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Pharmacology > Inflammatory Mediators > Flashcards

Inflammatory Mediators Flashcards

1
Q

storage of histamine

A
  • mast cells

- basophils

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2
Q

synthesis and release of histamine

A
  • in epidermal cells
  • gastric mucosa
  • CNS
  • regenerating or rapidly growing tissues
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3
Q

synthesis of histamine from

A

histidine

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4
Q

function of endogenous histamine

A
  • allergic hypersensitivity response
  • gastic acid secretion (by H2 receptors on gastric parietal cells)
  • gastric carcinoid tumors (proliferation of mast cells and basophils)
  • CNS neurotransmitter
  • myenteric plexus
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5
Q

endogenous histamine inhibited by

A
  • cromolyn sodium
  • nedocromil
  • moderated by beta-2 agonists
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6
Q

what non-immune compounds can release histamine

A
  • organic bases
  • venoms
  • several drugs
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7
Q

metabolism of histamine

A

can occur by 2 different pathways:

  1. N-methyltransferase
  2. diamine oxidase
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8
Q

pharmacologic effect of H1 receptor

A
  • vascular/extravascular smooth muscle
  • nerves
  • glands
  • some CNS
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9
Q

pharmacologic effect of H2 receptor

A
  • vascular/smooth muscle
  • gastric parietal cell
  • cardiac
  • some CNS
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10
Q

pharmacologic effect of H3 receptor

A
  • CNS
  • dampening
  • negative feedback
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11
Q

pharmacologic effect of H4 receptor

A

WBC

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12
Q

effects of histamine on the cardiovascular system

A
  • vasodilation
  • increased “capillary” permeability
  • cardiac stimulation; arrhythmias
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13
Q

what is the “triple response” of Lewis (wheal and flare)

A
  • Localized red spot
  • Brighter red flush/flare
  • Wheal that is noticeable in 1-2 mins that occupies the original red spot
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14
Q

extravascular effect of histamine

A
  • bronchoconstriction
  • intestinal smooth muscle contraction
  • cause nerve ending pain or itch
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15
Q

Histamine Antagonists (ie. Antihistamines) are available as

A

drug block H1 and H2 receptors

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16
Q

how are H1 blockers divided

A
  • older (1st) generation

- newer (2nd) generation agents

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17
Q

2nd generation H1 receptors

A
  • penetrate CNS poorly

- are non sedating

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18
Q

H2 blockers (OTC) used to deccrease

A

gastric acid secretion

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19
Q

what are H1- Receptor Antagonists

A

-REVERSIBLE, competitive inhibitors of the H1 receptor (act like an inverse agonist)

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20
Q

1st generation H1 receptors are

A
  • sedative

- anticholinergic

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21
Q

2nd generation H1 recptors are

A

-less or no sedation

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22
Q

what are the properties of H1 receptors

A
  • sedation (varies)
  • anticholinergic; some with alpha and 5-HT blocking action
  • central antinausea and antiemetic effects (some agents irritate GI)
  • mild antiparkinsonian effects (anticholinergic)
  • local anesthetic effects (structural features of local anesthetics)
  • drug allergy from topical administration
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23
Q

clinical uses of H1 Antagonists

A
  • allergies
  • allergic reactions
  • pruritus
  • itching
  • motion sickness
  • vestibular disturbances
  • OTC sleep aid
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24
Q

function of H2 Receptor Antagonists

A

block histamine - induced gastric acid secretion

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25
Q

H2 receptor antagonists have a larger effect on

A

nocturnal acid secretion

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26
Q

all drugs in H2 receptor antagonists are available OTC to reduce

A

gastric acid secretion

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27
Q

name 4 H2 receptor antagonists

A
  1. cimetidine
  2. ranitidine
  3. famotidine
  4. nizatidine
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28
Q

function of cimetidine

A

inhibits p450 and may cause confusion in ELDERLY patient receiving larger doses

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29
Q

what are kinins

A

are peptide autocoids that act locally to produce pain, vasodilation, increased vascular permeability
-synthesize vasoactive substances (ie. prostaglandins)

30
Q

kinins are activated by

A
  • tissue damage
  • allergic rxns
  • viral infection
  • inflammatory events
31
Q

kinins are cleaved from

A

alpha 2 globulins (kininogens)

32
Q

bradykinin and kallidin are cleaved by

A

plasma or tissue kallikrein

33
Q

plasma killikrein activated by

A

factor XII

34
Q

kinins are inactivated by

A
  • ACE (kininase II)

- inactivated by conversion to active Des-Arg metabolites by other peptidases

35
Q

bradykinin and kallidin are cleaved from

A
  • HMW or LMW kininogens by plasma

- tissue kallikrein

36
Q

B1 (kinin receptor) binds to

A

des-Arg metabolites

37
Q

B1 (kinin receptors) are present in what cells

A

normal vascular smooth m.

38
Q

B1 (kinin receptors) are unregulated during

A

inflammation by cytokines, GF and endotoxins

39
Q

function B2 (kinin receptors)

A
  • mediate the effects of bradykinin in the absence of inflammation
  • activate proinflammatory transcription factors, NO synthesis, prostaglandin synthesis
40
Q

pharmacological function of kinins

A
  • pain
  • inflammation - increase permeability
  • respiratory disease - provokes bronchospasms
  • kidney function - regulate urine volume and composition
41
Q

drugs affecting kinins

A
  • ACE inhibitors
  • investigational bradykinin agonists and antagonisists
  • kallikrein inhibitors
42
Q

what are eicosanoids

A
  • prostaglandins

- leukotrienes

43
Q

eicosanoids are derived from

A

20-C essential F/A that contain 3,4 or 5 double bonds

44
Q

where are eicosanoids found

A

in almost every tissue and body fluid

45
Q

eicosanoid production increases in response to

A

diverse stimuli

46
Q

what are the 2 routes of metabolism of arachidonic acid

A
  1. lipoxygenase

2. cyclooxygenase

47
Q

lipoxygenase pathway leads to

A

HPETEs
HETEs
leukotrienes

48
Q

cyclooxygenase pahtway leads to

A
  • cyclic endoperoxides (PGG and PGH)

- metabolic products

49
Q

how many active sittes does cyclooxygenase have

A

2

50
Q

expression of cyclooxygenase-1 (COX-1)

A

constitutively expressed

51
Q

where is COX-2 expressed

A
  • endothelial cells
  • kidney
  • brain
52
Q

COX-2 induced by

A
  • cytokines
  • GF
  • endotoxin
  • an effect that is blocked by glucocorticoids
  • laminar shear force
53
Q

function of eicosanoids

A
  • inflammation
  • smooth muscle tone
  • hemostasis/thrombosis
  • paturation (labor delivery)
  • gastrointestinal secretion
  • renal function
54
Q

what blocks Eicosanoids

A

NSAIDs

55
Q

what drugs decrease the effect of leukotrienes

A

Leukotriene receptor antagonists

5-Lipoxygenase inhibitor

56
Q

Name the Leukotriene receptor antagonists

A
  1. Zafirlukast

2. Montelukast

57
Q

name the 5-Lipoxygenase inhibitor

A

zileuton

58
Q

what is zileuton used to treat

A
  • asthma

- block leuoktriene derivatives

59
Q

what are the effects of Eicosanoids on the Cardiovascular system

A
  • vasodilate (PGI2, PGE2, PGD2)
  • hypotension (LRC4, LTD4)
  • vasoconstrict (TXAs, PGF2; endoperoxides)
  • increase C.O (PGE2m PGF2)
  • increase capillary permeability (LTC4, LTD4)
60
Q

what are the effects of Eicosanoids on Blood Elements

A
  • platelet aggregation (PGI2 inhibits; TXA2 promotes)
  • chemotaxis (LTB4)
  • inhibit lymphocyte function (PGE2)
61
Q

postaglandins contract or relax what type of muscle

A

extravascular smooth muscle

62
Q

leukotrines contract what kind of muscle

A

smooth muscle

63
Q

broncoconstriciton caused by

A

LTC4
LTD4
PGF2
PGD2

64
Q

uterine contraction caused by

A

PGE2

PGF2

65
Q

gastrointestinal smooth muscle contraction caused by

A

LTC4
LTD4
PGE2
PGF2

66
Q

effect of prostaglandins on GI

A
  • decrease gastric secretion
  • increase mucus
  • promote local blood flow
  • stimulate epithelial growth (PGE2 PGI2)
67
Q

effect of prostaglandins on kidney and urine formation

A
  • increase renal blood flow
  • decrease chloride reabsorption
  • increase renin secretion
68
Q

affects of prostaglandins on afferent nerves

A
  • direct pain producer

- hyperalgesia

69
Q

effect of prostaglandins on CNS

A
  • elevate body temp

- modulate NT

70
Q

effect of prostaglandins on eye

A

PGF decrease intraocular pressure

71
Q

what are the therapeutic uses of prostaglandins

A
  • cervical ripening (PGE2)
  • therapeutic abortion - stimulate uterine contraction)
  • gastric cytoprotection (Misoprostol; PGE1 analog)
  • maintenance of patent ductus arterioles
  • primary pulmonary hypertension

Pharmacology (23 decks)

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