Pathology 4 Ex 1

Front 1

Histamine source

Back 1

Mast cells/basophil degranulation

Front 2

Serotonin source

Back 2

Platelets

Front 3

Platelet activating factor, prostaglandins, leukotrienes source

Back 3

inflammatory cells

Front 4

Nitric Oxide, Platelet activating factor, prostaglandins source

Back 4

endothelium

Front 5

Histamine

Back 5

-synthesized and stored in mast cells and basophils
-diffuses rapidly through the blood stream
-promotes vasodilation, and increased vascular permeability
-recognized by specific receptors (H1, H2 and H3)

Front 6

Serotonin (5-HT)

Back 6

Stored in platelets, mast cells and enterochromaffin cells of the GI tract
Vasoactive mediator
Role in inflammation unclear

Front 7

Platelet activating factor (PAF) in cellular

Back 7

it is found in endothelial cells, where it has a role in
neutrophil – endothelial cell adhesion

Front 8

Platelet activating factor (PAF) in circulation form

Back 8

it induces platelet aggregation and degranulation

Front 9

PAF causes

Back 9

vasodilation and increased vascular permeability in low
concentration, though at higher concentration may cause
vasoconstriction and bronchospasm.

Front 10

Prostaglandins are

Back 10

oxidized derivatives of AA produced via cyclooxygenase pathway using 2 different
enzymes. COX-1 is constitutively expressed and COX-2 is inducible

Front 11

major sources of prostaglandins in the acute inflammatory response include

Back 11

monocytes, macrophages,
endothelial cells and platelets

Front 12

Prostaglandins are augmented by

Back 12

a number of stimuli including: bacterial endotoxin, immune complex
formation, C3a, bradykinin and IL-1

Front 13

Prostaglandins promote

Back 13

pain (PGE2), fever, vasodilation and increased vascular permeability

Front 14

Leukotrienes are oxidized derivatives of

Back 14

AA produced via lipoxygenase pathway

Front 15

Leukotrienes are released from

Back 15

neutrophils, basophils and mast cells

Front 16

LTA4 taken up by RBC and endothelial cells and converted to LTB4 and LTC4
Promotes

Back 16

vasoconstriction, increased vascular permeability, endothelial adhesion, bronchoconstriction, neutrophil activation and chemotaxis
(leukotrines do bad things)

Front 17

Lipoxins are derived from

Back 17

Lipoxygenase pathway

Front 18

Neutrophils produce intermediates in lipoxin synthesis, which are converted to

Back 18

LXA4 and LXB4 by platelet 12-lipoxygenase.

Front 19

Lipoxins inhibit

Back 19

leukocyte recruitment and cellular components of inflammation.
-Opposite role to leukotrienes

Front 20

Nitric Oxide May be released from

Back 20

from endothelial cells upon stimulation by ACh and bradykinin where it leads to vasodilation and inhibition of platelet aggregation

Front 21

NO also released by macrophages in response to

Back 21

to IFN-gamma, GM-CSF and TNF-alpha

Front 22

Nitric Oxide (NO) synthesized from L-arginine by

Back 22

nitric oxide synthase (NOS

Front 23

Pulmonary Hypertension of the Newborn (PPHN) is caused by the persistence of fetal circulation after birth with right to left
shunting of blood through fetal channels (foramen ovale and ductus ateriosus) secondary to elevated pulmonary vascular resistance and consequently reduction of pulmonary blood flow and can be treated with

Back 23

Inhaled Nitric Oxide

Front 24

Transmembrane protein expressed on monocytes and endothelial cells and it is the Main triggering element of the extrinsic clotting cascade after complex with factor VII

Back 24

Tissue Factor (TF)

Front 25

Proinflammtory; TF expression induced by

Back 25

endotoxin, TNF-alpha and IL-1

Front 26

Interleukin-1
primarily produced by

Back 26

monocytes and macrophages, though may be produced by nearly all nucleated cells

Front 27

IL-1alpha and IL-1beta produced

Back 27

increase local blood flow, production of other mediators, expression of adhesion molecules, growth factor secretetion, enzymes associated with matrix remodeling, loss of appetite, release of corticosteroids and fever

Front 28

Interleukin-4
produced by

Back 28

macrophages
Stimulate basophil development, eosinophil chemotaxis and granuloma formation (along with TNF-alpha and IFN-gamma)

Front 29

Interleukin-6
produced by

Back 29

T-lymphocytes, endothelial cells, monocytes and fibroblasts

Front 30

Interleukin-6 promotes

Back 30

monocyte differentiation and synthesis of acute phase reactants (fibrinogen) by the liver
promotes loss of appetite, release of corticosteroids and fever

Front 31

Interleukin-8
produced by

Back 31

monocytes, lymphocytes and neutrophils upon stimulation by IL-1 and TNF

Front 32

Interleukin-8 enhance

Back 32

PMN chemotaxis; limited effect on monocytes and eosinophils

Front 33

TNF is primarily produced by

Back 33

activated macrophages

Front 34

TNF- produces

Back 34

fever, promotes increased expression of other proinflammatory mediators, loss of appetite and corticosteroid release.
Promotes lipid and protein mobilization by appetite suppression (may lead to cachexia)
may induce apoptosis

Front 35

Interferon-
produced by

Back 35

by Tcells and NK cells
antiviral agent
increases superoxide formation by macrophages

Front 36

C1-INH Inactivates

Back 36

C1 by binding to active sites on C1r and C1s. Inhibits kallikrein, plasmin, factor XIa and factor XIIa

Front 37

Hereditary angioedema may result from decrease 80% of affected individuals have
decreased

Back 37

C1 inhibitor while the remaining 20%
have dysfunctional inhibitor; patients may suffer
from periodic attacks of life-threatening edema

Front 38

C4 binding protein (C4bp):

Back 38

-circulates complexed with protein S
-accelerates the decay of C4b2a complex

Front 39

Decay accelerating factor (DAF):

Back 39

-accelerates the decay of C3bBb and C4b2a
-expressed on a wide variety of cells

Front 40

Paroxysmal Nocturnal Hemoglobinuria

Back 40

Gene defects clustered around PIG-A
Near complete or complete absence of phosphatidylinositol-anchored proteins such as CD55 (DAF), CD59 and C8bp
Increased complement mediated lysis of RBCs