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Phase 2a > Pathology and Immunology > Flashcards

Pathology and Immunology Flashcards

1
Q

What are the type types of autopsy?

A
  • Hospital

- Medico-legal

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2
Q

What deaths are referred to the coroner?

A

Presumed natural - cause of death not known, not seen doctor in last 14 days

Presumed iatrogenic - peri/postoperative, anaesthetic deaths, abortion, complication of therapy

Presumed unnatural - accidents, industrial death, unlawful killing, neglect, custody deaths, war

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3
Q

Who makes referrals to coroner?

A 
Doctors  
Registrar of BDM 
Relatives 
Police 
Anatomical pathology technician 
Other properly interested parties
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4
Q

Who performs autopsies?

A

Histopathologists = hospital autopsies, coronial autopsies

Forensic pathologists = coronial autopsy

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5
Q

What is the role of the coronial autopsy?

A
  • Who was the deceased?
  • When did they die?
  • Where did they die?
  • How did they die?
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6
Q

What does an autopsy consist of?

A
  1. History/Scene
  2. External examination
  3. Evisceration
  4. Internal examination
  5. Reconstruction
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7
Q

What does an external examination consist of in an autopsy?

A

Identification ( formal, body modification, gender, jewellery, clothing) - WHO

Disease and treatment - WHY

Injuries - WHY ME

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8
Q

What does evisceration consist of?

A
  • Y shaped incision
  • Open all body cavities
  • Examine all organs in situ
  • Remove thoracic and abdominal organs
  • Remove brain
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9
Q

What does the internal examination consist of?

A

Heart and great vessels

  • Lungs, tracheal, bronchi
  • Liver, gallbladder, pancreas
  • Spleen thymus and lymph nodes
  • Genitourinary tract
  • Endocrine organs
  • Central nervous system
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10
Q

What is a coronial autospy

A

The coronial autopsy is a systematic scientific examination that helps the coroner determine who the deceased was, when and where they died and how they came about their death.

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11
Q

Who instructs the majority of autopsies?

A

Medico-Legal authority

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12
Q

When is inflammation good and when is it bad?

A

Good - infection and injury

Bad - autoimmunity

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13
Q

What are the classifications of inflammation?

A

ACUTE:

  • sudden onset
  • short duration
  • usually self resolving

CHRONIC:

  • slow onset or sequel to acute
  • Long duration
  • may never resolve
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14
Q

Name the cells involved in inflammation?

A 
Neutrophil polymorphs 
Macrophages 
Lymphocytes
Endothelial cells 
Fibroblasts
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15
Q

Describe neutrophil polymorphs in inflammation?

A

Short lived, usually first on the scene and die at the scene, attract other inflammatory cells such as macrophages

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16
Q

Describe macrophages in inflammation?

A

Long lived cells, phagocytic properties, ingest bacteria and debris, may carry debris away, may present antigen to lymphocyte

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17
Q

Describe lymphocytes in inflammation?

A

Long lived (years) produce chemicals which attract in other inflammatory cells, immunological memory

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18
Q

Describe endothelial cells in inflammation?

A

Line blood vessels, make become sticky in areas of inflammation and inflammatory cells adhere to them, become porous to allow inflammatory cells to pass into tissues

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19
Q

Describe fibroblasts in inflammation?

A

Long lived cells, form collagen in areas of chronic inflammation and repair

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20
Q

What would a group of macrophages surrounded by lymphocytes be?

A

A granuloma

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21
Q

What is used to treat inflammation?

A

NSAIDS - inhibit prostaglandin synthase

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22
Q

Define: resolution?

A

Initiating factor removed, tissue undamaged or able to regenerate

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23
Q

Define: Repair?

A

Initiating factor still present, tissue damaged and unable to regenerate - replacement of damaged tissue by fibrous tissue, collagen produced by fibroblasts

e.g.

Heart after MI
brain after CI

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24
Q

Name some cells that do regenerate?

A 
hepatocytes 
pneumocytes 
all blood cells 
gut epithelium 
skin epithelium 
osteocytes
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25
Q

Name some cells that do not regenerate?

A

myocardial cells

neurones

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26
Q

Define: thrombosis?

A

A solid mass of blood constituents formed within an intact vascular system during life

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27
Q

What are the three things that can predispose for thrombosis?

A
  1. change in vessel wall
  2. change in blood flow
  3. change in blood constituents
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28
Q

What two factors cause blood clots to be rare?

A
  1. Laminar flow - cells travel in the centre of the arterial vessel and dont touch the sides
  2. Endothelial cells that line the vessels are not sticky when they are healthy
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29
Q

Define: embolus?

A

a mass of material in the vascular system able to become lodged within a vessel and block it

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30
Q

Define: ischaemia?

A

A reduction on blood flow to a tissue without any other implications

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31
Q

Define: infarction?

A

The reduction in blood flow to a tissue that is so reduced that it cannot support the maintenance of cells in the tissue so that they die (subset of ischaemia)

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32
Q

What is end arterial supply?

A

Organ supplied by only one artery

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33
Q

What organs have more than one artery supplying them?

A

Lungs, liver and parts of the brain

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34
Q

What is an embolism?

A

The process of a solid mass in the blood being carried in the circulation to a place where it gets stuck and blocks the vessel

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35
Q

Describe the process

A
  1. Platelet aggregation, as platelets release chemicals when they aggregate which cause other platelets to stick to them starting off the cascade
  2. Once the clotting cascade has started there is formation of the large protein molecule fibrin which ,makes a mesh in which red blood cells can become entrapped
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36
Q

What are some risk factors of atherosclerosis?

A
  • Cigarette smoking
  • Hypertension
  • Diabetes
  • Hyperlipidaemia
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37
Q

How does hypertension increase the risk of atherosclerosis?

A

Shearing forces damage endothelial cells from hypertension

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38
Q

What is apoptosis?

A

Programmed cell death

BcL12 inhibits caspases
Bax+ stimulates caspases

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39
Q

What is HIV? (apoptosis)

A

Too much apoptosis

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40
Q

What is necrosis?

A

Traumatic cell death

e.g. caseous necrosis - looks like soft cheese - TB

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41
Q

Define: Hypertrophy?

A

It is an increase in the size of a tissue caused by an increase in the size of constituent cells (if they can’t divide then they can only hypertrophy)

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42
Q

Define: Hyperplasisa?

A

It is an increase in the size of the tissue caused by an increase in the number of constituent cells

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43
Q

Define: Metaplasia?

A

A change in the differentiation of a cell from one fully differentiated type to a different fully differentiated type

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44
Q

Dysplasia?

A

An imprecise term for the morphological changes seen in the progression of cells becoming cancer

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45
Q

Define:
Congenital
Inherited
Acquired

A

Congenital = present at birth

Inherited = is caused by a genetic abnormality

Acquired = caused by non environmental factors

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46
Q

Name some of the components in the pathology of ageing?

A
  • Dermal elastosis
  • Osteoporosis
  • Cataracrs
  • Senile dementia
  • Sarcopenia
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47
Q

Define: carcinogenesis?

A

It is the transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations –> applies to malignant neoplasms

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48
Q

Define: oncogenesis?

A

Benign and malignant tumours

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49
Q

What are the differences between:
Carcinogenic
Oncogenic
Mutagenic

A 
Carcinogenic = cancer causing 
Oncogenic = tumour causing 
Mutagenic = acts on DNA
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50
Q

What percentage of cancer risk is environmental?

A

85%

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51
Q

What are the problems with working out what is carcinogenic:

A
  • Latent intervals may be decades
  • Complexity of environment
  • Ethical constraints
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52
Q

What is some epidemiological evidence for some carcinogens?

A

Hepatocellular carcinoma: uncommon in the UK/USA and common in areas with increased hepatitis B/C and mycotoxins

Oesophageal carcinoma: increased incidence in Japan, China Turkey and Iran - dietary factors (hot coffee and Linhsien chickens

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53
Q

Name the five classes of carcinogens and give an example for each?

A
  1. Chemical e.g. polycyclic aromatic hydrocarbons
  2. Viral e.g. HPV
  3. Ionising and non ionising e.g. thyroid cancer in Ukrainian children
  4. Hormones, parasites and mycotoxins e.g. oestrogen and breast cancer
  5. Miscellaneous e.g. asbestos and metals
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54
Q

What are the different types of chemical carcinogen and what tumours do they cause?

A
  1. Polycyclic aromatic hydrocarbons: lung and skin cancer (smoking and mineral oils)
  2. Aromatic amines: bladder cancer (rubber/dye workers)
  3. Nitrosamines: gut cancer (proven in animals)
  4. Alkylating agents: leukaemia (small risk in humans)
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55
Q

What are some of the host factors that can increase the risk of cancer?

A 
Race: melanin 
Diet 
Constitutional factors e.g age and gender 
Premalignant lesions 
Transplacental exposure
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56
Q

What does leukaemia effect?

A

Blood

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57
Q

What does lymphoma effect?

A

Lymphocytes

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58
Q

What does sarcoma effect?

A

Connective tissue

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59
Q

What does carcinoma effect?

A

Epithelial tissue

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60
Q

Define: neoplasm?

A

A lesion resulting from the autonomous or relatively autonomous abnormal growth of cells which persists after the initiating stimulus has been removed

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61
Q

What is neoplasia? (4)

A

Autonomous
Abnormal
Persistent
New growth

62
Q

How does neoplasia affect the population?

A

25% of the population effected at some point in lifetime

Risk increases with age

Accounts for 20% of all deaths

63
Q

Describe the structure of neoplasms?

A

Neoplasm = neoplastic cells + stroma

Neoplastic cells: derive from nucleated cells, usually monoclonal, growth pattern related to parent cells, synthetic activity related to parent cell e.g. collagen, mucin, keratin hormones etc

Stroma: connective tissue framework, mechanical support, nutrition

64
Q

Describe tumour angiogenesis?

A
  1. Transformed cell
  2. Avascular tumour nodule
  3. Vascularised tumour
  4. Vascularised tumour with central necrosis
65
Q

Why classify neoplasms?

A
  1. To determine appropriate treatment

2. To provide prognostic information

66
Q

What are the methods of classification?

A

Behavioural: benign/malignant
Histogenetic: cell of origin

67
Q

Describe a benign neoplasm?

A 
Localised
Non-invasive 
Slow growth rates 
Low mitotic activity 
Close resemblance to normal tissue 
Circumscribed or encapsulated
68
Q

Why worry about benign neoplasms?

A 
Pressure on adjacent structures 
Obstructs flow 
Production of hormones 
Transformation into malignant neoplasms 
Anxiety
69
Q

Describe malignant neoplasms?

A

Invasive

Metastases

Rapid growth rate

Variable resemblance to normal tissues

Poorly defined or irregular borders

Hyperchromatic nuclei, pleomorphic nuclei, increased mitotic activity , necrosis common, ulceration, growth on mucosal surfaces and skin often endophytic

Encroach upon and destroy surrounding tissue, are poorly circumscribed and have crab like cut surface

70
Q

Why worry about malignant neoplasms?

A 
Destruction of adjacent tissue
Metastasies 
Blood loss from ulcers 
Obstruction of plow 
Hormone production 
Paraneoplastic effects 
Anxiety 
Pain
71
Q

Define: histogenesis?

A

The specific cell origin of a tumour

72
Q

What may neoplasms arise from?

A
  • Epithelial cells
  • Connective tissue
  • Lymphoid / haemopoetic
73
Q

What is a papilloma?

A

A benign tumour of the non glandular, non secretory epithelium, prefixed with the cell type of origin e.g. squamous cell papilloma

74
Q

What is an adenoma?

A

A benign tumour of glandular or secretory epithelium e.g. colonic adenoma

75
Q

What is a carcinoma?

A

A malignant tumour of epithelial cells, prefixed by the epithelial cell type

76
Q

Give some examples of benign epithelial neoplasms?

A

Lipoma - adipocytes
Chondroma - cartilage
Osteoma - bone
Angioma - vascular

77
Q

What is a rhabdomyoma?

A

Benign neoplasm of striated muscle

78
Q

What is a leiomyoma?

A

Benign neoplasm of smooth muscle

79
Q

Give some examples of some malignant neoplasms? (6)

A
  1. Liposarcoma - adipose tissue
  2. Rhabdomyosarcoma - striated muscle
  3. Leiomyosarcoma - smooth muscle
  4. Chondrosarcoma -cartilage
  5. Osteosarcoma - bone
  6. Angiosarcoma - blood vessel
80
Q

What is an anaplastic tumour?

A

Where the cell type is unknown

81
Q

Give some examples of -omas that are NOT neoplasms?

A

Granuloma
Mycetoma
Tuberculoma

82
Q

What is a melanoma?

A

Malignant neoplasm of melanocytes

83
Q

What is a mesothelioma?

A

Malignant tumour of mesothelial cells

84
Q

What is a lymphoma?

A

Malignant neoplasm of lymphoid cells

85
Q

What is a teratoma?

A

Embryonal tumours

86
Q

What is a basal cell carcinoma?

A

It only invades skin locally and never spreads to other parts of the body - complete local excision means total cure

87
Q

What cancers most commonly spread to bone?

A
  1. Breast
  2. Prostate
  3. Lung
  4. Thyroid
  5. Kidney
88
Q

Describe a treatment plan for breast cancer?

A
  1. Confirm diagnosis
  2. Has it spread to the axilla? - axillary node clearance needed
  3. Has it spread to the rest of the body? - chemotherapy
89
Q

What is adjuvant therapy?

A

Extra treatment given after surgical excision (micrometastasies)

90
Q

Which tumours commonly metastasise to the liver?

A
  • Colon
  • Stomach
  • Pancreas
  • Intestine
91
Q

Describe how cancer metastasises?

A
  1. invasion of the basement membrane
  2. Tumour cell motility
  3. Intravasation
  4. Evasion of the host immune defence
  5. Growth at the metastatic site
  6. Anigogenesis
92
Q

Define: innate immunity?

A

Instinctive, nonspecific, doesnt depend of lymphocytes and present from birth

93
Q

Define: adaptive immunity?

A

Specific accquired/learned immunity requires lymphocytes and antibodies

94
Q

Which cells are the polymorphonuclear leukocytes?

A

Neutrophil
Eosinophil
Basophil

95
Q

Which cells are the mononuclear leukocytes?

A

Monocytes - macrophage in tissue
T-cells
B-cells - plasma cell in tissue

96
Q

What are the different types of T-cells?

A

T-regs
T helper (CD4)
Cytotoxic (CD8)

97
Q

What are the dendritic cells?

A

Kupffer and Langerhans

98
Q

What is compliment?

A

A group of 20 serum proteins that need to be activated in order to be functional, activated only as a part of the immune response

They can

  1. Lyse microbes directly
  2. Chemotaxis
  3. Opsonisation (ketchup on chips)
99
Q

Describe igG?

A

most predominant Ig in human serum - 70-75%

100
Q

Describe IgM?

A

accounts for for 10% of Ig in serum, pentamer formation requires J chain, mainly found in the blood as its too big to cross endothelium, mainly primary immune response

101
Q

Describe IgA

A

accounts for 15% of Ig in serum, it is a monomer, predominant Ig in mucous secretion, sIgA held together with a J chain

102
Q

Describe igD?

A

Accounts for 1% of Ig in serum

103
Q

What are cytokines?

A

Proteins that are secreted by immune and non immune cells e.g.. inferons and interleukins

104
Q

Function of interferons?

A

Interferons induce as state of antiviral resistance in uninfected cells and limit the spread of a viral infection

105
Q

Function of interleukins?

A

Interleukins are produced by many cells and can be pro inflammatory or anti-inflammatory and can cause cells to divide, differentiate and to secrete factors

106
Q

What are colony stimulating factors?

A

Involved in directed the division and differentiation of bone marrow cells - precursors of leukocytes

107
Q

What are tumour necrosis factors?

A

TNFα & β Mediate inflammation and cytotoxic reactions

108
Q

What are chemokines?

A

Chemotaxic cytokines

Group of approx. 40 proteins that direct the movement of leukocytes and other cells from the blood stream into the tissues of lympth organs by binding to specific receptors on the cells

109
Q

Give some examples of chemokines?

A

CXCL – mainly neutrophils
CCL –monocytes, lymphocytes, eosinophils, basophils
CX3CL – mainly T lymphocytes & NK Cells
XCL – mainly T lymphocytes

110
Q

Give some characteristics of innate immunity?

A

innate - non specific

  • 1st line of defence
  • Provides barrier to antigen
  • Instinctive
  • Present from birth
  • Slow response
  • No memory
111
Q

Give some characteristcs of adaptive immunity?

A

adaptive - specific

  • response to specific antigen
  • learnt behavior
  • memory specific to antigen
  • quicker response
112
Q

What is innate immunity composed of?

A
  • Physical and chemical barriers e.g. skin, mucous, pH
  • Phagocytic cells e.g. neutrophils and macrophages
  • Blood proteins e.g. compliment and acute phase
113
Q

Define inflammation?

A

Inflammation is a series of reactions that brings cells and molecules of the immune system to sites of infection or damage

114
Q

What are the hallmarks of infection?

A
  1. Increased blood supply
  2. Increased vascular permeability
  3. Increased leukocyte transendothelial migration
115
Q

What is the response to tissue damage?

A
  1. Coagulation - stop bleeding
  2. Leukocyte recruitment - acute inflammation
  3. Kill pathogens, neutralise toxins, limit pathogen spread
  4. Clear pathogens/ dead cells - phagocytosis
  5. Proliferatoin of cells to repair damage
  6. Remove blood clot - remodel extracellular matrix
  7. Re-establish normal structure/function of tissue
116
Q

Describe: acute inflammation?

A

Complete elimination of a pathogen followed by resolution of damage, disappearance of leukocytes and full regeneration of tissue

117
Q

Describe: chronic inflammation?

A

persistent unresolved inflammation

118
Q

What senses microbes in:
blood?

tissues?

A

blood- Monocytes and neutrophils

tissues - Macrophages and dendritic cells

119
Q

What are the different types of compliment?

A

Classical - Ab bound to microbe
Alternative - C’ binds to microbe
Lectin - activated by mannose binding lectin bound to microbe

120
Q

What are the stages of phagocytosis?

A
  1. binding
  2. engulfment
  3. phagosome engulfment
  4. Phagolysosome
  5. membrane disruption
121
Q

What are the mechanisms of microbial killing?

A

O2 dependent - Reactive Oxygen Intermediate

  • Super oxides converted to H2O2 and then .OH free radical
  • Nitric oxide = vasodilation, increased extravasation but also antimicrobial

O2 independent

  • Enzymes e.g. lysosomes
  • Proteins e.g. defensins into membranes
  • pH
122
Q

Types of adaptive immunity?

A

Cell mediated - t cells - intracellular microbes

Humoral Ab - B cells - extracellular microbes

123
Q

What is cell mediated immunity and what does it require?

A

Interlay between antigen presenting and T cells

Requires intimate cell to cell contact

  • To control Ab responses via contact with B cells
  • To direct recognise and kill viral infected cells
124
Q

Describe the features of T lymphocytes?

A
  • do not response to soluble antigens only intracellular presented antigens
  • T cells that recognise self are kills in the foetal thymus as they mature - T cell selection
  • T cell receptor recognises foreign antigens in association with major histocompatibility complex
125
Q

Describe the major histcompatability complex?

A
  • Displays peptides from self or non self proteins e.g. degraded microbial proteins on the cell surface - invasion alert
126
Q

Describe the Major Histocompatability Complex I?

A

MHC I coded by HLA (A, B & C genes) - glycoproteins on ALL nucleated cells (graft rejection).

127
Q

Describe the Major Histocompatability Complex II ?

A

MHC II - coded by HLA (DP, DQ& DR) - glycoproteins ONLY on APC (antigen presenting cells

128
Q

Describe the relationship between intrinsic antigens and MHC?

A

Antigen: Intrinsic antigen (intracellular e.g. virus)

MHC: Class I (all cells)

T cells: Tc (CD8)

Function: kill infected cell with intracellular pathogen

129
Q

Describe the relationship between extrinsic antigens and MHC?

A

Antigen: extrinsic antigen (extracellular e.g. phagocytosis)

MHC: Class II (apc only)

T cells: Th (CD4)

Function: Help B cells make Ab to extracellular pathogen, can help directly kill

130
Q

Describe secreted and circulating Pattern Recognition Receptors? (PRRs)

A

Antimicrobial peptides secreted in lining fluids from epithelia and phagocytes e.g. defensins and phagocytes

  • Lectins and collectins: carbohydrate containing proteins that bind carbohydrates or lipids in microbe walls, activate compliment and improve phagocytosis e.g. mannose binding lectin, surfactant proteins A and D
  • Pentraxins. Proteins like CRP, which have some antimicrobial actions, can react with the C protein of pneumococci, activate complement, and promote phagocytosis.
131
Q

Describe Cell associated Patter Recognition Receptors (PRRs)?

A

Receptors that are present on the cell membrane or in the cytosol of the cells

  • Recognise a broad range of molecular patterns
  • TLRs are the main family
132
Q

Describe TLRs?

A
  • Family of receptors that may participate in pathogen recognition and particularly in pathogen phagocytosis
    e. g.
  • Mannose receptor on macrophages
  • Dectin-1. Widespread on phagocytes, helps recognise beta glucans in fungal walls
  • Scavenger receptors on macrophages
133
Q

Describe NLRs?

A

(type of PRR) Named after the first members of the family, NODs, Nod-like receptors.

Rapidly expanding family of another 22 human proteins that detect intracellular microbial pathogens.

Detection of peptidoglycan, muramyl dipeptide, Best known are NOD1, NOD2, NLRP3 etc

134
Q

Describe NOD2?

A

(type of PRRs) Widespread expression

Recognises muramyl dipeptide MDP a breakdown product of peptidoglycan

Activates inflammatory signalling pathways

Non-functioning mutations: Crohn’s disease

Hyperfunctioning mutations: Blau syndrome (rare, chronic granulomatous inflammation of skin, eyes and joints)

135
Q

Describe RLRs?

A

Named after first members of the family: Rig-I. Rig-like helicases = RLRs

Best known are RIG-I and MDA5, who’s roles are to detect intracellular double-stranded viral RNA and DNA.

They couple effectively to activation of interferon production enabling an antiviral response

NOD2 can also activate anti-viral signalling

136
Q

What are some damage molecules?

A

Extracellular molecules: fibrinogen, hyaluronic acid, tenascin C

Intracellular molecules: for example, HMGB1, mRNA, heat shock proteins, uric acid (and uric acid crystals), stathmin

137
Q

How can TLRs recognise damage?

A

TLRs also adapted to recognise a range of endogenous damage molecules, which may share characteristics of hydrophobicity.

Appearance of host molecules in unfamiliar contexts can activate TLRs.

TLR signalling by cellular damage products activates immunity to initiate tissue repair and perhaps enhance local antimicrobial signalling.

138
Q

How are PRRs relevent to disease?

A

Recognition of host molecules in autoimmune disease
Failure to recognise pathogens or increased inflammatory responses

Atherosclerosis, arthritis, COPD, inflammatory bowel disease, etc.

139
Q

How can PRR function translate to therapy?

A

Enhance TLR signalling: improve immunity, adjuvants

Inhibit TLR signalling: sepsis syndromes, inflammation, arthritis

Modify adaptive immune response: bias Th and Treg responses

140
Q

Describe the differences between immediate and delayed drug hypersensitivity?

A

Immediate - less than one hour, urticarial, anaphylaxis

Delayed - more than one hour, other rashes, hepatitis, cytopenias

141
Q

What are the four types of hypersensitivity?

A

Type 1 - IgE mediated drug hypersensitivity
Type 2 - IgE mediated cytotoxicity
Type 3 - Immune complex deposition
Type 4 - T cell mediated

142
Q

Describe type 1 hypersensitivity?

A

Type 1 - acute anaphylaxis

  • Prior exposure to antigen//drug
  • IgE antibodies formed after exposure to molecule
  • IgE becomes attached to mast cells or leucocytes, expressed as cell surface receptors
  • Re-exposure causes mast cell degranulation and release of pharmacologically active substances such as histamine, prostaglandins, leukotrienes, platelet activating factors et c
143
Q

Describe type 2 hypersensitivity?

A

Type 2 - antibody dependent cytotoxicity

  • Drug or metabolite combines with a protein
  • Body treats it as a foreign protein and forms antibodies (IgG IgM)
  • Antibodies combine with the antigen and complement activation damages the cells e.g. methyl-dopa-induced haemolytic anaemia
144
Q

Describe type 3 hypersensitivity?

A

Type 3 - immune complex mediated

  • Antigen and antibody form large complexes and activate complement
  • Small blood vessels are damaged or blocked
  • Leukocytes attracted to the site of reaction release pharmacologically active substances leading to an inflammatory process
  • Includes glomerulonephritis
145
Q

What are the main features of anaphylaxis?

A
  • Exposure to drug, immediate rapid onset
  • Rash (absent in 10%)
  • Swelling of the lips, face, oedema, central cyanosis
  • Wheeze/SOB
  • Hypotension
  • Cardiac arrest
146
Q

What drug is intially administered for anaphylaxis?

A

Adrenaline IM 500 micrograms (300mcg epi-pen)

147
Q

Describe the management of anaphylaxis?

A
  1. Commence basic life support ABC
  2. Stop the drug if infusion
  3. Adrenaline IM 500 micrograms
  4. High flow oxygen
  5. IV fluids
  6. IV antihistamine
  7. IV hydrocortisone
148
Q

Describe effects of adrenaline?

A
  • VASOCONSTRICTION as increase in peripheral vascular resistance, increased BP and coronary perfusion via alpha 1 adrenoreceptors
  • Stimulation of Beta-1 adrenoceptors, positive inotropic and chronotrpic effects on the heart
  • Reduces oedema and brochodilates via beta-2-adrenoceptors
  • Attenuates further release of mediatiors from mast cells by basophils by increasing intracellular c-AMP and so reducing the release of inflammatory mediators
149
Q

What are the medicine risk factors for hypersensitivity?

A
  • Protein or polysaccharide based macromolecules
150
Q

What are the host risk factors for hypersensitivity?

A

Females > males
EBV, HIV
Previous drug reactions
Uncontrolled asthma

151
Q

What are the genetic risk factors for hypersensitivty?

A

Certain HLA groups

Acetylator status

152
Q

What is the clinical criteria for an allergy to a drug?

A
  1. Does not correlate with the pharmacological properties of the drug
  2. No linear reaction with dose
  3. Reaction similar to those produced by other allergens
  4. Induction period of primary exposure
  5. Dissapearance on cessation
  6. Reapperance on re exposure
  7. Occurs in a minority of patients on the drug

Phase 2a (13 decks)

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