Immunological Pathology Flashcards

1
Q

Allergic disease - definition

A

Innocuous antigens - not harmful

In sensitized host - mast cells primed with IgE

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2
Q

Antibody mediated hypersensitivity reactions?

A

Type 1 - 3

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3
Q

Cell mediated hypersensitivity reactions?

A

Type 4

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4
Q

Type 1 hypesensitivity also known as?

A

Anaphylatic

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5
Q

Type 2 known as?

A

Cytotoxic

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6
Q

Immune complex hyper sensitivity reaction?

A

Type 3

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7
Q

Type 4 hypersensitivty is also known as?

A

delayed type

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8
Q
Antibodies involved in the hypersensitivity reactions:
Type 1
Type 2 
Type 3
Type 4
A

1 = Ige
2 and 3 = IgG and IgM
4 = NONE

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9
Q

Diseases that cause each type of hypersensitivity reaction

A

Type 1 - allergic asthma - hay fever
Type 2 - autoimmune, penicillin allergy
Type 3 - lupus and vascilitis
Type 4 - RA, MS and IBD

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10
Q

Signs of each hypersensitivity reaction?

A

Type 1 - weal and flare
Type 2 - lysis and necrosis
Type 3 - Erythema and odema
Type 4 - oedema

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11
Q

Immune cells involved in each type of hypersensitivity?

A

Type 1 - eosinophils and basophils
Type 2 - compliment + natural killers
Type 3 - complement + neutrophils
Type 4 - lymphocytes and monocytes

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12
Q
Components of the immune response that normal combat parasites? (4)
Antibodies
Inflammatory
Lymphocytes
Interleukins
A

IgE antibodies
Inflammation = eosinophils, mast cells basophils
Lymphocytes = T cells CD4+ type 2
Interleukin = 4, 5, 13

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13
Q
Hygiene theory (3)
Body creating Th2 > Th1
A

More siblings = less allergies
More parasitic infections = less allergies (geographic)
More infection ‘experience’ = body is able to dampen down immune response –> no ‘over the top’ reaction

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14
Q

Genetic predisposition to allergies?

A

Polymorphisms in IL 4, 5, and 13 and receptors to IgG

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15
Q

Th2 cells release which cytokines?

- Type one reaction

A

IL 4 and 5

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16
Q

Affect of IL (in sensitization)
4
5

A
4 = class switching from IgM to IgE
5 = degranulation of eosinophils
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17
Q

What do cytokines stimulate the release of in the ‘Late phase’ of type 1 sensitivity reaction

A

Leukotrines and prostaglandins

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18
Q
Affects of an allergic reaction?
Eyes
nose
mouth
airways
Skin
GI
A
eyes = conjunctivitis
nose = rhinitis
mouth = oral allergy syndrome - tingling
airways = asthma - bronchospasm, constrictions and mucosal hyperplasia
skin = dermatitis
GI = food allergies - V&D
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19
Q

Atopic triad?

A

Asthma
Atopic dermatitis (eczema)
Rhinitis

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20
Q

Diagnosis what kind of hypersensitivity?

A

TIME AFTER exposure to the allergen

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21
Q

Test of allergies? (6)

Gold standard?

A

Blood test - IgE specific
Skin Prick - response > 3mm
Intradermal
Oral challenge - GOLD STANDARD for food allergy
Basophil Activation test - culture basophils
Component resolved diagnosis - test specific parts of proteins against IgEs

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22
Q

Treatments for allergies (in order of increasing severity) (4)
+ Specific immunotherapy (sublingual and subcutaneous) = just for bee stings, animal hair and hay fever

A

Avoidance
Antihistamines
Steroids
Adrenaline

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23
Q

Food allergies most common in children (80% grow out of)

A

milk and eggs

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24
Q

Food allergies that you don’t grow out of

A

Soya beans and peanuts

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25
Q

Signs of food allergies (no seen in food intolerance)

NOTE: V&D seen in both

A

Bronchospasm
Oral symptoms
Rhinitis
Urticaria - bumpy rash that itches

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26
Q

Autoimmunity is what type of immune response?

A

Adaptive

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27
Q

Roll of
T cells
B cells

In autoimmiune disease?

A

T cells = recognize self antigens

B cells and plasma cells = make Auoantibodies

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28
Q

When does inflammatory response start in autoimmune diseases?

A

After the action of lymphocytes and autoantibodies

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29
Q

Genetic component of autoimmune disease?

A

MHC Class II polymorphism = predispose

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30
Q

Environmental components (environmental triggers) of autoimmune disease? (3)
Reason it present later in life
Trigger a genetic factor

A

Infection (eg. Rheumatoid disease)
Trauma
Smoking - replaces AA in the bodies proteins so they are recognized as non self

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31
Q

Immunoregulation (physiological) component of autoimmune disease

A

Autoimmunity attacks cancer cells that present with self antigens = protective

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32
Q

Process of developing tolerence

A

Lymphocytes produces to be nondescriminant
Exposed to self antigens
Either destroyed or mature depending on response

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33
Q

during the development of tolerance:

Negatively selected?
Positively selected mean?

A

Negatively selected = cell response to the self antigens and is destroyed

Positively selected = cell doesn’t respond to self antigens and matures to a T/B Cell

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34
Q

Regulatory T cells - results in developing tolerance?

Action in immune response?

A

Has slight reaction to self antigen - is kept

Regulate an immune response

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35
Q

where is central tolerance developed in
B cells
T cells

A

B cells = bone marrow

T cells = Thymus

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36
Q

Regulatory T cells are coded for by which gene

A

FOXP3

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37
Q

Causes of autoimmune disease (6)

A

Genetics - MHC class II
F>M
Age - advanced
Sequestered self antibodies - lymphocytes that aren’t exposed to pathogens very often (Eg. in eye)
Environmental trigger
Continuation of inflammation - uncontrolled immune response

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38
Q

2 classifications of autoimmune disease

A

Organ specific

Systemic

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39
Q

Organ specific autoimmune diseases

A

Hashimoto thyroiditis - hypothryoid
Graves disease - hyper thyroid
Myasthenia Gravis - neuromuscular junction
Pernicious anaemia - low B12

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40
Q

Action of autoantibodies in

Hashimoto thyroiditis

A

Cause inflammation

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41
Q

Action of autoantibodies in Grave’s disease

A

Mimic TSH and stimulates the thryoid gland

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42
Q

Action of autoantibodies in Myasthenia Gravis

A

Mimics ATcH and blocks receptors at neruomuscular jnct = can’t move facial muscles

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43
Q

Action of autoanitbodies in Pernicious aneamia

A

Bind to intrinsic factor so B12 can’t be taken up

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44
Q

Systemic autoimmune conditions (2)

A

Systemic Lupus erythematous (SLE or Lupus)

Connective tissue disorders eg. Scleroderma

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45
Q

Disease process of lupus? (2 processes)

A

UV light –> damages skin –> releases nucleic contents –> stimulates sequestered antinucleaic self antibodies = rash

Antibodies + antigen immune complex accumulate in the blood vessels = type 3 hypersensitivity and kidney damage

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46
Q

Autoinflammatory disorders?
Eg. Polygenic crohn’s
Cause?

A

Rare disease with an overactive innate immune response
No source of infection
Due to polymorphism in Compliment and cytokines

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47
Q

Serum compliment (C4 and C5) is a measure for?

A

Flare ups of Lupus

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48
Q

Elevated ferritin in the blood signifies?

A

an inflammatory response

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49
Q

ANA? what does it stand for? What does it diagnose?

A

Antinucelar antibodies
Diagnoses Lupus

NOTE: is an immunofluorescence assay that shows there are antinuclear antibodies present NOT their specific targets

50
Q

Muliplex? what is it for?

A

Identifying the type of aninucleaic antibodies in lupus

NOTE: uses Synthetic Extractable nucleaic Antigens (ENA) incubated with the patient serum

51
Q

Rheumatoid factor in the blood - what is it? what does it diagnose?

A

Antibody Vs Fc protein on IgG antibodies

Non specific for Rheumatoid arthritis and also vascilitis

52
Q

Serum Anti - CCP - what is it? What does it diagnose? what is it used for?

A

Immunoassay for antibody against CCP
Specific for Rheumatoid arthritis
Prognostic measure

53
Q

Anti- neutrophillic cytoplasmic antibodies (ANCA) - diagnoses what? 2 types of staining

A

Vascilitis

Cytoplasmic or perinuclear = type of antibodies involved

54
Q

Organ specific autoimmune testing method for liver disease?

A

Tissue block - using rodent tissue and ELISA (enzyme linked immuno assay)

55
Q

Organ specific test for Primary biliary sclerosis?

A

Anti-mitochondrial antibodies assay

56
Q

Organ specific test for Autoimmune hepatitis?

A

Anti-smooth muscle antibodies assay

57
Q

Immunodeficiency definition?

A

The immune system is not effective enough to clear a pathogen

58
Q

What is
Primary
Secondary
Immunodeficiency?

A

Primary - inherted/ genetic cause = RARE

Secondary - due to external cause = more common

59
Q

Causes of Secondary immunodeficiency (5)

A
Break down of physical barriers - CF, Burns, Age = thin skin
Drugs
Protein loss eg. Burns
Malignancy - lymphomas and myeloma
Infection - HIV and TB
60
Q

Drugs that cause secondary immunodeficiency (6)

A

Steroids
Disease modifying Anti-Rheumatic drugs (DMARD)
Anticonvulsants
Myelinsupressants - Chemo
Rituximab
Antibiotics = kills of commensal gut flora

61
Q

MyD88 and IRAK4 - in the innate immune response

A

intracellular signal proteins that cause cytokines to be produced

62
Q

IRAK4 deficiency (genetic) results in

A
Recurrent infections (staph and strep)
NO raised CRP
63
Q

Chronic Granulomatous disease - what is? what does it result in?

A

Lack of NAPDH complex in the phagolysomes

Phagocytosis can’t occur –> granulomas of macrophages not able to perform an immune response

64
Q

Common sites of Granulomas

Common bugs in granulomas

A

Lung, liver, skin and gut

Staph, Kelbsiella and aspergillus

65
Q

Test for Chronic Granulomatous disease

A

Blood serum + Nitroblue Tetrazolium chloride –> goes dark blue

66
Q

C4 and C5 compliment deficiency results in?

A

SLE, infection and myositis (muscle inflammation)

67
Q

C5-C9 (in MAC) compliment deficiency results in?

A

recurrent meningitis - N. meningitis

68
Q

X - linked agammaglobinaemia? Adaptive immune system genetic mutation
What is it? - what Igs are lost?
Results in?

A

Lack of maturation of Bcells = no IgA or IgG

Recurrent infections

69
Q

Treatment of X linked agammaglobinaemia?

A

Subtaneous IgG injections

70
Q

CVID - what does it stand for? what is it? eg.

A

Common variable immunodeficiency
Other B cell abnormalities
Eg. IgA deficiency

71
Q

X-linker hyper IgM syndrome
What doesn’t happen?
What are the effects?

A

Class switching can’t occur

Loss of antibody secretion + recurrent sinopulmonary infections

72
Q

SCID - what does it stand for?

A

Severe combined immunodeficiency

73
Q

SCID what is it? (3)

A

Loss/ reduced B and T cells
Loss/defected t cells molecules
Loss/ defected MHC II proteins

74
Q

SCID effect?

A

VERY RARE and severe
Frequent opportunistic infections

‘Bubble babies’ - only survive with haemopoietin stem cell transplant

75
Q

Action of Rituximab? = Secondary immundeficiency

A

Targets CD20 on Bcells –> kills them

76
Q

Action of HIV? = secondary immunodeficiency

A

Kills CD4+ T helpers

77
Q

Role of immunotheraputics?

A

Manipulate immune response to achieve desired immune response

78
Q

Actions of immunotheraputics? (5)

A

Suppress
Stimulate
Guide in a certain way
Induce tolerance

79
Q

Biologic drugs

A

Genetically engineered proteins made from human genes

Target the immune system

80
Q

3 classes of biologic drugs?

A

Mimic proteins - replace, increase amount or more potent
Monoclonal antibodies
Fusion proteins

81
Q

Immunopoteniation mean?

A

To stimulate the immune system

82
Q

Examples of immunopoteniation therapy? (2)

A

Vaccinations - Live (attenuated) and inactivated (suspensions)
Replacement therapy

83
Q

Examples of Replacement Therapies (4)

A

HNIG - human normal immunogloblin (injection supplement Ig against specific pathogen)

G-CSF and GM-CSF = injected into bone marrow to create neurophils

IL-2 = T cell activation

Interferons - Hep C, B and MS

84
Q

Immunosupression? when used?

A

Reducing the immune response

Autoimmune disease, Transplants

85
Q

Effects of Cortico steroids (immunosupressors)
On Innate system (3)
On Adaptive system (3)

A

Innate = decrease:

  • neutrophil migration
  • Cytokine production
  • Arachidonic acid production for phagocytosis

Adaptive = decreases:

  • Lymphocytes levels - lymphopenia
  • T cells proliferation
  • Ig Production
86
Q

Side effects of Corticosteroids? (7)

A
Diabetes
Hypolipideamia
Reduced protein synthesis
Reduced wound healing
psychiatric issues
Cataracts
osteoporosis
87
Q

Uses of Corticosteroids? (4)

A

Autoimmune disease = CTD, Vasculitis, RA
Inflammatory disorders = Crohns, polymyalgia Rheumatic
Lymphoma
Allograft rejections

88
Q

What results in reversible immunosurpession by target transcriptional factors that activate T cells

A

Calcinerurin in inhibitors and Tacrolimus

89
Q

Examples of mTOR (prevent t cell proliferation)

A

Sirolimus and Rapamycin

90
Q

Cytotoxic immunosupressors: antimetabolites - what do they do?
Examples?

A

Prevent DNA replication

Methrotroxate (folate)
cyclophosphamide (DNA cross linking)

91
Q

Uses of antimetobilte immunosupressive drugs?

Side effects?

A
Methrotroxate = RA
Cyclophosphamide = IBD

Also SLE and vascilitis

Attack other fast dividing cells - bone marrow, GI

92
Q

Types of DMARDs (5)

Usually monoclonal antibodies

A
Anti-cytokines (TNF, IL6 and IL1)
Anti-B therapies - Rituximab
Anti T cell activation
Anti-adhesion
Complement inhibitors
93
Q

Adoptive immunotherapy - include?

Used for?

A

Bone marrow and stem cell transplants

Lymphomas and Leukaemias

94
Q

Immunomodulatory therapy - used to treat?

What types?

A

Allergies
Steroids
Allergen specific immunotherapy
Monoclonal antibodies against immunogloblins

95
Q

Allergen specific immunotherapy - what is it/ how does it work?

A

switching from Th2 - Th1 T cells = more regulatory cells and tolerance

Sublingual and subcutaneous

NOTE: side effects = anaphylaxis

96
Q

Examples of Monoclonal antibodies against Immunoglobins - What Ig and what for?

A

Omalizumab - IgE. Vs. Asthma and chronic hives

Mepolizumab - IL-5 prevents eosinophil activation

97
Q

Opportunistic infections - what are they?

A

Are infections causes by pathogens with low pathogenicity

98
Q

Why are babies considered immunocompromised?

A

Under developed immune system

99
Q

Pathogens that commonly infect burns (2)

A

Psuedomonas and Group A strep

100
Q

Neutropenia? what causes this?

A

Low Neutrophils

Cancer treatments

101
Q

Results of Neutropenia? (5)

A
Prolong infection
Lethal psuedomona infections
Ulcerations in mouth and bowel
Systemic Candida and aspillergillus 
Recurrent skin infections - coagulase negative staph
102
Q

Treatments for Neutropenic patients (3)

A

Prophylatic penicillin (in case of psuedomonas)
Gentamicin
Broad spectrum carbapenem

103
Q

T cell deficiency are either?

A

Acquired
Congenital
Gestational - last trimester

104
Q

Opportunistic infections in T cell deficient patients? (4)

A

Intracellular bacterial infections - listeria monocytogenes and TB
Viruses in transplant patients HSV, CMV, VZV
Candida
Cryptococcal Menengitis in HIV

105
Q

Treatment of infections in T cell deficient patients?

A

Same AnitB’s used in healthy patients

Prophylactic acyclovir and ganciclovir in transplant patients

106
Q

Opportunistic infections in hypogammaglobinaemias (low antibodies - genetic)?

A
Encapsulated bacteria (S. Pneumonia)
Parasites - Giardia Lamblia
107
Q

Opportunistic infections in Compliment deficiencies?

A

Neisseria Meningitis

Recurrent S. Pneumonia

108
Q

Splenotomy patients - opportunistic infections?

A

Strep Pneumoniae
Haemophillus influenza type A and B
N. meningitis
Malaria

109
Q

Treatments for splenotomy patients?

A

Vaccinate against HIB and malaria

Prophylaxis penicillin

110
Q
Organ transplant patients - infections when:
incision made?
From organ
Early immunosupression
Later immunosupression
A
Incision = s. Aureus 
Organ = toxoplasmosis and CMV
Early = CMV and aspergillus
Late = zoster virus and listeria
111
Q

MHC - major histocompatability complex - purpose?

A

On the cell service of all body cells to express self and non self antigens for inspection by T cells receptors

112
Q

MHC are coded for on which chromosome and by which group of genes?

A

6p21.3

HLA - human leukocyte antigen

113
Q

Class I gene regions code for which HLAs? + what type of MHC?

A
HLA -  A, B and C antigens
MHC class I proteins - on all body cells
114
Q

Class II gene region codes for which HLAs and what MHC type?

A

HLA - DR, DQ and DP

MHC Class II dedritic cells –> APC

115
Q

Inheritance of MHCs?

A

Mendelian
Co -dominant

1 set of A, B, C, DR, DQ and DP from farther, one from mother - ALL are expressed

116
Q

Chance of being a:
Mismatch
Half match
Full match

with sibling MHC and thus organ donations?

A

Mismatch = 1/4
Half match = 1/2
Full match = 1/4

117
Q

Polymorphisms for each HLA allow?

A

capacity for individual to mount an immunological response against a antigen challenge

118
Q

Test the donors MHC to determine mismatch (mm). what does 0mm mean?
6mm mean?

A

All 6 alleles of the HLAs are the same

All 6 of the alleles of the HLAs are different

119
Q

Immune response during transplant
Direct?
Indirect?

A

Direct? = interaction with the donors immune system eg. Donors dendrites present to recipients T cells

Indirect = the normal immune response to a endothelial damage due to surgical stress

120
Q

Reaction frequency (%) ?

A

Compare the recipients antibody screen to the Donors database of antigens - to see the likely hood of a mismatch (a reaction)

121
Q

Cross match test? - what is it? what does it test?

A

Donor lymphocytes + recipients serum –> immunofluescent assay

Shows whether there would be a hyperacute reaction (eg. to blood group)