Diabetes

Question 1

Criteria for diagnosing diabetes (4)

Answer 1

• A1c > 6.5%
• Fasting plasma glucose (FPG) >125 mg/dL (no calories for 8 hours)
• 2 hour glucose >200 during 75 gm OGTT (oral glucose tolerance test)
• Classic sxs of hyperglycemia + random glucose >200 mg/dL

Question 2

3 criteria for prediabetes

Answer 2

• Impaired fasting glucose (IFG) = FPG 100-125 mg/dL
• Impaired glucose tolerance (IGT) = 2 hour glucose between 140-200 on 75 gm OGTT
• A1c 5.7-6.4%

Question 3

DKA triggers (5)

Answer 3

Omission of insulin, infection, medical illness / trauma, initial manifestation of type 1 DM

Question 4

Pathophysiology of DKA

Answer 4

Lack of insulin → lipolysis → FFAs → ketogenesis → metabolic acidosis, electrolyte depletion, and dehydration. Dehydration → decreased GFR → higher glucose levels → further dehydration. Viscious cycle. Often lose 7-10L of free water. Hypovolemia also exacerbates acidosis by decreasing perfusion → lactic acid production, which can’t be excreted due to low GFR.

Question 5

4 counter-regulatory hormones that make DKA worse

Answer 5

• Glucagon stimulates hepatic production of glucose and ketones
• Catecholamines stimulate GNG, glycogenolysis, and ketogenesis. 2 main ketones are betahydroxybutyrate and acetoacetic acid.
• Cortisol decreases peripheral glucose utilization
• Growth hormone stimulates lipolysis, hepatic glucose, and ketone production

Question 6

Treating DKA

Answer 6

• Treat in ICU. Replace insulin / fluids. Correct acidosis (done by insulin), dehydration, and hyperglycemia, and ketosis. Monitor electrolytes.
• Just because you have fixed hyperglycemia, it doesn’t mean you have fixed their DKA. Glucose may normalize but acidosis may still be present. Continue to give them insulin, but also give them glucose at the same time.

Question 7

General characteristics of HNKS
What is HNKS?
Pathogenesis

Answer 7

• Hyperosmolar non-ketotic syndrome
• Acute hyperglycemic complication of DM2. BG often >800 mg/dL.
• Pathophysiology is similar to DKA, but without ketoacidosis. Have enough insulin to prevent lipolysis / ketosis

Question 8

Treating HNKS

Answer 8

Treat in ICU. Correct dehydration, electrolyte imbalance, and hyperosmolality. Glucose improves w/ hydration + insulin. Look for precipitating factor.

Question 9

DKA vs HNKS
Age
Duration of sxs
Glucose concentration
Bicarb
Serum osmolality
Prognosis

Answer 9

Age: under 40 for DKA, over 40 for HNKS
Duration: less than 2 days for DKA, >5 days for NKS
Glucose concentration: less than 800 for DKA, >800 for HNKS
Bicarb concentration: low in DKA, normal in HNKS
Osmolality: less than 350 in DKA, >350 in HNKS
Prognosis: 3-10% mortality in DKA, 10-20% mortality in HNKS

Question 10

Treating hypoglycemia

Answer 10

15g oral fasting-acting carb (1/2 cup juice, 3 glucose tablets). If unconscious, give 1mg glucagon SQ or 50 mL IV dextrose (not IM b/c it is necrotic to tissues).

Question 11

What causes diabetic retinopathy?

Answer 11

Damage is due to retinal ischemia → abnormal vascular permeability and thickening of basement membrane.

Question 12

3 stages of diabetic retinopathy

Answer 12

• Stage 1: Non-proliferative type shows microaneurysms, hard exudates, and dot / blot hemorrhages
• Stage 2: Pre-proliferative type shows above + cotton wool spots (leaked cytoplasm) and intra-retinal microaneurysms (IRMA)
• Stage 3: Proliferative type shows neovascularization. Eye tries to compensate for ischemia by forming new vessels, but they are poorly formed and more prone to hemorrhage, which then causes vision loss.

Question 13

Pathophysiology of diabetic nephropathy

Answer 13

• Key event is basement membrane damage / thickening → glomerular leakage, loss of glomerular charge selectivity, and reduced size selectivity. Also see increased mesangial matrix material.
• HTN → Glomerular hyperfiltration. GFR increases initially, then decreases w/ time.

Question 14

Treating diabetic nephropathy

Answer 14

Treat hyperglycemia, HTN (ACE / ARB), and possibly transplant for ESRD

Question 15

4 types of autonomic diabetic neuropathies

Answer 15

• Cardiovascular
• Resting tachycardia due to parasympathetics being involved first.
• Damaged sympathetics → can’t vasoconstrict when stand up → orthostasis. Also causes decreased exercise tolerance. Occurs later.
• Markedly increased risk of sudden death.
• Gastrointestinal – gastroparesis, vomiting, diarrhea, bloating, persistent fullness. Difficult to match digestion of food w/ action of insulin.
• Genito-urinary (ED)
• Sudomotor (sweat glands)

Question 16

Somogyi Effect vs Dawn Phenomenon

Answer 16

• Somogyi Effect – fasting hyperglycemia that occurs as a rebound response from an overnight episode of hypoglycemia. Treat by decreasing night dose of insulin.
• Dawn Phenomenon – fasting hyperglycemia due to normal peaking counter-regulatory hormones in the morning (cortisol). Treat by increasing night insulin dose.

Question 17

Insulin receptor-mediated hypoglycemia vs Non-insulin receptor-mediated hypoglycemia

Answer 17

• Insulin receptor-mediated hypoglycemia
• Excess insulin may be from an insulin-producing tumor, exogenous insulin, or oral DM meds.
• Stimulation of insulin receptor by things other than insulin. Ex: insulin-like growth factor 2 (IGF2), which is produced by some tumors.
• Non-insulin receptor mediated hypoglycemia
• Impaired liver glucose production / output, such as impaired glycogenolysis.
• Impaired GNG from alcohol

Question 18

Which cause of hypoglycemia has increased ketones?

Answer 18

Impaired hepatic glucose production / output

Question 19

Which parent is more likely to pass on DM1?

Answer 19

Dad

Imprinting

Question 20

3 ketone bodies

Answer 20

beta hydroxybuterate, acetoacetate, and acetone

Question 21

Insulin effect on K

Answer 21

Insulin causes potassium to shift into cells, so rapid and severe hypokalemia can occur with DKA treatment if not replaced

Question 22

How do ketone bodies help determine efficacy of insulin?

Answer 22

If insulin is low or is not working, then ketone bodies are going to be made. If ketone bodies are absent, then insulin is working.