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Case 16 & 17 - Diabetes > CHEMPATH - DM > Flashcards

CHEMPATH - DM Flashcards

1
Q

Age of onset (1)

A

Type I in first 2 decades of life, type II typically later

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2
Q

Plasma insulin levels prior to treatment (1)

A

Absent in type I, often normal or even high in type II (depending on extent of insulin resistance)

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3
Q

Association with obesity (1)

A

Type I typically thin, type II frequently obese (obesity plays a central role in causation of type II)

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4
Q

Tendency to develop ketoacidosis (1)

A

Type I develop ketoacidosis more often

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5
Q

Tendency to develop hyperosmolar non-ketotic coma (HONK) (1)

A

HONK commoner in type II

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6
Q

Need for insulin therapy (1)

A

Type I have absolute insulin requirement, type II not.

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7
Q

Likelihood of developing long-term complications (retinopathy, nephropathy, etc.) (1)

A

Both are equally likely

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8
Q

Explain why a diabetic patient may be dehydrated, and why the serum Na concentration may underestimate the extent of his dehydration (2)

A

Glucose lost in the urine carries water with it (by osmotic diuresis).

Consequent hypernatraemia may be masked by a shift of water from cells into the serum induced by the elevated blood glucose.

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9
Q

List four (4) counter-regulatory hormones (4x½ = 2)

A

Glucagon, Cortisol, Growth hormone, Adrenaline

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10
Q

State three (3) criteria that can be used to confirm a diagnosis of diabetes mellitus (3) (NB)

A

Symptoms of hyperglycaemia and random plasma glucose ≥ 11.1 mmol/l

Fasting blood glucose of ≥ 7.0 mmol/l
Glucose tolerance test:

Blood glucose 2h after a standard oral glucose load of ≥ 11.1 mmol/l

Glycated haemoglobin (Hb A1c) ≥ 6.5%

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11
Q

Name the additive that is present in tubes used to collect samples for glucose analysis (grey top tube) and state the function of this additive (1)

A

Sodium fluoride. Inhibits glycolysis (prevents decreases in glucose)

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12
Q

Comment on the diagnostic relevance of an elevated blood glucose level in a known type 2 diabetic (1)

A

Uncontrolled diabetes

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13
Q

Would you expect to find glycosuria? Justify answer (1)

A

Yes. Because renal threshold for glucose exceeded (normal ~10mmol/l)

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14
Q

Name a common test used to monitor diabetic control over the long term (½) (NB)

A

Glycosylated haemoglobin (HbA1c)

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15
Q

Biochemically define HbA1c/ Give the chemical structure of HbA1C (2) (Super NB)

A

Glucose covalently (irreversibly) bound to the N-terminal valine (aminoacid) of the β-chain of the haemoglobin molecule. Normal range is 4-6%.

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16
Q

Explain why HbA1c is clinically useful (2) (NB)

A

It is a marker of glucose control over a 3-month period (lifespan of red blood cells) and is therefore used for long term assessment of glucose control.

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17
Q

A patient’s HbA1c was measured and found to be 8.0%. State why it is not useful to remeasure HbA1c one week later (1)

A

Red blood cells have a life span of 3 months, HbA1c is stable for the life span of the red blood cells.

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18
Q

Explain why HbA1c is typically elevated in poorly controlled diabetes. Give a situation in which its measurement at an out-patient clinic may be more useful than a simultaneously performed measurement of blood glucose (3)

A

The rate of haemoglobin glycosylation depends on the prevailing blood glucose at the time. Hence it gives an integrated reflection of blood glucose over the previous few months (RBC lifespan = 3 months). Not affected by short term fluctuations in blood glucose as might occur in a patient attempting to impress by lowering his/her blood glucose on the day of the visit.

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19
Q

List three (3) conditions where it cannot be used as a marker of glycaemic control. Outline reason for each (1½x3 = 4½) (NB) [HbA1c]

A

Haemoglobinopathy: Analytic error due to change in end-terminal valine

Haemolysis: Reduced RBC half-life (decreased HbA1c) e.g. thalassaemia, G-6-PD deficiency, Pyruvate Kinase

Iron deficiency: Increased RBC half-life (increased HbA1c)

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20
Q

Apart from hyperglycaemia, name three (3) conditions that can cause an elevated HbA1c (1½)

A

Abnormal Hb, Iron deficiency anaemia, Aplastic anaemia, Splenectomy, Renal failure, Pregnancy

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21
Q

Name a clinical condition that can result in a spuriously low HbA1C (2) (Super NB)

A

Haemolysis, blood transfusion, slow-migrating haemoglobin mutants (HbS, HbC)

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22
Q

Outline why the use of this marker is invalidated by the presence of haemolytic anaemia (like G6PD deficiency) that selectively targets old erythrocytes (2)

A

Haemolysis decreases mean RBC lifespan resulting in a spuriously low HbA1c.

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23
Q

Name an alternative test to HbA1c (½)

A

Fructosamine

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24
Q

State the marker used to differentiate between exogenous insulin administration and endogenous production in a patient with hypoglycaemia, where the plasma insulin level is elevated (½)

A

C-peptide

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25
Q

Define ‘C-peptide’ and give an example of its diagnostic value (4)

A

C-peptide is a peptide fragment derived from cleavage of proinsulin into insulin and is co-secreted with insulin. Plasma levels distinguish endogenous insulin secretion (e.g. from insulinoma) from exogenous insulin administration in hypoglycaemic individuals with an elevated plasma insulin.

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26
Q

Name a biochemical test for the early detection of microvascular disease in diabetes (1)

A

Microalbuminuria

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27
Q

Define microalbuminuria. Briefly explain its diagnostic value (2)/ Explain why this test is superior to routine urine dipstix testing (2) (Super NB)

A

The presence of albumin in the urine in insufficient quantity to be detected by routine dipstick testing but nevertheless pathological (between 20 and 200mg/day). Value = Timeous detection of early diabetic nephropathy (while it is still reversible with better glycaemic control).

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28
Q

State the likely significance of microalbuminuria in this patient (1). How can microalbuminuria be reversed, if at all? (1)

A

Indicates early diabetic nephropathy. By improved glycaemic control.

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29
Q

Name a cause for microalbuminuria in a non-diabetic patient (1)

A

Hypertension

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30
Q

What other analyte (chemical) might be useful to test for in a type 2 diabetic’ urine, and explain its diagnostic significance (2)

A

Microalbumin. Early detection of diabetic nephropathy while it is still potentially reversible by better glycaemic control.

31
Q

Explain the underlying defect in DM type 1 (1)

A

Absolute lack of insulin due to auto-immune β-cell destruction

32
Q

Other than type 1 diabetes mellitus, name another cause for ketonuria (ketones in the urine) / In non-diabetics (1) (NB)

A

Fasting, starvation

33
Q

State why type 1 diabetes mellitis (IDDM) and prolonged fasting in a healthy subject are both associated with elevated plasma ketone body levels (1)

A

Both the result of low plasma insulin levels

34
Q

Comment on any difference between the two situations above in terms of the resulting ketoacidosis (1)

A

In IDDM, insulin is totally absent (hence ketoacidosis much worse), whereas in prolonged fasting insulin is low but still sufficient to prevent ketogenesis spiralling out of control.

35
Q

Explain the mechanism resulting in ketosis in untreated type 1 DM (2)

A

No insulin so lipolysis is not inhibited by malonyl CoA

36
Q

Describe the acid-base findings (including anion gap) in DKA (2) (NB)

A

Partially compensated metabolic acidosis with high anion gap

37
Q

Define the term anion gap and calculate it in the above case. Name the likely cause for the increased anion gap in DKA (3) (NB)

A

Difference between the commonly measured cations and anions in the plasma = (Na+K) – (Cl -HCO3) = (130+6) - (90+5) = 41
Elevated due to presence of anion keto-acids (β-hydroxybutyrate, acetoacetate)

38
Q

Explain the low PCO2 in the blood gas results (1)

A

Hyperventilation in compensation for a metabolic acidosis

39
Q

List 3 biochemical hallmarks (typical characteristics) of DKA [3]

A

Compensated metabolic acidosis on blood gas analysis. Very elevated blood glucose levels (>20mmol/l, normal 5mmol/l). Ketones in blood (ketonaemia)

40
Q

Give the biochemical explanation for DKA [2]

A

Lack of insulin enhances free fatty acid release from adipose tissue and enhances beta-oxidation of these fatty acids to ketone bodies (acetoacetate and ß-hydroxybutyrate) by the liver (low hepatic malonyl CoA permits entry of fatty acids into mitochondria).

41
Q

Suggest a reason for the initially slightly high plasma Na (1)

A

Glucose-induced osmotic diuresis depleting body water and thus concentrating plasma Na

42
Q

Outline the reason for an apparently low sodium in patients with DKA (2x1 = 2) (Super NB)

A

Dilutional hyponatraemia caused by the increased osmolality in the extra cellular fluid compartment caused by the elevated glucose [1], which leads to movement of water from the intra cellular fluid compartment [1]

43
Q

Sodium was 120mmol/L (N = 135 – 145) & glucose 57 mmol/L (N = 7). Explain the finding of the low sodium using calculations to illustrate your answer (3)

A

Dilutional hyponatraemia due to elevated glucose. For every 10mmol increase in glucose, 3 mmol decrease in sodium. Therefore, sodium decreases related to glucose increase = (57 – 7)/10 x 3 = 15mmol/L.

44
Q

State two (2) reasons for the high plasma K (2) (Super NB)

A

Any two: Acidosis displacing K from intracellular binding sites. Loss of intracellular K-binding sites, including protein and phosphorylated glycolytic intermediates. Renal impairment.

45
Q

Does the high serum potassium in DKA reflect the whole-body potassium stores? Justify your answer (1)

A

No, in fact the patient is markedly potassium depleted intracellularly.

46
Q

State two (2) reasons for the disproportionate increase in urea over creatinine (simply stating ‘renal failure’ is not enough) (2)/ Name the abnormality in renal function and explain how this has come about (1½)

A

Pre-renal failure due to dehydration and reduced glomerular filtration rate (accelerated protein catabolism?)

47
Q

Name three (3) factors that must be corrected urgently in the treatment of DKA (1½) (NB)

A

Dehydration (Hypotonic fluid replacement), Electrolytes (Potassium), Hyperglycaemia (Insulin)

48
Q

Explain the typical changes in plasma Na and K observed during the resuscitation of a patient with DKA (with insulin) (4) (Super NB)

A

Na rises as glucose enters cells under influence of insulin, lowering plasma osmolality and causing water to shift into cells, thereby ‘concentrating’ plasma Na. Plasma K falls, since both correction of acidosis and entry of glucose into cells and its subsequent phosphorylation (creates intracellular binding sites) causes a shift of K from ECF into ICF.

49
Q

Outline the mechanism for the potential drop in plasma phosphate, magnesium and potassium levels after insulin administration in the treatment of a patient with hyperglycaemia (3)

A

Glucose that enters insulin sensitive cells is immediately phosphorylated to glucose-6-phosphate, this increases demand for phosphate within cells. As phosphate enters insulin sensitive tissues, an increased amount of negative charge across the cell membrane increases uptake of cations such as K and Mg and plasma levels can decrease if a whole-body deficiency exists.

50
Q

List any two (2) treatment options for lowering potassium and the mechanisms by which they operate (3)

A
  • Loop diuretics and fluids  renal potassium loss
  • Glucose and insulin  glycolysis  increased phosphorylation of glucose  increased negative charge intracellularly  increased binding sites for cations  increased uptake of potassium intracellularly
  • Dialysis diffusion of potassium into dialysate (out of body) across a concentration gradient
  • Kayexalate  cation binding resin
  • Salbutamol  β-2 agonist stimulates glycogenolysis  increased phosphorylated metabolites  increased negative charge intracellularly  increased binding sites for cations  increased uptake of potassium intracellularly
51
Q

Do you think the DKA patient will require potassium replacement at some stage? Justify your answer (1)

A

Yes, during treatment with insulin when potassium re-enters cells.

52
Q

Explain how DKA treatment causes a decrease in serum urea (1)

A

Dehydration has been corrected, which has restored renal perfusion, hence renal function

53
Q

Explain how the patient’s blood pH improved without any apparent change in the serum ketones (2)

A

The ketone test only detects acetoacetate, while the severity of acidosis is determined by the sum of both ketoacids (acetoacetate plus beta-hydroxybutyrate). While treatment leads to a rapid fall of betahydroxybutyrate, acetoacetate lags behind (due to improvement in pH and tissue oxygenation). Hence the ketone test remains positive for a considerable period.

54
Q

Indicate the biochemical result that would show that adequate insulin has been given and that further insulin treatment can be slowed down (1)

A

Disappearance of ketones (rather than normalisation of blood glucose)

55
Q

How would you calculate his serum osmolality? (1)

A

[2 x (Na + K)] + glucose + urea]

56
Q

Explain why HCO3 replacement may not be necessary, despite his greatly reduced plasma HCO3 at presentation (1)

A

Metabolism of ketone bodies regenerates HCO3

57
Q

Suggest two common reasons for the deterioration in his diabetic control (1)

A

Infection, physical stress, poor compliance with diet or insulin dose (rebellious teenager?)

58
Q

What is responsible for the smell on his breath? (1)

A

Acetone, a volatile ketone body

59
Q

Name a likely cause for intermittent dizzy spells in a poorly controlled diabetic (1)

A

Hypoglycaemia due to insulin overdose

60
Q

State how the disorder described above can be confirmed, and distinguished from an insulinoma (3)

A

Inappropriately high plasma insulin in the context of hypoglycaemia. C-peptide measurement.

61
Q

State why Type 2 diabetics are usually obese (1)

A

Obesity causes insulin resistance. Insulin resistance increases such that pancreatic insulin production is insufficient to regulate blood glucose levels and chronic hyperglycaemia ensues

62
Q

Explain why obesity predisposes to the development of type 2 diabetes (NIDDM) (2)

A

Deposition of triglyceride in extra-subcutanous adipose tissue sites (e.g. liver, muscle, visceral fat) promotes insulin resistance, as does decreased secretion of insulin-sensitizing hormones like adiponectin from over-filled adipocytes.

63
Q

Indicate how the biochemical features of lipodystrophy support this explanation (2)

A

In lipodystrophy, lack of subcutaneous adipose tissue results in both of the above effects and profound insulin resistance despite a lean phenotype (low BMI).

64
Q

Outline the origin of the ketonuria in a type 2 diabetic (2). Explain why ketonuria is relatively uncommon in type 2, as opposed to type 1, diabetes (3) [5] (NB)

A

Insufficient insulin to prevent lipolysis in adipose tissue and β-oxidation of the fatty acids released to form ketone bodies by the liver (2)
Insulin deficiency in type 2 diabetes is relative rather than absolute as it is in type 1. Thus, though insulin production in type 2 is insufficient to inhibit gluconeogenesis by the liver, and hence hyperglycaemia, it is generally adequate to prevent ketogenesis, since the latter process is very sensitive to inhibition by insulin.

65
Q

Name the type of diabetes (type 1 or type 2) suggested by the absence of urine ketones. Include the underlying biochemical explanation for your answer (1+2 = 3)

A

Type 2. Both types are hyperglycaemic (hence glycosuric) but only type 1 with an absolute insulin deficiency typically develop ketosis. Ketogenesis is very sensitive to inhibition by insulin, whereas gluconeogenesis is less so. Hence residual insulin production in type 2 sufficient to inhibit ketogenesis but not gluconeogenesis.

66
Q

Outline the biochemical steps that prevent ketone production in type 2 diabetics (4)

A

Insulin present increases production of malonylCoA [1] which inhibits carnitine palmitoyl transferase (CPT) activity. This in turn inhibits transport of fatty acids into mitochondria [1], inhibiting break down of fatty acids [1] and therefore inhibits ketone synthesis [1].

67
Q

List three (3) biochemical abnormalities of HONK (3)

A

Hyperglycaemia (>33 mmol/L) [mentioning glycosuria alone is not sufficient]

Increased urea (Severe dehydration including intracellularly, i.e., pre-renal)

Metabolic acidosis (due to lactic acidosis) [If they say pH can be decreased or normal – allowed]

Increased blood viscosity – thrombosis

Increased plasma osmolarity (> 320 mOsm/kg)

Whole body electrolyte losses of Potassium, Phosphate and Magnesium despite normal plasma levels

68
Q

Explain how it is possible to be dehydrated in the presence of a normal serum sodium concentration (3)

A

Elevated glucose levels increases ECF osmolality (1) and causes flow of water from the ICF into the ECF, which tends to decrease the serum sodium concentration and offsets the hypernatraemia which would otherwise result from water loss into the urine (2).

69
Q

Outline the mechanism for the glycosuria present in this patient (1)

A

Renal glucose threshold of 10mmol/L has been exceeded.

70
Q

Explain the absence of ketones in the urine in this patient (1)

A

Sufficient insulin present to inhibit fatty acid breakdown and ketogenesis but not enough to inhibit hepatic glucose output (gluconeogenesis)

71
Q

List three (3) reasons for the elevated serum potassium concentration (1½)

A

Renal failure; acidosis displacing K+ from ICF into ECF; inability of glucose to enter cells depletes the pool of phosphorylated glycolytic intermediates which provide K+ binding sites; similarly, enhanced intracellular (IC) protein catabolism means loss of IC K+ binding sites

72
Q

The patient was treated with insulin and intravenous fluids. List two (2) complications of insulin therapy in this setting (1)

A

Hypokalaemia and hypoglycaemia

73
Q

Readmitted with HONK and no ketoacidosis. Three months later Mr Williams presents to the emergency unit semi-conscious, with severe dehydration. Blood tests are performed. The following are his results: Sodium = 149 mmol/L, Potassium = 4.7 mmol/L, HCO3 = 18 mmol/L, Urea 35 = mmol/L, Creatinine = 180 umol/L, Osmol = 400 mosm/kg, Glucose = 55 mmol/L
• State and calculate the “true” sodium concentration in this patient given that normal glucose is 5 mmol/L (2)
• Calculate the amount of water replacement required, given that the total body water in an average male is 40L and normal sodium is usually 140 mmol/L (3)
• Calculate the osmolarity using the biochemical results provided (2)

A

“True” sodium: Sodium decreases by 3 mmol/L for every 10 mmol/L increase in glucose [1]
Therefore “true”sodium = 149 + 3 x (55-5)/10 = 164 mmol/L [1]

Change in volume/TBW = [(1-normal sodium)/ “true” sodium] [1]
Change in volume = TBW x [(1-normal sodium)/ “true” sodium] = 40 x [(1-140)/164] [1] = 40 x [(164-140)/164] = 4.9L [1]

Osmolarity = 2(Na + K) + Urea + Glucose [1] = 2 (149 + 4.7) +35 + 55 = 397 mosm/kg [1]

Case 16 & 17 - Diabetes (9 decks)

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