Exudate and leuk migration Flashcards

1
Q

Exudate fx

A

Dilute toxins
Distribute clotting factors and mediators around tissues
Distrib complement and Ab
Continuosly drained by lymphatics

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2
Q

Describe serous

A
Abundant
Watery
Clear/cloudy
Low pro and cell
Can coag at necropsy form loose jelly dep on fibrinogen content
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3
Q

Wear is serous found

A

Mild react involving serous mem synovial men and CT

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4
Q

Describe fibrinous

A

Abundant
Fibrinogen rich (most go to fibrin (can form yellow white elastic shaggy deposit))
Serous component w/in fibrin mesh pockets or accum as collections of clear yellow watery exudate

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5
Q

Where fibrinous found

A

More severe react involv serous mem CT alveoli

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6
Q

Describe catarrhal

A

Varies: Abundant cloudy thin mucinous to restricted thick sticky white mucinous
Large mucinous content
Rich in desquamated epi cells and neutrophils

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7
Q

Where cattarhal found

A

Assoc with inflam of muc mem of nasopharynx uterus airways mucous glands and lower alimentary tract

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8
Q

DescribeSuppurative/purulent

A

Opaque variable colour viscosity odour
Cont dead/dying neutr nevrotic tissue debris partly liquiefied
Breakdown products presenr eg fats soaps cholesterol
Colour dep onRBC presence and haemoglob breakdown and chomagenic bact pigments
Odour dep on breakdown products
Viscosity dep on DNA content

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9
Q

Where suppurative found

A
Usually localised (diffuse - cellulitis)
Assoc with pyogenic bact
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10
Q

Describe haemorrhagic and where found

A

Frank haemorr may occur and dom exudate appearance esp in organ rich in vascular supply
Esp if agent dam vessel walls and alter coag mech

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11
Q

How necrotising arise and where

A

Result of ischaemia after vasc spasm or thrombosis or of acute venous congestion and stasis post strangulation or thrombosis of venous return
Vasc crisis may result from combination with necrotising toxins

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12
Q

Cause of incr lymphatic flow

A

Distension if tissue space by exudate cause wall of lymphatics to open wide

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13
Q

Drainage interference of lymphatic cause

A

Severe react - fibrin coag in lymphatics

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14
Q

Result of incr lymph flow

A

Bact or agent can be circulated around the body and set up 2o infect site (maybe in lymphatic tissue) or spread further and reach blood. Lymphatic vessels can become inflamed themselves

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15
Q

2 stages of leuk migration

A

Neutro margination on changed vasc endo acoimpanied by slowing blood flow
Active emigration through gaps between endo cells through Bm perivasc sheath and into tissue spaces

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16
Q

Neutro arrest immediate pathway (mins)

A

Histamine PAF C5a cause rapid p selectin expr on endo cells which interact with rec on neutro
Cause tethering and rolling
Chemoattractants released cause neutro act and adhesive LFA-1 expr whih bind ICAM-1 on endo

17
Q

Monocyte adhesion

A

Express selectin rec
MCP-1 activate blood monocyte
LFA-1 bund ICAM-1!to mediate arrest

18
Q

Neutro arrest delayed pathway (2-8hr)

A

IL1 and TNF alpha cause E selectin expr by endo bund rec on neutro cause tether and roll
LTB4 and IL8 cause neutr to express LFA-1 which bind ICAM-1 mediate arrest

19
Q

Where is MCP-1 made

A

Synth and secr by resident macrophages at dam site

20
Q

Why monocyte adgesion slow

A

MCP-1 prod is slow

21
Q

Why neutro delayed pathway slow

A

All molecules in it need synthing

22
Q

Chemotactic and migration promoting factors for neutrophils

A

C3/5a PGE1/2 IL8 LTB4 bact products

23
Q

Req for neutro and mono phagocytosis (key inflam role)

A

Opsonins and suitable scaffolding to facilitate contact

24
Q

Neutro v mono

A

N: short lived end stage, no resynth lysosomal enz
M: long lived, resynth lys enz

25
Q

Macro role in acute inflam

A

Phagocyt by scavenger fc and complement rec
Secr toxic factors chemok and cytok to stim other effector cells
Secr colony stim factors