ADEGOKE ADEGBITE

DM CASE STUDIES
A. CASE STUDY 1
A man with type 2 diabetes mellitus presents for his regular physical
FBS 99mg/dl, HBa1c- 13 %
1. I wont congratulate him exactly
2. The FBS is within normal limit but only reflective of the particular day in
question, the upper limit for FBS is 110mg/dl, while the glycosylated
hemoglobin is used to determine the level of glycemic control over a
period of 6-8weeks; values less than 6.5% signifies a good glycemic
control over that period, hence 13% shows the glucose control has not
been optimum

B. CASE STUDY 2
Type 1 DM often results from autoimmune destruction of B islet cells leading
to lack of insulin, while, Type 2 DM results from reduced sensitivity of tissue
to insulin; hence insulin is not reduced in concentration in Type 2 DM(exact
pathophysiology is unknown but a number theories have been postulated :
roles of adipokines, oxidative and ER stress.
C. CASE STUDY 3
1. Hyperglycemic hyperosmolar state, precipitated by UTI
2. Firstly, the result shows hyperglycemia( 900mg/dl), high osmolality (390
mOsm/l), Significant E coli in urine( 100 CFU/ml),fever( on-going infection),
no acetone breathe and no significant ketones in urine and serum ( would
have thought of DKA) in a known type 2 DM
3. Fluid management to curb dehydration; it could also help in bringing down
the elevated glucose
D. CASE STUDY 4
1. The anion gap abnormality is high anion gap metabolic acidosis (usually >
16 mEq/L). As a result of osmotic diuresis that occur when the threshold of
renal glucose absorption is exceeded ( glucosuria): dehydration,
hyperosmolar state and metabolic acidosis( HCO3 is usually < 12 M
ensue.
2. The best way to correct metabolic acidosis is to correct the underlying
cause, in which case is hyperglycemia in DKA. Insulin therapy drives
potassium into the cell leading to hypokalemia (reduced serum K). The
resulting increased in intracellular potassium will lead to the cardiac cells
to easily depolarize, leading to arrhythmias
3. The hyponatremia in DKA is translational; there is movement of fluid from
the cells into the ECF due to hyperglycemia, hence serum Na
concentration falls in proportion to the fluid. Correction of the elevated
glucose level reverses this movement and Na concentration increases
E. CASE STUDY 5
- Early hyperglycemia can be explained by:
1. Dawn phenomenon- Normal rise in blood sugar early in the morning
resulting from hormones( GH, cortisol, catecholamines) mobilizing
glucose from the liver; in normal subject, insulin release counters this
 elevated plasma glucose but hyperglycemia results in diabetes with
lack of insulin
2. Somogyi effects occur when the hypoglycemia occur in the early
hours of the morning, hormones( GH, cortisol, catecholamines) help to
mobilize glucose from the liver, and the resulting effect is elevated
plasma glucose than normal in the morning. In the case of Mr Jones,
doubling his insulin dose probably tipped him into hypoglycemia, and
counter- regulatory hormones brought about hyperglycemia by
mobilizing glucose from the liver.
Prior hypoglycemia should always be suspected when abnormally high
elevated plasma glucose concentration in a patient taking insulin
therapy