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Principles of disease > Acute Inflammation 2 > Flashcards

Acute Inflammation 2 Flashcards

1
Q

What is the name of inflammation at these various sites?
Peritoneal cavity
Meninges
Appendix
Lungs
Pleural cavity

A

Peritonitis
Meningitis
Appendicitis
Pneumonia
Pleurisy

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2
Q

What do neutrophils do?

A

Recognise foreign antigen
Move towards it - chemotaxis
Adhere to organism
Phagocytose and destroy foreign antigen (mobile phagocytes)

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3
Q

What do the granules possess

A

oxidants - H202 and enzymes (proteases)

(oxidants - reactive molecules)

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4
Q

When does a neutrophil die?

A

When granule contents are released

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5
Q

What is pus?

A

Produced by neutrophils - fluid mixture, bits of cells, organisms, endogenous proteins

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6
Q

What is fibrinogen?

A

Plasma protein - coagulating factor forming fibrin and clots exudate
Localises inflammatory process

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7
Q

What plasma protein is responsible for humoural immune response?

A

Immunoglobulins

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8
Q

What does humoural mean?

A

immune response involves release of antibodies in circulating bodily fluids

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9
Q

Where are the mediators of acute inflammations?

A

Molecules released from endothelial membrane
Molecules in plasma and cells

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10
Q

What are endothelial cells?

A

Line walls of blood vessels

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11
Q

What the collective effects of mediators?

A

Vasodilation
Increased permeability
Neutrophil adhesion
Chemotaxis
Itch and pain

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12
Q

Describe the action of adhesion molecules that appear on endothelial cells

A

Help neutrophils stick
ICAM-1 (intracellular adhesion molecule)

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13
Q

Describe the function of P-Selectin

A

Interacts with neutrophil surface

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14
Q

What releases histamine?

A

Mast cells beside vessels
platelets
basophils

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15
Q

When is histamine released?

A

result of local injury

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16
Q

What is the effect of histamine?

A

Vasodilation
increases permeability
Act on H1 receptors (histamine receptors) on endothelial cells

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17
Q

Where is seratonin released from?

A

Platelets - degranulate in coagulation
Vasoconstriction - keep useful materials in correct place

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18
Q

What are the immediate systemic effects of inflammation?

A

Pyrexia - increase body temp
Feel unwell - malaise, anorexia, nausea, abdominal pain, vomiting in chilrdren
Neutrophilia - raised WBC count

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19
Q

What are the long term effects of inflammation?

A

Lymphadenopathy - lymph node enlargements
Anaemia
Weight loss - catabolic process

20
Q

Describe suppuration

A

Pus formation
Pyogenic membrane surrounds pus (capillary sprouts neutrophils, fibroblasts - walls off pus)

(Forms small, raised, and red bumps on the skin)

21
Q

What is an abscess?

A

Collection of pus under pressure

22
Q

What is a multiloculated abscess?

A

Pus bursts through the pyogenic membrane - forms new cavities

23
Q

What is empyema

A
  • pus in hollow body cavities (gall bladder, pleural cavity)
24
Q

What is pyaemia

A

Discharge of pus to blood stream

25
Q

What is organisation?

A

Healing and repair - fibrosis and scar formation

Granulation tissue characteristic

26
Q

What is granulation tissue?

A

Universal patch

formed of new capillaries
Fibroblasts
Collagen
Macrophages

27
Q

Describe the outcome of dissemination

A

Spreads to bloodstream (patient is septic)

28
Q

What is the difference between bacteraemia and septicaemia?

A

Bacteraemia - bacteria in blood
Septicaemia - Growth of bacteria in blood

29
Q

What is toxaemia?

A

Toxic products in blood

30
Q

How do you calculate cardiac output?

A

Stroke volume x heart rate

(stroke volume = volume of blood pumped out left ventricle of heart during each systolic cardiac contraction)

31
Q

How can you calculate blood pressure?

A

Cardiac output x systemic vascular resistance

32
Q

Define SVR

A

amount of force exerted on circulating blood by the vasculature of the body

33
Q

What is the effect of systemic infection?

A

Shock - inability to perfuse tissue (supply with fluid)

34
Q

What is the clinical picture of early septic shock

A

Peripheral vasodilation
Tachycardia
Hypotension
Pyrexia
Haemorrhagic skin rash - blood vessels leaking

35
Q

What is the effect of bacterial endotoxin?

A

Pyrexia
Interleukin- 1 released
Acts on hypothalamus

36
Q

What is the effect of prostglandins? (archidonic acid metabolite)

A

Histamine effects and inhibit inflammatory cells

Thromboxan A2 - promotes platelet aggregation and vasoconstriction

37
Q

What is a leukotriene? (archidonic acid metabolite)

A

substance derived from leucocytes (WBCs)

38
Q

What is the effect of omega 3 polyunsaturated fatty acids?

A

Decrease synthesis of inflammatory mediators derived from arachidonic acid

39
Q

What is the function of platelet - activating factor?

A

Produced by mast cells and basophils
Lipid molecule responsible for platelet aggregation degranulation
Releasing factors - histamine and serotonin

40
Q

What are cytokines and chemokines?

A

Small molecules produced by macrophages, lymphocytes , endothelium in response to inflammatory stimuli

attract inflammatory cells

41
Q

What is the function of NO?

A

Released by various cells
Smooth muscle relaxation
Anti-platelet
Regulate functional activity
Growth/death of macrophages, T cells, APC, mast cells, neutrophils and NKC
Regulates leukocyte recruitment to inflammatory focus

42
Q

What are the effects of oxygen free radicals and what are their names?

A

H2O2, OH-, O2-

Released by neutrophils on phagocytosis

Amplify other mediator effects

43
Q

What are the different plasma enzymes involved?

A

Blood coagulation pathways - clotting fibrinogen in exudate
Fibrinolysis - breaks down fibrin maintaining blood supply, breakdown products are vasoactive
Kinin system - bradykinin responsible for pain
Complement cascade - Increase permeability, chemotaxis, phagocytosis, cell breakdown

44
Q

What is the pathogenesis of septic shock?

A

Release of chemical mediators from cells into plasma
Mediators cause vasodilation
Loss of SVR
Catecholamine (adrenaline and noradrenaline release)
Tachycardia - maintain cardiac output
Bacterial endotoxins released (interleukin- 1 - pyrexia)

45
Q

The increased heart rate is insufficient to maintain cardiac output during septic shock, what is the effect of this?

A

Bp drops due to reduced SVR

reduced perfusion of tissues, hypoxia and loss of cell, tissue, organ function

46
Q

What is the outcome of septic shock

A

Rapidly fatal
Tissue hypoxia
Haemorrhage
Requires immediate intervention and support

Principles of disease (47 decks)

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