Diabetes 2

Question 1

Name the acute and chronic complications of DM.

Answer 1

acute: DKA, hyperosmolar nonketotic syndrome, hypoglycemia
chronic: microvascular (retinopathy, nephropathy, neuropathy); microvascular (CAD, PVD and CVD)

Question 2

Name the acute and chronic complications of DM.

Answer 2

acute: DKA, hyperosmolar nonketotic syndrome, hypoglycemia
chronic: microvascular (retinopathy, nephropathy, neuropathy); microvascular (CAD, PVD and CVD)

Question 3

Describe the imbalances found in DKA.

Answer 3

(insulin imbalance is the primary abnormality)
hyperglycemia
ketosis
metabolic acidosis
electrolyte depletion 
dehydration/ volume depletion

Question 4

What are the counter-regulatory hormones and their purpose?

Answer 4

glucagon (only anabolic): simulates hepatic production of glucose and ketone
catecholamines: stimulate gluconeogenesis and glycogenolysis and ketogenesis
cortisol: decreases peripheral glucose utilization
growth hormone: sub acutely stimulate lipolysis, hepatic glucose and ketone production

Question 5

Describe the electrolyte abnormalities seen in DKA.

Answer 5

sodium: total body depletion from osmotic diuresis
potassium: lost in diuresis and shifted to extracellular spaces
phosphate: lost in urine and shifted like K
bicarbonate: consumed in buffering acidosis`

Question 6

What are the presenting symptoms of DKA?

Answer 6

polyuria, polydipsia (osmotic diuresis, dehydration and hyperglycemia)
NV, anorexia, abdominal pain
weakness/lethargy
dyspnea- respiratory compensation

Question 7

What are the presenting symptoms/ signs of DKA?

Answer 7

polyuria, polydipsia (osmotic diuresis, dehydration and hyperglycemia)
NV, anorexia, abdominal pain
weakness/lethargy
dyspnea- respiratory compensation
dehydration
acetone breath
hypothermia (fever means infection)
mental status changes

Question 8

What are the key points of DKA treatment?

Answer 8

monitoring in an ICU (telemetry)
correct hyperglycemia and ketosis/acidosis with insulin
treat hypovolemia with free water and supplement electrolyte losses

Question 9

What are the key characteristics of hyperosmolar nonketotic syndrome?

Answer 9

pathophysiology is similar to DKA but without ketoacidosis
severe hyperglycemia, often >800
hyperosmolality >350
severe dehydration
mortality rate >25% esp since it effects population with complicating conditions

Question 10

What are the key characteristics of hyperosmolar nonketotic syndrome?

Answer 10

pathophysiology is similar to DKA but without ketoacidosis
severe hyperglycemia, often >800
hyperosmolality >350
severe dehydration
mortality rate >25% esp since it effects population with complicating conditions

Question 11

What causes HNKS? (esp. inciting meds)

Answer 11

infection
other severe medical illness or injury
medication: glucocorticoids, niacin and thiazide diuretics
omission of diabetes meds
as a manifestation of DM2

Question 12

What are the presenting symptoms and signs of HNKS?

Answer 12

more gradual onset (3-6days)
polyuria/ polydipsia
altered mental status
occasional nausea vomiting, typically no respiratory symptoms
SEVERE dehydration 
increased sensorium, not uncommonly with focal neurologic signs
seizures
hyperpnea possible

Question 13

What is the focus of HNKS treatment?

Answer 13

correcting dehydration and hyperosmolality is the key
glucose will improve with hydration, insulin will help to resolve faster
tx in ICU, look for precipitating factor

Question 14

Define hypoglycemia.

Answer 14

generally a blood glucose

Question 15

What is the physiologic response to hypoglycemia?

Answer 15

low glucose is sensed in hypothalamus and results in release of counter-regulatory hormones (in adrenals and alpha cells)

Question 16

What is the physiologic response to hypoglycemia?

Answer 16

low glucose is sensed in hypothalamus and results in release of counter-regulatory hormones (in adrenals and alpha cells)

Question 17

List examples of the adrenergic and neuroglycopenic complications of hypoglycemia

Answer 17

adrenergic: sweating, tachycardia, tremor, anxiety, irritability

Question 18

List examples of the adrenergic and neuroglycopenic complications of hypoglycemia

Answer 18

adrenergic: sweating, tachycardia, tremor, anxiety, irritability
neuroglycopenic: decreased concentration, visual disturbance, confusion, seizures, coma

Question 19

List examples of the adrenergic and neuroglycopenic complications of hypoglycemia

Answer 19

adrenergic: sweating, tachycardia, tremor, anxiety, irritability
neuroglycopenic: decreased concentration, visual disturbance, confusion, seizures, coma

Question 20

What are the factors predisposing to hypoglycemia?

Answer 20

excessive injected insulin, increased physical activity, delay/missed meal or snack, lower A1c, diabetic gastroparesis, alcohol ingestion (suppresses glucose production), sulfonylureas, impaired renal function

Question 21

Contrast Somogyi effect and Dawn effect.

Answer 21

somogyi: fasting hyperglycemia that occurs as a rebound response from overnight low (decrease PM insulin)
dawn: normal peaking of counter-regulatory hormones in the AM (increase PM insulin)

Question 22

How does hemoglobin A1c relate to blood glucose level?

Answer 22

change in A1c by 1% represents a 30-40 mg/dL change in blood glucose

Question 23

What different syndromes can cause hypoglycemia?

Answer 23

insulin receptor mediated hypoglycemia (excess insulin- tumor (c-peptide) or exogenous); stimulation of insulin receptor by substances other than insulin (ILGF2-tumors)

impaired liver glucose production/output (ie. impairment of glycogenolysis); accompanied by rise in ketones

impairment of glyconeogensis (alcohol)

Question 24

What different syndromes can cause hypoglycemia?

Answer 24

insulin receptor mediated hypoglycemia (excess insulin- tumor (c-peptide) or exogenous); stimulation of insulin receptor by substances other than insulin (ILGF2-tumors)

impaired liver glucose production/output (ie. impairment of glycogenolysis); accompanied by rise in ketones

impairment of glyconeogensis (alcohol)

Question 25

Describe the different types of diabetic retinopathy and their pathophysiology.

Answer 25

general retinopathy generally due to ischemia, abnormal vascular permeability and thickening of the basement membrane (early management is important)

dot and blot hemorrhages due to leaky vessels
hard exudates due to lipids that leak out of vessels
cotton wool spots- ischemia of retina
vessel proliferation- ischemia causes growth of more fragile vessels; can progress to sudden serious damage with major hemorrhage and blindness

Question 26

What factors predispose patients to diabetic nephropathy?

Answer 26

appears to have a genetic predisposition; occurs in both type 1 and 2 and non0caucasians have a higher risk;

increased risk with poor glycemic control and hypertension

Question 27

What factors predispose patients to diabetic nephropathy?

Answer 27

appears to have a genetic predisposition (50% seem to have a higher risk); occurs in both type 1 and 2 and non-caucasians have a higher risk;

increased risk with poor glycemic control and hypertension

Question 28

What is the key event in the pathophysiology of nephropathy?

Answer 28

basement membrane damage: leads to basement membrane thickening, increased glomerular leakage, loss of charge and size selectivity

combined with glomerular hyperfilitration or intraglomerular HTN

Question 29

How do we screen for and treat diabetic nephropathy?

Answer 29

patients should be screened annually with urine micro albumin:creatinine ratio

documented microalbuminuria should be aggressively treated with tight glucose control (ACEI and ARBs) w/ or w/o HTN; in addition HTN should be aggressively treated

ESRD best treated with transplantation