Hyperglycemia Flashcards
Diabetes mellitus
Etiopatho
- Chronic metabolic disease characterized by
hyperglycemia as a cardinal biochemical feature
Pathophysiology of DM
Pathophysio
- Insulin inhibits glycogenolysis, gluconeogenesis,
lipolysis and ketogenesis.
- Hunger in the midst of plenty: hyperglycemia without
cellular uptake of glu because of receptor resistance or
hyposensitivity.
- Reactivation of counterregulatory hormones (in order
of activation): glucagon –> epinephrine –> cortisol –>
GH
- Patient remains hyperglycemic despite poor oral intake
and increased losses because of counterregulatory
hormone effect, causing lipolysis and ketogenesis = net
effect is hyperglycemia, ketoacidosis, and
hyperthyroidisemia
- Kidney max glu 180mg/dL, beyond that result to
glucosuria resulting to polyuria and hypotension,
ketonuria
Clinical manifestations of DM
CM
Mnemonic: 3P’s+weight loss/ 4T’s: Toilet, Thirsty, Tired, Thinner
1. Polydipsia, polyuria, nocturia
2. Unexplained weight loss
3. Glucosuria, ketonuria
4. Monilial vaginitis – among F with chronic glucosuria
5. Polyphagia/ Hyperphagia
6. BOV, mood changes, skin infections, oral thrush,
abdominal pain
7. Ketoacidosis
Diagnostics
Impaired fasting glucose Tolerance
Fasting glucose: 100-125 mg/dl (5.6-7.0 mmol/L)
2-hr Plasma glucose (OGTT):
≥140mg/dL but <200 (≥7.8 mmol/L)
HBA1C: 5.7-6.4%
Diabetes Mellitus
≥126 mg/dL (7.0mmol/L)
2hr Plasma glucose (OGTT): ≥200 mg/dL (≥11.1mmol/L)
HBA1C: ≥6.5%
others: symptoms of DM + random blood glucose ≥200mg/dL (≥11mmol/L)
Management
Mgt
1. Glycemic control – gycohemoglobin (HbA1c)
monitoring
- Reliable index of long-term glycemic control
- Reflects the ave blood glu concentration of the
preceding 2-3 months
- For known diabetics:
o 6-7.5%: good diabetic control
o 7.6-9.9%: fair
o >10%: poor
Rapid acting
Aspart
Glulisine
Lispro
Short acting
regular Humulin R
Intermediate
NPH
Long-acting
Detemir
What is the “honeymoon period”?
reduced exogenous insulin needs shortly
after starting tx due to residual B-cell function. Usually fades
within a few months reflected as steady increase in insulin
requirements and wider glu excursions.
What is the usual regimen?
Usual regimen:
- 4 injection regimen: basal bolus regimen at night that
is slow-onset, long duration for between mean glucose
control (glargine/detemir) (40-50% of total dose) +
rapid-onset insulin at each meal (Lispro/aspart) (50-
60% of total dose div by 3)
- 3 injection regimen: NPH + rapid analog bolus at
breakfast à rapid-acting bolus analog at supper à
glargine at bedtime
- Insulin pump therapy/ continuous SC insulin infusion
(CSII)
Other medications for DM?
Metformin – insulin sensitizer; usual starting dose 500mg OD, may
be inc to 1500-2500mg/d BID-TID
- AE: GI disturbance, lactic acidosis. Avoid in hepatic or
renal impairment
Sulfonylureas – occasionally used when metformin monotx
unsuccessful or contraindicated
- 1st gen: Acetohexamide, Chlorpropamide, Tolbutamide
- 2nd gen: Glipizide, Glyburide, Glimepiride
2. To ensure N growth (height and weight)
- CHO counting: allows patients to adjust insulin dosage
to their mealtime CHO intake
- Exercise. WOF hypoglycemia post workout
3. To prevent acute complications – DKA, cerebral edema
4. To prevent long-term vascular complications –
retinopathy, nephropathy, CAD, CV ds, neuropathies
- Diabetic retinopathy: leading cause of blindness
- Diabetic nephropathy: leading known cause of ESRD
5. Refer to endo/multidisciplinary specialists (ophtha,
nephro, cardio, neuro)
What is dawn phenomenon?
Elevated blood glu early morning before breakfast:
Dawn phenomenon – due to overnight GH secretion à inc insulin
clearance
What is Somogyi phenomenon?
Somogyi phenomenon – theoretical rebound from late-night or
early-morning hypoglycemia (exaggerated counterregulatory
response)
What is etiopathogenesis of DKA?
Etiopatho
- End result of metabolic abN due to severe deficiency of
insulin or severe insulin ineffectiveness
- Effects of insulin deficiency:
o Glu utilization by muscle and fat decreases
o Excess glu production via glycogenolysis and
gluconeogenesis –> leading to
hyperglycemia
o Resultant osmotic diuresis produces
polyuria, urinary losses of e’ and
dehydration
o Combination of insulin deficiency + elevated
counterregulatory hormones = accelerated
lipolysis and impaired lipid synthesis
o Increased plasma cholesterol and FFA –>
leads to ketone body formation
(acetoacetate & beta-hydroxybutyrate) à
resulting in metabolic acidosis