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Pharmacology 1 > adernergic agonists > Flashcards

adernergic agonists Flashcards

1
Q

where can you find adrenergic receptors?

A

post synaptic in the sympathetic effector organs
or pre synaptic on the neuron

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2
Q

what are the steps of neurotransmission at the adrenergic neurons?

A

The process involves 5 steps: synthesis, storage, release, and receptor binding of norepinephrine, followed by removal

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3
Q

what are the two types of adrenergic receptors and how where they classified

A

alpha (a) and beta (b)

alpha has high affinity for epinephrine>norepinephrine>isoproterenol

beta has high affinity for isoproterenol>epinephrine>norepinephrine

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4
Q

where are alpha1 receptors located and what G protein do they activate

A

found on thr postsynaptic membrane if the effector organs.

they activate Gq protein—–> phospholipase C which increase IP3 and DAG

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5
Q

where are alpha 2 located and what result from their activation?

A

they are located on the sympathetic and parasympathetic presynaptic nerve endings.

they control the release of norepinephrine (inhibitory heteroreceptors) and acetylcholine (inhibitory heteroreceptors).

they work by GI protein—–inhibits adenylyl cyclase—–fall in cAMP levels.

MAO—-when norepinephrine binds to the alpha2 receptors it sends an inhibitory signal to stop the release of norepinephrine (auto inhibition) or acetylcholine (hetero inhibiton)

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6
Q

what are the further subdivisions of alpha receptors

A

alpha1—-a,b,c,d

alpha2—–a/b/c

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7
Q

what are the differences between beta1 and beta2 receptors

A

beta 2 has a higher affinity for epinephrine than norepinephrine while beta1 has the same affinity

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8
Q

what is the G protein for beta receptors

A

Gs proteins——-activates and increases adenylyl cyclase—–more cAMP

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9
Q

remember that

A

Adrenergically innervated organs and tissues tend to have a predominance of one type of receptor.
example: skeletal muscles have both a1 and B2 but B2 predominantes

Other tissues may have one type of receptor exclusively, like the heart which have B1 only

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10
Q

what does the simulation of ALPHA1 leads to

A

vasoconstriction

increased peripheral resistance

increased blood pressure

mydriasis (dilated pupils)

increased closure of internal sphincter of the bladder

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11
Q

what does alpha2 activation leads to

A

inhibition of norepinephrine and acetylcholine and insulin release

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12
Q

what does the activation of beta1 receptors lead to

A

tachycardia

increased lipolysis

increased heart contractility

increased release of renin

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13
Q

what does the activation of beta2 lead to

A

vasodilation

decreased peripheral resistance

bronchodilation

increased glycogenolysis

increased glucagon

relaxed uterine smooth muscle

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14
Q

what are the three mechanisms that explains the desensitization of adrenergic receptors

A

1) sequestration of the receptors so that they are unavailable for interaction with the ligand

2) down-regulation, that is, a disappearance of the receptors either by destruction or by decreased synthesis

3) an inability to couple to G-protein, because the receptor has been phosphorylated on the cytoplasmic side.

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15
Q

what do adrenergic agonists look like and what are the important structural features

A

they look like b-phenylethylamine derivatives

•1) the number and location of OH substitutions on
the benzene ring

•2) the nature of the substituent on the amino
nitrogen.

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16
Q

what are the properties of catecholamines

A

high potency

rapid inactivation

poor penetration into the cns

17
Q

how do non-catecholoamines differ from catecholamines

A

they lack the catechol hydroxyl groups

have a longer half life

cant be inactivated by COMP

can go through theCNS

18
Q

what does the subsititutions on the amine nitrogen determine

A

the Beta selectivity

19
Q

answer the following about Epinephrine

is it a direct or indirect acting

where is it secreted from

compare the actions at low and high dose

what are the effects on the
heart,renin,arterioles,bp,respiratory,blood sugar

what are the therapeutic uses

what are the side effects

A
  1. direct acting

2.from the adrenal medulla

3.at low doses effects beta receptors (vasodilation), at high doses effects the alpha receptors (vasoconstriction)

4.increases the contractility(b1)
increases heart rate (b1)
increases cardiac output and oxygen consumptions
increases renin releases
vasodilators
increases systolic bp while lowers diastolic
powerful bronchodilation
hyperglycemia (increased glucagon and glycogenolysis)
increased lipolysis

5.used for bronchospasm, anaphylactic shock, cardiac arrest,improving local anesthesia at low conc( by causing vasoconstriction at the site of injection thus reducing the systemic absorption and giving a longer effect) , and intraocular surgery to maintain mydriasis

6.cns effects that include anxiety, fear, tension,headache, and tremor.
cardiac arrhythmias
pulmonary edema
have an increased CV actions with patients with hyperthyroidism
Inhalation anesthetics also sensitize
the heart to the effects of epinephrine, which may lead to tachycardia
increases the release of endogenous stores of glucose. In diabetic patients, dosages of insulin may have to be increased

can be given by IV, SC and inhalation

20
Q

answer the following about norepinephrine

is it direct acting?

affinity for what receptor?

what are the actions

what is the drug interaction with atropine

what are the therapeutic uses

how is it given\ what is the duration

what are the side effects

A
  1. yes
  2. alpha
  3. a) vasoconstriction
    b) baroreceptor reflex ( causes a reflex bradycardia effect)
  4. when atropin is given before norepinephrine it causes tachycardia
  5. used for treating shocks like septic shocks
  6. given by IV lasts for 1-2 mins
  7. similar to epinephrine, can cause blanching and sloughing of the skin along the injected vein due to it bring a potent vasoconstrictor, If extravasation occurs, it can cause tissue necrosis
21
Q

answer the following about Isoproterenol

is it direct acting

stimulate which receptors

is it used therapeutically

what are the effects

what are the side effects

A
  1. direct acting synthetic
  2. beta 1 and 2
  3. rarely used due to it nonselectivity
  4. on the heart—-it increases the HR, contractility and output

on the arterioles of skeletal muscle& peripheral
resistance——-dilates the artioles and decreases the resistance

slightly increases the systolic BP and greatly reduces the diastolic BP

it is a potent bronchodialter and may be useful in AV shock

  1. similar to Beta receptor-related side effects of epinephrine
22
Q

answer the following about Dopamine

which receptors are activated by it

what are the effects on high and low doses

it binds to D1 and D2 where are they located and what are the effects

what are the actions

what are the therapeutic uses

what are the side effects

A
  1. alpha and beta
  2. at high doses—-causes vasoconstriction (alpha)
    at low —- causes tachycardia (beta)
    note: its similar to norepinephrine
  3. they are located in the peripheral mesenteric and renal vascular beds, where binding of dopamine produces vasodilation. D2 receptors are also found on presynaptic adrenergic neurons, where their activation interferes with norepinephrine release.
  4. on the CVs—–low dose—-beta1 stimulation
    at high dose—-alpha 1 stim—vasoconatruction

on the renal and visceral—dilation of the renal arterioles—increses bloodflow (by effecting the D receptors)

5.cardiogenic and septic shocks, and hypotension and severe HF

6.has the same effects as sympathetic stimulation such as nausea,hypertension,arrhythmias by its short lived due to the rapid metabolizim by MAO and COMT

23
Q

answer the following about Fenoldopam

agonist of what receptor

what is the clinical use

what is the effect on the arterioles, and mesenteric arteries?

what is the half time after IV

A
  1. D1
  2. used ad a vasodilator to treat sever hypertention
  3. dilates them
  4. 10 mins

extra notes from the book

R-isomer is active
Headache, flushing, dizziness, nausea, vomit and tachycardia( due to vasodilation

24
Q

answer the following about Dobutamine

is it synthetic

agonist to what receptor

what are the major effects

what are the therapeutic uses

what are the adverse effects

A
  1. yes
  2. majorly Beta1 but with minor Beta2 and Alpha1 effects

3.increses heart rate and cardiac output

  1. It is used to increase CO in acute CHF as well as for inotropic support after cardiac surgery.

5.the same as those for epinephrine.
• Avoid in atrial fibrillation because it increses AV conduction
tolerance my be developed

25
Q

answer the following about oxymetazoline

its a direct synthetic agonist to what receptor

what are the efffects

found in what?

what is the MAO

what are the side effects if it entered the systemic circulation

what are the long term side effects

A
  1. alpha 1 and 2
  2. vasoconstrction and decreases congestion

3.found in many over-the-counter nasal spray
decongestants, as well as in ophthalmic drops for the relief of redness of the eyes associated with swimming, colds, and contact lenses.

4.stimulates the the alpha receptors on the blood vessels supplying the nasal mucosa and conjunctiva and causing vassoconstriction

5.nervousness, headaches, and trouble sleeping (cns)

6.Use for greater
than 3 days is not recommended, as rebound congestion and depen-
dence may occur.

26
Q

answer the following about phenylephrine

• It is a direct-acting drug that binds primarily to which α receptors?

• What is its effect on blood vessels and systolic and diastolic BP?

used for the treatment of what

used in nasal and ophthalmic solutions for what

A
  1. alpha 1
  2. vasoconstrictor that raises both systolic and diastolic blood pressures. It has no effect on the heart itself but, rather, induces reflex bradycardia
  3. used to treat hypotension

4.nasal decongestant and for mydriasis

note— has been replaced by pseudoephedrine due to the misuse to make crystal meth (walter white)

27
Q

answer the following about Midodrine

its a prodrug of what

agonist to what receptor

used for what

whats the dose

A
  1. desglymidodrine

2.selective alpha1

  1. acts in the periphery to increase arterial and venous tone. Midodrine is indicated for the treatment of orthostatic hypotension.

4.3 times daily

28
Q

answer the following about Clonidine

agonist to what receptor

used for what disease

what are the other uses

how How does Clonidine decrease sympathetic outflow to the periphery?

A
  1. alpha 2

2.used in managment of ADHD

3.the treatment of hypertension. It can also be used to minimize symptoms of with drawal from opiates, tobacco smoking, and benzodiazepines.

4.Clonidine acts centrally on presynaptic~ receptors to produce inhibition of sympathetic vasomotor centers, decreasing sympathetic outflow to the periphery.

29
Q

answer the following about Albuterol ,metaproterenol& terbutaline

what are the uses

what are the side effects

what happens when they are systemically administered

A
  1. they are SABA bronchodilators (metered dose MDI)
  2. tremor, but patients tend to develop tolerance to this effect. Other side effects include restlessness, apprehension, and anxiety.

3.tachycardia or arrhythmia (due to B1 receptor activation), especially in patients with underlying cardiac disease

30
Q

answer the following about Salmeterol and formoterol

what are the used for

how do they differ from SABA

are they used as monotherapy

A

1.they are LABA

  1. the dose last longer
  2. not recommended as monotherapy but are
    highly efficacious when combined with a
    corticorsteroid.
31
Q

answer the following about Mirabegron
•Is an agonist at which receptor?

•What is its effect on the urinary bladder?

•It is used for patients with what disorder?.

•It may increase BP and should not be used in patients
with uncontrolled HTN.

•Dose higher than (200 mg) are not recommended why?

A
  1. beta 3
  2. relaxes the detrusor smooth muscle and creases the capacity

3.overactive bladder

4.It increases levels of digoxin and inhibits the CYP2D6 isozyme, which may enhance the effects of other medications metabolized by this pathway for example, metoprolol

32
Q

answer the following about amphetamine

is it direct acting?

what are the CNS effects

whats the bp effect

what is the mao

A
  1. no, indirect acting

2.stimulates the brain and abused by drug abusers

  1. increases the bp and heart rate

4.by increasing the release of catecholamines such as dopamine and norepinephrine

33
Q

answer the following about tyramine

is it direct acting

is it clinically useful

where is it found

how is it metabolized

whats the moa

What happens if a patient taking is MAOIs and takes it

A
  1. no, indirect

2.no

  1. in fermented food

4.oxidized by MAO in the GIT

  1. increases the release of catecholamines
  2. it can precipitate serious vasopressor episodes
34
Q

answer the following about Cocaine

is it indirect

what the moa

A
  1. yes
  2. blocks the sodium-chloride dependent norepinphrine transporter thats required for uptake of norephinphrine
    cause norepinephrine accumulates in the synaptic space
    resulting in enhancement of sympathetic activity

• Therefore, small doses of the catecholamines produce greatlymagnified effects in an individual taking cocaine.
• In addition, the duration of action of epinephrine and
norepinephrine is increased

35
Q

answer the following about ephedrine and pseudoephedrine

what does mixed agonist means

why do they have a long duration

can they get into the cns

whats the effects

A

1.They not only enhance release of stored norepinephrine from nerve endings but also directly stimulate both a and p receptors

  1. they are are poor substrates for COMT and MAO. Therefore, these drugs have a long duration of action.
  2. yes ephidrine more the pseudo

4.Ephedrine raises systolic and diastolic blood pressures by vasoconstriction and cardiac stimulation and it is indicated in anesthesia-induced hypotension. Ephedrine produces bronchodilation, but it is less potent and slower acting than epinephrine or isoproterenol.

Oral pseudoephedrine is primarily used to treat nasal and sinus congestion.

thier usage has been limited due to the usage in making crystal meth

Pharmacology 1 (10 decks)

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