Misc Flashcards
Which one of the following cells of the immune system is most reliant on its release of mediators into the extracellular fluid surrounding the organism in order to carry out its role in eradication of foreign organisms? A. Neutrophils. B. Eosinophils. C. Macrophages. D. Cytotoxic T lymphocytes. E. Natural killer cells.
B
Which of the following cytokines when secreted in an acute phase inflammatory response is most responsible for stimulating hepatocytes to synthesise acute phase proteins such as CRP? A. IL‐6 B. IL‐12 C. IL‐17 D. Interferon gamma E. Transforming growth factor beta
IL-6
Which of the following most accurately reflects the mechanism of complement consumption induced by complement component 3 (C3) nephritic factors?
A. Activation of the classical complement pathway.
B. Stabilisation of the membrane attack complex, C5-9.
C. Amplification of C3 “tickover”.
D. Stabilisation of the C3 convertase, C3bBb.
E. Inhibition of the complement regulator, Factor I.
D. Stabilisation of the C3 convertase, C3bBb.
immunodeficiency/Which of the following conditions is most likely to cause recurrent mild meningitis?
A. CD4
B. CD8
C. Neutrophil
D. Total haemolytic complement level (CH50)
E. Immunoglobulins
CH50
Recurrent infections with which of the following organisms is most characteristic of a disorder of neutrophil phagocytic function (such as chronic granulomatous disease)? A. Non-tuberculous mycobacteria B. Pseudomonas aeruginosa C. Nocardia species D. Pneumocystis jiroveci (carinii) E. Staphylococcus aureus
E
A defect in elimination of which of the following is most likely to occur post-splenectomy? A. Polysaccharide antigens. B. T cell-dependent antigens. C. Intracellular microbes. D. Protein antigens. E. Staphylococcus aureus.
Polysaccharide antigens (make up capsule)
Common variable immunodeficiency (CVID) is the most common primary immunodeficiency in adults. What best explains its pathogenesis?
A. Absence of co stimulatory signal between B and T cells (CD40/CD40L)
B. Absent neutrophil respiratory burst
C. Dysfunctional T cell signalling cascade
D. Maturation arrest during B cell development
E. Absent or reduced circulating B cells
Answer: D. Maturation arrest during B cell development
Common variable immunodeficiency (CVID) is a heterogeneous immune disorder characterized by recurrent sinopulmonary infections, autoimmune disorders, granulomatous disease, and an enhanced risk of malignancy. CVID is defined by the following:
• Markedly reduced serum concentrations of IgG, in combination with low levels of IgA and/or IgM
• Poor or absent antibody response to infection or immunization, or both
• An absence of any other defined immunodeficiency state
Treatment with IVIg is of most benefit in which of the following conditions?
A. CVID – Common variable immunodeficiency
B. CIDP – Chronic inflammatory demyelination polyneuropathy.
C. Wegener’s granulomatosis
D. pemphigus vulgaris
E. IgG subclass deficiency
CVID
Tumours of the immune system developing in patients with immune dysregulation due to immune deficiency (including human immunodeficiency virus (HIV) infection) and autoimmune disease are most likely to arise from which cell lineage?
A. B cell.
B. CD4 positive (CD4+) helper T cell.
C. CD8 positive (CD8+) cytotoxic T cell.
D. Monocyte.
E. Thymocyte.
B cell
HAE angioedema
Antihistamines and corticosteroids have no role in the management of HAE related angioedema. The role of adrenaline in the treatment of HAE is not well established. Use C1 inhibitor concentrate. Otherwise FFP
Type I HAE
Low C1 esterase, Low C4
Type II HAE
Normal C1 esterase, but functional defect. Low C4
Type II HAE
Normal C1 esterase, but functional defect. Low C4. Usually present <40
Autoimmune or inherited defect of C4
Low C4, Normal C1NH and normal function
Which of the following best describes the toxicological mechanism of recurrent acute angioedema related to the use of angiotensin converting enzyme (ACE) inhibitors?
A. IgE (immunoglobulin E) mediated hypersensitivity.
B. Delayed-type hypersensitivity.
C. Enhancement of complement activation.
D. Disruption of endothelial tight junctions.
E. Impairment of bradykinin catabolism.
Impairment of bradykinin catabolism
• ACE inhibitors and ARBs may also unmask deficiencies of C1-INH