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A 65-year-old man with a history of myocardial infarction four years earlier was admitted with progressiveshortness of breath and decreasing exercise tolerance. He has smoked 40 cigarettes per day for the last 45years.

He takes lansoprazole, aspirin and lisinopril.

Which of the following laboratory tests would help identify the reason for his symptoms?

(Please select 1 option)

Brain natriuretic peptide (BNP)

Clotting screen

C reactive protein

Full blood count

Urea and electrolytes

Question: 1 of 10 Time taken: 00:18 Session Analysis

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A 65-year-old man with a history of myocardial infarction four years earlier was admitted with progressiveshortness of breath and decreasing exercise tolerance. He has smoked 40 cigarettes per day for the last 45years.

He takes lansoprazole, aspirin and lisinopril.

Which of the following laboratory tests would help identify the reason for his symptoms?


Brain natriuretic peptide (BNP) Correct

Clotting screen

C reactive protein

Full blood count


This patient has features of heart failure which appear to be related to underlying ischaemic heart disease. Thedifferential diagnosis is COPD, given his extensive smoking history.

Heart failure is a clinical syndrome characterised by dyspnoea, fatigue and ankle oedema. Signs which canpoint towards the diagnosis are pulmonary rales, pleural effusion, raised jugular venous pressure andperipheral oedema. Objective evidence is gained from echocardiogram, and raised natriuretic peptideconcentration. Cardiomegaly, third heart sound and murmurs can be suggestive of cardiac failure. TheEuropean Society of Cardiology guidelines state there must be symptoms, signs AND objective evidence beforea diagnosis of heart failure can be made. It is important to always attempt to identify the underlying cause.

BNP is a biologically active peptide, which has vasodilator and natriuretic properties. It is synthesised in thecardiac ventricles and correlates with left ventricle (LV) pressure, degree of dyspnoea, and state ofneurohormonal modulation. Levels increase markedly in left ventricular dysfunction, and the level correlateswith symptom severity (and decrease after effective treatment). It is raised in right or left systolic or diastolicheart failure. As such, it is an important clinical marker for the diagnosis of heart failure in patients withdyspnoea that could be attributed to a number of causes. Its use as a prognostic marker, therapy guide orscreening marker is under investigation. One note of caution, however, as levels can be raised in comorbidillness, age, renal failure and obesity and therefore correlation should be made with the clinical scenario.

In practice as this patient has had a previous MI, according to the current NICE guidelines he needs specialistassessment and Doppler echocardiography within 2 weeks. However, as this is not an option, BNP is the bestavailable answer. BNP is used first line in patients who have not had a previous MI. Levels >400pg/ml warranturgent specialist assessment and echocardiography; intermediate levels (100-400pg/ml) should be investigatedwithin six weeks.

FBC, U&E and creatinine, CRP and clotting screen are non-specific investigations which are unlikely to directlylead to a diagnosis in this case.

References & Further Reading:Chronic heart failure: management of chronic heart failure in adults in primary and secondary care. NICEClinical Guidelines CG108, August 2010.

Question: 1 of 10 Time taken: 01:09

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Which of the following is most likely be associated with hyperkalaemia?


Bartter's syndrome

Beta adrenergic stimulation

Cushing's syndrome

Cyclosporin

Mannitol


Score: 70.37%

Total Answered: 27

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Which of the following is most likely be associated with hyperkalaemia?


Bartter's syndrome

Beta adrenergic stimulation

Cushing's syndrome

Cyclosporin Correct

Mannitol

Common causes of hyperkalaemia include:

1. Impaired renal excretion: renal failure, hyporeninaemic hypoaldosteronism (type IV renal tubular acidosis),Addison's, C-21 hydroxylase deficiency.

2. Cellular changes: acidosis, rhabdomyolysis, tumour lysis, malignant hyperthermia, burns.3. Drugs: potassium retaining diuretics, angiotensin-converting enzyme (ACE) inhibitors, non-steroidal anti-

inflammatory drugs (NSAIDs), cyclosporin, succinyl choline, beta-blockers.

Related Articles (BMJ)

BASL abstracts -- 52 (5): e1 -- Gut Read article

Interstitial lung disease guideline -- Wells and Hirani 63 (Suppl 5): v1 -- Thorax Read article

Abstracts -- 53 (suppl 3): a1 -- Gut Read article


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Web(4) Angiotensin convertingenzyme inhibition and chroniccyclosporine ...ndt.oxfordjournals.orgndt.oxfordjournals.org/content/1






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Which of the following statements is true concerning gamma glutamyl transferase (GGT)?


Increased GGT is found in fatty liver

Isolated elevation of gamma GT in a patient with prostatic carcinoma Indicates the presence of hepatic metastases.

It is a better indicator of infectious hepatitis than of cholestasis

It is only present in the liver

Serum activity is typically elevated in pregnancy


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Which of the following statements is true concerning gamma glutamyl transferase (GGT)?


Increased GGT is found in fatty liver This is the correct answer

Isolated elevation of gamma GT in a patient with prostatic carcinoma Indicates the presence of hepatic metastases.

Incorrect answer selected

It is a better indicator of infectious hepatitis than of cholestasis

It is only present in the liver

Serum activity is typically elevated in pregnancy

GGT is found in muscle, prostate as well as liver.

Increased levels of GGT are found in cholestatic liver disease and in hepatocellular disease when there is anelement of cholestasis.

Levels are increased with chronic intake of excess alcohol and with certain drugs (especially phenytoin), as aresult of enzyme induction. Pancreatitis and prostatitis may also be associated with increased levels.

Levels may be normal early in the course of acute hepatocellular damage, for example, acute viral hepatitis,paracetamol hepatotoxicity.

Elevations in pregnancy would suggest liver disease.


Antidepressant induced cholestasis: hepatocellular redistribution of multidrug resistant protein (MRP2)-- Milkiewicz et al. 52 (2): 300 -- Gut Read article

Acute hepatocellular and cholestatic injury in a patient taking celecoxib -- Nachimuthu et al. 77 (910):548 -- Postgraduate Medical Journal Read article

Cholestatic hepatitis in association with celecoxib -- Mohammed et al. 325 (7357): 220 -- BMJ Read article


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A 46-year-old man was seen for an insurance medical examination.

He was entirely asymptomatic, but his serum urate concentration was noted to be 0.5 mmol/L (0.23 - 0.46).

What is the most appropriate management for this patient?


Allopurinol

Colchicine

Ibuprofen

Lifestyle intervention

Sulphinpyrazone


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A 46-year-old man was seen for an insurance medical examination.

He was entirely asymptomatic, but his serum urate concentration was noted to be 0.5 mmol/L (0.23 - 0.46).

What is the most appropriate management for this patient?


Allopurinol

Colchicine

Ibuprofen

Lifestyle intervention Correct

Sulphinpyrazone

Uric acid is the major product produced from the catabolism of purines, adenosine monophosphate (AMP) andguanosine monophosphate (GMP) from nucleic acids.

GMP and AMP are catabolised by a series of enzymes which remove a single phosphate group and the ribosesugar, eventually forming xanthine. Xanthine is then converted to uric acid by the enzyme xanthine oxidase.Uric acid can then be excreted by the kidneys.

When uric acid levels are high, there is a risk of developing gout, which causes monoarticular inflammation,gouty arthropathy and tophaceous deformity. Xanthine oxidase inhibitors are used in the treatment of gout, toreduce the amount of uric acid formed.

The patient above requires lifestyle advice about reducing intake of substances containing high purines(including some alcohol and red meat). Should he become symptomatic, treatment would be advisable. Inacute gout, treatment is with NSAIDs or other anti-inflammatories such as colchicine.

A xanthine oxidase inhibitor such as allopurinol should be started after the acute attack to reduce the risk ofrecurrence.

Causes of hyperuricaemia include:

Increased formation of uric acid:

Primary:

Idiopathic and inherited metabolic disease

Secondary:

AlcoholPsoriasisIncreased nucleic acid turnover: leukaemia and myelomaTissue hypoxiaExcess dietary purine intake.

Decreased excretion of uric acid:

Primary:

Idiopathic


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Web(4) Goutwww.els.netwww.els.net/WileyCDA/ElsArticle/refId-a0002311.htmlGout






Secondary:

Acute or chronic renal diseaseOrganic acidosis: lactate, ketonesLead poisoningDrugs: aspirin and thiazidesDown's syndrome.


Treatment of inflammatory myopathies -- Cordeiro and Isenberg 82 (969): 417 -- PostgraduateMedical Journal Read article

Efficacy of allopurinol and benzbromarone for the control of hyperuricaemia. A pathogenic approachto the treatment of primary chronic gout -- Perez-Ruiz et al. 57 (9): 545 -- Annals of the RheumaticDiseases Read article

Colchicine in acute gout -- Morris et al. 327 (7426): 1275 -- BMJ Read article

... tophi; xanthine oxidase; purine;oxipurine; allopurinol; uricosuric;probenecid; ... colchicine;hypoxanthine-guanine-phosphoribosyl-transferase;allantoin; ...www.els.netwww.els.net/WileyCDA/ElsArticle/refId-a0002311.htmlclipped from Google - 8/2012The Gout Clinical Companion:www.francefoundation.comwww.francefoundation.com/gout/pdf/gout_monograph.pdfThe Gout Clinical Companion:File Format: PDF/Adobe Acrobatcolchicine during initiation ofallopurinol was provided by a studyof 43 .... Allantoin. XO. XO. GMP.Guanosie. Guanine. Uricase. Figure8. Purine metabolism ...www.francefoundation.comwww.francefoundation.com/gout/pdf/gout_monograph.pdfclipped from Google - 8/2012Pharmacy Times CE: TheContemporary Management ofGout ...secure.pharmacytimes.comsecure.pharmacytimes.com/lessons/201105-CS2.aspPharmacy Times CE: TheContemporary Management of Gout...Apr 27, 2011... of a readilyabsorbable purine called guanosine,which may explain the higher risk ...Colchicine has been used since the6th century AD as a treatment forgout. .... Allopurinol (Zyloprim) is anoral xanthine oxidase inhibitor.secure.pharmacytimes.comsecure.pharmacytimes.com/lessons/201105-CS2.aspclipped from Google - 8/2012The management ofhyperuricemia and gout inpatients with heart ...eurjhf.oxfordjournals.orgeurjhf.oxfordjournals.org/content/4/4/403.fullThe management of hyperuricemiaand gout in patients with heart ...Urate is the catabolic end-product ofadenine and guanine, the purinebases .... Colchicine was introducedfor the specific treatment of acutegout almost 250 years ago. ...Allopurinol, the only xanthineoxidase inhibitor in clinical use,inhibits ...eurjhf.oxfordjournals.orgeurjhf.oxfordjournals.org/content/4/4/403.fullclipped from Google - 8/201212345678Book(4)

Principles ofpharmacology: thepathophysiologic basis ofdrug therapyby David E. Golan2008- 985 pagesbooks.google.com

clipped from Google - 8/2012Biochemistry for thePharmaceutical Sciencesby Woodbury2011





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Metabolic alkalosis is characteristically found in which of the following?


An infusion of sodium chloride

Ileostomy

Mineralocorticoid deficiency

Pyloric stenosis

Salicylate poisoning


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Metabolic alkalosis is characteristically found in which of the following?


An infusion of sodium chloride

Ileostomy

Mineralocorticoid deficiency

Pyloric stenosis Correct

Salicylate poisoning

Pyloric stenosis is associated with vomiting and the loss of stomach content - hence a metabolic alkalosis.

Normal saline has a pH of 5 and may produce a mild metabolic acidosis with significant infusions.

Ileostomy may be associated with a loss of bicarbonate ions and hence acidosis.

Mineralocorticoid excess (Conn's syndrome) is also associated with a metabolic alkalosis.

Salicylates are themselves acidic and produce a metabolic acidosis.


Bacteria as the cause of ulcerative colitis -- CAMPIERI and GIONCHETTI 48 (1): 132 -- Gut Read article

Dietary salicylates -- Hare et al. 56 (9): 649 -- Journal of Clinical Pathology Read article

Topical choline salicylates implicated in Reye's syndrome -- Oman et al. 336 (7657): 1376 -- BMJ Read article


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A 75-year-old man presents with a long history of shortness of breath and ankle oedema.

His serum biochemistry shows sodium 122 mmol/L (137-144) and potassium of 2.9 mmol/L (3.5-4.9). He nowcomplains of weakness.

Which of the following is likely to explain the above biochemical picture?


Addison's disease

Diuretic therapy

Nephrotic syndrome

Primary hyperaldosteronism

SIADH


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A 75-year-old man presents with a long history of shortness of breath and ankle oedema.

His serum biochemistry shows sodium 122 mmol/L (137-144) and potassium of 2.9 mmol/L (3.5-4.9). He nowcomplains of weakness.

Which of the following is likely to explain the above biochemical picture?


Addison's disease

Diuretic therapy Correct

Nephrotic syndrome

Primary hyperaldosteronism

SIADH

The long history of his symptoms and serum biochemistry suggests that his condition is due to treatment withfurosemide for congestive cardiac failure (CCF).

Primary hyperaldosteronism is associated with high aldosterone, suppressed renin, low potassium andnormal/high sodium. Clinically it causes hypertension and is often asymptomatic.

Addison's disease - glucocorticoid and mineralocorticoid deficiency - is classically associated with low sodiumand high potassium.

Nephrotic syndrome is not associated with hyponatraemia and hypokalaemia in early stages although if there isreduced glomerular filtration rate (GFR) hyperkalaemia can result. Glomerular disease allows the release ofproteins into the urine but electrolytes are reabsorbed.

SIADH would not explain the hypokalaemia.


Understanding the risk of hyperkalaemia in heart failure: role of aldosterone antagonism -- Poggio etal. 86 (1013): 136 -- Postgraduate Medical Journal Read article

Combined versus sequential diuretic treatment of ascites in non-azotaemic patients with cirrhosis:results of an open randomised clinical trial -- Angeli et al. 59 (01): 98 -- Gut Read article

Ultrafiltration for decompensated heart failure: renal implications -- Kazory and Ross 95 (13): 1047 --Heart Read article


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A 72-year-old man is found to have the following biochemistry:

Calcium 1.98 mmol/L (2.2-2.6)

Phosphate 0.55 mmol/L (0.8-1.4)

Alkaline phosphatase 450 U/L (60-110)

Which of the following is the most likely explanation for his biochemistry?


Osteomalacia

Osteoporosis

Paget's disease

Renal failure

Tertiary hyperparathyroidism


Score: 71.88%

Total Answered: 32

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A 72-year-old man is found to have the following biochemistry:

Calcium 1.98 mmol/L (2.2-2.6)

Phosphate 0.55 mmol/L (0.8-1.4)

Alkaline phosphatase 450 U/L (60-110)

Which of the following is the most likely explanation for his biochemistry?


Osteomalacia Correct

Osteoporosis

Paget's disease

Renal failure

Tertiary hyperparathyroidism

Osteomalacia is associated with low calcium and phosphate with raised alkaline phosphatase. Parathyroidhormone (PTH) would be high.

Serum biochemistry is normal in osteoporosis, although alkaline phosphatase can be elevated following afracture.

Paget's disease is associated with normal calcium and phosphate with raised alkaline phosphatase.

In chronic renal failure there is inadequate 1-alpha hydroxylation of vitamin D, preventing the formation ofactive 1,25 dihydroxy vitamin D. This results in a low serum calcium and a compensatory high PHT (secondaryand tertiary hyperparathyroidism). Phosphate is elevated due to altered excretion.


An inborn error of bile acid synthesis (3-hydroxy-5-C27-steroid dehydrogenase deficiency)presenting as malabsorption leading to rickets -- Akobeng et al. 80 (5): 463 -- Archives of Disease inChildhood Read article

Mutations in SRD5B1 (AKR1D1), the gene encoding 4-3-oxosteroid 5-reductase, in hepatitis andliver failure in infancy -- Lemonde et al. 52 (10): 1494 -- Gut Read article

Hereditary hypophosphataemic rickets: report of a family from the Indian subcontinent -- Zargar et al.75 (886): 485 -- Postgraduate Medical Journal Read article


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An Afro-Carribean male aged 48 years presents with gradual onset of exertional dyspnoea, non-productivecough, malaise, weight loss and polyarthralgia.

Schirmer's test indicates a dry eye. x Ray of the hand shows punched out osteopenic lesions.

Which of the following investigations is unlikely to be helpful in establishing the diagnosis of this condition?


Quantitative immunoglobulins.

Serum calcium

Serum phosphorus

Thallium scan



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An Afro-Carribean male aged 48 years presents with gradual onset of exertional dyspnoea, non-productivecough, malaise, weight loss and polyarthralgia.

Schirmer's test indicates a dry eye. x Ray of the hand shows punched out osteopenic lesions.

Which of the following investigations is unlikely to be helpful in establishing the diagnosis of this condition?


Quantitative immunoglobulins. Incorrect answer selected

Serum calcium

Serum phosphorus

Thallium scan This is the correct answer


This condition is sarcoidosis.

Serum calcium, serum phosphorus, chem7 and chem 20 and quantitative immunoglobulins are all used inestablishing the diagnosis. Gallium scan is helpful in sarcoidosis. ( Radiology of extrathoracic sarcoid ...)

Gallium scan vs. Thallium scan.

Gallium scan (radioactive 67

Ga) is used to detect inflammation - such as in inflammatory disorders ormalignancy.

Thallium (radioactive 201

Tl) is a potassium analogue and is used to demonstrate areas of poor perfusion. It isparticularly used in cardiology to detect areas of ischaemia.


An unusual case of congenital short trachea with very long bronchi mimicking bronchial asthma --Ravenna et al. 57 (4): 372 -- Thorax Read article

Pseudoaneurysm of the thoracic aorta presenting with angina: a late complication of aortic valvereplacement -- HAMILTON et al. 79 (3): 310 -- Heart Read article

Reference intervals for serum creatine kinase in athletes -- Mougios 41 (10): 674 -- British Journal ofSports Medicine Read article


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With which of the following is lipoprotein lipase deficiency associated?


Abetalipoproteinaemia

Combined hyperlipidaemia

Familial combined hyperlipidaemia

Familial hypercholesterolaemia

Marked hypertriglyceridaemia


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With which of the following is lipoprotein lipase deficiency associated?


Abetalipoproteinaemia

Combined hyperlipidaemia

Familial combined hyperlipidaemia

Familial hypercholesterolaemia

Marked hypertriglyceridaemia Correct

Lipoprotein lipase deficiency is autosomal recessive and associated with increased chylomicrons and markedhypertriglyceridaemia.


Investigation and management of hypertriglyceridaemia -- Ferns et al. 61 (11): 1174 -- Journal ofClinical Pathology Read article

Pathology -- 90 (suppl 2): A64 -- Archives of Disease in Childhood Read article

Ataxia with isolated vitamin E deficiency presenting as mutation negative Friedreichs ataxia --Hammans and Kennedy 64 (3): 368 -- Journal of Neurology, Neurosurgery Psychiatry Read article


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Web(4) Chylomicron retention disease- Genetics Home Referenceghr.nlm.nih.govghr.nlm.nih.gov/condition/chylomicron-retention-disease






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Which of the following medications can cause hypomagnesaemia?


Aminophylline

Amitriptyline

Cisplatin

Co-trimoxazole

Lithium


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Which of the following medications can cause hypomagnesaemia?


Aminophylline

Amitriptyline

Cisplatin Correct

Co-trimoxazole

Lithium

Most of the body's magnesium is intracellular with only 1% being extracellular, in blood and interstitial fluid.This means that blood magnesium levels do not necessarily correspond with whole body magnesium status.

Causes of hypomagnesaemia include:

Drugs including cisplatin, diuretics, cyclosporine and cardiac glycosidesMalabsorption syndromesDiarrhoeaHypercalcaemiaAlcoholMetabolic acidosisRenal diseases - pyelonephritis, glomerulonephritis, acute tubular necrosis and interstitial nephritis.

Profound hypomagnesaemia can cause tetany, seizures and cardiac arrhythmias and needs to be treatedintravenously.

Lithium can cause hypermagnesaemia.


Serotonergic modulation of visceral sensation: lower gut -- Camilleri 51 (suppl 1): i81 -- Gut Read article

Other articles noted -- 13 (4): 127 -- Evidence-Based Medicine Read article

BTS statement on malignant mesothelioma in the UK, 2007 -- 62 (Suppl 2): ii1 -- Thorax Read article


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Web(4) DRUG INTERACTIONSwww.med.unc.eduwww.med.unc.edu/medicine/edursrc/drug_int.htmDRUG INTERACTIONS






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Which of the following are antibodies to which enzymes involved in glucose metabolism may be found inprimary biliary cirrhosis?


All of the following

Glucokinase (generates glucose-6-phosphate from glucose)

Lactate dehydrogenase (generates lactate from pyruvate)

Pyruvate dehydrogenase (generates acetyl-coA from pyruvate)

Pyruvate kinase (generates pyruvate from phosphoenolpyruvate)


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Which of the following are antibodies to which enzymes involved in glucose metabolism may be found inprimary biliary cirrhosis?


All of the following

Glucokinase (generates glucose-6-phosphate from glucose) Incorrect answer selected

Lactate dehydrogenase (generates lactate from pyruvate)

Pyruvate dehydrogenase (generates acetyl-coA from pyruvate) This is the correctanswer

Pyruvate kinase (generates pyruvate from phosphoenolpyruvate)

Pyruvate dehydrogenase (PD), required for the generation of acetyl-CoA from pyruvate for entry into thetricarboxylic acid (TCA) cycle, is found in the mitochondria.

Anti-mitochondrial antibodies (AMAs) - the serological hallmark of primary biliary cirrhosis (PBC) - are oftentargeted against pyruvate dehydrogenase.

The other enzymes listed are involved in glycolysis, which takes place in the cytosol.

Pyruvate dehydrogenase is crucial for aerobic respiration. Inherited deficiencies / defects of PD are rare butoften present with severe lactic acidosis in neonates. When this occurs, there can be no generation of acetyl-CoA for the Krebs cycle. Anaerobic glycolysis occurs, as the cell attempts to make adenosine triphosphate(ATP), but lactate is formed creating an acidosis.

In health, PD competes with pyruvate carboxylase (PC) for their common substrate, pyruvate. PD producesacetyl-CoA for the Krebs cycle, whereas PC produces oxaloacetate, a substrate for gluconeogenesis.

Acetyl-CoA regulates the balance between these two reactions (and thus the balance between anabolic andcatabolic pathways) by activating PC - so that in 'energy-rich' states, where acetyl-CoA is in abundance,gluconeogenesis will be favoured.

References

Ah Mew et al. MRI Features of 4 Female Patients With Pyruvate Dehydrogenase E1 alpha Deficiency. PediatrNeurol (2011) vol. 45 (1) pp. 57-9

http://themedicalbiochemistrypage.org/tca-cycle.html (an excellent source for biochemical pathways withdiagrams).


Altered glucose metabolism and proteolysis in pancreatic cancer cell conditioned myoblasts:searching for a gene expression pattern with a microarray analysis of 5000 skeletal muscle genes --Basso et al. 53 (8): 1159 -- Gut


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A 43-year-old woman presents with weight gain and menstrual irregularities.

Her BMI is 29 kg/m2, blood pressure is 150/90 mmHg and urinalysis shows + glucose.

Which of the following investigations should be performed initially?


24 hour urine cortisol

Aldosterone

HbA1c

Plasma testosterone

Prolactin


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A 43-year-old woman presents with weight gain and menstrual irregularities.

Her BMI is 29 kg/m2, blood pressure is 150/90 mmHg and urinalysis shows + glucose.

Which of the following investigations should be performed initially?


24 hour urine cortisol Correct

Aldosterone

HbA1c

Plasma testosterone

Prolactin

This history is suggestive of Cushing's syndrome: hypertension, adiposity, menstrual irregularities and impairedglucose homeostasis or diabetes. It is caused by overproduction of cortisol. Other features are recurrentinfections, osteoporosis, hypokalaemia and psychiatric disturbance.

Cushing's syndrome can be challenging to diagnose as it often requires several different diagnostic tests.

The 24 hour urine free cortisol (UFC) is a good initial screening test. Borderline results can occur with stress. Ifthe UFC is elevated, consider repeating it and consider the overnight or low-dose dexamethasone suppressiontests. Investigations are then often needed to localise the cause of Cushing's syndrome.

If Cushing's syndrome is excluded, serum prolactin, testosterone and HbA1c are all reasonable tests todo. The patient may have polycystic ovarian syndrome (PCOS) with impaired glucose tolerance or diabetes.The presence of clinical or biochemical evidence of hyperandrogenism is useful in the diagnosis of PCOS -serum testosterone would be useful here. A prolactinoma can cause menstrual disturbance but is notparticularly associated with weight gain or diabetes.

The correct answer remains UFC however, as you do not want to miss Cushing's syndrome.


Recurrence of adrenal aldosterone-producing adenoma -- Calvo-Romero and Ramos-Salado 76(893): 160 -- Postgraduate Medical Journal Read article

What is the rationale for hydrocortisone treatment in children with infection-related adrenalinsufficiency and septic shock? -- Aneja and Carcillo 92 (2): 165 -- Archives of Disease in Childhood Read article

Adrenal incidentaloma: evaluation and management -- Singh and Buch 61 (11): 1168 -- Journal ofClinical Pathology


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Which of the following statements regarding myosin is correct?


Contains an cAMP-binding sites

Forms filaments in a pentameric array with two heavy chains and three light chains

Has no function when not part of a filament

It drives smooth muscle contraction

Myosin heavy chain mutations are associated with development of familial hypertrophic cardiomyopathy


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Which of the following statements regarding myosin is correct?


Contains an cAMP-binding sites

Forms filaments in a pentameric array with two heavy chains and three light chains Incorrect answerselected

Has no function when not part of a filament

It drives smooth muscle contraction

Myosin heavy chain mutations are associated with development of familial hypertrophic cardiomyopathy

This is the correct answer

Myosin drives striated muscle contraction, and can be divided into two groups :

Conventional (class II myosins) which form filaments in a hexameric array of two heavy chains and twopairs of light chains.

Unconventional myosins do not form filaments and perform varied functions in a broad range of cells (forexample, organelle transport, endocytosis).

Myosin contains adenosine triphosphate (ATP) and actin-binding sites.

Other myosin related genetic disorders besides the heavy chain mutations in cardiomyopathy include Carney'scomplex (trismus-pseudocamptodactyly), type 1b Usher syndrome and non-syndromic deafness.


A mutation in the gamma actin 1 (ACTG1) gene causes autosomal dominant hearing loss(DFNA20/26) -- van Wijk et al. 40 (12): 879 -- Journal of Medical Genetics Read article

Novel association of hypertrophic cardiomyopathy, sensorineural deafness, and a mutation inunconventional myosin VI (MYO6) -- Mohiddin et al. 41 (4): 309 -- Journal of Medical Genetics Read article

Current perspectives in diastolic dysfunction and diastolic heart failure -- Leite-Moreira 92 (5): 712 --Heart Read article


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Web(4) Familial hypertrophiccardiomyopathy can becharacterized by a ...www.ncbi.nlm.nih.govwww.ncbi.nlm.nih.gov/pubmed/


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onexamination 2012 - clinical biochemistry & metabolism - (www.mymrcp.blogspot.com)

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