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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
What does fibrinolysis do?
Breaks down fibrin clots to help maintain blood supply Products of fibrin breakdwon are vasoactive (affect vessel diameter)
26
Qhat are the conseueuncecs of the complement cascade?
Activated complement proteins can: - Increase permeability - Stimulate chemotaxis - Phagocytose antigens - cause cell lysis ofpathogens.
27
What is pyrexia?
Endogenous pyogenes released from white cells -> Cause raised temperature
28
What is malaise?
General feelin of unwell
29
What symptoms do children with inflmaation show specially?
Abdominal pain vomiting
30
Define Neutrophilia:
A high number of neutrophils in the blood Bone marrow produces more white cells.
31
What is suppuration?
An outcome of inflammation Pus formation surrounded by a pyogenic membrane
32
What is an abscess?
Suppuration under pressure, clumps in one spot then discharges (popping) Single locale, if pus bursts pyogenic membrane becmes multiloculate
33
What is it called when pus ends up int he bloodstream?
Pyaemia, when pus is in the blood
34
What is empyema?
Pus ending up in a hollow viscus (hollow organ) e.g. gall bladder or pleural cavity
35
What is organisation?
Formation of granulation tissue followed by fibrosis forming a scar
36
What makes up granulation tissue?
New capillaries Fibroblasts & collagen MAcrophages
37
What is dissemination?
Spread of the acute inflammatory process to the blood i.e. pateint is septic
38
Define bacteraemia:
Bacteria in blood Often happens & ususally cleared harmlessly
39
Define Septicaemia:
Bacteria growing in the blood
40
Define Toxaemia:
Toxic products in the blood e.g. lipopolysaccharides from gram negative bacteria
41
Define Shock:
The inability to perfuse (deliver blood to capillary beds) tissues,
42
What are the symptoms of early septic shock?
- Peripheral Vasodilation - Tachycardia - Hypotension (Low BP) - Pyrexia (raised temp) - Sometimes haemorrhagic skin rash
43
What does BP stand for?
Blood Pressure
44
What does CO stand for & how is it calculated?
Cardiac Output Stroke volume x Heart Rate
45
What does SV stand for?
Stroke Volume
46
What does HR stand for?
Heart Rate
47
What is SVR & how is it calculated?
Systemic Vascular Resistance, the resistance to blood flow offered by systemic vasculature. SVR = BP/CO
48
What happens to Stroke volume during shock?
The stroke volume decreases during shock
49
How is cardiac output maintained during shock?
By increasing heart rate to balance lost stroke volume (CO = SVxHR)
50
How is pyrexia caused during septic shock?
- Bacterial endotoxin released -> Interleukin-1 acts on hypothalamus -> raised temperature (pyrexia)
51
How is haemorrhagic skin rash caused during septic shock?
Shock causes coagulation -> fibrin breakdown releases vasoactive chemicals that cause vasodilation -> Results in haemorrhagic rash
52
What happnes when heart rate cant be increased enough to maintain cardiac output?
Blood pressure falls (BP = CO x SVR)
53
Whats the effect of falling blood pressure?
Reduced tissue perfusion -> Tissue Hypoxia -> Loss of tissue & organ function
54
What is the outcome of septic shock?
Tissue hypoxia -> cell death Resulting in haemorrhage & death.

Year 1- PoD (47 decks)

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