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Journal questionnaire.

Below are ten questions based on articles from the April 2017 issue. Read the articles carefully as most questions require more than one answer.

Answers are to be submitted through the NZIMLS web site. Make sure you supply your correct email address and membership number. It is recommended that you write your answers in a word document and then cut and paste your answers on the web site.

The site has been developed for use with Microsoft's Internet Explorer web browser. If you are having problems submitting your questionnaire and you are using the Firefox web browser, try re-submitting using Microsoft's Internet Explorer.

You are reminded that to claim valid CPD points for successfully completing the journal questionnaire you must submit an individual entry. It must not be part of a consultative or group process. In addition, members who have successfully completed the journal questionnaire cannot then claim additional CPD points for reading the articles from which the questions were derived.

The site will remain open until Friday 7th July, 2017. You must get a minimum of eight questions right to obtain five CPD points.

The Editor sets the questions but the CPD Co-ordinator, Jillian Broadbent, marks the answers. Please direct any queries to her at cpd@nzimls.org.nz.

APRIL 2017 JOURNAL QUESTIONNAIRE

1. What is point 9 of the NZIMLS Code of Ethics.

2. What should members do with the returned answers to their journal questionnaire submissions, and why?

3. What is thought to be the mechanisms of sickle cell disease associated priapism?

4. What are the typical cavernous blood gas values in ischaemic priapism?

5. Define priapism, and where is the tem derived from.

6. What is antithrombin, and how does it act?

7. What are antithrombin deficient patients at increased risk of?

8. Inherited antithrombin deficiency Type IIb alters what and results in what?

9. Name the antithrombin heparin binding site methods that have been used.

10. Recent research has shown that vascular disease and hypertension are driven by what, and what was this associated with.

NOVEMBER 2016 JOURNAL QUESTIONNAIRE ANSWERS

1. At Aotea Pathology, what was their initial protocol for the cultivation and isolation of Salmonella and Shigella from clinical faecal specimens?

Directly plating faeces onto Hektoen enteric agar (half plate) and sub-culturing onto Xylose Lysine Deoxychocolate agar following enrichment in Selenite F broth after overnight incubation.

2. Both chronic and acute immune thrombocytopenia are caused by what? By increased platelet destruction in which anti-platelet antibodies sensitise circulating platelets marking them for removal by splenic macrophages bearing Fc[gamma] receptors.

3. Helicobacter pylori is what type of bacteria? Fastidious, microaerophilic, helical shaped Gramnegative bacteria.

4. Co-carriage of other resistant mechanisms in in Enterobacteriaceae and non-glucose-fermenting Gramnegative bacilli isolates can result in what? Compromised treatment options, and high mortality rates in patients with severe infections.

5. What was the current screening protocol at Canterbury Health Laboratories for the detection of carbapenemase producing organisms in routine faecal screening samples? CHROMagar[TM] ESBL and MacConkey agar with a 10 [micro]g meropenem disc.

6. Preparation of re-suspended red cells for transfusion involves what processes? Leucocyte depletion by high-efficiency filtration in an adsorption depth filter, followed by a centrifugation step and separation of the red cells and plasma. The red cells are then resuspended in saline, adenine, glucose and mannitol additive solution with only a minimal volume of plasma.

7. What are the principal constituents of aggregated material in unfiltered units of blood? Platelets, granulocytes and monocytes, together with small amounts of fibrin.

8. What concerns exists over the association of aggregated material with febrile transfusion reactions? Transmission of cell-associated cytomegalovirus, immunisation by transfused leucocytes resulting in HLA antibodies and refractoriness to platelet transfusion, post-transfusion thrombocytopenia, immunomodulation and potentially other adverse effects.

9. Juvenile myelomonocytic leukemia is characterised by what? Overproduction of granulocytic and monocytic cells that can infiltrate organs including the spleen, liver, gastrointestinal tract and lung.

10. What non-specific features on presentation of juvenile myelomonocytic leukemia are typically included? Fever, splenomegaly, cough, rash and a failure to thrive.
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Publication:New Zealand Journal of Medical Laboratory Science
Date:Apr 1, 2017
Words:671
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