Diabetes 2 Flashcards
Name the acute and chronic complications of DM.
acute: DKA, hyperosmolar nonketotic syndrome, hypoglycemia
chronic: microvascular (retinopathy, nephropathy, neuropathy); microvascular (CAD, PVD and CVD)
Name the acute and chronic complications of DM.
acute: DKA, hyperosmolar nonketotic syndrome, hypoglycemia
chronic: microvascular (retinopathy, nephropathy, neuropathy); microvascular (CAD, PVD and CVD)
Describe the imbalances found in DKA.
(insulin imbalance is the primary abnormality) hyperglycemia ketosis metabolic acidosis electrolyte depletion dehydration/ volume depletion
What are the counter-regulatory hormones and their purpose?
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
Describe the electrolyte abnormalities seen in DKA.
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`
What are the presenting symptoms of DKA?
polyuria, polydipsia (osmotic diuresis, dehydration and hyperglycemia)
NV, anorexia, abdominal pain
weakness/lethargy
dyspnea- respiratory compensation
What are the presenting symptoms/ signs of DKA?
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
What are the key points of DKA treatment?
monitoring in an ICU (telemetry)
correct hyperglycemia and ketosis/acidosis with insulin
treat hypovolemia with free water and supplement electrolyte losses
What are the key characteristics of hyperosmolar nonketotic syndrome?
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
What are the key characteristics of hyperosmolar nonketotic syndrome?
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
What causes HNKS? (esp. inciting meds)
infection other severe medical illness or injury medication: glucocorticoids, niacin and thiazide diuretics omission of diabetes meds as a manifestation of DM2
What are the presenting symptoms and signs of HNKS?
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
What is the focus of HNKS treatment?
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
Define hypoglycemia.
generally a blood glucose
What is the physiologic response to hypoglycemia?
low glucose is sensed in hypothalamus and results in release of counter-regulatory hormones (in adrenals and alpha cells)
What is the physiologic response to hypoglycemia?
low glucose is sensed in hypothalamus and results in release of counter-regulatory hormones (in adrenals and alpha cells)
List examples of the adrenergic and neuroglycopenic complications of hypoglycemia
adrenergic: sweating, tachycardia, tremor, anxiety, irritability
List examples of the adrenergic and neuroglycopenic complications of hypoglycemia
adrenergic: sweating, tachycardia, tremor, anxiety, irritability
neuroglycopenic: decreased concentration, visual disturbance, confusion, seizures, coma
List examples of the adrenergic and neuroglycopenic complications of hypoglycemia
adrenergic: sweating, tachycardia, tremor, anxiety, irritability
neuroglycopenic: decreased concentration, visual disturbance, confusion, seizures, coma
What are the factors predisposing to hypoglycemia?
excessive injected insulin, increased physical activity, delay/missed meal or snack, lower A1c, diabetic gastroparesis, alcohol ingestion (suppresses glucose production), sulfonylureas, impaired renal function
Contrast Somogyi effect and Dawn effect.
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)
How does hemoglobin A1c relate to blood glucose level?
change in A1c by 1% represents a 30-40 mg/dL change in blood glucose
What different syndromes can cause hypoglycemia?
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)
What different syndromes can cause hypoglycemia?
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)
Describe the different types of diabetic retinopathy and their pathophysiology.
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
What factors predispose patients to diabetic nephropathy?
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
What factors predispose patients to diabetic nephropathy?
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
What is the key event in the pathophysiology of nephropathy?
basement membrane damage: leads to basement membrane thickening, increased glomerular leakage, loss of charge and size selectivity
combined with glomerular hyperfilitration or intraglomerular HTN
How do we screen for and treat diabetic nephropathy?
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
