Diabetes

Question 1

How do u diagnose diabetes

Answer 1

Signs and symptoms 3P
RBG: >11mmol/mL
OGTT>11
FBG: >7
HbA1c >6.5
Increased in 3 occasions. 

Prediabetic -
Imparied fasting glucose: 6-7
Impaired glucose tolerance 7.8-11

Question 2

How to monitor glycemic control

Answer 2

Hba1c 
>10 poor control
8-10 fair control
6.5-8 good control
Fasting glucose 4-6
Peak postprandial glucose (postprandial 2-3hrs) has to be not more than 11

Question 3

Preoperative management of DM undergoing Sugical procedure under Ga

Answer 3

Aims at preventing hypoglycemia and excessive hyperglycemia.
For surgical diabetic patients periop
Fasting glucose 5-7
Random <11

1. 1 day preop admission
2. 6hourly glucose monitoring
3. Blood glucose should be corrected asap on sliding scale if necessary.
4. Normal saline as choice of fluid maintenance

Patients on OHAs to withhold OHAs and start on short acting insulin on a sliding scale or continuous infusion to maintain optimal control. Postop to continue OHA and insulin sliding scale stopped.

Patients on insulin to withhold their insulin as they start fasing 6hrs preop.
Start on iv dextrose 50% if necessary. Need glucose sliding scale
If hsrix 0-3 40cc of 50% dextrose
If hstix 3-10 normal saline fluid maintenance
If hstix > 11 2U actrapid sc
Recheck hstix 30mins after any treatment.

Question 4

Complications of diabetes

Answer 4

Acute

• DKA
• Hype osmotic hyperglycemic state (HHS)
• Hypoglycemia

Chronic

• microvascular retinopathy
• nephropathy,
• neuropathy
• macrovascular disease (accelerated artherosclerosis, coronary artery disease, MI, peripheral vascular disease)

Question 5

Emergency hypoglycemic

Answer 5

IM glucagon 1-2mg

IV 40cc Dextrose 50%

Question 6

What is metabolic syndrome

Answer 6

Any of these 3:

• elevated Tg
• low HDL
• abdominal obesity
• fasting glucose > 100mg/dL
• hypertension

Question 7

What is DKA.

Answer 7

Diabetic emergency resulting from an increase in the catecholamines, cortisol, growth hormone, and glucagon which stimulates gluconeogenesis, glycogenolysis, and lipolysis. 
Resulting in increase 
- blood glucose
- electrolytes
- ketones
-

Question 8

Diff dx of DKA

Answer 8

With increase glucose

• dawn phenomena (nocturnal rise in cortisol and growth hormone)
• Somogyi phenomena (midsleep hypoglycemia leading to increase in cortisol, GH, glucagon during sleep)

Without increase glucose

• methanol toxicity
• uremia
• paraldehyde ingestion
• isoniazid toxicity
• isopropyl alcohol toxicity
• salicylate toxicity

Question 9

Persentations of DKA

Answer 9

Acute (within 24hours)
Polyruia
Poluphagia
Polydipsia
Weakness
Fatigue
N&V 
Abdominal pain
Altered mental status
Dehydration
Fruity breath
kussmaul breathing

Question 10

Investigations for DKA

Answer 10

Bloods - Increase Hb and Hct
BUSE 
- hyperkalemia (due to exchange of intracell K+ with H+, K exit cell into blood)
- low bicarb (acidosis)
- ketones increase
ABG
- pH < 7.4
- HCO3 low
- pCO2 low (Kussmaul breathing to excrete co2 - respi compensation)

Urine analysis
- positive for ketones, proteins, glucose

ECG
- signs of hyperkalemia (peaked T, wide QRS, loss of P)

Question 11

Treatment of DKA

Answer 11

1. ABC
2. IV fluid with NS
3. Lytic cocktail for hyperkalemia (calcium gluconate + insulin actrapid + d5w) - glucose should be decreased at a rate of 100mg/dL per hour to reduce the osmolarity. In which rapid reduction can lead to cerebral edema. Also rapid glucose reduction leads to release of cortisol, glucagon and growth hormone - which then leads to further glucose increase and production of ketones
4. Monitor K+ closely. Insulin, saline, calcium gluconate can rapidly reduce K+
5. Monitor glucose closely

Question 12

What is HHS?

Answer 12

Hyperosmotic hyperglycemic state

• mild hyperglycemia
• glucosuria
• osmotic diuresis
• dehydration
• depletion of osmotic diuresis
• retention of glucose
• exacerbate hyperglycemia