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Principles > Pathology - Inflammation > Flashcards

Pathology - Inflammation Flashcards

1
Q

What are the four inflammatory responses to injury?

A

Vascular Changes
Cellular Changes
Chemical Mediators
Morphological Patterns

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2
Q

What vascular changes occur in response to injury?

A

Changes in flow and vessel calibre
Vasodilatation
First involves arterioles then capillary beds

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3
Q

What mediates vascular changes?

A

Histamine and nitric oxide

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4
Q

What is the result of vascular changes?

A 
Increased heat (calor) 
Redness/erythema (rubor)
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5
Q

What cellular changes occur in response to injury?

A 
Stasis 
White cell margination 
Rolling 
Adhesions 
Migration
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6
Q

What is white cell margination?

A

With vascular dilatation, blood flow slows down

Allows cells, especially large white cells, to move peripherally

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7
Q

What are selectins?

A

Expressed on endothelial cell surface

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8
Q

What are integrins?

A

Bind to vessels walls, cell matrix and other cells

Over 30 types

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9
Q

Why does rolling occur?

A

Integrin/selectin interaction with their ligands is of low affinity and binding on and off are fast

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10
Q

Which mediators increase selectin expression?

A

Histamine and thrombin from inflammatory cells

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11
Q

What mediators increase endothelial cell expression of VCAM and ICAM?

A

Tumour necrosis factor

Interleukin-1

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12
Q

What are VCAM and ICAM?

A

Vascular cell adhesion molecule

Intercellular adhesion molecule

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13
Q

What increases the affinity of VCAMs and ICAMs for integrins?

A

Proteoglycans on endothelial cell surface (only when bound to chemokines from site of injury)

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14
Q

What changes occur to vascular permeability?

A

Leaky vessels = loss of proteins
Change in osmotic pressure
Water follows protein = swelling (tumour)

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15
Q

Why do vessels become so leaky?

A

Endothelial contraction - Histamine, bradykinin, substance P, leukotrienes
Direct injury - toxins, burns
White cells - attack vessel wall (self harm)
Transcytosis - VEGF mediated
New verse formation - VEGF makes new vessels and increases leakiness

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16
Q

What is chemotaxis and which components act as “chemotaxis molecules”?

A 
Cells follow a chemical gradient and move along it 
Bacteria components 
Complement 
Leukotrienes 
Cytokines - interleukins
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17
Q

What are the three stages of phagocytosis?

A

Recognition and attachment
Engulfment
Killing and degradation

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18
Q

How does recognition and attachment occur?

A

Mannose receptors
Bacteria contain terminal mannose residues; mammalian cells do not

Scavenger receptors

Opsonins
Coated with proteins, including compliment cascade components and IgG

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19
Q

How does engulfment occur?

A

Pseudopods
Vesicle formation - phagosome
Joins with lysosome - phagolysosome

20
Q

How does killing and degradation occur?

A

Reactive oxygen species
NADPH oxidase

Reactive nitrogen species
Nitric oxide synthase

21
Q

What are the clinical features of acute inflmmation?

A 
Rubor
Calor 
Tumor 
Dolor
Loss of function
22
Q

What causes rubor?

A

Redness

Increased perfusion, slow flow, increased vessel permeability

23
Q

What causes calor?

A

Heat

Increased perfusion, slow flow rate, increased vessel permeability

24
Q

What causes tumor?

A

Swelling

Vascular changes

25
Q

What causes dolor?

A

Pain

Mediated by prostaglandins and bradykinin

26
Q

What is the microscopic appearance of the neutrophil?

A

Moly lobed nucleus (polmorph)
Granulocyte
Phagocytic and cytotoxic abilities

27
Q

What is the main cell of acute inflammation?

A

Neutrophil

28
Q

What are the potential outcomes of acute inflammation?

A

Resolution
Suppuration
Repair, organisation and fibrosis
Chronic inflammation

29
Q

What factors can influence the outcome of acute inflammation?

A

Site of injury
Type of injury
Duration of injury

30
Q

What is resolution?

A

Complete restoration of the tissue to normal after removal of inflammatory components

31
Q

What factors are needed for resolution to occur?

A

Minimal cell death
Tissue has capacity to repair
Good vascular supply
Injurious agent easily removed

32
Q

What is suppuration?

A

Formation of pus

33
Q

What is pus?

A

Contains living, dying and dead cells

Neutrophils, bacteria and inflammatory debris

34
Q

Why is an abscess difficult to get rid of?

A

No blood supply reaches the middle, and so antibodies cannot get in

35
Q

What is an empyema?

A

Walled off space filled with pus

36
Q

What factors might result in organisation?

A

Injury with lots of necrosis
Injury with lots of fibrin which isn’t easily cleared
Poor blood supply
Tissue type
Mucosa where damage goes beyond the basement membrane

37
Q

What is organisation?

A

Scarring

38
Q

What is an ulcer?

A

Erosion beyond the basement membrane

39
Q

What is granulation tissue?

A

Aids healing
Defect is slowly infiltrated by capillaries and then myofibroblasts
Deposit collagen and smooth muscle cells
Looks very red
Acts as a stop gap

40
Q

What is the main problem with scarring and fibrosis?

A

Loss of function

e.g. heart muscle that won’t contract, or tight skin

41
Q

When might chronic inflammation be favoured?

A

Suppuration, empyema, scarring
Persistence of injury - foreign material
Infectious agent - virus, persistent (mycobacterium)
Type fo injury - autoimmune, transplant injury

42
Q

What cells characterise chronic inflammation?

A

Lymphocytes and macrophages

43
Q

What might cause granuloma formation?

A 
Foreign bodies = Endogenous (e.g. keratin) or exogenous (e.g. asbestos) 
Specific infections
Parasites 
Worms, eggs 
Syphilis 
Mycobacterium
44
Q

What is a granuloma?

A

Aggregate of epthelioid histiocytes

45
Q

What granuloma is seen in TB?

A

Caseous necrosis

Principles (13 decks)

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