ANS Pharmacology Flashcards
Sympathetic Receptors in the eye
A1 –> Mydriasis
B2 –> inc Aq humor production
SNS receptors in the heart
B1, B2 in SA, AV, PK fibers, and ventricles increasing rate, contractility, automaticity and conduction velocity.
Mostly B1, B2 is stim by EPI from blood
SNS receptors in BV of mucosa, skin, and splanchnics
A1, A2- vasoconstriction
SNS receptors in BV or skeletal muscles
A1- constriction
B2- dilation
SNS receptors in Airway
B2- dilation
SNS receptors in GI
A2, B1, B2- relaxation
A1- sphincter contraction- decrease motility
SNS receptors Urinary blader wall
B2- relaxation
SNS receptors Urinary sphincter and prostate
A1- contraction
SNS receptors Kidney JG cells
B1- inc renin secretion
SNS receptors Uterus
A1- contraction
B2- relaxation (these accumulate as approach pregnancy)
SNS receptors Male sex organs
A1- ejaculation
SNS receptors- Liver
B2- inc glucose output
SNS receptors- adipocytes
B1- inc FA synthesis
SNS receptors Skin pilomotor
A1- contraction
SNS receptors sweat glands
M- synpathetic cholonergics, inc secretion
General function of A1 receptors
Contraction/ Constriction of tubules
Locations of A1 receptors
Pupil- Mydriasis
BV- skin, mucosa, splanchnics, skeletal muscle- Constriction
GI- sphincter constriction
Urinary sphincter and prostate- contraction
Uterus- contraction
Male sex organs- ejaculation
Skin- Pilomotor muscle contraction
Location of A2 receptors
Vascular smooth muscle of skin, mucosa and splanchnics- contraction
GI- relaxation
Location of B1 receptors
Heart- inc rate, contractility, automaticity, and conduction velocity
GI- relaxation
JG- inc renin release
Adipocytes- inc FA output
General function of B1 receptors
secretion/ output of heart and GI
General function of B2 receptors
relaxation and dilation, secretions, and the heart
Location of B2 receptors
Eye- inc Aq humor Heart- inc everything BV of skeletal muscle- dilation Airway- dilation Gi- relaxation Bladder wall- relaxation Uterus- relaxation Liver- inc glucose release
Non selective B1. B2 antagonists MOA
reversibly inhibit B receptors
Non selective B antagonists use
Tx glaucoma
Non selective B agonist properties
selectivity
membrane stabilitzaion- has to do with ability to be used as anesthetic
lipid solubitliy
TImolol
Non selective B antagonist
Timolol use
Glaucoma tx by blocking B2 in the eye –> dec in Aq humor production.
used b/c low membrane stabilization properties
Epi affinity
equal affinity for all receptors
Effect of low dose of Epi on HR and BP
A2 –> vasoconstriction
B2 –> vasodilation- this will be dom –> dec TPR –> dec diastolic BP
B2 –> inc HR and contractility –> inc systolic BP
no change in MAP, inc in PP
Effect of high dose of Epi on HR and BP
A1 and A2 –> tons of vasoconstriction –> TPR inc –> diastolic BP inc –> reflexive inc in BP
B1/ B2 –> inc in HR and contractility –> inc in systolic BP
MAP inc reflexive inc is overcome by B stim
Epi Uses
anaphylactic shock - high dose to restore BP and HR and open airway
Asthma- inhale to open airway
Cardiac arrest- high dose to get heart to pump and vasoconstriction sends blood to the right brain
A/V block- stim ventricular automaticity
anesthetics- high local dose for vasoconstriction
NE- affinity
everything EXCEPT B2
NE- effect of low dose on HR and BP
A2 –> vasoconstriction –> inc TPR –> inc diastolic BP –> inc in MAP (b/c diastolic inc also inc systolic) –> reflexive dec in HR
NE effect- high dose
same but more
NE Uses
Cardiogenic and Neurogenic shock- B1 and/ or A depending on dose
anaphylactic shock- early/ warm phase, low dose to after fluid replacement
During Spinal Anesthesia- support BP
anesthesia- alternative to E
Isoprotenolol - affinity
Affinity for B and but not A
Isoprotenolol- low dose effect on BP and HR
B2 –> inc HR, contractility– > inc PP
B2 –> vasodilation –> dec in diastolic BP
Systolic BP = DBP + PP –> SBP dec so does MAP
means reflexive inc in HR
Isoprotenolol- high dose
same but more, systolic P will be more unpredictable
Isoprotenolol uses-
bradyarrhythmias that are refractory to other tx
pharmacologic provocation on tilt table test for unexplained syncopes ie vasocagel syncope
Dopamine affinity
B1>A1»>all others
D low dose
Stims D receptors on renal and GI smooth muscle –> vasodilation
D intermediate dose
stims B1 cardiac receptors
D high dose
stims A1 receptors and this overcomes the effect of D receptors on for renal and GI BF so BP and TPR rise
D uses
Cardiogenic shock- int dose to stim heart
neurogenic shock- high dose for vasoconstriction and stimulate the heart
septic shock- early phase- high dose for vasoconstriction
septic shock- late phase- int to stim heart and improve flow to GI and renal
bradycardia
stim heart when coming out of Sx
Dobutamine- affinity
B1 agonist
Dobutamine- uses
stim heart when coming out os surgery
cardiogenic shock- ventricular muscle contraciton
septic shock- late phase counter low CO
CHF
B2 agonists- all have what in the name
ter
B2 agonists- are
Albuterol Metaproterenol Pirbuterol Salmetrol Terbutaline
B2 agonists- use
tx bronchoconstriction in ashtma, COPD, and exercise induced bronchoconstriction
Terbutaline- uses
prevent labor by stim B2 in the uterus
A1 selective agonists are
Phenylephrine and Midodrine
Phenylephrine- main effect
vasoconstriction
Phenylephrine uses
nasal decongestant- dec size and flow to BV in nose so dec size and mucus production
Mydriatic agent
Hemorrhoids- dec size of BV in hemorrhoids
neurogenic shock- maintain diastolic MAP
Maintain diastolic BP and MAp in theraputic spinral and general anesthesia
SVT
Midodrine- uses
orthostatic hypotention b/c causes venus and arteriolar constriction
Experimental use in urinary incontinence
Indirect Sympathomimetics
Cocaine
Pseudoephedrine
Ephedrine
Cocaine- MOA
Inhibits NE reuptake and has efect on CNS D receptors
Cocaine- use
good aneshtetic
local anesthetic for mucosal membranes and intubation for the trachea b/c of vasconstriction
Pseudoephedrine/ ephedrine MOA
Stimulate NE release w/o AP, may have direct stim effects, reverses NE reuptake pump
Pseudoephedrine/ Ephedrine- Uses
tx nasal congestion and promote sinus drainage and bronchial dilation trough B2 receptors
Timolol MOA
beta blocker
Timolo- use
tx glaucoma b/c has no membrane stabilizing ability
Alpha antagonist- non selective- start with
phen
Non selective alpha antagonists- names
Pehnoxybenzamine
Phentolamine
Selective alpha blockers- all end in
sin
Selective alpha blockers- names
Prazosin Doxazosin Tamsulosin Afluzosin Silodosin
Phentolamine- MOA
short acting reversible inhibitor of A1 and A2
Phentolamine- uses
prevent accidentally induced A agonist dermal tissue necrosis via vasodilation
Oraverse- block soft tissue anesthesia in dentistry
Prazosin, Doxazosin- MOA
prototype A1 agonist
Prazosin, Doxazosin- Uses
relax smooth muscle of bladder neck, urethra to relieve BPH
Raynauds- vasodilation
tx nightmares related to PTSD
Prazosin, Doxazosin AE
orthostatic hypotention with syncope on first dose
systemic fluid retention if not given with diuretetics
reflex tachycardia but not as much as with non selective agents
Famsulosin, silodosin- MOA
selective for A1 subtype A- concentrated in bladder
Famsulosin, silodosin- uses
more specific tx for BPH urine retention and less systemic side effects
Famsulosin, silodosin- AE
high incidence of abnormal ejaculation b/c A1 subtype is right there
Afluzosin- MOA
A1 blocker with uroselectivity so accumulates in prostate, so hits those A1 receptors first
Afluzosin- uses
BPH urine retention
