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Flashcards in Acute inflammation 2 Deck (32)
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1
Q

What are the immediate systemic effects of acute inflammation

A

Pyrexia
Nausea, feeling unwell etc
neutrophilia - raised WBC count

2
Q

What are the long term systemic effects of acute inflammation

A

lymphadenopathy - enlargement of lymph’s
Weight loss
anemia

3
Q

What are the five possible outcomes of acute inflammation

A
Resolution 
Suppuration 
Organisation 
Dissemination 
Chronic Inflammation
4
Q

What is the best possible outcome of acute inflammation

A

Resolution as inflammation is resolved and everything returns to normal

5
Q

What is Suppuration

A

Pus formation

6
Q

What is pus composed of

A

dead tissue, organisms, exudate, neutrophils, fibrin, red cells, debris

7
Q

What surrounds pus

A

Pyogenic membrane

8
Q

What causes an abscess

A

collection of pus under pressure

9
Q

What happens when multiloculated abscess is burst

A

pus bursts through pyogenic membrane and forms be cavity

10
Q

What happens when pus bursts through single locule

A

Pus bursts out and then collapses

11
Q

What is empyema

A

Pus in a hollow viscus

12
Q

What is pyaemia

A

Pus discharge into blood stream

13
Q

What is Organisation

A

Healing and repair of acute inflammation leading to fibrosis (scars)

14
Q

What tissue causes the formation of scars

A

granulation

15
Q

How is granulation tissue formed

A

New capillaries
Fibroblasts + collagen
Macrophages

16
Q

What is fibrosis

A

the thickening and scarring of connective tissue

17
Q

What is dissemination

A

Spread of acute inflammation to the bloodstream causing patient to become septic

18
Q

Define: Septicaemia

A

Growth of bacteria in the blood

19
Q

What are the clinical features of septic shock

A
peripheral vasodilatation
tachycardia - high heart rate
hypotension - low blood pressure
often pyrexia
sometimes haemorrhagic skin rash
20
Q

How does tacycardia occur in septic shock

A

Mediators enter plasma and cause vasodilation decreasing systemic vascular resistance, so stroke volume decreases therefore to maintain cardiac output heart rate must increases

21
Q

How is pyrexia caused in septic shock

A

By bacterial endotoxin acting on hypothalamus

22
Q

What happens when compensation fails in septic shock

A

The vascular resistance to low, BP falls and cardiac output cannot be maintained

23
Q

What is the result of septic shock

A

Tissue hypoxia (death)
Loss of organ function
Haemorrhage
Can be fatal

24
Q

What is mediators

A

important substances control the processes of acute inflammation

25
Q

Where can mediators be found

A

endothelial cells (lining the blood vessels)
Released from cells
Inacrive molecules in the plasma

26
Q

What are the effects of mediators

A
Vasodilation 
Increased permeability 
Cause adhesion of neutrophils 
chemotaxis 
itch and pain
27
Q

What is the two roles of plasma protein in inflammation

A

forms fibrin and clots exudate

immunoglobulins in plasma specific for antigen

28
Q

What do cell surface mediators do

A

Help neutrophils stick

29
Q

Give examples of molecules released as mediators

A
Histamine 
Serotonin (platelets) 
Cytokines 
Nitric oxide - smooth muscle relaxation 
oxygen free radicals
30
Q

Blood coagulating pathway which clots fibrinogen in exudate is in dynamic balance with what other pathway

A

Fibrinolysis

breaks down fibrin to helps maintain blood supply

31
Q

What does the kinin system do

A

trigger pain

32
Q

What does the complement cascade do

A

Increases permeability
Chemotaxis
phagocytosis
cell breakdown

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