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Flashcards in Inflammation Deck (88):
1

What is the main purpose of acute inflammation

- Protect homeostasis
- Response to injury

2

What are the 5 cardinal signs of acute inflammation?

Rubor - redness
Calor - temperature
Tumor - swelling
Dolor - pain
Loss of function

3

What are the possible causes of acute inflammation?

Biological (eg microorganisms)
Chemical (acids, alkali, urine, bile)
Physical (extreme cold/heat)
Mechanical (trauma, surgery)
Dead tissue (necrosis irrititates nearby tissue)
Hypersensitivity (reactions)

4

Where does acute inflammation occur?

Localised to affected area, occurs in capillary bed and surrounding ECF

5

What is the pathogenesis of acute inflammation?

1. Increased vessel radius - increased blood flow
2. Increased vessel permeability - increased exudate (protein leakage)
3. Neutrophil migration (through vessel and out)

6

Why does increased vessel radius cause increased flow in acute inflammation?

Increased vessel radius (dilatation, smooth muscle relaxed) --> Pouseuille's Law: 2x radius increase, x16 increase in flow

7

What type of leaking occurs in acute inflammation?

Exudation (high protein content)

8

What is found in the plasma exudate in acute inflammation?

Proteins, immunoglobulins (antibodies) and fibrinogen (clotting factor)

9

What happens as a result of increased vessel permeability?

- Exudative process (oedema)
- Increased viscosity and slower flow (stasis)

10

What is the sequence of events in exudate formation?

Normally neutrophils are in middle of lumen (surrounded by RBC)
During acute inflammation:
- Margination (neutrophils pushed towards vessel wall
- Pavementation (neutrophils adhere to endothelium)
- Emigration (neutrophils push out through vessel wall)

11

What are the benefits of acute inflammation?

- rapid response to non-specific injury
- neutrophil action: denature antigens/destroy organisms
- cardinal signs: short term tissue protection
- plasma proteins localise inflammation
- resolution of inflammation

12

What is the sequence of microvascular changes in acute inflammation?

- Increased radius (increased flow)
- Increased permeability (exudate)
- Neutrophil migration out of vessel

13

What is the role of neutrophils in acute inflammation?

To phagocytose and destroy foreign organisms
To denature antigens

14

How do neutrophils kill foreign antigens?

Phagocytosis - Release of granules (enzymes and oxygen free radicals) - digestion of foreign antigen

15

What is the fate of activated neutrophils?

Neutrophils die after having released their granules to digest foreign antigen

16

What is the role of plasma proteins in acute inflammation?

Fibrinogen - clotting factor: localises inflammation by walling off the area through production fibrin clots and stopping pus from leaking out of inflamed area
Immunoglobulins - trigger humoral immune response, antigen specific

17

Give examples of some acute inflammation mediators

Histamine, serotonin (5HT), prostaglandins and leukotrienes, NO, Platelet-activating factors (PAF), Reactive Oxygen Species (ROS)

18

What is the role of acute inflammation mediators broadly speaking?

- Produced by a number of cells
- Pro or anti inflammatory properties
- Vasoconstriction, vasodilatation, vessel permeability
- Histamine agonists or antagonists
- Some derived from arachidonic acid (leukotrienes and prostaglandins
- Some derived from platelets (serotonin)

19

Give examples of mediators derived from arachidonic acid

Leukotrienes and prostaglandins

20

Where is histamine produced?

In mast cells

21

What mediator can stop leukotrienes and prostaglandins from being formed?

Omega 3 fatty acids (stop arachidonic acid synthesis)

22

What are some of the immediate and long term systemic effects of acute inflammation?

Immediate: pyrexia, malaise/fatigue, neutrophilia
Long term: lymphadenopathy, anorexia, weight loss

23

What is pus?

It's a mixture of neutrophil and organism debris, RBC, exudate, proteins, fibrinogen etc

24

What is an abscess?

It's a collection of pus walled off by a fibrinogen-derived pyogenic membrane (membrane made of fibrin that walls off pus from surrounding area)

25

What is a multiloculated abscess?

An abscess in which pus breaks through the pyogenic membrane and deposits in a new cavity (second abscess) etc

26

What are different conditions related to pus collection in areas of the body?

Abscess - generic term for collection of pus
Empyema - pus deposited in body cavity (eg pleura, gall bladder)
Pyaemia - pus in the blood

27

What is the term used to describe pus formation?

Suppuration

28

What does the definition granulation mean?

It's the deposition of granulation tissue in reparation of inflamed area

29

What is granulation tissue composed of?

New capillaries (angiogenesis); fibroblasts and collagen; macrophages

30

What is sepsis?

Bacteria growing in the bloodstream causing a systemic acute inflammation response

31

What is bacteraemia?

Bacteria getting into the bloodstream

32

What are the signs of sepsis?

Tachycardia
Low blood pressure
Pyrexia
Haemorragic skin rashes

33

Why does low blood pressure occur in sepsis?

Because a widespread arteriolar vasodilatation (acute inflammatory response) causes the total peripheral resistance to decrease

34

Why does sepsis cause tachycardia?

Because CO is decreased by the fall in TPR, so to maintain it SV or HR have to be increased. SV remains unchanged, so HR compensates instead

35

Why does sepsis lead to death?

Because the body fails to compensate for reduction in CO (caused by reduction in TPR), leading to widespread hypoxia, cell death and multiple organ damage

36

What are the 4 outcomes of acute inflammation?

1. Resolution (healing)
2. Suppuration (pus formation)
3. Organisation (granulation tissue deposition)
4. Dissemination (sepsis)

37

What is disseminated intravascular coagulation (DIC) and why does it happen?

- DIC is the simultaneous haemorraging from vessels due to permeability and clotting action by fibrinogen.
- It occurs because fibrinogen is making clots to stop the permeability of vessels, but not fast enough so blood is getting out through the ruptured vessels

38

What processes cause hypoxia in sepsis?

Drop in TPR and reduced CO
Oedema and fluid leakage in ECF creating a barrier for O2 to cross to get to cells and tissues

39

What type of white blood cell is most prevalent in acute inflammation?

Neutrophil

40

What type of white blood cell is most important in chronic inflammation?

Macrophages, B/T lymphocytes, plasma cells, fibroblasts

41

What defines chronic inflammation?

Presence of macrophages, B and T lymphocytes, plasma cells
Presence of necrosis/organ damage and slowly progressive loss of function

42

What are some of the signs of chronic inflammation?

Non-specific malaise, unwell
Weight loss
Slow/progressive loss of function

43

What are the outcomes of chronic inflammation?

Ongoing tissue damage/necrosis
Granulation tissue and angiogenesis
Fibrosis and scarring
Granuloma formation

44

What are some examples of secondary chronic inflammation?

Acne; peptic ulcers; cholecystitis; osteomyelitis

45

What are some examples of primary chronic inflammation?

Autoimmune disorders (connective tissue diseases): SLE, rheumatoid disease, autoimmune thyroiditis
Endogenous and exogenous substances (surgical material, digestion-resistant organisms, necrosis)

46

What are the most prevalent infective granulomatous diseases globally?

Tuberculosis
Leprosy
Syphilis

47

What defines a granuloma?

Granulomatous inflammation caused by nondigestible pathogen
Epithelioid macrophages
Giant cells
Surround dead tissue
Surrounded by lymphocytes

48

What are examples of some known types of giant cell found in granulomas?

Langhans type (tuberculosis)
Warthin-Finkeldy type (measles, rarely)
Foreign Body type (pyogenic granulation tissue)
Silicone associated (burst implants)

49

What are examples of common types of non-infective granulomatous diseases?

Rheumatoid disease
Crohn's disease
Sarcoidosis

50

What is the sequence of events in wound healing?

Injury
Acute inflammation - fibrinogen (clotting)
Organisation - granulation tissue
Scar formation and healing

51

What promotes wound healing?

Good nutrition (vitamin A, C)
Clean wound
No/minimal bruising
Metabolic activity stable and normal
Local mediator activity

52

What impairs wounds healing?

Bad nutrition
Dirty gapind wound
Lots of hematoma
Edges not adjacent
Impaired angiogenesis
Metabolic imbalance

53

What differentiates normal wound healing with fracture healing?

Bone repair as well as tissue repair
Granulation tissue contains osteoblasts as well as fibroblasts
Macrophages remove dead bone debris

54

What molecule promotes angiogenesis and where is it secreted?

VEGF - vascular endothelial growth factor
Promoted by other enzymes
secreted by hypoxic cells to promote oxygen supply

55

What happens in callus formation?

Osteoblasts deposit woven bone with cartilage
Osteoclasts remove dead bone
Bone remodelling: Woven bone and cartilage replaced with lamellar bone

56

Give some examples of when angiogenesis occurs

Thrombosis - bypass occluded vessel
Cancer - provide steady oxygen supply to cancer cells
Wound healing

57

What is hypersensitivity?

Excessive/inappropriate response to antigens which would not normally cause an inflammatory response

58

What causes the damage in hypersensitivity reactions?

The inflammatory reaction to the antigen by the body, not the antigen itself

59

How many types of hypersensitivity are there?

4

60

What is Type 1 Hypersensitivity?

Allergy: excessive IgE production along with other factors

61

What is atopy?

It's the physiological increase in IgE production without showing the allergy hypersensitivity

62

What are the different ways allergens can come in contact with immune system?

through ingestion, inhalation, injection and physical contact

63

What molecule in the immune system is responsible for allergic reactions and why?

T Helper Cells, because they trigger inappropriate IgE production from B cells

64

Where are histamine and other mediators released from during a Type 1 Hypersensitivity reaction?

Mast cells

65

What are the reasons for the early and late phase of a Type 1 Hypersensitivity reaction?

The release of premade (early phase - histamine, heparin) and newly synthesised (late phase - prostaglandins, leukotrienes) inflammatory mediators

66

What is Type 2 Hypersensitivity?

An activation of IgM/IgG to antigens on cell surfaces or tissues, which may be self or foreign

67

What processes cause damage in Type 2 Hypersensitivity and what is the end result?

Complement pathway activation --> cell lysis
Fc receptor binding to IgM/IgG causes phagocytosis
Antibody-dependent cellular cytotoxicity
Results in damage of cell function (inhibition or stimulation of cell)

68

What is Type 3 Hypersensitivity?

Hypersensitivity reaction to pathological production of antibody/antigen immune complexes

69

What antibodies are normally involved in Type 3 Hypersensitivity reactions?

IgM, IgG or a combination of the two

70

What are the possible presentations of a Type 3 Hypersensitivity reactions?

Serum sickness - systemic deposition of immune complexes causing hypersensitivity reaction
Arthus reaction - localised reaction to immune complex deposition

71

What are the possible predisposing factors determining a Type 3 Hypersensitivity Reaction?

Predisposition to antigen, or abnormal immune reaction to antigen

72

What differentiates Hypersensitivity reaction 4 from 1-3?

It is T helper cell mediated rather than antibody mediated

73

What is another name for Type 4 Hypersensitivity?

delayed-type reaction

74

What normally causes Type 4 Hypersensitivity?

- Low molecular weight antigens which on their own cause no reaction, only when attached to a carrier protein
- organisms which evade digestion/destruction by immune system

75

What is a low molecular weight antigen called that causes Type 4 Hypersensitivity reactions?

Hapten

76

What is the overlap between type 4 hypersensitivity reactions and chronic inflammation?

- inability to remove an antigen
- the aggregation of giant cells and formation of granulomas

77

What is tolerance in the context of the immune system?

It's the ability of lymphocytes to ignore self/auto antigens

78

How is tolerance ensured in the body?

By killing off lymphocytes which are activated by self antigens, and "training" B cells (in bone marrow) and T cells (in thymus) to ignore self antigens

79

What is autoimmunity?

lymphocytes being activated by self antigens in the body and attacking them

80

What triggers autoimmunity?

A combination of predisposing factors and a breakdown in tolerance

81

What factors can contribute to autoimmunity?

Genetics
Environmental
Hormonal
Immune regulation

82

Broadly speaking, what are the two main categories of autoimmune diseases?

Organ specific (localised) and non-organ specific (widespread)

83

What types of radionuclides are usedin PET scanning, and what are their half lives?

F18 - 110min
C11 - 20 min
N13 - 10min
O15 - 2min

84

What are the ideal properties for a nuclear isotope?

- Half life long enough for length of investigation
- Emits gamma rays
- Readily available in hospital
- Easily bound to pharmaceutical molecules for tracking

85

What are the main types of nuclear imaging?

PET and SPECT

86

What are the properties of nuclear imaging?

- Pick up gamma rays emitted by radioisotopes in body
- Show functional/biological activity

87

What is 99m Technetium used for?

Bound to pharmaceutical molecules for bone, brain, lung, kidney and heart scans

88

What is an important consideration to make in nuclear imaging?

Exposure to ionising radiation