With a glucose challenge, how is insulin secreted?
1) within 3-5 mins it increases 10 fold, this is from the immediate dumping of preformed insulin from the beta cells of the islets of langerhans. This is not maintained as after 10 mins insulin concentration decreases halfway towards normal
2) after 15 mins, insulin concentration rises a second time, reaches a new plateau in 2-3 hours with a greater rate of secretion than the initial phase. Increased secretion results from add'l release of preformed insulin and new insulin production
what happens when BG levels decrease back to normal?
insulin secretion rapidly decreases as well (within 3-5 mins)
where is glucagon secreted from?
what kind of hormone is glucagon
what effects does glucagon have?
-opposite insulin's effects
-release is stimulated by hypoglycemia and inhibited by hyperglycemia
-increases BG concentration by glycogenolysis and gluconeogenesis
where is somatostatin secreted from?
delta cells of islets of langerhans
what kind of hormone is somatostatin?
polypeptide made up of 14 AA
what stimulates secretion of somatostatin?
-increased GI hormones
main role of somatostatin
increases the length of time that food is in the GI tract and prevents rapid exhaustion of food nutrients
what organ acts as a buffer for glucose control?
-after a meal excess glucose is stored in the liver as glycogen
-breaks down glycogen into glucose with hypoglycemia
-reduces BG fluctuations by 1/3 and helps to maintain tight control
what effect does epi have on carb and fat metabolism?
It will cause glycogenolysis (increase BG levels) and lipolysis (increased levels of FA), leading to both an increase in glucose and FA utilization
what happens if there is a high level of glucose in the ECF?
-cellular dehydration as glucose exerts a high osmotic pressure, water is drawn out of the cells into ECF by osmosis to try to normalize
-organ damage (DM pts)
type 1 DM
-lack of insulin secretion due to beta cell destruction (viral or autoimmune)
-5-10% of DM cases
type 1 DM patho
-glucose can't enter the cell due to lack of insulin secretion
-glucose accumulates in IVF, causing increased osmolarity, increased glucose level in urine and blood
-polyuria (osmotic diuresis)
-cells can't use glucose so proteolysis and lipolysis are stimulated
-AA and FA levels increase exceeding the liver's ability to metabolize them
-result is metabolic acidosis
type 1 DM s/sx
increased fat utilization
type 1 DM diagnosis
FBS> 120 mg /dl
random BG > 200 mg /dl
glycosuria (> 180 mg/ dl)
what does a FBS of 100-125 mg/ dl indicate?
T or F, the duration and degree of abnormal BG levels correlate with tissue injury associated with DM?
T! Exact mechanism unknown.
What type of tissue injury can result from chronically high BG levels?
-BV abnormalities, increased risk of MI, PVD, CVA, ESRD, retinopathy
-neuropathy (peripheral or autonomic)
-increased fat utilization leading to metabolic acidosis
-depletion of body proteins leading to tissue wasting
type 2 DM
-increased insulin secretion
-inadequate response of beta cells in response to glucose and decreased responsiveness of tissues to insulin
-90-95% of cases
-obesity is an important risk factor
-associated with metabolic syndrome
in type 2 DM is the up or down regulation of insulin receptors?
down regulation, the receptors are less sensitive to insulin
DM goals of therapy
-prevent end organ damage
-tight glycemic control delays onset of complications (esp microvascular)
What does Ha1C tell us
-reflects past 2-3 months of glucose control
-evaluates effectiveness current treatment
-glycosylated Hgb, glucose binds covalently to Hgb and stays attached for the life of the RBC which is about 120 days
non diabetic < 6%
goal of therapy < 7.5%
poor control 9%
-more common in DM1
-+ ketones in urine or blood
-hyperventilation, (respiratory compensation for metabolic acidosis- try to blow off excess CO2)
-replace volume with 1-2L, then 200-500 ml / hr of NS
-correct BG with insulin
-pt will likely need K+
Why do we want to avoid LR in DKA? What type of solution should be use
-Avoid LR because lactate can be converted to glucose
-Choose isotonic solutions
With DKA how quickly do we want to decrease the BG? How much insulin do we give to do this?
-Goal is to decrease BG by 75-100 mg/dl / hr or by 10%
-Usually give insulin 10 u / hr or 0.1 u/ kg
What is hyperosmolar nonketotic coma
-AKA hyperglycemia hyperosmolar state (HHS)
-there's enough insulin that ketone bodies aren't formed, but still get a hyperosmolar situation (dehydration)
-can cause RF, lactic acidosis, and vascular thrombosis
-osm > 360 mosm/L
-MS changes and possible seizures
BG often >600 mg/ dl
What BG level is considered hypoglycemia?
<50 mg /dl
-due to increased catecholamine release
-some s/sx may be masked by GA
Each ml of D50 increased BG by ___ mg / dl (for a 70 kg pt)
-can occur in DM 1 or 2
-affects CV, GI, and GU systems as all are innervated by the ANS
-present in 20-40% of all pts with DM1
-will see large fluctuations in BP as they can't compensate for changes in IV volume
autonomic neuropathy- CV effects
-CV effects include resting tachycardia, orthostatic hypotension, decreased HR response to both BB and atropine, HTN
autonomic neuropathy- GI effects
-gastroparesis (aspiration risk)
-occurs in 20-30% of all DM pts
autonomic neuropathy- GU effects
-nephropathy is the complication associated with highest mortality (40-50% of diabetics)
-micro or macro albuminuria may preceed steady decline in renal function
macrovascular complications of DM
microvascular complications of DM
Stiff joint syndrome- anesthesia implications
-limited atlantooccipital ROM
-30-40% of diabetics
What types of surgical procedures would alert us that the pt is likely a diabetic?