Receptors Flashcards

1
Q

Nicotinic receptors are located on cell bodies in ganglia of both PANS and SANS and in the adrenal medulla

A

Nn

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2
Q

Nicotinic receptors are located on the skeletal muscle motor end plate innervated by somatic motor nerves

A

Nm

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3
Q

Muscarinic receptors are located on all organs and tissues innervated by postganglionic nerves of the PNS and on thermoregulatory sweat glands innervated by the SNS.

A

M1-M3

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4
Q

Systemically, alpha-1 agonist increase mean BP via vasoconstriction
• Increased BP may elicit a reflex bradycardia
• Cardiac output may be ↓ but also offset by ↑ venous return
• Drugs and uses: nasal decongestant and ophthalmologic uses(Mydriasis without cycloplegia), hypotensive states

A

Phenylephrine

Alpha 1 agonist

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5
Q

α1:↑TPR,↑BP
• Potential reflex bradycardia
• No change in pulse pressure

A

A1 Agonist Phenylephrine

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6
Q

Alpha-2 agonists stimulate prejunctional receptors in the CNS to decrease
sympathetic outflow. Their primary use is for mild to moderate HTN.
• Drugs and uses: (mild to moderate hyper- tension)

A

clonidine and methyldopa

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7
Q
Systemically decrease mean BP via vasodilation (β2) and 
increase HR (β1)
  • β1: ↑HR,↑SV,↑CO, and ↑ pulse pressure
  • β2:↓TPR,↓BP
A

beta-agonists

– Isoproterenol (β1 = β2)
– Dobutamine (β1 > β2): congestive heart failure

Selective β2 agonists: salmeterol, albuterol, terbutaline (asthma); terbutaline(premature labor)

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8
Q

Mixed acting Agonists

(α1, α2, β1)

α1:↑TPR,↑BP
• β1: ↑ HR↑SV↑CO↑ pulse pressure 
• Potential reflex
bradycardia
• No effect on β2
A

Norepinephrine

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9
Q

(α1, α2, β1, β2)

β1:↑HR,↑SV,↑CO,
↑ pulse pressure

β2:↓TPR,↓BP

A

Epinephrine

Low-dose Epinephrine on HR and BP

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10
Q

β1:↑HR,↑SV,↑CO
↑pulse pressure

β2:↓TPR,↓BP
α1:↑TPR,↑BP

A

Epinephrine

Medium Dose on Heart Rate and Blood Pressure

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11
Q

α1:↑TPR,↑BP
Potential reflex
bradycardia

• β1:↑HR,↑SV,↑CO,
↑ pulse pressure
• β2:↓TPR,↓BP

A

Epinephrine

High Dose Epi/ Similar to NE

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12
Q

↓ HR, ↓ SV, ↓ CO

↓ renin release

A

β1 Blockade

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13
Q
May precipitate bronchospasm (in asthmatics) and vasospasm (in
patients with vasospastic disorders)
– ↓aqueous humor production
– Metabolic effects
o Blocks glycogenolysis, gluconeogenesis
o ↑ LDLs, TGs
A

β2 blockade

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14
Q

Activation of M receptors causes contraction of ciliary muscle, which increases flow through the canal of Schlemm

A

Cholinomimetic

ie Pilocarpine

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15
Q

Block actions of NE at ciliary epithelium * aqueous humor formation

A

Beta blockers

ie Timolol

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16
Q

α1-antagonists

A

doxazosin, prazosin, terazosin

17
Q

α2 antagonists

A

mirtazapine

18
Q

Mixed α antagonists:

A

phenoxybenzamine, phentolamine

19
Q

β1 (cardioselective) antagonists

A

acebutolol, atenolol, metoprolol

“A-M”

20
Q

β1, β2 (nonselective)

A

pindolol, propranolol, timolol

“N-Z”

21
Q

α1 and β antagonists

A

carvedilol, labetalol

22
Q

α1 agonists

A

phenylephrine

23
Q

α2 agonists

A

clonidine, methyldopa

24
Q

β agonists:

A

isoproterenol, (β1 = β2), dobutamine (β1 > β2)

25
Q

β2 agonists

A

albuterol, terbutaline, salmeterol

26
Q

Mixed Adrenergic Rc Activators

A

dopamine (D1, β1, α1),
epinephrine (α1, α2, β1, β2),
norepinephrine (α1, α2, β1)

27
Q

Indirect-acting adrenergics

A

amphetamine, cocaine, ephedrine, tyramine

28
Q

Muscarinic blockers

A

atropine, benztropine, ipratropium, scopolamine

29
Q

Ganglionic blockers:

A

hexamethonium, mecamylamine

30
Q

Direct Cholinergic activators

A

bethanechol (M), methacholine (M and N), nicotine (N), pilocarpine (M), cevimeline (M)

31
Q

Reversible AChE inhibitors:

A

reversible—edrophonium, physostigmine, neostigmine, pyridostigmine, donepezil, rivastigmine

32
Q

irreversible AChE inhibitors

A

irreversible—malathion, parathion