Glucose Flashcards
Diabetes Mellitus
chronic, body is unable to use glucose as it should to produce energy
Type 1
unable to produce insulin- irreversible disorder of pancreatic beta islet cells (severe insulin deficiency)- altered macronutrient metabolism- dependent on exogenous insulin
Type 2
unable to use insulin- pancreas doesn’t produce enough (deficiency)- cells don’t use insulin properly (resistance) majority- dysfunction of liver: excess glucose released
insulin role
- promotes uptake and storage of glucose from blood- promotes uptake and storage of glucose by other cellsminor- promotes fat deposition, amino acid transport- inhibits protein degradation
hyperglycemia pathophysiology
osmotic gradient shift - fluid from ICM -> ECM -> glomerular filtrateglucose > 180 mg/dl -> glucosuria, polyuria
diabetes clinical manifestations
- frequent urination- increased thirst, appetite- decreased energy- vision disturbances- abdominal pain
alpha cells
glucagon: acts on liver to release glycogen, increases blood sugar
beta cells
insulin: decreases blood sugar
delta cells
somatostatin: stops glucagon and GH, decreases blood sugar
type 1 etiology
Human Leukocyte Antigen (HLA) system- identifies cells to immune system as self or non. Certain patterns indiate a susceptibility to Type 1 DMautoimmune process- islet cell antibodies, insulin antibodiesenvironmental factors-viruses
diabetic ketoacidosis
BIGGEST ISSUE.- often presenting symptom in children- moderate to life threatning- caused by metabolism of fats for energy (source #2 for energy; ketones released; body at extremely high glucose for extended period for this to happen)
DKA lab findings
- hyperglycemia- glucosuria- ketonuria- metabolic acidosis/ketoacidosis
DKA s/s
- kussmaul respirations (deep, rapid)- dehydration- acetone breath (sweet, fruity)- poor perfusion- impaired consciousnessi
illness/stress response + diabetics
check blood sugar, monitor to prevent DKA
nursing interventions for DKA
- manage hyperglycemia(regular insulin, IV, 75 - 150 mg/dl/hr)- fluid and electrolyte(restore volume, maintain perfusion to brain/heart/kidneys)- education(reason for diagnosis, prevent further episodes)
Type 2 DM etiology
- strong genetic basis exacerbated by environment factors including inactivity, weight gain, stress- most people overweight at time of diagnosis; weight loss can prevent/delay development- all age groups
Type 2: increased risks
- overweight- parent/sibling with diabetes- 40+ yo- htn- African American, Latino, American Indian- diabetes during pregnancy- stress of illness, injury- had baby weighing more than 9 pounds at birth
hyperglycemic-hyperosmolar state (HHS)
mainly type 2- blood sugars EXTREMELY high (up to 600 mg/dl)- body tries to rid excess by passing through urine- initially lots of UOP, becomes dark- very thirsty- if condition continues: severe dehydration -> seizures, coma, death
nursing intervention of HHS
fluid therapy- replacement to increase blood volumemedical therapy- IV insulin after adequate fluid replacement. 50-70 mg/dL/hr
management of DM
meds (insulin + PO)monitoringmeal planexercise planEDUCATION!
medicinal management of Type 1
insulin: basal, rapid acting
basal insulin
Levemir, Lantus (work up to 24 hours)
rapid acting insulin
Novolog, Humalog (meal time and correction doses)
medicinal management of Type 2
biguanides: Metformin (glucophage) - increases insulin sensitivity; decreases hepatic production of glucose from glycogen; decreases absorption of glucose from small intestinesulfonylureas: Glyburide, Glucotrol (glipizide) - directly stimulate pancreas to secret insulin