Diabetes Flashcards
Glucose Regulation
High BGL–>promotes insulin release
Insulin (made in pancreas)
Glucagon maintains BGL when fasting & raise very low glucose levels (made by alpha cells, in islets of Langerhans in pancreas)
Glucagon –> released into the bloodstream. Glucagon-secreting alpha cells surround insulin-secreting beta cells.
Liver–> stores glucose as glycogen
Liver makes ketones from fats when glycogen storage is low–> ketones burned as fuel for muscles & other body organs, leaving sugar for brain, RBC, & kidney.
Type 1 Diabetes
Pancreas produces insulin–> insulin moves glucose to cells.
A diabetic pt–> immune cells destroy beta cells in the pancreas.
The pancreas cannot produce insulin, > glucose in the blood
Type 1 Diabetes
cause:
autoimmune destruction Beta cells in pancreas
earlier onset/younger patients
genetic & environmental factors
*Always requires Insulin!
Type I Diabetes
body’s response to insulin deficiency
glycogenolysis- glycogen is changed to glucose in the liver
gluconeogenesis- glucose is formed protein (release amino acids)
lipolysis- fats breakdown (free fatty acids released & converted to ketone bodies for energy–> can lead to ketoacidosis).
Type 1 Diabetes
sxs:
- Polyuria/polydipsia/polyphagia (DM “eating” own body once surpass state of DKA, will eat muscle, brain, etc until can’t fx)
- weight loss
- frequent infections (pathogens prefer warm, moist areas & lots of energy/sugar)
Type I Diabetes
complications:
DKA (diabetic ketoacidosis)
buildup of ketones in bloodstream
often brought on by a stressor, like infection
associated w/ severe hyperglycemia & dehydration
basic sxs: decreased LOC, Kussmaul’s respirations, fruity breath
(DKA= increased BGL & ketones)
DKA–> mostly Type I diabetics
[DM-II goes into HHS (Hyperosmolar hyperglycemic syndrome) > often than DKA]
Type II Diabetes
- stomach converts food to glucose
- glucose enters bloodstream
- pancreas produces insulin, but it’s resistant to effective use
- glucose unable to enter body effectively
Type II Diabetes
populations at risk:
Population @ risk for Type II DM:
- Native Americans
- Alaskan Indians
- African Americans
- Hispanic Americans
- White Americans
Type II Diabetes
R/F:
genetic adult onset HTN sedentary lifestyle certain ethnicities obesity poor diet
Metabolic Syndrome
Abd obesity (>40" men; >35 women) Hyperglycemia (FBS > or = 100; fasting >8 hr) HTN (BP > or = 130/80) Hyperlipidemia [trig > or = 150; hdl (healthy chol) < 50 men; < 40 women]
Diabetes
dx:
fasting plasma glucose > or = 126 twice or…
A1C > or = 6.5% or…
random BG > 200 or…
glucose tolerance test (given 75 g of glucose in 2 hr, should be < 200)
Diabetes
Determinants of good BG control:
Hgb A1C < 7
fasting blood glucose 70-130 mg/dL
post-prandial blood glucose < 180 mg/dL
Glucometer: steps for BG Monitoring
- wash hands
- Load new lancet & test strip
- prick finger at side
- squeeze finger
- touch tip against drop of blood
- clean finger, remove test strip
- dispose of lancet in sharps container
Diabetes Med Mgmt
Metformin: drug of choice for monotherapy (pill)
Tx DM-II
-avoids kidney dz
-monitor GFR for decreased levels
-monitor for increased BUN & creatinine levels
-IV contrast & anesthesia: hold metformin before & 48 hrs after
-metformin–> can cause kidneys to overwork & before restarting metformin check labs & I/Os
Sulfonylureas:
ends in “ides”
glipizide, glyburide, glimepiride
- used for DM-II
- give w/ or just before meals
Thiazolidinediones (TZDs):
pioglitazone, rosiglitazone
- Tx DM-II
- contraindicated for clients w/ HF
- monitor liver function
DPP-4 Inhibitors
Sitagliptin (Januvia), linagliptin Tx DM-II -rarely used (FDA warns s.e. joint pain, may be severe) -s.e. N/V common (warn pt in advance) -pancreatitis risk -taken PO -to block or slow lipoprotein in the gut
Summary of Insulin Tx
rapid
Rapid- aspart, lispro
onset: 15-30 min
peak: 30 min-3 hrs