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Written exam > Immunology > Flashcards

Immunology Flashcards

1
Q

What are the 4 types of immune hypersensitivity reactions?

A

1 - immediate: IgE mediated
2 - cytotoxic; IgG or IgM mediated
3 - immune complex mediated
4 - delayed; cell mediated

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2
Q

Mediators, effects and cells involved in a Type 1 (immediate) hypersensitivity reaction?

A

Mediators - allergen-specific IgEs
Effect - histamine, leukotrienes, prostaglandin D2, cytokines, enzymes
Cells - mast cells and basophils

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3
Q

Mediators, effects and cells involved in a Type 1 (late phase) hypersensitivity reaction?

A

Mediators - IgE
Effect - cytokines
Cells - eosinophils and basophils

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4
Q

Mediators, effects and cells involved in a Type 2 late phase hypersensitivity reaction?

A

Mediators - IgG, rarely IgM
Effect - opsonisation, complement activation
Cells - phagocytes

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5
Q

Mediators, effects and cells involved in a Type 3 late phase hypersensitivity reaction?

A

Mediators - IgG or IgA immune complex precipitation
Effect - complement activation
Cells - phagocytes

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6
Q

Mediators, effects and cells involved in a Type 4 late phase hypersensitivity reaction?

A

Mediators - T cells
Effect - cytokines
Cells - T cells, macrophages

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7
Q

Explain Type 1 acute phase response hypersensitive reactions

A

Occurs within minutes to an hour after exposure to an allergen.
Examples - systemic anaphylaxis, allergic rhino-conjunctivitis, allergic asthma, atopic dermatitis
Symptoms mostly due to release of histamine from mast cell and basophils
IgE antibodies are antigen specific and only occur in response to previous exposure

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8
Q

Effects of histamine

A

Vasodilation, increased vascular permeability, tachycardia, cardiac contraction, glandular secretion

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9
Q

What are the 4 histamine receptors

A

H1 - wheal and flare reaction, bronchoconstriction, pruritus
H2 - increased gastric acid secretion
H3 - decreased histamine synthesis and release (neg feedback)
H4 - chemotactic pathway for eosinophils

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10
Q

Explain Type 1 late phase response hypersensitive reactions

A

May start 2-12 hours after immediate reaction
Can last hours to days
Cytokine release from the acute phase causes an infiltration of eosinophils and basophils
The probability of LPR increases with the severity of the acute reaction

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11
Q

Explain Type 2 hypersensitive reactions

A

Cytotoxic hypersensitivity.
Common cause of autoimmune-mediated cell destruction.
Initiated when IgG or (rarely) IgM binds to an antigen on a cell (eg RBCs, plts), a fixed tissue antigen (eg basement membrane) or a cell receptor (eg thyroid hormone receptor).
These IgG and IgM antibodies are called autoantibodies.
Binding of the antibody results in target cell destruction by:
-> cells lysed by MAC due to complement activation
-> opsonisation from the production of C3b due to complement activation, therefore attracting phagocytes
-> phagocytes have a receptor for the Fc portion of the antibodies and attack antibody coated cells.

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12
Q

Examples of antibody mediated cell destruction (type 2 hypersensitivity reaction)

A

Immune thrombocytopaenia - plts
Autoimmune haemolytic anaemia - RBCs
Leukopaenia - WBCs
Goodpasture syndrome - basement membrane of kidneys and lungs
Myasthenia gravis - ACh receptor on muscle cells
Graves disease - thyroid hormone receptor

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13
Q

Explain type 3 hypersensitivity reactions

A

Immune complex hypersensitivity, seen in autoimmune diseases and drug reactions.
Due to accumulation of ICs not cleared by innate immune system. Abs (usually IgG but can be IgA) combine with an antigen and form an IC.
In contrast to type 2, antigens are soluble and not bound to cell surfaces.
Precipitation occurs with excess antigen to Abs (Ag:Ab>1). As more Abs are produced, a point is reached where there is only slight Ab excess. At this pt, the ICs interlace and become bigger and less soluble. These precipitate in small vessels -> activate complement -> cytokine release -> gathering of more inflammatory cells -> necrosis of small vessels.
Hallmark pathologic finding = leukocytoclastic vasculitis, identified by hemorrhagic indurated lesions ie palpable purpura.

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14
Q

What are the models of systemic v localised reaction in Type 3 hypersensitivity reactions?

A

Serum sickness (systemic) - non-immunised to antigen, see necrotic vasculitis. Also affects the joints and kidneys causing arthritis and nephritis.
Arthus reaction (cutaneous or localised) - hyperimmunised so that there are many circulating IgG Abs. A small intradermal injection of the Ag leads to complement cascade and activation at the site of injection. A painful indurated lesion develops in 4-6 hrs, can progress to sterile abscess.

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15
Q

Examples of autoimmune type 3 hypersensitivity reactions

A

SLE - SLE; nuclear materials eg dsDNA, Smith antigen
IgAV - respiratory pathogen
Pernicious anaemia - intrinsic factor
Rheumatoid arthritis - RA, rheumatoid factor

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16
Q

Examples of external antigen type 3 hypersensitivity reactions

A

Hepatitis antigen - associated serum sickness
Farmer’s lung - mould or hay dust
Tetanus and diphtheria immunisation
Local insulin reactions

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17
Q

Explain type 4 cell mediated reactions

A

T-cell mediated, antibody INDEPENDENT, delayed reaction.
Involves previously sensitised T cells interacting with an antigen, causing the attraction and activation of macrophages resulting in an inflammatory reaction.
Reaction peaks in 1-3 days.

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18
Q

Examples of type 4 hypersensitivity reactions

A

Positive tuberculin test
Allergic contact dermatitis - poison ivy, nickel, metals
Granulomatous disease - Crohns, sarcoidosis
Allograft rejection
Graft-versus-host disease

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19
Q

What are the allergic disorders?

A

Asthma, eczema, rhinitis, conjunctivitis, food allergy, urticaria

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20
Q

Explain anaphylaxis

A

An acute, severe, life-threatening reaction to an allergen that leads to the release of immune mediators from mast cells and basophils. At least 2 organ systems are involved, including the skin, resp, CVS, GI and neuro.
Symptoms that are similar but non-IgE mediated are called anaphylactoid or non-IgE mediated anaphylaxis.

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21
Q

What is DRESS?

A

Drug reaction with eosinophilia and systemic symptoms.
May begin 2-12 weeks after beginning treatment.

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22
Q

Explain drug desensitisation

A

Indicated if drug is the only known clinically effective therapy. Usually penicillins or cephalosporins in CF and multiple drug resistant pseudomonas.
Only effective for one course, must be repeated each time.
Contraindicated for severe cutaneous drug reactions.

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23
Q

Explain Vancomycin Redman syndrome

A

Vancomycin flushing syndrome.
Non immune-mediated, hypersensitivity syndrome.
Caused by stimulation of vasoactive mediators, resulting in flushing, erythema and upper body pruritus.
May also have chest pain, dizziness, hypotension.
Absence of anaphylactic signs - wheeze, swelling, hives, GI sx.
Treat by lowering the infusion rate, not decreasing the dose.
Other forms of vancomycin hypersensitivity include IgE-mediated anaphylaxis, nephrotoxicity, drug-induced fever, and DRESS syndrome.
May also get linear IgA bullous dermatosis.

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24
Q

Explain linear IgA bullous dermatosis

A

Associated with antibiotics, esp Vancomycin.
Clinical appearance similar to erythema multiforme.
Occurs 24 hrs - 1 mth post use.
Usually face, lower trunk and genitalia.
Rings of blisters - “string of pearls sign” - common on the trunk.
Spares conjunctiva and mucous membranes.
Dx via biopsy and direct immunofluorescence - shows linear IgA deposition at the dermal-epidermal junction.
Resolves with discontinuation of antibiotic.
If can’t discontinue drug, can use dapsone.

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25
Q

Explain DRESS

A

Drug reaction with eosinophilia and systemic syndromes.
T cell mediated.
10% mortality.
Usually occurs 2-6 wks post drug use, can be up to 12 wks.
Most common triggers are abx (vanc, minocycline, sulfonamides) but also aromatic antiepileptics and allopurinol.
May cause viral reactivation - HHV 6, HHV 7, EBV, CMV.
Sx: polymorphous rash, may be pruritic; fever; lymphadenopathy; facial swelling, arthralgias, multiorgan involvement (eg hepatitis, carditis, nephritis).
Ix: leukocytosis with peripherial eosinohilia, atypical lymphocytes, elevated serum transaminases.
Mx: cease drug (symptoms persist or worsen post), supportive care, glucocorticoids. In severe cases IvIG or immunosuppressants eg cyclosporine.

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26
Q

Explain a fixed drug reaction

A

Slightly oedematous and well-circumscribed lesions that usually occur at the same sight following reexposure to an agent.
Usually solitary lesions, may occur in small groups.
Occasionally get central blistering of the eruption, followed by desquamation, and crusting.
Usually resolves in 7-10 days but may have residual hyperpigmentation that can last for mths.
Usually occur in mouth, hands, trunk and genital area.
Initial lesions may not appear for a week or longer after agent is ingested by are visible 30 minutes to 8 hrs following repeat ingestion.
Mx: avoid offending agent.

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27
Q

SJS v TEN

A

SJS - < 10% BSA
SJS/TEN - 10-30% BSA
TEN - > 30% BSA

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28
Q

What is the Nikolsky sign?

A

Occurs in SJN/TEN.
Sloughing of the epidermis with slight tangential pressure.

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29
Q

Anaphylaxis diagnostic criteria

A
30
Q

Broad categories of immunodeficiencies

A

Adaptive
-> B-cell deficiencies
-> T-cell deficiencies
-> Combined B and T cell
Innate
-> Phagocytic disorders
-> Toll-like receptor defects
-> Complement deficiencies
Also
-> Immune dysregulatory diseases, autoinflammatory diseases, bone marrow failure syndromes

31
Q

Classic B-cell deficiency infections

A

Recurrent sinopulmonary infections (after maternal antibodies are depleted)
-> Bacteria: encapsulated (eg Strep pneumo Haem flu), staph aureaus, pseudomonas (no IgG, no IgM)
-> Virus: enterovirus (no IgA)
-> Protozoa: Giardia (no IgA, no IgE)

32
Q

Class T-cell deficiency infections

A

Intracellular organisms and opportunistic infections
-> Bacteria (mostly intracellular): Salmonella, syphilis
-> Mycobacteria: TB, mycobacterium avium complex
-> Viruses: CMV, HSV, VZV, EBV, hepatitis, HPV, molluscum contagioscum
-> Fungi: Candida, Aspergillus, coccidioidomycosis, Cryptococcus, histoplasmosis
-> Protozoa: Pneumocystis, toxoplasmosis, cryptosporidiosis, isosporiasis, microsporidiosis

33
Q

Classic phagocytic deficiency infections

A

Skin and organ abscesses
-> Bacteria: S aureus, Serratia, Nocardia

34
Q

Classic Toll-like receptor defect infections:

A

Recurrent severe infections (cellulitis, arthritis, meningitis, osteomyelitis, organ abscesses, sepsis)
-> Bacteria: pyogenic bacteria, mycobacteria
-> Virus: herpes virus

35
Q

Classic complement deficiency infections

A

Overwhelming sepsis
-> Bacteria: Neisseria meningitidis, S pneumoniae

36
Q

General features x-linked agammablobulinaemia (XLA)

A

Males only
Absent to low IGs of all classes
No IG-carrying B cells in peripheral circulation, but they’re normal in the bone marrow.
Due to mutation in the BTK gene (at Xq22) that encodes for Bruton tyrosine kinase, which is necessary for B-cell development.
Usually presents at 6mths once placental IgG has been consumed.

37
Q

XLA associated infections

A

Encapsulated bacterial infections of the respiratory tract are common (pneumonia, OM, sinusitis).
Also meningitis, sepsis, osteomyelitis or persistent/recurrent giariasis.
Predisposition to enterovirus infections, at high risk if given the live polio vaccine (an enterovirus).

38
Q

XLA - exam, diagnosis, treatment

A

Exam: small or absent lymph nodes and tonsils.
Investigations:
-> Flow cytometry: no mature B cells, deficiency in all Ig classes.
-> B lymphocytes are absent from the blood and lymph tissue, but present in bone marrow.
Management:
-> IVIG or subcut Ig (SCIG) + manage infections

39
Q

What are the live vaccines?

A

Bacille Calmette-Guerin
MMR
Varicella - may not be suitable in close contacts
Intranasal flu - also not suitable in close contacts
Rotavirus
Oral poliovirus - also not suitable in close contacts
Smallpox - not suitable in immune compromised or atopic dermatitis

40
Q

Groups to be aware of re vaccines

A

Immunocompromised
HSCT
Receiving steroids - 2mg/kg prednisolone for >14 days (should be off steroids for 3 mths before give vax)
HIV - receive MMR and VZV vax at age 12 mths, not for OPV

41
Q

Tests used for immunodeficiency screen

A

IgG, IgA, IgM levels - assess quantitative humoral defects
Specific antibody titres to vaccines - assess qualitative humoral defects
Flow cytometry - assesses cellular immunity (enumerates lymphocyte subsets)
Total haemolytic complement (CH50) - assesses complement function (all steps in the classical pathway (C1-C9) must be present to yield normal result
Genetic testing

42
Q

What are the key B-cell deficiencies?

A

XLA
CVID
Specific antibody deficiency
Selective IgA deficiency
Hyper IgM syndrome
X-linked lymphproliferative disease
Transient hypogammaglobulinaemia of infancy

43
Q

What are the key T-cell deficiencies

A

22q11.2 deletion (DiGeorge) syndrome - thymic hypoplasia, absent T-cells, B-cells can’t produce Abs due to lack of T-cell help
Nezelof syndrome - autosomal recessive form of thymic hypoplasia

44
Q

Features of immune deficiency in DiGeorge syndrome

A

Variable immune manifestations.
Low CD3+ T-cells.
If complete DiGeorge phenotype:
-> have absent T-cells, B-cells can’t produce antibodies due to lack of T-cell help
-> can have SCID, at risk of GVHD from nonirradiated blood and cells
If partial phenotype:
-> partial T-cell depletion and normal B-cell function
-> immune deficits can improve with time

45
Q

Describe transient hypogammaglobulinaemia of infancy

A

Diagnosis of exclusion.
Thought to be abnormal prolongation of physiological hypoIg that occurs normally between 4 and 6 mths.
Usually have normal IgG levels by 3-4 yrs of age.
Most do not need treatment, but consider IVIG if recurrent infections or markedly low IgG levels, or antibiotic prophylaxis (amoxicillin or cotrimoxazole) if frequent RTIs +/- OM.

46
Q

Describe x-linked proliferative disease (Duncan syndrome)

A

Causes severe or fatal infections with EBV.
Fulminant infectious mononucleosis results in hepatitis, B-cell lymphomas, agranulocytosis, aplastic anaemia, or acquired hypogammaglobulinaemia.
Pathophysiology -> EBV triggers a polyclonal expansion of B and T cells -> leads to NK or cytotoxic T-cell infiltration of organs.
Most common causes of death are hepatic necrosis and/or bone marrow failure.
If survive EBV infection, are at risk of malignancy esp Burkitt-type lymphoma.
Genetics - mutation of the SH2D1A gene on Xq25.
Mx: steroids, immunosuppressants, rituximab (anti-CD20 monoclonal antibody), cytotoxic agents, only cure = allogenic stem cell transplantation.

47
Q

Explain the pathophysiology of infectious mononucleosis

A

Mononucleosis = large amounts of cells with a single nucleus (ie T-cells)
Usually caused by EBV
EBV targets B cells - uses the surface glycoproteins to attach to the CD21 receptor, enter the cell and replicate.
This initiates a T-cell response, esp cytotoxic T-cells. This contributes to the symptoms of swollen lymph nodes, fever and fatigue.

48
Q

Hyper IgM syndrome - features

A

Normal or high IgM with low IgA, IgG and IgE
X-linked (more common, poor prognosis with high risk of malignancy) and AR forms.
Defect on x-chromosome encoding the CD40L on the T-cell, prevents Ig class switching from IgM to other classes.
Also impairs T-cell to macrophage signalling, therefore at risk of opportunistic infections.
Common infections: sinopulmonary with encapsulated bacteria, giardiases, bacterial and viral meningitis.
X-linked susceptible to PJP, or chronic parvovirus infection (leading to RBC aplasia).

49
Q

Hyper IgM syndrome - exam, diagnosis, treatment

A

Exam - hepatosplenomegaly, non-palpable to enlarged lymph nodes.
Investigations:
-> Bloods - high IgM, low IgG, IgA, IgE
-> Flow cytometry - normal T and B cell counts with lack of CD40L on activated CD4+ T cells, Ab responses decreased or absent
-> Genetic testing
Management:
-> IVIG/SCIG
-> prophylactic antiobiotics eg cotrimoxazole for PJP
-> HSCT for x-linked disease

50
Q

Common variable immunodeficiency (CVID) - features

A

Recurrent sinopulmonary infections with encapsulated bacteria.
Deficiency of at least 2 classes of IGs (IgG, IgA or IgM) AND poor IG function as demonstrated by IgG titres to vaccines (diptheria/tetanus for protein and pneumococcal for polysaccharide).
Most cases have an unknown genetic basis, M and F equally affected, sometimes familial.
Pathogenesis - B cells cannot or have impaired differentiation into plasma cells.
Can present at any age. Unlike other immunodeficiencies, most common in teens and 20s, rare in young children.

51
Q

CVID - exam, diagnosis, management

A

Exam:
-> sarcoid-like disease with non-caseating granulomas of the spleen, liver, lungs, skin - can present as hepatosplenomegaly
-> ITP, pernicious anaemia, haemolytic anaemia, malabsorption, pancytopaenia
-> polyarthritis
-> amyloidosis, HUS (more typical in CVID)
-> sprue-like illness common ie diarrhoea, malabsorpotion, steatorrhoea, protein-losing enteropathy

Other associated findings:
-> lymphoma
-> giardia infection
-> chronic enteroviral meningitis

Management:
-> IVIG/SCIG and infection-specific therapy

52
Q

Describe specific antibody deficiency

A

Like XLA and CVID, recurrent sinopulmonary infections with encapsulated organisms.
Poor functioning of Abs, despite B-lymphocytes and normal IG levels.
Will see poor reponse of IgG titres to vaccines.
Management: specific Ab therapy for infections +/- IVIG/SCIG.

53
Q

Describe IgA deficiency

A

Most common primary immune disorder, prevalence as high as 1:300.
Most patients asymptomatic.
1/3 have recurrent sinopulmonary or GI infections.
Associated with atopy and some autoimmune conditions eg coeliac, thyroid, autoimmune cytopaenias, JIA, SLE, T1D, IBD.
Rarely associated with malignancy.
Management:
-> prophylactic abx if recurrent infection
-> IVIG/SCIG is a relative contraindication, as pts can develop allergic reactions or anaphylaxis + have normal IgG levels.
-> If need IVIG due to progression to CVID, administer a product with low IgA content and administer cautiously with premeds of antihistamines +/- glucocorticoids.

54
Q

Characteristics of primary B-cell immunodeficiencies

A
55
Q

Tests for immunodeficiencies

A
56
Q

Overview of complement cascade

A

Classical, lectin and alternative pathways lead to:
-> production of C3
-> opsonisation (candy coating) of target cells with C3
-> formation of membrane attack complex (MAC)

57
Q

Describe the complement cascade

A
58
Q

Explain the classical complement pathway

A

Activated by IgG and IgM
1 IgM pentamer can initiate it, but normally takes at least 2 IgGs.
C1q subunit attaches to an Ab in an antigen-Ab complex -> C1q binds to the Fc portion of 2 IgGs (or 1 IgM penatmer) or to the pathogen’s surface -> binding changes the conformation of C1q -> activated C1 cleaves C4 then C2 to form C4b and C2a -> combine to form C4b2a (C3 convertase) which activates C3.

59
Q

Explain the lectin complement pathway

A

Activated by binding of lectins (mannose-binding lectins (MBLs) to mannose on surface of pathogens.
Associated proteases then cleave C2 and C4 -> similar mechanism then to classical pathway.
MBLs are produced by an acute-phase response and are fairly non-specific.

60
Q

Explain the alternative complement pathway

A

C3 is spontaneously cleaved by bacterial cell wall hydroxyl groups.
Cleaved C3 combines with factor B -> this complex activates more C3 and factor B -> leads to cascade normally regulated by H and I proteins.

61
Q

Explain the membrane attack complex (MAC)

A

C3, when combined with C4b2a or factor B, activates C5 -> causes the formation of C5-6-7-8-9 MAC.
The MAC forms holes in bacterial cell wall membranes, killing the bacteria.
MAC targets only the few bacteria not cleared by the C3b opsonisation and phagocytosis - mainly Neisseria.

62
Q

Explain atopic dermatitis

A

One of the many types of eczema (dermatitis).
Chronic, relapsing, inflammatory skin disease associated with allergy, but is not itself an allergy.
Known as the “itch that rashes”.
In older children presents on flexor surfaces (ACF, axilla, inguinal, behind the ears, around the eyes).
In infants, presents on the scalp, face and extensor surfaces.
Atopic dermatitis pts have higher rates of allergic diseases than general population
-> approx 50-75% develop asthma +/- allergic rhinitis
-> approx 1/3 have food allergies
Rountine food allergy not recommended due to false positive results, although may do prior to introduction of peanuts in 4-6 mth year olds with severe eczema and/or egg allergy.

63
Q

Eczema treatment

A

1) Moisturisers - 1st line, best applied to wet skin after short lukewarm baths
2) Immunomodulatory creams - topic corticosteroid, topical calcineurin inhibitor (pimecrolimus or tacrolimus), or crisaborole ointment. Topic calcineurin inhibitors don’t cause skin atrophy and can be prescribed for the face (if > 2 yrs).
3) Oral antihistamines - to help with pruritis.
4) Wet wraps - acts to keep skin moist, prevents trauma from further scratching, cooling effect during evaporation.
5) Antibiotics - required for superimposed infection (usually staph aureus).
6) Other - oral immune suppressants (cyclosporine and MTX) and phototherapy. Oral corticosteroids are NOT recommended in kids.

64
Q

Eczema - prevention

A

1) Maternal dietary restriction during pregnancy does not prevent the development of atopic disease.
2) Breastfeeding for at least 4 mths may decrease the risk of eczema, cow’s milk allergy, VIW.
3) If have high risk of atopy and not breastfed, hydrolysed formulas may delay onset of atopic disease.
4) There is NO evidence that delaying solids after 4-6 mths of age prevents the occurrence of atopic disease (and will likely increase food allergies).
5) Use of soy-based formula does NOT prevent atopic disease.

65
Q

Describe contact dermatitis

A

Subtype of eczema.
Typically a type 4 T-cell mediated hypersensitivity reaction.
Poison oak and ivy cause dermatitis in most individuals.
If makeup, hair product, nickel-containing jewellery or belt buckle cause the rash refer to dermatologist or allergist and avoid using the agent.

66
Q

HLA definition

A

Human major histocompatibility complex HLA antigen

67
Q

Explain HLA restriction

A

T cells recognise antigens if, and only if, Class I or Class II HLAs present them.
Binding of the T-cell receptor (TCR) to the antigen bound to the HLA on antigen presenting cells initiates TCR signalling that results in T-cell responses.

68
Q

Explain Class I HLAs (aka MHC - major histocompatibility complex)

A

On all cells except mature RBCs.
3 subtypes: HLA-A, HLA-B, HLA-C
Class I HLAs present non-self material to the CD8+ T cells and activate them.
Once activated the CD8+ cells will kill the attached cell - important in transplant rejection and fighting neoplasms and viral infections.

69
Q

Anaphylaxis - signs of mild to moderate allergic reactions

A

Swelling of lips, face, eyes
Hives or welts
Tingling mouth
Abdo pain, vomiting (also signs of severe allergic reaction to insects)

70
Q

Anaphylaxis - signs and symptoms of severe reaction

A

In setting of exposure to allergen…
Difficult talking, hoarse voice
Difficult/noisy breathing
Swelling of tongue
Swelling/tightness in throat
Wheeze, persistent cough
Dizziness, collapse
Pale and floppy (infants)
If insect bite - abdo pain,

Written exam (14 decks)

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