTIVE ADRENERGIC, both alpha and beta)
what are the SIX beta agonist? what are they selective for?
1. dobutamine (BETA 1)

2. isoproterenol (non selective beta agonist)

3. terbutaline, metaproterenol, albuterol, ritodine (BETA 2)
what is FENOLDOPAM
Dopamine 1 AGONIST
used in SEVERE HYPERTENSION

*the drug dopamine is a non selective dopaminergic agonist (obviously)
what will happen to the blood pressure if you give an pure alpha agonist to a patient
1. increase peripheral resistance
2. decrease venous capacitance
3. INCREASE IN BP
4. INCREASE VAGAL TONE (due to reflex arc)
5. will have normal CO because alpha receptor will INCREASE CONTRACTILITY of the heart
what will happen to a patient if you give them a non selective beta agonist?

give an example of a non-selective beta agonist
ISOPROTERENOL
BP DECREASE

1. increase cardia output (beta 1)
2. decrease peripheral resistance (beta 2)
what will happen to the IOP of the eye if you give a patient a non selective adrenergic agonist? (alpha and beta agonist)

what is an example of a non selective adrenergic agonist
DECREASE IOP
EPINEPHRINE

1. alpha 2: decrease aqueous production
2. beta: increase outflow
what is so special about CLONIDINE
it has an acute hypertensive effect followed by a LONGER HYPOTENSIVE EFFECT

1. it tricks the post ganglionic neuron into thinking that it is binding to Norepi or Epi.
2. this causes a decrease in NorEpi and Epi secretions
3. result in decrease in BP, HR, and PR.

only important adrenergic agonist that does this.
what is the purpose of MAO and COMT
inactivates catecholamines

should not given methamphetamines to a person taking MAOI
dopamine should ONLY be given
intravenously...

at low dose: will dilate renal, coronary, and mesenteric systems

at high dose: will activate beta1 and alpha receptors
what is Phentolamine? mechanism?
1. NON SELECTIVE ALPHA BLOCKER
2. reversible
3. competitive

1. vasodilation with increase in CO and heart rate
2. a1 blocker decrease peripheral resistance, decrease in BP cause reflex arc to increase sympathetic tone to heart (tachy). a2 inhibition cause INCREASE in norEPI and EPI (more tachy)
what is phenooxybenzamine?
mechanism
ALPHA 1 selective (irreversible) antagonist
what is Prazosin used to treat?
reversible alpha 1 antagonist

used to treat hypertension in Raynaud Syndrome and BPH

prazosin, terazosin, doxazozin, and tamsulosin (structurally different than others)
what is Yahimbine?
1. alkaloid, alpha 2 selective antagonist
what are the non selective beta blockers
1. PROPRANOLOL
2. carteolol
3. penbutolol
4. pindolol
5. timolol
what are the important FIVE beta 1 blocker
1. metoprolol
2. acebutolol
3. atenolol
4. esmolol
5. nebivolol
name a beta 2 blocker
butoxamine
what is special about labetalol and carvedilol
blocks both alpha 1 and beta receptors
what is special about nebivolol
1. blocks beta 1
2. vasodilation due to NO release
what TWO responses do ALPHA antagonists cause on the HEART
1. reflex response of alpha antagonist induce BP drop will INCREASE sympathetic tone causing tachycardia via B1
2. blocking alpha 2 receptors on the presynaptic ganglion will cause in INCREASE in nor EPI and EPI secretion.
what is epinephrine reversal
drop in PR and BP due to:

1. alpha 1 mediated vasoconstriction is blocked
2. beta 2 vasodilation in skeletal muscle in unopposed

*alpha antagonist is actually reversing the pressor effect of epinephrine
blockade of alpha 1 receptors in the veins can cause...
orthostatic hypotension
short term use of beta blockers will cause...
1. decreased CO due to reduced contractility and rate
2. decrease in BP will cause increase sympathetic tone (reflex arc)
3. PR is increase due to B2 blockade
what will happen in patients taking beta blockers chronically
1. total PR will return back to initial values
2. in hypertensive patients, PR will be reduced

used to treat:
supraventricular arrhythmias and ventricular arrhythmias
how should you go about taking someone off of a beta blocker
TAPER!!!

1. beta blockers should never be withdrawn abruptly
2. there is a upregulation of beta receptors when antagonists are used.
3. stopping abruptly will cause a severe arrhythmia
what precaution do you need to cardiovascular precautions should you consider when giving someone beta blockers
congestive heart failure and MI

1. these patients are rely on sympathetic outflow to regulate cardiac output.
2. removing this with beta blockers may cause them to bottom out.
if you have a life threatening adverse effect to beta blockers, what can you do to fix the situation
1. ISOPROTERENOL (non selective beta agonist)
2. GLUCAGON
neurlogically, what can beta blockers do therapeutically
1. reduce freq. and intensity of migraines
2. do not prevent or stop migraines when it has already happened...signal has already been sent

propranolol can be used to reduce performance anxiety