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Year 1- PoD > Acute inflammation 2 > Flashcards

Acute inflammation 2 Flashcards

1
Q

What is the suffix for inflammaiton?

A

-itis
e.g. meningitis (inflammation of meninges)
e.g. Appendicitis (inflammation of appendix)

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2
Q

Whats inflammation of lungs called?

A

Pneumonia

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3
Q

Whats inflammation of the pluera called?

A

Pleurisy

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4
Q

What is the function of a neutrophil?

A

They are mobile phagocytes

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5
Q

How do neutrophils move towards foreign antigens?

A

By chemotaxis

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6
Q

What do neutrophils use to digest ingested foreign particles?

A

Granules which contain oxidants & digestive enzymes (e.g. proteases)

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7
Q

What happens to neutrophils after they digest a foreign organism?

A

They die prodcuing pus made of fluid, cell parts & endogenous proteins.

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8
Q

What two plasma proteins are mainly involved in acute inflammation?

A

Fibrinogen
Immunoglobulins

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9
Q

What does Fibrinogen do?

A

Forms fibrin which clots around the area of inflammation, basically localising by blocking off the inflammatory process.

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10
Q

What do immunoglobulins do in acute inflammation?

A

Antibodies opsonize pathogens so phagocytes can more easily reconise/destroy them.
They also activate the complement system leading to lysis of pathogenic cells.

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11
Q

What are 3 locations/types of acute inflammatory mediators?

A
  • Molecuels on endothelial cell surface
  • Molecules in blood plasma
  • Molecules released from cells in infalmmatory tissue.
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12
Q

What 5 things do inflammatory mediators cause?

A

Vasodilation
Altered Vascular permeability
Chemotaxis
Neutrophil adhesion
Itch/Pain

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13
Q

What tye of inflammatory mediators cause neutrophil adhesion?

A

Cell surface mediators - Adhesion molecules
e.g. ICAM-1 helps in pavementing

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14
Q

What inflammatory mediator is released from Mast Cells?

A

Histamine

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15
Q

Why triggers histamine release?

A

IgE mediated reactions

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16
Q

What/how does histamine cause?

A

Vasodilation & increased vascular permability
Acts on H1 receptors on endothelial cells

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17
Q

Where is the inflammatory mediator 5-hydroxytryptamine made?

A

PLatelets

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18
Q

What is 5-hydroxytryptamine called?

A

Serotonin

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19
Q

What does serotonin cause & why?

A

Vasoconstriction to prevent leakage from a damaged vessel.

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20
Q

When is serotonin released? (5-hydroxytryptamine)

A

When platelets coagulate to reapir a damaged vessel (i.e. degranulate)

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21
Q

What are cytokines & chemokines?

A

Inflammatory Mediators
Small molecuels produced by endothelium ,macrophages & lymphocytes in response to inflammtory stimuli

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22
Q

Waht do cytokines & chemokines do?

A

Attract inflamatory cells and trigger action of some of them

23
Q

What are the 4 enzyme cascades that interact and make up plasma inflammatory mediators?

A

The blood coagulation pathway
Fibrinolysis
Kinin system
Complement Cascade

24
Q

What does the blood coagulation pathway do?

A

Forms fibrin from firbinogen & clots it around exudate to contain inflammation

25
Q

What does fibrinolysis do?

A

Breaks down fibrin clots to help maintain blood supply
Products of fibrin breakdwon are vasoactive (affect vessel diameter)

26
Q

Qhat are the conseueuncecs of the complement cascade?

A

Activated complement proteins can:
- Increase permeability
- Stimulate chemotaxis
- Phagocytose antigens
- cause cell lysis ofpathogens.

27
Q

What is pyrexia?

A

Endogenous pyogenes released from white cells
-> Cause raised temperature

28
Q

What is malaise?

A

General feelin of unwell

29
Q

What symptoms do children with inflmaation show specially?

A

Abdominal pain
vomiting

30
Q

Define Neutrophilia:

A

A high number of neutrophils in the blood
Bone marrow produces more white cells.

31
Q

What is suppuration?

A

An outcome of inflammation
Pus formation surrounded by a pyogenic membrane

32
Q

What is an abscess?

A

Suppuration under pressure, clumps in one spot then discharges (popping)
Single locale, if pus bursts pyogenic membrane becmes multiloculate

33
Q

What is it called when pus ends up int he bloodstream?

A

Pyaemia, when pus is in the blood

34
Q

What is empyema?

A

Pus ending up in a hollow viscus (hollow organ)
e.g. gall bladder or pleural cavity

35
Q

What is organisation?

A

Formation of granulation tissue followed by fibrosis forming a scar

36
Q

What makes up granulation tissue?

A

New capillaries
Fibroblasts & collagen
MAcrophages

37
Q

What is dissemination?

A

Spread of the acute inflammatory process to the blood i.e. pateint is septic

38
Q

Define bacteraemia:

A

Bacteria in blood
Often happens & ususally cleared harmlessly

39
Q

Define Septicaemia:

A

Bacteria growing in the blood

40
Q

Define Toxaemia:

A

Toxic products in the blood
e.g. lipopolysaccharides from gram negative bacteria

41
Q

Define Shock:

A

The inability to perfuse (deliver blood to capillary beds) tissues,

42
Q

What are the symptoms of early septic shock?

A
  • Peripheral Vasodilation
  • Tachycardia
  • Hypotension (Low BP)
  • Pyrexia (raised temp)
  • Sometimes haemorrhagic skin rash
43
Q

What does BP stand for?

A

Blood Pressure

44
Q

What does CO stand for & how is it calculated?

A

Cardiac Output
Stroke volume x Heart Rate

45
Q

What does SV stand for?

A

Stroke Volume

46
Q

What does HR stand for?

A

Heart Rate

47
Q

What is SVR & how is it calculated?

A

Systemic Vascular Resistance, the resistance to blood flow offered by systemic vasculature.
SVR = BP/CO

48
Q

What happens to Stroke volume during shock?

A

The stroke volume decreases during shock

49
Q

How is cardiac output maintained during shock?

A

By increasing heart rate to balance lost stroke volume (CO = SVxHR)

50
Q

How is pyrexia caused during septic shock?

A
  • Bacterial endotoxin released
    -> Interleukin-1 acts on hypothalamus
    -> raised temperature (pyrexia)
51
Q

How is haemorrhagic skin rash caused during septic shock?

A

Shock causes coagulation
-> fibrin breakdown releases vasoactive chemicals that cause vasodilation
-> Results in haemorrhagic rash

52
Q

What happnes when heart rate cant be increased enough to maintain cardiac output?

A

Blood pressure falls
(BP = CO x SVR)

53
Q

Whats the effect of falling blood pressure?

A

Reduced tissue perfusion
-> Tissue Hypoxia
-> Loss of tissue & organ function

54
Q

What is the outcome of septic shock?

A

Tissue hypoxia -> cell death
Resulting in haemorrhage & death.

Year 1- PoD (47 decks)

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