Exam (elaborations)
310 Diabetes
- Course
- Management 310 KU
- Institution
- Management 310 KU
Exam of 6 pages for the course Management 310 KU at Management 310 KU (310 Diabetes)
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310 Diabeteschildhood/adolescence
abrupt - ANS-Type 1 age/speed onset
autoimmune process/ loss of pancreatic beta cells (cells responsible for insulin synthesis and
release into the bloodstream, what matters is total carbs not type - ANS-type 1 etiology/primary
defect
reduced early in disease and completely absent later - ANS-Type 1 insulin levels
insulin replacement mandatory, strict diet control, no oral anti-diabetic drugs, prevent long term
damage, educate the patient, maintain weight, statins & colesyelam reduce high levels of LDL,
ACE inhibitor or ARB reduce risk of HTN and neuropathy - ANS-type 1 treatment
polyuria: excess urination volume
polydipsia: excessive thirst
polyphagia: excessive hunger/increased appetite
weight loss - ANS-type 1 symptoms
common, especially if insulin dosage is insufficient - ANS-Type 1 ketosis
usually over 40
gradual
family hx - ANS-type 2 age/speed onset
insulin resistance and inappropriate insulin secretion - ANS-type 2 primary defect
levels may be low(indicates deficiency), normal, high(indicates resistance) - ANS-type 2 insulin
levels
normally asymptomatic, s/s result from insulin resistance and impaired insulin secretion,
hyperinsulinemia - ANS-type 2 symptoms
1. reduced binding of insulin to its receptor
2. reduced receptor numbers
3. reduced receptor responsiveness - ANS-insulin resistance (pharmacodynamics)
most occur secondary to disruption of blood flow
micro/macro vascular damage - ANS-long term complications
, biguanide, initial treatment for type 2 diabetes, GI upset, absorbed in small intestine but not
metabolized so excreted in the kidneys, delay type 2 onset for high risk, can use for gestational
diabetes - ANS-Metformin (Glucophage)
General
1. inhibits glucose production in liver
2. reduces slightly glucose absorption in the gut
3. sensitizes insulin receptors in target tissues (fat &skeletal), thereby increasing glucose uptake
Does not stimulate insulin release from pancreas - ANS-metformin MOA
1. nausea
2. diarrhea
3. anorexia/decreased appetite - ANS-Metformin side effects
1. kidney failure because increase lactic acid toxicity
2. deficiency of B12 and folic acid
3. liver disease, HF, prone to lactic acid production
4. reduce consumption of OH - ANS-metformin contraindications
alpha-glucosidase inhibitor
type 2 diabetes w/ diet & exercise third line drug, PO, minimal systemic effects, DOES NOT
DEPEND ON PRESENCE OF INSULIN - ANS-Acarbose(precose)
delays absorption of dietary carbs and thereby reduces postprandial rise in blood glucose -
ANS-Acarbose MOA
flatulence, cramps, abd distention, borborygmus(rumbling), diarrhea
risk of anemia due to poor iron absorption
hypoglycemia when combo
void with metformin due to both GI upset
long term/high dose=liver dysfxn. - ANS-Arcabose side effects/contraindications
2nd generation sulfonylureas, onset 15-30 min, less drug-drug interactions, type 2 diabetes with
calorie restriction and exercise, duration 10-24 hours - ANS-Glipizide (Glucotrol)
stimulating release of insulin from pancreatic islets (no type 1 because no insulin production)
Bind & block ATP-sensitive channels in cell membrane, membrane depolarize-permit influx of
CA+=insulin release - ANS-Glipizide MOA
hypoglycemia*--> will make glucose go lower no matter the level, more likely in pt with
liver/kidney dysfxn (hepatic/renal metabolism), possible cardiac death, teratogen=no
pregnancy/breast feeding (make baby hypoglycemic) - ANS-Glipizide side
effects/contraindications
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