Final: Ch 33 DM & Metabolic Syndrome Flashcards
fasting level of blood glucose
80-90mg/dl
a high blood glucose (like after a meal) stimulates release of what
insulin release –> increased uptake and use of glucose and aa
carbohydrates are stored as ________ in the ______ and ______ _______
glycogen, liver, skeletal muscle
excess glucose is converted to what
fat and stored in adipose
a low blood glucose stimulates release of what
glucagon –> glycogenolysis and gluconeogenesis
what are triglycerides used for
energy or stored in adipose
glycerol + 3 FA
excess aa are used for what
energy
glycogenolysis
glycogen –> glucose
when blood sugar is low
stimulated by glucagon to raise blood sugar
glycolysis
glucose –> pyruvate
gluconeogenesis
aa or FA –> glucose
by liver
the exocrine pancreas produces what
digestive enzymes
endocrine pancreas has what types of cells
islets of langerhans - hormone production
alpha cells - glucagon
beta cells - insulin
is release of insulin biphasic?
yes
immediately with a meal and then hrs later
3 ways insulin lowers blood sugar
raises glucose uptake, glycolysis, glycogen synthesis
lowers lipolysis, glycogenolysis
lowers gluconeogensis
insulin promotes ___ storage by increasing….
fat, increasing glucose uptake by adipose
insulin is produced as proinsulin and cleaved to _____ and _-______ prior to release
insulin, C-peptide
how does insulin reach the liver
portal circulation
1/2 used or degraded
insulin binds to the _-subunits of the membrane insulin receptor
alpha-subunits
causes beta-subunits to be autophosphorylated (activated kinase activity)
GLUT4 transporter
gets translocated to membrane to take in glucose
glucagon
produced by alpha-cells
released when blood sugar falls
maintains blood sugar during fasts
stimulates glycogenolysis, gluconeogenesis, lipolysis
somatostatin
secreted by delta cells in response to food
inhibits insulin and glucagon release –> slow GI activity
prolongs energy availibility
counter-regulatory hormones
catecholemines: stim glycogenolysis/lipolysis
GH: lowers glucose uptake
steroids: stimulate gluconeogenesis
classifications of DM
Type 1: Beta-cell destruction
Type 2: 9/10 cases - insulin resistance
gestational: glucose intolerance beginning in pregnancy
Dx of DM
depends on stages of glucose intolerance
pre-diabetes 3 levels
fasting plasma glucose 100-125mg/dl
plasma glucose 140-199 2 hrs after oral glucose load
hemoglobin A1C 5.7-6.4
type 1 DM
autoimmune destruction of beta-cells
absolute lack of insulin
requires insulin to avoid ketosis
progression of type 1 DM
triggering event activates immune system
anti-insulin and B-cell Ab appear
GTT abnormal
overt DM
is there genetic predisposition in type 1 DM
some
type 2 DM
impaired insulin secretion (B-cell failure)/insulin resistance
hepatic release of glucose is high
uptake of glucose by tissues is low
plasma glucose is high
early insulin resistance causes…
more insulin secretion, which further increases insulin resistance
patients with type 2 DM are usually
older and obese
but young people get it now too
strong genetic (not HLA) links
risks for type 2 DM
central obesity/lack of activity
high free fatty acids (FFA)
3 effects of high FFA on type 2 DM
increases insulin secretion –> B-cell failure
block peripheral glucose uptake
lower hepatic insulin sensitivity
is insulin resistance linked to other metabolic abnormalities in addition to hyperglycemia
yes, metabolic syndrome
metabolic syndrome
central obesity
high triglycerides
low HDL
HTN
other causes of DM
endocrine: cushing’s syndrome or pheochromocytoma
meds: streptomycin, diuretics, antiretrovirals
gestational DM
glucose intolerance 1st detected in pregnancy
after pregnancy, woman has higher risk of getting real DM
risks for gestational DM
family history of DM
glucosuria
obesity
previous large baby
previous stillbirth/miscarraige
Rx of gestational DM
close observation
nutritional counseling
insulin
symptoms of DM
polyuria: a lot of urine b/c glucose is an osmotic diuretic
polydipsia: thirst (diuresis –> dehydration)
polyphagia (type 1): cells depleted of nutrients
hyperglycemia: blurred vision, fatigue, skin infections
fasting blood glucose normal/DM
normal: less than 100mg/dl
DM: greater than 126
casual blood glucose DM
greater than 200mg/dl w/ symptoms
OGTT
test plasma glucose 1-2 hrs after 75g of glucose
glycosalated Hb
Hb acquires glucose during life of RBC
normal is 4-6%
recommendation is less than 7%
urine tests
ketones?
self-monitoring of blood glucose
lancet to obtain blood
drop of blood on test strip
put strip in meter
record results in a log
dietary management goals
maintain normal blood glucose and lipids
attain reasonable weight
restrict fat/Na to avoid cardiovascular complications
type 1 DM dietary management
assess food and adjust insulin
type 2 DM dietary management
weight loss
lower blood glucose/lipids
low affinity glucose transporter
GLUT2 found in beta cells
high blood glucose increases glucose entry into beta cells and metabolism for ATP
oral (non-insulin) hypoglycemics are used mostly in type what
2
insulin secretogogues
biguanides
alpha-glucoside inhibitors
thiazolidendones
incretin-based agents
biguanides
metformin
lowers hepatic glucose output
alpha-glucoside inhibitor
acarbose
slow carb metabolism in small intestine
thiazolidendones
lower insulin resistance by up-regulating GLUT4
sodium glucose cotransporter 2 (SGLT2) inhibitors
glucose diffuses out of the cell
insulin is always required in type __ and sometimes needed in type __
1, 2
short acting insulin
works in minutes
action for 5 hrs or less
intermediate acting (NPH) insulin
onset in several hours
action for up to a day
multiple daily injections (MDI) of insulin
long or intermediate acting insulin 1-2x per day
short-acting before meals
continuous subcutaneous insulin infusion (CSII)
insulin pump
basal and bolus injections
acute complications of DM
ketoacidosis
hyperosmolar state
hypoglycemia
ketoacidosis is most common in which type
1
ketoacidosis
FA converted to ketones by liver
metabolic acidosis (pH and bicarb low)
intracellular acidosis –> K+ shift out of cells
Symptoms of ketoacidosis
fruity breath
tachycardia
hypotension
Rx of ketoacidosis
give insulin and IV fluids + K+
hyperosmolar hyperglycemic state (HHS)
extreme hyperglycemia (BG > 600mg/dl)
plasma osmolarity > 310mOsm/L
extreme cellular dehydration
can exist without ketoacidosis
symptoms of hyperosmolar hyperglycemic state
neuro from aphasia
hallucinations to seizures
treatment of hyperosmolar hyperglycemic state
replace water carefully to avoid hypokalemia and cerebral edema
grave prognosis
hypoglycemia
usually seen in people with DM who use insulin
rapid onset when BG less than 50-60mg/dl
precipitating factors of hypoglycemia
increased exercise
missing a meal
decrease in insulin requirement
alcohol (reduces gluconeogenesis)
symptoms of hypoglycemia
headache
decreased mentation
anxiety
tachycardia, sweating, shaking
treatment of hypoglycemia
eat 15-20g of concentrated glucose
Somogyi effect
hypoglycemia increases stress hormones –> hyperglycemia
people at risk for hyperglycemia after an episode of hypoglycemia
Dawn effect
high blood glucose early in the morning
circadian GH release
microvascular complications of chronis DM
nephropathies
retinopathies
macrovascular complications of chronic DM
CHD
stroke (CVA)
PVD (PAD)
other complications of chronic DM
neuopathies
foot ulcers
infections
sorbitol pathway in hyperglycemia
glucose –> sorbitol within cells
breakdown is slow
excess –> swelling of lens
depletes ATP
causes schwann cell damage/neuopathy
advanced glycation end products
hyperglycemia –> higher glycoproteins
glycoproteins damage basement memb of small vessels
neuropathies in DM
schwann cell damage
damage to nerve nutrient vessels
somatic neuopathies
distal and symmetric
stocking-glove pattern
sensory loss
painful
autonomic neuopathies
low cardiac, GI, GU, sexual function
nephropathies
leading cause of end stage renal disease
thickening of capillary basement membrane
sclerosis of glomerulus
risks for nephropathies
HTN (goal is 130/80)
poor glycemic control
microalbuminura
prevention of nephropathy
BP control using ACEI or ARB
glycemic/A1C control
stop smoking
treat hyperpilidemia
retinopathies
DM is #1 cause of new blindness
microaneurysm
neovascularization
bleeding/scarring
cataracts
other risks of macrovascular complications
high BP, lipids, glucose, CRP
poor endothelial function
type 1 DM macrovascular complications
develop with age
type 2 DM macrovascular complications
often have at diagnosis
prevention of macrovascular complications in DM
manage risk factors aggressively
BP/lipid management
stop smoking
diabetic foot ulcers
caused by a combination of neuropathy, vascular lesions, and infections
common cause of amputation
distal symmetric neuropathy
major risk factor for foot ulcers
sensory loss allows tissue damage without pain
pressure points common at sites of ulcers
prevention of diabetic foot ulcers
foot exams
test sensory function of the feet
check feet for infection
stop smoking
infections in DM
more serious and common in DM
sensory loss –> people ignore symptoms
hyperglycemia stimulates bacterial growth
