Guess the drug (autonomic nervous system version)) Flashcards
I am a drug that inhibit the rate limiting step of synthesis of Ach
Hemicholinium
I am a drug that block Ach release while my brother causes the release of Ach
Botulinium
Spider venom (black widow)
I am an enzyme found in plasma but I don’t play a significant role in termination of Ach effect
Pseudocholinesterase
I am a drug that inhibit the movement of Ach into the vesicles
Vesamicol
An alkaloid present in poisonous mushrooms
muscarine
How many muscarinic subclasses do we have
5 (only 3 being functionally characterized)
M1 receptors are on——-
M2 receptors are on——-
M3 receptors are on ——-
Gastric parietal cells
Cardiac and smooth muscle
Bladder, exocrine and smooth muscle
T or F
drugs with Muscarinic act can’t stimulate nicotinic receptors
false
at high concentration they do
Muscarinic receptors are G-coupled receptors with — or —- being excitatory ( G–) while —– being inhibitory (G–)
G coupled
M1 and M3 Gq
M2 inhibitory (Gi)
nicotinic receptors are —–gated —- that have (rapid\slow)—– action
ligand gated ion channels (Na+ or Ca2+)
rapidddd
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
I am an alkaloid, stable to hydrolysis by AChE, uncharged used mainly in ophthalmology
pilocarpine
I am a poor substrate for ACHE positively charged and i have nicotinic action
Carbachol
I am rarely therapeutic except in the eye because of my high potency , non selective binding and long duration of action
Carbachol
I lack nicotinic action and not hydrolized by ACHE i have a duration of action about 1 hr
bethanechol
My major actions are on SMC of bladder and GI
Bethanecol
I am primarily used as miotic for treating glaucoma or during ophthalmic surgery
Carbachol
From my side effects:
Cause marked diaphoresis
enter brain and cause CNS disturbances
pilocarpine
From my usages:
tx of xerostomia
tx of open angle glaucoma
miosis and contraction of ciliary muscle
Pilocarpine
I am administered as intraocular solution or injection
Carbachol
I am used to treat megacolon and atonic bladder
Bethanecol
Iam a useless drug
ACH
I am a tertiary amine that make a stable carbmaminoylated compound with ACHE then make it reversibly inactive
physostigmine
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
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
NE
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
T
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