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93 Cards in this Set
- Front
- Back
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what are the catecholamines |
1. epinephrine
2. NE 3. isoproterenol |
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isoproterenol is what
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catecholamine
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what are the alpha agonists
what are the alpha 2 agonists |
Alpha
1. Phenyephrine 2. Pseuduephedrine Alpha 2 Agonists 1. Cloidine 2. apraclonidine |
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what are the b1 agonists
what are hte b2 agonists |
Beta 1
1. Dobutamine Beta 2 Albuterol Terbutaline Ritrodine |
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what are the dopamine agonists
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dopamine
fenodolpam D R are in brain adn kidney D1: dilates renal BV D2: inhibits NT release |
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what are 5 'other" adrenergic agonists
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1. Ephedrine
2. amphetamine 3. methylphenidate 4. cocaine 5. tyramine |
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what branch of the ANS is turned on in response to blood loss
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SNS
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NE stim what R
Epi stim what R |
alpha
B1, NO b2 stim released form adrenal medulla in stress and acts on B1/B2 and alpha |
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with SNS stim what happens, include R type responsible
1. BV in skin, kidney, mucous membranes 2. BV in sk mm 3. sweat glands, salivary glands 4. Bronchioles 5. heart 6. metabolism 7. insulin, renin 8. CNS 9. NT release |
1. BV in skin, kidney, mucous membranes constrict (a1)
2. BV in sk mm dilate (b2) 3. sweat glands, salivary glands a, M 4. Bronchioles dilate (B2) 5. heart increased HR,icnrease force of contraction (B1,B2) 6. metabolism: increased glycogenolysis and gluconeogenesis (b2) lipolysis (b3) 7. insulin, renin modulation (b1, a1, a2) *prime for NE, no B2 here 8. CNS stimulaiton 9. NT release is inhibited (a2 presynaptic R) |
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what receptor modulates...
1. BV constriction in skin 2. BV constriction in Kidney 3. BV constriction in mucosa 4. BV dilation in kidney 4. BV dilation in SK mm 5. bronchiole dilation 6. glycogenolysis 7. lipolysis 8. inhibit NT release 9. Salivation 10. sweat lots 11 HR increase, force of contraction |
1. BV constriction in skin- a1
2. BV constriction in Kidney- a1 3. BV constriction in mucosa- a1 4. D1 4. BV dilation in SK mm- b2 5. bronchiole dilation- b2 6. glycogenolysis- b2 7. lipolysis- b3 8. inhibit NT release- a2, D2 9. Salivation, a1 10. sweat M 11. b1 and some b2 |
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what are 3 ways adrenergic agonists can act INDIRECTLY
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1. Inhibit metabolism of NE/Dopamine, MAO inhibitor
2. inhibit reuptake of dopamine (cocaine) 3. Increase release/displacement of NE from nerve endings (tyramine, dopamine) **Drugs that affect INDIRECTLY loose effect when there is denervation or depletion of NE stores. the drug reserpine will also do this **indirect acting drugs are increased to normal |
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what does denervation do to adrenergic agonists
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inhibits indirect acting agonists (depleting NE stores with reserpine will do the same thing)
**direct acting drugs are increased to normal Recall indirect acting drugs act via 1. decrease reputake of NE/dopamine 2. inhibit breakdown of NE and dopamine (MAOI) 3. increase release/displacement of NE from nerve terminal |
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depleting NE stores with the drug _____ will cause ____ which is simliar to _____
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reserpine
inhibition of drugs that act INDIRECTLY (displace NE or increase its release, inhibit catabolism/reuptake of NE & dopamine) denervation will also inhibit indirectly acting drugs **direct acting drugs are increased or normal |
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what does denervation do to direct acting drugs
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nothing, slight enhanced effects
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if a drug has a mixture of direct and indirect effects what happens with denervation
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blunted effect
**we know denervation will inhibit indirectly acting drugs |
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a receptors are more responsive to what NT
what about b1 b2 and b3 |
ALPHA
Epi > NE >>> Isoproterenol BETA b1: Isoproterenol > Epi = NE b2: isoproterenol > Epi >> NE b3: isoproterenol = NE > Epi |
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what NT loves a receptors the most
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Epi, then NE then last is isoproterenol
*isoproterenol has a higher affinity for b receptors (b1/2/3) |
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a1 R are excitatory/inhibitory
a2 R are excitatory/inhibitory |
a1: excitatory, PLC --> IP3 + DAG --> PKC
a2 inhibitory, decrease cAMP, presynaptic and decrease NT release |
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what R will act presynaptically to inhibit NT release via PLC --> IP3 + DAG
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a2
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what are some things a1 R do
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BV: constriction, increase TPR
Mucosa: constriction, decreased nasal congestion EYE: mydriasis, contract radial mm Heart: Prostate: contraction Lung: none GI: relax SM GU: inhibit peeing, contract sphincters Hair: contract erector pili metabolism: small increase in glycogenolysis/gluconeogenesis (mainly b2) |
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what R is responsible
1. dilate renal BV 1. relax respiratory epithelium 2. contract some vascular SM 2. relax BV in Sk mm 3. constrict BV everywhere else 4. relax GI/GU including uterus 5. increase force/rate of heart contraction 6. increase renin secretion 6. inhibit NT release 7. decongestion via constrication nasal mucosa 8. dilate eye, contract radial iris mm 9. increase AV conduction/automaticity 10 contract prostate 11. goose bumps 12. glycogenolysis, gluconeogenesis 13. promote K uptake in sk mm 14. decrease insulin secretion |
1. D1
1. b2 2. a2 2. b2 3. a1 4. b2 5. b1 6. b1 6. a2, D2 7. a1 8. a1 9. b1 10. a1 11. a1 12. b2 13. b2 14 a2 |
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what R increases renin release
what inhibits insulin release what stim lipolysis |
b1
a2 b3 *a2 also inhibits lipolysis |
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a1 receptors are selectively stim by...
adn cause... |
Phenyephrine
1. vasoconstriction, increase TPR 2. nasal vasoconstriction, decongestant 3. mydriasis 4. contract prostate 5. contract GU sphincters 6. Relax GI SM 7. erector pili to make hair stand up 8. glycogenolysis, gluconeogenesis (kinda, the real player is b2) |
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a2 Receptors are selectively stim by..
and cause... (4) |
Clonidine
1 presynaptic nerve terminals, inhibits NT release 2. contract some vascular SM 3. decrease insulin secretion 4. platelet aggregation |
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what r when stim will do this?
aggregation of platelets decrease insulin contract SOME vascular SM and... |
a2, presynaptic to decrease NT release
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whats the NT affinity for the b1/b2/b3 receptors
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isoproterenol likes them all most (contrast to a where is was least)
b1: iso > epi=NE b2: iso>Epi >>NE b3: iso = NE >epi |
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NE wont bind to...
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b2 R
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whats hte 2 messenger for ALL b receptors
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increase cAMP
Gs: B Gi: a2. M2 Gq: M1 M3 a1 |
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what is the selective B1 agonist, what will it stim
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doputamine
1. increase HR/force of contraction, increase AV conduction 2. increase renin |
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whats the b2 selective agonist, what will it stim
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Albuterol
1. relax bronchioles 2. glycogenolysis/gluconeogenesis 3. relax BV in sk mm, increase K uptake in Sk mm 4. increase HR/force of contraction but not as much as b1 |
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what do b3 R do
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stim lipolysis
*lipolysis is inhibited by a2 (no surprise here, we know a2 are inhibitory, also inhibit renin and insulin) |
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where are D receptors?
what do they do |
Brain
Kidney: D1: stim cAMP, dilate renal BV D2: inhibit cAMP, inhibits NT release |
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what is the backbone for catacholamines
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phenylethylamine
catecholamines like: dopamine NE Epi isoproterenol metabolized by: MAO and COMT |
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what are catecholamines metabolized by?
oral abs |
MAO
COMT NO oral abs, given IV (think epi pen) |
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if a adrenergic stim is not technically a catecholamine but some synthetic molecule what can be said about it
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not degraded by COMT so...
increased bioavailability after oral ingestion (catecholamiens MUST be IV) longer duration of action, less potent |
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the effects of adrenergic agonists depend on what
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1. distribution of A/B R in the tissue
2. drugs selectivity for A/B R 3. reflex responses |
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alpha r stimulation cases what in the heart
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recall a1 vasoconstrict BV including nasal mucosa
recall a2 inhibit NT release and contract some vascular SM EFFECT: increase arterial resistance in small vessels to increase BP, baroreceptors do reflex bradycardia **in artherosclerosis the baroreceptor response is impared and we get HUGE increase in BP |
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what R was stim
increase BP with reflex brady cardia |
alpha agonist
*alpha recetors vasoconstrict small arteroiles and cause increase TPR, there is then reflex bradycardia via baroreflex **imparied baroreceptor reflex in ppl with srtherosclerosis,. their BP skyrockets |
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whats the effect of a agonist in ppl with artherosclerosis
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typical to have increase BP due to increased TPR via vasoconstriction, with reflex bradycardia via baroreceptors
**in artherosclerosis the baroreceptor is defetive and we have huge increase in BP |
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what do alpha agonists do in the eye
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mydriasis, contract radial mm
NO AFFECT in accomidation decrease production of and increase removal of aqueous humor so used to tx glaucoma |
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stim of what will cause mydriases w/o affecting accomidation? what is the effect on intraocular pressure
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alpha agonist
no effect on accomadation (ciliary mm) just the radial iris mm **also increases removal of aqueous humor so used to tx glaucoma |
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what does a R stim do in the lungs
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nasal vasoconstriction for decongestion
a R are in the mucous membranes of the upper airway, the B2 receptor does bronchodilation |
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what effect does a 1 stim have in the GI
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constrict the sphincters
ejaculation contract the prostate |
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what are hte metabolic effects of A 1 stimulaiton
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metabolic effects are seen better with B R stim
*a1 stim glycogenolysis/gluconeogenesis *a2 inhibit lipolysis in fat cells * a2 inhibits insulin/renin *overall minor effects |
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what is the cardiovascular effect of B stimulation
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1. b1 increase HR (increased conduction velocity) and force of contraction (b2 also but less)
-conduction is increased so refractory period decreases. automaticity increases 2. increased O2 repuirements 3. increased coronary blood flow 4. b2 relax BV in SK mm (decreased diastolic pressure) |
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what might increase the O2 demand of the heart and increase coronary artery blood flow while decreasing diastolic BP . what other effects are seen
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beta receptor stimulation
b1 increase HR and contractility, this increases O2 demand and coronary blood flow. AV conducatnace is increased so automaticity increases b2 will dilate sk mm and decrease diastolic pressure |
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what bappens in the eye with a beta agonist
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b2 increase aquesous humor production in the eye, increased intraoculat pressure
A beta BLOCKER will be used to tx glaucoma |
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how is intraocular pressure changed with adrenergic stimulation
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b2 increase aquesous humor production and increase intraocular pressure
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what type of b drug will help with asthma
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b2 when stim will dilate the bronchioles so b2 can be used to tx asthma
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whats the b effect int he GU/GI
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b2 relax uterine contractions and so can prevent premature labor
b2 will relax hte bladder only slightly |
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what are the b effects on metabolism
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BETA 1
-renin release BETA 2 -glycogenolysis -uptake of K -insulin BETA 3 -lipolysis |
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what happens to BP and HR
a stimulation, phenylephrine |
a1- vasoconstriction
reflex brady cardia Increase BP, decrease HR |
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what happens to BP and HR
b stim, isoproterenol |
b1- increase HR, contraction
b2- vasodilation in sk mm Increase HR, slight diastolic decrease |
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what does NE do to HR and BP
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stim a and b1
a1- vasoconstriction b1- increased HR, contractility increased BP with slight reflex bradycardia even with b1 stimulation |
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how powerful is baroreceptor reflex bradycardia, use a adrenergic stim to illustrate
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STRONG
when we give NE it stim b1 and a1 mainly and the result is increaased BP via a1 and DECREASED HR due to reflex bradycardia even through there is direct stim of b1 now with phenylephrine there is just a1 stim and we get increased BP and total reflex bradycardia. the effects of b1 stim with NE will give a higher hr with NE than phenylephrine |
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what will cause selective a and b1 stimulation
what will cause stim of a and b1/2 |
NE
increased BP with some reflex brasycardia even with b1 stim EPI stim all, |
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what does Epi do
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stim EVERYTHING, but we know R have dif affinities so there is a dose related response
alpha1/2 like Epi most beta 1/2 like epi seccond b3 like epi last Low dose: -b1 HR and conduction increase -a1 constriction -b2 sk mm dilation increased BP, then decreased diastolic bc of b2. Overall increased pulse pressure, increased HR High Dose: stronder pressor effect |
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lets talk about NE
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stim a and b1, not b2
increrased BP with little effect on pulse pressure baroreceptor reflex keeps HR low (atropine will inhibit this and HR increases) causes such vasoconstriciton that necrosis can occur at site of injection |
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what might haappen if you inject your finger with NE, how to reverse
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necrosis from vasoconstrication
give alpha antagonist |
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what happens when atripone is give before NE
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atropine (muscarinic antagonist) will block vagal response and baroreceptor effect isnt seen
**NE will then increase BP (expected) AND HR (new and exciting) |
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how is the effect of Epi determined
what happens with a low dose given slowely what happens with a high dose given fast |
on dose, Epi stim it ALL!!!
Low and slow - b1 increase HR -a vasoconstrict -b2 dilate sk mm (decrease diastolic, this is unique to epi be NE wont stim b2) *bc diastolic decreases Pulse pressure increases but mean pressure stays the same...SO this means there is no baroreceptor adn HR stays high with b1 stim *CO and O2 requirement are increased *sk mm get more blood but skin and kidney get less HIGH FAST DOSE -LOTS of a1 consrticiton -increased blood sugar (b2 glycogenolysis, a2 inhibition of insulin) - renin increases b1 - increased FFA b3 lipolysis |
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what happens with a slow does of EPI
HR and BP |
b1- increase HR and conduction, CO and O2 consumption increase
a- constrict skin, kidney, mucosa. increased BP b2- dilate sk mm BV, decrease diastolic. increased pulse pressure --> all of this together means that mean pressure is the same and we have NO baroreceptor mediated bradycardia nad HR is increased HR and BP increase *decreased Blood to skin adn kidney |
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an increase in HR and BP is seen when
an increase in BP with only a slight increase in HR is seen when |
low dose of epi is given
hard and fast epi **the difference is with a low dose you can have the b2 stim that decreases diastolic by letting blood get to mm, this keeps MAP the same and NO baroreceptor bradycardia. When epi is given really fast we get an overwhelming pressor effect and the baroreceptor bradycardia occurs |
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what happens with a hard and fast injection of epi
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hard adn fast pressor effects right away so we get reflex bradycardia
BP increases, HR not as increased |
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what is Epi used for
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1. anaphylactic shock- restore BP, decrease BP
2. Cardiac Arrest/Complete heart block 3. given with other drugs to cause Vasoconstriction so that the drug wont diffuse 4. glaucoma- decrease intraocular pressure (alpha decrease intraocular pressure, b2 will increase intraocular pressue) not used much for this 5. bronchodilation for asthma |
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what does Epi do to
1. effect on other drugs 2. shock 3. heart 4. glaucoma 5. asthma |
1. is vasoconstricts so that the intended drug wont diffuse out
2. tx for anaphylactic shock, restore BP, decrease bronchospasm, decreasd edema, restore heart 3. in complete block or cardiac arrest it can stim the heart 4. a stim will decrease intraocular pressure. (increase removal and decrease produciton of humor) 5. bronchodilate via b2 (NE will NEVER work for this) |
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what are some of the toxicities assocated with EPI
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1. tremor
2. headache (no CNS effects) 3. increased BP, tachycardia (DUH) 4. angina- increased O2 demands 5. vasopressor effect is HUGE, esp at high dose 6. at low dose the sk mm dilate BV. the sk mm do have both a and b but b are more sensitive to epi |
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who should NEVER have a huge old dose of epi
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ppl on b blockers!
there will be unopposed a effects and HUGE amts of a constriction |
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what are some toxicities associated with HIGH Epi doses
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a receptos dominate and we get massive constrictions
can cause LARGE increase in BP cerebral hemmorage vent arrhythemias contraindicated in ppl on b blockers bc then the a effects are unopposed!!! |
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whats ephedrine
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one of those "other" adrenergic stimulants
_its the junk in diet pills, its like EPI but has a more modest effect, higher bioabilibility and longer duration. - mixed acting on b and a R so in cases of denervation it still has some effects - CNS stimulant, increased HR and BP, bronchodilation - deaths due to hypertension prevent it in diet pills |
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whats the drug that acts like EPI but i sa bit more moderate, we know it has longer bio effects but can cause severe HTN and even hemmorage. how can we get this crud out of our bodies
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ephedrine
*renal excretion is increased by acidifying the urine |
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what does phenylepherine do
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alpha 1 agonist
*vasoconstriction with increased BP and reflex bradycardia (obviously dont use in ppl with HTN) *used to increase BP in hypotensive emergency *can cause vasoconstriction in the nose so works as a decongestant, but we get a rebound effect *dilate eye w/o affecting accomadation, no a receptors on ciliary mm |
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what are the 2 alpha agonists
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phenylepherine a1 selective (increased BP, refelx bradycardia, used to tx hypotension, decongestant, mydriasis. careful in ppl with HTN)
pseudoepherine |
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what does pseudoephedrine do
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a agonist, simliar to phenylephrine
**used as a decongestant, sudafed, *careful in ppt with HTN it can increase BP *meth precurson, restrictions in sales |
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what is teh widely used decongestant that is an adrenergic agonist, how does it work
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pseudoepherine
**its an a agonist that causes vasoconstriction in teh nose and leads to DECONGESTION! cool |
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whats xylometazoline and oxymetaxoline
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a agonists are arent bold!
topical agents to decrease congestion used in the eye **dont use in ppl with narrow angle glaucoma, hypertension |
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whats clonadine
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a2 agonist that works in the brain
* decrease CNS NE release so decreased SNS to periphery (presynaptic a2) -decreased BP, tx HTN - reduce cravings in addicts -decrease hot flashes -preanesthetic, to sedate you and dry secretions Transdermal Patch Side Effects: dry mouth, sedation, sexual dysfx, dont get it hot bc youll get a big release |
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whats the transdermal a2 agonist that prevents cravings and hot flashes. what are some of its more intuitive effects
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clonidine
*a2 agonist in the CNS so will decrease NE release to the periphery. effectively decreasing SNS tone - decreased BP, tx HTN. if you stop drug abruptly you can get HTN also causes dry mouth, sexual dysfunction, sedation |
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so i know clonidine is an a2 agonist, whats the other
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apraclonidine
used in teh eye to tx glaucoma a receptrs decrease production of aquesous humor (the b2 will increase it) |
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whats isoproterenol
agonist of what R causes what in BP and HR used for |
b agonist (b1 and b2)
-b1 increase HR and contraction -b2 dilate sk MM--> decrease in BP with reflex tachycardia initial increase in BP (b1) and HR followed by decrease in BP (b2 dilation) and increased HR (reflex tachy) used for - cardiac arrest, heart block -asthma, but replaced by b2 selective like albuterol can lead to tachycardia, palpitations, arrhythemias |
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whats dobutamine
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b1 agonist
*increase HR, used in cardiac stress tests when ppl cant be on treadmil *really short half life 2 min |
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whats albuterol
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selective b2 agonist
help ppl with asthma by acting on b2 in the lungs to bronchodilate terbulatine is an oral b2 for asthma |
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wahts terbulatine
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b2 agonist that is sometimes given orally for asthma
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whats ritodine
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selective b 2 agonist that is used to relax the uterus
*prevent premature birth |
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whats dopamine
what does it do at normal, and high doses side effects |
its a D R agonist
recall D1- dilate renal BV D2- inhibit NT release sooo.. DOpamine will increase blood Flow to kidney to increase GFR and Na excretion HIGH DOSE can stim b1 also to increase HR and contractility, given in cardiac shock to increase heart rate w/o causing constriction will affect a1 receptors and have effects simliar to epi nausea, vomit |
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why are large doses of dopamine, though ineffective, used to treat cardiagenic shock
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increased dose of dopamine will act on B receptors to increase HR and CO w/o vasoconstriction side effects
high doses can also increase release of NE and stim a1 so the effects are smiliar to epi |
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whats henoldopam
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D1 agonist
increase blood flow to kidney, increased GFR increased Na excretion dilate vascular beds to decrease HTN |
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whats amphetamine
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indirect acting drug that increases NE release from vesicles
1. CNS stimulant: increased alterness, decreased appetite, decreased need for sleep, euphoria, psychosis 2. tachycardia 3. HTN 4. contracts bladder sphincter methyphenidate (rifalin) is a type of amphetamine and is used for kids with ADD, causes a paradoxical decrease in hyperactivity |
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how do amphetamine, cocaine, and tyramine work, what does this implicate
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indirect acting stimulants
if there is denervation or depletion of NE by reserpine the effects are diminished. if the drug works on more than 1 receptor there can be blunted affects still denervation enhances the effect of drugs that bind directly |
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s methyogenudate
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ritalin, its a type of amphetamine
*tx kids with ADHD, paradoxical decreasei n hyperactivity |
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what indirect adrenergic agonist increases NE release from vesicles, what does it cause
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amphetamine
CNS effects are great: euphoria, decreased appetite/sleep, increased motor activity, psychosis tachycardia HTN methyphenidate, ritalin is in this category |
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what does cocaine do
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blocks reuptake of dopamine/NE, more dopamine/NE is available.
really addictive, causes short lasting amphetamine effects cause HTN, stroke, MI/arrhythemia psychosis |
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whats tyramine
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indirect actine sympathomimetics
increase relase of catecholamine from nerve terminal. replaces NE with octopamine (a false NT) causes tachyphylasis (really fast sensitization) tyramine is normal in food digestion but is hydrolyzed by MAO, when ppl are on MAO inhibots tyramine can be a prble and cause HTN crisis |
