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Principles of Disease > Inflammation > Flashcards

Inflammation Flashcards

1
Q

List 6 causes of acute inflammation.

A
  1. Micro-organisms
  2. Mechanical
  3. Chemical
  4. Physical
  5. Dead tissue
  6. Hypersensitivity
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2
Q

What are the benefits of acute inflammation?

A
  1. Rapid response
  2. Cardinal signs and loss of function
  3. resolution and return to normal
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3
Q

What is the function of neutrophils?

A

Destroy organisms and denature antigens for macrophages.

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4
Q

What is the function of neutrophils?

A

Destroy organisms and denature antigens for macrophages.

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5
Q

What is the function of plasma proteins in acute inflammation?

A

Localise process.

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6
Q

Describe the three main steps in the sequence of microvascular change.

A
  1. Change in vessel radius and blood flow
  2. Increase permeability of vessel wall.
  3. Movement of neutrophils from the vessel to the extracellular compartment.
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7
Q

What changes occur with the vessel radius and blood flow during inflammation>

A
  • Transient arteriolar constriction and local arteriolar dilatation.
  • relaxation of smooth muscle
  • increase blood flow to local tissues
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8
Q

What causes endothelial leak?

A

Released during the localised vascular response when the permeability of the cell wall is increased.

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9
Q

What are the effects of endothelial leak?

A

Net movement of plasma from capillaries to extravascular space (exhudation) causes OEDEMA, PAIN and REDUCES FUNCTION.

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10
Q

Describe the main three steps regarding the movement of neutrophils.

A
  1. Margination (move to endothelial aspects of lumen)
  2. Pavementing (neutrophils adhere to endothelial aspects)
  3. Emigration (neutrophils squeeze between endothelial cells to extravascular tissues)
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11
Q

What is exudate composed of?

A

Protein, plasma, immunoglobulins and fibrinogen.

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12
Q

What is the result on blood after fluid loss?

A

Increased viscosity and slows rate of flow.

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13
Q

What are the local effects of acute inflammation?

A

Redness and heat, swelling, door (pain) and loss of function.

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14
Q

List the immediate systemic effects of acute inflammation.

A

Pyrexia, feel unwell (malaise, anorexia, nausea, abdominal pain and vomiting in children) and neutrophilic (increased WBC)

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15
Q

List the longer term systemic side effects of acute inflammation.

A

Weight loss, lymphadenopathy, anaemia.

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16
Q

Describe complications of acute inflammation.

A

Dissemination i.e septic shock.

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17
Q

Describe dissemination.

A

Inflammation spread to bloodstream (bacteraemia in blood, toxaemia with toxic products in blood or septicaemia with growth in blood). Shock prevents perfusion of tissues, causing vasodilatation.

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18
Q

What are the signs of shock.

A

Increase HR, decrease BP, increase temperature, rash

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19
Q

What is the cause of dissemination.

A

Chemical release mediators from cells to plasma

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20
Q

What chemical mediators are released by bacterial endotoxins?

A

IL-1

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21
Q

What is the result of compensation failure?

A

Septic shock (unable to perfuse tissues)

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22
Q

Summarise the cell-surface mediators of acute inflammation?

A

ICAM-1 and P-selectin

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23
Q

Summarise the mediators released from cells.

A

Histamine, 5-hydroxytryptamine, prostaglandins, leukotrienes, omega-3 polyunsaturated fats, platelet-activating factor, cytokines and chemokine, NO, oxygen free radicals.

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24
Q

Name three process of acute inflammation that can be altered to the detriment of patients.

A

Suppuration (pus formation), Organisation (granulation tissue - fibrous and scar), Dissemination (spread to bloodstream)

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25
Q

List the cell types involved in chronic inflammation.

A

Lymphocytes, plasma cells, macrophages, fibroblasts, NK cells, T cells.

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26
Q

What are the major causes of chronic inflammation?§

A
  1. From acute inflammation

2. Arising as a primary lesion

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27
Q

Describe the effects of chronic inflammation.

A

Long term, tissue or organ damage, no specific “for bit”, malaise and weight loss, loss of function.

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28
Q

Describe organisation.

A

Granulation tissue, healing and repair, fibrosis and scar.

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29
Q

What is the function of fibroblasts?

A

Produce collagens to form matrix and replace exudate to form a scar.

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30
Q

Describe adverse effects of tissue scarring.

A

Structural and functional deterioration.
E.g peptic ulcer, cholecystitis, osteomyelitis, pain or numbness, hair follicles don’t grow back, loss of muscle power (after MI).

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31
Q

List factors involved in promoting healing and repair.

A
  • cleanliness
  • apposition of edges
  • sound nutrition
  • metabolic stability
  • normal inflammatory and coagulation mechanisms.
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32
Q

Describe the role of angiogenesis in healing and repair.

A

New vessels form (capillary beds), VEGF released by hypoxic cells stimulates proliferation, enzyme secretion aids progression, enabled blood supply to enter damaged tissue.

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33
Q

Describe instances where angiogenesis occur.

A
  1. In thrombosis to reinstate flow
  2. In malignant tumours as tumour grows
  3. In atherosclerosis for fibrosis and scarring
34
Q

Name factors that impair healing.

A

Dirty, gaping wound, large haematome, poorly nourished, abnormal CHO metabolism, diabetes, corticosteroid therapy, inhibition of angiogenesis.

35
Q

What is the role of histamine?

A

Relaxes vascular smooth muscle in acute inflammation.

36
Q

what does hypoxia impede?

A

Wound healing.

37
Q

What cells are a major component of the acute inflammatory response?

A

Neutrophil polymorphs.

38
Q

What hypersensitivity reaction requires immune complex formation?

A

Type III.

39
Q

What hypersensitivity reaction requires local IgG or IgM production?

A

Type II.

40
Q

What hypersensitivity reaction is the basis of allergy and requires inappropriate IgE synthesis?

A

Type I

41
Q

What hypersensitivity reaction is not antibody mediated?

A

Type IV

42
Q

What hypersensitivity reaction is mediated by the inappropriate action of Th1 cells and cytokine products?

A

Type IV

43
Q

What cells are responsible for the inappropriate synthesis of IgE in type I hypersensitivity reactions?

A

Mast cells.

44
Q

What hypersensitivity reaction causes complement activation?

A

Type II

45
Q

What hypersensitivity reaction is caused by the abnormal deposition of fomed Ag-Ab complexes?

A

Type III

46
Q

What hypersensitivity reaction results in Antibody dependent cellular cytotoxicity (ADCC)?

A

Type II

47
Q

Give two examples of type III hypersensitivity reactions.

A

Serum sickness (systemic) or Arthus (local)

48
Q

What reaction involves the binding of hapten and a carrier host protein to produce antigenic stimuli?

A

Type IV.

49
Q

what hypersensitivity reaction has a 48-72 hour delay?

A

Type IV.

50
Q

Describe the pathophysiology of early phase allergic reactions.

A

Occurs in minutes and involves preformed mast cell mediators.

51
Q

Describe the pathophysiology of late phase allergic reactions.

A

Occurs in hours and involves newly synthesised mediators e.g Th2 cytokines and eosinophil mediators.

52
Q

Define atopy.

A

A genetic tendency to produce IgE to normally innocuous, common environmental allergens.

53
Q

Define allergy.

A

Clinical expression of atopic tendency with inappropriate production of IgE.

54
Q

What is used in type IV hypersensitivity to direct immune response?

A

Haptens

55
Q

What is the purpose of carrier proteins in type IV hypersensitivity reactions?

A

Produce sufficient antigenic bulk.

56
Q

Define the two mechanisms of immunological tolerance.

A
  1. Central tolerance (deletion of auto reactive b and T cells during maturation)
  2. Peripheral tolerance ( inhibit activity of autoreactive cells which escape central tolerance processes)
57
Q

What results in the breakdown of tolerance?

A

Autoimmune disease.

58
Q

Define autoimmune disease.

A

Large group of clinical disorders which are characterised by tissue or organ damage mediated through aberrant immunological mechanisms which are directed against autoantigens.

59
Q

What 5 factors are involved in the aetiology of autoimmune disease.

A
  1. Genetic factors (e.g inheritance of particular HLA genes)
  2. Immune regulatory factors
  3. Hormonal factors
  4. Environmental factors
  5. ‘Other’ factors
60
Q

What are the pathogenetic mechanisms involved in autoimmune disease?

A
  • Genetic Background & environmental factors (e.g infection)
  • Effector mechanisms = cellular or antibody mediated, autoAb activation of complement-mediated inflammation, immune complex formation, recruitment of innate immune components.
61
Q

Can organ specific and non-organ specific autoimmune diseases overlap in one patient?

A

No. Overlap of different ends rarely found however, overlap of disorders found at same side of spectrum can be found e.g thyroid and gastric organ specific disorders in one patient.

62
Q

What imaging techniques are used in inflammatory disorders?

A

PET, CT, SPECT

63
Q

Outline the scientific basis of a PET scan.

A

Use nucleotides that decay by positron emission (proton to neutron + positron)

64
Q

What is the main isotope used for PET?

A

18F with a half-life of 110mins.

65
Q

State the properties of an ideal isotope for labelling.

A
  • Half-life similar to length of examination.
  • Radionuclides should be readily available at hospital.
  • Easily bound to pharmaceutical component.
  • Radiopharmaceutical should be easy to repair.
66
Q

What type of radiation is used in PET scanning.

A

Gamma emitter.

67
Q

Explain detection of gamma radiation and production if digital image by digital camera, PET, SPECT.

A

Occurs due to radioactive decay of unstable isotopes.

68
Q

Put these steps in order. Light electromagnetic energy, electrical energy, nuclear energy and gamma electromagnetic energy.

A
  1. Nuclear Energy
  2. Gamma electromagnetic energy
  3. Light electromagnetic energy
  4. Electrical energy.
69
Q

What is the function of the gamma camera?

A

Rotates around the patient for 25 minutes and detects gamma radiation being admitted.

70
Q

What is SPECT?

A

Single Photon Emission Computed Tomography (Ct version of nuclear medicine).

71
Q

List typical effective doses.

A

4mSV = bone scan, 10mSV = CT abdomen/ pelvis), 18mSV = myocardial perfusion

72
Q

What is the UK average for natural background radiation.

A

2.2mSV/year.

73
Q

Explain the role of diagnostic imaging in the diagnosis, monitoring and treatment of inflammatory/infectious conditions.

A
  • Need to know normal distribution of tracers to determine abnormal distribution.
  • Identifies tissue type
  • Show anatomical changes therefore, late/chronic stages.
  • Detect biological and biochemical changes in earliest phase of disease (increase specificity and diagnostic accuracy)
74
Q

What does a high neutrophil count indicate?

A

Acute inflammation.

75
Q

What does a high amylase suggest?

A

Pancreatitis (caused by alcohol, gall stones or idiopathic).

76
Q

Is acute inflammation specific?

A

No.

77
Q

What hypersensitivity reaction is interleukin-4 associated with?

A

Type II

78
Q

What are type IV hypersensitivity reactions also known as?

A

Delayed-type hypersensitivity.

79
Q

What hypersensitivity reaction is associated with the production of gamma-interferon?

A

Type IV (delayed type)

80
Q

What does rubber mean?

A

Redness

81
Q

What does dollar mean?

A

Pain

Principles of Disease (9 decks)

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