Acute Inflammation 2 Flashcards

1
Q

What is inflammation named according to?

A

The anatomical location if occurs at

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2
Q

How is inflammation named?

A

‘Structure’-itis

Such as:
Peritonitis (perioneal cavity)
Meningitis (meninges)
Appendicitis (appendix)

Except for:
Lungs
Pleural cavity

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3
Q

What is inflammation of the lungs known as?

A

Pneumonia

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4
Q

What is inflammation of the pleural cavity known as?

A

Pleurisy

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5
Q

What is the process of neutrophils destroying pathogens?

A

1) Recognise foreign anitgens
2) Move towards it
3) Adhere to it
4) Release oxidants (such as hydrogen peroxide) and enzymes (such as proteases) and destroy the pathogen

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6
Q

What is the consequence of neutrophil action?

A

Once they die they release their granules, producing pus which might extend to other tissues and cause further inflammation

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7
Q

What is pus?

A

A soup of fluids, containing bits of cells, organisms and endogenous proteins

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8
Q

What are the main plasma proteins in inflammation?

A

Fibinogen

Immunoglobulin

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9
Q

What is the role of fibrinogen?

A

Forms fibrin and clots exudate (localising the process)

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10
Q

What is the role of immunoglobulins?

A

Specific for antigen, humoral immune response

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11
Q

What are mediators of acute inflammation?

A

Molecules on endothelial cell surface

Molecules released from cells

Molecules in the plasma

Molecules inside cells

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12
Q

What are the collective effect of mediators?

A

Vasodilation

Increased permeability

Neutrophil adhesion

Chemotaxis (movement of motile cell)

Itch and pain

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13
Q

What is chemotaxis?

A

Movement of motile cell

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14
Q

What helps neutrophils stick?

A

Cell surface mediator ICAM-1 which appears on endothelial cells

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15
Q

What are mediators released from cells?

A

Histamine

Serotonin

Prostglandins

Cytokines

Nitric oxide

Oxygen free radicals

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16
Q

What cells release histamine?

A

Mast cells

Platelets

Basophils

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17
Q

What does histamine cause?

A

Vasodilation

Increased permeability

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18
Q

What releases serotonin?

A

Plateletes

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19
Q

What does serotonin do?

A

Causes vasoconstriction

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20
Q

What do prostgandlins do?

A

Promote histamine effect

Inhibit inflammatory cells

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21
Q

What produces cytokines?

A

Macrophages

Lymphocytes

Endothelium

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22
Q

What effects do cytokines have?

A

Both pro and anti-inflammatory

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23
Q

What do cytokines do?

A

Stimulate extracellular pathways and signilling

24
Q

What does nitric acid do?

A

Smooth muscle relaxation

Anti-platelet

Regulate lymphocyte recruitment

25
What releases oxygen free radicals?
Neutrophils on phagocytosis
26
What do oxygen free radicals do?
Amplify other mediatory effects
27
What are molecules released inside cells for?
Signilling
28
What do are mediators released inside the cell?
Pathogen associated molecular pattern Danger associated molecular pattern
29
What do mediators released inside the cell do?
Activate inflammatory response
30
What are the 4 purposes of plasma molecules?
Blood coagulation pathways Fibrinolysis Kinin system Compliment cascade
31
What are blood coagulation pathways?
Ones which clots fibrinogen in exudate
32
What is fibrinolysis?
Break down of fibrin to help maintain blood supply
33
What are fibrin breakdown products?
Vasoactive
34
What does the kinin system do?
Bradykinin causes blood vessels to dilate
35
What does the compliment cascade do?
Ties inflammaiton with the immune system Active components stimulate increased permeability, chemotaxis, phagocytosis and cell breakdown
36
What are the systematic effects of inflammation?
Pyrexia (raised temperature) Feel unwell (malaise, anorexia, nausea, abdominal pain and vomiting) Neutrophilia (raised white blood cellcount)
37
What is pyrexia?
Raised temperature
38
What could long term effects of inflammation be?
Lymphadenopathy (regional lymph node enlargement) Weight loss Anaemia
39
What is pus surrounded by and what does this do?
Pyogenic membrane which contains it
40
What is an abscess?
Collection of pus under pressure
41
What happens if pus breaks through the pyogenic membrane?
New cavities can be formed
42
What is an outcome of pus breaking through pyogenic membrane?
Formulation of granulation tissue which heals and leads to fibrosis and formation of a scar
43
What can granulation tissue be described as?
A universal patch, a repair kit for all damage
44
What does granulation tissue lead to the formation of?
New capillaries (angiogenesis) Fibroblasts and collagen Macrophages
45
What may occur after acute inflammation?
Dissemation
46
What are different kinds of dissemation after acute inflammation?
Patient septic (spreads to the bloodstream) Bacteraemia (bacteria in blood) Septicaemia (growth of bacteria in blood) Toxaemia (toxic products in blood)
47
What are some basic cardiovascular terms?
Blood pressure (BP) Cardiac output (CO) Stroke volume (SV) Heart rate (HR) Systematic vascular resistance (SVR)
48
49
What is a formula that describes cardiac output?
CO = SV x HR
50
What is a formula that describes blood pressure?
BP = CO x SVR
51
What could systematic infection lead to?
Shock
52
What is shock?
The inability to perfuse tissues (passage of fluid through the circulatory system)
53
What are clinical symptoms of shock?
Peripheral vasodilation Tachycardia (high heart rate) Hypotension (low blood pressure) Often pyrexia (raised body temperature)
54
What is tachycardia?
High heart rate
55
What is the pathogenesis of shock?
1) Systematic release of chemical mediators into plasma, causing vasodilation and loss of systematic vascular resistance 2) Increased heart rate to maintain cardiac output 3) Bacterial endotoxin is released which acts on hypthalamas and causes pyrexia 4) Activation of coagulation (liquid changes to solid state) 5) When increased heart rate cannot maintain cardiac output, blood pressure falls 6) Reduced perfusion of tissues which leads to loss of tissue and organ function
56
What are the outcomes of shock?
Quickly fatal Tissue hypoxia (cell death) Haemorrhage
57
What is a summary of acute inflammation outcomes?
Resolution Suppuration Organisation Dissemation Chronic inflammation