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Foundation of Medicine > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

Define acute inflammation

A

Immediate & early response to injury (transient- last short time)

To deliver leukocytes to site of injury

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2
Q

What is ‘itis’ vs ‘osis’ at the end of conditions

A

itis= Inflammation of
osis= Is a disease/condition

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3
Q

What are the 5 causes of inflammation

A

Infections
Hypersensitivity reactions
Physical agents e.g. trauma
Necrosis
Chemicals

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4
Q

What are bacterial exotoxins

A

Chemical released by bacteria stimulating inflammation

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5
Q

What are bacterial endotoxins

A

Associated in cell walls which get released and stimulate inflammation

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6
Q

What is hypersensitivity

A

Excess immune response due to altered immunological state

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7
Q

How does physical agents and chemicals cause inflammation

A

Tissue damage provokes inflammatory response

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8
Q

How does tissue necrosis trigger inflammation

A

Dead tissue releases peptides which trigger inflammatory response

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9
Q

What are the Cardinal signs of acute inflammation (diagnostic features)

A

Redness(rubor)
Heat (calor)
Swelling (tumour)
Pain (dolar)
Loss of function (functio laesa)

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10
Q

What is redness and heat caused by in inflammation

A

Dilation of blood vessels leading to increased blood flow and increased vessel permeability

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11
Q

What causes pain in inflammation

A

Distortion of tissue and release of chemical mediators-
Prostaglandins & Bradykinins

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12
Q

What is swelling caused by in inflammation

A

Accumulation of fluid & increased inflammatory cells migrating to the area

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13
Q

What are the 6 stages of inflammation

A
  1. Chemical mediator release
  2. Vasodilation
  3. Increased vascular permeability
  4. Fluid accumulation
  5. Cellular recruitment (neutrophils)
  6. Phagocytosis
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14
Q

What are the 2 major components of early inflammation

A

Vascular changes (change in vessel calibre)
Cellular events (forms cellular exudate)

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15
Q

How does the vascular calibre change in acute inflammation

A

initial transient constriction then vasodilation occurs

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16
Q

What is exudation

A

Vascular permeability increases which increases net flow of fluid out of the vessels

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17
Q

What processes are involved in forming cellular exudate

A

Margination
Adhesion
Emigration

To accumulate neutrophil polymorphs

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18
Q

What is margination

A

Neutrophils marginate out by inflammation site losing intravascular fluid to slow flow of blood to site

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19
Q

What is adhesion

A

Neutrophils adhere to vascular endothelium
-interaction between paired adhesion molecules on neutrophils and endothelial surface

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20
Q

What is emigration

A

Neutrophils pass between endothelial cells through basil lamina and into the adventitia

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21
Q

What are the components of cellular exudate

A

Cells (endothelial & inflammatory)
Chemical agents (Cytokines, complements, histamine & prostaglandins)

22
Q

What are the early chemical mediators of inflammation

A

Histamine & Thrombin & Neutrophils

23
Q

What chemical mediators of inflammation are released by cells

A

Histamine
Lysosomal compounds
Leukotrienes
Prostaglandins
Serotonin
Chemokines

24
Q

What does histamine cause

A

Vascular dilation and increased permeability

(Released by mast cells)

25
Q

What do lysosomal compounds cause

A

Increasing vascular permeability and stimulated histamine release from mast cells

(released by neutrophils)

26
Q

What do leukotrienes cause

A

Vasoactive properties

(made in neutrophils)

27
Q

What do prostaglandins do

A

Increase vascular permeability and cause platelet aggregation

28
Q

What does serotonin do

A

Vasoconstrictor

(released by platelets)

29
Q

What do chemokines do

A

Attract more WBC to site of infection
-Common one is Il-8 which attracts neutrophils

30
Q

What are the enzyme cascade systems in plasma

A

Coagulation system
Kinins
Fibrinolytic system
Complement System

31
Q

What are some Inflammation benefits

A

Entry of antibodies
Dilution of toxins
Drug transport
Stimulates immune response

32
Q

What are harmful effects of inflammation

A

Digestion of normal tissue

Swelling can compromise airways and cause brain damage

Can cause anaphylaxis if
inappropriate

33
Q

What are systematic manifestations of acute inflammation

A

Fever
Malaise
Loss of appetite
Nausea

34
Q

What are outcomes of acute inflammation

A

Resolution
Suppuration
Scarring/fibrosis
Chronic inflammation

35
Q

What is resolution of acute inflammation

A

Everything goes back to normal with mininal tissue damage and good vascular drainage to remove fluid & debris

36
Q

What is suppuration

A

The formation of pus

-Mixture of neutrophils (dead & alive), debris & bacteria

-Walled off pus forma and abcess

37
Q

What causes scarring/fibrosis

A

New capillaries lead to more macrophages proliferating more fibroblasts

38
Q

What types of skin healing are there

A

By primary intention
By secondary intention

39
Q

What is healing by primary intention

A

2 edges of wound brought together an fibrin joins weakly at edges

-Over time epidermal re-growth and collagen synthesis makes stronger join

40
Q

What is healing by secondary intention

A

Tissue defect filled by granulation tissue and epithelial re-growth occurs over surface

-Fibrous scar forms contracting over time

41
Q

How does acute inflammation progress to chronic

A

If causative agent is not removed, cellular exudate changes lymphocytes, plasma cells and macrophages replace neutrophils

42
Q

What are macroscopic signs of chronic inflammation

A

Chronic ulcer
Chronic abscess cavity
Fibrosis/tissue thickening

43
Q

what do the cells of chronic inflammation look like

A

Lymphocytes- Small circular purple dots
Plasma cells- fried eggs
Macrophages- Big and blobby
Eosinophils- Tomato with sunglasses

44
Q

What do lymphocytes do in chronic inflammation

A

B- turn into plasma cells then produce antibodies

T - Killer T cells (CD8+) – cytotoxic function. Helper T cells (CD4+) – Activate killer T and plasma cells

45
Q

What are macrophages good at

A

Eating things i.e. phagocytosis
-Not killed in the process like neutrophils

Produce cytokines

46
Q

what do cytokines do in chronic inflammation

A

Small proteins which enhance cell mediated immunity and antibody response - cell signalling and promote apoptosis

47
Q

What is a granuloma

A

Collection of histocytes
-stationary phagocytic cell present inconnectivetissue

48
Q

what are giant cells

A

Macrophages collide (potentially when both trying to eat same particle) producing huge multi-nucleated cells

49
Q

What 3 types of giant cells are there

A

Foreign body type
Langhans
Touton type

50
Q

What are foreign body type giant cells

A

Have random nuclei scattering

51
Q

What are Langhans giant cells

A

Has a horseshoe nucleus often seen in TB

52
Q

What are touton type giant cells

A

Lipid breakdown with neat circle of cells

Foundation of Medicine (23 decks)

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