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Pathological Processes > 3. Acute Inflammation > Flashcards

3. Acute Inflammation Flashcards

1
Q

What is inflammation?

A

The response of living tissue to injury, initiated to limit the tissue damage

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2
Q

Name 5 causes of acute inflammation

A 
Microbial infections
Hypersensitivity reactions
Physical agents
Chemicals
Tissue necrosis
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3
Q

What are the 5 clinical features of acute inflammation?

A 
Rubor - redness
Tumour - swelling
Calor - heat
Dolor - pain
Loss of function
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4
Q

What changes happen to blood flow in acute inflammation?

A

Transient vasoconstriction of arterioles, then vasodilation of arterioles and then capillaries.
Increased permeability of blood vessels (exudation of protein-rich fluid into tissues and slowing of circulation (stasis)).

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5
Q

What is the earliest chemical mediator in inflammation?

A

Histamine

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6
Q

What cells is histamine released from?

A

Mast cells, basophils, platelets

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7
Q

What is histamine released in response to?

A

Physical damage, immunological reactions, C3a, C5a, IL-1, factors from neutrophils and platelets

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8
Q

What does histamine cause in acute inflammation?

A

Vascular dilation
Transient increase in vascular permeability
Pain

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9
Q

What causes oedema in acute inflammation?

A

Arterioles vasodilate, increased hydrostatic pressure in capillaries, and increased leakyness of venules due to chemical mediators.
Fluid containing plasma proteins moves out of vessels, increasing colloid osmotic pressure of interstitium, increasing flow out of vessel further.

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10
Q

What is the definition of oedema?

A

Excess of fluid in interstitium

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11
Q

What is transudate? What does it occur

A

Extravascular fluid with low protein content

Fluid loss due to hydrostatic pressure imbalance only

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12
Q

What is exudate? When does it occur?

A

Extravascular fluid with high protein content

Inflammation

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13
Q

What plasma protein avoids excessive blood loss in acute inflammation on serosal surfaces?

A

Fibrin - causes blood clotting and so keeps inflammation localised

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14
Q

What is the primary type of WBC involved in inflammation?

A

Neutrophils

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15
Q

How can neutrophils be identified on a histology slide?

A

Multiple nuclei

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16
Q

What are the 4 stages of infiltration of neutrophils? What happens in each stage?

A

Margination - stasis causes neutrophils to line up at edge of blood vessel along endothelium.
Rolling - roll along endothelium, sticking intermittently.
Adhesion - stick more avidly.
Emigration - through blood vessel wall via digestion of the vascular basement membrane by proteases (diapedesis).

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17
Q

What signals do neutrophils follow?

A

Chemotaxis

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18
Q

Give 4 examples of chemicals that neutrophils move towards

A

Endotoxins
Thrombin in blood clots
Complement especially C5a
Leukotriene B4, produced by leukocytes

19
Q

Name 2 opsonins that neutrophils attach to on targets for phagocytosis

A

IgG antibody - not present when a bacterium is encountered for the first time.
C3b fragment of complement - released when complement is activated.

20
Q

What happens if opsonins aren’t present?

A

Phagocyte (eg neutrophil) recognises microbial surface antigens

21
Q

What do the oxygen-dependant and oxygen-independant mechanism of killing in phagocytosis involve?

A

Oxygen-dependent - using oxygen derived free radicals

Oxygen-independent - using enzymes

22
Q

What do the inflammatory mediators histamine, prostaglandin, bradykinin and complement fragments cause in inflammation?

A 
Vasodilation
Increased vascular permeability
Chemotaxis
Phagocytosis
Pain
23
Q

How does exudation of fluid combat injury in inflammation?

A

Delivers plasma proteins (eg immunoglobulins, inflammatory mediators and fibrinogen) to area, dilutes toxins, increases lymphatic draining (delivering micro-organisms to phagocytes and antigens to the immune system)

24
Q

How does the infiltration of cells in inflammation combat injury?

A

Neutrophils remove pathogenic organisms and necrotic debris

25
Q

How does vasodilation combat injury in inflammation?

A

Increases delivery of cells, increases temperature

26
Q

How does pain and loss of function in inflammation combat injury?

A

Enforces rest, so reduced change of further traumatic damage

27
Q

Give 4 local complications of acute inflammation

A

Damage to normal tissue due to substances produced by neutrophils.
Obstruction of tubes eg bile duct due to swelling.
Loss of fluid eg burns.
Pain and loss of function.

28
Q

One systemic effect of acute inflammation is fever, what causes fever?

A

Pyrogenic cytokine production by macrophages eg IL-1

29
Q

What reduces fever? Why?

A

Aspirin as inhibits prostaglandin synthesis in the anterior hypothalamus.

30
Q

What happens in leukocytosis (a systemic effect of acute inflammation)?

A

Number of circulating leukocytes increases. Macrophages and lymphocytes produce colony-stimulating factors or more leukocytes released from the bone marrow.

31
Q

In what type of infection does the number of neutrophils increase?

A

Bacterial infections

32
Q

In what type of infection does the number of lymphocytes increase?

A

Viral

33
Q

What is the acute phase response (a systemic effect of acute inflammation) produced by?

A

Cytokines released during inflammation

34
Q

What is the acute phase response?

A

Change in the levels of some plasma proteins eg more fibrinogen and CRP (an opsonin) made, less albumin made

35
Q

Shock ism a systemic effect of acute inflammation, what is shock and what causes it?

A

Dramatic drop in BP. Bacterial or inflammatory mediators spread around the body in the blood stream, causing inflammation to occur throughout the body.

36
Q

What happens in resolution after acute inflammation?

A

Inflammation stops, as initial stimulus has been removed.
Exudate drains into lymphatic,
Fibrin is degraded.
Neutrophils apoptose and are phagocytosed.
Damaged tissue regenerates if some tissue architecture remains.

37
Q

Name 3 mechanisms of resolution after acute inflammation.

A

(Mediators of acute inflammation have short half lives.)
May be inactivated by degradation.
Inhibitors may bind.
May be diluted in exudate.

38
Q

What is pus/abscess?

A

Creamy/white exudate as is rich in neutrophils. Typical of infections by chemotactic bacteria.

39
Q

What is haemorrhagic exudate?

A

Inflammation where significant vascular damage has occurred. Contains lots of RBC’s. seen in destructive infections or where exudate is. Result of infiltration by a malignant tumour.

40
Q

What is serous exudate?

A

Contains plasma proteins but few neutrophils, so occur where no infection eg in a blister after a mild burn.

41
Q

What is a fibrinous exudate?

A

Exudate with significant fibrin deposition. When occurs in the pericardial or pleural spaces, serosal surfaces no longer slide smoothly over each other, this can be heard as a rubbing sound.

42
Q

Name 3 clinical examples of acute inflammation

A

Bacterial meningitis - cause vascular thrombosis, reduce cerebral perfusion and cause swelling in brain.
Lobar pneumonia - streptococcus pneumoniae, alveoli fill with exudate.
Liver abscess or acute appendicitis.

43
Q

What is an abscess?

A

Occurs in solid tissues, where inflammatory exudate forces the tissue apart, and liquefactive necrosis occurs in the centre. High pressure and so painful, cause tissue damage and squash adjacent structures.

44
Q

Give an example of a disorder of acute inflammation, and what causes it

A

Alpha1-antitrypsin deficiency.
Autosomal recessive.
Low levels of a1-antitrypsin, protease inhibitor that deactivates enzymes released from neutrophils at site of inflammation.
Develop emphysema, as proteases released by neutrophils within lungs act unchecked and destroy normal parenchyma tissue.
Liver disease as hepatocytes produce an abnormal version of the protein, which builds up in hepatocytes causing cirrhosis.

Pathological Processes (14 decks)

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