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23 Cards in this Set

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What is diabetes?
Normally, insulin allows glucose to travel into cells. There, it is used for enery and stored as glycogen. Ketone (acidic)can poison the body and cause confusion.
What are S/S of DM
Polyuria,polydipia,polyphagia,vision changes,(tiny blood vessels in retina get blocked dec. blood flow,blood escapes into eye)
fatigue,argumentitive,unexplained wt.loss,loss of feeling in limbs
Type 1 (IDDM)(juvenile onset)
Body does not make insulin. Pt needs exogenous insulin by injection. Body mistakenly attacks insulin factors in the pancreas.
Type 2 (NDDM)(adult onset)
Body does make 60-70% of insulin needed, May have insulin resistance,develops over time,Requies diet and exercise(helps body use insulin more efficiently) May turn into type 1 down the road, may need some insulin now and then
Insulins and times TYPE 1, SQ injections, only use insulin syringe
name onset peak duration
Lispro 5-15m 1-2h 4-6h
Regular 30-60m 2-4h 6-10h
NPH 1-2h 4-8h 10-18h
ultrale 2-4h 8-14h 18-24h
Lantus 1-2h flat 24hrs
Type 2 meds, PO
Sulfonures (Micronase)
(glucotrol)
stimulates beta cells to secreate more insulin,^ sensitivity of the cells of the muscles,liver,fat to effects of insulin.
s/effects: hypoglycemia, sore throat,dec. WBC,nausea,photosensitivity
Type 2 meds
Meglinides(Prandin)
stimulates beta cells produce more insulin
s/effects; same as suflonureas
Type 2 meds
Amino Acid Dervitives (starlix)
Stimulate beta cells to produce more insulin
s/effect same as sulfonureas
Type 2 meds
Biguanides (Glucophage)
Decreases overproduction of glucose by the liver;dec. intestinal absorption of glucose;dec. insulin resistance
s/effects; nausea,bloating,lactic acidoisis(fatal) muscle pain
Type 2 meds
Alpha Glucosiase inhib.(Precose)
Delay glucose absorption in small intestine
s/effect; farts,diarrhea, abdominal pain
Type 2 meds
TZD (Avandia)
(Actos)
^sensitivity of liver and skeletal muscle insulin recep.
s/effects: Wt. gain,edema,mild anemia,hepatic toxicity (need liver panels)
Hypoglycemia(insulin shock)
Too much insulin for level of glucose.
S/S of Hypoglycemia
Diaphoresis(sweating),pallor,hunger,weak,anxious,confusion,tingling in mouth,tachy,
BLOOD GLUCOSE <50mg/dl
Can develop neroglycopenia
double vision
headache
lethargy
Body response of hypoglycemia
Glucogon, epinephrine,GH,cortisol
Management of hypoglycemia
ABC,IV dextrose-critical to prevent damage to CNS in unconscious pt.
15g (1/2 glass of OJ)
may dev. hyperglycemia rebound 2-12 hrs
Hyperglycemia
(Diabetic Ketoacidosis-DKA)
Def. of insulin-glucose can't enter cells;glucose in urine(blood glucose level exceeds renal threshold)Osmotic diuresis leads to ^excretion of H2O,Na+,K+,Fluid and electrolyte imbalances occur
S/S hyperglycemia
BG=300-800mg/dl
fruity(acetone)breath
Blood ph=<7.35=metabolic acidosis
dehydration(poor skin turgur)
Body attempts to compensate
Kussmauls respirations
H+ go into cells K+ moves out
kidneys eliminate excess glucose and K+
Management of hyperglycemia
Regular insulin
Glucose moves into cells
Body stops using fat for egy
H+can come out of cells
K+ can return (supplement?)
Fluid and electrolyte replacement
Large vol. of NSS IV (1L/hr)
Caution to avoid CHF,edema
Monitor BG and electrolytes
May need K+
What is Hyperosmolar Hyperglycemic state (HHS)
{Body dosen't make Ketones}
Pt. has enough insulin but body does not burn fat, not enough insulin to dec. blood glucose levels, BG=>800mg/dl, Body diureses water w/electrolytes,pt. doesn't drink fluids=dehydration(10L).
HHS can be precipitated by
Type 2 DM, elderly w/chronic illness or acute inf(pneumonia),dialysis,tube feedings,burns,heat stroke,dilantin,Lasix
S/S of HHS
^TPR,lung crackles,dilute urine,glycosuria w/o detonuria,serum Na+ and K+ ^,
Management of HHS
Replace fluids
NSS over 1-2hrs
Then order 0.45%NSS as BG approaches normal
Reverse hyperglycemia
IV push regular insulin
followed by more insulin
K+ almost always necessary, due to ^ renal excretion