adrenergic quiz Flashcards
2 main adrenergic neurotransmitters
epi and NE
Epi is syn and stored in the
adrenal medulla (making it a neurohormone)
Epi has a different response at different levels meaning it is
concentration dependent
Epi at low concentrations
has predominant beta effects more than alpha
Epi at high concentrations
engages beta and alpha receptors at the same degree
in the heart, Epi
increases HR, FOC, SV, CO, BP
in the lungs, Epi
bronchodilation occurs
in the vasculature, Epi
low concentrations = beta = vasodilation (decrease TPR)
high concentrations = alpha engaged = constriction (increase TPR)
is epi appropriate for asthma attack
yes B2 engaged = bronchodilation
epi with an anesthetic
vasoconstriction; anesthetic is kept localized; good for prolonged procedures
NE is synthesized and stored
sympathetic post ganglionic neuron
NE targets which receptors
beta1, alpha1, alpha2
NE at the heart
increases HR, FOC, CO
NE at the lungs
no clinical observation is observed
NE in the vasculature
vasoconstriction (alpha1)
Dopamine is syn and stored in the terminal of the
sympathetic postganglionic neuron
DA targets which receptors at different concentrations meaning it is
D1, beta1, alpha1; concentration dependent
at low concentrations DA
has the highest affinity (lowest kd); leads to vasodilation of gut and renal by lowering TPR; good for maintaining good kidney function
at mild concentrations DA
engages B1 receptors as well as D1; leads to vasodilation, increasing HR and CO
at high concentrations DA
engages alpha1 (B1 and D1 also); it causes vasoconstriction, increasing TPR, CO; it can be effected by vagal response
at the kidney DA
increases RBF and increases GFR (only at low doses due to D1)
at the heart DA
increases HR, FOC, (through B1 engagement at mid to high conc)
at the vasculature
decreases TPR (some due to D1) increases TPR (alpha1 engagement)
therapeutic uses for dopamine
shock, hypotension, poor tissue perfusion, low CO
sympathomimetics
synthetic receptor agonists mimic the actions of catecholamines
alpha 1 receptor agonists
phenylephrine
naphazoline
oxymetazoline
tetrahydrozoline
topical, decongestants, vasoconstrictors in cornea
alpha 2 receptor agonists
clonidine
guanfacine
methyldopa
activate alpha 2 and therefore decrease SNS outflow
decrease HR, TPR, BP
upregulation of peripheral B1 and alpha1
beta 1 agonists
dobutamine
IV only; preserves CO; increases HR and FOC; decompensated heart failure; low CO = risk to vital organs; can only use for 3 days due to downregulation
Beta 2 agonists
albuterol (SABA)
terbutaline
salmeterol (LABA)
good for bronchodilation; good for patients with asthma
isoproterenol
non selective B1 and B2 agonist
beta blockers are used to treat
hypertension, chronic angina, heart failure
in treating hypertension and chronic angina, beta blockers work to
decrease CO, FOC, HR; block the effects of NE on the heart; improve blood flow and decrease oxygen
beta 1 antagonists also effect the RAA system
block the beta 1 receptors on the JG cells of the kidney which are responsible for the activation of the RAA pathway
cardioselective beta blockers are more selective for
B1 than B2
why would these agents be favored over non selective
they specifically block B1 more than B2 good for patients that have COPD or asthma or diabetes
diabetes blocking B2 would lead to decreased insulin secretion and decreases tissue sensitivity to insulin
nonselective B blockers increase the change of developing
type 2 diabetes
ISA
intrinsic sympathomimetic activity; partial agonist
agents with ISA include
pindolol, acebutolol, labetalol
bind to the receptor and have the same ability to turn it on but not to the same ability; could be used to reduce the degree of bradycardia or limit the effect on lipid profile
Labetalol has ISA at beta 2 receptors
will cause B2 stimulation and vasodialate reducing TPR and reducing BP; nonselective; don’t want to mess with B2 still full agonist to open airways is always better
carvedilol
blocks alpha 1, blocks L type CC, anti-oxidant
vasodilation, decreased HR, limited oxidative damaged seen in heart failure
nebivolol
increased NO production in vasculature
causes vasodilation; maybe B3
labetalol
B1 antagonist; B2 ISA; alpha1 blocked
affects glucuronidation pathway; gives vasodilation, happens on JG cells good at lowering BP
nearly all B blockers are eliminated by
the liver 2D6
which B blockers are eliminated by the kidney
nadolol and atenolol and 50% of bisopropol
esmolol
has a half life of 10 minutes; metabolized by gut (plasma) esterases; shorter half life = quicker response; given IV
nadolol has a half life of ___
24 hours; making it the longest for a B blocker
most hepatically cleared have a half life of
4-6 hours
atenolol has a half life of
12 hours
4 diff types of adverse effects associated with B blockers
lipids CNS sexual dysfunction, hypoglycemia
lipid adverse effect
increased LDL, increased VLDL; decreased HDL
wouldn’t use this medication on statin therapy
glaucoma
role of beta receptors on aqueous humor production
thyrotoxicosis
thyroid hormone increases the expression of beta receptors
increase production of thyroid hormone by way of B1
tremor
activation of B2 receptors can cause tremors; trigger for excess symp activity
migraine
beta blockers; mechanism is unknown; effective in preventing migraines
alpha blockers are primarily used in the treatment of
BPH and hypertension (not as good as others)
the least selective of alpha antagonists
phent, PB2 outside vasculature decreases blood to tissues necrosis occurs give an IV of alpha blocker around site where it occurs
the first alpha 1 selective antagonists ___ led to the development of ___ and ___
prazonsin; terozosin and doxazosin
alpha 1 antagonist use in treating BPH
decrease growth and contraction of prostatic tissues
the different types of alpha 1 receptor subtypes include
A, B, D
the most predominant subtype in the prostate is the
alpha 1 a
the most predominant alpha 1 receptor subtype in the vasculature is
B and D
what counseling would you give to someone on an alpha 1 antagonist
get up slowly; take a bedtime; due to orthostatic hypotension (dilates arterioles and effects venous tone)
what is an ADR associated with tamsulosin
floppy iris syndrome
alpha 1 A receptors are located on the dilator muscles of the iris and it can lead to atrophy of the muscle
which neurons use ACh
parasymp, nicotinic, muscarinic, neuromuscular
cholinergic
any system affected by or involving ACh
M3
“secretory” (SLUD)
any muscle
contraction including smooth muscle
circulatory muscles in the eye constrict
M2
“cardiac”
decrease HR
slows SA node
slows down AV node
M1
cholinergic pathways
Alzheimer’s; circuits involved in memory and cognition
neural receptor
muscarinic agonist would lead to what
increased SLUD and decreased HR
muscarinic agonists would treat
tachycardia, dry mouth, constipation, glaucoma
muscarinic antagonists would lead to
decreased SLUD and increased HR
muscarinic antagonists would treat
urinary urgency
eye surgery
IBS (type D)
nicotinic receptors
ligand gated Na+ ion channels
nicotinic receptors are found in (2)
autonomic ganglia
neuromuscular junction
autonomic ganglia
Ng
parasymp or symp
neuromuscular junction
some selective nicotinic
Nm
could paralyze someone with a nicotinic blocker
AChE
where ACh is released, this enzyme is present, highest turnover rate of all enzymes
lack of AChE
lack of breakdown of ACh
increase SLUD
decrease HR
in brain = increase cholinergic activity (treatment of Alz)
ACh antagonist could treat
COPD/asthma
quaternary ammonium compound is (in ACh and choline)
unable to get into the CNS
unable to cross BBB
rotamers
rotational conformers of norepinephrine
play a role in which receptors are activated
beta 1, alpha 1, and alpha 2
can twist to activate all three receptors despite it being 1 molecule
Receptors use __ to define a ligand binding site
side chains of AA
interactions of drugs with ligand binding site (3)
- H bonds - one of the polar groups needs an H to donate to form the H bond
- ionic bond - very strong (not as covalent) can help hold drugs in receptor active site
- van der waals - hydrophobic interactions; lipid or nonpolar areas of a molecule interacting with non polar
affinity (B2 adrenergic agonists)
want a highly potent agent / low dose
activation (B2 adrenergic agonists)
full or partial agonist
lipophilicity (B2 adrenergic agonists)
does play a role in B2 receptor selectivity and for some of the long acting beta 2 agonists (LABA)
