Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/174

Click to flip

174 Cards in this Set

  • Front
  • Back
What NT and receptor are used in the synapse between the pre and post ganglions of the PS and SNS?
NT: ACh
Receptor: Nn
NT and receptor at the post-ganglionic synapse of PS?
NT: ACh
Receptor: M
NT and receptor at the post-ganglionic synapse of SNS on smooth muscle?
NT: NE
Receptor: α & β
NT and receptor at the post-ganglionic synapse of SNS on sweat gland?
NT: ACh
Receptor: M
NT and receptor of a somatic motor neuron?
NT: ACh
Receptor: Nm

(only 1 neuron)
What is the precursor to NE?
Tyrosine
What is the main mechanism for NE inactivation in a sympathetic synapse?
uptake by the norepinephrine transporter (NET) on the pre-synaptic varicosity
-inside it is either reused or degraded by MAO
Where is NE converted to Epi and by what enzyme
In the Adrenal Medulla by PNMT
Relative sympathetic receptor affinity for NE and EPI
NE α1=α2 β1>>β2
EPI α1=α2 β1=β2
What 2 receptors are found on blood vessels?
α1 and β2
What does low dose EPI do to blood vessels?
Activates β2 receptors causing vasodilation and decreased PVR
Main mechanism for the inactivation of ACh?
acetylcholinesterase (AChE) in the synaptic cleft
3 locations for a N receptor
skeletal m., parasympathetic and sympathetic ganglia
Gs (G-protein)
s for stimulate
(activates adenylyl cyclase)
Gi (G-protein)
i for inhibits
(inhibits adenylyl cyclase)
Gq (G-protein)
activated Phospholipase Cβ
What is interesting with regard to β2 receptors and their G-protein?
β2 receptors are coupled with Gs protiens with cause stimulate but ultimitely cause relaxation
Where are β1 receptors found and what is the result of activation?
heart: inc. HR, inc. force of contraction
kidney: renin release
Where are β2 receptors found and what is the result of activation?
smooth m.: relaxation
liver: glycogenolysis, gluconeogenesis
Where are β3 receptors found and what is the result of activation?
lipolysis
What is the mechanism of activation for nicotinic receptors?
ligand gated ion channel
(note: not G-protein)

-> results in depolarization
Where are M3 receptors found?
smooth muscle and secretory glands

-> cause contraction/ secretion
->Gq
Where are M2 receptors found?
heart

-> causes decreased activity
-> Gi
What happens to the permeabitlity of K+ upon ligand binding to M3?
increase permeability of K+ which results in hyperpolarization -> longer to reach threshold
What happens to receptor number upon chronic exposure to an antagonist?
receptor up-regulate
(issue when drug is taken away)
What happens to receptor number upon chronic exposure to an agonist?
receptor down-regulation
What is the effect of PS stimulation of the iris sphincter smooth muscle?
contraction and constriction (miosis)
What is the effect of sympathetic stimuation of the iris radial smooth muscle?
contraction and dilation (mydriasis)
What is the effect of PS stimulation to the ciliary muscle?
contraction of the ciliary m. -> unflatten the lens -> accomodation for near vision
How does the ciliary muscle allow for far vision?
relation of the ciliary muscle -> flattening the lens

(note: no ANS stimulation needed for this)
What are the PS and S receptors found on bronchial smooth muscle?
M3 and β2

(note: β2 receptors have no innervation, rather react to circulating EPI)
What receptors are on the bronchial glands?
M3
-cause secretion
PS stimulation to the lungs causes bronchoconstriction or bronchodilation?
bronchoconstriction
(M3 receptors)
3 effects of parasympathetic stimulation to the GI system
1. gastric secretions
2. relax sphincter
3. contraction - increase tone and motility
2 effects of sympathetic stimulation of the GI system
1. contract sphincter
2. relaxation - decrease tone and motiltiy
What would be used to stop gastric secretions?
muscarinic antagonist
Describe parasympathetic stimulation to the bladder
Micturation
-contraction of the detrusor m.
-relaxation of the trigone m.
Describe sympathetic stimulation to the bladder
Urinary retention
-relax detrusor m. (β2)
-contract trigone m. (α1)
Describe the effect of ACh within the lumen of a blood vessel on the endothelial cell?
ACh binds to M3 receptor -> endothelial cell releases NO -> NO activates guanylyl cyclase in smooth m.
3 examples of blood vessels innervated by parasympathetic nerves?
-erectile tissue
-salivary glands
-GI glands
What sympathetic receptor is more prevalent on blood vessels to liver/skeletal m.?
β2 -> vasodilation
What sympathetic receptor is more prevelant on blood vessels to the rest of the body other than liver/skeletal m.?
α1 -> vasoconstriction
3 effects of parasympathetic stimulation to the heart
1. decrease HR
2. decrease force of contraction
3. decrease conduction velocity
3 effects of sympathetic stimulation to the heart
1. increase HR
2. increase conduction velocity
3. increase force of contraction (atria and ventricles)
-> β1 receptors
Does isoproterenol have more affinity for β or α receptors?
β

β=β>>>>>α
What 2 secretory glands are innervated by parasympathetics?
salivary and nasopharyngeal glands
-> secretion M3
Describe sympathetic innervation of sweat glands
2 types
-thermoregulatory sweating - M3
-palms of hands - α1
Describe sympathetic innervation to a fall cell
NE -> β3 -> lypolysis to provide energy
Describe the effect of low plasma glucose on the adrenal medulla and liver and skeletal m. cells
low plasma glucose -> causes release of EPI from adrenal medulla -> EPI activate β2 receptors on liver and skeletal m. -> glycogenolysis and gluconeogenesis
How does sympathetic stimulation cause a decrease in insulin release?
Sympathetic innervation to α2 receptor
How does sympathetics cause an increase in insulin release?
circulating EPI activates β2 receptors
How does sympathetics cause renin release?
sympathetic innervation to β1 receptors on the kidney causing an increase in renin release
EPI activation of β2 receptors shift K (into or out) of the cell.
into the cell
Would a β2 agonist be used to treat hyperkalemia or hypokalemia?
hyperkalemia
-bring K into the cell
What does overstimulation of skeletal m. due to EPI cause?
tremors
Adrenalin
epinephrine
Which receptor on blood vessels has a greater sensitivity for EPI?
β2

-> at low dose of EPI vessel will vasodilate and decrease PVR
What does high dose of EPI do the PVR in blood vessels?
causes increased PVR due to the amount of α1 receptors compared to β2
Dipivefrin
-prodrug converted into epinephrine
-topical, opthalmic agent
Dopamine
-activates dopamine, β1, α receptors
Phenylephrine
α1 selective agonist
-sudafed PE
Dipivefrin
-prodrug converted into epinephrine
-topical, opthalmic agent
Xylometazoline
α1 selective agonist
-nasal
Dopamine
-activates dopamine, β1, α receptors
Phenylephrine
α1 selective agonist
-sudafed PE
Oxymetazoline
α1 selective agonist
-also activated α2
-nasal
Xylometazoline
α1 selective agonist
-nasal
Oxymetazoline
α1 selective agonist
-also activated α2
-nasal
Midodrine
α1 selective agonist
-oral
-orthostatic hypertension
Brimonidine and Aprachonidine
α2 selective agonist
-topical
-eye (glaucoma)
Isoproterenol
non-selective β agonist
-parenteral
Dobutamine
(+) isomer - β1 agonist, α1 antagonist
(-) isomer - α1 agonist
-parenteral
β2 selective agonist (3)
-Albuterol
-Metaproterenol
-Pirbuterol

(inhalation, some oral)
Terbutaline
β2 selective agonist
-oral/parenteral
Salmeterol, Formoterol, Arformoterol
β2 selective agonist
-inhalation
Drug for hemorrhage from a minor cut
EPI
-activate α1 receptor -> vasoconstrict blood vessels in the area
What is the difference btwn Phenylephrine and Xylometazoline and Oxymetazoline
Phenylephrine has a short 1/2 life (4 hrs)
Xylometazoline and Oxymetazoline have a long duration of action (overnight)
Describe rebound nasal congestion
down regulation of α1 receptors with chronic use of nasal decongestant -> in absence of drug NE has low affinity for α1 receptors -> nasal congestion
Describe the reactions of Anaphylaxis and the effects of EPI
Angioedema -> α1 constrict capillary beds
Bronchoconstriction -> β2 bronchodilation
Pruritus, Urticaria -> β suppress release of mediators from mast cells
Hypotension -> α1 β1 raise BP
How does Phenylephrine correct paroxysmal supraventricular tachycardia?
-convert arrhythemia to NSR
-PE (α1 agonist) causes vasoconstriction -> increase BP -> decrease firing of baroreceptor -> decrease HR and decrease conduction
How does Phenylephrine effect hypotension?
activates α1 receptors that cause vasoconstriciton leading to an increase in BP
3 locations of dopamine receptors and effects of activation
1. renal vasculature -> vasodilation, increase renal blood flow
2. β1 receptos -> increase CO and BP
3. α1 receptors -> increase PVR and BP
3 drugs to treat shock (hypovolumic, cardiogenic, distributive)
dopamine, dobutamine, NE
Drug to treat AV Block
EPI, isoproterenol
β1 agonist, increase AV conduction
Drug to treat Ventricular fibrillation/ Pulseless ventricular tachycardia
EPI
Short acting drugs for Asthma/COPD
albuterol, metaproterenol, pirbuterol, terbutaline
Long acting drugs for Asthma/COPD
salmeterol, formoterol, arformoterol
Drug to stop premature labor
Terbutaline
-activation of β2 receptors cause uterine smooth muscle relaxation -> stop uterine contractions
What drug is used to dilate the pupil?
Phenylephrine
-α1 agonist
-contraction of the iris radial smooth muscle
-dilation without cycloplegia (paralysis of the ciliary m.)
Adverse effects from α adrenergic activation
-reduced peripheral blood flow (α1 on blood vessels)
-excessive contraction of blood vessels at infusion site (ischemia/necrosis)
-rebound nasal congestion
-mydriasis (dilation of pupils)
Adverse effects from β1 adrenergic activation
β1 receptors on the heart
-increase HR (palpitations, tachycardia, cardiac arrhythmias)
-increase force of contraction -> increase work load -> angina
Adverse effects from β2 adrenergic activation
-hyperglycemia (β2 receptor activation on the liver stimulates glycogenolysis)
-tremor (over activation of skeletal m.)
Contraindications of direct acting adrenomimetics
-cardiovasuclar disease
-hyperthyroidism
-diabetes
4 indirect acting adrenomimetics
-Tyramine
-Amphetamine
-Methylphenidate
-Atomoxetine
(last 3 CNS stimulants and/or used for ADHD)
Tyramine
NOT A DRUG
-comes from gut bacteria and fermented food
-normally is metabolized in the liver by MAO
-if not... found in blood and promotes release of NE from sympathetic nerve terminal
2 mixed acting adrenomimetic agents
Ephedrine, Psudoepedrine
-release NE from the nerve terminal and activate both α and β
-cross the blood/brian barrier
Approved uses from Ephedrine
Asthma, COPD, nasal congestion
Adverse effects of Ephedrine
-cardiovascular (excessive stimulation of the heart)
-CNS (insomnia, nervousness, anxiety)
Actions of Pseudophedrine
-directly activates α and to a lesser extent β receptors
-release NE from nerve terminal
-less CNS effects than ephedrine
-nasal decongestant
α1 selective antagonist, reversible
all end in -osin
-Prazosin
-Terazosin
-Doxazosin
-Tamsulosin
-Alfuzosin
-Silodosin
Non-selective α antagonist, reversible
Phentolamine
Non-selective α antagonist, non-reversible
Phenoxybenzamine
3 α antagonists used to treat hypertension
Prazosin, Terazosin, Doxazosin
2 α antagonist used to treat Pheochromocytoma
Phentolamine, Phenoxybenzamine
(both α1 blockers)
-goal is to reduce the BP caused by an increase in EPI in the system due to a tumor on the Adrenal Medulla
6 α antagonist used to treat Benign Prostatic Hyperplasia (BPH)
Prazosin, Terazosin, Doxazosin, Tamsulosin, Alfuzosin, Silodosin
-increases urine flow by blocking α1 receptors and relaxing smooth m. in the base of bladder and the prostate
3 α antagonist used to treat Raynaud's disease
Raynaud's disease: cold induced vasospasm in fingers and toes

Prazosin, Terazosin, Doxazosin
-block the α1 receptors on fingers and toes -> maintain circulation
What is the 1st dose effect with regard to orthostatic hypotension?
With the 1st dose of the α antagonist medication profound orthostatic hypotension with syncope is observed (also occurs when increase dose)
What is the mechanism for orthostatic hypotension with regard to α antagonist
Prazosin inhibits the α1 receptors on blood vessels -> no vasoconstriction -> blood pools in the veins -> decrease CO -> hypotension with syncope
How does Prazosin (α antagonist) cause reflex tachycardia?
Prazosin blocks the α1 receptors on the blood vessels -> decreased BP -> stimulate baroreceptors -> reflex tachycardia
6 Non-selective, competitive, reversible β receptor antagonists
Propranolol, Nadolol, Timolol, Pindolol, Carteolol, Levobunolol
(all end in olol)
6 β1 selective, competitive, reversible β receptor antagonist
Metoprolol, Atenolol, Acebutolol, Betaxolol, Bisoprolol, Esmolol

(all end in olol and begin with BEAM)
What cardiovascular diseases are treated with β receptor antagonists?
Hypertension, Ischemia, Arrhythmias, MI, Heart failure
Are β antagonists used to treat Pheochromocytoma?
Yes in conjunction with α blocker

(Pheochromocytoma - excessive EPI and NE release caused by adrenal tumor)
What is typically used to treat migraines?
β receptor antagonists
-used only to prevent rather than treat (prophylactic)
What is used to prevent Esophageal variceal bleeding?
non-selective β blockers
Describe the adverse effects of β receptor antagonist with regard to the heart
inhibition of β1 receptors on the heart lead to bradycardia, AV block, decreased contractile force => hypotension and heart failure
What 2 β receptor antagonists are able to cross the blood brain barrier and cause adverse effects?
Propranolol and Metoprolol

-cause: nightmares, lassitdue, mental depression, insomnia
What is the issue with having your diabetic pt on β receptor antagonists?
hypoglycemia activates the sympathetic NS to release EPI to act on the liver (glycogenolysis, gluconeogenesis) and heart (inc. HR)
-> eliminate these responses
Why are both non-selective and β1 selective blockers contraindicated in a pt with asthma?
non-selective: block the β2 receptors on the lungs -> bronchoconstriciton
(β1 selective lose their selectivity at higher doses)
What happens when a pt with peripheral vascular disease is on a β receptor antagonist?
unopposed vasoconstriction
-no β2 activity
Describe rebound hypertension with regard to β receptor antagonists
chronic therapy up regulates β receptors
abrupt withdrawal from β blocker causes rebound hypertension, nervousness, tachycardia, angina
6 direct acting muscarinic agonists
Acetylcholine, Bethanechol, Pilocarpine, Carbachol, Cevimeline
Upon activation of M receptors...
heart, blood vessels, ciliary body, iris sphincter, GI tract, bladder
Heart- decrease HR
Blood vessels - vasodilate via NO
Ciliary muscle - contraction/near vision
Iris sphincter - miosis
GI tract - increase activity
Bladder - micturition
2 therapeutic uses of Bethanechol
muscarinic agonist
1. post operative abdominal distension and urinary retention
2. neurogenic atony of the urinary bladder with retention
(non-obstructive retention)
Therapeutic uses for Pilocarpine, both topical and oral
muscarinic agonist
Topical: miotic, open angle glaucoma, narrow angle glaucoma
Oral: Sjogren's syndrome, radiation induced dry mouth
Therapeutic use of Cevimeline
muscarinic agonist
-newer drug from Sjogren's syndrome (autoimmune disorder against moisture producing gland)
Is Muscarine a drug?
No, present in mushrooms
Adverse effects of direct acting muscarinic agonists with regard to salivary glands, sweat glands, GI tract, Stomach
salivary gland - salivation
sweat glands - sweating
GI tract - intestinal cramps/NVD
stomach - aggravate ulcer
Adverse effects of direct acting muscarinic agonists with regard to CV system
blood vessels - dilation (via NO)
heart - bradycardia -> reflex tachycardia
How do direct acting muscarinic agonists adversely affect the lungs and eye
Lungs: bronchoconstriction (difficulty breathing/asthma attack)
Eyes: near vision and miosis
Reversible AChE inhibitors
Physostigmine, Neostigmine, Edrophonium, Edrophonium + Atropine, Pyridostigmine
Work in the CNS:
Donepezil, Tacrine, Rivastigmine, Galantamine
What drug would be used or an overdose of a muscarinic blocker?
Physostigmine
(note: it is lipid soluble and can cause severe adverse effect -> only used when absolutely needed)
2 topical uses from Physostigmine
miotic (constriction of the pupil) and treatment of glaucoma
Which would be used for postoperative urinary retention and abdominal distension (Neostigmine or Pyridostigmine)
Neostigmine
Which 2 drugs could be used to treat Myasthenia gravis and why?
Pryidostigmine and Neostigmine
-they are non-lipid soluble and are more selective in the neuromuscular junction
Drug used as a diagnostic test for myasthenia gravis
Edrophonium (analog of neostigmine)
-shorter acting, 3-4 minutes
-IV only
Name 2 irreversible AChE inhibitor therapeutic agents
Echothiophate [+ charged, not volatile, used over DFP]
Diisoprophyl flourophosphate (DFP) [high lipid solubility, volatile]
-only given topically on the eye
3 irreversible AChE inhibitor insecticides
Tetraethyl pyrophosphate (TEPP), Parathion, Melathion
3 Nerve Gases
Sarin, Soman, Tabun
(irreversible AChE inhibitors)
Which insecticide is used to treat head lice?
Melathion
-low dermal absorption
Toxicity of irreversible AChE inhibitors
Malathion < Parthion <<<< Sarin (nerve gas, micogram dose)
3 adverse effects of AChE inhibitors
1. lens opacities
2. chronic neurotoxicity
3. cholinergic crisis
Differentiate Neostigmine, Physostigmine, Organophosphates with regard to reversibility and ability to cross the BBB
Neostigmine: reversible and does not cross BBB
Physostigmine: reversible but does cross the BBB
Organophosphates: irreversible and crosses the BBB
What drug is used to treat a Cholinergic crisis?
Atropine: muscarinic blocker
(remember it does not act on the Nicotinic receptors in the skeletal m. Neuromuscular junction)
Pralidoxime: cholinesterase reactivator
(NMJ, used only for organophosphate poisoning)
7 non-depolarizing neuromuscular blocking agents
Tubocuraine, Atracurium, Cisatracurium, Mivacurium, Pancuronium, Rocuronium, Vecuronium
-all have curoni in the name
1 depolarizing neuromuscular blocking agent
Succinylcholine
Sequence of paralysis with non-depolarizing neuromuscular blockers
eyes, face, limbs, abdominal, intercostals, diaphragm
(small m. first, recover is the reverse order)
How would you reverse the effects of a non-depolarizing neuromuscular blocker
AChE inhibitor
3 characteristics of all neuromuscular blockers
1. do not enter the CNS
2. do not affect sensory neurons
3. are not anesthetic or analgesic
Describe phase I block of Succinylcholine
-acts as ACh to depolarize the cell
-resistant to AChE -> repetitive excitation that may elicit fasciculations
-depolarization block that leads to flaccid paralysis
Describe phase II block of Succinylcholine
continuous exposure causes re-polarization of the receptor which resembles desensitization
-difficult for the receptor to be depolarized again
Which is short acting agent and which a long acting agent (Pancuronium & Succinylcholine)
Succinylcholine - short 1/2 life, 5 minutes
Pancuronium - long 1/2 life, 120-180 minutes
Adverse effects of non-depolarizing neuromuscular blockers
-histamine release - really bad for asthmatics
-block autonomic ganglia - vasodilation, hypotension, tachacardia
-block muscarinic receptor - tachacardia
Describe the adverse effects of Succinylcholine with respect to hyperkalemia
In pts with denervation supersensitivity upon exposure to Succinylcholine there is a large efflux of potassium resulting in hyperkalemia -> cardiac arrest =(
Describe the adverse effects of Succinylcholine with regard to Malignant hyperthermia
causes an excessive release of calcium from the SR -> potentially fatal
List of Muscarinic Antagonists
Atropine, Scopolamine, Tropicamide, Cyclopentolate, Ipratropium bromide, Tiotropium bromide, Tolterodine, Fesoterodine, Oxybutynin chloride, Darifenacin HBr, Solifenacin, Trospium Chloride
What 3 drugs are used to achieve Mydriasis and cycloplegia
Tropicamide (short duration)
Atropine and Scopolamine (long duration)
What are 2 methods for treating acute rhinitis
1. muscarinic antagonist - get rid of snot
2. alpha agonist - constrict blood vessels
What are the differences between Ipratropium bromide and Tiotropium bromide for the treatment of Asthma/COPD?
Ipratropium - short duration of action, usually given 4x/day
Tiotropium - longer duration of action, once a day
(both inhaled muscarinic antagonists -> inhibit bronchoconstriction)
Which is more lipid soluble Atropine or Ipratropium bromide
Atropine
Which preoperative drug has more sedative and amnesia effects (Atropine or Scopolamine)
Scopolamine > Atropine
-a much higher dose of atropine is needed
-both result in less oral secretions
How are muscarinic antagonists used to treat hyperactive carotid sinus syndrome?
inhibit the excessive PS stimulation to the heart -> stopping bradycardia and AV block -> guy with very tight tie does not have an episode of syncope =)
What is used to treat motion sickness
Scopolamine
-put behind the ear
-inhibit stimulation of the vomit center in the medulla, which has M receptors
Does atropine effect ventricular arrthymias?
No, because there aren't any M receptors on the ventricles
-able to act on the AV node
Main agents used to treat urinary incontinence due to detrusor overactivity
Tolterodine, Oxybutynin Chloride, Darifenacin, Solifenacin, Trospium Chloride
List the order of severity of adverse effects of mucarinic antagonists with regard to the CNS
(Atropine, Scopolamine, Ipratropium)
Scopolamine > Atropine >>>> Ipratropium (does not cross the BBB)
When is it not appropriate to use Muscarinic antagonists
pt with narrow angle glaucoma
What produces Aqueous Humor in the eye?
Ciliary Body
2 ways to treat open angle glaucoma
1. decrease aqueous humor production -> β antagonist to decrease production or α2 agonist to decrease production
2. clear the trabecular meshwork -> α2 agonist
2 α2 agonists used to treat open angle glaucoma
Brimonidine and Apraclonidine
(both end in nidine)
What type of drug is used to open the hole within the trabecular meshwork of open angle glaucoma
Muscarinic agonist
-contraction of the ciliary m.
-Pilocarpine
What is the first choice for treatment of open angle glaucoma
beta blocker
-then alpha agonists, EPI, and cholinomimetrics
Describe the Cholinomimetics used for Glaucoma
Muscarinic agonists (Pilocarpine, Carbachol)
Reversible Acetylcholinesterase Inhibitors (Physostigmine(
Irreversible Acetylcholinesterase Inhibitors (Echothiophate)
-preferably used in that order
Is Pilocarpine used for Narrow Angle Glaucoma
yes, contract the iris sphincter m. -> move iris out of the way