13. Diabetes CPC

Question 1

What is the definition of diabetes?

Answer 1

• A fasting plasma glucose > 7 mmol/L
• A 2 hour plasma glucose in a GTT > 11.1 mmol/L
• HbA1c > 6.5% (48 mmol/mol)
• NOTE: with HbA1c, the original method of quantifying it was using a percentage, but this has since changed to mmol/mol
• Non-diabetic HbA1c < 42 mmol/mol

Question 2

Case 1: Mrs GB. First presented in February 2002. 48 y/o unconscious. Acutely unwell for a few days. Vomiting. Polyuria and polydipsia. Breathless. Dehydrated. PMH: appendicectomy, osteoporosis, poorly controlled HTN. DHx: amlodipine 10mg, atenolol 100mg. Examination: obese, very dehydrated, BP 80/40, urine dip: 4+ glycosuria. What Ix to do next?

Answer 2

ABG

Question 3

Case 1: Mrs GB. First presented in February 2002. 48 y/o unconscious. Acutely unwell for a few days. Vomiting. Polyuria and polydipsia. Breathless. Dehydrated. PMH: appendicectomy, osteoporosis, poorly controlled HTN. DHx: amlodipine 10mg, atenolol 100mg. Examination: obese, very dehydrated, BP 80/40, urine dip: 4+ glycosuria. ABG: pH = 7.65; PCO2 = 6.1 kPa N 4.7 - 6.0); PO2 = 15kPa. What is this?

Answer 3

Metabolic alkalosis (high pH = alkalosis, thus high CO2 = metabolic)

Question 4

What are the causes of metabolic alkalosis?

Answer 4

H+ loss (i.e. vomiting), hypokalaemia, ingestion of bicarbonate. NOTE: high bicarbonate will cause a slightly raised CO2 - this is due to a shift in the equilibrium and is NOT a form of compensation. H+ + HCO3- H2CO3 CO2 + H2O

Question 5

How does compensation occur in metabolic alkalosis?

Answer 5

Metabolic alkalosis will inhibit ventilation which will drive the CO2 up further. The extent of this compensation is limited because ventilation needs to remain sufficient to maintain good oxygen levels. So, there is relatively little respiratory compensation for alkalosis

Question 6

Case 1 patient results: Na = 145; K = 2.5; U = 40; pH = 7.65; glucose = 46; bicarb = 55 mM (high). What is the osmolality?

Answer 6

• Osmolality = charged molecule + uncharged
• Osmolality = cations + anions + urea + glucose
• since cations = anions,, osmolality = 2(Na + K) + U + G
• Osmolality = 381 mosm/kg

Question 7

Case 1 patient results: Na = 145; K = 2.5; U = 40; pH = 7.65; glucose = 46; bicarb = 55 mM (high); chloride = 80. Osmolality is 381 mosm/kg. What is the anion gap?

Answer 7

Anion gap = Na + K - Cl - bicarb

Anion gap = 145 + 2.5 - 80 - 55

Anion gap = 12

Suggest no extra anions

Question 8

Case 1: Mrs GB. First presented in February 2002. 48 y/o unconscious. Acutely unwell for a few days. Vomiting. Polyuria and polydipsia. Breathless. Dehydrated. PMH: appendicectomy, osteoporosis, poorly controlled HTN. DHx: amlodipine 10mg, atenolol 100mg. Examination: obese, very dehydrated, BP 80/40, urine dip: 4+ glycosuria. Why is she unconscious? A. DKA, B. Hyperosmolar non ketotic coma, C. Severe hypotension, D. Stroke, E. Renal failure

Answer 8

C. Severe hypotension (first two can cause the third option?)

Question 9

Case 1 patient results: Na = 145; K = 2.5; U = 40; pH = 7.65; glucose = 46; bicarb = 55 mM (high); chloride = 80. Osmolality is 381 mosm/kg. Anion gap = 12. Is this DKA?

Answer 9

No. Ketones are anions and would result in a high anion gap. This is a hypokalaemic alkalosis.

Question 10

What are the causes of longstanding hypokalaemia?

Answer 10

1. Intestinal loss: diarrhoea, vomiting, fistula. 2. Renal loss: mineralocorticoid excess, hypoaldosteronism, diuretics, renal tubular disease. 3. Redistribution: insulin, beta-agonists, alkalosis (4. decreased intake - rare!)

Question 11

How does hypokalaemia lead to alkalosis?

Answer 11

1. Low K+, 2. shift of H+ into cells, 3. extracellular alkalosis. Hypokalaemia causes alkalosis and alkalosis causes hypokalaemia

Question 12

Case 1 further history. Longstanding HTN and diabetes, previous fractured hip, slowly worsening obesity, wound on shin that did not heal. What is the diagnosis? A. Cystic fibrosis, B. SLE, C. Cushing’s syndrome, D. Sjogren’s, E. Osteoporosis

Answer 12

C. Cushing’s syndrome

Question 13

What are the possible causes of Cushing’s syndrome?

Answer 13

Pituitary, ectopic ACTH, adrenal tumour

Question 14

Case 1: ACTH: 250 (very high) and cortisol 3120 nM (very high). Dexamethasone failed to suppress. Low dose dex cortisol = 3100 nM and high dose dex cortisol = 2990 nM (totally failed to suppress). What is the cause? A. pituitary Cushing’s B. Ectopic ACTH C. adrenal tumour

Answer 14

B. Ectopic ACTH. With high dose dex, pituitary Cushing’s would suppress a bit. Not adrenal tumour because ACTH would have been suppressed. Also because ectopic ACTH gives the lowest level of potassium. Because very high levels of cortisol bind to the aldosterone receptor. It saturates the renal enzyme 11HSD, and cortisol starts to behave like aldosterone, which means you retain sodium and lose potassium. As that keeps happening, pt becomes more and more cushingoid, and becomes more hypokalaemic.

Question 15

What are the causes of ectopic ACTH

Answer 15

lung cancer, other cancers

Question 16

Case 1: Respiratory examination. Examination reduced on right. Percussion dull on right. Vocal resonance increased on right. What is the diagnosis? A. pleural effusion, B. pneumothorax, C. collapse and consolidation, D. COPD, E. bronchiectasis

Answer 16

Answer is C. collapse and consolidation (pneumonia). Vocal resonance on the right makes pleural effusion wrong.

Question 17

Case 1 patient - CXR resolved with ABX, possible small endobronchial lesion was causal but not identified. Patient was very hypotensive, why?

Answer 17

Patient very dehydrated. Rehydrate cautiously and replace potassium (caution).

Question 18

Case 1: hypotensive patient is being rehydraed cautiously. She does not pass any urine. What should you do? Na 145, K 4.0, U 45, Creat 450. What are the differential diagnoses?

Answer 18

Acute renal failure (dehydration), chronic renal failure (diabetes).

Question 19

Case 1: BP recovers to 130/80, JVP starts to rise, risk of pulmonary oedema. Remains anuric for 24h. How can we distinguish acute renal failure (ATN) and chronic renal failure (diabetic renal disease)?

Answer 19

Renal biopsy needed. See notes for images. If ATN, then dialyse for 3 weeks (will recover). Diabetic glomerular kidney disease is end stage renal failure and will need lifelong dialysis. Fortunately this was acute tubular necrosis due to dehydration. She made full recovery after dialysis for 3 weeks.

Question 20

Case 1: what was done about the ectopic ACTH? CT thorax showed possible (***inoperable) small lesion in hilum close to mediastinum. Probable very slow growing multiple metastases. CT abdomen showed bilateral adrenal hyperplasia.

Answer 20

Bilateral adrenalectomy.

Question 21

Case 1: Recovered fully from surgery and back to complete normal fitness despite metastases from ectopic ACTH. Patient elected to have no further treatment. As adrenals are out, she then goes on low dose hydrocortisone. She’s got lung cancer making ACTH but no adrenals, so it doesn’t matter. Patient said she was fine, there were no clever mabs at the time, and chemo looked toxic to her, so she said ‘leave me alone’. It grew pretty slowly so she did well for a while. 3 months later, chest pain on exertion. ECG shows inferior stemi, with true posterior extension (see notes). What is the treatment?

Answer 21

Aspirin, GTN, beta blocker, pain relief, thrombolysis/primary angioplasty

Question 22

Case 1: patient remained well for 1 year after treating inferior stemi. Then she had new onset difficult walking, tone increased on the right, power reduced on the right, brisk reflexes on the right. Diagnosis?

Answer 22

Right upper motor neurone signs. Metastasis to brain. 6 months later, developed recurrent neurological signs, known metastatic disease, deteriorated, found dead in bed at home. Post mortem: due to coronary thrombosis.