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304 Cards in this Set
- Front
- Back
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What are uses of Non-selective adrenoceptor agonits
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Shock, Cardiac dystrhymias, and allergice reactions
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What is shock chacterized by
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inadeuate perfusion of tissues
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What happens with inadeuate perfusion of tissues
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Decreased O2 and nutrietns, and organ system failue and associated hypotension
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Shock is associated with hypotensive, a decreased BP causes
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Increased sympathetic dischange
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An increase sympathetic dischange causes
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vasoconstrtion, increase HR and contracility to maintain BP to cerberal blood flow
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If shock causes is result of hypotensiion, and results in increased sympathetic dischange, cerberal blood flow is mantained, but
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blow flow dereases to other organs, and decrease renal filtration
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What are used to treat shock
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adrenergic agoinsts
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How do non-selective agrenegic agoinst treat shock
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increase cardiac contractility (B1), adn modify vascular resistance
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What icnrease vasulcar resistance
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a1--phenylephrine
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What happens if you treat an MI with an adrenergic agoinst
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B-activation increases O2 consumptions, and alpha activation increases PVR and decreases CO
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What aderenergic agoinst is used to treat shock
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dopamine--in high doses cause activate of al--constrction increases BP, and cause renal perfusion
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What is used to treat cardiac arrest
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Epinehprine and other alpha agoinsts
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What do alpha agoinsts do
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vasconstriction which increase PVR increases BP
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What does epinehepinre do in treatmetn of cardiac arrest
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Increases daistolic BP and increase cornary perfusion
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What are the B effects of epinehpine
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thought to make ventricular fibrillation more susceptible to conversion by electrical countershock
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When paroxysmal atrial tachcardia is under conditions of, and should be treated
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mild hypotension, aplha agoinst
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What does alpha agoinst do
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Constricts BV, increases BP which decreases sympathetic response which decrease HR or tachycardia
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What are drugs that treat paroxysmal atrial tachycardia
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methoxamine and phenylephrine
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What are allergic reactions caused by
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acture hypersensity reaction by a string or allergy to food or drugs
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What happesn in an allergic reaction
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Mast cells release a mediator that decreases BP, and broncoconstriction
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How are allergic reactions treated
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epinehprine
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What does epinehrine do in allergic reactions
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reverse hypotension and shock decrease icching and swelling of lips tondue and eyes and decreases edema of glottis
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What does epinherine have on activated B2
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decreases mediator release and broncodialtion
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What are adrenoceptor antagoinistis
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inhibit the actions of epinephrien and norepinephrine
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Where is norepinehprien released
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symhatetic postganliionic nerves
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Where is epienphrien released from
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chormaffin cells of adrenal medulla
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What are alpha non-selective antagonists
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phentolamine, tolazoline, and phenoxybenzamine
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What are special properties of phentolamine
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bloacks muscarinic H1
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What are special properties of phenoxybenzamine
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irresible antagoinst, and also blakcs muscarinic H1
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What are alpha 1-selective antagoinnt drugs
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prazoin, alfuzosin, doxazosin, tamsulosin, and terazosin
new cavediolol, and labetolol |
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What are special proterioes of tamsulosin
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al selective antagoinst, and selective inhibitor of Alpha1A in prostate)
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What are special properties of carvedilol
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Al antagoinst and B antagonist
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What are special properties of labetolol
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Al antagoinst, and Beta antagoinst
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What do alpha 1 antagoinst hav ean effect on
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blood vessels, and urinary tract relaxation
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What are alpha 1 antagoinst effects on blood vessel
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dilates aterioles and venules,whicn decrease venous return and decreases BP
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Special properties of prazosin
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acts on baroeceptor and CNS to decreases sympathetic outfolw and decrease BP
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What is side effect of alpha 1 antagoinst on blood vessels
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reflex tachycardia, and A1 diatles BV, decrease BP, which increases sympathetic response and increase Hr
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Alpha 1-seleective inhibitors do not produce as great a relfex tachycardia as non selective alpha antagoinst
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NON-selective block presynaptic A2 receptors and increases increase NE release increases reflex tachycardia
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A1 adrenoceptor antagoinsts are used for in
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primary systmeic hypertension, Raynaud's disease, and phaeochromocytoma
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How do alpha 1 antagoinsts used to treat pimrary systemic hypertension
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dilates ateriolies and venules, and decrease PVR, and venous return adn decrease BP
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How do Alpha 1 agtagoinsts work on HF
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Dilation of veins decreases preload, and ateriolaor dilation that decreases afterload (SHORT-TERM)
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What is result of decrease preload and afterload for alpha1 antagoinsts
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increases CO and decreases pulmonary congestion
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What happens with long term use of prazosin for HF
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tolerance, kidenys reatin fluid and BP increases again
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What is Raynaud;s disease
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painful vasoconstrition of digits
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What does an alpha 1 antagoinst do to Raynaud's disease
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decreases incidence of digtial vasospasms
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What is phaeochromocytoma
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tumor of adernal medulla, that cause severe hypertesion from all the CCAs's
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What treats phaeochromocytoma
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phenoxybenzamine
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Is phaeochromocytoma treated with phenoxybenzamine in prepartion for sruget
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YES
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What are effects of Al antagoinsts on urinary tract--and results
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relaxes trigone muscle, bladder neck, prostate capsule, and and neck--which decreases resistance ot urine flow
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What does Al antagoinsits treat when relaxing trigone muscle, bladder neck, and prostrate capsule and neck?
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tresat Benign prostatic hypertrophy or imparied bladder empptying
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Do Al antagoinsts decrease uriany resistance in spinal injury
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YES
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What are side effects of alpha 1 antagoinsts
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first dose phenomenon and postrual hypotension
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What is first dose phenomenon
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posturla hypotnesion and syncope afterin inital dose occurisn 30-90 minutes after dosing
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What causes the first dose phenomenon
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tdrugs prevent symathetic control on BP on ateries and veins
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What causes postural hypotension
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prevent symathetic constriction of veins
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How do fix the side effect of first dose phenomenon and postural hypotension
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taking a night, adn increase dose slowly
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What are selective A2 antagoinsts, and system affecting
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yohibmbine---cardio and penile function
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What happens with A2 receptor antagoinsts
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increases NE--leads to activation of A1 and B2, and increase symaatheic outflow
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What are result of A2 receptor antagoinst on heart and blood vessels
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Increases HR and contracility and consticts BV both directly and indirectly, --increasesing sympatehtic outflow which increase BP
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What is A2 antagoinst Yohimbine's effect on penile function
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increases penile blood inflow, and decrease penile blood outflow leading to erection
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What is use of alpha antagoinst +pataverine ---and where
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impotence--injected in corpus collusom
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Non-selective B-antagonists end in OLOL---what are parital agoinsts
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cateolol, penbutolol and pindolol
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What are B1 selective antagonits
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MAE
metorporlol atenolol acebutolol and esmolol |
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What are special propteries of acebutolol
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some ISA (partial agoinst) and membrane stabilizing activity
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What are special propteries of esmolol
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Short DOA, inactivated by esterases, and use when need esaily controlled B-blockcade
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What B-antagoisnts have an influence on the heart
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Both B1 adn B2
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What are B1 and B2 antagoinsts affect on heart
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B1--decrease HR, contractility and conduction
B2 decrease HR |
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Do Beta antagoints have affect on HR in individuals with norma heart
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NO
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Beta antagoinsts only have effect in HR when
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there is INCRASE symathetic drive (hypertension)
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Partial agoinst sare less likely to cuse profound bradycardia or negative inotropy WHY?
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prevent receptor from being fully activiate (better)
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What are B anatgoinst affectso on cardiac conduction
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Decrease depoliation of ectopic pacemakers
decrea rate condutin in Atria and AV node, increases refractory period fo AV node, and decrease Sinus Rate |
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A dcrease sinus rate =
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decreased HR
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What are effects of B antagoinism on blood vessels
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B2---cause vasoconstriciton
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What are effect of B1 antagoinism on kidney
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decrease renin release, which decrease Angiotension II, and aldoster which decrease fluid renention and decreases BP
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Beta antagoinsts are used in heart for
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hypertension, exterional angina, acute MI, and superventricular dysrhythmias
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Why would yo upredict B1 adrenceptor antagoinst to be more effective antihypertensive agents than non-selelctive B- antagoinstis
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Non-selective block B2 receptors which causes vasoconstriction, and increase PVR and BP
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What causes angina
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decrease O2 to heart
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What happens with exertional angina
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decreased O2 to heart, so chest pain
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With exertinoal angina you have increase O2 demand, what do B antagoinsts do
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Block CCA decrease chornortirpic and ionotropic effect, which decresase mycardial demand for O2
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What is benefit of B antagoinsts in acute MI
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decrease Oxygen demand,
decrease plasma FFA antidyrhtmic action redistributino of myocardial flow |
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What is benefit of decrease oxtgen demand and work-load on heart
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limit the size of the infartion
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How are supraventicular dysrhytmias treated generally
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slow ventricular rate by Decreasing AV conduction
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WHat are effects of B antagoinsits on supraventriuclar dysrhytmias
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decrease rate of conductino in atria and Av node
increase refaractory period of Av node, and decrease sinus and decreases HR |
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What is B2 antagoisms effect on airways
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broncoconstriction in asthamics
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Are even B1 selective antagoinist only relavitvely selecitve--what makes them even less selecitve
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HIGH DOSES
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What are metabolic effects of B2 antagoinst
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decrease gluconeolysis and gluconeoensis
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What inviduals may have a slow response to recover from hypoglycemia
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insulin-dependent diabetics (type 1)
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What are effects of B2 that can cover an importatnt indicator of hypoglycemia in diabetes?
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B2 can prevent tachcardia and tremor occuring during hypoglycemia
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What are effects of B3 antagonists
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inhibits hormone lipase,increases LDL decrease HDL and increases TG
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What happens with increase LDL, decreases HDL and increased TGs
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increased risk for CAD
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Problesm with non-selective B antagoinsts like propranolol do,
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increase risk for CAD--b/c increase LDL, decrease HDL and increases TGas
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What is associated with plasma K+
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Beta 2 agonints/antagoinsts
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What happens normally in exericse
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increased K+ release from SKM
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What happens with B2 antagoinist of plasma K+
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decrease K+ uptake into cell,and increased K+ in blood
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What are Beta antagonits effect on eye
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decrease aquesous humor production, decreases IP{
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What beta antaagoinst treat open angle glacuoma
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bextaolol, levobetaxolol. leveobunolol, and carteolol and timolol
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Beta antagoinst can also treat pheochromoctyome--what else treats
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Alpha antagoints, and Beta antagoinist
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Beta antagoinists are administred in phaechromocytoma only AFTER an alpha antagoinst==why
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Blockagde of B2 receptor could lead to exacerbation of HTN--dialates BV
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What happens in hyperthyroidsism
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increases B receptor expression and increase symphatetic effects
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What does pronaolol do in hyperthyroidism
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prevents T4-T3--
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Are Beta antagoinsts used to in prophylaxis of migraine
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YES--atenolol, metroprol,
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B1 seceltive drugs should be used from patients with
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diabetes, PVD, or Raynauds disases--all are assoicated with vasoconstrtion--using nonselecitve antagoinsit-could block B2 causingmore constriction
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Should B-antagoinst be used carefully in asthmatics
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YES
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B-antagoinsit may induce HF in patietns whre
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cardiac performace is supported by sympathetic drive
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What do B-antagoinsts do in patients with partial or complete AV conduction defects
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B-antagoinst may induce life threating bradycarida
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What happens with abrupt discontinuation of long term therapy with B-antagonist
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may worsen angina or lead to sudden death
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Where is AcH released from
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all preganglioinic nerves, all somatic all parasympathetic postgandlionic
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What happen in you blocked the effect of Ach at the gnaglia
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block all autonomic,
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What happen if you bloack Ach at neuroeffector cell
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parasympathetic
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What would happen if you block Ach at SKM
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paralysis
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Synthesis of CHOLINERGIC NT
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occurs by acetylation of choline by choline acetyltranferase
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Choline in diet from
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lechin
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Choline is concnetgrates in
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cytoplasm of nverve terminal by a carrier mediated high affinity choline uptake process
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What is the rate limiting step in ACh syntehtiss
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uptake of choline in nerval terminal cytoplasm is rate-limiting step
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Hemicholinum is a drug that inhibt the HIGH affinity uptake of choline, how would this agent affect chlinergic transmission
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Decrease choline uptake, and ACh synthetsis, and leads to depletion of Ach--and blockage of cholinergic transmission
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Where is Ach storged
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ACh is tkaen up into vesicles in verve termine
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What is uptake in a vesicle dependent on
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H+ dpenednent antiporter carrier mechanism
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What else is in the Ach vesicle
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ATP, VIP, and proteoglycan are also stored with ACh and all are released
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What causes the release of ACh
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influx of sodium into the axon from an AP
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What does tetrodotoxin do
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blocks fast Na+ channels--so prevents AP condution
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After nerver terminal depolarization from Na+, what happens
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open volatage sensitve Ca+ channel N-type Ca+2 channels
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THe opening of N-type Ca+2 channels does what
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vesicle mirgrate and fuse with terminal ,and contents are rlease into NE junction
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What does w-conotoxin do
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Bloack N-type Ca+2 channels and prevents NT release
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What are inhibitors of release
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Botulinum toxin A
Alpha-Latrotoxin presynatic receptors |
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What produces botulinum toxin A
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produced by Clostridium Botulinum, from improperly canned food
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What does Botulimum toxin A do
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binds to synaptobrevin on vesicle membrane, and inbhits Ach rlease paralysis of SKM (weakens w/ low doses)
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Is botulium toxin irreversible
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YES, unit new synthetisis of synatobrevin (1 month time)
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Where is botiumun toxin administered to
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orbital muscle for spasmodic ocular movement or dystonia, cosmetic purposes, and excessive sweating, migrane and dystonic muclse
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Alpha latrotoxin (black widow spider) does what
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prmotes Ca++ influx into nerve terminal, massive AcH release, followed by cholinegic transmission failure
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Presynatic receptors are located on nerve terminal and what receptor inhibit rlease of ACh
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M2
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What are inhibitors of NE release
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A2
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What are inbhitors of opiates
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u receptors
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Ach released from nerve temrinal mustb e in sufficnet amounts to activate postjunctional receptors, however is must be rapidly
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degraded to prevent 'OVERACTIVATION"
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If AcH is inactive too quickly
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no postjunctional response
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If acetylcholic is inactivated too slowly
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excessive respones and loose fine control
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What does Cholinesterase do (ChE)
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hydrolyzes ACh to choline and acetic acid
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Where is Cholinesterase in greatest conc
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NMJ>NEJ>ganglion
NMJ (muscle) |
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2 types of chloinesterase
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Acetylcholinesterase and butylcholinesterase
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Where is acetylcholinesterase
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on pre-or post juctional membrnaes of cholinergic NEJ or NMJ
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Whre is butyrlcholinesterase
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plasma and liver,
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What does butyrlcholineastease do
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metabolized any ciruclating choline estera dn esters from plant sources
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What happens with inhibition of mettabolism of ACH
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enchancement of ACH mediated responses adn overactivity of parasyathic/ somatic responses
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What do indirectly-activyt cholinomimetics do
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inhbit cholinestases, to increase AcH resposne
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What are indirectly-aciting cholinomemetics
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neostrigmine,and phyostighmine--useing in increase cholingergic resposne
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Neostigmine and phyostigmine are have been used in nerve gases, what would signs of toxcity be
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parasymthatic--salviation, dirrahea, urination, and broncontrstiction
SKM---muslce fasciculation (twicthcing) CNS --respiraotry depression |
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What are lipid solulbe drugs more deadly
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good absorption thourgh skin, get in CNS more redaily
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What are the cholinergic receptors (Ach receptors)
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Nicontic receptors and
Muscarinic receptors |
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What are nicotinic receptors activated by
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nicotine
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Where are nicotinic receptors located
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all postganglionic cell bodies
adrenal medulla cells and SKM NMJ |
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Muscarinic are activated by
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muscarine
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Where are muscarinic receptors located
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paprasympathetic effect cells or/and sympathetic cholinergic
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Peripheran nerves (autonomic and somatice leaving the CNS are
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cholinergic
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Released acetylcholine acts on
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NICOTINIC recpetors
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What are types of Nicotinic receptors
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NM
NN |
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Where is NM
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muscle nicotnic--SKM
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What is NN
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neuronal--postganglion cells, and adrenal medullary cells
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What type of drugs target NM
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neuromusclar blocking drugs
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What types of drugs target NN
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ganglionic bloacking drugs
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The receptor subunit for nicontics is pentameric, there are 2 alpha subunits, wehre does ach bind
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to both A subunits--for channel to open
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After Ach binds to both alpha subunits what happens for SKM
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opeing of Na+ channel and depolariation of motor endplate
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What happens with porloneg exposure to nicotinic agoinst
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recpetor desensitization--where receptor will change in conformation and b/c inactiveted
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What is denervation supersensitivity
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when motor nerve cut--results in nicotinic receptors expressed outstide motor end plate
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What are muscarinic receptors divided into
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M1-M5
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M1-M4 were identified through
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molecular cloning techniques
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Where are M1 located
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postganlionic cells CNS and gastric glands (secrete acid)
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Where are M2
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heart, and presynatic receptor, and slows down HR, and inhibits release ACH
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Where are M3
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smooth muscle and secretory glands
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The majority of Muscarinic cells are
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M3
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Muscarinic effect on cell by a G-protein linked transduction mechanism--which stimulate phosphliase C
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M1, M3, and M5
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Which muscarinic receptor are involed with K+ channel activate, and inhibition of Adeylate cyclase
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M2 and M4
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What are cholinoceptor agoinsts
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mimic the effects of cholinergic receptor activation
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What is Nm, NN agoinst
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Nicotine
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What is M receptor agoinst
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muscarine
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What activates both Nicotinic and Muscarinic receptors
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Ach
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What response would you expect to see upon administration a ganglionic nicotinic agoinst
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increase parasympathteic and increase sympathetic, no effect on SKM
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What is a NN antagoinst
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hexamethonium
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What is a NM agtagoinst
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tubocurarine
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What is M antagoinst
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atropine
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Bloack of NN receptors results in
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autonomic blockage
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What is result on Muscarinic blockage
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parasympatethic blockage
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What is result on NM blockade
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paraylsis
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What causes autonomic blockage
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Nn--hexamthetonium
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What causes parasympathetic blackage
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atropine
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What causes paraylsis
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NM--tubocurarine
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AcH release from all preganglion nerves affect
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NN
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ACH released from all somatic nerves affects
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NM
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ACH from all parasympathetic postganglionic
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M (M3)
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ACH rleased from some symahteitc postganglionic nerves
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M (M3)
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NN stimulations
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autonomic acitvation (paprasymathic/ sympathetic)
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NM stimulation
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SKM movement
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M stimulation
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all effector tiisue innervated by para/sympathetic nerves
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What are the cholinomemetics
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AM
BCP CMA AcH methacholine Bethanechol carbachol pilocarpine cevimeline muscarine aceclidine |
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What cholinomemetics are sensitive to cholinesterase
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Ach (+++), and methacholine (+)
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What cholinomemetics have effects on muscarinic receptors
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ALL
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What cholinommetics have an effect on nioctinic receptors
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Ach (+++), methacholine (+), and carbachol, and acelidine
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Is methacholine hydrolyzed more slow by cholinesterase than Ach
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YES
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Is methacholine affect by Butyncholinesterase
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NO
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What are idela cholinommimetics for bladder
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bethanechol, and carbachol
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The pharmacological actions of ACH are mainly thoruigh
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muscarinic q
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What are Ach (parasympathetic effects on heart)
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Negative chronotropic (HR)
Negative ionotropic Negative conduction |
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What are effects of Ach on negative chronotropic
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K+ channel activation, which hyperpolarizes SA, and decreases rate of depolarization
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WHat are effects of Ach on negative inotropic
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K+ channel activation--mebrane hyperpolization, decreases excitiability of heart, and decreases CCA release by presynatic action
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What are Ach effects on conduction
|
K+ channel activation, which decreases Av node conduction
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Cardiac glycosides protect the ventricle from aberrant atrial impulses by
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enchancing parasymathetic drive to heart--and decreasing Av node contion
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What affect does Ach have on blood vessels ( what receptor type
|
releaxs blood vessels--through muscarinic
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How does Ach relax blood vessels
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endothetlial part of cell release NO--which dialtes vessel, and inhibition of NE from adrenergic nerves
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What are Ach effects on BP
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Decreases BP
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What are Ach effects on GI system
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contracts GI and increase peristatic acivity, and relaxes spincters
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What is used for GI atony (without tone)
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Bethanechol
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What is bethanechol used
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more selecive, and no nicotinic actiivty
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What are side effects of bethanechol
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uriary urgency
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What happens with increasing doses of bethanechol
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mimics parasympathic--miosis and blurry vision
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Carbachol has similar selectivity as bethanechol-why is it less preferable
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Nicotinic side effects
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What are Ach effects on Glands
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increase gland secretion
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What drugs are used to treat xerostomia
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cevimeline, and pilocarpine
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Cevimeline/pilocarpine is contraininaidated in
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peptide ulcer
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Why are cevimeline and pilocarpine contraindicated in peptic ulcer
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b/c increase digestive gland secretion and increases acid--bad on ulcers
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What are Ach effects on urinary tract
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Increase uretal peristalis, and relaxes tirgone
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What also relaxes trigone
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Al and parasymathic
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What drug is used to treat urinary retention
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bethanechol
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Bethanechol is used to treat
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GI atony, and urinary retention
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May bethanechol be given mutiple time ntil voding begins
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YES
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What are Ach actions on airway smooth muscle
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bronconstrition contrainatic in asthma (like B-antagoinsts) and promotes mucus secretion
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What is Ach use for airways
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bronchial provocation test
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What is bronchial provocation test
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NOT THERAPY--TEST to determine if asmatic
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What drug is used in bronchial provocation test
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methacholine
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Methacholine is given as an aerosol, why
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decrease systemic effects
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Why isnt bethanechol used instead of methacholine for bronchial provcation
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methacholine is senstive to cholinesterases
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What are Ach effects on eye
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contacts iris-miosis and contract ciliary muscule results in cyloplegia
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What is use of Ach in eye
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induction of miosis and reversal of mydriasis
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What is used for short duration of miossi
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Ach
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What is used for long term miosis
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carbachol
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What is used for reversal of mydriasis
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pilocarpine
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What causes Glucoma
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increase IOP, and altered aquesou humor production and outflow
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Increase IOP does what
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optic nerve damange, and blindness
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What cuases narrow-angle glucoma
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iris obsution of trabecular network, blocks aqeuous hmor outflow
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What is used to treat Narrow angle glucose
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pilcarpine causes contraction of circular muscles ciciular muscle and increases outflow
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What causes open-angle glucoma
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invloes loss of trabecular network, and blackage of aqeous humor outflow
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Does pilocarpine treat both open angle and narrow angle glucoma
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YES
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Does pilocarpine a miotic agent htat cuases minimal cyclopelgia
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YES
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Why is polcarpine applied topically
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local constriciton of eye decrease SEs
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What are anticholinesterase agents
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inbhit cholinesterase by binding to the enzyme at active site or peripheral anionic site revsible or irreversible
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Agents degraded by cholinesterase--effects will be ptentiated by cholinestease inbhitiors--what does it amplify
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cholinergic nerve-mediated response, succinylchlone, and local anestetics
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What are the reversible anticholineserase agents
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Neostigmine
Physostigmine pyridostigmine edrophonium admbedonium demecarium |
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What are the revesilbe anticholinesase LIPID soluble
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RDGT
Rivastigmine Donepezil Rivastigmine tacrine |
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Rivastigamine, donepezil, galantamine, and tacrine all are lipid soluble this means
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enters the CNS
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Special features of neostigmine
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cholinergic agoinst, and direct nicotinic agoinst
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Specal feautures of physostigmine
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lipid sobule and 3N
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Special features of pyridostigmine
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NONE
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Speical features of ambedonium
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NON
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Special features of edrophonium
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short-acting
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What are special features of demecarium
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long-acting
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What makes anticholinesterase agents irreversible
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phosphorlated active stie,
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The agents are not truly iirevisble until---
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the phosphrlated enzyme loos an ALCOXY group
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What are the irrversible agents
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DFP
parathion malathion echotiophate |
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Which irrversible antiocholinestase agents are lipid soluble--and excesive consumption leads to CNS convulsions
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DFP
parathion malathion |
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What are special properties of DFP
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volatine and very lipid soluble
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What are special propteris of parathion
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insecticie, and pro drug--metabolized to paraoxan
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What are special propteries of malathion
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insecticide and active metabolite, and rapidly detoxified in vertebrate (not in insects)
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What irrvesible is the safest to use
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echothiophate
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What are properties of echothiophate
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low toxicity and postively charge, low volatility
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Poorly lipid soluble inhibitors show selectivity for
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TISSUES NMJ>ganglia>NEJ
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Lipid soluble inhbitors show selectivity for
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NOT tissue-penetrate easily rather CNS
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What are cholinesterase inhibitior actions onf postganlionic chlinergic nerves
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increases parasympathetic M
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What are cholinesterase inhibitior actions on autonimic ganglia
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increase para and symahaptic response (N)
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What are cholinesterase inhibitior actions on NMJ
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increase SKM resposnes (NM)
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Despression occurs by persistent depolarizastion of nicontinic receptors leads to
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tachyphylacixs (receptor desensitization)
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What are cholinesterase inhibitior actions on heart
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negative chronotropic by parasymathetic effects
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What are cholinesterase inhibitior actions on blood vessels
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dilate by action on vasomotor center
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Why don't cholinesterase inbhitiors induce vasodialtion by amplifying cholinergic affects
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BV do nto have cholingeric innervation
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What are cholinesterase inhibitior actions on BP
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decreases BP
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What are cholinesterase inhibitior actions on GI system
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same as directly-acting cholinomimetics
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What are cholinesterase inhibitior actions mediated at in GI
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ganglia of Auerbach's plexus, and increases parasympathetic NEJ
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What anticholinesertase treats gastroinetninal atony
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neostigmine
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What chohlinommeitc treats GI atony
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bethanachol
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What anticholinesterase treasts narrow-angle Glaucoma
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physostigmine
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What cholinommetic treats narrow-angle Glucoma
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pilocarpine
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What anticholinesterase treats open angle Gluacoma
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physotigmine, demacarium and echothiphate
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Long acting antichoinestrase--Demecarium side effects
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increased risk of cataracts greater than 6 months
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Systmeic absoprtion of eye drops is through
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nasolacrimal ducts
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What anticholinesterase treats unrinary retention vs. cholinommetic treat urinary retnetion
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neostigmine---bethanacol
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What are actions of anticholinerase inbhitiors at NMJ
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Increase Ach--strong contraction, and decreaseed decay result in unncordinated SMK contraction
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ChE inhbiitiosn results in doplorization of motor end plate and presynaptic effect---
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antidromic impluses--activate assoicated nerves--and causes faciculation of MOTOR UNIT
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What Neuromuscular disorders does anticholinesterase treat
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Myasthenia gravis and Lambert Eaton syndrome
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What happens in myasthenia gravis
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autoimmune disease taht antiboides bind to Nm receptors--result in muscle weakness and fatigue
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What happens in Lambert-eaton syndrome
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antibiotic bind to Ca++ channels--preventing Ach release leading to muscle weakness and fatigue
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What drugs treat myasthenia gravis and Lambert-eaton syndrome
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Neostigmine, pyridostigmien, and ambedonium
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What is benefits of Neostigmien, pyridostigmine and ambedonium in myastenia gravis, and Lambert-eaton
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Increases NM activation, increases SKM response and strength
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What is initally given with neostigmine, pyridostigmine,and ambedonium
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muscarinic antagoinst (atopriine) to decrease parasympathetic SEs
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What can be used for DIAGNOSIS of myasthenia gravis
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edrophonium
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What does endrophonium do to diagnossis myasthenia gravis
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Increases muscle strenth means myasthenia gravis
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What happens when you take endrophonium and DO NOT have mystehinia gravis
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decreased strenght and lingual fasciculations
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Excessive cholinesterase inbhitior acutally will aggrave and mimic myathenia gravis--why
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persistane depolarizstion of nicotinic receptors results in tachpyhlaxisi
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Several drugs exhibit anti-muscarinic side effect those effects can be reversed by
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cholinerstase inbhitiors-physotigmine
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Paralysis induced by competive neuromuscle blocking drugs can be reversed by
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neostigmine--choinerstase inhibitors
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Che inbhitiors do NOT reverse paralsis induced by
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depolarizing neuromuscular blocking drugs
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Physostigmine is used reverse anti-muscarinic side effects in
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CNS (lipid soluble)
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Neostimigne is poorly lipid soluble and shows most activity at
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NMJ
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What are cholinesterase reactivators
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pralidoxime and obidoxime
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What do praildoxamine and obidoxmine do
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reverse inhibition of irrversible inbhitiors--NO effect in CNS
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When are pralidoxime and obidoxmine most effective
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given minstures after exposure to irreversible ChE inbhtiors
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What makes prailodxime and obidoxmine ineffective on ChE inbitiors
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after loss of alkoxy group
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Do Cholinesterase reactivators posses weak cholinertease inbhitiory activity and neuromuscle blackage at supratherapetic doses
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YES
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Why wouldnt use pralidoxime and obidoxmine on neostimine or phyostigmien
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they are not irrervesible inbiotrs
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