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D&T2 Exam 2 > Kinins, Serotonin and Drug Therapy of Migraine headache -Salisbury > Flashcards

Kinins, Serotonin and Drug Therapy of Migraine headache -Salisbury Flashcards

1
Q

what are 3 biological effects of Kinins

A

autocoids that induce inflammation, pain and vasodilation

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2
Q

what are two kinins

A

Bradykinin

kallidin

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3
Q

what is the precursor for kinin

A

Kininogens

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4
Q

what are Killikerins

A

serine proteases that cleave Kininogens into kinins

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5
Q

High molecular weight kininogens HMWK is cleaved by what and gets turned into what?

A

Plasma Kallikrein into bradykinin

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6
Q

Low Molecular weight Kininogen LMWK is cleaved by what

A

Tissue Kallikrein into kallidin which is then cleaved by Aminopeptidase into Bradykinin

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7
Q

Autoactivation of Factor XII (Hageman factor) turns into what

A

factor XIIa

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8
Q

Factor XIIa converts what into what

A

plasma Prekallikrein to plasma Kallikrein

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9
Q

what is the role of Plasma Kallikrein (2)

A
  1. converts high molecular weight kininogen HMWK to Bradykinin
  2. activates factor XIIa
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10
Q

the first step in the intrinsic clotting cascade enhances what

A

Bradykinin synthesis

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11
Q

Are tissue and plasma Kallikrein the same thing

A

no

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12
Q

Tissue Kallikrein converts what

A

Low Molecular Weight Kininogen LMWK to Kallidin

Aminopeptidase converts kallidin to Bradykinin

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13
Q

Role of Carboxypeptidase N and M (CPN, CPM)

A

cleave kinins into active kinin metabolites

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14
Q

what is another name for carboxypeptidase N and M CPN, CPM

A

kinase I

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15
Q

another name for Angiotensin I-converting Enzyme (ACE_)

A

Kinase II

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16
Q

Role of ACE kinase II

A

hydrolyzes Bradykinin into inactive products

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17
Q

when people take ACE inhibitors for lowering blood pressure and cardioprotective reasons, what effect does this have on Bradykinins

A

increases

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18
Q

Name two Kinin receptors? what kind of receptors are they

A

B1 and B2

G coupled receptors

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19
Q

Native Bradykinin and Kallidin activate what receptor

A

B2

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20
Q

Active metabolites of Bradykinin and Bradykinin activate what receptor

A

B1

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21
Q

where is B2 mostly expressed

A

in most tissues

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22
Q

B1 receptor is induced by what

A

tissue damage and inflammation

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23
Q

activation of B receptors stimulates increase synthesis of what

A

prostaglandins
NO
EDHF

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24
Q

What effect do NSAIDS have on bradykinin and kallidin and prostaglandin

A

decreases Bradykinin and Kallidin

increases prostaglandin by blocking cyclo-oxygenase

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25
Q

What effect do corticosteroids have on bradykinin and kallidin and prostaglandin

A

decreases Bradykinin and Kallidin

increases prostaglandin by stimulating Lipocortin ( phospholipase A2 inhibitor)

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26
Q

what are 4 effects of kinins

A

pain
inflammation
cardiovascular
respiration

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27
Q

what is the most potent vasodilator peptide in the trigeminal system

A

CGRP

induced by kinins

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28
Q

Kinins can induce what in the respiratory tract

A

bronchospasms

kinin levels can be elevated in asthma

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29
Q

what do kinins do to the cardiovascular system

A

vasodilation and lower BP

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30
Q

what are 4 biological effects of Serotonin

A

platelets
cardiovascular
GI
CNS

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31
Q

what role does serotonin play in platelets

A

platelets do not synthesize serotonin
platelets actively take up serotonin
Serotonin release during platelet aggregation promotes platelet aggregation and vasoconstriction

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32
Q

what role does serotonin play in cardiovascular

A

induces vasoconstriction

positive inotropic and chronotropic effects on heart

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33
Q

what role does serotonin play in GI

A

Enterochromaffin cells release 5-HT in response to vagal stimulation and stretching with food digestion
5-HT regulates GI motility

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34
Q

5-HT producing carcinomas will induce what

A

diarrhea and abdominal cramps

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35
Q

where are 5-HT found in the CNS? role?

A

raphe nuclei of brain stem

regulates sensory perception and nociception

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36
Q

Serotonin is inactivated by what

A

monamine-oxidase A (MAO-A)

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37
Q

what only expresses MAO-B isoform

A

platelets

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38
Q

what is a urinary metabolite of 5-HT

A

5-HIAA

5-Hydroxyindoleacetic acid

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39
Q

what serotonin receptors play a role in migaine

A

5-HT 1B/1D

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40
Q

role of 5-HT 1D

A

induces vasoconstriction of cranial blood vessels

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41
Q

role of 5-HT1B

A

autoreceptor

inactivation inhibits nociceptive trigeminal afferents which controls acute migraine attacks

42
Q

what drug are 5-HT1B/1D agonist that controls/reverses acute migraine attacks

A

Triptans

43
Q

common migraine

A

headache

44
Q

classic migraine

A

aura and headache

45
Q

what are the 4 stages of migraine

A

prodome ( 1-2 days prior to attack) GI effects mood changes
aura (20-60 min prior to attack)
attack ( 4 hrs - 3 days)
postdrome

46
Q

what is a characteristic of a migraine attack

A

POUND

Pulsating headache lasting 4-72 hOurs that is Unilateral, Nauseating and Debilitating

47
Q

can patients be genetically susceptible to migraine

A

yes

48
Q

what is neurovascular headache

A

disorder in which neural events results in further dilation of cranial blood vessels, which in turn, results in pain and further nerve activation

49
Q

can a migraine be caused by a primary vascular event?

A

no

50
Q

what causes a migraine

A

brain-stem nuclei that normally mediate sensory input and exerts neural effects on cranial vessels

51
Q

Beta blockers are what kind of agents for migraines

A

prophylactic

52
Q

name 2 beta blockers

A

Propranolol and Atenolol

53
Q

Propanolol and Atenolol is contraindicated in who

A

patients with ashtma

54
Q

Name two tricyclic antidepressants

A

Amitriptyline

Nortriptyline

55
Q

what are side effects of Amitriptyline and Nortriptyline

A

limit use

- significant anti-muscarinic properties, weight gain, tiredness

56
Q

tricyclic antidepressants- how are they used to treat migraines

A

prophylactic agent

57
Q 
Valproic acid 
Topiramate
Gabapentin 
Levetiracetam 
are what type of drug and use
A

Anticonvulsants

prophylactic

58
Q

who is Valporic acid contraindicated in

A

pregnant patients

59
Q

Anticonvulsants are typically prescribed to who

A

migraine patients with epilepsy or anxiety disorders

60
Q

name a calcium channel blocker and its use

A

Verapamil

prophylactic

61
Q

what are side effects of Verapamil

A

negative inotropic cardiac effects

hypotension

62
Q

MOA for Cyproheptadine

A

antagonist of histamine, acetylcholine, serotonin

Prophylactic

63
Q

side effects of Cyproheptadine

A

CNS depression

sleepiness

64
Q

what is used to abort mild to moderate migraines ( rescue)

A

Acetaminophen, aspirin NSAIDS

65
Q

what is used to abort moderate to severe migraines? how can you administer it? what the longest length of time you can use it? (rescue)

A

Ketorolac ( IV or oral)

max 5 days

66
Q

what is used to abort migraines in children ( rescue)

A

Acetaminophen and ibuprofen

67
Q

what is used to abort migraines in pregnant ladies ( rescue)

A

Ibuprofen and acetaminophen

all NSAIDS should be avoided in last trimester

68
Q

Same 2 Ergot alkaloids

A

Ergotamine and Dihydroergotamine

69
Q

what is MOA for Ergot Alkaloids

A

agonist effects at 5-HT1 receptors

70
Q

what are the routes of administration of Ergotamine and Dihydroergotamine

A

Ergotamine- sublingual

Dihydroergotamine: nasal spray, injection

71
Q

what are side effects of Ergot Alkaloids

A

Nausea and vomiting

generalized vasoconstriction

72
Q

Ergotamine and dihydroergotamine are contraindicated in who

A

pregnancy
peripheral vascular disease
ischemic heart disease

73
Q

Ergot alkaloids can be combined with what to treat what

A

antiemetic

curve nausea

74
Q

what cannot you not combine ergotamine and dihydroergotamine with

A

Triptans

75
Q

compare side effects of Triptan and Ergot alkoids

A

Triptan causes less nausea and generalized vasoconstriction

76
Q

MOA of Triptan

A

5-HT 1B/1D receptor agonists

77
Q

Triptan effect on vascular

A

vasoconstriction of cranial vessles

78
Q

Triptan effect on neurogenic

A

reduction of trigeminal sensory nerve activation

inhibition of vasoactive neuropeptide release

79
Q

Triptan effect on central

A

-inhibition of neurotransmitter release from activated trigeminal nerve in the brainstem and upper cervical spinal column

80
Q

what are good things about Sumatriptan

A

short onset

relief within 1hr

81
Q

limitations of Sumatriptan

A

short duration
low bioavailability
short plasma half life

82
Q

Good things about Naratriptan and Zolmitriptan

A

lipophilicity: greater distribution to brain
greater bioavailability
longer half life

83
Q

draw back of Naratriptan and Zolmitriptan

A

onset of action 1 hours

84
Q

what drugs get metabolized by P450

A

Naratriptan and Zolmitriptan

85
Q

what patients should receive lower doses of Naratriptan and Zolmitriptan

A

renal dysfunction

86
Q

what has the longest acting Triptan, higher affinity for 5-HT 1B/1D

A

Frovatriptan

87
Q

How is Rizatriptan given

A

sublingual

88
Q

adverse effect of Rizatriptan

A

headache recurrence

tingling, paresthesia, dizziness, flushing, neck pain, and drowsiness

89
Q

contraindications of Rizatriptan

A

dont use ergot alkaloid within 24 hrs

  • peripheral vascular disease
  • ischemic heart disease
90
Q

Drug interactions of Rizatriptan

A

dont use with SSRI

- restlessness, hallucinations, loss of coordination, diarrhea

91
Q

Episodic severe unilateral stabbing headaches that tend to appear at the same each ( circadian Rhythm)

A

cluster headace

92
Q

acute treatment options for cluster headache attacks

A

oxygen

triptans

93
Q

prophylactic options for cluster headaches

A

high dose prednisone

calcium channel blockers ( verapamil)

94
Q

Headache pain is a squeezing or pressure felt around the head that is not associated with nausea or vomiting

A

tension

95
Q

abortive medications for tension headaches

A

acetaminophen and NSAIDS

96
Q

prophylactic medications for tension headaches

A

tricyclic antidepressants

antiepileptic gabapentin

97
Q

pain due to increases in intracranial pressure and disorder occurs most frequently in obese young women

A

idiopathic intracranial hypertension

98
Q

Drug therapy for idiopathic intracranial hypertension includes

A

carbonic anhydrase inhibitors

Acetazolamide and Topiramate

99
Q

what is MOA of Acetazolamide and Topiramate

A

function as carbonic anhydrase inhibitor that reduce CSF production

100
Q

side effects of carbonic anhydrase inhibitors

A

nausea, tingling in hands and feet, altered taste

D&T2 Exam 2 (14 decks)

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