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MOD 2 > Session 2 (1) - Acute inflammation > Flashcards

Session 2 (1) - Acute inflammation Flashcards

1
Q

Define acute inflammation

A

Response of living tissue to injury initiated to limit tissue damage

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2
Q

In general, what occurs in acute inflammation?

A

Vascular and cellular reactions controlled by a variety of chemical mediators derived from plasma or cells. Protective function, but can lead to complications and systemic effects

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3
Q

What are five causes of acute inflammation?

A
  • Microbial infections e.g. pyogenic organisms
  • Hypersensitivity reactions
  • Physical agents e.g. heat and trauma
  • Chemicals
  • Tissue necrosis – elicits inflammatory reaction
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4
Q

What are the five macroscopic features of acute inflammation?

A
  • Rubor – redness
  • Tumor – swelling
  • Calor – heat
  • Dolor – pain
  • Loss of sensation
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5
Q

What are the three main tissue changes in acute inflammation?

A

Changes in blood flow (vasodilation)
Exudation of fluid into tissues (oedema)
Infiltration of inflammatory cells

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6
Q

What are the four microscopic features of acute inflammation?

A

Oedema
Vasodilation
Neutrophil margination and migration

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7
Q

What is the purpose of oedema in acute inflammation?

A

Delivers plasma proteins to point of inflammation (immunoglobulin, inflammatory mediators, fibrinogen (localizes inflammation due to sticky nature)
Dilutes toxins
Increases lymphatic drainage (delivers MO’s to phagocytes and antigens)

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8
Q

What is the purpose of vasodilation in acute inflmamation?

A

Increases delivery of antibodies, nutrients, oxygen and cells AND increases temperature

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9
Q

What is the purpose of neutrophil margination and emigration in acute inflammation?

A

Removes pathogenic organismsand necrotic debris

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10
Q

What is rubor a result of?

A

Vasodilation

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11
Q

What is tumour a result of?

A

Oedema/infiltration of neutrophils

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12
Q

What is calor due to?

A

Vasodilation

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13
Q

What is dolor caused by and why is it useul?

A

Chemical mediators such as bradykinin involved in pain mechanism.
Dolor is useful as it enforces rest and reduces chance of further traumatic damage.

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14
Q

What causes loss of sensation in actute inflammation?

A

Neurologic response to pain

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15
Q

What is oedema?

A

Excess fluid in intersitium, can be transudate or exudate.

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16
Q

What is exudate oedema?

A

Fluid loss in inflammation, high in protein

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17
Q

What are three chemical mediators involved in oedema formation in acute inflammation?

A

Histamine (transient), bradykinin (maintains permeability) and leukotrienes

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18
Q

What is histamine produced by and why?

A

Mast cells, basophils and platelets, in response to

  • physical damage
  • immunologic reactions
  • C3a, C5a and IL-1 factors from neutrophils and platelets
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19
Q

What does histamine do?

A

Causes vascular dilation, a transient increase in vascular permeability and pain

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20
Q

What response are histamines a part of?

A

The immediate early response

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21
Q

Give two chemical mediators involved in the persistent response

A

Leukotrienes and bradykinin

22
Q

How is oedema caused in acute inflammation?

A

Chemical mediators cause

  • Arteriolar dilation, which leads to increase in hydrostatic pressure
  • Increased permeability of vessel walls >loss of protein into interstitium > increased colloid osmotic potential of interstitium
  • Net flow of fluid out of vessel > oedema
23
Q

What are the three chemical mediators involved in vasodilation?

A

Histamines, prostaglandins, nitric oxide

24
Q

How does vasodilation take place? What are its two main effects?

A

Chemical mediators cause expansion of arterioles and then capilaries

Increase in blood flow to injured tissues
Increased transport of chemical mediators

25
Q

What is transudate oedema?

A

Fluid loss due to hydrostatic imbalance only, low protein content in fluid (found in cardiac failure of venous outflow obstruction)

26
Q

Give three mechanisms of vascular leakage

A

Endothelial contraction –> gaps (histamine, leukotrienes)

Cytoskeletal reorganisation –> gaps (cytokines IL-1 and TNF)

27
Q

What are the three chemical mediators involved in neutrophil margination and emigration?

A

C5a,leukotrieneB4 and bacterial products

28
Q

What are the five steps of neutrophil margination and emigration?

A

Increased concentration of RBCs in small vessels (due to vasodilation) leads to stasis - increased viscosity of blood

2) Stasis causes neutrophils to line up at the edge of blood vessels along endothelium (MARGINATION)
3) Neutrophils roll along endothelium, sitcking to it intermittently (rolling)
4) They stick more avidly (adhesion)
5) Neutrohphils EMIGRATE through the blood vessel wall into interstitium

29
Q

What does vasodilation allow?

A

Delivery of antibodies,nutrients and oxygen

30
Q

What does oedema cause?

A

Dilution of toxins, maintenance of temperature, stimulation of immuneresponse

31
Q

What are neutrophils and what do they do?

A

Primary type of white blood cell involved in inflammation.

Destroy and remove dead or foreign material

32
Q

How do neutrophils EMIGRATE?

A

Relaxation of interendothelial cell junctions
Digstion of vaascular basement membrane
Movement via chemotaxis (along concentrationgradient of chemoattractant)

33
Q

How do neutrophils perform phagocytocis?

A

Recognition is facilitated by opsonins

Phagosomes fuse with lysosomes to produce secondary lysosomes

34
Q

What are two killing mechanisms of polymorphs?

A

O2 dependent - superoxide and hydrogen peroxide produced
O2 independent
- lyzozyme and hydrolases
- Bacteriacidal Permeability Increasing Protein (BPI)
- Cationic Proteins (defensins)

35
Q

What are the the three systemic consequences of acute inflammation?

A

Fever, Leukocytosis, Acute phase response

36
Q

How is fever produced?

A

Endogenous pyrogens produced (IL-1 and TNF a) which act on thermoregulatroy centre in hypothalamus to raise core temperature > increases activity of immune response

37
Q

What is Leukocytosis and how is it caused?

A

IL-1 and TNF - a produce an accelerated release of WBC from marrow
- Macrophages and T lymphoctes produce CSF (colony stimulating factor)

38
Q

What is the acute phase response in acute inflammation?

A
  • Decreased appetite
  • Altered sleep patterns
  • Change in plasma concentrations of:
  • C-reactive protein - marker for inflammation
  • Fibrinogen
39
Q

How is acute inflamation resolved?

A

Exudate drainage to lymph system
Fibrin degraded by plasmin and other proteases
Neutropils die and are removed
Damaged tissue may be able to regenerate

40
Q

Give 6 possible complications of acute inflammation

A 
Swelling - Blockage of tubes
Exudate - Compression (cardiac tamponade)
Loss of fluids
Pain
Pyrexia
Shock (circulatory failure)
41
Q

Give three categories of chemical mediators

A

Proteases
Prostaglandins (metabolites of arachidonic acid)
Cytokines

42
Q

Give two chemicalmediators which increaseblood flow

A

Histamine

Prostaglandin

43
Q

Give two chemical mediators which increase vascular permeability

A

Histamin

Leukotrienes

44
Q

Give three chemical mediators which guide neutrophil chemotaxis

A

C5a, LTB4 and bacterial peptides

45
Q

Give one chemical mediator resonsible for phagocytosis

A

C3b

46
Q

What is a clinically useful acute phase protein?

A

C-reactive protein

47
Q

What are the four possible clinical sequlae of acute inflammation?

A

Complete resolution

Continued acute inflammation with chronic inflammation = abscess

Chronic inflammation and fibrous repair with tissue regeneration

Death

48
Q

What is Lobar Pneumonia?

A

Caused by streptococcus pneumoniae
Causes inflammation in lungs > alveoli contain exudate istead of air > hypoxaemia/ dry cough
Immune response > sudden improvement

49
Q

What is acute appendicitis?

A

Often triggered by faecolith which occludes blind ended tube
Swells due to infiltration of cells and exudate
Abcess forms, forces tissues apart, liquefactive necrosis occurs
Bacterial substance could leak out into abdominal cavity > peritonitis

50
Q

What is hereditary angioedema?

A

Autosoma dominant disorder of C1 inhibitor > uncontrolled activation of the classical complement pathway
Causes recurrent episodes of oedema of the skin, URT and GI tract
Increased levels of vasoactive mediators of anaphylaxis
May be mediated by such factors as minor trauma, suddent changes in temperature and emotional stress

51
Q

What can the spread of microorganisms and toxins cause in the body?

A

Shock, a clinical syndrome of circulatory failure

52
Q

Why is aspirin used as an anti inflammatory?

A

It is an anti-pyretic and analgesic which acts via the irreversible inhibition of of COX, an integral part of the prostaglandin system.

MOD 2 (16 decks)

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