Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
43 Cards in this Set
- Front
- Back
What types of receptors does acetylcholine interact with?
|
this neurotransmitter interacts with
-nicotinic receptors -muscarinic receptors |
|
Which muscarinic/nicotinic agonists are acetylcholinesterase substrates? (short action duration) Why?
|
-acetylcholine
-methacholine both have an ester group |
|
Which muscarinic/nicotinic agonists are not acetylcholinesterase substrates? (long action duration) Why?
|
-carbachol
-bethanechol both have an amide group instead of an ester group |
|
What is edrophonium?
|
this drug is:
-reversible competitive inhibitor of cholinesterase (very short duration) -used in diagnosis of myasthenia gravis |
|
What is DFP (diisopropyl-fluorophosphate)?
|
this drug is an irreversible inhibitor of cholinesterase (long term inhibition)
|
|
What is neostigmine?
|
this drug is:
-carbamate inhibitor of cholinesterase (intermediate duration of action) -binds covalently but bond is readily hydrolyzed |
|
Which drugs are antimuscarinic (anticholinergic) agents?
|
-atropine
-scopolamine -methylatropine -ipratropium |
|
What is trimethaphan?
|
this drug is:
-short acting ganglionic blocking agent -used during surgery to produce controlled hypotension |
|
What is atypical plasma cholinesterase?
|
-lacks the ability to hydrolyze carboxylic ester bonds in drugs
-causes slowed metabolism of drugs containing carboxylic esters |
|
Why does methacholine at low doses produce miosis in dysautonmia patients but not in normal patients?
|
this disease involves small-fiber peripheral neuropathy → supersentized to methacholine (normal patients are not supersensitized)
|
|
What are common effects of muscarinic agonists?
|
this category of drugs often causes:
-bradycardia (direct effect) -vasodilation -reflex tachycardia (indirect effect) -increased secretions of fluids → dehydration -bronchoconstriction -increase in peristaltic activity → diarrhea -pupillary constriction -loss of accomodation → blurred vision |
|
What are common side effects of antimuscarinic (anticholinergic) agents?
|
side effects of this type of drug:
-paralysis of accomodation to near objects (cycloplegia) -increased heart rate -reduced secretion of fluids -reduced GI/bladder motility → constipation, urinary retention -reduced bronchial mucous secretion -bronchodilation -CNS: sedation, memory loss, psychosis (high doses) |
|
What types of receptors does norepinephrine interact with?
|
this neurotransmitter:
-interacts with α and β1 receptors at low dose -interacts with β2 receptors at high dose |
|
What types of receptors does epinephrine interact with?
|
this neurotransmitter:
-interacts with β1 and β2 receptors at low dose -interacts with α receptors at high dose |
|
What types of receptors does isoproterenol interact with?
|
this drug interacts with β1 and β2 receptors only
|
|
What is phenylephrine?
|
-this drug is an α1-agonist
-causes vasoconstriction → reflex bradycardia |
|
Which drugs are usually given as bronchodilators?
|
β2 agonists are usually used for this purpose.
examples: -terbutaline -albuterol |
|
What is dobutamine?
|
this drug is:
-β1 agonist -increases force and rate of heart contraction |
|
What is the mechanism of action of amphetamine?
|
-indirect acting sympathomimetic
-displaces NE, Epi, DA from storage sites in presynaptic nerve terminals |
|
What is phentolamine?
|
-direct receptor sympatholytic
-α blocker |
|
What is propanolol?
|
-direct receptor sympatholytic
-β blocker (non selective) |
|
What is clonidine?
|
-central sympathetic depressant (sympatholytic)
-α2 agonist |
|
What is reserpine?
|
-adrenergic neuronal blocking agent (sympatholytic)
-interferes with synthesis and release of NE consequent to nerve stimulation |
|
What are two examples of MAO inhibitors? What is their effect?
|
-parglyine
-tranylcypromine this category of drugs enhances NE and Epi effects |
|
What is the mechanism of action of cocaine?
|
this drug causes strong dopamine reuptake inhibition → exaggerate adrenergic response
|
|
What is the mechanism of action of tricyclic antidepressants?
|
these category of drugs causes strong NE and/or 5-HT reuptake inhibition → exaggerate adrenergic response
|
|
What is yohimibine?
|
-indirect acting sympathomimetic
-α2 blocker -increase NE release -increase sympathetic tone (CNS) |
|
What are general sympathomimetic effects on nonvascular smooth muscle?
|
these drugs have the following effects on nonvascular smooth muscle:
-bronchial smooth muscle (β relax, α constrict) -stomach and intestine (α and β, relax) -contraction of anal sphincter -pupil dilation -urinary retention -increase force and rate of heart contraction -uterus (β2, relax) |
|
What are general sympathomimetic effects on vascular smooth muscle?
|
these drugs have the following effects on vascular smooth muscle:
-vessels of skin, brain, splanchnic, mucus membranes (α, constrict) -vessels of visceral organs including kidney and skeletal muscles (β2, dilate) |
|
What are side effects of all sympatholytic agents?
|
side effects of this category of drugs include:
- ↓GFR → increase in blood volume and NA+ retention -sedation and depression (if it gets in CNS) |
|
What are side effects of α-blockers, CNS sympathetic depressants, and adrenergic neuronal blockers?
|
these categories of drugs have the following side effects:
-nasal stuffiness - ↑GI motility and diarrhea |
|
What side effects occur only with α-blockers?
|
these drugs have the following side effects:
-postural hypotension → reflex tachycardia -impaired ability to ejaculate -in CNS: akinesia, loss of spontaneous motion, rigidity, tremor |
|
What are the effects of β blockers?
|
these drugs have the following effects:
-bradycardia -decreased cardiac output -impairment of insulin release (sometimes) -bronchoconstriction -blocks some symptoms of hyperthyroidism -increase in triglycerides and decrease in HDL -cold extremities |
|
How does digitalis increase cardiac contractility?
|
this drug:
-inhibits Na/K pump -causes higher intracellular Ca2+ |
|
How do β adrenergic agonists increase cardiac contractility?
|
these stimulate Ca channel and SR Ca pump via cAMP (G protein pathway)
|
|
How does caffeine increase cardiac contractility? What is another drug that has the same mechanism of action?
|
-this drug stimulates Ca channel and SR Ca pump via cAMP (phosphodiesterase inhibition)
-milrinone works the same way |
|
Which types of drugs decrease MVO2 (myocardial oxygen consumption)?
|
-β1 blockers (decrease cardiac output)
-nitrates (vasodilate peripheral resistance) -diuretics (decrease afterload) -ACE inhibitors (decrease afterload) |
|
What is captopril?
|
this drug is an example of an ACE inhibitor
|
|
Which types of drugs increase MVO2 (myocardial oxygen consumption)?
|
-β1 agonists (increase cardiac output)
-vasoconstrictors |
|
What are furosemide and bumetanide? What is their mechanism of action and what side effects do they produce?
|
-these drugs are loop diuretics; they inhibit the NKCC2 transporter in the thick ascending limb
-side effects: hypokalemic metabolic acidosis |
|
What is the mechanism of action of thiazide diuretics? What side effects do they cause?
|
-these drugs inhibit the Na-Cl transporter in the distal convoluted tubule and collecting duct
-side effects: hypokalemic metabolic alkalosis |
|
What is acetazolamide? What are the side effects?
|
-this drug blocks carbonic anhydrase in the proximal tubule → blocks absorption of HCO3-
-side effects: acidosis, urine increases in K+ and PO4- |
|
What is aldactone? What side effects does it produce?
|
-this drug blocks aldosterone in the distal tubule and collecting duct
-spares K+ and enhances Na+ loss → diuresis -side effects: hyperkalemic metabolic acidosis |