Diabeetuhs Flashcards
insulin does…
lowers blood glucose by moving it into target cells (fat, liver, muscle, brain)
insulin released from which cells
beta cells
glucagon does what
stimulates glycogenolysis –> causes sugar to be released from liver when serum glucose is low
(it’s elevated in diabetes so releasing sugar into blood when there’s already too much)
what do beta cells release
insulin and amylin
what do alpha cells release
glucagon
what does the liver store?
glycogen
What’s the half life of A & B chains in insulin, and why is this important?
very short half-life so insulin can be very quickly regulated
What’s c-peptide
chain in proinsulin that’s cleaved out;
has a long half life and measured to check insulin levels
What is the net effect of insulin resistance?
hyperinsulinemia (make more insulin so you have higher levels because it takes more insulin to do the same job)
what happens when the pancreas burns out and can’t produce insulin anymore?
diabetic and resistant
considered diabetes once fasting sugar is…
> 125
126 or higher
acanthosis nigricans is a sign of
insulin resistance
fat and gut peptides are
central problems in type II
what does amylin do
co-released w/insulin from beta cells;
slows gastric emptying and promotes satiety
What are the incretin peptides
Glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide 1 (GLP1)
what are incretin peptides released in response to
released from nutrient and neural stimulation (eating)
not dependent on glucose levels so much as eating itself
What does GLP1 do?
incretin hormone that inhibits glucagon release, so lowers sugar
-also slows gastric emptying and promotes satiety
GLP1 analog
name, etc
Exenatide/Byetta is analog used for type II;
ddp-iv resistant so lasts longer; may promote beta cell regeneration
What is DPP-IV and what does the inhibitor do
degrades natural incretins;
so dppiv inhibitors prolong the action of endogenous incretins and used for type II
diabetic symptoms
- polydipsia/polyuria
- fatigue
- weight loss
- non-healing ulcers
- blurred vision
macrovascular disease examples
Atherosclerosis, CAD, peripheral vascular dz
microvascular dx examples
retinopathy & blindness, nephropathy/renal failure
What is the PRIMARY TARGET in controlling diabetes?
glycemic control! control blood sugar
What is Metabolic Syndrome, aka..
Metabolic Syndrome = Global CV Risk
- increased waistline> 40in men, >30 women
- fasting glucose >100
- Elevated BP >130/85
- elevated TG >150
- decreased HDL
DKA
severe hyperglycemia (>250) in type I
- common presentation for new-onset type I
- lack of insulin causes fat metabolism, produces ketones in urine, fruity breath
- diuresis and fluid shifts cause **confusion, coma, dehydration
treatment DKA
REHYDRATION!! some insulin & electrolyte correction
HHNK
Hyperglycemic Hyperosmolar Nonketotic State
(hyperglycemia type II) WITHOUT ketones
-much higher glucose >600
Tx HHNK
fluids, **monitor K+
Dawn effect
wake up in AM w/ high sugar b/c cortisol spike in morning
*without preceding hypoglycemia
Somogyi effect
insulin too high overnight so become hypoglycemic which causes compensatory hyperglycemia
hypoglycemia usually from…
therapies, so try to avoid these meds
-insulin and sulfonylureas are really only two that risk hypoglycemia
sx of hypoglycemia
confusion, HA, seizures, tachy
Tx hypoglycemia
glucose, IV glucose/glucagon for severe
sx hyperglycemia
polydipsia/polyuria, blurred vision, weight loss, fatigue
When to screen for diabetes if no other risk factors
every 3 yrs >45yo
when to screen for DM2 under 45yo?
Screen for DM2 BMI >25 AND
physically inactive, high risk, HTN, high HDL, A1C > 5.7%, etc
type I problem/cause
- beta cells destroyed by insulitis so no insulin made
- autoimmune problem, vitamin D linked
type I usually seen in
young/children with acute onset
what is serious problem with type I
HYPOglycemia
markers seen in type I but not type II
IA2 islet cell antibodies, and Anti-GAD65 (glutamic acid decarboxylase)
type 1.5
person doesn’t fit mold of either, sort of in-between, may be in 30s and not sure which type
Basal bolus
- usually strategy for insulin tx
- basal glucose steady plus
- bolus of insulin for spike in glucose at mealtime
native human insulin
hexamer, made as proinsulin in pancreatic cells then cleaved
-kick in w/in 1/2-1hr, lasts 4-8hrs
rapid-acting insulin
dimer, quicker uptake
-kick in 15mins, lasts 3-5 hrs
(kicks in fast so take right before meals)
longer acting insulin
NPH - mix of regular insulin and protamine
- slows absorption
- lasts several hours
ultra-long acting insulin
very slow uptake
- *Lantus/Glargine has 24hr half life so great basal insulin
- starts working 4-6 hrs, no peak, lasts 24 hrs
Basal dosing starts at ____u and what is goal?
10u QHS to keep sugar b/t 80-140
Rule of 1800 does what
predicts how much glucose will be reduced by rapid acting insulin
What’s the rule of 1800 formula
1800/total daily insulin dose = amt BS lowered for each unit injected
if total daily insulin is 60, BS is 210, and goal is BS 150
1800/60=30, so each unit will reduce glucose by 30. If sugar is 210, then need to reduce by 60, so give 2 units in addition to regularly scheduled bolus
insulin pumps give what kind of insulin/schedule
rapid acting insulin
-basal rate and bolus given based on carb intake
Normal BS range
up to 100, usually 70-100
Prediabetes levels
- Impaired Fasting Glucose 100-125,
- Impaired Glucose Tolerance 140-199 (BS stays up longer than normal after a meal)
- A1C 5.7-6.4%
Risks-fam hx, obesity
ADA Criteria for Diabetes
- A1C 6.5% or higher
- Fasting BS 126 or higher
- Random BS 200 or higher WITH DIABETIC SX
- OGTT oral gluc tolerance test BS 200 or higher at 2 hrs
which type of diabetes is strongly influenced by family history
Type II
What is the approach to treating diabetes?
diet & exercise
What is the primary TARGET in treating diabetes?
glycemic control is primary target
1 drug treatment for Type II
Metformin
starting dose for metformin, and up to how much
500mg QHS, up to 2500g (or 1g BID)
Sulfonylureas
- stim pancreas to make insulin
- cause severe hypoglycemia
biguanides
and give drug name
-and when to avoid
- Metformin
- lowers blood glucose (reduces hepatic glucose output)
- **avoid if high creating levels or impaired renal fxn (lactic acidosis)
alpha glucosidase inhibitors
decrease breakdown of disaccharides therefore lower BS
Thiazoladinediones (“glitazones”)
increase insulin sensitivity
Incretin analogs
increase insulin release from B cells, slow gastric emptying, inhibit glucagon
-increase satiety, decrease food intake
DPP-IV inhibitors
allow incretins to act longer
DPP-IV normally degrades incretins
amylin analogs
and give drug name
Pramlinitide
decrease gastric emptying, increase satiety signals
SGLT2 inhibitors
increase sugar output in urine
-**lower BP, weight loss, decreases insulin resistance!
What can you do to decrease risk of getting diabetes in someone at risk or pre diabetic?
- diet/exercise
- ACE/ARBs
- metformin
- TZD
UKPDS
-what is it and what are the findings/recommendations?
study on Type 2
- lower A1C
- lower BP/ control HTN
how much body weight to lose?
decrease by 7%
Type I drug tx is…
insulin
Type II drug tx is..
metformin
CVD & Risk management diabetes pdf thing
- lower BP & tx HTN
- statin therapy to manage lipids
- low dose aspirin antiplatelet preventative
how much physical activity for children and adults?
children 60min/day
adults 150min/week
What is A1C goal?
7%
