3 glucose dysregulation 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 cells
minor
- promotes fat deposition, amino acid transport
- inhibits protein degradation
hyperglycemia pathophysiology
osmotic gradient shift - fluid from ICM -> ECM -> glomerular filtrate
glucose > 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 DM
autoimmune process
- islet cell antibodies, insulin antibodies
environmental 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 volume
medical therapy
- IV insulin after adequate fluid replacement. 50-70 mg/dL/hr
management of DM
meds (insulin + PO) monitoring meal plan exercise plan EDUCATION!
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 intestine
sulfonylureas: Glyburide, Glucotrol (glipizide) - directly stimulate pancreas to secret insulin
