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75 Cards in this Set

  • Front
  • Back
glucose
produces energy
you need insulin to
transport glucose across cell membranes
small glands of pancreas
islets of Langerhans
two types of islet cells
alpha cells- produce glucagon


beta cells- produce insulin and amylin
glucagon
"counterregulatory" hormone

actions opposite of insulin

causes release of glucose from cell storage sites whenever blood glucose levels are low

prevents hypoglycemia
type 1 diabetes
insulin dependent

no cure- but can be managed
type 2 diabetes
more common

resistant to insulin

body isn't making enough insulin
signs and symptoms- absence of insulin
hyperglycemia

polyuria, polydipsia, polyphagia

presence of ketone bodies
fat broken down- fatty acids- ketones released
how is metabolic acidosis caused
the excess acids caused by absence of insulin increase hyrogen ions and carbon dioxide levels in the blood
Kussmaul respiration (metabolic)
increased rate and depth (deep and rapid)

an attempt to excrete more carbon dioxide and acid
arterial blood gas studies showing metabolic acidosis and compensatory respiratory alkalosis
metabolic acidosis-
decreased pH
decreased arterial bicarbonate

compensatory resp alkalosis-
decreased carbon dioxide
(shallow and rapid resp)
potassium could be
low, high, or normal depending on hydration, acidosis, and response to treatment

low- insulin lack causes low potassium (increased fluid loss)

high- shift of potassium from inside the cells to blood (acidosis)
Diabetic Ketoacidosis (DKA)
manifestations:
fruity breath because acetone is being exhaled
nausea, ab pain, dehydration or electrolyte loss, dry skin, sunken eyes, soft eyeballs, lethargy, coma, Kussmaul respiration

Precipitation factors:
infection, other stressors, inadequate insulin dose

Onset: sudden

Labs:
glucose- over 300
pH- less than 7.35
HCO3- less than 15
positive for ketones- 1:2 dilutions
Diabetic Ketoacidosis is caused by
lack of insulin and ketosis

sudden
treatment for DKA
fluid replacement
insulin (insulin pushes K+ into cells)
Hypoglycemia- signs and symptoms
confusion
cold clammy skin
diaphoresis
irritable
tremors
treatment for hypoglycemia
if alert- juice (not OJ if renal pt)

if not alert- dextrose 50% IV push
Hyperglycemic - Hyperosmolar state
caused by insulin deficiency and profound dehydration

Onset- gradual

Precipitating factors:
infection, other stressors, poor fluid intake

Labs:
blood sugars over 600
osmolarity- over 320
pH- over 7.4
HCO3- more than 20
no ketones
Hyperglycemic - Hyperosmolar state- signs and symptoms
difficulty breathing
coma
dehydration
altered central nervous system
treatment for hyperglycemic - hyperosmolar state
insulin
always is dehydrated- lots of fluids 0.9 normal saline
replace electrolytes
Macrovascular chronic complications
large blood vessel disease -

coronary heart disease
cerebrovascular disease
peripheral vascular disease

fat, blood clots stick to walls- MI and stroke
Common macrovascular disease-
CDV
Cardiovascular disease- most common complication

Myocardial infarction- leading cause of death- affects women more

(Hyperglycemia, hypertension, hyperlipidemia, obesity, smoking, renal)
Common macrovascular disease-
cerebrovascular disease
damages cerebrovascular and arterial circulation

Stoke (CVA)
complications makes diabetes a major risk factor for
higher mortality and morbidity rates
Microvascular chronic complications
small blood vessels

nephropathy
neuropathy
retinopathy

increased for fall
diabetic retinopathy
after 20 years of diabetes- nearly all pt with type 1 have some degree

block retinal blood vessels and cause them to leak, leading to retinal hypoxia

25x more likely- blindness

NPDR and PDR

linked to fasting blood glucose levels above 129mg/dL
Nonproliferateive diabetic retinopathy
causes structural problems in retinal vessels

growth of new blood vessels is not stimulated

develops slowly and rarely causes blindness
predictor of PDR
venous beading- abnormal appearance of retinal veins in which areas of swelling and constriction along a segment of vein resemble links of sausage. it occurs in areas of retinal ischemia
Proliferative diabetic retinopathy
growth of new retinal blood vessels (neovascularization)

when hypoxia develops- growth factor secreted- stimulates new blood vessels in eye

new vessels thin and fragile- bleed easily

fibrous tissues bands- retinal detachment and permanent vision loss
hyperglycemia causes _ vision

hypoglycemia causes _ vision
hyperglycemia causes blurred vision

hypoglycemia causes double vision
diabetic neuropathy
progressive deterioration of nerves that results in loss of nerve function

damage to:
sensory nerve fibers- pain or loss of sensation

motor nerve fibers- muscle weakness

nerve fibers in autonomic nervous system- dysfunction in every part
signs and symptoms- neuropathy
tingling, numbness, ulcers, foot ulcers
erectile dysfunction in neuropathy
poor glucose control
hypertensive
smoke
50% of men have it
nephropathy
microabluminuria
type 1- yearly screening after 5 years
type 2- annual
risk factors for diabetes
age, obesity, family history, having 9lb baby

american indian, african american, hispanic
genetics
type 2 -
offspring 15% chance of having it
30% of glucose intolerance
plays major role

type 1
HLA-DR and HLA-DQ
risk but not all
health promotion type 1
tight control of blood sugar control
vision checked yearly
microalbumin levels
early diagnosis of change allows adjustment of treatment
health promotion type 2
exercise
weight loss

risk- triglycerides, hypertension, tobacco
testing
fasting blood glucose- no caloric intake for 8 hours, preferred test, over 126 two times for confirmed, over 100 but less than 126 is glucose intolerance

oral glucose tolerance- most sensitive, inconvenient, costly, fast 10-12 hours before, drinks glucose load, then check hourly, for gestational, 75g 2 hr, 100g 3 hr, greater than 140mg/dL and less than 200 is impaired glucose intolerance, greater than 200 is diabetes

HBA1C- best indicator of compliance, 8% is poor glucose control, goes back 120 days
urine test- ketones
presence of moderate to high urine ketones indicates a severe lack of insulin

should be performed during acute illness, stress, pregnant, weight loss program, levels consistently over 300
urine glucose
quick screening- should not be used for monitoring diabetes
drug therapy
for type 2
small dose,1-2 weeks work way up

based on cost, ability to manage multi dose, age, response to drugs

older adults, irreg eating pattern- shorter acting are preferred
insulin is prescribed after
2 or 3 drugs don't work
Sulfonylurea agents
should never be taken with NSAID because of hypoglycemia
Meglitinide Analogues
Starlix (Nateglinide)
teach pt to take the drug 3 times daily, 1-30 min before meals

teach pt to omit the drug when skipping a meal, and instruct them to add a dose if an extra meal is eaten
Thiazolidinediones
Pioglitazone (Actose)
emphasize the need for liver function tests as recommended. Instruct pt to report symptoms of unexplained nausea, vomiting, ab pain, fatigue, anorexia, or dark urine

advise women of the need for effective contraception during therapy

monitor weight; assess for edema and shortness of breath

stress importance of continuing therapy even if a response is not evident within 2 weeks
Fixed combos
Glucovance
(glyburide/metformin)

teach pt to prevent and treat hypoglycemia

taken with sulfonylurea can cause hypoglycemia
insulin is available in
100 and 500 units
antidiabetic drugs are not a sub for
dietary modification and exercise

consult dr with otc meds
rapid acting insulin
insulin aspart (Novolog)
onset- 15 mins
peak- 1-3 hours
duration- 3-5 hours

clear-IV

human lispro injection (humalog)
onset- 15 min
peak- .5-1.5 hour
duration- 5 hour
short acting insulin
regular human insulin injection (Humulin R) (Novolin R) (ReliOn R)
onset- 30 minutes
peak- 2-4 hours
duration- 5-7 hours

clear- IV

draw first with other insulin
intermediate acting insulin
isophane insulin (Humulin R) (Novolin R) (RelioOn R)
onset- 1.5 hr
peak- 4-12 hr
duration- 16+24 hr

basal rate, for btwn meals
long acting insulin
insulin glargine injection (Lantus)
onset-2-4 hours
peak- NONE
duration- 24 hours

once a day at bedtime
dont hold
never mix
insulin teaching
roll, don't shake
good for 28 days
assess for cloudiness, clumping, frosting, precipitation,
right syringe to buy
1ml -100, .5ml-50, 3/10 ml-30
.5 inch or 5/16 inch
28-31 gauges
factors affect insulin absorption and availability
injection site, timing, type, dose of insulin, physical activity
fastest injection site absorption
abdomen (preferred)
followed by deltoid, thigh, and buttocks
lipohypertrophy
increased fat deposits under skin
lipoatrophy
loss of fatty tissue, leaving uneven appearance
rotation within one site is
preferred

because of day to day changes in absorption
factors that increase blood flow
local application of heat, massage of area, exercise of injected area
scarred sites
become favorite
usually slower rate of absorption
dawn phenomenon
results from nighttime release of growth hormone that causes blood glucose elevations at about 5-6am

managed by more insulin at night
Samogyi phenomenon
spike glucose in morning

managed by exercise, diet, more insulin
protein
15-20%
kidney problems- 10% lower intake
carb
45-65%
fruit, vegetables, whole grains, legumes, and low-fat milk

amount and types of carb consumed have the greatest impact on after-meal blood glucose levels
saturated fatty acids and trans fatty acids
restricted
fiber
legumes, fiber rich cereals, fruits, veg, and whole grain products

add gradually

increase fast- hypoglycemia
sweeteners
sucrose
cover with insulin
alcohol
only with or shortly after meals
men- 2 bev
women- 1 bev

12 ounce beer, 5 ounces of wine, 1.5 ounces of distilled spirits

hypoglycemia

not good for high triglycerides
exercise
lowers insulin requirements for type 1

prevents and delays for type 2
guidelines for exercise
based on blood glucose levels and urine ketone levels

type 1-
80-250 and no ketones than it is ok
hypoglycemia
cool clammy skin

no dehydration

profuse perspiration

anxious, nervous, irritable, mental confusion, seizures, coma

weakness, double vision, blurred vision, hunger, tachycardia, palpitations

glucose- less than 70

negative ketones
hyperglycemia
hot dry skin

dehydration

rapid, deep, kussmaul type, fruity odor

varies to alert to stuporous, obtunded, or frank coma

acidosiss, hypercapnia, ab cramps, nausea, vomiting, dehydration- decreased neck vein filling, thostatic hypotension, tachycardia, poor skin turgor

glucose- more than 250

positive ketones
neuroglycopenic symptoms
warmth, weakness, fatigue, difficulty thinking, confusion, behavior changes, emotional lability, seizures, loss of consciousness, brain damage, death
neurogenic symptoms
adrenergic- shaky/tremulous, heart pounding, nervous/anxious

cholinergic- sweaty, hungry, tingling