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Year 2 Pharmacology > Autonomic pharmacology III > Flashcards

Autonomic pharmacology III Flashcards

1
Q

what is the mechanism of atropine?

A

competes with Ach at M receptors (does not discriminate between M1, M2, M3)

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2
Q

what are the pharmacological effects of atropine?

A
  1. decreased secretions
  2. mydrisasis and cycloplegia
  3. hyperthermia
  4. tachycardia
  5. sedation
  6. urinary retention and constipation
  7. behavioral excitation and hallucination
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3
Q

what are the clinical uses for atropine?

A
  1. antispasmotic
  2. antisecretory
  3. management of AchE inhibitor overdose
  4. antidiarrheal
  5. opthamology
  6. prevent vagal reaction in some procedures
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4
Q

what are the properties of ipratropium?

A
  1. nonselective muscarinic antagonis
  2. mainly acts on M3 in bronchial SMCs and glands when inhaled
  3. no CNS absorption
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5
Q

what are the pharmacological effects of ipratropium in the lungs?

A
  1. decreases bronchoconstriction

2. decreases bronchial secretions

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6
Q

what are the clinical uses of ipratropium?

A
  1. COPD

2. asthma

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7
Q

what are the properties of benztropine?

A
  1. CNS absorption
  2. acts on muscarinic receptors in the brain
  3. PNS effector sites
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8
Q

what are the pharmacological effects of benztropine?

A
  1. reestablishment of dopaminergic-cholinergic balance in patients with Parkinson’s Disease
  2. decreased GI/GU secretions, decreased motility
  3. increased HR
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9
Q

what are the clinical uses for benztropine?

A

Parkinson’s Disease

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10
Q

what are the effects of the ganglion blocking agents?

A
  1. reduce predominant autonomic tone

2. prevent baroreceptor reflex changes in HR

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11
Q

what determines whether or not a neuromuscular blocking drug is depolarizing or non-depolarizing?

A

whether they are a real blocker of the channel or actually an agonist (activator) of the channel

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12
Q

what is the mechanism for neuromuscular blocking drugs?

A

compete for receptor and interfere with transmission at the neuromuscular endplate

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13
Q

what are the clinical uses for neuromuscular blocking drugs?

A
  1. facilitate tracheal intubation

2. optimize surgical conditions while ensuring adequate ventilation

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14
Q

what is the prototypical non-depolarizing neuromuscular blocking drug?

A

tubocurarine

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15
Q

what is the mechanism for non-depolarizing neuromuscular blocking drugs?

A
  1. prevent opening of channel when bound to receptor
  2. small dose - compete with Ach
  3. large dose - enter pores
  4. can also block pre-junctional Na channel to decrease Ach release
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16
Q

what is the prototypical depolarizing neuromuscular blocking drug?

A

succinylcholine

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17
Q

what is the mechanism for depolarizing neuromuscular blocking drugs?

A
  1. phase I - bind to Nm, persistent depolarization, paralysis, augmented by AchE inhibitors
  2. phase II - end plate desensitization
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18
Q

what are the clinical uses for depolarizing neuromuscular blocking drugs?

A
  1. decrease neuromuscular transmission during anesthesia
  2. intubation
  3. ventilation control
  4. anticonvulsive
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19
Q

what are the side effects of depolarizing neuromuscular blocking drugs?

A
  1. hypotension (histamine release)
  2. high dose - ganglion blockade - severe hypotension
  3. hyperkalemia
  4. increased intraocular pressure
  5. increased gastric pressure
  6. muscle pain
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20
Q

what is the rate limiting step of catecholamine synthesis?

A

tyrosine hydroxylase

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21
Q

which step of catecholamine synthesis occurs only in the medulla?

A

NE to EPI via phenylethanolamine-N-methyltransferase

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22
Q

what is the function of metryrosine?

A

tyrosine hydroxylase inhibitor

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23
Q

what is the function of reserpine?

A

inhibitor of VMAT

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24
Q

what is the effect of reserpine on BP?

A

decrease (decreases secretion of NE)

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25
Q

what is the function of bretylium?

A

VAMP inhibitor - prevention of exocytosis

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26
Q

what are the three fates of catecholamines following exocytosis?

A
  1. diffusion - metabolized by catechol-O-methyltransferase
  2. autoreceptor - decreased release
  3. reuptake via NET - repackaged and metabolized by MAO
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27
Q

what is the function of MAO inhibitors?

A

increases NE

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28
Q

what are the factors that determine adrenoceptor responses?

A
  1. receptor specificity
  2. receptor density
  3. NET
  4. receptor regulation
29
Q

what is the mechanism of a1 activation?

A
  1. GPCR - Gq associates with phospholipase C
  2. increase in IP3 and activation of PKC
  3. increase in calcium concentration
  4. increase in vasoconstriction, smooth muscle
30
Q

what is the primary receptor in the vasculature?

A

a1

31
Q

B1 and B2 receptors activate what kind of G protein subunit?

A

Gs

32
Q

a2 receptors activate what kind of G protein subunit?

A

Gi

33
Q

what is the end result of B1 and B2 receptor activation?

A

increase in cAMP

34
Q

what is the end result of a2 receptor activation?

A

decrease in cAMP

35
Q

what is the autoreceptor of the adrenergic system?

A

a2

36
Q

what is the autoreceptor of the cholinergic system?

A

M2

37
Q

which receptors activate Gq protein subunits?

A

H1, a1, V1, M1, M3

38
Q

which receptors activate Gs protein subunits?

A

B1, B2, D1, H2, V2

39
Q

which receptors activate Gi protein subunits?

A

M2, a2, D2

40
Q

what is the result of Gq activation?

A
  1. phospholipase C
  2. PIP2 - IP3 + DAG
  3. increased calcium (IP3)
  4. PKC activation (DAG)
41
Q

what is the result of Gs activation?

A
  1. adenylyl cyclase
  2. conversion of ATP to increased cAMP
  3. increased PKA activity
42
Q

what is the result of Gi activation?

A
  1. inhibition of adenylyl cyclase
  2. decreased cAMP
  3. decreased PKA activity
43
Q

what is the result of Nm and Nn activation?

A
  1. no second messenger

2. activation (opening) of Na/K channels

44
Q

what is the effect of a1 receptor activation on the eye?

A

contraction - mydriasis (radial dilator)

45
Q

what is the effect of a1 receptor activation on arterioles?

A

contraction - increased TPR, diastolic pressure, afterload

46
Q

what is the effect of a1 receptor activation on veins?

A

contraction - increased venous return and preload

47
Q

what is the effect of a1 receptor activation on the bladder and sphincter?

A

contraction - urinary retention

48
Q

what is the effect of a1 receptor activation on the male sex organs?

A

ejaculation

49
Q

what is the effect of a1 receptor activation on the liver?

A

increased glycogenolysis

50
Q

what is the effect of a1 receptor activation on the kidney?

A

decreased renin release

51
Q

what is the effect of a2 receptor activation on the prejunctional nerve terminal?

A

decreased release and NE synthesis

52
Q

what is the effect of a2 receptor activation on platelets?

A

aggregation

53
Q

what is the effect of a2 receptor activation on the pancreas?

A

decreased insulin secretion

54
Q

what is the effect of B1 receptor activation on the SA node?

A

increased HR

55
Q

what is the effect of B1 receptor activation on the AV node?

A

increased conduction velocity (positive dromotropy)

56
Q

what is the effect of B1 receptor activation on atrial and ventricular muscle?

A

increased force of contraction (positive inotropy), conduction velocity, CO, and oxygen consumption

57
Q

what is the effect of B1 receptor activation on the His-Purkinje system?

A

increased automaticity and conduction velocity

58
Q

what is the effect of B1 receptor activation on the kidney?

A

increased renin release

59
Q

what is the effect of B2 receptor activation on the vasculature (all)?

A

vasodilation - decreased TPR, diastolic BP, afterload

60
Q

what is the effect of B2 receptor activation on the uterus?

A

relaxation

61
Q

what is the effect of B2 receptor activation on the bronchioles?

A

dilation

62
Q

what is the effect of B2 receptor activation on skeletal muscles?

A

increased glycogenolysis and contractility

63
Q

what is the effect of B2 receptor activation on the liver?

A

increased glycogenolysis

64
Q

what is the effect of B2 receptor activation on the pancreas?

A

increased insulin secretion

65
Q

what is the effect of D1 receptor activation on renal, mesenteric, and coronary vasculature?

A

vasodilation - in kidney - increased GFR, RBF, and sodium excretion

66
Q

which receptors are typically activated first in response to endogenous catecholamines?

A

beta

67
Q

how are TPR, CO, HR, and SV related to control BP?

A

control of BP is through TPR and CO

CO = HR x SV

68
Q

what are the results of activating or inhibiting a1 receptors in the heart?

A

activation - increased TPR - reflex bradycardia

inhibition - decreased TPR - reflex tachycardia

69
Q

what is the best course of action for a patient with hypertension / ischemic heart disease and considering a1 receptor blockers and/or beta blockers?

A

use B1 receptor antagonist in conjunction with a1 receptor antagonist in order to counteract the reflex tachycardia

Year 2 Pharmacology (70 decks)

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