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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
what is the function of bretylium?
VAMP inhibitor - prevention of exocytosis
26
what are the three fates of catecholamines following exocytosis?
1. diffusion - metabolized by catechol-O-methyltransferase 2. autoreceptor - decreased release 3. reuptake via NET - repackaged and metabolized by MAO
27
what is the function of MAO inhibitors?
increases NE
28
what are the factors that determine adrenoceptor responses?
1. receptor specificity 2. receptor density 3. NET 4. receptor regulation
29
what is the mechanism of a1 activation?
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
what is the primary receptor in the vasculature?
a1
31
B1 and B2 receptors activate what kind of G protein subunit?
Gs
32
a2 receptors activate what kind of G protein subunit?
Gi
33
what is the end result of B1 and B2 receptor activation?
increase in cAMP
34
what is the end result of a2 receptor activation?
decrease in cAMP
35
what is the autoreceptor of the adrenergic system?
a2
36
what is the autoreceptor of the cholinergic system?
M2
37
which receptors activate Gq protein subunits?
H1, a1, V1, M1, M3
38
which receptors activate Gs protein subunits?
B1, B2, D1, H2, V2
39
which receptors activate Gi protein subunits?
M2, a2, D2
40
what is the result of Gq activation?
1. phospholipase C 2. PIP2 - IP3 + DAG 3. increased calcium (IP3) 4. PKC activation (DAG)
41
what is the result of Gs activation?
1. adenylyl cyclase 2. conversion of ATP to increased cAMP 3. increased PKA activity
42
what is the result of Gi activation?
1. inhibition of adenylyl cyclase 2. decreased cAMP 3. decreased PKA activity
43
what is the result of Nm and Nn activation?
1. no second messenger | 2. activation (opening) of Na/K channels
44
what is the effect of a1 receptor activation on the eye?
contraction - mydriasis (radial dilator)
45
what is the effect of a1 receptor activation on arterioles?
contraction - increased TPR, diastolic pressure, afterload
46
what is the effect of a1 receptor activation on veins?
contraction - increased venous return and preload
47
what is the effect of a1 receptor activation on the bladder and sphincter?
contraction - urinary retention
48
what is the effect of a1 receptor activation on the male sex organs?
ejaculation
49
what is the effect of a1 receptor activation on the liver?
increased glycogenolysis
50
what is the effect of a1 receptor activation on the kidney?
decreased renin release
51
what is the effect of a2 receptor activation on the prejunctional nerve terminal?
decreased release and NE synthesis
52
what is the effect of a2 receptor activation on platelets?
aggregation
53
what is the effect of a2 receptor activation on the pancreas?
decreased insulin secretion
54
what is the effect of B1 receptor activation on the SA node?
increased HR
55
what is the effect of B1 receptor activation on the AV node?
increased conduction velocity (positive dromotropy)
56
what is the effect of B1 receptor activation on atrial and ventricular muscle?
increased force of contraction (positive inotropy), conduction velocity, CO, and oxygen consumption
57
what is the effect of B1 receptor activation on the His-Purkinje system?
increased automaticity and conduction velocity
58
what is the effect of B1 receptor activation on the kidney?
increased renin release
59
what is the effect of B2 receptor activation on the vasculature (all)?
vasodilation - decreased TPR, diastolic BP, afterload
60
what is the effect of B2 receptor activation on the uterus?
relaxation
61
what is the effect of B2 receptor activation on the bronchioles?
dilation
62
what is the effect of B2 receptor activation on skeletal muscles?
increased glycogenolysis and contractility
63
what is the effect of B2 receptor activation on the liver?
increased glycogenolysis
64
what is the effect of B2 receptor activation on the pancreas?
increased insulin secretion
65
what is the effect of D1 receptor activation on renal, mesenteric, and coronary vasculature?
vasodilation - in kidney - increased GFR, RBF, and sodium excretion
66
which receptors are typically activated first in response to endogenous catecholamines?
beta
67
how are TPR, CO, HR, and SV related to control BP?
control of BP is through TPR and CO CO = HR x SV
68
what are the results of activating or inhibiting a1 receptors in the heart?
activation - increased TPR - reflex bradycardia inhibition - decreased TPR - reflex tachycardia
69
what is the best course of action for a patient with hypertension / ischemic heart disease and considering a1 receptor blockers and/or beta blockers?
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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