Acute Inflammation Flashcards
(40 cards)
0
Q
What is acute inflammation’s primary role?
A
- Initiated to limit tissue damage
1
Q
What is the definition of acute inflammation?
A
- Response of living tissue to injury
2
Q
Want are the main features of acute inflammation?
A
- Innate
- Immediate
- Stereotyped (always the same response)
- Short duration (mins/hrs/days)
3
Q
How is acute inflammation controlled?
A
- Variety of chemical mediators derived from plasma cells
4
Q
What are the two main features of inflammation that would be seen on a histological slide?
A
- Exudate
- Neutrophils
5
Q
What are the main causes of acute inflammation?
A
- Microbial infections
- Hypersensitivity reactions
- Physical and chemical agents
- Tissue necrosis
6
Q
Why can’t we tell the cause by the response?
A
- Stereotyped, so all reactions are the same
7
Q
What are the main clinical signs of inflammation?
A
- Rubor: redness
- Tumor: swelling
- Calor: heat
- Dolor: pain
- (Loss of function)
8
Q
What are the main changes in tissues that are undergoing acute inflammation?
A
- Change in blood flow (more vasodilation hence redness)
- Exudation of fluid into tissues
- Infiltration of inflammatory cells
9
Q
Outline why there’s a change in blood flow during acute inflammation.
A
- Vasodilation of blood vessels hence heat and redness.
- Increased permeability of blood vessels:
Exudation of fluid into tissues
Slowing of circulation (swelling) - Conc of RBCs in small vessels and increase in viscosity of blood leading to stasis
10
Q
What are the characteristic of the chemical mediators used in acute inflammation?
A
- Immediate early response (½ hr)
- Histamine release in response to stimuli e.g physical damage
- Persistent response: many and varied mediators interlinked
11
Q
From what is histamine released and what does histamine cause?
A
- Released from: mast cells, basophils and platelets
- Causes: vascular dilation, increased vascular permeability, pain
12
Q
Why is pain caused?
A
- Possibly a response by the body to try and cause rest so no further damage is caused.
13
Q
What is Starling’s law?
A
- Fluid flow across vessel walls determined by hydrostatic and colloid osmotic pressure.
- Increased hydrostatic pressure -> increased fluid flow out of vessels
- Increased colloid osmotic pressure of interstitium -> increased fluid flow out of vessels.
14
Q
How do oedemas form due to acute inflammation?
A
- Arteriole dilation -> increased hydrostatic pressure -> increased permeability of vessel walls -> loss of protein into interstitium -> leakage -> oedema (excess fluid in interstitium)
15
Q
What is an exudate?
A
- High protein content fluid loss
16
Q
What is a transudate?
A
- Fluid loss due to hydrostatic pressure imbalance only
- Low protein content
17
Q
What are the different mechanisms for vascular leakage?
A
- Endothelial contraction leads to gaps
- Cytoskeletal reorganisation leads to gaps
- Direct injury
- Leukocyte dependent injury (toxic O2 species and enzymes from leukocytes)
- Increased transcytosis (channels across endothelial cytoplasm)
18
Q
What are neutrophils and what are they also known as?
A
- Primary type of WBC involved in inflammation
- Type of granulocyte
- Polymorphs
19
Q
How do neutrophils infiltrate the inflamed tissue?
A
- Stasis causes neutrophils to line up at edge of bv along endothelium, (MARGINATION)
- Neutrophils roll along endothelium sticking intermittently (ROLLING)
- Sticking more avidly (ADHESION)
- Followed by EMIGRATION of neutrophils through bv wall
20
Q
How does emigration occur?
A
- Relaxation of inter-endothelial cell junctions
- Digestion of vascular basement membrane
- Movement
21
Q
How do neutrophils move?
A
- Emigration and diapedesis (migration)
- Chemotoxis: movement along conc gradient of chemoattractants
- e.g of chemotoxins: C5a, LTB4, bacterial peptides
- Receptor-ligand binding
- Rearrangement of cytoskeleton
- Production of pseudopod (arms to engulf during phagocytosis)
22
Q
What is the main role of neutrophils?
A
- Phagocytosis
- Contact, recognition, internalisation
- (Phagosomes fuse with lysosomes to produce secondary lysosomes)
23
Q
What are the killing mechanisms for neutrophils?
A
- O2 dependent: Super oxide radicals, H2O2, HOCl
- O2 independent: Lysozyme and hydrolyases, bactericidal permeability increasing protein (BPI), cationic proteins (defensins)
24
What are the chemical mediators of acute inflammation?
```
- Proteases (plasma proteins produced in liver)
Kinins
Complement system
Coagulation
- Prostaglandins/Leukotrienes
Metabolites of arachidanic acid
- Cytokines (produced by WBC)
- Increased blood flow
- Vascular permeability
- Neutrophil chemotoxis
- Phagocytosis
```
25
What are the responses to a combat injury?
- Exudation of fluid
- Infiltration of cells (removes pathogenic organisms and necrotic debris)
- Vasodilation (increases delivery and temperature)
- Pain and loss of function
26
What is the role of exudation of fluid?
- Delivers plasma proteins to injury area
- Immunoglobulins
- Inflammatory mediators
- Fibrinogen
- Dilutes toxins
- Increases lymphatic drainage (delivers microorganisms to phagocytes and antigens)
27
Give examples of local complications of acute inflammation.
- Swelling: blockage of tubes (e.g. Bile duct/intestine)
- Exudate: compression, serositis
- Fluid loss: burns
- Pain and loss of function
28
What is serositis?
- Inflammation of serous tissue
| - E.g: pleura, pericardium
29
Give examples of systemic effects of acute inflammation
- Fever, endogenous pyrogens
- Leukocytosis
- Acute phase response
- Spread of microorganisms and toxins
- Shock (lack of O2 to major organs)
30
What is Leukocytosis?
- IL-1 and TNF alpha cause accelerated released of WBC from marrow
- Macrophages and T lymphocytes produced
- Can be due to bacterial infections
31
What is acute phase response?
- Change in plasma conc of acute phase proteins
| - Leukocytes/neutrophils produce more cytokines -> more phase proteins produced by the liver
32
What are the possible sequelae of acute inflammation?
- Complete resolution
- Continued acute inflammation leading to chronic and abscesses
- Chronic inflammation and fibrous repair -> scarring
- Death
33
What is the main mechanism of resolution?
- Morphology: changes gradually reverse
| - Vascular changes stop: neutrophils no longer marginate, vessel permeability and calibre returns to normal.
34
What are the changes that occur during recovery from inflammation?
- Exudate drains to lymphocytes
- Fibrin degraded by plasmin (proteases)
- Neutrophils die and break up - carried away/phagocytosed
- Damaged tissues MAY repair
35
How are acute inflammation mediators removed?
- Short half life
- May be inactivated by degeneration
- Instability
- Diluted in exudate
- Binding of inhibitors
36
What is lobar pneumonia?
- Strep. Pneumonia
- Alveoli filling with exudate not air
- Fever, hypoxanaemia, dry cough, breathlessness
37
How do skin blisters form?
- Causes: heat, sunlight, chemical
- Pain and profuse exudate
- Collection of fluid strips off epithelium
- Inflamed cells
- Resolution: scarring
38
What are abscesses?
- Solid tissues
- Inflamed exudate forces tissues apart
- Liquefactive necrosis in centre
- May cause high pressure leading to pain
- May cause tissue damage and squash adjacent structures
39
What are the symptoms of acute phase response?
- Decreased appetite
- Increased pulse rate
- Altered sleep patterns
