Acute Inflammation 2 Flashcards

1
Q

<p>What is inflammation named according to?</p>

A

<p>The anatomical location if occurs at</p>

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2
Q

<p>How is inflammation named?</p>

A

<p>'Structure'-itis</p>

<p>Such as:<br></br>Peritonitis (perioneal cavity)<br></br>Meningitis (meninges)<br></br>Appendicitis (appendix)</p>

<p></p>

<p>Except for:<br></br>Lungs<br></br>Pleural cavity</p>

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3
Q

<p>What is inflammation of the lungs known as?</p>

A

<p>Pneumonia</p>

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4
Q

<p>What is inflammation of the pleural cavity known as?</p>

A

<p>Pleurisy</p>

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5
Q

<p>What is the process of neutrophils destroying pathogens?</p>

A

<p>1) Recognise foreign anitgens</p>

<p>2) Move towards it</p>

<p>3) Adhere to it</p>

<p>4) Release oxidants (such as hydrogen peroxide) and enzymes (such as proteases) and destroy the pathogen</p>

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6
Q

<p>What is the consequence of neutrophil action?</p>

A

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

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7
Q

<p>What is pus?</p>

A

<p>A soup of fluids, containing bits of cells, organisms and endogenous proteins</p>

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8
Q

<p>What are the main plasma proteins in inflammation?</p>

A

<p>Fibinogen</p>

<p>Immunoglobulin</p>

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9
Q

<p>What is the role of fibrinogen?</p>

A

<p>Forms fibrin and clots exudate (localising the process)</p>

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10
Q

<p>What is the role of immunoglobulins?</p>

A

<p>Specific for antigen, humoral immune response</p>

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11
Q

<p>What are mediators of acute inflammation?</p>

A

<p>Molecules on endothelial cell surface</p>

<p>Molecules released from cells</p>

<p>Molecules in the plasma</p>

<p>Molecules inside cells</p>

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12
Q

<p>What are the collective effect of mediators?</p>

A

<p>Vasodilation</p>

<p>Increased permeability</p>

<p>Neutrophil adhesion</p>

<p>Chemotaxis (movement of motile cell)</p>

<p>Itch and pain</p>

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13
Q

<p>What is chemotaxis?</p>

A

<p>Movement of motile cell</p>

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14
Q

<p>What helps neutrophils stick?</p>

A

<p>Cell surface mediator ICAM-1 which appears on endothelial cells</p>

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15
Q

<p>What are mediators released from cells?</p>

A

<p>Histamine</p>

<p>Serotonin</p>

<p>Prostglandins</p>

<p>Cytokines</p>

<p>Nitric oxide</p>

<p>Oxygen free radicals</p>

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16
Q

<p>What cells release histamine?</p>

A

<p>Mast cells</p>

<p>Platelets</p>

<p>Basophils</p>

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17
Q

<p>What does histamine cause?</p>

A

<p>Vasodilation</p>

<p>Increased permeability</p>

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18
Q

<p>What releases serotonin?</p>

A

<p>Plateletes</p>

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19
Q

<p>What does serotonin do?</p>

A

<p>Causes vasoconstriction</p>

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20
Q

<p>What do prostgandlins do?</p>

A

<p>Promote histamine effect</p>

<p>Inhibit inflammatory cells</p>

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21
Q

<p>What produces cytokines?</p>

A

<p>Macrophages</p>

<p>Lymphocytes</p>

<p>Endothelium</p>

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22
Q

<p>What effects do cytokines have?</p>

A

<p>Both pro and anti-inflammatory</p>

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23
Q

<p>What do cytokines do?</p>

A

<p>Stimulate extracellular pathways and signilling</p>

24
Q

<p>What does nitric acid do?</p>

A

<p>Smooth muscle relaxation</p>

<p>Anti-platelet</p>

<p>Regulate lymphocyte recruitment</p>

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

What is a formula that describes cardiac output?

CO = SV x HR

49

What is a formula that describes blood pressure?

BP = CO x SVR

50

What could systematic infection lead to?

Shock

51

What is shock?

The inability to perfuse tissues (passage of fluid through the circulatory system)

52

What are clinical symptoms of shock?

Peripheral vasodilation

Tachycardia (high heart rate)

Hypotension (low blood pressure)

Often pyrexia (raised body temperature)

53

What is tachycardia?

High heart rate

54

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

55

What are the outcomes of shock?

Quickly fatal

Tissue hypoxia (cell death)

Haemorrhage

56

What is a summary of acute inflammation outcomes?

Resolution

Suppuration

Organisation

Dissemation

Chronic inflammation