- StudyBlue
- Michigan
- Michigan State University
- Pharmacology
- Pharmacology 340
- Cobbett
- Pharmacology Exam 1
Pharmacology Exam 1
Pharmacology 340 with Cobbett at Michigan State University
About this deck
By: Tom Centofanti
Created: 2012-02-18
Size: 173 flashcards
Views: 27
Created: 2012-02-18
Size: 173 flashcards
Views: 27
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Pharmacodynamics
Decribe mechanisms of drug effect and the relationship of drug concentration and intensity of drug effect
Why does a drug do what it does?
Why does a drug do what it does?
Pharmacokinetics
describe the action of a drug is time dependent and how the factors controlling this time dependence also affect the intensity of desired and undesired effects of that drug
How to drug is handled and processed
How to drug is handled and processed
ADME
Absorption, Distribution, Metabolism, Excretion
Metabolism and Excretion can be combined into Elimination
Metabolism and Excretion can be combined into Elimination
Enteral
Route of administration of a drug
Into the GI tract
Into the GI tract
Parenteral
Route of administration of a drug
outside GI tract
outside GI tract
Absorption
the process by which a drug molecule reach the plasma from original site of administration
Absorption rate dependent on what?
surface area of absorption surface
vascularization of absorption surface
blood flow within blood vessels of absorption
vascularization of absorption surface
blood flow within blood vessels of absorption
Bulk Flow
Mechanism of absorption
Movement of water and solutes across blood vessel wall due to openings of wall
driven by hydrostatic and osmotic pressure
Movement of water and solutes across blood vessel wall due to openings of wall
driven by hydrostatic and osmotic pressure
Transportation
Mechanism of absorption
Molecule moved across membranes by transporter molecule embedded in plasma membrane
rarely a mechanism
Molecule moved across membranes by transporter molecule embedded in plasma membrane
rarely a mechanism
Endocytosis
Mechanism of absorption
Molecule moved into cytoplasm from extracellular space by being enveloped by membrane invagination
Molecule moved into cytoplasm from extracellular space by being enveloped by membrane invagination
Exocytosis
Mechanism of absorption- goes with endocytosis
Molecule moved out of cytoplasm by being packaged in vesicle and the vesicle contents being released after vesicle-plasma membrane fusion
Molecule moved out of cytoplasm by being packaged in vesicle and the vesicle contents being released after vesicle-plasma membrane fusion
Diffusion
Mechanism of absorption
molecules cross membrane in both directions, into and out of cells
molecules cross membrane in both directions, into and out of cells
Ionization
Charged molecule
One Chamber. Solution is Acidic. What drug is ionized?
Weak base drug mostly ionized
Weak acid drug not ionized
Weak acid drug not ionized
One Chamber. Solution is Basic. What drug is ionized?
Weak acid drug is ionized
Weak base drug not ionized
Weak base drug not ionized
Ion Trapping
Weak acid drug accumulates in more basic compartment
Weak base drug accumulates in more acidic compartment
Weak base drug accumulates in more acidic compartment
Factors which prevent uniform distribution
Time
Ion Trapping
Preferential drug accumulation
Barriers to uniform distribution
Ion Trapping
Preferential drug accumulation
Barriers to uniform distribution
Metabolism
to remove active form of drug from the body
Non synthetic or phase 1 of a reaction
Oxidation, Reduction, and Hydrolysis
Oxidation
Addition of atom of oxygen, hydroxylation
Reduction
Addition of hydrogen atom
Replacement of hydroxyl (-OH) by hydrogen atom
Replacement of hydroxyl (-OH) by hydrogen atom
Hydrolysis
Enzyme catalyzed cleavage of molecule with water being added to the drug molecule to split active molecule into two inactive parts
Synthetic or phase II of a reaction
Conjugation
Conjugation
adds chemical from body to the drug molecule to form a new compound
Drug metabolism following first order kinetics
So much enzyme, that the enzyme is never the rate limiting factor
Changes in amount of enzyme may not affect rate of drug metabolism
Changes in amount of enzyme may not affect rate of drug metabolism
Drug metabolism following zero order kinetics
amount of enzyme limited so that enzyme amount is rate limiting factor
Changes in amount of enzyme will affect rate of drug metabolism
Changes in amount of enzyme will affect rate of drug metabolism
Routes for excretion of drugs
Urine, Feces, Respiratory gases, milk, saliva, tears, sweat and hair
Elimination equation
E = Cp * CV
Elimination equals plasma concentration times clearance volume
Elimination equals plasma concentration times clearance volume
Time response of drug actions
The sum of ADME determine the profile of plasma concentration of the drug over time after administration
K_a
rate of absorption
K_e
rate of elimination
Therapeutic Threshold Concentration
minimal plasma drug concentration to produce desired therapeutic response
Toxic Threshold Concentration
Minimal plasma drug concentration to produce undesired or toxic effect
Therapeutic range
Range of plasma concentration in which a drug produces a therapeutic effect without producing undesired side effects or toxic effects
Bioavailability
measure of the total amount of administered drug that reaches the desired site of action
Multiple Drug effects
a drug does not have a single effect because
a drug interacts with a single type of receptor located on different cell types
a single type of receptor may be coupled to multiple response mechanisms
a drug interacts with multiple types of receptors
a drug interacts with a single type of receptor located on different cell types
a single type of receptor may be coupled to multiple response mechanisms
a drug interacts with multiple types of receptors
Direct drug actions
if a drug has effect on organ A, and if that effect is mediated by receptors for drug A in organ
Indirect drug actions
if drug A has direct effect on organ A and the body responds by altering activity in organ B
Association
Binding of molecule to a receptor
Dissociation
Unbinding of molecule to a receptor
Affinity
the ease with which a molecule can bind to a receptor and the tenacity with which the bond is maintained
High Affinity
occupation of receptors is high with low drug concentration
Low affinity
High occupation requires high drug concentration
equation for affinity
1/K_d (dissociation constant)
Modulation
raises binding rate due to changing receptor to look more appealing
agonist
drug that binds to a receptor and activates it, and induces a response from the tissue/celss on which the receptors are located
Antagonist
drug that binds to a receptor and does not induce response
Pharmacological efficacy
ability of molecules of a particular type to bind and activate a population of receptors and induce a maximal response from the tissue/cells on which the receptors are located
Agonist Potency
measure designed to compare the effect of two or more drugs acting as antagonists through a single set of receptors at a given site
EC50
concentration of drug required to produce 50% of maximal response
Antagonist Potency
Measure designed to compare the effect of two or more drugs acting as antagonists through a single set of receptors at a given site
IC50
concentration of drug required to reduce the effect of full agonist by 50%
ED50
does at which drug has desired therapeutic effect in 50% of people
TD50
dose at which drug as toxic effect in 50% of people
LD50
Dose at which drug has lethal effect in 50% of people
Therapeutic index
a measure of drug safety
Ratio LD50/ED50
higher numerical value, safer the drug
Ratio LD50/ED50
higher numerical value, safer the drug
Standard Safety Margin
a relatively more useful measure of drug safety which relates difference in drug dose to cause a toxic effect in 1% of population and the drug dose required to produce desired therapeutic effect in 99% of population
TD1/ED99
TD1/ED99
Muscarinic ACh
actions mimicked by muscarine
actions blocked by atropine
actions not mimicked by nicotine
receptor coupled to effector mechanism by G-protein
actions blocked by atropine
actions not mimicked by nicotine
receptor coupled to effector mechanism by G-protein
Cholinergic Receptors
M1 - CNS
M2 - Heart
M3 - Glands and Smooth muscle
M2 - Heart
M3 - Glands and Smooth muscle
ACh Actions
Eye - Miosis, cyclospasm
Glands - Increase secretion
Heart - decrease HR, decrease conduction rate, decrease contractility
GI tract - increase motility with relaxation of sphincters
Urinary Bladder - Bladder wall contraction and relaxation of sphincter
Bronchioles - Constrict
Blood Vessels - Vasodilation
CNS - Multiple
Glands - Increase secretion
Heart - decrease HR, decrease conduction rate, decrease contractility
GI tract - increase motility with relaxation of sphincters
Urinary Bladder - Bladder wall contraction and relaxation of sphincter
Bronchioles - Constrict
Blood Vessels - Vasodilation
CNS - Multiple
Nicotinic ACh
ACh mimicked by nicotine
ACh not blocked by atropine
ACh not mimicked by muscarine
agonists induce desensitization
receptor integral part of effector mechanism
ACh not blocked by atropine
ACh not mimicked by muscarine
agonists induce desensitization
receptor integral part of effector mechanism
Nicotinic ACh actions
Skeletal Muscle - N_M - Membrane depolarization with increase AP frequency and contraction
Autonomic Ganglia - N_N - membrane depolarization with increase AP frequency
CNS - N_N - Membrane depolarization with increase AP frequency
Autonomic Ganglia - N_N - membrane depolarization with increase AP frequency
CNS - N_N - Membrane depolarization with increase AP frequency
ACh
activates N and M cholinergic receptors
Charged molecule so not absorbed across mucosa or skin
rapidly metabolized by ChEases in plasma
not used systemically (does not reach sites of action)
ONLY used in eye surgeries through direct application
Charged molecule so not absorbed across mucosa or skin
rapidly metabolized by ChEases in plasma
not used systemically (does not reach sites of action)
ONLY used in eye surgeries through direct application
Choline Esters
Bethanechol
Succinylcholine
Succinylcholine
Bethanechol
Charged Choline Ester - enters CNS and crosses GI tract SLOWLY
Slower degradation than ACh - insensitivity or resistant to AChEase and CHEases, longer actio than ACh
Muscarinic Receptor Selective
Slower degradation than ACh - insensitivity or resistant to AChEase and CHEases, longer actio than ACh
Muscarinic Receptor Selective
Uses of Bethanechol
Postoperative GI atony
Paralytic ileus
Postoperative UB atony
Postpartum UB atony
Paralytic ileus
Postoperative UB atony
Postpartum UB atony
Cautions of Bethanechol
System administration
DO NOT USE if GI or UT obstructed
DO NOT USE if GI or UT obstructed
Succinylcholine
Two AChs together
Charged Choline Ester - enters CNS and GI tract very slowly
Slower Degradation than ACh - resistant to ChEases, longer action than ACH
Nicotinic N_M receptor selective
Charged Choline Ester - enters CNS and GI tract very slowly
Slower Degradation than ACh - resistant to ChEases, longer action than ACH
Nicotinic N_M receptor selective
uses of Succinylcholine
Muscle relaxant - by desensitizing the N receptors
Cautions of Succinylcholine
Paralysis of diaphragm
Paralysis without anesthetic effect
Paralysis without analgesic effect (still feel pain)
Paralysis without anesthetic effect
Paralysis without analgesic effect (still feel pain)
Non Choline Ester, Synthetic Cholinomimetics
Varenicline
Pilocarpine
Pilocarpine
Varenicline
Uncharged molecule - crosses GI tract and into CNS
Non Choline Ester - insensitive to ChEases
Nicotinic N_N receptor selective, partial agonist
Non Choline Ester - insensitive to ChEases
Nicotinic N_N receptor selective, partial agonist
Uses of Varenicline
Nicotine addiction
Pilocarpine
uncharged molecule - crosses GI tract and into CNS
Non choline ester - insensitive to ChEase
Muscarinic receptor specific
Non choline ester - insensitive to ChEase
Muscarinic receptor specific
Uses of Pilocarpine
Glaucoma
Cautions of Pilocarpine
Systemic administrations
CNS effects
CNS effects
Non choline ester, non-synthetic cholinomimetics
Nicotine
Nicotine
Crosses GI tract, lung air-blood interace, into CNS
Non choline ester - not ChEase substrate
Nicotinic receptor specific - N_N more than N_M
Non choline ester - not ChEase substrate
Nicotinic receptor specific - N_N more than N_M
uses of Nicotine
Treatment of nicotine addiction
Insecticide
Insecticide
Symptoms of OD muscarinic receptor stimulation
GI cramps, diarrhea
Urinary incontinence
Vasodilation
Hypotension
sweating and salvation
bronchoconstriction and secretion
burred vision
parkinson's disease like symptoms
Urinary incontinence
Vasodilation
Hypotension
sweating and salvation
bronchoconstriction and secretion
burred vision
parkinson's disease like symptoms
Symptoms of OD nicotnic receptor stimulation
CNS effects - various effects
Autonomic ganglia - variable effects
NMJ - muscle weakness
Autonomic ganglia - variable effects
NMJ - muscle weakness
Treatment of muscarinic OD
Use of antimuscarinic - atropine
use of epinephrine if bradycardia and brochoconstriction are escessive
administer fluids and electrolytes
use of epinephrine if bradycardia and brochoconstriction are escessive
administer fluids and electrolytes
Treatment of Nicotinic OD
no drug based treatment
requires time without agonist
requires time without agonist
Reversible, non substrate for ChEase cholinesterase inhibitor
Edrophonium
Edrophonium
Non substrate for ChEase
Ionized - must be injected intravenously and low CNS effects
short acting
Ionized - must be injected intravenously and low CNS effects
short acting
Uses of Edrophonium
Diagnosis of Myasthenia gravis (muscle weakness disease)
Reversible, substrate for ChEase cholinesterase inhibitor
Physostigimine
Pyridostigmine
Tacrine
Donepezil
Neostigmine
Pyridostigmine
Tacrine
Donepezil
Neostigmine
Physostigmine & Pyridostigmine
Non ionized
absorbed thru GI tract
crosses into CNS
medium duration of action
absorbed thru GI tract
crosses into CNS
medium duration of action
uses of Physostigmine & Pyridostigmine
GI atony - M
UB atony - M
Glaucome - M
Atropine poisoning - M
Reversal of M antagonist (OD) - M
reversal of N_M antagonists - N
Treatment of Myasthenia gravis - N
UB atony - M
Glaucome - M
Atropine poisoning - M
Reversal of M antagonist (OD) - M
reversal of N_M antagonists - N
Treatment of Myasthenia gravis - N
Tacrine & Donepezil
Non ionized
absorbed through GI tract
cross into CNS
Medium duration of action
absorbed through GI tract
cross into CNS
Medium duration of action
Uses of Tacrine & Donepezil
Alzheimer's disease (makes symptoms less intense)
Neostigmine
ionized
slow oral absorption
slow CNS access
Medium duration of action
slow oral absorption
slow CNS access
Medium duration of action
uses of Neostigmine
GI atony - M
UB atony - M
Glaucome - M
Atropine poisoning - M
Reversal of M antagonist (OD) - M
reversal of N_M antagonists - N
Treatment of Myasthenia gravis - N
BUT
Does not enter CNS
Not well absorbed orally
UB atony - M
Glaucome - M
Atropine poisoning - M
Reversal of M antagonist (OD) - M
reversal of N_M antagonists - N
Treatment of Myasthenia gravis - N
BUT
Does not enter CNS
Not well absorbed orally
Irreversible, substrate for ChEase cholinesterase inhibitor
Organophosphates
- Echothiophate
- Malathion
- Parathion
- Echothiophate
- Malathion
- Parathion
uses of Organophosphates
Glaucoma
Insecticides
Nerve Gases
Insecticides
Nerve Gases
Side effects of ChEase Inhibitors
Equivalent to M and N agonist OD - muscle weakness and fatigue
Parasympathetic activation
Parasympathetic activation
Treatment for side effects of ChEase Inhibitors
Atropine for muscarinic receptor based effects
artificial ventilation resulting from N receptor desensitization in diaphragm
Pralidoxime
artificial ventilation resulting from N receptor desensitization in diaphragm
Pralidoxime
Atropine
M Antagonist
absorbed across mucosal membranes
Enters CNS
absorbed across mucosal membranes
Enters CNS
Actions of Atropine
Heart - increase HR, increase myocardial contractility
Eye - Mydriasis, cycloplegia, increase intraocular pressure
GI tract - decrease secretions, decrease motility, sphincters contracted
UB - Decrease bladder wall contractility, sphincter constrictions
Bronchioles - Decrease muscle tone, dilation of airways
Salivary - decrease secretion
CNS - no effect at therapeutic doses
Eye - Mydriasis, cycloplegia, increase intraocular pressure
GI tract - decrease secretions, decrease motility, sphincters contracted
UB - Decrease bladder wall contractility, sphincter constrictions
Bronchioles - Decrease muscle tone, dilation of airways
Salivary - decrease secretion
CNS - no effect at therapeutic doses
Cautions of Atropine
systemic use
Uses of Cyclopentolate & Tropicamide
Ophthalmology - retinal exam
uses of Ipratropium & Tiotropium
Treatment of Asthma
Uses of Glycopyrrolate & Atropine
Preanesthetic agent
Uses of Trihexyphenidyl, Benzytropine, & Biperidine
Treatment of Parkinson's Disease
Uses of Flavoxate, Toleridine, & Darifenacin
Treatment of UB spasm and urinary incontinence
Symptoms of Muscarinic Antagonist OD
Dry mouth
hot, dry skin
blurred vision, photophobia
increase intraocular pressure
Constipation
urine retension
Tachycardia
Delirium
hot, dry skin
blurred vision, photophobia
increase intraocular pressure
Constipation
urine retension
Tachycardia
Delirium
Treatment of Muscarinic Antagonist OD
M agonists
antiChEase - Physotigmine and Neostigmine
antiChEase - Physotigmine and Neostigmine
NMJ nicotinic competitive blockers
Gallamine
Atracurium
Tubocurarine (Curare)
Antagonists - Long Duration
Atracurium
Tubocurarine (Curare)
Antagonists - Long Duration
Autonomic Ganglia nicotinic competitive blocker
Trimethaphan
NMJ nicotinic non competitive blocker
Succinylcholine
Agonist - Short Duration
Agonist - Short Duration
Uses of NMJ blockers
Surgery
Orthopedic procedures
Ventilator Control
Tracheal intubation
muscular convulsions
affect site of highest innervation first
Orthopedic procedures
Ventilator Control
Tracheal intubation
muscular convulsions
affect site of highest innervation first
Use of AG blockers
Difficult to use
Effect dependent on PNS/SNS tone
Effects on cardiovascular system - Heart - decrease PS input to heart
- decrease sympathetic input to heart
- net effect is dependent on situation
Blood vessels - decrease S input to arterioles - vasodilation
Effect dependent on PNS/SNS tone
Effects on cardiovascular system - Heart - decrease PS input to heart
- decrease sympathetic input to heart
- net effect is dependent on situation
Blood vessels - decrease S input to arterioles - vasodilation
Types of adrenoreceptors
A1 - postsynaptic
A2 - presynaptic
B1 - postsynaptic
B2 - postsynaptic
A2 - presynaptic
B1 - postsynaptic
B2 - postsynaptic
Fast/strong effects of adrenoreceptor
Heart, eye, lungs, blood vessels
Slow/Medium effects of adrenoreceptor
GI tract, Bladder
Very Slow/Weak effects of adrenoreceptor
Blood Glucose (pancreatic hormones)
Blood Volume (RAS)
Blood Volume (RAS)
Blood pressure effects of B1
Increase HR and SV
Increase CO
Increase water reabsorption, increase blood volume, increase cardiac filling, increase CO
Vasoconstriction, increase TPR
Increase CO
Increase water reabsorption, increase blood volume, increase cardiac filling, increase CO
Vasoconstriction, increase TPR
Blood Pressure effects of B2
Vasodilation (heart, skeletal muscle)
Decrease TPR
Decrease TPR
Blood pressure effects of A1
Vasoconstriction
increase TPR
Venoconstriction
increase cardiac filling
increase CO
increase TPR
Venoconstriction
increase cardiac filling
increase CO
A1 activation
Vasoconstriction
Increase TPR and Increase BP
Mydriasis
Bladder sphincter constriction
Bladder wall relaxation - urine retention
decrease inestinal motility
increase intestinal sphincter constriction - feces retention
Uterine contraction in pregnant female
Decrease rennin secretion from kidney
Increase TPR and Increase BP
Mydriasis
Bladder sphincter constriction
Bladder wall relaxation - urine retention
decrease inestinal motility
increase intestinal sphincter constriction - feces retention
Uterine contraction in pregnant female
Decrease rennin secretion from kidney
A2 activation
Reduction of NE release
B1 activation
Increase HR
Increase heart contractility (SV)
increase conduction rate - increase CO and BP
increase increase rennin secretion from kidney
Increase heart contractility (SV)
increase conduction rate - increase CO and BP
increase increase rennin secretion from kidney
B2 activation
Vasodilation in skeletal muscle
Vasodilation of coronary arteriole - decrease TPR and BP
Bronchial Dilation
Increase Lipolysis
Increase glycogenolysis
Increase Glucagon Secretion - causing hyperglycemia
Increase Insulin secretion - causing hypoglycemia
Uterine relaxation in pregnant female
Vasodilation of coronary arteriole - decrease TPR and BP
Bronchial Dilation
Increase Lipolysis
Increase glycogenolysis
Increase Glucagon Secretion - causing hyperglycemia
Increase Insulin secretion - causing hypoglycemia
Uterine relaxation in pregnant female
Catecholamines
E
NE
Dopamine
Isoproterenol
Dobutamine
NE
Dopamine
Isoproterenol
Dobutamine
Non Catecholamines
Phenylephrine
Methoxamine
Terbutaline
Albuterol
Clonidine
Methoxamine
Terbutaline
Albuterol
Clonidine
Affinity of E
A1
A2
B1
B2
A2
B1
B2
Affinity of NE
A1
A2
B1
A2
B1
Affinity of Dopamine
A1
B1
B1
Affinity of Isoproterenol
B1
B2
B2
Affinity of Dobutamine
B1
Affinity of Phenylephrine
A1
Affinity of Methoxamine
A1
Affinity of Terbutaline
B2
Affinity of Albuterol
B2
Affinity of Clonidine
A2
Catecholamine agonist
Transmitters and synthetic agents
Short half-life
non oral
Short half-life
non oral
non catecholamines agonist
plant derived and synthetic agents
long half life
oral
long half life
oral
Cardiovascular effects of E
Increase CO, increase BP
Increase HR, contractility, and conduction velocity
Decrease TPR, decrease BP
constriction of skin and mesentery, dilation of heart and skeletal muscle
Increase systolic BP, decrease diastolic BP, no change in mean BP
Increase HR, contractility, and conduction velocity
Decrease TPR, decrease BP
constriction of skin and mesentery, dilation of heart and skeletal muscle
Increase systolic BP, decrease diastolic BP, no change in mean BP
Non cardiovascular effects of E
A1 - mydriasis, relaxation of GI tract and UB, contraction of GI and UB sphincters, decrease rennin secretion from kidney
B1- Increase increase rennin secretion from kidney
B2- Bronchodilation and decreased bronchosecretion, Hyperglycemia, increase lipolysis, decrease intestinal and bladder motility
B1- Increase increase rennin secretion from kidney
B2- Bronchodilation and decreased bronchosecretion, Hyperglycemia, increase lipolysis, decrease intestinal and bladder motility
Cardiovascular effects of NE
Increase CO, increase BP
B1- Increase HR, increase contractility, increase conduction velocity
Increase TPR
A1- vasoconstriction of skin and mesentery, increase systolic BP, increase diastolic BP, increase mean BP
B1- Increase HR, increase contractility, increase conduction velocity
Increase TPR
A1- vasoconstriction of skin and mesentery, increase systolic BP, increase diastolic BP, increase mean BP
Non cardiovascular effects of NE
A1- Mydriasis, relaxation of GI tract and UB, constriction of GI and UB sphincters, decrease renin secretion from kidney
B1- increase increase rennin secretion from kidney
B1- increase increase rennin secretion from kidney
Cardiovascular effects of Isoproterenol
Increase CO, increase BP
B1- increase HR, increase contractility, increase conduction velocity
Decrease TPR and decrease BP
B2- vasodilation of heart and skeletal muscle
increase systolic BP, decrease decrease diastolic BP
decrease mean BP
B1- increase HR, increase contractility, increase conduction velocity
Decrease TPR and decrease BP
B2- vasodilation of heart and skeletal muscle
increase systolic BP, decrease decrease diastolic BP
decrease mean BP
Non cardiovascular effects of Isoproterenol
B2- Bronchodilation and decrease bronchosecretion, increase glucose availability to skeletal muscle, decrease intestinal and bladder motility
B1- increase increase rennin secretion from kidney
B1- increase increase rennin secretion from kidney
Cardiovascular effects of Dopamine
increase CO, increase BP
B1- increase HR, increase contractility
Increase TPR, increase BP
A1- vasoconstriction
increase systolic BP, increase diastolic BP, increase mean BP
B1- increase HR, increase contractility
Increase TPR, increase BP
A1- vasoconstriction
increase systolic BP, increase diastolic BP, increase mean BP
non cardiovascular effects of Dopamine
B1- increase increase rennin secretion from kidney
A1- decrease rennin secretion from kidney
A1- decrease rennin secretion from kidney
Cardiovascular effects of Dobutamine
short but potent effect
B1- increase contractility, small effect on HR
A1- increase TPR and increase BP
B1- increase contractility, small effect on HR
A1- increase TPR and increase BP
non cardiovascular effects of Dobutamine
B1- increase increase renal rennin secretion
Cardiovascular effects of Phenylephrine & Methoxamine
Increase TPR, increase BP
A1- vasoconstriction of skin and mesentery, increase BP
reflex bradycardia and decrease CO
A1- vasoconstriction of skin and mesentery, increase BP
reflex bradycardia and decrease CO
non cardiovascular effects of Phenylephrine & Methoxamine
A1- mydriasis, relaxation of GI tract and UB, contraction of GI and UB sphincters
Effects of Terbutaline & Albuterol
B2- Bronchodilation, Uterine relaxation in pregnant female
Effects of Clonidine
A2- Effects in CNS, decrease SNS output, causing decrease BP
Cardiac (A1) Therapeutic Actions
Paroxysmal atrial tachycardia (PAT)
- vasoconstriction causes increase TPR causes reflex bradycardia
Methoxamine & Phenylephrine
- vasoconstriction causes increase TPR causes reflex bradycardia
Methoxamine & Phenylephrine
Cardiac (B1) Therapeutic Actions
Cardiogenic shock
decrease BP due to decrease CO
Dopamine and Dobutamine
Anaphylactic Shock
Decrease BP due to vasodilation
E & Isoproterenol
decrease BP due to decrease CO
Dopamine and Dobutamine
Anaphylactic Shock
Decrease BP due to vasodilation
E & Isoproterenol
Vasoconstriction (A1) Therapeutic Actions
Local Actions
Decongestants - Phenylephrine
Hemostat - E
Local Anesthetics - E
Systemic Actions, Cardiac Arrest, Acute/chronic hypotension, anaphylactic shock - E, NE, and Phenylephrine
Decongestants - Phenylephrine
Hemostat - E
Local Anesthetics - E
Systemic Actions, Cardiac Arrest, Acute/chronic hypotension, anaphylactic shock - E, NE, and Phenylephrine
Bronchodilation (B2) Therapeutic Actions
Allergic Reactions
Asthma - E, Ephedrine, Albuterol, Terbutaline
Asthma - E, Ephedrine, Albuterol, Terbutaline
Mydriasis (B2) Therapeutic Actions
Retinal Exam - Phenylephrine, E
CNS (A1, B1, B2) Therapeutic Actions
Appetite suppression
Management of Narcolepsy
Management of ADD
Phenylpropanolamine & Methylphenidate
Management of Narcolepsy
Management of ADD
Phenylpropanolamine & Methylphenidate
Uterus (B2) Therapeutic Actions
Premature Labor, causes uterine relaxation, causes some vasodilation and reflex tachycardia
Albuterol & Terbutaline
Albuterol & Terbutaline
Side Effects of Sympathomimetics
Hypertension
Arrhythmias
Vasoconstriction related ischemic damage in brain; stroke
Vasoconstricion related ischemic muscle damage in heart; myocardial infarction
Restlessness
Anxiety
Arrhythmias
Vasoconstriction related ischemic damage in brain; stroke
Vasoconstricion related ischemic muscle damage in heart; myocardial infarction
Restlessness
Anxiety
A receptor Antagonists
Phentolamine
Prazosin
Prazosin
Phenotolamine
A1 Block causing artiole dilation, decreases TPR, decrease BP, causing reflex tachycardia
A2 block produces tachycardia, inducing hypotension, postural hypotension
A2 block produces tachycardia, inducing hypotension, postural hypotension
Uses of Phenotolamine
Pheochromocytoma
Essential Hypertension
Essential Hypertension
Prazosin
A1 selective
similar to phenotolamine
except increase HR through increase NE release
similar to phenotolamine
except increase HR through increase NE release
Uses of Prazosin
Essential hypertension
Benign prostate hyperplasia
Pheochromocytoma
Benign prostate hyperplasia
Pheochromocytoma
Side effect of Prazosin
Reflex tachycardia
B receptor antagonists
Propranolol
Metaprolol, atenolol, pindolol
Labetolol, carvedilol
Metaprolol, atenolol, pindolol
Labetolol, carvedilol
Propranolol
B1 and B2 adrenoreceptor mediated effects - first antagonist for sympathetic effects in controlling cardiac activity
Cardiodepressant
asodilation
Decrease rennin secretion
Hyperglycemia
Block effect of E to release insulin
Cardiodepressant
asodilation
Decrease rennin secretion
Hyperglycemia
Block effect of E to release insulin
uses of Propranolol
Antiarrhythmic
Antianginal
Antihypertensive
Antianginal
Antihypertensive
Side effects of Propranolol
Agina - block of effect of E to dilate coronary vessels
Asthma-like symptoms - block NE induces bronchodilation
Hyperglycemia - block E induce insulin release
Asthma-like symptoms - block NE induces bronchodilation
Hyperglycemia - block E induce insulin release
Metaprolol, Atenolol, & Pindolol
B1 selective
cardiovascular selective - decrease cardiac work and O2 demand, decrease rennin secretion
Unlike propranolol, no hyperglycemia or bronchiole constriction
cardiovascular selective - decrease cardiac work and O2 demand, decrease rennin secretion
Unlike propranolol, no hyperglycemia or bronchiole constriction
Uses of Metaprolol, Atenolol, & Pindolol
Hypertension
Tachyarrhythmias
Angina Pectoris
Tachyarrhythmias
Angina Pectoris
Labetolol, Carvedilol
A1, B1, and B2
Equivalent to prazosin plus propranolol in therapeutic effect and some but not all side effects
Equivalent to prazosin plus propranolol in therapeutic effect and some but not all side effects
Uses of Labetolol, Carvedilol
Antihypertensive
About this deck
By: Tom Centofanti
Created: 2012-02-18
Size: 173 flashcards
Views: 27
Created: 2012-02-18
Size: 173 flashcards
Views: 27
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