Guess the drug (autonomic nervous system version)) Flashcards by Mahdi Akoush

I am a drug that inhibit the rate limiting step of synthesis of Ach

Hemicholinium

How well did you know this?

Not at all

Perfectly

I am a drug that block Ach release while my brother causes the release of Ach

Botulinium
Spider venom (black widow)

How well did you know this?

Not at all

Perfectly

I am an enzyme found in plasma but I don’t play a significant role in termination of Ach effect

Pseudocholinesterase

How well did you know this?

Not at all

Perfectly

I am a drug that inhibit the movement of Ach into the vesicles

Vesamicol

How well did you know this?

Not at all

Perfectly

An alkaloid present in poisonous mushrooms

muscarine

How well did you know this?

Not at all

Perfectly

How many muscarinic subclasses do we have

5 (only 3 being functionally characterized)

How well did you know this?

Not at all

Perfectly

M1 receptors are on——-
M2 receptors are on——-
M3 receptors are on ——-

Gastric parietal cells
Cardiac and smooth muscle
Bladder, exocrine and smooth muscle

How well did you know this?

Not at all

Perfectly

T or F
drugs with Muscarinic act can’t stimulate nicotinic receptors

false
at high concentration they do

How well did you know this?

Not at all

Perfectly

Muscarinic receptors are G-coupled receptors with — or —- being excitatory ( G–) while —– being inhibitory (G–)

G coupled
M1 and M3 Gq
M2 inhibitory (Gi)

How well did you know this?

Not at all

Perfectly

nicotinic receptors are —–gated —- that have (rapid\slow)—– action

ligand gated ion channels (Na+ or Ca2+)
rapidddd

How well did you know this?

Not at all

Perfectly

I am a drug that block the nicotinic receptors at the ganglia level while my brother blocks it at the level of neuromuscular junction

Hexamethonium
Tubocurarine

How well did you know this?

Not at all

Perfectly

I am an alkaloid, stable to hydrolysis by AChE, uncharged used mainly in ophthalmology

pilocarpine

How well did you know this?

Not at all

Perfectly

I am a poor substrate for ACHE positively charged and i have nicotinic action

Carbachol

How well did you know this?

Not at all

Perfectly

I am rarely therapeutic except in the eye because of my high potency , non selective binding and long duration of action

Carbachol

How well did you know this?

Not at all

Perfectly

I lack nicotinic action and not hydrolized by ACHE i have a duration of action about 1 hr

bethanechol

How well did you know this?

Not at all

Perfectly

My major actions are on SMC of bladder and GI

Bethanecol

How well did you know this?

Not at all

Perfectly

I am primarily used as miotic for treating glaucoma or during ophthalmic surgery

Carbachol

How well did you know this?

Not at all

Perfectly

From my side effects:
Cause marked diaphoresis
enter brain and cause CNS disturbances

pilocarpine

How well did you know this?

Not at all

Perfectly

From my usages:
tx of xerostomia
tx of open angle glaucoma
miosis and contraction of ciliary muscle

Pilocarpine

How well did you know this?

Not at all

Perfectly

I am administered as intraocular solution or injection

Carbachol

How well did you know this?

Not at all

Perfectly

I am used to treat megacolon and atonic bladder

Bethanecol

How well did you know this?

Not at all

Perfectly

Iam a useless drug

ACH

How well did you know this?

Not at all

Perfectly

I am a tertiary amine that make a stable carbmaminoylated compound with ACHE then make it reversibly inactive

physostigmine

How well did you know this?

Not at all

Perfectly

I am a quaternary amine that enters the CNS poorly from my uses:
gastric contractions and secretions
motor act of small intestine and colon
treating bladder atony and symptomatic myasthenia gravis

neostigmine

How well did you know this?

Not at all

Perfectly

we are 4 drugs for alzheimer's but we cant stop the disease progression one of us is hepatotoxic from our side effects is---

galantamine, tacrine, donepezil, rivastigmine tacrine is the toxic GI distress

I am used to diagnose myasthenia gravis but i am a short acting agent that cause cramping for only few minutes

Edrophonium

we are 2 drugs used to treat myasthenia gravis

neo and pyridostigmine

we are 2 drugs used as antidotes for tubocurarine

neostigmine and edrophonium

i m an intermediate acting agent used to increase intestinal and bladder motility and produce miosis and spasm accomodation as well as lowering intraocular pressure

physostigmine

i am used for overdoses of atropine phenothiazines or TCAs

physostigmine

I am a synthetic organophosphate that bind covalently to serine OH of AchE

Echothiophate

I can reverse the action of echothiophate only before aging (loss of alkyl group)

Pralidoxime

We can reverse the actions of echothiophate

Pralidoxime and atropine

T or F Echothiophate is the first line tx for glaucoma

False only in chronic tx of open angle glaucoma

Tor F the actions of echothiophate may last up to 3 weeks

false 1 week

T or F Pralidoxine can penetrate CNS

F It can reverse echothiophate effects except in the CNS

I am an alkaloid act both centrally and peripherally my actions last about 4 hrs while placed topically in the eye its action last for days

Atropine

I have longer duration of action than atropine and greater action on CNS

Scopolamine

I am used to treat asthma who are unable to take adrenergic agonist also used in COPD

Ipratropium

I produce mydriasis for 6 hrs while my brother produce it for 24 hrs

tropicamide cyclopentolate

I am an important adjunct in anesthetic procedures and effective prophylactically for motion sickness I can produce sedation, excitement and euphoria

scopolamine

The most effective anti motion sickness drug and i block short term memory

scopolamine

low doses of me may overcome atropine toxicity

physostigmine

I reduce gastric acid secretion but i dont antagonize other systems

Pirenzepine

used as mydriatic and cyclopegic agent , anti spasmodic, antidote for cholinergic agonist and anti secretory

atropine

T or F nicotine is a nondepolarizing competiitive antagonist

false all except nicotine

I depolarize ganglia first in stimulation then in paralysis

nicotine

at low doses i increase Bp and HR and increase peristalsis and secretions while at high doses the pressure falls and activity of both GI and bladder ceases

nicotine

I am the only ganglion blocker other than nicotine used for emergent hypertensive situations and my action lasts for 10 hrs

Mecamylamine

I block skeletal neuromuscular junction largely replaced because i am a potential allergen, less anesthetic is required when i am administered.

tubocurarine

mode of action of competitive blockers at low and high doses

low: binds to the receptor administration of AchE inhibitors can overcome the effect of tubocurarine high: binds to the ion channel reducing the ability of AcHE inhibitors to overcome its effect

we are 3 drugs that cause the release of histamine and cause fall in blood pressure flushing and bronchoconstriction adjuvants of anesthesia during surgery and useful in intubation

tubocurarine mivacurium atracurium

we are 3 drugs that cause the release of histamine and cause fall in blood pressure flushing and bronchoconstriction adjuvants of anesthesia during surgery and useful in intubation

tubocurarine mivacurium atracurium

I am degraded by plasma by ester hydrolysis i provoke seizures

atracurium

we are 2 drugs excreted in the urine unchanged

tubocurarine and mivacurium

the fam of 3 drugs exhibit 3 important characteristics 1-------- 2------- 3.......

orally ineffective (quaternary amines bulky) dont enter cells or cross BBB not metablized (terminated by redistribution)

I am in the same family as atracurium but i have less side effects

cisatracurium

We belong to the aminosteroid family excreted unchanged in bile

Vecoronium and rocuronium

nondepolarizing blockers drug drug interctions (3)

-Cholinesterase inhibitors can overcome their actions but with increased dosage they cause depolarizing block -aminoglycosides (tobramycin and genta) enhance the blockage -Calcium channel blockers increase neuromuscular block

I am depolarizing agent that cause constant stimulation and depolarization of the receptor then gradual repolarization then flaccid paralysis

succinylcholine

I block the the transport of dopamine to the vesicle

reserpine

we block the release of NE from the neurons

Guanethidine and bretylium

we inhibit the reuptake of NE

Cocaine and imipramine

I increase the cardiac contraction decrease the peripheral resistance

Epinephrine

I am used in anaphylactic shock cardiac arrest anesthetics and bronchospasm

epinephrine

T or F in emergency NE have the most rapid onset of action

F Epi

Mode of administration of epi

topical SC Iv

Epi adverse effects

CNS disturbances (anxiety fear tremor headache) Hemorrhage Cardiac arrhythmias (with digitalis)

Epi interactions

with coc: exagerrated CV action Can cause diabetes B-blockers: leads to increased Bp

I work on alpha1 alpha2 b1 I increase the peripheral resistance but cause reflex bradycardia

T or F NE is well absorbed SC NE can cause necrosis duration of action 4-5 mins Used to treat shock

false poorly T F: 1-2mins T

i work on B1 and b2 only

isoproterenol

I significantly decrease peripheral resistance and increase cardiac force used in atrioventricular block

Isoprotenerol

Uses of isoprotenerol

rarely as bronchodilator stimulate heart in emergency

Mode of adminstration of iso

sublingual inhaled IV

I work on a1(at high doses) and b1(on low doses) but also 2 other receptors iam the best in tx of shock

dopamine

I am a selective B1 agonist used in congestive heart failure and does not sigficantly increase oxygen demand

Dobutamine

I am a a1 a2 agrenergic agonist used as ophthalmic drops to treat eye redness and as a decongestant i can cause rebound congestion in long term use with burning of mucosa and sneezing

oxymetazoline

I am selective a1 agonist acting as a vasoconstrictor i can cause reflex bradycardia when given IV i have local effects as a decongestant and cause mydriasis

phenylephrine

a1 favored over a2 used in supraventricular tachy used to ovrcome hypotensive effect of halothane

Methoxamine

a2 selective agonist used in essential hypertension and to minimize withdrawal of opiates or benzo

Clonidine

B2 non selective used as bronchodilator in tx of asthma and reverse bronchospasm ------- inhalation aerosol is indicated

Metaprotenerol Alupent

short acting B2 agonists (3)

Albuterol Pirbuterol Terbutaline

LABAs: duration of action not recommended as monotherapy usually accompanied with--- uses:

Salmeterol and formoterol 12 hr compared to 3 hr for SABAs ICS Nocturnal asthma

I cause release of stored catecholamines Used in ADHD narcolepsy and apetite control should be avoided in pregnancy

Amphetamine

Can cause hypertension when taken with MAO inhibitors because it causes release of NE from nerve terminals

Tyramine

I block the NA+/K+ pump

Cocaine

Ephedrine and pseudoephedrine Mode of action

Release both stored NE and E and also stimulate A and B receptors

T or F Ephedrine and pseudoephedrine both are well absorbed orally and penetrate CNS

Ephedrine works on ------- receptors and used in----- while pseudoephedrine is used in --------

a1 a2 b1 b2 mild stimulation of CNS asthma,nasal decongestant, raise BP nasal and sinus congestion

I am used to treat ADHD patients by inhibiting reuptake of dopamine and NE

Methylphenidate

I block a1 and a2 covalently irreversibly and in a noncompeyitive manner I prevent vasoconstriction and cause relfex tachycardia I reverse the effect of epi Used in pheochromocytoma and raynaud's disease

Phenoxybenzamine

Adverse effects of phenoxybenzamine

Inhibit ejaculation Postural hypotension Nausea and vomiting Reflex tachy

I am a competitive antagonist for a1 and a2 My action last for 4 hr Used for short term pheo Can trigger arrhytmias and anginal pain (contraindicated in patients with decreased perfusion)

Phentolamine

We are both in the competitive antagonists for a1 but we are used in tx of hypertension

Prazosin doxazosin

We belong to the competitive antagonist a1 but we are used mainly for tx of BPH

Tamsulosin Alfusozin

T or F Tamsulosin have the most effect on HtN Tamsulosin binds on a1B receptors

Falseee least Falseeeee a1A found on SMc of prostate

Adverse effects of -sin family

Orthostatic htn Retrograde ejaculation and inhibition of ejaculation Drowsinnes dizziness Lack of energy Nasal congestion Headache

I am a a2 competitive blocker I increase the sympathetic flow

Yohimbine

Uses of B blockers

HTN Dont induce hypotension Angina Cardiac arrythmias MI CHf Hyperthyroidism Glaucoma Migrain prophylaxis