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M2 Mechanisms of Disease > Adrenergic Agonists > Flashcards

Adrenergic Agonists Flashcards

1
Q

What diseases are associated w/ adrenergic agonists? Why are they difficult drugs to use?

A
  • blood pressure, adhd, asthma, COPD

- reflex responses to drug

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2
Q

What are Noepi and Epis affinity for the various adrenoreceptors? TRICKY TRICKY

A

NE: alpha1>alpha2>beta 1&raquo_space;»> beta 2
Epi: alpha2>alpha1 and beta 1=beta2

Alpha1: NE > Epi
Alpha 2: NE=Epi
Beta1: NE=Epi
Beta2: Epi>>> NE
Beta3: NE>>> EPi
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3
Q

What is the solubility of Norepi and epi? What does this mean for CNS affects?

A

-epi is slightly more lipid soluble than Norepi but neither cross BBB. when epi is released, there is a pereception of anxiety that is a consequence of CNS but not epi entry into the CNS

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4
Q

What is dopamines affect on sympathetics? At low levels? High levels? other affects?

A
  • vasodilates renal arterioles and preserve renal function through DA receptors located in the arterioles
  • low levels: stimulates natriuresis and diuresis via second messengers, acts as a natriuretic hormone by increasing sodium excretion by diminishing reabsorption in the proximal tubule, also dilates coronary vessels
  • high levels: has inotropics effects mediated by beta 1 receptors. at higher doses, stimulates alpha 1
  • also present in the chain ganglia in small intensely fluorescent (SIF) cells and used for shock treatment secondary to severe blood loss
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5
Q

Why is dopamine used in emergent situations?

A
  • dopamine increases cardiac output while maintaining kidney perfusion (doesn’t cause renal arteriolar constriction like alpha and beta drugs)
  • kidney sparing!
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6
Q

What areas are not protected by the BBB and what receptors are rich there?

A

-hypothalamus and area postrema which are rich in DA receptors and initiates emesis

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7
Q

What are the 9 locations and functions of alpha 1 receptors when stimulated?

A
  1. vascular smooth muscle contraction (arterioles and venules): increased TPR
  2. pupillary dilator contraction: mydriasis (dilation)
  3. heart: mild positive inotropy
  4. bladder trigone and sphincter contraction: urinary retention
  5. ENS sphincter contraction: increased transit time/reduced motility
  6. arrector pili muscle: erects hair
  7. apocrine gland secretion: stress related sweating
  8. penis and seminal glands: ejaculation
  9. adipose tissue: glycogenolysis and gluconeogenesis
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8
Q

How do heteroreceptors and autoreceptors work on alpha 2 receptors? What are the functions of alpha 2?

A
  • autoreceptors function ot reduce future NE release
  • heteroreceptors function to reduce release of Ach and other neurotransmitters.
  • functions: decrease symp outflow, decrease insulin release, decrease lipolysis, increase platelet aggregation
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9
Q

Where does beta 1,2,3 receptors work and what is function?

A

Beta 1

  1. heart: positive inotropy, chronotropy, and dromotropy
  2. juxtaglomerular cells: increased renin release

Beta 2:
1. bronchioles: reduced airway resistance
2. arterioles in muscle: increased vascular flow to striated muscles
3. liver: glycogenolysis
(First aid, increased heart rate, contractility, lipolysis, insulin release, aqueous humor production. decreased uterine tone, ciliary muscle relaxation)

Beta 3:
fat lipolysis

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10
Q

How does magnitude of SANS response affect receptors and neurotrasmitters released?

A
  • lower levels of SANS activation initiated release of NE producing alpha 1 effects similar to beta 1 and much more than beta 2
  • further increases in SANS activation leads to Epi release which brings in full beta 1 and beta 2 stimulation
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11
Q

What is the difference between receptor specificity and preference? What is the specificity of NOepi and Epi

A
  • specificity means there is a 1000 fold more affinity for one receptor versus another
  • Noepi: alpha selective over beta
  • Epi: beta selective over alpha
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12
Q

How does SANS affect blood flow to the brain?

A
  • little to none
  • SANS controls brain through regulating TPR.
  • vascular flow within the brain is regulated locally by CO2 and by release of NO and angiotensin
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13
Q

What is homologous desensitization? Heterologous desnitization?

A
  • homolgous: tolerance of the receptor to which the agonist or natural ligand binds
  • heterologous: effect of an agonist or natural ligand that acts through its receptor to affect the function of another receptor or system (hetero or auto receptors)
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14
Q

What is the prototypical drug of the alpha 1 direct acting receptor agonists? What receptor does it prefer? MOA? Effects? Clinical use? Toxicity? Pharamcokinetic consdieration?

A
  • Phenylephrine (alpha 1 > alpha 2)
  • MOA: competitive agonist
  • Effects: smooth muscle contraction and other alpha 1 effects
  • clinical use: most widely used decongestant, hypotension (vasoconstrictor), priapism to treat ED, to induce mydriasis (don’t use in narrow angle glaucoma!), enters CNS to enhance alertness
  • toxicity: hypertension and seizures
  • pharacokinetic considerations: significant first pass effect because it is a substrate for MAO-A
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15
Q

What is midodrine?

A

prodrug to desglymidodrine used to treat hypotension

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16
Q

What is the baroreceptor reflex? How does adding an alpha 1 agonist affect the reflex

A
  • aortic arch and carotid bodies monitor pulse pressure through stretch receptors and reduce stretch (reduce TPR) leading to reflex increasing in SANS outflow (increase NE release producing vasoconstriction) to compensate. Vagal afferents reflexicvely reduce vagal activation leading to increased HR (reduction in vagal tone, which is the primary mediator of HR).
  • adding an alpha 1 agonst will increase TPR leading reflexively to reduced SANS and icnrease vagal outflow reflexively reducing HR. a new steady state will be reached
17
Q

What is the alpha 2 prototypical drug? other drugs? MOA? effects? clinical use? toxicity? pharmacokinetic considerations?

A
  • clonidine: sympatholytic effects
  • other drugs: methyldopa, guanfacine and guanabenz
  • MOA: direct acting competitive agonist
  • effects: reduces NE release and activated alpha 2 receptors. oral admin leads to mild reduction in SANS outflow from CNS and alpha 2 reducing NE release leading to hypotensive affects. IV will lead to mild vasoconstriction due to direct effects on alpha 2 receptors located post-synaptically.
  • clinical use: ADHD, anxiety effect of opiate withdrawal, antihypertensive by reducing NE release, mild sedation w/ reduction in ventral alertness system
  • toxicity: orthostatic hypotension, dizziness, palpitations, tachycardia. Headaches, depression, loss of appetite, fatigue, nasal congestion.
  • pharmacokinetic considerations: highly orally bioavailable. methyldopa is an aromatic aminod acid decarboxylase inhibitor and reduces syn of Da, NE, and Epi
18
Q

What is isoproterenol? MOA,effects, clinical use, toxicity?

A
  • non specific beta receptor agonist
  • MOA: direct acting, beta 1,2,3 agonist
  • effects: activates all beta receptors directly w/ very little if any alpha actiation
  • clincal: use to be used for asthma but beta 1 reaction was issue w/ asthmatics w/ heart problems
  • toxicity: high dose cause significant initial increase in BP w/ concomitant marked reduction in HR that can be problematic and can produce fatal arrhythmias
19
Q

How does the barorecetor reflex affect isoproterenol administration?

A
  • initial increase in systolic blood pressure
  • increased CO leads to reflex activation to bring down systolic BP
  • beta 2 effects cause vasodilation of large striated muscle vessels reducing TRP and dropping systolic n diastolic pressure
  • this drop leads to increased HR
20
Q

What are the affects of isoproterenol on the following: Sa node, atria, AV node, His-purkinje system, ventricles, kidney, arterioles and veins, tracheal and bronchiolar muscle, gut motility and tone, urinary bladder, skeletal muscle, liver?

A

beta 1
-SA node: increase chronotropy
-atria: increase inotropy and dromotropy
-av node: increased chrontropy and dromotropy
-his-purkinje system: increase dromotropy
-ventricle: increased inotropy and dromotropy
-kidney: renin secretion up
Beta 2
-arterioles and veins: dilation
-tracheal and bronchiolar muscle: relax
-gut motility and tone: decrease
-urinary bladder: detrusor relaxation
-skeletal muscle: increase contractility, glycogenolysis, k uptake
-liver: increase gluconeogensis, glycogenolysis

21
Q

What is dobutamine? Receptor specificity? How is it used? Side effects?

A
  • beta 1 selective agonist (b1> b2, alpha)
  • used to treate acute heart failure (inotropic > chronotropic), and used to induce cardiac stress in stress testing
  • side effects: angina, hypertension, tachycardia, arrhythmias
22
Q

What are the beta 2 selective agonists? MOA? effects? clinical use? toxicity? pharmacokinetic considerations?

A
  • albuterol, terbutaline, salmeterol (b2>b1)
  • MOA: R isomer is active ingrediate. S is inactive and produces inflammation leading to levalbuterenol
  • effects: albuterol for acute asthma, salmeterol for long term asthma or COPD control; terbutaline to reduce premature uterine contractions.
  • toxicity: polymorphisms can lead to albuterol tolerance
  • pharmacokinetics: 10 min to achieve max effect and 3-4 of relief.
23
Q

Salmeterole is combined w/ ___ and formoterol is combined w/ ____

A
  • advair (fluticasone): corticosteoid

- Symbicort

24
Q

____ produces full agonist action at all receptor subtypes (alpha and beta)

A

epi

25
Q

What is amphetamine? MOA? substrate? effects? clinical use? toxicity? pharmacokinetic?

A
  • amphetamine: structural similar to catechol nuclear (NE,DA,EPIC) and mimicks its action.
  • MOA: indirect agonist, competitive reuptake inhibitor
  • substrate: NET=DAT>SERT. As a substarte, it carries the transporter into the cytosolic side of the membrane where the “mobile pool” ligands can bind and be transported back out of the cell into the synaptic pool. Ca independent release.
  • blocks monamino oxidase
  • effects: increase the synaptic pool of NE=DA>5HT, increasing HR and TPR. crosses BBB (increased alertness, increase motor activity, increased body temperature, dependence liabiliity, and reduced appetite) (First aid: used in narcolepsy, obesity)
  • clinical: improve attention in face of fatigue, improved reaction time in face of fatigue, increased motor activity, increased anxiety, reduced appetite, increased body temperature, increased respiratory rate
  • toxicity: schedule 2 drug, stimulant vasulitis (prolonged vasoconstriction w/ eventual ischemia and necrosis esp in gut), hyperthermia, and metabolic acidosis.
  • pharmacokinetics: 14 hrs half life. excreted unchanged
26
Q

What is the ceiling effect?

A

cause of death in amphetamine due to increasing dosing. mobile pool amphetamine starts to compete w/ neurotransmitter for access to the reuptake pump reducing ca independent release.

27
Q

What is methamphetamine?

A

meth is biotransformed in the liver to amphetamine with more 5ht effects

28
Q

What is ephedrine?

A

indirect general agonist, releases stored catecholamines. used as a nasal decongestion, urinary incontinency, hypotension medications

29
Q

What is cocaine? MOA? effects? clinical? toxicity? pharmacokinetics? other cocaine drugs?

A
  • drug represent a group of non-related chemical structures that inhibit NET and DAt without acting as a ligand for the transport protein. since these chemical are not ligands, they are not transported into the mobile pool and therefore do not facilitate Ca independent release of neurotransmitter. they vary in their specificty for NEt
  • MOA: binds allosteric regulatory site on reuptake pumps (NET=DAT»SERT). alters the tertiary structure of the pump.
  • effects: similar to amphetamine except that the drug potentiates the actions of neurotransmitters that are released. can’t induce release of itself
  • clincal: nasal surgeries for cain properities.
  • toxicity: NE vasoconstrictive properties limit its bioavailability. continued use can lead to perforated septa.

M2 Mechanisms of Disease (13 decks)

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