Leeds metropolitan university

Notes to Candidates:
Answer ALL questions in Section A (contributes 50% of total mark)
Answer ONE question in Section B (contributes 50% of total mark)
Use separate answer books for Sections A and B
You may consult your Practical Portfolio for Section B only after handing in your Section A

Answer ALL questions in your first answer book

You must select a confidence value for each answer
Marks will be awarded according to the following table:

Confidence level
A1 Which one of the following statements concerning allergic disease is NOT true?
(a) polymorphism of the IL-9 gene is associated with asthma (b) the loci of genes regulating IgE have been identified on C9 (c) HLA has been linked to some allergen sensitivities (d) genetic susceptibility to allergic disease has not been clearly defined (e) high levels of serum IgE are found in all allergic families
Which one of the following statements concerning late phase allergic reaction is NOT
(a) it typically occurs >12 hours after exposure (b) it is characterised by cellular infiltrations of CD4+ cells, monocytes and (c) release of TH2 - type cytokines results in further inflammation at the site of (d) late phase reaction resembles type IV hypersensitivity due to the presence (e) the presence of eosinophils and TH2 cells distinguishes late phase reaction Which one of the following statements concerning allergic food allergy is NOT true? (a) some food allergy may involve sensitisation via breast milk (b) the mechanism involves T cells in the GI tract (c) changes in gut permeability may result in systemic reactions (d) local reactions result in diarrhoea and vomiting (e) typical food allergic reactions are provoked by e.g. shellfish, nuts, eggs,
A4 Type III hypersensitivity reactions are the direct result of interaction between which
(a) sensitised T lymphocytes and antigen (b) pre-formed antibodies and antigens (c) mast cells and antigen (d) plasma cells and antigen (e) histiocytes and antigen
A5 Primary immunodeficiencies are commoner than secondary causes of
immunodeficiency. Which single statement is true? (a) This statement is only true for adults (b) This statement is true at all ages (c) This statement is totally untrue for all ages (d) Secondary immune deficiencies are rarely due to drugs (e) Vegetarians are particularly at risk of immune suppression
A6 Jane, a 15-month-old infant, was brought to her family practice clinic for her routine
well-child examination. During the course of her office visit, Jane received her first measles immunisation. For successful immunisation leading to formation of specific memory cells, all of the following cell types would need to be activated except: (d) Eosinophils (e) Natural killer cells A7 Which of the following diseases usually occur in ‘atopic’ individuals? (multiple options

A8 Systemic anaphylaxis can be caused by: (multiple options may be correct)

A9 Hyposensitisation is of proven benefit in which one of the following conditions:
(b) house dust mite allergy (c) wasp venom hypersensitivity (d) coeliac
A10 Asthma is characterised by: (multiple options may be correct)
(a) response to cyclosporin therapy in severe disease (b) reversible (c) TH2 cells in bronchoalveolar lavage fluid (d) affecting 5% of the population (e) being diagnosed routinely by the use of rast
A11 Which one of the following statements is true? Autoimmune diseases:
(a) affect about 1 person in every thousand (b) are more common in women (c) tend to begin in childhood (d) are an inevitable consequence of autoimmune responses (e) are
A12 Which one of the following statements is true?
(a) the thymus controls peripheral tolerance of T cells (b) no self-reactive T cells can be found in healthy normal subjects (c) naive T cells need more than one signal in order to become activated (d) B-cell tolerance is more important than T-cell tolerance in the prevention of (e) class II MHC molecules are expressed on most cells
A13 Which one of the following is NOT true? Autoimmune diseases:
(a) can cluster within families (b) are often associated with particular HLA alleles (c) are usually mediated by type 1 hypersensitivity (d) may occur in humans or animals with inherited defects in apoptosis (e) may occur in inherited complement deficiencies A14 Which of the following agents are known to be immunosuppressive? (multiple options
(a) Levamisole (b) Corticosteroids (c) Azathioprine (d) Cyclosporin (e) Total lymphoid irradiation
A15 Which of the following are live vaccines? (multiple options may be correct)
(b) Diphtheria (c) Tetanus (d) BCG (e) Hepatitis
A16 In the UK, immunisation schedules are routinely started at which one of the

A17 Which of the following sets of antigens are important in relation to successful renal
grafting? (multiple options may be correct) (a) MHC class II antigens (b) Lewis red cell antigens (c) Rhesus red cell antigens (d) Sex antigens (products of X and Y chromosomes) (e) ABO red cell antigens
A18 Which of the following factors may indicate renal graft rejection? (multiple options
(a) fever (b) increase in serum IgG level (c) tender (d) rise in urine volume (e) rise in creatinine
A19 Which of the following statements regarding graft-versus-host disease (GVHD) are
(a) Occurs in only a minority of patients receiving allogeneic bone marrow (b) May occur mildly following bone marrow transplantation between HLA- (c) May occur following unirradiated blood transfusion in babies with severe (d) Is preventable by depleting T cells from donor blood marrow (e) Clinically involves the skin, liver and intestine A20 The administration of vaccines is not without hazard. Which one of the following
vaccines is least likely to affect adversely an immunocompromised host? (a) recombinant hepatitis B protein (b) Bacille Calmette-Guerin (BCG) (c) Sabin SECTION B:
Answer ONE question in your second answer book. You
may now consult your practical portfolio.

Miss Jacob, a 30-year-old Caribbean woman, had been visiting her doctor for some time with aches and pains in her joints. The year before, following a flight from the Caribbean, she developed a severe pain in her left leg and was found to have a deep vein thrombosis. The cause of the venous thrombosis was thought to be venous stasis because of the long plane flight and she was treated with anticoagulants. She then developed other symptoms such as headache, occasional bouts of acute abdominal pain - all this being associated with lethargy, occasional fever and some loss of weight. She had just returned from holiday when she was sent to the rheumatologist who found that she had a rash on her face and some patchy hair loss on her scalp. Her joints were tender but not very swollen. Her muscles ached and she complained of chest pain. The results of investigations are shown below. A diagnosis of systemic lupus erythematosus (SLE) was made. Miss Jacob was treated in the first instance with chloroquine, an antimalarial, for the rash on her face and chest. She was strongly advised to have an examination of her eyes every 6 months because of the potential side effects of the chloroquine treatment. At a follow-up appointment, she was found to have pain in the calf of her leg, and further information of her medical history was obtained. Three years previously she had suffered a spontaneous abortion. Although not commonly associated with SLE, she was then diagnosed as having the antiphospholipid syndrome and treated with anticoagulants. Her renal function showed an elevated serum creatinine with red cells and protein in her urine. This prompted a renal biopsy which gave the histological picture of diffuse proliferative lupus nephritis. She was then treated with oral corticosteroids, immunosuppressants and an antihypertensive drug. Ten years later, she was still attending the clinic and still required treatment. No evidence of thalassaemia or sickle cell disease Skin biopsy from unaffected Deposition of complement and IgG at dermoepidermal area (a) Comment on the (i) clinical signs (10 marks) and the (ii) results of the laboratory investigations (20 marks) with respect to the patient’s condition. (b) What methods would you use to estimate (i) serum complement components (15 marks), and (ii) serum autoantibodies (15 marks) in this case? Briefly describe the methods with comments on their relative strengths and weaknesses. (c) What information can be obtained from autoantibody tests in patients with SLE? (10 (d) What is the immunopathological mechanism leading to the glomerulonephritis? (10 (e) What are the main characteristics of the antiphospholipid syndrome (APS)? (10 Is SLE a classic autoimmune disease? (10 marks) Mr Jackson, a 31-year-old Irishman, presented to his GP with a 3-month history of malaise, anorexia, weight loss, mild diffuse abdominal pain and diarrhoea. Over the last fortnight he had vomited every other day and had developed an itchy, blistering rash on the extensor surfaces of his knees and elbows. He had not vomited any blood or had any obvious bleeding from the gut. Recently, mealtimes were accompanied by bloating and he noted his stools were also paler than normal. He was not taking any medication and had not travelled abroad. His relatives lived in Ireland and he was unable to recall any family history of disease. He did not complain of muscle cramps, paraesthesia or bruising. On examination, Mr Jackson was underweight for his height and had finger clubbing, several aphthous mouth ulcers, and angular cheilitis (inflammation of the lip). He had a vesicular rash on the extensor surfaces of his elbows and knees. There was no jaundice or oedema, but he was clinically anaemic. He had a mildly distended and nOI1- tender abdomen and normal bowel sounds. No masses were felt OD palpation or on rectal examination, and there was no evidence of per rectum bleeding. Mr Jackson's doctor decided to refer him to a gastroenterologist for further evaluation. The results of investigations are shown in below. Mr Jackson had combined iron and folate deficiency anaemia and low serum albumin. His mild hypocalcaemia was compensated by a degree of secondary hyperparathyroidism. The gastroenterologist identified his rash as dermatitis herpetiformis, and this, combined with the history and laboratory evidence of malabsorption, led to a provisional diagnosis of coeliac disease (gluten enteropathy). A jejunal biopsy was performed and the sample sent for histological examination, The presence of subtotal villous atrophy, elongated crypts and dense inflammatory infiltrate was strongly suggestive of coeliac disease. The diagnosis was further confirmed by positive enzyme-linked immunosorbent assays (ELISAs) for serum IgA antibodies to endomysium, gliadin and reticulin. Mr Jackson was referred to a dietician who outlined a gluten-free diet and provided calcium, folate and iron supplements. In the next 3 months he gained several kg in weight and his oilier symptoms improved considerably. At a follow-up appointment his endomysium, gliadin and reticulin antibody levels were lower than those at presentation and a repeat biopsy showed an improvement in jejunal architecture. Other indices, including his serum albumin, calcium, haemoglobin and clotting, were within normal limits, Mr Jackson was advised to observe a gluten-free diet for life and regular follow-up appointments were arranged because of the increased risk of small bowel malignancy in patients with coeliac disease. Microcytes Oval macrocytes Howell-Jolly bodies Activated partial thromboplastin time (secs) (a) Comment on the (i) clinical signs (10 marks) and the (ii) results of the laboratory investigations (20 marks) with respect to the patient’s condition. (b) What methods would you use to estimate (i) white cell counts (15 marks), and (ii) serum immunoglobulins (15 marks) in this case? Briefly describe the methods with comments on their relative strengths and weaknesses. (c) What is the aetiology of coeliac disease? (15 marks) (d) What is the immunopathology of coeliac disease? (10 marks) (e) Is the patient's antibody status sufficient to make the diagnosis of coeliac disease? Can other foods cause the same clinical picture? (5 marks)

Source: https://x-stream.leedsmet.ac.uk/bbcswebdav/institution/Exam_Papers/Faculty%20of%20Health%20and%20Social%20Sciences/2009-10%3B%2082%20papers%20received/Clinical_Immunology_JAN_2010_Mod8617.pdf

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The Soapmakers Store Web-Site: Material Safety Data Sheet Section 1 – Chemical Product and Company Identification Product/Chemical Name: Melt & Pour Soapbase, Natural INCI Name: Glycerin, Aqua, Sodium Stearate, Sodium Oleate, Sorbitol, Sodium Laurate, Sodium Myristate, Stearic Acid, Lauric Acid, Pentasodium Pentetate, Tetrasodium Etidronate Product c

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Publications 1. Cintora-Gonzalez, O., Estournes, C., Guille, J.L., Grob, J.J., Honerlage, B., Lemoigne, J., Levy, R., Lutz, T., Merle, J.C., Muller, D., Richard, M., Rehspringer, J.L., Schell, J., Viart, N. "Aggregates in silica based matrices." Analusis 28 109 - 113, 2000. 2. Felder, D., Guillon, D., Levy, R., Mathis, A., Nicoud, J.F., Nierengarten, J.F., Rehspringer, J.L., Schell,

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