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Inflammation Flashcards

1
Q

Rubor

A

redness

  • vasodilation via relaxation of arteriolar smooth muscle
  • histamine/PGs/bradykinin-mediated
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2
Q

Tumour

A

swelling

  • edema via leakage from post-capillary venule -> interstitial space
  • histamine and tissue damage-mediated
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3
Q

Calor

A

heat

  • vasodilation via relaxation of arteriolar smooth muscle
  • histamine/PGs/bradykinin-mediated
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4
Q

Dolor

A

pain

  • sensitization of sensory nerve endings
  • bradykinin and PGE2-mediated
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5
Q

Fever

A
  • pyrogens stimulate macrophages to release IL-1, TNF -> increase COX in perivascular cells of the hypothalamus -> increases PGE2 -> raises temperature set point
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6
Q

Factors of the extrinsic pathway (of the coagulation cascade)

A

III (Thromboplastin)
VII

IIa (Thrombin)

*Note: activated VII (VIIa) can convert IX to IXa

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7
Q

Factors of the intrinsic pathway (of the coagulation cascade)

A

XII (Hageman factor)
XI
IX
VIII

IIa (Thrombin)

*Activated XI (XIa) converts IX to IXa

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8
Q

Factors of the common pathway (of the coagulation cascade)

A 
X
V
II (Prothrombin) 
I (Fibrinogen)
XIII

IIa (Thrombin)
* the common pathway uses thrombin, and also generates thrombin

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9
Q

Aspirin

A

COX-1 inhibitor

  • prevents formation of thromboxane in platelets
  • permanent action on platelets
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10
Q

Heparin

A

Binds and inactivates thrombin (factor IIa)
Binds and activates antithrombin III

  • low molecular weight heparins only bind antithrombin III
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11
Q

Warfarin

A

Oral anticoagulant

- blocks epoxide reductase in liver -> prevents regeneration of active form of Vitamin K

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12
Q

Streptokinase

A

Thrombolytic agent

  • plasminogen activator
  • converts plasminogen -> plasmin
  • enables dissolution of clots
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13
Q

Bleeding time

A
  • time taken from initial injury to the formation of the primary hemostatic plug (plug formed prior to incorporation of fibrin)
  • indicator of PRIMARY HEMOSTASIS

Prolonged bleeding time indicates:

  • low platelet count
  • vWF deficiency
  • platelet receptor defects
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14
Q

Clotting time

A
  • time taken for the formation of the stable hemostatic plug (incorporation of fibrin into the plug)

Prolonged clotting time indicates:

  • defects in coagulation pathway
  • specific defects of either the intrinsic or extrinsic pathway are indicated by:
  1. Prothrombin time (PT)
  2. Activated partial thromboplastin time (APTT/PTT)
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15
Q

Prothrombin time (PT)

A
  • tests extrinsic and common coagulation pathways

Measures defects in:

  • thromboplastin
  • VII
  • X
  • V
  • prothrombin (II)
  • fibrinogen (I)
  • XIII
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16
Q

Activated partial thromboplastin time (APTT)

A
  • tests intrinsic and common pathways

Measures defects in:

  • XII
  • XI
  • IX
  • VIII
  • X
  • V
  • prothrombin (II)
  • fibrinogen (I)
  • XIII
17
Q

E selectin (what does it bind? what does it facilitate? how is it regulated?)

A
  • endothelial molecule (ELAM-1)
  • facilitates ROLLING adhesion
  • binds Sialyl-Lewis X-modified proteins on leukocytes
  • TNF, IL-1 stimulate DE NOVO synthesis of E selectin
18
Q

P selectin (what does it bind? what does it facilitate? how is it regulated?)

A
  • endothelial molecule
  • facilitates ROLLING adhesion
  • binds Sialyl-Lewis X-modified proteins on leukocytes
  • histamine stimulates release of P selectin from Weibel-Palade bodies

*Weibel-Palade bodies also contain von Willebrand factor

19
Q

ICAM-1 (what does it bind? what does it facilitate? how is it regulated?)

A
  • integrin ligand/ endothelial adhesion molecules
  • facilitate Adhesion & Emigration
  • binds LFA-1 (CD11a/CD18) - integrin
  • binds Mac1 (CD11b/CD18) - integrin
  • TNF stimulates DE NOVO synthesis of ICAM-1
20
Q

VCAM-1 (what does it bind? what does it facilitate? how is it regulated?)

A
  • integrin ligand/ endothelial adhesion molecules
  • facilitate Adhesion & Emigration
  • binds VLA-4 (CD49d/CD29) - integrin
  • upregualted by TNF
21
Q

Chemotactic factors for PMNs

A
  1. Bacterial products (i.e. E. coli, Staph. aureus)
  2. C5a
  3. LTB4
  4. IL-8
22
Q

Chronic Granulomatous Disease

A

NADPH Oxidase deficiency
- increased infection by catalase + microbes (because they can convert hydrogen peroxide to water, thereby protecting themselves)

23
Q

Conditions in which you see granulomatous inflammation

A
  1. Tuberculosis (Caseating granuloma)
  2. Cat-scratch disease
  3. Syphilis
  4. Fungal
  5. Protozoan
  6. Foreign body granuloma
  7. Rheumatic fever (Aschoff body)
  8. Rheumatoid arthritis
  9. Sarcoidosis
  10. Granuloma annular of skin

Pathology (2 decks)

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