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63 Cards in this Set

  • Front
  • Back
Insulin
Anabolic hormone secreted by the beta cells of the islets of Langerhans in the pancreas
transports glucose across cell membranes to be used for energy
Insulin Actions
promotes glycogenesis
inhibits glycogenolysis
inhibits ketogenesis
inhibits gluconeogenisis
glycogenesis
promotes the production and storage of glycogen in the liver
glycogenolysis
glycogen breakdown to glucose
ketogenesis
conversion of fats to fatty acids
gluconeogenisis
conversion of protein to glucose
Counterregulatory Hormones definition
counter act the insulin to maintain homeostasis
counterregulatory hormones
glucagon
cateholamines
growth hormones
cortisol
glucagon
changes glycogen back to glucose
epinephrine and metabolism
triggers liver to turn glycogen into glucose
promotes glycogenolysis
Growth hormones and diabetes
also triggers release of glucose, ussually happens at night
cortisol
causes release of some sugar. Increase thru day and decrease at night
Maintain 70-110
BG maintainance
Maintain 70-110
Diabetes Mellitus Definition
a chronic metabolic disorder marked by hyperglycemia resulting from failure of the pancreas to produce insulin or from insulin resistance.
Absence of Insulin
P3+A+K2+H6
Poly uria
polydipsia
Polyphagia
Acidosis
Kussmaul respirations
K changes (hypokalemia)
Hemoconcentration
Hyperviscosity
Hyperglycemia
Hypovolemia
Hypperfusion (poor perfusion to tissues)
Hypoxia
Type 1
inherited
destruction of beta cells in pancreas
autoimmune
viral
type 2
insulin resistance
insulin secretory defect
gestational
insulin resistance increases in pregnancy- due to insulinase from placenta
Maternal insulin demands triple
Type 1 characteristics
acute onset
young age
white population
primary relative with type 1
presence of 1 or more autoantibodies
prone to ketoacidosis
5-10% of all cases of diabetes
goals
must integrate diabetes management with the complicated physical and emotional growth needs of children, adolescents and their families
Promote normalcy
Type 2 diabetes mellitus characteristics
insidious onset
elevated Post Pranial glucose before elevated FBS
Probably genetically based w/ a strong behavioral component
Family history of type 2
Older age
history of metabolic disorders
Diagnosing type 2 DM
Impaired GTT
Impaired FBS
Glycosylated Hemoglobin
glucose permanently attaches to hemoglobin over time
more accurate indication of glycemic control
A1C norms
below 5.7: Normal
5.7-6.6 Pre
6.0-6.4 High risk
greater than 6.5 diabetic
>7.0 poor control
HHS
Hyperglycemin-hyperosmolarity Syndrome
Diabetic Ketoacidosis
usually precipitated by concurrent illness
infection
environmental concern
emotional stress
Lab findings of DKA
BS > 300mg/dl
Decreased Na+ <120
Urine and serum ketones are present
K+ changes
HHS
Hyperglycemic Hyperosmolar Syndrome
no significant ketosis
does not occur in adequately hydrated clients
higher hyperglycemia
higher blood osmolarity
HHS Triggers
Mi
Sepsis
pancreatitis
stroke
drugs
HHS diagnostics
Blood sugar>800
serum osmolarity >350
Urine and serum ketones negative
treatment for DKA and HHS
Frequent VS
Fluid replacement
insulin
glucose monitoring
K+ replacement
SQ heparin for blood viscosity
Hypoglycemia
brain is dependent on continuous supply of glucose
counterregelatory response may be impaired
may be a side effect of treatment
Hypoglycemia manifestations
brain damage
seizures
Jittery
Hypoglycemia treatment for IV
50% dextrose (25gms) IV
Glucogon 1.0 IM/SQ
Macrovascular Complications
cardiovascular disease
cerebrovascular disease
peripheral vascular disease
Microvascular complications
retinopathy
diabetic neuropathy-nerve cells
Diabetic nephropathy-kidneys
Goals of Medical management of chronic disorders
Glucose monitoring
regular checkups
exercise
drug therapy
education on glycemic control
Gestation diabetes high risk ethnic factors
native american
african american
Gestational Diabetes Prevalence
7% of all pregnancy
Gestational Risk Factors
Maternal age >30
obesity
polyhydramnios
unexplained stillbirth
Miscarriages
Maternal Complications of GDM
Hypertensive disorders of pregnancy
Infections: Monilial vaginitis, bladder infections
Perineal trauma
fetal complications
Macrosomias-large head and shoulders
shoulder dystocia-shoulders are stuck
hypoglycemia
hypocalcemia
hyperbilirubinemia
Thrombocytopenia
polycythmia
RDS-Resp Distress Syndrome-underdeveloped lungs
Gestational diabetes-interventions during pregnancy
blood glucose control
diet
exercise
insulin therapy-not oral hypoglycemics
fetal surveillance
Gestational Diabetes-intrapartum interventions
monitor glucose 2qh
fetal heart monitoring
Dextrose can be given for IV maintenance fluids
Gestational diabetes- postpartum interventions
assess for CHO intolerance in 6-12 weeks and after cessation of breastfeeding
Insulin--Rapid acting
onset 15-60 minutes
peaks 1-4 hours
Duration 2-7 hours
rapid acting names
humulin
novolog
humalog
apidra
Intermediate Acting
Onset 1-4 hours
Peak 6-12 hours
duration 18-28 hours
Long acting insulin
Onset: 1-6 hours
Peak 18-plateau
Duration 24-36 hours
Insulin combinations
Humulin 50/50
Humulin 70/30
Novolin 70/30
Pharmacokinetics of insulin
inection site
absorption rate
inection depth
time of injection
mixing insulins
complications of insulin therapy
hypoglycemia
lipoatrophy-deteriation of adipose tissue
dawn phenomenon
somagyi's phenomenon-rebound from hypo
alternative methods of insulin therapy
continuous subcutaneous infusion of unsulin
implanted insulin pumps
injection devices
inhaled insulin
transdermal patch
sulfonylureas
enhances release of insulin from beta cells
increases cellular sensitivity
first generation (diabenese)
second generation (last longer and fewer side effects
Biguanides
metformin
decrease hepatic glucose production
increase action of insulin on the cells
decrease gi glucose absorption
glucoside inhibitors
delay digestion and absorption of CHO
causes flatulance, cramping, diarrhea
acarbose
miglitol
Meglitinides
stimulates beta cells to produce insulin
short acting and excreted faster
good for irregular eating patterns
thiazolidinediones
decreases insulin resistance
resensitizes body to own insulin
strong and can cause liver damage, is used as a last resort
noninsulin polypeptide analogues
released by beta cells shortly after eating
decreases glycogen stores
decreases appetite
slows gastric emptying
risk for hypo
Symlin
Herbs that enhance hypo effect
cinnamon
garlic
bilberry
therapeutic management
exercise therapy
Whole-pancreas transplantation
operative procedure
rejection management
islet cell transplatation hindered by limited supply of beta cells and problems caused by antirejection drugs
Wound care
debridement
elimination of pressure on infected area
growth factors applied to wounds