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Arjun's Copy- Owen's Path > Immunology > Flashcards

Immunology Flashcards

1
Q

What type of virus is HIV

A

RNA retrovirus single stranded
Belongs to lentivirus family

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2
Q

Which cells do HIV infect

A

CD4+
- t helper cells
- macrophages

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3
Q

Pathogenesis of HIV

A

Attaches to CD4 via GP120 (ie glycoprotein) but uses co receptor either CCR5 or CXCR4
Replicates via a DNA intermediate
Integrates into host genome
HIV DNA transcribed to viral mRNA
Viral RNA translated to viral proteins
Packaging and release of mature virus

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4
Q

What can predict HIV disease progression

A

Initial viral burden after primary infection settles

set point?

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5
Q

What CD4 count defines AIDS

A

Less than 200

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6
Q

Response when recognise PAMP

A

Th1 and Th17 (from Th1 cells)

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7
Q

How does immune system respond to toxins and helminthes (parasitic worm)

A

Detect a loss of function then get Th2 response - IL-5 causes eosinophilia

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8
Q

What are inborn errors of immunity

A

Heterogenous group of genetic disorders resulting in immune dysfunction and ill health
485 single defects already identified

group of genetic disorders that result from defects in biochemical pathways responsible for the synthesis, breakdown, or transport of molecules within cells. These disorders are typically caused by mutations in genes encoding enzymes or transport proteins - e.g. PKU, Gaucher’s, MSUD etc.

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9
Q

What is the most common form of inborn errors of immunity

A

Antibody deficiency or B cell function

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10
Q

What gene defects result in suceptibility to mycobacterial and BCG infection

A

Gene defects in generation of IL-12 adn response to IFN-gamma
Leads to reduced production of TNF to activate oxidative pathways

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11
Q

What gives rise in critical influenza pneumonia susceptibility

A

Defects in TLR3 which is sensor of influenza A

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12
Q

What is in mucous from membranes which protects against microorganisms

A

IgA prevents bacteria and viruses from binding to epithelial cells
Lysozyme which breaks down cell walls
Lactoferrin which starves bacteria of iron

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13
Q

Which cells form part of innate immune response

A

Polymorphonuclear cells
Dendritic cells
Monocytes and macrophages
NK cells (lymphoid cell involved)

NK cells is KEY!

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14
Q

Where are granulocytes produced

A

Bone marrow then migrate to site of injury

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15
Q

Other than cells what is included in the innate immune system

A

Complement
Acute phase proteins
Cytokins and chemokins

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16
Q

What are examples of pattern recognition receptors

A

TLR
RIG-1

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17
Q

What are monocytes and macrophages

A

Monocytes are produced by bone marrow and migrate to tissues where differentiate into macrophages

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18
Q

Function of macrophages

A

Phagocytosis
Present processed antigens to T-cells

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19
Q

What are mannose receptors

A

C-type lectin receptor found innate cells which detects pattern

expressed predominantly by most tissue macrophages, dendritic cells (DCs) and selected lymphatic or liver endothelial cells

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20
Q

What type of receptors are those detecting PAMPs

A

Fc receptors

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21
Q

What is opsonisation

A

Enables phagocytosis by marking the pathogen and making a bridge between it and phagocyte receptor

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22
Q

What are examples opsonins

A

Antibodies
Complement components
Acute phase proteins

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23
Q

What are 2 types of microbial killing

A

Non-oxidative- release bacteriocidal enzymes into phagolyosome
Oxidative- produce hydrochlorous acid

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24
Q

What forms pus

A

Phagocytosis depletes neutrophil glycogen store which results in cell death
As cell dies enzymes are released causing liquefaction of adjacent tissue

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25
Q

What is function of dendritic cells prior to phagocytosis

A

Found in peripheral tissue
Express Fc receptors for Ig to detect immune complexes

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26
Q

What mediates migration of dendritic cells to lymph node

A

CCR7

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27
Q

What are the components of the adaptive immune system

A

Humoral immunity
Cellular immunity
Chemokines and cytokines

T,B cells, NK cells are INNATE immunity even though lymphoif lineage!

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28
Q

What makes up humoral immunity versus cellular

A

Humoral- B lymphocytes and antibodies
Cellular- T lymphocytes

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29
Q

What are the primary lymphoid organs

A

Organs where lymphocytes develop
Bone marrow- both T and B haemopatoetic stem cells and where B cells mature
Thymus- where T cells mature

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30
Q

What are the secondary lymphoid organs

A

Sites where naive lymphocytes and microorganisms interact
Spleen
Lymph nodes
MALT

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31
Q

What do all T cells express

A

CD3+

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32
Q

When is the thymus most active

A

Foetal and neonatal stages of life (as developing immunity)
Involutes after pregnancy

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33
Q

HLA class 1 proteins

A

A, B, C

1 letter

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34
Q

HLA class 2 proteins

A

DR, DQ, DP

2 letters

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35
Q

Most important HLA matches

A

In order
DR
B
A
When matching donors you want to minimise HLA differences

Dr BA

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36
Q

transplants- What does
- isograft
- allograft
- xenograft
- split graft mean

A

Iso- from a twin
Allo- from same species
Xeno- from different species
Split- shared by 2 recipients (liver transplant)

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37
Q

Complications of SCT

A

Graft failure
Infections
GVHD
Relapse

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38
Q

What is GVHD

A

Where donor cells recognise the patient as foreign

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39
Q

Acute GVHD presentation

A

Rash which can blister
GI- D&V with bloody diarrhoea
Liver- jaundice
Days to weeks

red,green, yellow (rash, D&V, jaundice)

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40
Q

How is acute GVHD prevented

A

Methotrexate
Corticosteroids
Cyclosporin

also leukodepletion?

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41
Q

Main prognostic factor for acute GVHD

A

Previous acute GVHD

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42
Q

What is pathology behind allergic reaction triggering

A

Normal epithelial function affected- breaking of epithelial barrier

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43
Q

Which route of transmission promtoes IgE sensitisation

A

Skin
Resp tract
If its oral it promotes IgG immune tolerance

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44
Q

What causes rapid onset symptoms in allergic reactions

A

Cross linking of IgE on the surface of mast cells and basophils
- release of histamine from granules
- release and synthesis of leukotrienes and prostaglandins
- pro-inflam cytokines which recruits inflam cells
- increases lymphatic flow to regional lymph nodes
- contraction of muscles in lungs and activation of sneezes and itches

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45
Q

What results in delayed symptoms of allergic reactions

A

Eosinophlic related tissue damage and cytokine release from Th2 T-cells (IL4, IL5, IL13)

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46
Q

What is most appropriate initial investigation for suspected peanut allergy giving urticaria and angioedema

A

Skin prick test

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47
Q

What allergic diseases will present in infancy and childhood

A

Dermatitis
Food allergy

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48
Q

Presentation of IgE allergic responses

A

Within 3-4 hours after exposure
Skin-angioedema, urticaria
Resp tract- cough, wheeze, nasal congestion
GI- D&V
Blood vessels- fainting, sense of impending doom

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49
Q

What is refractory anaphylaxis

A

No improvement in resp and cardio symptoms in response to 2 doses of IM adrenaline

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50
Q

What is the best lab test to diagnose anaphylaxis

A

Mast cell tryptase taken 30mins-2 hours after the initial symptoms start

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51
Q

What demotes a positive skin prick test

A

Wheal 3mm greater than negative control

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52
Q

What do sensitisation blood tests do

A

Detect IgE to whole allergen or a component of the allergen

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53
Q

What is function of compnoent resolved diagnostics

A

Test for IgE against the specific protein within a whole allergen
In essence identifies the exact protein to which someone is allergic to

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54
Q

How are allergic diseases diagnosed

A

Is made by a clinican based on epidemiology, history, exam, SPT etc NOT a blood sensitisation test
These are necessary but not sufficient

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55
Q

If have a raised mast cell tryptase which fails to return to baseline afer anaphylaxis what could be causes

A

Systemic mastocytosis
Hereditary alpha tryptassaemia

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56
Q

What is gold standard for diagnosing food and drug allergies

A

Double blind oral food challenge tests

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57
Q

Anaphylaxis guidelines

A

ABCDE
Call for HELP
Remove trigger
Lie patient flat
IM adrenaline in anterolateral aspect of thigh
Establish airway and give oxygen
If no response
-IM adrenaline
- fluid bolus

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58
Q

Difference between food allergy and food intolerance

A

Allergy- adverse health effect arising from a specific immune response
Food intolerance- non-immune reactions which include pharmacological, metabolic

Food intolerance does not involve the immune system. It occurs when the body is unable to properly digest certain foods, usually due to a deficiency in enzymes or sensitivity to food additives.

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59
Q

Examples of food intolerances

A

Food poisoning
Enzyme deficiencies- lactase
Pharmacological- caffeine, tyramine

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60
Q

Allergy mechanism in atopic dermatitis

A

IgE

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61
Q

Allergy mechanism in contact dermatitis

A

T cell mediated

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62
Q

What can differentiate between IgE sensitisation and IgE mediated allergy

A

Component resolved diagnostics

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63
Q

What can give delayed food induced anaphylaxis

A

Occur 3-6 hours after eating red meat
IgE antibody to alpha-1-3-galactose

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64
Q

What mechanism is oral allergy syndrome

A

When have haye fever, get cross reaction to some homologous proteins in apples, pears, carrots and nuts but not cooked

heat labile so fine if cooked

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65
Q

Presentation of oral allergy syndrome

A

Swelling and itch of lips and mouth

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66
Q

What does a positive blood sensitisation/SPT suggest

skin prick test

A

Sensitisation not allergy!

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67
Q

Most commmon cause of secondary immunodeficiency worldwide

A

Malnutrition

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68
Q

Causes of secondary immunodeficiency

A

Malnutrition
Measles- get immune defects lasting months to years
TB
HIV
COvid
Haem cancers
Drugs

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69
Q

Drugs which cause immunodeficiency

A

Steroids
Cytotoxic agents- methotrexate, mycophenolate, cyclophosophamide, azathioprine
Calcineurin inhibitors- cyclosporine, tacrolimus
Anti-epileptics
DMARD
JAK inhibitors
Biologics

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70
Q

What is good s syndrome

A

Combined T and B cell defect with thymoma and antibody deficiency

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71
Q

What infections are those with Goods syndrome susceptible to

A

CMV
PJP
Mucocutaneous candida

opportunistic?

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72
Q

Natural history of HIV

A

Acute phase where can have flu like illness
Asymptomatic but progressive
AIDS

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73
Q

Difference in transmission of HIV across disease course

A

Related to viral load in plasma
High in acute and aids but drops in asymptomatic

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74
Q

What is acute immune response to HIV

A

Induction of HIV-1 antibodies
CD8 T cell activation

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75
Q

How is HIV diagnosed if child under 18 months

A

HIV RNA or DNA tests

serology not useful as maternal ABs

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76
Q

What tests are done which can determine HIV treatment

A

Test for HLAB5701 to avoid prescribing abacavir as severe risk of SJS
Tropism test for CCR5 to determine if CCR5 antagonist therapy would work - e.g. miraviroc?

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77
Q

What is first line for HIV in the UK

A

2 NRTI and 1 NNRTI
OR
2NRTI and INI
Mainly will change treatment due to drug toxicity rather than response

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78
Q

When likely to see PJP, toxoplasma and mycobacterium avium complex in HIV

A

PJP- CD4 less than 200
Toxoplasma- 100
MAC- 75

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79
Q

What is chronic benign neutropenia

A

Get a mild/moderate neutropenia common in african and middle eastern groups
Asymptomatic with no further investigation required

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80
Q

What is familial neutropenia

A

Adult onset severe neutropenia
Specific organ autoimmune disease
No increased infection risk?

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81
Q

Which conditions give a severe congenital neutropenia

A

Kostmann syndrome
Cyclic neutropenia

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82
Q

What is genetic defect in cyclic neutropenia

A

Autosomal dominant- Neutrophil elastase

ELA-2

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83
Q

What is genetic defect of Kostmann syndrome

A

Autosomal recessive- HCLS-1 associated protein X-1 which prevents maturation of neutrophils

HAX-1

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84
Q

How do severe congenital neutropenias present

A

Present in first 3 months
Susceptible to oral, cutaneous and epithelial s. aureus infections, g-enteric bacteria and fungal infections

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85
Q

How are severe congenital neutropenias treated

A

G-CSF support
Stem cell transplantation

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86
Q

Pathophysiology of neutrophil leukocyte adhesion deficiency

A

Deficiency in CD18 which is used to remove neutrophils from circulation

i.e. how neutrophils leave blood (ICAM-1 etc.)

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87
Q

What is result of luekocyte adhesion deficiency

A

delayed separation of umbilical cord
very high neutrophil counts in blood (20-100 x106/L)
Absence of pus formation

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88
Q

Pathophysiology of chronic granulomatous disease

A

Deficiency in NADPH oxidase which used to generate free radicals as such fail to kill certain bacteria
Get excessive inflammation from persistent recruitment of neutrophils and phagocytes causing granuloma formation

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89
Q

Presentation of chronic granulomatous disease

A

Granulomas
Hepatomegaly and lymphadenopathy
Recurrent infections from PLACESS (catalase +ve bact) often affecting skin
Pseudomonas
Listeria
Aspergillosis
Candida
Ecoli
S aureus
Serratia

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90
Q

Treatment of chronic granulomatous disease

A

Interferon gamma

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91
Q

Test for chronic granulomatous disease

A

Dihydrorhodamine (DHR) flow cytometry test. DHR is oxidized to rhodamine, which is strongly fluorescent, following interaction with hydrogen peroxide.

NBT(stays yellow- doesnt go blue)

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92
Q

What are the 3 triggers for complement pathway

A

Immune complexes (antigen-antibody) - classical
Bacterial endotoxin (alternative e.g. LPS)
Mannose binding lectin (directly C2, 4 - misses C1q)

Upon binding to pathogens, MBL can activate the complement system, a cascade of proteins that enhances the immune response against invading microorganisms. MBL activates the lectin pathway of the complement system, leading to the deposition of complement proteins on the surface of pathogens and promoting their elimination by phagocytic cells or direct lysis.

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93
Q

How does classical complement system work

A

Immune complexes trigger C1 which begins cascade involving C1, C2 and C4. Ultimately activate C3

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94
Q

Pathophysiology of classical component deficiencies

A

These include deficiencies in C1q,2 and 4
This means that is failure to activate the complement system causing increased susceptibility to infections

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95
Q

What is link of classical complement deficiencies and SLE

A

If have deficiency of classical complement pathway then is accumulation of immune complexes which can deposit in the joints, skin and kidneys

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96
Q

Presentation of classical complement deficiencies

A

Susceptibility to infections namely Hib and strep pneumoniae
Severe skin disease
Co-existing SLE

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97
Q

Pathophysiology of alternative pathway deficiencies

A

Lack of factor B, D and P (properdin) mean less activation of terminal pathway from alternative pathway

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98
Q

Susceptibility of alternative pathway deficiencies

A

Encapsulated bacteria

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99
Q

Presentation of C3 deficiency

A

Increased suscpetibility to encapsulated bacteria infection

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100
Q

What are the types of C3 deficiency

A

Primary from genetic deficiency
Secondary- get autoantibodies against C3 (e.g. nephritic factor - MPGN)

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101
Q

What is associated with C3 deficiency

A

Membranoproliferative glomerulonephritis

nephritic factors-autoABs against C3

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102
Q

What is significance of mannose binding lectin deficiency

A

Very common however does not affect susceptibility to infection unless coinciding factor causing immunodeficiency like chemo or premature infant

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103
Q

Pathophysiology of SCID

A

Encompassing term for various mechanistic pathways however all relate to defects in the generation of lymphoid precursors in the bone marrow

rememebr reticular dysgenesis - msot severe form (adenylate kinase 2 mutation, autosomal recessive!)

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104
Q

Presentation of SCID

A

Present by 3 months of age
Opportunistic infections
Live vaccine infected (BcG and rotavirus)
Persistent candida infection
Failure to thrive
Peristent diarrhoea

SPUR (severe, persistent, unusual, recurrent)

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105
Q

Which infections are SCID normally susceptible

A

Opportunistic- candida, PJP, CMV
Viral chest and GI infections- adenovirus, parainfluenza
RARELY BACTERIAL

An eczema like rash is often present. Failure to thrive or systemic Candida infections (rare in normal ppl for candida to disseminate) may also be present.

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106
Q

Treatment for SCID

A

Stem cell transplant

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107
Q

Pathophysiology of DiGeorge syndrome

A

22q11.2 deletion

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108
Q

Congenital features of DiGeorge syndrome

A

CATCH
Cardiac abnormalities (TOF) - also interrupted aortic arch
Atresia (oesophageal) and abnormal facies
Thymic aplasia
Craniofacial defects (cleft palate)
Hypocalcaemia from hypoparathyroidism

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109
Q

Immune problems of DiGeorge syndrome

A

Thymic hypoplasia leading to reduced T cell counts
Increased incidence of autoimmune conditions and sino-pulmonary infections

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110
Q

How is IgA deficiency diagnosed

A

Serum IgA under 0.07g/L with normal Ig and B cell counts

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111
Q

Presentation of IgA deficiency

A

Most asymptomatic
Increased prevalence of allergic disorders and autoimmune diseases (e.g. more commonly have coeliac etc.)
Recurrent sino-pulmonary and GI infections

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112
Q

What is pathogenesis of common variable immune deficiency

A

Heterogenous conditions were is defect in B cell develpoment, maturation or function and fail to produce protective antibodies

MHC III mutation

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113
Q

Presentation of CVID

A

PRESENTS IN ADULTS (need to over 4 for diagnosis, mean age is 26)
Recurrent sino-pulmonary infections with encapsulated bacteria
These can be so bad get bronchiectasis
Otitis media
Hib conjunctivitis
Enteric infections
Skin cellulitis, abscess HSV and VZV
Viral resp infections
Granulomatous infiltration
Autoimmune conditions common
Increased risk of B cell NHL and gastric cancers

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114
Q

Hallmarks of CVID

A

Increased infection susceptibility
Autoimmune conditions more prevalent
Granulomatous infiltration
Lymphoproliferative conditions common

can occur in older ppl - dx > age of 4

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115
Q

Management of CVID

A

Normal human IVIG

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116
Q

Pathogenesis of X-linked agammaglobulinaemia

A

Mutation in bruton tyrosine kinase which is key in maturation of B cells

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117
Q

Presentation of x-linked agammaglobulinaemia

A

Presentation under 5
Recurrent bacterial infection of ENT, resp and GI
Encapsulated bacteria

in boys only as x linked

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118
Q

Management of x linked agammaglobulinaemia

A

Normal human IVIg

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119
Q

Blood findings of x linked agammaglobulinaemia

A

Neutropenia
Reduction or absence of b cells
Absent of all Ig

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120
Q

MOst common cause of death in X linked agammaglobulinaemia

A

Acute or chronic lung disease

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121
Q

MOst common antibody deficiency

A

Selective IgA deficiency

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122
Q

What is immunopathology

A

Damage to the host caused by immune system

123
Q

Difference between auto-inflammatory and auto-immune

A

Auto-inflammatory get activation of immate immune cells such as macrophages and neutrophils resulting in tissue damage
Auto-immune get activation of T and B cell responses in primary and secondary lymphoid organs

124
Q

Genetic defect in familial mediterranean fever

A

Autosomal recessive loss of function mutation in MEFV which encodes pyrin-marenostrin
Leads to uncontrolled IL-1 production

125
Q

Investigations for familial mediterranean fever

A

High CRP
High serum amyloid A
Send off to genetics lab for confirmation

126
Q

Presentation of familial mediterranean fever

A

Periodic fevers lasting 48-96 hours associated with:
Abdominal pain due to peritonitis
Chest pain due to pleurisy and pericarditis
Arthritis
Rash

127
Q

Treatment of familial mediterranean fever

A

Colchicine
IL-1 blocker (anakinra)

128
Q

What does IPEX stand for

A

Immune dysregulation polyendocrinopathy enteropathy X-linked syndrome

129
Q

Pathophysiology of IPEX

A

Mutations in Foxp3 which is needed for the development of CD25+ T reg cells. Menas is failure to negatively regulate T cell responses

130
Q

How does IPEX present

A

Increased prevalence of autoimmune diseases
- DM
- Hypothyrodism
- enteropathy
- eczema
(Diarrhoea, DM, dermatitis)

131
Q

What does ALPS stand for

A

Auto-immune lymphoproliferative syndrome

132
Q

Pathophysiology of ALPS

A

Mutation in FAS pathway which is involved in apoptosis of lymphocytes

133
Q

Presentations of ALPS

A

Very high lymphocytes
Splenomegaly and enlarged lymph nodes
Auto-immune diseases (typically cytopenias)
Lymphoma

134
Q

Inheritance of ALPS

A

Autosomal dominant

135
Q

What mutations is associated with Crohns disease

A

IBD1 gene of chr 16- NOD2 (most common)
CARD15

136
Q

What are mixed pattern diseases

A

Involve mutations in both the innate and adaptive immune system

137
Q

Main genetic allele associated with ank spond

A

HLA B27

138
Q

Presentation of ank spond

A

Back pain worse in morning with stiffnesss
Large joint arthritis
Enthesitis- pain where ligaments/tendons insert

139
Q

Management of ank spond

A

NSAIDS
Anti-TNF alpha (e.g. etanercept)
Anti- IL17 (secukinumab)

140
Q

What are the types of immunological diseases

A

Monogenic auto-inflammatory
Polygenic auto-inflammatory
Mixed pattern diseases
Polygenic auto-immune diseases
Monogenic auto-immune diseases

141
Q

What is the genetic association of goodpasture syndrome

A

HLA-DR15

and HLA-DR2 as well?

142
Q

What are 2 examples of genetic polymorphisms seen in polygenic autoimmune disease

A

Protein tyrosine phosphatase non-receptor 22
Cytotoxic t lymphocyte associated protein 4

(PTPN22 and CTLA-4)

143
Q

What is Protein tyrosine phosphatase non-receptor 22 polymorphism (PTPN22) associated with

A

SLE
RA
T1DM

144
Q

What is Cytotoxic t lymphocyte associated protein 4 polymorphism associated with

A

Hashimotos
SLE
T1DM

i.e. CTLA4 mutation - so T cells uncontrolled

145
Q

What are the 4 hypersensitivity reactions

A

Type 1- IgE
Type 2- antibody reacts with cellular antigen
Type 3- antibody reacts with soluble antigen to form immune complex
Type 4- T-cell mediated/delayed type

146
Q

What is autoantigen in goodpastures

A

Noncollagenous domain of basement membrane collagen type IV
Anti glomerular basement membrane

147
Q

What is the autoantigen in pemphigus vulgaris

A

Epidermal cadherin
Anti-desmoglein

148
Q

Antibody in hashimotos

A

Anti thyroid peroxidase antibodies
Can get antithyroglobulin
NOTE IS VERY COMMON FOR PEOPLE IN GENERAL POPULATION TO HAVE

149
Q

What type of immunological reaction is T1DM

A

Type IV
Get T cell infiltration of the pancreas

150
Q

What are some of the antibodies in T1DM

A

Anti-islet cell antibodies
Anti-glutamic acid decarboxylase antibodies
Often predate the development of DM and do not play a role in diagnosis

151
Q

Antibodies in pernicious anaemia

A

Anti gastric parietal cells - more common
Anti intrinsic factor- most specific

152
Q

Presentation of B12 deficiency

A

Macrocytic anaemia
Degeneration of spinal chord subacute (SACD)
Peripheral neuropathy
OPtic neuropathy

153
Q

Antibodies in coeliac

A

Anti tissue transglutaminase
Anti endomysial

154
Q

Which antibody can be seen in IBD

A

P-ANCA
MORE UC THAN CROHNS

155
Q

What are antibodies in primary biliary cholangitis

A

Anti mitochondrial antibody
ANA

156
Q

Antibodies in Myasthenia gravis

A

Anti acetylcholine receptor
Anti-striational (if with myositis)

157
Q

What antibody is seen in myasthenia gravis if concurrent myositis

A

Anti-striational

158
Q

What antibody is seen in neuromyelitis optica spectrum

A

Anti aquaporin 4

159
Q

What antibody is seen in optic neuritis

A

Anti myelin oligodendrocyte glycoprotein

160
Q

What antibodies can be seen in encephalitis

A

Anti NMDA receptor

161
Q

What antibodies can be seen if seizures (in AI enceph)

A

Anti GABA receptor
Normally underlying malignancy too

162
Q

What are genetic predispositions to RA

A

HLA DR4 (and 1 i think)
Peptidyl arginine deaminase as increases citrullination of proteins

4 walls in a ‘rheum’

163
Q

Environmental predispositions to RA

A

Smoking
Gum infection with porphyromonas gingivalis as expresses peptidyl arginine deaminase which promotes citrullination

164
Q

Which antibodies are present in RA

A

Anti cyclic citrullinated proteins- most sensitive
Rheumatoid factor- antibody against Fc portion of IgG

165
Q

What are the antibodies present in SLE

A
  • ANA
  • Anti DsDNA
  • anti Ro
    -anti La
  • anti Sm
  • anti U1RNP
166
Q

What are the investigations done if psoitive ANA

A

Will do dsDNA
And extractable nuclear antigens
- anti Ro
-anti La
- anti Sm
- anti U1RNP
- scl70
- centromere

167
Q

What are Ro, La, Sm and U1RNP all

A

Ribonucleoproteins (ie proteins and RNA)- extractable nuclear antigens

RNPs: Specific complexes of RNA and protein in the nucleus, targeted by anti-RNP antibodies, particularly associated with mixed connective tissue disease (MCTD) and also found in SLE.
ENAs: A broader group of nuclear antigens, including RNPs, targeted by various autoantibodies associated with different autoimmune diseases such as SLE, Sjögren’s syndrome, systemic sclerosis, and myositis.

168
Q

What are the complement profiles of C3 and C4 in SLE

A

C4 reduced in active disease and severe disease
C3 only reduced in severe disease

169
Q

What is seen in antiphospholipid syndrome

A

Recurrent thromosis
Recurrent miscarriage
Can get valvular disease

170
Q

What antibodies test for in antiphospholipid syndrome

A

Anti-cardiolipin
Lupus anticoagulant
Anti beta 2 glycoprotein 1

171
Q

Presentation of sjogrens

A

Dry eyes
Dry mouth
Arthralgia
Fatigue

172
Q

Lip biopsy finding in sjogrens

A

B cell and T cell infiltration
CD4+ most prominent

173
Q

What antibodies seen in sjogrens

A

Anti-Ro
Anti La
Speckled staining

174
Q

What is risk of sjogrens or SLE with anti Ro antibodies during pregnancy

A

Can cross react with foetal cardiac tissue causing neonatal heart block

175
Q

What antibody seen in polymyositis and dermatomyositis

A

Anti Jo-1 (anti t-RNA synthetase)
Speckled pattern

176
Q

What are second line immune deficiencies tests

A

Measure concentration of vaccine antibodies
If antibodies are low then can offer vaccination wit pneumovax II and tetanus and measure response
This is a criteria for IgG in replacement some conditions

177
Q

Which vaccines are used to investigate immune deficiency

A

Pneumovax II
Tetanus

In individuals suspected of immune deficiency, vaccines can be used as part of diagnostic investigations to assess the functioning of the immune system. The response to certain vaccines can provide valuable information

178
Q

How is HIV diagnosed (options available)

A

4th gen ELISA then to confirm use western blot (need pt to have seroconverted - happens at around 10wks)
Rapid point of care tests available which provide answer in 20 minutes however less sensitive than 4th gen test

179
Q

If in acute HIV have suspicion of HIV but serological tests negative what use

A

HIV RNA tests

180
Q

How is HIV monitored

A

Viral load
CD4 count

181
Q

What is viral load set point

A

3-6 months after initial infection a steady state HIV-1 viral concentration is observed in blood
Used to predict long term outcomes

182
Q

When is ART offered to prevent infection

same as PEP?

A

Prevent transmission to seronegative partners
Pregnancy (zidovudine)
Following inadvertant exposure follwoing occupational exposure or high risk sex

183
Q

What are the phases of T cell mediated transplant rejection

A

Phase 1- presentation of donor HLA by an APC
Phase 2- T cell activation and inflammatory cell recruitment
Phase 3- effector phase with organ damage

184
Q

What are phases of antibody mediated rejection

A

Phase 1- B cells recognise foreign HLA
Phase 2- proliferation and maturation of B cells with anti HLA antibodies
Phase 3- effector phase where antibodies bind to graft endothelium

185
Q

Graft biopsy of t cell mediated rejection

A

Inerstitial inflammation and tubulitis
Arteritis

186
Q

Graft biopsy of antibody mediated rejection

A

Antibody deposition
Complement deposition
All in endothelium

187
Q

Which antibodies can exist in antibody mediated rejection

A

Anti-HLA
Anti-A or anti-B

ABO natural, anti-HLA not - so from this Tx or prev events (blood transfusions etc.)

188
Q

Where can anti-HLA antibodies seen in organ rejection arise from

A

Anti-HLA are not naturally occuring
- pre formed- prev transplant, pregnancy, transfusion
- post formed- arise from transplant

189
Q

How can rejection be prevented by tissue typing

A

ABO and HLA tissue-matching
Screen for anti-HLA antibodies

190
Q

What induction agents are given for baseline suppression in prevention of graft rejection

prevent so pre-Tx

A

Anti CD52- alemtuzumab
OKT3- muronomab-CD3
Anti-CD25 (IL2-R)- daclizumab

ABC - alemtuzumab, basiliximab, CD3 inhib

191
Q

As well as induction agents which baseline immunosuppression agents are given to prevent SOT rejection

i.e. post Tx

A

Calcineurin inhibitor
Mycophenolate or azathioprine
+/- steroids

SAC mnemonic

192
Q

How can organ rejection be detected

A

Monitor organ function ie creatinine
Screen for antibodies (anti-HLA)

193
Q

How is T cell mediated organ rejection treated

A

IV steroids
OKT3- muronomab-CD3

194
Q

How is antibody mediated rejection treated

A

IVIG
PLasma exchange
Rituximab

195
Q

How is drug toxicity treated of immunosuppressive agents treated

A

Reduce dose

196
Q

If are immunocompromised and then contract a viral infection how is it treated

A

Reduce dose

197
Q

What is moa of tacrolimus and cyclosporin

A

Calcineurin inhibitor- needed for T cell proliferation

i.e. blocks IL-2 production?

198
Q

What is MOA of azathioprine

A

Prevents purine (adenine and guanine) synthesis

199
Q

What is moa of mycophenolate motefil

A

Prevents guanine synthesis by inhibiting inosine-5’-monophosphate dehydrogenase (5-IMD)
Anti-proliferative affecting T>B cells

200
Q

What is MOA of methotrexate

A

Inhibits dihydrofolate reductase which so is anti folate

201
Q

What is MOA of daclizumab

A

IL-2 receptor antibody, targets CD25

i think IL-2 and CD25 are same/v related

202
Q

What is MOA of rituximab

A

Anti-CD20 which depletes mature B cells but not plasma cells

203
Q

What is MOA of muromonab-CD3

aka OKT3

A

Blocks CD3 on T cells

204
Q

What is MOA of alemtuzumab

A

Binds to CD52- blocks all lymphocytes (B, NK, T cell production)

205
Q

Which immunosuppressive agent is strongly linked with JC virus

A

Mycophenolate motefil

(MFM and pMl)

and natalizumab!

206
Q

What is main side effect of calcineurin inhibitors

A

Gingival hypertrophy

mainly ciclosporin - ciclo’sore’in i.e. sore gums

207
Q

What is main side effect of cyclophsophamide

A

Haemorrhagic cystitis due to excretion product acrolein

i.e. not BK virus!

208
Q

What is MOA of cyclophoshamide

A

Alkylates guanine which inhibits DNA synthesis

209
Q

What is MOA of corticosteroids

A

Inhibits phospholipase A2

210
Q

What is MOA of infliximab

A

TNF-alpha inhibitor

211
Q

What is MOA of denusomab and what used in

A

Anti-RANK ligand
Osteoporosis

212
Q

How is contact dermatitis diagnosed

A

Patch testing

213
Q

What is immunopathology of an allergic reaction

A

if an allergen is taken up by a macrophage, it is processed
intracellularly and peptides are presented via major histocompatibility
complex on the cell surface to T cells of the TH2-cell (E) subclass. TH2-
cell secrete IL-4, which stimulates B cell (B) proliferation. TH1-cells (D)
do not play a role in the pathogenesis of type I hypersensitivity but do
contribute to type IV hypersensitivity reactions. B cells in turn produce
allergen-specific antibodies of the IgE variety. IgE binds to mast cells
(A) via the Fc receptor.

214
Q

Which C proteins involved in membrane attack complex

A

C5b through to 9

215
Q

What is presentation when defect in terminal pathway forming membrane attack complex

A

Defects in C5b through to 9 lead to recurrent infection with encapsulated bacteria

216
Q

What is difference between a mature and immature dendritic cell

A

Immature- phagocyte
Mature- antigen presenting cell

217
Q

Which cells derive from monocytes

A

Macrophages

218
Q

When on what drug do you get repeated mouth and lip swelling after procedures

A

ACEi

drug induced angiooedema

219
Q

Which vaccines are given to the elderly

A

Pneumococcal PPV
Shingles
Flu

Don’t break your HIP

H for herpes zoster = shingles

220
Q

Which cells are involved in adaptive immune response to vaccines

A

APC presents to specific receptor effector T-cell
which then proliferate
Specific antigen binds to b-cells release IgM, which undergo proliferation to memory b-cells and plasma cells with high affinity antibodies

rememebr T cells stim B cell (CD40/28 complex)

221
Q

Which antigen confers immunity to Influenza vaccine

A

Haemoagglutinin

222
Q

How does tuberculin test work

A

Inject tuberculin into arm and measure induration width 48 hours later

223
Q

How do conjugate vaccines work

A

Contain a weak antigen alongside a stronger antigen to trick immune system into generating stronger response to weaiker antigen

e.g. diphtheria toxin = strong immunogenic toxin

224
Q

When is interferon alpha given to boost immune response

A

Hep B and C

ABC- ifn-A for hep B, C and CML

225
Q

When is IL-2 given to stimulate T cell response

A

Renal cell cancer

2 kidneys

226
Q

When are haematopoietic stem cells given

A

SCID
Leukocyte adhesion defect
Haem malignany

227
Q

Which organisms are bloods for IVIG screened for

A

HIV
Hep B and C

228
Q

Indications for antibody replacement

A

Primary AB deficiency
- X linked agammaglobulinaemia
- X linked hyper IgM syndrome
- CVID

Secondary deficiency
- CML? CLL
- myeloma

229
Q

When are specific abs given

A

Hep B exposure from sex/needlestick etc HBSag
Rabies exposure from a bite
VZV in pregnant women
Suspected tetanus exposure

230
Q

What is adoptive cell transfer

A

Can give specific T cells to a recipient

231
Q

Types pf adoptive cell transfer

A

Virus specific T cells
Tumour infiltrating T cells
Tcell receptor T cells
Chimeric antigen T cells

CaVITy

232
Q

What is virus specific t cell therapy

A

Take allogenic or autologous T cells
Expose to antigen
Grow them and give back to recipient

233
Q

When is virus specific T cell therapy used

A

EBV related B cell lymphoproliferative disease
Persistent viral infection in immunocompromised

e.g. post Tx LPD?

234
Q

How does tumour infiltrating lymphocyte therapy work

A

Excise a tumour
Identify lymphocytes which have infiltrated tumour and expand them with IL-2 and reinfuse

235
Q

Blood features of coeliac

A

IDA
- hypochromic and microcytic
Megaloblastic? B12 abs in ileum (crohn’s?)
- hypersegmented
- macrocytosis
Hyposplenism
- howell-jolly bodies

i guess general inflammation reduces absorption!

236
Q

Hyposplenism causes

A

Coeliac
SLE
SCD
IBD

coeliac and IBD i always forget!

237
Q

What exact antigen does anti-tissue transglutaminase respond to

A

Gliadin

238
Q

What type of antibodies are anti-TTG and endomysial

A

IgA

239
Q

Where take biopsy in coeliac

A

Deeper duodenum as presence of brunners gland distorts biopsy

or jejunal biopsy

240
Q

Define atopy and anaphylaxis

A

Atopy- tendancy to produce IgE
Anaphylaxis- allergic reaction with an A,B or C definition

241
Q

Person had anaphylaxis then a few hours later has same symptoms, what cause

A

Anaphylaxis is biphasic

242
Q

What is used to measure complement

A

C3 and C4
CH50
AP50

243
Q

What is livedo reticularis seen in

A

Antiphospholipid- net like discolouration of legs

244
Q

Non serological blood findings of APL

A

Thrombocytopenia
Prolonged APTT

mnemonic = CLOTS (coagulopathy, livedo reticularis, obstetric complications, thrombocytopaenia, SLE (can be with or w/o it!))

245
Q

How is renal disease monitored in SLE

A

Urine dip

246
Q

Why get recurrent infections in myeloma

A

Suppression of BM expansion by IgG

247
Q

Why get anaemia in myeloma

A

Plasma cells crowd out the BM

248
Q

What are T-cell receptor T cells and chimeric antigen receptor cell therapy

A

Involves the insertion of genes into T-cells which provokes development of T cell receptors on their surface which can bind to ligands on tumour cells

249
Q

Difference between chimeric antigen receptor cell therapy and t-cell receptor T cell therapy

A

In chimeric the genes inserted are made up of recombinant genes

250
Q

Use of chimeric antigen receptor T cells

A

Can get T cells to express receptors which bind to CD19 of some non-hodgkin lymphomas and b lymphocytes in ALL

251
Q

Which cell is most affected by steroids

A

CD4+

i think steroids initially cause neutrophils to rise as blocks them entering tissues!

252
Q

Side effects of antiproliferative immunosuppressants

A

BM suppression
Infection
Malignancy

253
Q

What is MOA of rapamycin/sirolimus

A

mTOR inhibitor which prevents T cell proliferation via IL-2

254
Q

What is MOA of jakinibs

A

Inhibit JAK-STAT signalling which prevents production of cytokines

255
Q

What are JAKinibs used in

A

Psoriasis
RA
Ank spond

256
Q

What are PDE4 inhibitors used in

A

Psoriasis

e.g. apremilast

257
Q

What is MOA of PDE4 inhibitors

A

Modulates cytokine release

258
Q

MOA of basilixumab and daclizumab

A

Binds to IL2R/CD25 reducing T cell proliferation

259
Q

MOA of abatecept

A

Reduces costimulation of T cells via CD28

260
Q

MOA of vedolizumab

A

Binds to alpha 4 beta 7 integrin which inhibits leukocyte adhesion

261
Q

MOA of tocilizumab

A

IL-6 receptor antibody

262
Q

What is tocilizumab (IL-6 antibody) used for

A

RA

263
Q

MOA of secukinumab

A

Anti-IL17

264
Q

MOA of guselkumab

A

Anti-IL23

265
Q

MOA of mepolizumab

A

Anti-IL5

266
Q

Use of mepolizumab

A

Eosinophilic asthma

267
Q

What is most common classical pathway deficiency

A

C2

268
Q

What are the most common SCIDs

A

X-linked SCID most common
Adenosine deaminase deficiency 2nd most common

269
Q

Pathophysiology of X-linked SCID

A

Defective gamma chain on IL-2 leading to no t-cells and NK cells but immature B-cell production

270
Q

Blood findings of x-linked SCID

A

Low T-cells and NK cells
Normal B cells

271
Q

Pathophysiology of ada deficiency

A

Adenosine deaminase deficiency which is enzyme involved in leukocyte deficiencies
Low all b and t cells

272
Q

Blood findings of ADA deficiency

A

Low T and NK cells
Low B cells

273
Q

Inheritance of hyper IgM syndrome

A

x-linked recessive

274
Q

Presentation of hyper IgM

A

Failure to thrive
Recurrent bacterial infections
PJP infection

275
Q

What are the polygenic auto-inflammatory disease

A

IBD
Osteoarthritis
GCA
Takayasus arteritis

276
Q

What are the mixed pattern disease

A

Ank spond
Psoriatic arthritis
Behcets disease

277
Q

What does speckled mean when it comes to antibodies

A

Under immunofluorescence it means the nucleus is speckled with antibodies

278
Q

What ENA have speckled appearance

A

Ro
La
U1RNP

extractable nuclesar AGs

279
Q

What gel and coombs in RA

A

4
3 if RF positive

280
Q

Difference between direct and indirect antigen detection in transplant rejection

A

Direct- donor APC presents foreign antigen to host T cells (acute)
Indirect- host APC presents foreign antigen to T cells like in infection

281
Q

How to remember which cells antiproliferative agents affect the most

A

B cells
- cyclophosphamide
T cells- ones which have T in
- azathioprine
- mycophenolate motefil
Can include tacrolimus here too

282
Q

MOA of ustekinumab

A

Anti-IL12 and IL-23

283
Q

Name for beef tapeworm

A

Taenia saginata

284
Q

What is the target of the antibody P-ANCA?

A

Myeloperoxidase

285
Q

What is the target of the antibody C-ANCA?

A

Proteinase 3

286
Q

What hematological cells create a “respiratory burst” in order to kill phagocytosed pathogens?

A

Neutrophils- done by NADPH oxidase

287
Q

What is the worst SCID

A

Reticular dysgenesis

288
Q

What is the minimum number of Fc receptors on the surface of mast cells that must bind to an antigen to cause mast cell degranulation

A

2

289
Q

Which cell surface receptor allows cells of the innate immune system to bind to immunoglobulins?

A

Fc

290
Q

What test can be used to identify the allergens in allergic rhinitis?

A

Skin prick

291
Q

Antibodies in diffuse systmeic sclerosis

A

Topoisomerase (Scl70)
Fibrillarin

292
Q

What is the maximum number of viral capsids that a molecule of IgM, IgA and IgG may bind to?

A

IgM- 10
IgA- 4
IgG- 2

293
Q

What is use of natalizumab

A

Relapsing remitting MS

294
Q

MOA of natalizumab

A

Targets alpha4integrin

295
Q

T helper cells involved in bacterial versus allergies

A

Bacterial infections- T helper 1 cells
Allergies- T helper 2 cells

296
Q

Monoclonal vs polyclonal antibodies

A

Monoclonal antibody = a solution of identical antibodies Polyclonal antibody = a solution of mutliple antibodies with different affinities for the same antigen (or target molecule)

297
Q

What is example of integrase inhibitor

A

Dolutegravir

298
Q

What chemical is responsible for urticaria and swelling in allergy

A

Histamine

299
Q

What is latex food syndrome

A

Latex food syndrome is an IgE mediated type 1 hypersensitivity reaction to fruits and seeds, that is caused by cross-reactivity to latex antigens.

300
Q

HLA association of DM

A

DR3 and DR4

301
Q

HLA association of goodpastures

A

DR15

302
Q

Presentation of hereditary angioedema

A

Recurrent bouts of swelling around mouth and neck

303
Q

Pathophysiology of herditary angioedema

A

Acquired C1-inhibitor deficiency

Arjun's Copy- Owen's Path (8 decks)

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