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normal range of glucose
70-100 mg/dL
fasting plasma glucose
no caloric intake for at least 8 hours
impaired fasting glucose = 100-126
critical values
<60 mg/dL or >500 mg/dL
random glucose
can be drawn any time
meals, drugs, stress can cause increase
critical values
>180 mg/dL on two occasions
>200 mg/dL with s/s of hyperglycemia
two hour oral glucose tolerance test (OGTT)
Fasting and then consuming sugary drink
Multiple blood draws over 2 hours after a glucose load of 75 g
Critical values
200 mg/dL or more = diabetes
>140 and <199 = prediabetes
glycosylated hemoglobin A1c (HbA1c)
tests to see blood glucose in last 3 months
glycosylated hemoglobin is glucose that has attached to the hemoglobin protein
normal range: 4 - 5.6%
pre-diabetes: 5.7 - 6.4%
diabetes: 6.5% or higher
other diagnostic testings
urine - protein and ketones
kidney function test
BMI - concern with >25
lipid levels - metabolic syndrome
C-reactive protein (CVD)
hypoglycemia
cause: alcohol stops releasing glucose
collaborative care:
conscious - rule of 15
unconscious - glucagon 1 mg IM or Sc or 50% dextrose (D50) 25-50 mL IV push
have nothing but patient is unconscious - put sugar under their tongue
diabetes mellitus causes
obesity
not enough insulin
steroids
hormones
type 1.5
LADA - latent autoimmune diabetes in adults
slow-progressing form of autoimmune diabetes
body destroys cells that produce insulin
type 3
alzheimer’s disease
insulin deficiency and insulin resistance as mediators of AD
MODY
maturity onset diabetes of the young
autosomal dominant
leads to beta cell dysfunction
occurs before age of 25
not associated with obesity or hypertension
treatment depends on genetic mutation
pre-diabetes
hbA1c = 5.7 - 6.4%
fasting plasma glucose level is above 100
studies show prevention with lifestyle change of weight loss and regular exercise
studies show long-term damage of CV system already may be occurring
type 1 diabetes
progressive destruction of pancreatic B cells
risk of DKA
manifestations - 3 P’s, and weight loss
type 2 diabetes
insulin resistance
can result in HHNK - hyperosmolar hyperglycemia nonketotic state
manifestations - gradual 3 P’s, fatigure, recurrent infections, visual changes, prolonged healing times
metabolic syndrome
cluster of abnormalities working together to increase risk for CV disease and DM
elevated insulin levels
decreased HDL (good cholesterol)
increased LDL (bad cholesterol)
hypertension
obesity
sedentary lifestyle
treated with weight loss and exercise
hyperglycemia short and long-term consequences
short term - inadequate glucose reaching cells, dehydration
long term - end organ disease, macrovascular angiopathy (atherosclerosis)
why cant’t exogenous insulin be taken orally?
insulin can’t be absorbed and broken down in stomach if taken orally
hyperglycemia collaborative care nutritional therapy
CHO - includes fruits, veggies, whole grains and low fat milk
high protein diets for weight loss not recommended
eliminate fats
limit alcohol, if consumed then with food!
hyperglycemia collaborative care exercise
best done after meals
if BS <100 mg/dL - delay exercise
if BS >250 mg/dL and with ketones in urine - postpone exercising
hyperglycemia collaborative care while patient is ill
regular diabetic diet
increase non-caloric fluids
continue with oral agents and/or insulin
monitor BS every 4 hours
if >240 check urine for ketones and report
hyperglycemia collaborative care foot care
risk of amputation up to 40x higher in diabetics
foot care/assessment
proper footwear
podiatrist
somogyi effect
overdose of insulin causes low BS in middle of night and morning hyperglycemia
treatment:
check BS between 2 AM and 4 AM, if low then reduce PM dose of insulin OR eat a bedtime snack
dawn phenomenon
hyperglycemia at night in the AM due to release of hormones in predawn hours
GH, cortisol, glucagon are factors
affects majority of diabetics but most severe in adolescence and young adulthood
high BS after 3 AM
treatment: if BS is high between 2AM and 4AM then increase insulin and eat bedtime snack
DKA
inadequate insulin for cells does not allow body to obtain energy
body attempt to obtain energy by rapid breakdown of fat in liver and form ketone bodies (acidic)
caused by:
missed insulin dose, inadequate insulin, increased insulin needs
new diagnosis of type 1 DM
stress/illness
HHNK
hyperglycemia hyperosmolar non-ketotic state
produce enough insulin to prevent DKA
not enough insulin to prevent osmotic diuresis, hyperglycemia, or ECF depletion
increase in serum osmolarity
BS >400 mg/dL
ketones ABSENT
treatment of DKA and HHNK
med emergency
IV administration of NSS or ½ NSS (first thing you do)
regular insulin IV
when glucose falls <250 add IV glucose
electrolyte replacement
bicarbonate for pH <7.10 (FOR DKA)
cardiac monitoring - dysrhythmias - worried about hypokalemia
monitor potassium levels