T12 DM and Hypoglycemia Flashcards
How do we diagnosis DM?
Symptoms of diabetes with - random plasma glucose >11.1 - fasting plasma glucose >7mmol/L - 2hr OGTT >11.1 mmol/L at least 2 separate measurements taken
- secondary causes excluded e.g. hypercortisolism
Definition of impaired fasting glucose?
Fasting plasma glucose = 5.6-7
Definition of impaired glucose tolerance
2hr OGTT 7.8-11.1
Patient 45/M, random plasma glucose is 12 mmol/L, is the patient diabetic?
No.
Patient is asymptomatic, requires further additional investigations.
- random glucose > 11.1 is compatible with DM, but an additional abdominal glucose measurement is needed before DM is diagnosed
Patient 45/M, random plasma glucose is 12 mmol/L, is the patient diabetic?
What other tests should be considered? (3) Give some benefits or cons for each)
HbA1c
- high precision
- no need overnight fasting
- low sensitivity
Fasting glucose
- second most sensitive
- requires overnight fasting
OGTT
- most sensitive
- highest pick up rate but most tedious
- requires overnight fasting
- requires exact timing of 2 hours
All of the above requires second measurement
Patient has massive myocardial infarct, random plasma glucose is 12 mmol/L.
Is the patient diabetic?
If not, how to further investigate?
Inconclusive
- Immense physical stress causes increased cortisol, thus increased glucose.
- To comment on his glucose tolerance, proper testing should be performed one-month after his recovery?
20/M with fasting plasma glucose 6.8 mmol/L
Is the patient diabetic?
No
- only impaired fasting glucose
- although no DM now, there is 50% chance of developing DM over next 10 years since IFG
20/M with fasting plasma glucose 6.8 mmol/L
What other tests to consider?
- HbA1c
- C-peptide
(very young! look for any familial/genetic causes)
OGTT
0 min: 6
60 min: 9.1
120 min: 8.3
Interpret the OGTT results.
Patient management?
Normal:
0: <5.1
60: <11.1
120: <8.5
The 2 hour glucose level is <11.1 but >7.8, thus this is a case of impaired glucose tolerance.
In addition, fasting plasma glucose is 6, indicating impaired fasting glycemia.
Lifestyle modification (dietary advice)
Known Type I diabetic in semi-conscious state,
2 day history of diarrhoea, vomiting.
Dehydrated, coarse crackles in both upper zones of her lungs.
Low Na+ High K+ High urea and creatinine High glucose Urine ketones ++
Blood gas
- acidemia
- low HCO3-
- low PCO2
- high pO2
What is the diagnosis?
Explain
Dehydrated, coarse crackles in both upper zones of her lungs. = pneumonia
High urea and creatinine = dehydration
Diabetic ketoacidosis
- type I DM
1. the patient was too sick to take insulin injections > hyperglycaemia > osmotic diuresis > dehydration and pre-renal failure (high urine/creatinine ratio)
- lack of insulin = uninhibited lipolysis with ketone production > high anion gap metabolic acidosis with respiratory compensation
- acidosis and lack of insulin causes reduced cell uptake of K+, thus hyperkalemia (but total body K+ is low)
- Dilution hyponatremia due to hypertonicity from the presence of glucose
Treatment for DKA?
- rehydration with normal saline
- insulin administration
- monitor glucose and K+ levels
- give DKI drip + phosphate
- (Dextrose + K+ + insulin): bring down glucose levels
- phosphate is for ionising glucose > won’t leave cell
In a patient with DKA,
glucose is 45.4 mmol/L
while Na+ is 122 mmol/L
Na+ is affected by glucose and needed to be recalculated. Describe how.
During osmotic diuresis, high level of glucose causes water loss, and dehydration will cause Na+ loss too due to no time for reabsorption.
Actual Na+ is calculated by
(122+45.5)/3 = 15
15+122 = 137
A 79/F with type II DM found lying on floor in semi-conscious state.
- Na+ high
- K+ normal
- Cl- high
- HCO3- borderline high
- Urea high
- Creatinine high
- Anion gap = 17
- Glucose - very high
- Osmolality = 393 mmol/L
Urine ketons -ve
Why is osmolarity high?
Explain this case.
Osmolarity is high due to high Na+ and glucose.
Patient with Type II DM, with insulin production but resistance.
There is insulin to suppress lipolysis thus ketone production - thus not DKA.
Insulin cannot suppress gluconeogenesis
This is case of Hyperosmolar non-ketotic coma.
Dehydration is marked (urea/creatitine)
Diuretic diuresis, with hyperglycaemia, hyperosmolality, hypernatraemia, with no ketones.
Normal anion gap.
Management for patient with Hyperosmolar hyperglycaemic state?
DKI drip and phosphate
35/F with known Type I DM, drowsy.
Glucose is 1.5 mmol/K.
Interpretation?
Common causes for such condition?
Hypoglycemic, <2.5 mmol/L
Whipple’s triad:
- hypoglycaemic symptoms
- hypoglycemic shown in laboratory results
- symptoms reversed with administration of glucose
Causes
- overdose of oral hypoglycemic agents
- insulin overdose
- eaten less, exercised more
DDx
- Insulin overdose
- Reactive hypoglycaemia
