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PRINCIPLES > Pathology- Inflammation > Flashcards

Pathology- Inflammation Flashcards

1
Q

What mediates vasodilation/ vasoconstriction?

A

Histamine and nitric oxide

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2
Q

Cellular change involves which 5 processes?

A 
Stasis
White cell margination
Rolling
Adhesions
Migration
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3
Q

what chemicals increase selectin expression?

A

histamine and thrombin

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4
Q

What cells increase V+ICAM expression?

A

TNF and IL-1

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5
Q

Where is selectin expressed?

A

on endothelial cells and white cells

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6
Q

Where do integrins bind to?

A

vessel walls, cell matrix, ICAM, VCAM

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7
Q

Rolling

A

integrin-selectin interaction with their ligands is low affinity therefore binding on and off is fast

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8
Q

Role of chemokines in response to injury

A

they bind to proteoglycans on endothelial cell surface, which increase the affinity of V+ICAMs for interns

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9
Q

How is swelling caused?

A

increased vascular permeability-> loss of proteins-> change in osmotic pressure-> water follows protein-> swelling

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10
Q

3 phases of phagocytosis

A
  • Recognition and attachment
  • Engulfment
  • Killing and degradation
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11
Q

Dolor

A

Pain

mediated by prostaglandins and bradykinin

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12
Q

Function laesa

A

loss of function

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13
Q

Main inflammatory cell in acute inflammation

A

neutrophil

  • many lobes, granulocytic and has phagocytic and cytotoxic abilities
  • mops up dead cells
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14
Q

Types of changes in acute inflammation

A

Vascular and cellular changes

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15
Q

Resolution

A

complete restoration of tissue to normal after inflammatory components are removed

minimal cell death

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16
Q

Why must there be a good vascular supply for resolution to occur

A

delivery of WBC and rapid removal of injurious agent

17
Q

Suppuration

A

Production and accumulation of purulent exudate (pus)

18
Q

What is pus comprised of?

A

living, dying and dead cells

neutrophils, bacteria, fibrin

19
Q

empyema

A

walled off space filled with pus

20
Q

Organisation

A

mucosa where damage goes beyond basement membrane

occurs if injury produces lots of necrosis, fibrin (that cant be cleared) and has a poor blood supply

21
Q

Granulation tissue formation

A

Defect slowly infiltrated by capillaries then myofibroblast-> collagen and smooth muscle cells accumulate-> redness

22
Q

Result of fibrosis

A

loss of function

23
Q

cirrhosis

A

scarring and fibrosis in liver

24
Q

cell which is characteristic of chronic inflammation

A

lymphocyte

small, round, blue cell

25
Q

Chronic inflammation

A

not related to time

occurs in cases of persistent injury/ infection

26
Q

This type of cell is granulated and an aggregate of epithelial histiocyte. It is involved in chronic inflammation.

A

Macrophage (type of monocyte)

27
Q

Examples of endogenous foreign bodies which cause granulomatous inflammation

A

keratin, bone, crystal

28
Q

Examples of exogenous foreign bodies which cause granulomatous inflammation

A

talc, asbestos, suture material, oil

29
Q

Examples of infections which cause granulomatous inflammation

A

parasites, worms, mycobacterium (eg TB), eggs, syphylis

30
Q

Changes within first 20 mins of MI

A

No macro/microscopic changes; there are changes on ECG

31
Q

First signs of cell death

A

pyknosis, erythema, nucleus shrinks and darkens, marginal contraction bands appear

32
Q

Changes within first 24hrs of MI

A

cell contents leak, complement cascade is initiated and acute inflammation occurs

wall of heart at its weakest, risk of cardiac rupture

33
Q

Changes within first 48hrs of MI

A

neutrophils are replaced by macrophages, changes seen at autopsy-> macrophages create yellow appearance

34
Q

Restitution

A

A gradual process in which progressive scarring occurs.

macrophages are replaced by fibroblasts over 6 weeks

35
Q

Role of fibroblasts

A

gradually lay down collagen from wks 2-6.

this is why after the 6 week mark, an MI cannot be dated

PRINCIPLES (21 decks)

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