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Pharmacology > Autocoids > Flashcards

Autocoids Flashcards

1
Q

What are the Autocoids

A

Naturally available substances

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2
Q

Examples of autocoids

A

Eicosanoids
Angiotensin
Nrurotensin
NO
Kinins
Histamine
Serotonin
Endothelins

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3
Q

Features of the Eicosanoids

A

Oxygenation products of AA
Wide range of therapeutic usefulness
Prostaglandins
Thromboxanes
Leukotrienes

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4
Q

AA libearted from where

A

Cell membrane phospholipids

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5
Q

Which enzyme is responsible for the generation of AA from the cell membrane

A

Phospholipase A

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6
Q

What are the forms of PLA

A

Cardiac
Cytosolic— Ca dependent
Secretory— Ca dependent

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7
Q

Pathways of AA

A

1-COX Pathway
2- 5-Lipoxygenase pathways

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8
Q

How is the COX pathway occur

A

COX coverts AA to PGG2 and then Eicosanoids

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9
Q

Isoforms of COX

A

COX-1= always secreted, important for physiological situations.
COX-2=specific for pathological situations, secreted when needed
COX-3

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10
Q

COX-2 inhibitors

A

NSAIDs
Rofecoxib
Celecoxib
Nimesulide

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11
Q

Side effects of COX-1 inhibitors

A

COX is responsible for inhibition of gastric acid secretion and helps to secrete gastric mucus
Inhibiting COX-1 can result with decrease in mucus secretion and cause ulcers

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12
Q

COX enzymes converts AA to what?

A

Prostaglandin G2
Which is an unstable cyclic endoperoxide and coverts to PGH2
PGH2 also unstable and yields to PGI2,PGE2,PGF2a,PGD2, Thromboxane A2 and Thrombaxe B2.

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13
Q

Why corticoids are used as an anti-inflammatory drug?

A

They induce the formation of lipocortin that inhibts PLA
They can also inhibit COX-2 gene expression

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14
Q

What are the general effects of Eicosanoids

A

Effect on
Vascular
Airway
Reproductive
GI smooth muscles

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15
Q

Vasoconstrictor Eicasonids

A

TXA2
PGF2a

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16
Q

Vasodilator prostaglandins

A

PGI2
PGE2

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17
Q

GI smooth muscle contractor Eicosanoids

A

PGs
TXA2

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18
Q

Constrictor of bronchial smooth muscles

A

TXA2
PGE2
PGF2a

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19
Q

Bronchodilator Eicosanoids

A

PGI2
PGE2
PGE1

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20
Q

Inhibitors of platelet aggregation

A

PGE1
PGI2

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21
Q

Enhances the Platelet aggregation

A

TXA2

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22
Q

Role of aspirin

A

Aspirin inhibts TXA2 formation only in platelets
Inhibits vasodilator PGI2 formation
Antiaggregant

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23
Q

Kidney synthesizes which Eicasonoids

A

PGs— PGE1,PGE2,PGD2— for glomerular filtration due to their vasodilator effect

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24
Q

Effects of PGs in the reproductive system

A

PGE2 and PGF2a are oxytocic molecules— normal delivery
Used for the abortion and initiation of labor
PGE1 helps erection
Seminal vesicles, prostate and testes produce PGs

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25
Q

Eicasonoids involved in fever

A

PGE1
PGE2

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26
Q

Eicasonoid that regulates natural sleep

A

PGD2

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27
Q

Eicosanoids that decrease the intraocular pressure

A

PGE
PGF

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28
Q

Dinoprostone

A

Synthetic analogue of PGE2
Produces contraction of uterine muscles

29
Q

Alprostadil

A

PGE1 analogue
Used for the treatment of erectile dysfunction in men

30
Q

Epoprostenol

A

PGI2 analogue
Uses for pulmonary hypertension

31
Q

Eicosanoids that involved in Patent Ductus Arteriousus

A

PGE2 and PGI2
NSAIDs are used for the duct closure
If duct should remain open Alprostadil is administered

32
Q

Misoprostol

A

PGE1 analogue
Used for ulcer treatment
COX-1 effects are minimized where administered with NSAIDs

33
Q

How is the Lipoxygenase Pathway

A

AA— Leukotriene A4—Leukotriene B4—Leukotriene C4—Leukotriene D4—Leukotriene E4

34
Q

Which Leukotriene types are Bronchoconstrictors

A

LTC4
LTD4

35
Q

Zileuton and Zafirkulast used in which disease

A

Asthma

36
Q

Features of Lipoxins

A

Derived from AA
Gamma-6 fatty acid
2 types= LXA and LXB
Formed by platelets but platelets cannot synthesize them alone.
Inhibit chemotaxis,transmigration,superoxide generation and NF-kB activation.
Antagonize the receptors of cysteine leukotrienes so that inflammation stop.
Signal macrophages to phagocyte the remains of these cells.

37
Q

LTA4 will form bc of platelets?

A

LTA4 converted to LXA4 and LXB4 by 12-Lipoxygenase.
LTA4 will form LTC4,LTD4,LTE4 which are synthesized in platelets.

38
Q

LXA4 will form?

A

Cysteinyl-Lipoxins— LXC4,LXD4,LXE4

39
Q

Lipoxins act on which receptors?

A

LXA4R and inhibit chemotaxis,transmigrationisuperoxide generation and NF-kB activation

40
Q

Lipoxins antagonize which receptors?

A

Cysteinyl Leukotrienes receptors so that inflammation can stop

41
Q

During the acute inflammatory process, the pro inflammatory cytokines such as IFN-y and IL-1beta can induce the expression of?

A

Anti-inflammatory mediators such as Lipoxins and IL-4, which promote the resolution phase of ingfalmmation.

42
Q

How is the production of Histamine

A

B-imidazoleethylamine = Histamine
Histidine———— Histamine by Histidine Decarbozylase

43
Q

What inhibits the conversion of Histidine to Histamine

A

Alpha-fluoromethyl histidine
Tritocaline

44
Q

Histamine is present in

A

Mast cells— as a complex with heparin
Neuronal histamine
Enterokromaffine cells (APUD cells)

45
Q

How is the liberation of Histamine from Mast cells

A

Mast cells contain IgE as receptors on their surface. As the ag interacts with IgE, histamine liberated.

46
Q

Can Histamine be absorbed?

A

Yes but the microorganisms in the GIT metabolism histamine.
Histamine is metabolized by histamine N-methyl transferase or diamond oxidase.
End product is methyl imidazole acetic acid

47
Q

Histamine receptors

A

H1—G protein coupled receptor — produces phosphoinositidyl hydrolysis
H2— G protein coupled receptor — inhibition of Adenylate cyclase activity.
H3— inhibits Acetyl Choline release

48
Q

Agonists do H1,H2,H3

A

H1: 2-methyl histamine
H2: 4-methyl histamine
H3: alpha-methyl histamine

49
Q

Betazole used in?

A

H1 analogue
Meniere’s Disease

50
Q

Pharmacological effects of histamine

A

Decrease in blood pressure
Vasodilation (sometimes vasoconstriction)
Increase PGI2 secretion
Increase in capillary permeability
Lewis’ triple response: edema, flare and urticaria
Increases leukocyte infiltration to the tissues during inflammation. Contracts uterus smooth muscle
Increases gastric acid secretion via H2 receptor stimulation.

51
Q

Role of histamine in endogenous pathological situations

A

Systemic or local reaction
Allergic reactions due to physical factors
Drug mediated allergic reactions
Histamine mediated headache
Mast cell or basophil tumors
Peptic ulcer
Prutitus,flare,pain sensation
Tissue proliferation and repair
H1 involved in awakefulness

52
Q

Serotonin formed from

A

Tryptophan— tryptophan hydroxylase— 5-hydroxytryptophan— l-aromatic acid decarboxylase— serotonin

53
Q

Serotonin present in

A

Enteric NS
Thrombocytes
Enterokromaffin cells (APUD cells)

54
Q

Serotonin receptor subtypes

A

5-HT1a— regulation of sleep
5-HT1b
5-HTm
5-HT2a
5-HT2b
5-HT2c
5-HT3—should not used in pregnant women
5-HT4
5-HT6
5-HT7

55
Q

Pharmacological effects of serotonine

A

Produces severe vasoconstriction
Migraine
Renal vessels are sensitive to serotonin
Decrease cardiac rate suddenly
Stimulates respiration but the bronchi are not sensitive to serotonine
Increases peristaltic movements in small intestine
Mediates pain sensation
Initiates emesis
Dumping syndrome

56
Q

Kinins produced from

A

Prekallikrein— activated haegeman— kaliikrein
Kallikrein converts Kininogens to Kinins

57
Q

Pharmacological effects of Kinins

A

Dilation of arterioles
Constriction of venules
Contracts intestinal muscles
Stimulate pain receptor in the tissues
B1 and B2 receptors.
Tachykinins and bradykinins

58
Q

Which drug inhibits kallikrein

A

Aprotinin

59
Q

Endothelia secreted from where and how?

A

Vascular endothelium
Synthesized as pre-pro-endothelin
Endothelia-1— Endothelin-2— Endothelin-3

60
Q

Receptors of Endothelin

A

ETa
ETb

61
Q

Antagonist of endothelin receptor

A

Bosentan— pulmonary hypertension

62
Q

Pharmacological effects of endothelins

A

Vasoconstriction
Renal vascular bed is very sensitive endothelins
Bronchoconstriction occurs
Mito genie activity occurs
In hypertension,myocardial infraction, pulmonary hypertension, chronic renal failure— ET-1 increases
ET-1 RECEPTOR ANTAGONISTS DO NOT DECREASE THE VASCULAR TONUS

63
Q

Features of Urotensin-2

A

Strongest vasoconstrictor
Effect on BV
May help to depression

64
Q

NO synthesized from?

A

L-arginine by nitric oxide synthase

65
Q

Forms of Nitric Oxide Synthase

A

NNOS
ENOS
Both constitutive
INOS is Inducible NOS

66
Q

NOS inhibitor

A

L-NAME

67
Q

How does NO causes vasodilation in vascular smooth muscles?

A

NO binds to Guanylate Cyclase and cGMP is formed
CGMP deactivates MLCK
MLCK cannot phosphorylated MLC
Myosin and actin cannot combine to form the contracted muscle filaments

68
Q

Clinical implications of NO system

A

Hypertension
Atherosclerosis
Immune system
Excitotoxicity, ischemia
Neurotransmitter release
Impotence

69
Q

Features of Neurotensin

A

Acts as a neuromodilator of neurotransmitter
Vasodilation
Increased vascular permeability
Anterior pituitary hormones
Hyperglycemia
Inhibition of gastric acid
3 types of receptors
Therapeutic potential in Parkinson’s and schizophrenia

Pharmacology (6 decks)

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