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Foundations of Medicine > Acute Inflammation 2 > Flashcards

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
Q

<p>What releases oxygen free radicals?</p>

A

<p>Neutrophils on phagocytosis</p>

26
Q

<p>What do oxygen free radicals do?</p>

A

<p>Amplify other mediatory effects</p>

27
Q

<p>What are molecules released inside cells for?</p>

A

<p>Signilling</p>

28
Q

<p>What do are mediators released inside the cell?</p>

A

<p>Pathogen associated molecular pattern</p>

<p>Danger associated molecular pattern</p>

29
Q

<p>What do mediators released inside the cell do?</p>

A

<p>Activate inflammatory response</p>

30
Q

<p>What are the 4 purposes of plasma molecules?</p>

A

<p>Blood coagulation pathways</p>

<p>Fibrinolysis</p>

<p>Kinin system</p>

<p>Compliment cascade</p>

31
Q

<p>What are blood coagulation pathways?</p>

A

<p>Ones which clots fibrinogen in exudate</p>

32
Q

<p>What is fibrinolysis?</p>

A

<p>Break down of fibrin to help maintain blood supply</p>

33
Q

<p>What are fibrin breakdown products?</p>

A

<p>Vasoactive</p>

34
Q

<p>What does the kinin system do?</p>

A

<p>Bradykinin causes blood vessels to dilate</p>

35
Q

<p>What does the compliment cascade do?</p>

A

<p>Ties inflammaiton with the immune system</p>

<p>Active components stimulate increased permeability, chemotaxis, phagocytosis and cell breakdown</p>

36
Q

<p>What are the systematic effects of inflammation?</p>

A

<p>Pyrexia (raised temperature)</p>

<p>Feel unwell (malaise, anorexia, nausea, abdominal pain and vomiting)</p>

<p>Neutrophilia (raised white blood cellcount)</p>

37
Q

<p>What is pyrexia?</p>

A

<p>Raised temperature</p>

38
Q

<p>What could long term effects of inflammation be?</p>

A

<p>Lymphadenopathy (regional lymph node enlargement)</p>

<p>Weight loss</p>

<p>Anaemia</p>

39
Q

<p>What is pus surrounded by and what does this do?</p>

A

<p>Pyogenic membrane which contains it</p>

40
Q

<p>What is an abscess?</p>

A

<p>Collection of pus under pressure</p>

41
Q

<p>What happens if pus breaks through the pyogenic membrane?</p>

A

<p>New cavities can be formed</p>

42
Q

<p>What is an outcome of pus breaking through pyogenic membrane?</p>

A

<p>Formulation of granulation tissue which heals and leads to fibrosis and formation of a scar</p>

43
Q

<p>What can granulation tissue be described as?</p>

A

<p>A universal patch, a repair kit for all damage</p>

44
Q

<p>What does granulation tissue lead to the formation of?</p>

A

<p>New capillaries (angiogenesis)</p>

<p>Fibroblasts and collagen</p>

<p>Macrophages</p>

45
Q

<p>What may occur after acute inflammation?</p>

A

<p>Dissemation</p>

46
Q

<p>What are different kinds of dissemation after acute inflammation?</p>

A

<p>Patient septic (spreads to the bloodstream)</p>

<p>Bacteraemia (bacteria in blood)</p>

<p>Septicaemia (growth of bacteria in blood)</p>

<p>Toxaemia (toxic products in blood)</p>

47
Q

<p>What are some basic cardiovascular terms?</p>

A

<p>Blood pressure (BP)</p>

<p>Cardiac output (CO)</p>

<p>Stroke volume (SV)</p>

<p>Heart rate (HR)</p>

<p>Systematic vascular resistance (SVR)</p>

48
Q

<p>What is a formula that describes cardiac output?</p>

A

<p>CO = SV x HR</p>

49
Q

<p>What is a formula that describes blood pressure?</p>

A

<p>BP = CO x SVR</p>

50
Q

<p>What could systematic infection lead to?</p>

A

<p>Shock</p>

51
Q

<p>What is shock?</p>

A

<p>The inability to perfuse tissues (passage of fluid through the circulatory system)</p>

52
Q

<p>What are clinical symptoms of shock?</p>

A

<p>Peripheral vasodilation</p>

<p>Tachycardia (high heart rate)</p>

<p>Hypotension (low blood pressure)</p>

<p>Often pyrexia (raised body temperature)</p>

53
Q

<p>What is tachycardia?</p>

A

<p>High heart rate</p>

54
Q

<p>What is the pathogenesis of shock?</p>

A

<p>1) Systematic release of chemical mediators into plasma, causing vasodilation and loss of systematic vascular resistance</p>

<p>2) Increased heart rate to maintain cardiac output</p>

<p>3) Bacterial endotoxin is released which acts on hypthalamas and causes pyrexia</p>

<p>4) Activation of coagulation (liquid changes to solid state)</p>

<p>5) When increased heart rate cannot maintain cardiac output, blood pressure falls</p>

<p>6) Reduced perfusion of tissues which leads to loss of tissue and organ function</p>

55
Q

<p>What are the outcomes of shock?</p>

A

<p>Quickly fatal</p>

<p>Tissue hypoxia (cell death)</p>

<p>Haemorrhage</p>

56
Q

<p>What is a summary of acute inflammation outcomes?</p>

A

<p>Resolution</p>

<p>Suppuration</p>

<p>Organisation</p>

<p>Dissemation</p>

<p>Chronic inflammation</p>

Foundations of Medicine (167 decks)

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