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ZGoljan Pathology > Ch3 Acute Inflammation EC > Flashcards

Ch3 Acute Inflammation EC Flashcards

1
Q

What are the cardinal signs of acute inflammation? What are their mediators?

A

Rubor/Calor - Histamine mediated vasodilation of arterioles
Tumor - Histamine mediated increase in venular permeability (contract endothelial cells)
Dolor - PGE2/Bradykinin
Functio laesa (loss of function)

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2
Q

Is edema fluid an exudate or a transudate?

A

Transudate (low protein and cell levels)

moves across intact BM

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3
Q

What is margination and what its mechanism?

A

PMNs pushed to periphery
~liver releases fibrinogen
~RBCs form rouleaux
~forces PMNs into periphery

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4
Q

Describe the rolling of PMNs

A

Occurs in venules
L-selectin on PMNs binds E&P selectins on endothelial cells
IL-1 and TNF stimulate expression of selectins

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5
Q

L-selectin

A

selectin ligand on Leukocytes (rolling)

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6
Q

E-selectin and P-selectin

A

selectins on endothelial cells (rolling)

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7
Q

Weibel-Palade bodies

A

“glue factory” in endothelial cells
~P-selectin
~vWF
~platelet adhesion molecules

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8
Q

Describe firm adhesion in PMN extravasation

A

Beta2 integrin activated by C5a and LTB4

Activation of ICAM by IL-1 and TNF

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9
Q

What substances inhibit activation of Beta-2 integrins?

A

Corticosteroids and Catecholamines

Reason PMN levels increase w/ corticosteroids and during MI - all in blood because they can’t stick

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10
Q

What substances increase activation of Beta-2 integrins?

A

Endotoxins

causes circulating PMN level to decrease

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11
Q

Delayed separation of umbilical cord

A

Leukocyte adhesion defect due to selectin deficiency

also see severe gingivitis, poor wound healing, peripheral blood leukocytosis

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12
Q

Transmigration

A

Movement of PMNs from venules into interstitial space (via type IV collagenase and binding of PECAM-1)

Formation of pus (dilutes toxins and provides opsonins)

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13
Q

Chemotactic mediators

A

C5a
IL-8
LTB4
Kallikrein

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14
Q

Opsonins

A

IgG and C3b

Enhance PMN ability to ingest bacteria

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15
Q

Bruton agammaglobinemia

A 
Opsonization defect (lack of IgG) 
Cannot mature B cells
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16
Q

Describe neutrophil ingestion

A

Engulf bacteria in phagosomes

Lysosomes combine and empty hydrolytic enzymes (forming phagolysosome)

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17
Q

Chediak-Higashi syndrome

A

Cannot form phagolysosomes due to a defect in microtubule function

18
Q

What cells contain the MPO system?

A

PMNs and monocytes (NOT macrophages)

19
Q

NADPH oxidase complex

A

Converts O2 to superoxide

20
Q

SOD

A

Converts superoxide to H2O2

21
Q

MPO system

A

Combines H2O2 with Cl to make COCl

22
Q

Chronic Granulomatous Disease

A 
XR mutation in CYBB 
Defective NADPH oxidase
Absent respiratory burst
MPO present
Susceptible to Cat+ infections (others can be killed because they supply the H2O2 for MPO to generate HOCl)

Pneumonia, Skin, Visceral organs, and Bones

NBT dye test (turns blue if superoxide present)
Oxidation of dihydrorhodamine to fluorescent rhodamine used more commonly now

23
Q

Myeloperoxidase deficiency

A

Superoxide and H2O2 are produced (normal respiratory burst)

Can’t make HOCl

24
Q

G6PD deficiency

A

Lack of NADPH interferes with normal function of O2 dependent MPO system

25
Q

Lactoferrin

A

(Oxygen independent killing)
Binds Fe that is necessary for normal bacterial growth and production

lactoFERRIN

26
Q

Major Basic Protein

A

(oxygen independent killing)

Eosinophil product that is cytotoxic to helminths

27
Q

Prostaglandins source and function

A

Source: Macrophages, endothelial cells, platelets, (PGH2 major precursor of PGs and thromboxanes)

PGE2: Vasodilation, pain, fever

PGI2: Vasodilation, inhibition of platelet aggregation

28
Q

Thromboxane A2 source and function

A

Platelets (converted from PGH2 by thromboxane synthase)

Vasoconstriction, platelet aggregation

29
Q

Leukotrienes source and function

A

Leukocytes

LTB4 chemotaxis and activation of adhesion molecules
LTC4/LTD4/LTE4 vasoconstriction, increased venule permeability, bronchoconstriction

Zileuton inhibits 5-lipoxygenase

Montelukast is a LTE receptor antagonist

30
Q

Bradykinin source and function

A

Product of kinin system activated by factor XII

Vasodilation, increased venular permeability, pain

31
Q

Chemokines source and function

A

Leukocytosis, endothelial cells

Activate PMNs and stimulate migration

32
Q

C3a/C5a

A

Stimulate mast cell release of histamine

C5a also activation of adhesion molecules/chemotaxis

33
Q

C3b

A

Opsonization

34
Q

C5-C9

A

MAC and cell lysis

35
Q

IL-1, TNF source and function

A

Macrophages

Initiates PGE2 synthesis in anterior hypothalamus leading to fever
Activates adhesion molecules/chemotaxis

TNF promotes apoptosis

36
Q

IL-6 function

A

Increases liver synthesis of acute phase reactants

37
Q

IL-8 function

A

Chemotaxis

38
Q

Histamine source and function

A

Mast cells

Vasodilation, increased venular permeability

39
Q

NO source and function

A

Endothelial cells, macrophages

Vasodilation, bactericidal

40
Q

Why is fever beneficial in acute infection?

A

Right shifts OBC enhances delivery of O2 for killing

Decreases viral replication also

41
Q

Lipoxins

A

Resolution of acute inflammation

inhibit chemotaxis and promote apoptosis

42
Q

Resolvins

A

Resolution of acute inflammation

Inhibit recruitment of inflammatory cells

ZGoljan Pathology (9 decks)

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