Vasoconstrictors Flashcards
where does the SNS originate?
Thoracolumbar T1-L2
what converts dopamine to norepinephrine ?
dopamine beta hyroxylase
norepinephrine is metabolized by ___ and ___
MAO and COMT (monamine oxidase and catecholo-methyltranseraese
what are the 4 adrenergic receptors
alpha 1&2, beta 1&2
alpha 1 Is located in the ___
periphery
alpha 2 is located ___
centrally (negative feedback like precedex)
beta-1 is located in the ___
heart
beta-2 is located in the ___
smooth muscle (some beta 2 can be on the heart)
T/F Even though Beta1 and Beta2 share g-protein type mechanism and the end result is increasing cyclic AMP, the end product is different
TRUE . beta1: contraction. beta2: vasodilation
T/F Alpha-1 leads to bronchodilation
FALSE- bronchoconstriction - no good!
Alpha 1 inhibits or promotes insulin secretion?
inhibits
Alpha 1 causes smooth muscle ____
contraction
Alpha 1 receptor is PRE or POST synaptic?
post
Alpha1 causes peripheral vaso____
constriction
what is Alpha 1’s relationship to glucose
stimulates glycogenolysis and gluconeogenesis - by inhibiting insulin, there is more glucose in the blood to use, more ATP, more energy
Alpha 1 effect on pupils?
mydriasis. pupil dilation - open up the eyes more so you can see surroundings
Alpha 1 causes GI contraction or relaxation ?
relaxation
Alpha 2 is pre or post synaptic?
PREsynaptic in the PNS, POSTsynaptic in the CNS
Alpha 2 MOA in PNS
post-synaptic - decreases entry of CA into the cell, limits the release of nor-epi
alpha 2 MOA in the CNS
sedation, decreased sympathetic outflow, decreased BP, platelet aggregation
BETA1 receptor is ____synaptic
POST
what does Beta1 do to HR, conduction velocity, and myocardial contractility ?
Increases.
Beta1–more complete and faster heartbeat to get more blood out into the circulation faster
BETA2 is ____synaptic
post
beta 2 stimulation leads to smooth muscle contraction or relaxation?
relaxation
beta 2 leads to peripheral vasoconstriction or vasodilation?
vasodilation.
think: more of a surface area in the periphery for o2 exchange
T/F Beta 2 receptor decreases BP
TRUE
Beta2 causes broncho____
dilation
Beta 2 ___ insulin secretion, but also ____ glycogenolysis and gluconeogenesis
increases.
seems counter intuitive but does both
Beta 2 ____ GI motility
decreases
The PNS has a ____ origin.
craniosacral (III, V VII, X)
PNS - preganglia near _____
organs of innervation
PNS - postganglia secrete _____
Ach
T/F acetylcholine activates both arms of the ANS
TRUE
acetylcholine participates in a ____ ____ action potential
calcium mediated
Cholinergic receptors can be ___ or ____
nicotinic, muscarinic
SNS affects on urinary bladder: smooth muscle ____, sphincter ____
relaxation, contraction
SNS affects on urinary bladder: smooth muscle ____, sphincter ____
contraction, relaxation
SNS cause bronchial smooth muscle ___, while PNS causes bronchial smooth muscle ____
relaxation, contraction
SNS stim causes gallbladder ____, while PNS causes ____
relaxation, contraction
PNS affects on GI tract - motility and sphincter
increases motility, secretion, sphincter relaxation
PNS stim causes ___ of the eye
miosis (constriction)
T/F both SNS stim and PNS stim increase salivary secretions, but PNS has a marked increase
TRUE
SNS stim causes ___ beta cell secretion
decreased - (fight/flight)
T/F PNS stim causes glycogen synthesis
true (rest/digest)
T/F SNS stim of beta causes constriction of coronary arterioles
FALSE.
stim of ALPHA causes constriction of coronary arterioles
stim of BETA causes relaxation of coronary arterioles
same idea with skeletal muscle arterioles.
T/F PNS stim causes relaxation of : coronary arterioles, skin and mucous arterioles, and skeletal muscle arterioles , and pulmonary arterioles.
TRUE
T/F SNS stim causes constriction of all the arterioles, except when beta is stimulated.
TRUE
Down regulation is a reduction in the ____ of receptors
number.
Reduces the number, but not their response.
when you’re using an agonist for a very long time, overstimulating the receptors, eventually your body realizes something is wrong so it will begin to break down and remove your receptors.
T/F Up regulation results in tachyphylaxis
FALSE
down regulation results in tachyphylaxis.
Chronic depletion of catecholamines or use of antagonists increases the number of receptors, but not their sensitivity… otherwise known as?
up regulation
T/F Up-regulation may account for withdrawal syndrome with beta blockers
TRUE
what is receptor uncoupling?
inability of the receptor to bind G protein (alters the function of the receptor)
occurs rapidly (minutes to hours)
movement of receptors from the cell surface to intracellular compartments is
sequestration
occurs more slowly (couple of days)
the movement of receptors from the cell surface to intracellular compartments, but then destroyed = _____
downregulation
prolonged process (weeks to months)
what results in uncontrolled release of catecholamines due to an adrenal gland tumor?
pheochromocytoma
catecholamines can be either ___ or ____
neurotransmitters and hormones
T/F All catecholamines are sympathomimetics but not all sympathomimetics are catecholamines
TRUE
what are compounds that resemble catecholamines except that hydroxyl groups are not present in both the 3 and 4 positions of the benzene ring
sympathomimetics
all sympathomimetics are derived from ____
B phenylethylamine (ring)
T/F Presence of hydroxyl groups on the 3 and 4 position of the benzene ring of the B phenylethylamine creates a catachol
TRUE
sympathomimetics ___ skeletal muscle
dilate
T/F sympathomimetics increase vulnerability to dysrhythmias
TRUE
sympathomimetics have what effect hepatically?
glycogenolysis (glucose going up bc glycogen is broken down into glucose)
sympathomimetics cause CNS ____
stimulation
the only time a vasopressor should be used is when….
the patient’s BP must be increased immediately to avoid pressure-dependent reductions in organ perfusion with subsequent ischemia
T/F sympathomimetics are used as additive to LA to slow systemic absorption of LA from site of infiltration or injection
TRUE
The ____ of alpha and beta receptors influences the response evoked by the sympathomimetic
anatomical distribution.
(the primary action at the organ has to do with the amount of that type of receptor that is there, and what the affinity for that receptor is.
T/F norepinephrine has minimal effects on airway resistance because adrenergic receptors in bronchial smooth muscle are mostly beta-2 and thus not stimulated by catecholamine.
TRUE
T/F Epi and isoproterenol are potent bronchodilators as a result of their ability to activate beta2 receptors
TRUE
where is MAO located?
Monoamine oxidase in an enzyme present in liver, kidneys, GI tract that catalyzes oxidative deamination
COMT methylates the _____ of catecholamines
hydroxyl group
If it’s a catecholamine its metabolized by ___, if its non-catecholamine its just ____`
both, MAO
T/F inhibition of the reuptake of catecholamines produces a greater potentiation of effects of epinephrine than does inhibition of either enzyme.
TRUE
how is completeness of the reuptake mechanism and metabolism evidenced?
presence of unchanged catecholamines in the urine
why are PO catecholamines ineffective
because of metabolism of these compounds by enzymes in the GI mucosa and liver before reaching the systemic circulation
what routes can epi be given
sq, IV
what routes can dopamine and norepi be given
IV
T/F patients on MAO inhibitors may manifest reduced responses when treated with synthetic non-catecholamines
FALSE - exaggerated responses
what are the reflexive changes of vasoconstrictors
decreased HR, decreased conduction, occasionally decreased contractility
vasoconstrictors broncho____
dilate
T/F non cardiac effects of vasoconstrictors include glycogenolysis and CNS stimulation
true
risk of end organ damage with a MAP <65 occurs after how long
13-28min
risk of end organ damage with a map <50 occurs after how long
1 min
vasoconstrictors contraindications:
can worsen LV failure, can exacerbate RV failure, can decrease RBF, can mask hypovolemia
what are the 3 natural catecholamines
epi, norepi , dopamine
what receptors does epi stimulate
alpha 2, beta 1, beta 2
what drug is the most potent activator of alpha1?
epi. 2-10x more potent than NE
epi ____ blood sugar
increase
epi ____ secretion of insulin (promotes or inhibits?)
inhibits
epi ___ lipolysis
increases
epi __ glycogenolysis
increases
how does epi decrease renal blood flow?
potent renal vasoconstrictor (alpha-1 effect)
stimulates renin release
what effects do low dose EPI have? (1-2mcg/min)
beta 2 in peripheral vasculature predominates- the net effect is decreased SVR and distribution of blood to skeletal muscle.
map remains essentially the same
what effects do intermediate dose epi have? (4mcg/min)
beta1
increased HR and contractility and increased C.O.
increased automaticity (may lead to dysrrhythmias)
what effects do high doses of epi have (>10mcg/min)
alpha 1
at this point A1 overrides any B1 effects and you can see slight reflect bradycardia, bradyarrthmia.
potent vasoconstrictor including cutaneous, splanchnic and real vascular beds. (no significant effect on cerebral arterioles)
used to maintain myocardial and cerebral perfusion.
reflex brady can occur
racemic epi is a mixture of ___ and ___ that constrict edematous mucousa
levo and dextrorotatory isomers that constrict edematous mucousa
what effect does epi have on coagulation
platelet aggregation
what does epi do to pupils
dilate - mydriasis
norepinephrine is primarily an ___ agonistt
alpha 1
T/F both epi and norepinephrine have the potential to interact with all the receptors, but norepinephrine does not interact with all the receptors. these drugs have different affinities to for the same receptors
TRUE
norepinephrine is primarily an alpha-1 agonist
beta-1 effects are overshadowed by its alpha 1 effects
beta 2 effects are minimal
at higher doses of norepinephrine, what happens to cardiac output?
decrease. because of increased afterload and baroreceptor-mediated reflex bradycardia.
explains refractory hypotension
T/F norepinephrine has greater metabolic effects than epi
false. LESS
they both share the property of creation of glucose and liberation of glucose (glycogenolysis and gluconeogensis). but when you dont have the beta2 effect you might lose some of those metabolic effects (not gone just lesser than)
