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PHAR2002 > Inflammation > Flashcards

Inflammation Flashcards

1
Q

An inflammatory reaction is

A 
A pathophysiological process which 
i) destroys
ii) dilutes
iii) walls off  
an inflammatory initiating agent: 
-> microbrial infection, noxious stimuli, neoplasm trauma
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2
Q

Basic physiological events:

A
  1. Vascular- dilation
  2. Cellular- anti-microbial
  3. Induction - antigen presents
  4. Effect - lymphocyte recruitment
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3
Q

Outline vascular - dilation phase

A
  1. Increased vasodilation increases vascular permeability
  2. Fluid extravasation
  3. Endothelial cell activation -> express CAMS
  4. Leukocytes in blood vessel adhere to endhothelium
  5. Transmigrate to site inflammation
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4
Q

Cellular response involves which 2 types of cells :

A
  1. Polymorph nuclear cells (PMN’s) e.g. neutropil
    - > phagocytosis microbial nature -> respiratory burst
    - > proteases/ recruit more leukocytes
  2. Monocytes -> differentiate into macrophages which
    i) phagocytose
    ii) release host inflammation mediators
    - > reactive o2 species
    - lipid mediators
    - cytokines/ chemokines
  3. Present antigen to lymphocytes
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5
Q

Henry Dale’s criteria for chemical mediator:

A

Be present, cause inflammation, releived if synthesis. release manipulated

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6
Q

Histamine is released from _____ or ____ by a variety of stimuli including XYZ

A

Mast cells/ basophilis by
X: IGE cross linking
Y: Amphylation C5a and C3a
Z: Morphine

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7
Q

H1 mediates

A

endo cell activation by rounding up -> I.C. spaces form, arteriolar and arterial relaxation

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8
Q

Histamine is formed by

A

Histidine by histidine decarboxylase

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9
Q

H1 antagonists that cross BBB and what they’re used for:

A

Gaq - diphenhydramine, chlopheniramine

-> sedation, motionsickness, allergies (but drowsy)

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10
Q

H1 antagonists that don’t cross BBB

A

Cetirizine, terfenadrine

-> allergies (partially effective)

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11
Q

H2 antagonists

A

Gas
e.g. rantidine
suppression gastrin secretion
-> heals duodenal ulcers

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12
Q

Types of kinins and origins

A

Bradykinins + kallidin (lys-bradykinin)

-> formed from plasma protein precursors (kinninogens)

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13
Q

Kallikans

A

Enzymes that produce kinin from kinnogens

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14
Q

Kinin is destroyed by X and Y with a plasma half life of

A

X- Carboxypeptidase N
Y- Angiotensin coverting enzyme
20 minutes

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15
Q

Kinin functions and mediators

A
  1. Vasodilators, increase venular permeability, cause pain + contract smooth muscle
  2. Actions mediated by B2 receptors but B1 also exist/ histamine. prostaglindin release
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16
Q

How does beta 2 mediate kinin function?

A
  • constitutive
  • acts through other mediators
  • NO + prostaglandins
  • agonist: bradykinin, kalidin
  • antagonist : icibant HOE140
17
Q

How does beta 1 mediate kinin function?

A
  • induced via cytokines
  • not internalised
  • agonist: des-arg kalidin DABK (des-arg bradykinin)
  • antagonist: des-arg icibant
18
Q

Prostaglandin characteristics

A

20 carbon with HO group at C15

19
Q

Prostaglandin E.synthase:

A

1) cytosolic: constituitive production

2) membrane: inflammatory mediators e.g. arachindonic acid -> prostenoid + relevant synthase (COX)

20
Q

How do the EP receptors differ?

A
  1. Bronchial G.I, sm mu contraction, pain
  2. Bronchodilation, vasodilation, stimulation of intestinal fluid secretion + G.I. sm. muscle relaxation
  3. Intestinal Sm. mu. contraction gastric acid secretion inhibition, increase gastrine mucus secretion
  4. Bronchial constriction + vaso D, leukocyte suppression
21
Q

How does PGE2 cause fever?

A

Hypothalamus

22
Q

How does PGE2 cause pain?

A

Induces hyperalgesia at peripheral terminals of primary afferent nociceptors and spine

23
Q

How does PGE2 cause oedema?

A

Synergy with other mediators

24
Q

PGE2 and leukocytes

A

Inhibits leukocytes

25
Q

PGD2

A

Synthase found predominantly in mast cells and brain
DP- receptors: Vasodilatation, inhibit platelet aggregation, Relaxation GI muscle & uterine
TP-receptors:- Bronchoconstrictor
CRTH 2:- Chemoattractant for Th2 cells

26
Q

PGF2

A

FP-receptors:- Smooth muscle contraction, Bronchoconstriction, Reproductive physiology

27
Q

PGI2

A

prostacyclin

  • > synthase found in vascular endothelium
  • IP- receptors: Vasodilatation, Inhibit platelet aggregation, renin release
28
Q

Thromboxane A2

A

Synthase found in platelets

TP receptors: Vasoconstriction, platelet aggregation

29
Q

Cytokine + Chemokine characteristics

A

Simple polypeptides/ glycoprotein with molecular weight <30KD -> production transient

  • bind to high affinity CS receptors
  • > alter gene expression in target cells
30
Q

Binding affinity of cytokine + chemokines

A

10-9 - 10-12 M

PHAR2002 (14 decks)

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