Immunology COPY Flashcards
Which one of these statements about mucosal surfaces is NOT true?
(a) Lysozyme and antimicrobial peptides directly kill invading pathogens
(b) Lactoferrin acts to starve invading bacteria of iron
(c) Secretory IgA prevents bacteria and viruses attaching to and penetrating epithelial cells
(d) Physical barrier to trap invading pathogens
(e) Mucous contains IgM to effectively bind pathogens before they can invade the epithelial cells.
The statement that is incorrect is (e). Mucous contains secretory IgA as detailed in option (c), IgM is not inherent in mucous itself.
Which one of these immune cells is the odd one out?
(a) Kupffer Cell
(b) Microglia
(c) Langerhans Cell
(d) Mast Cell
(e) Mesangial cell
The correct answer is (d), mast cell.
Mast Cell is the odd one out because all the others are macrophages. Kupffer is from the liver, microglia the brain, Langerhans the skin and mesangial cell the kidney.
Regarding polymorphonuclear cells, what statement is false?
(a) Express Fc receptors for immunoglobulin – to detect antigens on pathogenic cells
(b) Express pattern recognition receptors – to detect pathogens
(c) Capable of non-oxidative killing
(d) Express receptors for cytokines and chemokines to detect inflammation
(e) Release lipid mediators of inflammation from granules
The statement that is incorrect is (a). Polymorphonuclear cells do express Fc receptors for immunoglobulin, but their role is to detect immune complexes, not the antigens on pathogenic cells themselves.
In the thymus, if a T cell has an intermediate affinity for HLA class I, what will happen to that T cell?
(a) Differentiate as a CD4+ T cell
(b) Not be selected due to not having high enough reactivity.
(c) Not be selected due to negative selection to avoid autoreactivity
(d) Differentiate as a CD8+ T cell
(e) It will acquiesce until it gets a higher affinity for HLA class I
The correct answer is (d), it will differentiate as a CD8+ T cell.
If it had low affinity for HLA it would not be selected due to inadequate reactivity, and if it had high affinity it would face negative selection to avoid autoreactivity. If the cell had intermediate affinity for HLA class II instead it would differentiate as a CD4+ T cell.
Which of the following statements about B cells are true?
(a) Can express IgG with stimulation by an antigen, requires cd4 t cell help to produce IgM and IgD
(b) Can express IgM with stimulation by an antigen, requires cd4 t cell help to produce IgA and IgG
(c) Can express IgA with stimulation by an antigen, requires cd4 t cell help to produce IgM and IgD
(d) Can express IgE with stimulation by an antigen, requires cd4 t cell help to produce IgA and IgM
(e) Can express IgD with stimulation by an antigen, requires cd4 t cell help to produce IgE and IgM
The correct answer is (b).
B cells can express IgM when stimulated by an antigen, this causes the early IgM response. If the B cells are provided with appropriate signals from CD4+ T cells in secondary lymphoid tissue, they proliferate and undergo genetic rearrangements. This involves isotype switching to IgG, IgA or IgE and somatic hypermutation to generate high affinity receptors. B cells can also undergo further differentiation into plasma cells with product IgG, IgA or IgE antibody or to long-lived memory cells.
Which of the following statements about complement activation is false?
(a) Opsonisation of pathogens promotes phagocytosis
(b) Promotes and activates mast cell/basophil degranulation
(c) Decreases vascular permeability and inhibits cell trafficking to the site of inflammation
(d) Form/punch holes in pathogen membranes
(e) Opsonisation of immune complexes keeps them soluble
The statement that is incorrect is (c). Instead, complement activation increases vascular permeability and stimulates cell trafficking to the site of inflammation.
Regarding phagocyte function, which of the following statements is true?
a. In Kostmann syndrome the neutrophil count is normal but the leukocyte adhesion markers are deficient in CD18.
b. In Chronic granulomatous disease the neutrophil count is normal and the nitroblue test is positive.
c. In a patient with leukocyte adhesion deficiency the neutrophil count is low during infection.
d. In a patient with leukocyte adhesion deficiency the dihydrorhodamine test is abnormal
e. In Kostmann syndrome both the nitroblue test and dihydrorhodamine test are negative
The correct answer is (e), in Kostmann syndrome both the nitroblue test and dihydrorhodamine test are negative.
In Kostmann syndrome the neutrophil count is absent but there are no deficiences in leukocyte adhesion markers; option (a) is describing leukocyte adhesion deficiency instead.
In chronic granulomatous disease, the neutrophil count is normal but both the nitroblue and dihydrorhodamine test are negative due to failure of oxidative killing so (b) is incorrect.
In a patient with leukocyte adhesion deficiency, the neutrophil counts are high during infection, but both the nitroblue and dihydrorhodamine tests are normal so both (c) and (d) are incorrect.
Finally, in Kostmann syndrome both the nitroblue test and dihydrorhodamine test are negative because there are no neutrophils so (e) is the correct answer.
Which of the following statements is true for dendritic cells?
(a) Present within blood and may migrate to inflamed tissue.
(b) Express inhibitory receptors for self-HLA molecules to prevent damage to healthy self cells and inappropriate activation by normal self.
(c) Express a range of activatory receptors including natural cytotoxicity receptors that recognise heparan sulphate proteoglycans.
(d) Cytotoxic capacity - kill ‘altered self’ as in malignant of virus infected cells.
(e) Express cytokine and chemokine receptors to detect inflammation.
The correct answer is (e) Express cytokine and chemokine receptors to detect inflammation.
All the other options describe natural killer cells, not dendritic cells.
Which of the following statements about cytokine production by immune cells is true?
(a) Th1 cells produce il-2, ifnγ and lymphotoxin
(b) Th2 cells secrete il-17 and il-22
(c) Th17 cells secrete il-4, il-5 and il-10
(d) Tregs secrete il-10 and tgf beta
(e) Tr1 cells express cd25 and foxp3 and secrete il-10
The correct answer is (a) Th1 cells produce il-2, ifnγ and lymphotoxin.
As for the other answers they’ve been switched around, so option (b) describes Th17 cells, (c) describes Th2 cells, (d) describes Tr1 cells and (e) descrives Tregs.
(I apologise for this question)
Which of the following statements about complement activation is true?
(a) The classical pathway relies on the binding of C2 to the binding site on antibodies which result in activation of the cascade.
(b) The mannose binding lectin (MBL) pathway is activated by direct binding of MBL to specific antigen receptors on microbial cells.
(c) The MBL pathway directly stimulates the classical pathway, involving C4 and C1, but not C2.
(d) The alternative pathway is directly triggered by binding of C3, C4 and C5 to bacterial cell wall components.
(e) Activation of C3 is the major amplification step in the complement cascade which triggers the formation of the membrane attack complex via C5-C9.
The correct answer is (e) Activation of C3 is the major amplification step in the complement cascade which triggers the formation of the membrane attack complex via C5-C9.
With regards to (a), the classical pathway relies on C1 binding to the binding site on antibodies which causes activation of the cascade, not C2.
For (b) MBL binds to microbial cell surface carbohydrates, not specific antigen receptors on microbial cells.
The MBL pathway stimulates the classical pathway involving C4 and C2, but not C1, so (c) is wrong.
The alternative pathway is directly triggered by binding of C3 to bacterial cell wall components, not C4 and C5 too so (d) is also wrong.
Which of these statements regarding the clinical phenotype of severe combined immunodeficiency (SCID) with combined B and T cell deficiencies is false?
(a) Unwell by 12 months of age.
(b) Infections of all types.
(c) Failure to thrive.
(d) Persistent diarrhoea.
(e) Family history of early infant death.
The correct answer is (a) unwell by 12 months of age. The clinical phenotype of SCID is that the child is unwell by 3 months of age. Before this, the neonate is protected by maternal circulating IgG.
All the other options are true for SCID.
A 6 month baby boy presents to A&E with a fever and difficulty breathing. This is his 4th visit in the past month, and he’s had recurrent infections since he was about 3 months old. His mother says that her uncle died when he was very young from an infection. The boy has dropped from 50th centile to 14th in both height and weight. Investigations reveal that the CD4 count is low, but the CD8 count is normal. Levels of IgG and IgA are both low but IgM is normal. What condition does this child have?
(a) HIV.
(b) Severe combined immunodeficiency (SCID).
(c) Bare lymphocyte syndrome type 1.
(d) Bare lymphocyte syndrome type 2.
(e) DiGeorge Syndrome.
The correct answer is (d) bare lymphocyte syndrome(BLS) type 2.
This child has the classical clinical phenotype of BLS, and with the investigation results showing CD4 is low and CD8 count is normal we can conclude that it is BLS type 2.
Which of the following vignettes matches the disease correctly in the following options?
(a) Adult with bronchiectasis, recurrent sinusitis and development of atypical SLE - IgA deficiency
(b) Recurrent bacteral infections in a child, episode of pneumocystis pneumonia, high IgM, absent IgA and IgG - Severe combined immunodeficiency
(c) 1 year old child, recurrent bacterial infections, CD4 and CD8 T cells present. B cells absent, IgG, IgA and IgM absent - Bruton’s X-linked hypogammaglobulinaemia.
(d) Recurrent respiratory tract infections, absent IgA, normal IgM and IgG - Common variable immunodeficiency,
(e) 1 year old boy, recurrent bacterial infections as a child as well as some atypical fungal infections. Absent IgM, normal IgA and high IgG - X-linked hyper IgM syndrome due to CD40 ligand mutation.
The correct pairing is (c) 1 year old child, recurrent bacterial infections, CD4 and CD8 T cells present. B cells absent, IgG, IgA and IgM absent - Bruton’s X-linked hypogammaglobulinaemia.
As for the others, (a) describes an adult with common variable immunodeficiency.
(b) describes a child with X-linked hyper IgM syndrome.
(d) describes a patient with IgA deficiency.
(e) Is wrong because in hyper IgM syndrome you’d see what is described in (b), not absent IgM and high IgG. (I don’t even know whether that’s a thing)
Which of the following statements about complement deficiencies is incorrect?
(a) Membranoproliferative nephritis and bacterial infections is seen in C3 deficiency with presence of a nephritic factor.
(b) Meningococcus meningitis with family history of sibling dying of same condition aged 6, the deficiency is in C9.
(c) Severe childhood onset SLE with absent levels of C3 and C4 is seen in C1q deficiency.
(d) Recurrent infections when receiving chemotherapy but previously well occus in MBL deficiency.
(e) Normal levels of C3, C4 and CH50 but reduced levels of AP50 on a background of recurrent infections with encapsulated bacteria points to a Factor B deficiency.
The correct answer is (c) Severe childhood onset SLE with absent levels of C3 and C4 is seen in C1q deficiency. This is incorrect as the levels of C3 and C4 are normal in C1q deficiency.
All the other statements about complement deficiencies are correct.
In GP practice you see a 54 year old female patient who has come in for review of her medications. She’s taking Colchicine 500μg BD, as well as Anakinra and Etanercept. She’s currently undergoing regular renal tests to rule out nephrotic syndrome and renal failure. When she first had symptoms she had periodic fevers that lasted for 48-96 hours and abdominal pain. She says she has a genetic condition, and when asked she reveals that she was born in Turkey. What condition is this patient most likely to have?
(a) Muckle Wells Syndrome.
(b) Familial cold auto-inflammatory syndrome.
(c) TNF receptor associated periodic syndrome.
(d) Hyper IgD with periodic fever syndrome.
(e) Familial Mediterranean fever.
The patient is most likely to have (e) Familial Mediterranean fever.
This is an autosomal recessive condition with a mutation in MEFV gene which affects neutrophils, causing a failure to regulate cryopyrin activation of neutrophils.
Epidemiology wise it affects Sephardic>Askhenazy Jews, and Armenian, Turkish and Arabic people mostly.
The clinical presentation is periodic fevers lasting 48-96 hours associated with abdominal pain due to peritonitis, chest pain due to pleurisy and pericarditis, and arthritis.
Long term risk of amyloidosis hence this patient receiving renal check ups to rule out nephrotic syndrome and renal failure.
Treatment is Colchicine 500μg BD which binds to tubulin in neutrophils and disrupts neutrophil functions including migration and chemokine secretion, Anakinra which is an interleukin 1 receptor antagonist, etanercept which is a TNF alpha inhibitor and Type 1 interferon.
You’re on the ward trying to look busy in order to dodge questions when the consultant barks at you and asks you what the classic presentation triad of auto-immune polyendocrine syndrome type 1 (APS1) is, What is it?
(a) Arthritis, hyperparathyroidism, diabetes mellitus.
(b) Diabetes mellitus, hypoparathyroidism, Addison’s disease.
(c) Arthritis, diabetes mellitus, Addison’s disease.
(d) Candidiasis, Arthritis, diabetes mellitus
(e) Candidiasis, hypoparathyroidism, Addison’s disease.
The correct answer is (e) candidiasis, hypoparathyroidism and Addison’s disease syndrome. Also referred to as APECED.
APS1 is an autosomal recessive disorder where there is a defect in auto-immune regulator (AIRE) which is a transcription factor involved in development of T cell tolerance in the thymus.
The triad comes from antibodies against parathyroid and adrenal glands which lead to dysfunction (hypoparathyroidism and Addison’s) and mild immune deficiency which leads to candida infections.
74 year old female presents with a painful headache that gets worse when she eats food. She rates the pain at 9/10. Which of the options below would you expect to find given this history?
(a) Low CRP and ESR, abnormal temporal artery biopsy with intimal proliferation, disrupted internal elastic lamina, and neutrophils throughout the vessel wall.
(b) Normal CRP and high ESR, abnormal temporal artery biopsy with intimal proliferation, disrupted external elastic lamina, and mononuclear cells throughout the vessel wall.
(c) High CRP and ESR, abnormal temporal artery biopsy with intimal proliferation,disrupted internal elastic lamina, and neutrophils throughout the vessel wall.
(d) High CRP and normal ESR, abnormal temporal artery biopsy with intimal proliferation, disrupted external elastic lamina, and mononuclear cells throughout the vessel wall.
(e) High CRP and ESR, abnormal temporal artery biopsy with intimal proliferation, disrupted internal elastic lamina, and mononuclear cells throughout the vessel wall.
The correct answer is (e) High CRP and ESR, abnormal temporal artery biopsy with intimal proliferation, disrupted internal elastic lamina, and mononuclear cells throughout the vessel wall.
This presentation is classical for giant cell arteritis which is the most common systemic vasculitis in the elderly. Usually affects the temporal artery like with this patient, and the opthalmic artery which can present with visual loss.
Treatment is immunosuppression with corticosteroids.
30 year old man presents with low back pain and stiffness. He finds that this gets worse after periods of rest so tries to keep active all day, which makes it better. He also has painful and swollen knees, and sausage-like fingers. His doctor has previously prescribed Ibuprofen, but he asks you what else can be used to treat his condition?
Choose the most appropriate treatment from the list below.
(a) Oral prednisolone
(b) Corticosteroid injections
(c) Etanercept
(d) Colchicine
(e) Anakinra
The correct answer is (c) Etanercept. Etanercept is TNF alpha antagonist which works well in the treatment of ankylosing spondylitis, which this patient has.
Treatment with corticosteroid injections or steroids have not been shown to be more effective in treatment and reduction of symptoms than NSAIDs in ankylosing spondylitis.
Which of the following is not an example of type II antibody driven auto-immune disease?
(a) Auto-immune haemolytic anaemia
(b) Goodpasture disease
(c) Pemphigus vulgaris
(d) Rheumatoid arthritis
(e) Myaesthenia gravis
The correct answer is (d) Rheumatoid arthritis. RA is an example of type III immune complex driven auto-immune disease. In RA the auto antigen is the Fc region of IgG and the main pathology is arthritis.
All the other options are examples of type II antibody driven auto-immune disease.
In auto-immune haemolytic anaemia (a) the auto antigen is the rhesus blood group antigen or I antigen and the pathology is destruction of red blood cells causes anaemia.
In goodpasture disease (b) the auto antigen is noncollagenous domain of basement membrane collagen type IV and the pathology is glomerulonephritis and pulmonary haemorrhage.
In pemphigus vulgaris (c) the auto antigen is epidermal cadherin and the pathology is blistering of the skin.
In myaesthenia gravis (e) the auto antigen is the acetylcholine receptor and the pathology is muscle weakness.
Which of the following statements about investigations in autoimmune disease is correct?
(a) Only 50% of patients with rheumatoid arthritis are ever positive for rheumatoid factor(RhF) so absence of RhF is insufficient to rule out rheumatoid arthritis.
(b) Anti-cyclic citrullinated peptide (CCP) antibodies are much less specific than RhF but more sensitive so more useful as a diagnostic test for rheumatoid arthritis.
(c) Anti-DNA antibodies are highly specific for SLE (95%) so are useful for diagnosis, but high titres are not shown to correlate with more severe disease, so they aren’t useful for disease monitoring.
(d) Unactivated C3 and C4 levels inversely reflect the magnitude of immune complex deposition, so serial measurement of C3 and C4 is used in routine monitoring of SLE as a surrogate marker of presence of circulating immune complexes.
(e) p-ANCA is associated with antibodies to Proteinase 3 and occurs in most patients with Wegener’s granulomatosis, especially where there is renal involvement.
The correct answer is (d) Unactivated C3 and C4 levels inversely reflect the magnitude of immune complex deposition, so serial measurement of C3 and C4 is used in routine monitoring of SLE as a surrogate marker of presence of circulating immune complexes.
In terms of (a) 50% of patients with rheumatoid arthritis are positive for RhF at the time of diagnosis, a further 25% will become seropositive in the first 2 years of disease.
(b) was wrong because CCP antibodies are as sensitive as RhF but much more specific as a diagnositic test for rheumatoid arthritis.
(c) is wrong as very high anti-DNA antibody titres are often associated with more severe disease, therefore, they are useful in disease monitoring as an increase in antibody titre is associated with disease activity and may precede disease relapse.
(e) describes c-ANCA not p-ANCA.
Which of the following statements about connective tissue disease is incorrect?
(a) Anti-centromere is associated with the diffuse cutaneous form of systemic sclerosis.
(b) Anti-Ro may be positive in either SLE or in Sjogren’s syndrome.
(c) Anti-Jo-1 (t-RNA synthetase) is sometimes positive in patients with immune mediated myositis particularly if they have interstitial lung disease.
(d) ANA is used as a screening test for a connective tissue disease.
(e) Anti-dsDNA is highly specific for diagnosis of SLE, present in 70% of patients.
The correct answer is (a) Anti-centromere is associated with the diffuse cutaneous form of systemic sclerosis. Anti-centromere antibodies are associated with the limited cutaneous form of systemic sclerosis, anti-Scl70 is the antibody associated with the diffuse cutaneous form.
All the other options are correct.
Which of the following is not a possible cause of IgE-mediated mast cell degranulation?
(a) Peanut
(b) Intravenous contrast media
(c) Penicillin
(d) Wasp or bee venom
(e) Latex
The answer is (b) intravenous contrast media. This is a cause of non- IgE mediated mast cell degranulation.
Anaphylaxis is best diagnosed in the laboratory by measuring which of the following analytes?
(a) Tryptase
(b) IgE
(c) Histamine
(d) IgG
(e) Eosinophilic cationic protein
The correct answer is (a) Tryptase. Histamine is massively increase in anaphylaxis but peaks and drops almost to normal within 30-60 minutes, whereas tryptase peaks at roughly 60 minutes after exposure to the allergen, and slowly decreases, still measurably high at 4 hours after the exposure.
A 20 year old male presents to his GP with a two year history of nasal itch, sneezing and a clear discharge in the summer months. He also finds that his nose is usually blocked. He gets some syptomatic relief from anti-histamine tablets which he buys in Boots.
For each scenario choose the most appropriate answer from the following list. Each option may be used once, more than once or not at all.
(a) Acute urticaria
(b) Allergic asthma
(c) Allergic rhinitis
(d) Anaphylaxis
(e) Chronic urticaria
(f) Chronic sinusitis
(g) Idiopathic angioedema
(h) Latex allergy
(i) Oro-genital allergy
(j) Panic attack
(k) Physical urticaria
The correct answer is (c) allergic rhinitis.
A 40 year old lady is admitted to A&E with swelling of her lips, tongue, throat and difficulty in breathing. Clinical examination reveals an urticarial skin rash and low blood pressure. She is unable to talk to tell you what happened.
For each scenario choose the most appropriate answer from the following list. Each option may be used once, more than once or not at all.
(a) Acute urticaria
(b) Allergic asthma
(c) Allergic rhinitis
(d) Anaphylaxis
(e) Chronic urticaria
(f) Chronic sinusitis
(g) Idiopathic angioedema
(h) Latex allergy
(i) Oro-genital allergy
(j) Panic attack
(k) Physical urticaria
The correct answer is (d) anaphylaxis.
A 22 year old student experiences an urticarial skin rash when he uses condoms for sexual intercourse. He also gives a history of lip irritation and swelling when he blows up balloons.
For each scenario choose the most appropriate answer from the following list. Each option may be used once, more than once or not at all.
(a) Acute urticaria
(b) Allergic asthma
(c) Allergic rhinitis
(d) Anaphylaxis
(e) Chronic urticaria
(f) Chronic sinusitis
(g) Idiopathic angioedema
(h) Latex allergy
(i) Oro-genital allergy
(j) Panic attack
(k) Physical urticaria
The answer is (h) Latex allergy.
A 25 year old woman presents to her GP complaining of itchy, red wheals on her torso which have been present for 8 weeks. She can not remember how they started but she says that the skin rash is worse in the heat and when she exercises.
For each scenario choose the most appropriate answer from the following list. Each option may be used once, more than once or not at all.
(a) Acute urticaria
(b) Allergic asthma
(c) Allergic rhinitis
(d) Anaphylaxis
(e) Chronic urticaria
(f) Chronic sinusitis
(g) Idiopathic angioedema
(h) Latex allergy
(i) Oro-genital allergy
(j) Panic attack
(k) Physical urticaria
The correct answer is (e) chronic urticaria.
A 44 year old woman comes into A&E sobbing and breathing very fast. She tells you she’s just accidentally consumed a strawberry and she’s allergic to strawberries. On examination there is no swelling on her lips, tongue or throat, blood pressure is normal, but heart rate is high.
For each scenario choose the most appropriate answer from the following list. Each option may be used once, more than once or not at all.
(a) Acute urticaria
(b) Allergic asthma
(c) Allergic rhinitis
(d) Anaphylaxis
(e) Chronic urticaria
(f) Chronic sinusitis
(g) Idiopathic angioedema
(h) Latex allergy
(i) Oro-genital allergy
(j) Panic attack
(k) Physical urticaria
The correct answer is (j) panic attack. 20% of adults believe they have a food allergy whereas a lot of it is intolerances and the real figure of allergy is closer to 6%.
Which of the following vaccines is not a live vaccine?
a) MMR
(b) Typhoid
(c) Pertussis
(d) Tuberculosis (BCG
(e) Polio (Sabin)
The correct answer is (c) Pertussis. This is instead an inactivated vaccine.
All the others are live vaccines, although it’s important to note that the Sabin Polio vaccine is live but the Salk Polio vaccine is an inactivated vaccine.
Which of the following vaccines is a live vaccine?
(a) Hepatitis B
(b) Pneumococcus
(c) Tetanus
(d) Yellow Fever
(e) Cholera
The correct answer is (d) Yellow fever.
Hepatitis B (a) is a component/subunit vaccine, specifically the HbS antigen.
Pneumococcus (b) is a conjugate vaccine.
Tetanus (c) is a toxoid vaccine.
Cholera (e) is an inactivated vaccine.
State three routes of infection for HIV.
Sexually, through infected blood, i.e. transfusion, sharing needles or blood products, and mother to child, either before or during birth or via breast milk.
Which of the following would be the most appropriate treatment to boost the immune response in a patient suffering from post-transplant lymphoproliferative disorder?
(a) IFN alpha
(b) Bone marrow transplantation
(c) IFN gamma
(d) EBV- specific CD8 T cells
(e) Human normal immunoglobulin
The correct answer is (d) EBV- specific CD8 T cells.
IFN alpha (a) would be useful as part of the treatment for Hepatitis C.
Bone marrow transplantation (b) is appropriate in patients with X linked SCID.
IFN gamma (c) can be given to patients with chronic granulomatous disease.
Human normal immunoglobulin (e) should be given to patients with x-linked hyper IgM syndrome.
