5: Diabetes Clinical Cases

Question 1

Acid-base balance schematic

Answer 1

If you generate CO2, pH will fall as H+ and HCO3- will be formed

CO2 ALWAYS CORRELATES WITH BICARB (low CO2 = low bicarb, high CO2 = high bicarb)

H+ HCO3- = CO2 + H2O

Question 2

Case 1: A 16-year-old was found unconscious. He had been acutely unwell for a few days, vomiting. His mother also reported that he had been breathless.

pH: 6.85 – low pH = acidosis (i.e. excess H+ ions)

PCO2: 2.3 kPa (4.0 – 5.0)

PO2: 15 kPa

Sodium: 145

Potassium: 5.0

Urea: 10

Glucose: 25

Chloride: 96

Bicarbonate: 4.0

Answer 2

Metabolic acidosis

If the COs is low, the bicarbonate will be low (diffuses over to the right side of the equilibrium equation).

The acid-base abnormality is an acidosis (low pH). According to the low the equilibrium equation, bicarbonate will be low (due to a low CO2). This is therefore a metabolic acidosis. This patient is unconscious because brain enzymes cannot function at such an acidic pH.

Question 3

calculating osmolality

Answer 3

osmolality = 2 (Na + K) + urea + glucose

Question 4

Anion gap formula

Answer 4

There should always be a small mismatch between the anions and cations because of the contribution of the anions that are not measured and taken into account.

anion gap = (Na + K) – (Cl + HCO3)

Normal anion cap: (140 + 4) – (102 + 24) = 18 mM

A high anion gap is suggestive of there being some other form of toxin in the patient’s blood (e.g. ketones, lactic acid, methanol, ethanol). Ethylene glycol poisoning can cause a high anion gap.

Question 5

Osmolality and Anion gap for case 1

Case 1: A 16-year-old was found unconscious. He had been acutely unwell for a few days, vomiting. His mother also reported that he had been breathless.

pH: 6.85 – low pH = acidosis (i.e. excess H+ ions)

PCO2: 2.3 kPa (4.0 – 5.0)

PO2: 15 kPa

Sodium: 145

Potassium: 5.0

Urea: 10

Glucose: 25

Chloride: 96

Bicarbonate: 4.0

Answer 5

Osmolality of Case 1 patient: 335

Anion Gap of Case 1 patient: 50 – this is high (suggests extra anions – ketones)

Question 6

What condition usually causes a high anion gap in a young patient with acidosis?

Answer 6

DKA

ketones in the blood cause an increase in the anion gap.

Question 7

Case 2: A 19-year-old known to have T1DM for several years presents unconscious.

pH: 7.65

pCO2: 2.8 kPa

Bicarbonate: 24 mM (normal)

pO2: 15 kPa

Sodium: 140

Potassium: 4.0

Chloride: 100

Glucose 1.3 mM – hypoglycaemia

Answer 7

This is a respiratory alkalosis (CO2 is low, and pH is high)

This is probably due to primary hyperventilation (due to hypoglycaemia-induced anxiety)

In hyperventilation, CO2 is blown off and as a result, bicarbonate will fall

When your pH increases, plasma proteins start to stick to calcium more than usual

The plasma calcium will appear normal, however, there will be less free ionised calcium

A fall in free ionised calcium will result in tetany (which can make patients hyperventilate more)

Also, the patient is very hypoglycaemic; this can induce anxiety

Low glucose causes a surge in adrenaline, which can also cause hyperventilation

• NORMAL anion gap = 20

Question 8

Case 3: A 60-year-old man presents unconscious to casualty, with a history of polyuria and polydipsia. Investigations reveal:

osmolality?

what is wrong with the patient?

Sodium: 160

Potassium: 6.0

Urea: 50

pH: 7.30

Glucose: 60

Answer 8

442 = very high

very dehydrated

Question 9

T1DM vs T2DM regarding acidosis

what condition can result in T2DM

why not normalise fast

Answer 9

T1DM first present with acidosis

• DKA

T2DM

• increasing hyperglycaemia –> dehydration –> collapse (HHS)
• DO NOT normalise too quickly –> cerebral oedema
• treat with gentle 0.9% saline (enables a slower reduction in plasma sodium concentration)
• Observe the patient – they will manage on diet alone eventually

Question 10

Case 4: A 59-year-old man known to have type 2 diabetes on a good diet and metformin presents to casualty unconscious.

anion gap? what is causing this?

Urine is negative for ketones (not DKA)

Sodium: 140

Potassium: 4.0

Urea: 4.0

pH: 7.10

Glucose: 4.0

pCO2: 1.3 kPa

Chloride: 90

Bicarbonate: 4.0 mM

Answer 10

This is a metabolic acidosis because the pH and pCO2 are low

The osmolality in this patient is 296

The anion gap is 50 – there are NO ketones, so there must be another acid involved:

Other acids that could be involved: methanol, ethanol, lactate

Metformin overdose can cause LACTIC ACIDOSIS – this is rare (normalised with bicarbonate)

Lactic acidosis is also seen in patients taking metformin with metabolism impairment/renal failure

Question 11

The cori cycle

Answer 11

Metformin can cause lactic acidosis because it inhibits hepatic gluconeogenesis of lactate to glucose (one of its mechanisms of action). Normally, excess lactate will be cleared by the kidneys, but in patients with renal failure, the kidneys cannot handle the excess lactic acid. This is seen very rarely.

Question 12

T2DM definition

Fasting blood glucose and OGTT

HbA1c

Answer 12

Fasting Blood Glucose > 7.0 mM – if you get this result, no need to do an OGTT

Oral Glucose Tolerance Test (75 g of glucose given at time 0)

• Diabetes = plasma glucose > 11.1 mM at 2 hours
• Impaired Glucose Tolerance = plasma glucose 7.8 – 11.1 mM at 2 hours
• Impaired glucose tolerance patients tend to develop diabetes if we are not careful

NOTE: plasma glucose is different from whole blood glucose

HbA1c

• 42 or more impaired flucose tolerance
• 48 or more diabetes

Question 13

what happens in DKA?

Answer 13

The liver produces ketones deliberately, which are acidic (pH goes down)

There is no compensation; by equilibrium, as bicarbonate falls, CO2 drifts to the left

The CO2 will be low

Supposing you have a metabolic acidosis, mechanisms for compensation will occur

Compensation has to occur; the brain will not survive the acidosis

Compensation: improving the pH at the expense of making the CO2 worse

In a DKA, the patient will breathe faster to increase pH -> compensated metabolic acidosis

Kussmaul breathing (deep, laboured) seen in metabolic acidosis (particularly in DKA)

The pH improves, but the pCO2 further deteriorates in compensated metabolic acidosis

Question 14

what happens in acute respiratory acidosi?

Answer 14

CO2 will rise rapidly and that is usually because you have stopped breathing entirely (we see a high CO2 and a low pH).

Question 15

What happens in COPD (chronic respiratory acidosis)?

Answer 15

COPD leads to the development of a chronic respiratory acidosis

In COPD, the lungs fail over a long period of time and the pCO2 begins to drift upwards

As CO2 drifts upwards, the patient becomes very breathless (CO2 is a potent respiratory stimulus)

If this goes on for long enough, the kidneys will retain bicarbonate -> which increases CO2 further

Compensated respiratory acidosis: improved pH but very high CO2

Question 16

pink puffers and blue bloaters

Answer 16

Pink puffers are very breathless because they are still sensitive to this raised CO2 - hyperventilation is one technique that the body uses to compensate the acidosis (more CO2 blown off).

• There will eventually come a point when your brain has had enough of puffing
• The brain then becomes unresponsive to CO2
• Then, the CO2 is no longer a potent driver to breathe

This makes you a nice, calm blue bloater – you are not breathless, but your CO2 will continue to rise.

The kidneys will try to compensate by retaining HCO3-.

Question 17

compensation

Answer 17

: it is theoretically possible to compensate for a respiratory alkalosis – if you over breathe (and continue to do so), the kidneys can compensate (in reality, they do not compensate because the patient will calm down before they take action). We also wouldn’t see a compensated metabolic alkalosis (e.g. milk-alkali syndrome). The only compensation we see is for DKA and COPD.