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
What causes dolor?
Pain | Mediated by prostaglandins and bradykinin
26
What is the microscopic appearance of the neutrophil?
Moly lobed nucleus (polmorph) Granulocyte Phagocytic and cytotoxic abilities
27
What is the main cell of acute inflammation?
Neutrophil
28
What are the potential outcomes of acute inflammation?
Resolution Suppuration Repair, organisation and fibrosis Chronic inflammation
29
What factors can influence the outcome of acute inflammation?
Site of injury Type of injury Duration of injury
30
What is resolution?
Complete restoration of the tissue to normal after removal of inflammatory components
31
What factors are needed for resolution to occur?
Minimal cell death Tissue has capacity to repair Good vascular supply Injurious agent easily removed
32
What is suppuration?
Formation of pus
33
What is pus?
Contains living, dying and dead cells | Neutrophils, bacteria and inflammatory debris
34
Why is an abscess difficult to get rid of?
No blood supply reaches the middle, and so antibodies cannot get in
35
What is an empyema?
Walled off space filled with pus
36
What factors might result in organisation?
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
What is organisation?
Scarring
38
What is an ulcer?
Erosion beyond the basement membrane
39
What is granulation tissue?
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
What is the main problem with scarring and fibrosis?
Loss of function | e.g. heart muscle that won't contract, or tight skin
41
When might chronic inflammation be favoured?
Suppuration, empyema, scarring Persistence of injury - foreign material Infectious agent - virus, persistent (mycobacterium) Type fo injury - autoimmune, transplant injury
42
What cells characterise chronic inflammation?
Lymphocytes and macrophages
43
What might cause granuloma formation?
``` Foreign bodies = Endogenous (e.g. keratin) or exogenous (e.g. asbestos) Specific infections Parasites Worms, eggs Syphilis Mycobacterium ```
44
What is a granuloma?
Aggregate of epthelioid histiocytes
45
What granuloma is seen in TB?
Caseous necrosis