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Principles of Disease > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What is the main purpose of acute inflammation

A
  • Protect homeostasis

- Response to injury

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2
Q

What are the 5 cardinal signs of acute inflammation?

A 
Rubor - redness
Calor - temperature
Tumor - swelling
Dolor - pain
Loss of function
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3
Q

What are the possible causes of acute inflammation?

A 
Biological (eg microorganisms)
Chemical (acids, alkali, urine, bile)
Physical (extreme cold/heat)
Mechanical (trauma, surgery)
Dead tissue (necrosis irrititates nearby tissue)
Hypersensitivity (reactions)
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4
Q

Where does acute inflammation occur?

A

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

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5
Q

What is the pathogenesis of acute inflammation?

A
  1. Increased vessel radius - increased blood flow
  2. Increased vessel permeability - increased exudate (protein leakage)
  3. Neutrophil migration (through vessel and out)
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6
Q

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

A

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

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7
Q

What type of leaking occurs in acute inflammation?

A

Exudation (high protein content)

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8
Q

What is found in the plasma exudate in acute inflammation?

A

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

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9
Q

What happens as a result of increased vessel permeability?

A
  • Exudative process (oedema)

- Increased viscosity and slower flow (stasis)

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10
Q

What is the sequence of events in exudate formation?

A

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)

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11
Q

What are the benefits of acute inflammation?

A
  • 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
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12
Q

What is the sequence of microvascular changes in acute inflammation?

A
  • Increased radius (increased flow)
  • Increased permeability (exudate)
  • Neutrophil migration out of vessel
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13
Q

What is the role of neutrophils in acute inflammation?

A

To phagocytose and destroy foreign organisms

To denature antigens

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14
Q

How do neutrophils kill foreign antigens?

A

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

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15
Q

What is the fate of activated neutrophils?

A

Neutrophils die after having released their granules to digest foreign antigen

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16
Q

What is the role of plasma proteins in acute inflammation?

A

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

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17
Q

Give examples of some acute inflammation mediators

A

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

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18
Q

What is the role of acute inflammation mediators broadly speaking?

A
  • 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)
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19
Q

Give examples of mediators derived from arachidonic acid

A

Leukotrienes and prostaglandins

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20
Q

Where is histamine produced?

A

In mast cells

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21
Q

What mediator can stop leukotrienes and prostaglandins from being formed?

A

Omega 3 fatty acids (stop arachidonic acid synthesis)

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22
Q

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

A

Immediate: pyrexia, malaise/fatigue, neutrophilia

Long term: lymphadenopathy, anorexia, weight loss

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23
Q

What is pus?

A

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

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24
Q

What is an abscess?

A

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)

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25
Q

What is a multiloculated abscess?

A

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

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26
Q

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

A

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

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27
Q

What is the term used to describe pus formation?

A

Suppuration

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28
Q

What does the definition granulation mean?

A

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

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29
Q

What is granulation tissue composed of?

A

New capillaries (angiogenesis); fibroblasts and collagen; macrophages

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30
Q

What is sepsis?

A

Bacteria growing in the bloodstream causing a systemic acute inflammation response

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31
Q

What is bacteraemia?

A

Bacteria getting into the bloodstream

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32
Q

What are the signs of sepsis?

A

Tachycardia
Low blood pressure
Pyrexia
Haemorragic skin rashes

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33
Q

Why does low blood pressure occur in sepsis?

A

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

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34
Q

Why does sepsis cause tachycardia?

A

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

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35
Q

Why does sepsis lead to death?

A

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

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36
Q

What are the 4 outcomes of acute inflammation?

A
  1. Resolution (healing)
  2. Suppuration (pus formation)
  3. Organisation (granulation tissue deposition)
  4. Dissemination (sepsis)
37
Q

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

A
  • 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
Q

What processes cause hypoxia in sepsis?

A

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
Q

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

A

Neutrophil

40
Q

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

A

Macrophages, B/T lymphocytes, plasma cells, fibroblasts

41
Q

What defines chronic inflammation?

A

Presence of macrophages, B and T lymphocytes, plasma cells

Presence of necrosis/organ damage and slowly progressive loss of function

42
Q

What are some of the signs of chronic inflammation?

A

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

43
Q

What are the outcomes of chronic inflammation?

A

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

44
Q

What are some examples of secondary chronic inflammation?

A

Acne; peptic ulcers; cholecystitis; osteomyelitis

45
Q

What are some examples of primary chronic inflammation?

A 
Autoimmune disorders (connective tissue diseases): SLE, rheumatoid disease, autoimmune thyroiditis
Endogenous and exogenous substances (surgical material, digestion-resistant organisms, necrosis)
46
Q

What are the most prevalent infective granulomatous diseases globally?

A

Tuberculosis
Leprosy
Syphilis

47
Q

What defines a granuloma?

A 
Granulomatous inflammation caused by nondigestible pathogen
Epithelioid macrophages 
Giant cells
Surround dead tissue
Surrounded by lymphocytes
48
Q

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

A 
Langhans type (tuberculosis)
Warthin-Finkeldy type (measles, rarely)
Foreign Body type (pyogenic granulation tissue)
Silicone associated (burst implants)
49
Q

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

A

Rheumatoid disease
Crohn’s disease
Sarcoidosis

50
Q

What is the sequence of events in wound healing?

A

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

51
Q

What promotes wound healing?

A 
Good nutrition (vitamin A, C)
Clean wound
No/minimal bruising
Metabolic activity stable and normal
Local mediator activity
52
Q

What impairs wounds healing?

A 
Bad nutrition
Dirty gapind wound
Lots of hematoma
Edges not adjacent
Impaired angiogenesis
Metabolic imbalance
53
Q

What differentiates normal wound healing with fracture healing?

A

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

54
Q

What molecule promotes angiogenesis and where is it secreted?

A

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

55
Q

What happens in callus formation?

A

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

56
Q

Give some examples of when angiogenesis occurs

A

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

57
Q

What is hypersensitivity?

A

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

58
Q

What causes the damage in hypersensitivity reactions?

A

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

59
Q

How many types of hypersensitivity are there?

A

4

60
Q

What is Type 1 Hypersensitivity?

A

Allergy: excessive IgE production along with other factors

61
Q

What is atopy?

A

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

62
Q

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

A

through ingestion, inhalation, injection and physical contact

63
Q

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

A

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

64
Q

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

A

Mast cells

65
Q

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

A

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

66
Q

What is Type 2 Hypersensitivity?

A

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

67
Q

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

A

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
Q

What is Type 3 Hypersensitivity?

A

Hypersensitivity reaction to pathological production of antibody/antigen immune complexes

69
Q

What antibodies are normally involved in Type 3 Hypersensitivity reactions?

A

IgM, IgG or a combination of the two

70
Q

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

A

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

71
Q

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

A

Predisposition to antigen, or abnormal immune reaction to antigen

72
Q

What differentiates Hypersensitivity reaction 4 from 1-3?

A

It is T helper cell mediated rather than antibody mediated

73
Q

What is another name for Type 4 Hypersensitivity?

A

delayed-type reaction

74
Q

What normally causes Type 4 Hypersensitivity?

A
  • 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
Q

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

A

Hapten

76
Q

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

A
  • inability to remove an antigen

- the aggregation of giant cells and formation of granulomas

77
Q

What is tolerance in the context of the immune system?

A

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

78
Q

How is tolerance ensured in the body?

A

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
Q

What is autoimmunity?

A

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

80
Q

What triggers autoimmunity?

A

A combination of predisposing factors and a breakdown in tolerance

81
Q

What factors can contribute to autoimmunity?

A

Genetics
Environmental
Hormonal
Immune regulation

82
Q

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

A

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

83
Q

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

A

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

84
Q

What are the ideal properties for a nuclear isotope?

A
  • Half life long enough for length of investigation
  • Emits gamma rays
  • Readily available in hospital
  • Easily bound to pharmaceutical molecules for tracking
85
Q

What are the main types of nuclear imaging?

A

PET and SPECT

86
Q

What are the properties of nuclear imaging?

A
  • Pick up gamma rays emitted by radioisotopes in body

- Show functional/biological activity

87
Q

What is 99m Technetium used for?

A

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

88
Q

What is an important consideration to make in nuclear imaging?

A

Exposure to ionising radiation

Principles of Disease (3 decks)

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