disease that disrupts the bodys ability to produce and properly use insulin

**disruption in the normal metabolism of the pancreatic hormones of glucagon and insulin

limit cost by prevention and containment of complications

**challenge is achieving and maintaining meticulous blood glucose control so that long term complications can be prevented

destruction of alpha and beta cells in the pancreas

**may lead to failure to produce insulin or

production of excess glucagon

elevated blood glucose---->increases osmolarity

glucosuria, polydipsia, polyphagia, polyuria

weight loss

accelerated atherosclerosis, impaired immune function

small vessel disease which may lead to diabetic neuropathy, diabetic nephropothy, diabetic retinopathy

what might a production of excess glucagon lead to

(production of glucose from protein and fat stores)

increased ketones--ketonuria

acidosis--acetone breath

wasting of lean body mass--weight loss, fatigue

blood glucose testing

glycosylated hemoglobin (HgA1c)

hyeprglycemia

polyuria

polydipsia

polyphagia

glucosuria

ketosis

DKA

what is.....

polyuria

polydipsia

polyphagia

glucosuria

osmotic dieresis that can lead to severe dehydration

increased thurst

increased appetite

excess glucose secreted into the urine--(bg over 180)

lipid panel(elevated with DM)

total cholesterol <200

tryglycerides <200

HDL >45 in women >35 in men

LDL <100

urine test for protein

kidney function

liver function tests

accumulation of ketone bodies during the breakdown of fats and proteins when insulin levels are insufficient for the body's needs

**can increase in the blood and spill over into the urine

when there is insufficient insulin body breaks down fats and proteins for energy causing acidic ketone bodies to build up

**causes systemic acidosis and requires hospitalization

BUN and creatinine

every 6 months

defect, failure or destruction in beta cells of pancreas--

little or no production of insulin

**beta cells destroyed by genetics, autoimmunity, and environmental factors

pancreas secretes inadequate amounts of insulin

**starts 5-10 yrs prior to symptoms

***rountine screening for at risk pts

form of type 2 that increases insulin resistance

**treated with multiple oral antidiabetic meds and eventually insulin

pregnancy induces hyperglycemia

body unable to produce enough insulin for mother and baby

impaired glucose tolerance

prediabetes

borderline diabetes

blood glucose level higher than normal but not high enough to be classified as DM----(at increased risk for developing diabetes later)

type 1 DM

etiology

juvenile diabetes, insulin dependent diabetes

genetics, immunologic factors(antibodies against insulin), environmental factors(response to virus exposure)

onset under 30yrs

weight loss-thin, catabolic

sudden onset of----

fatigue

blurred vision

infections

ketosis

DKA

hypovolemic shock

diabetic coma

severe acidosis leads to coma and death

SMBG

insulin required to survive

oral anti diabetic meds(not usually effective bc they stimulate beta cells in pancreas)

nutritional therapy

exercise

type 2 DM

etiology

adult onset, non insulin dependent

heredity(100% correlation in twins)

obesity

insulin resistance--insulin less effective in liver and peripheral tissue= higher blood glucose

muscle and fat tissue unable to uptake glucose for energy

desensitization---beta cells chronically exposed to high glucose

over 30 yrs

fatigue

decreased wound healing

weight gain

obese at diagnosis

blurred vision

infections

parathesias

sexual dysfunction

SMBG

weight mgmt

oral anti diabetic meds---to help control blood glucose

nutrional therapy

exercise

insulin therapy

heart disease

HTN

hyperlipidemia

left ventricular hypertrophy

SMBG

weight loss

oral anti diabetic meds

monitor cardio status

nutritional therapy--low fat low cholesterol meal plan

onset in 2-3rd trimester

caused by hormone secreted by placenta that inhibits insulin action

pregnant over 30yrs

obesity

family history of DM

previous large baby--over 9 pounds

increased neonatal mortality

insulin therapy--oral anti diabetic meds cannot be used

nutritional therapy

exercise

SMBG

careful bg mgmnt to protect mother and baby

s/s of impaired glucose tolerance

fasting blood glucose 110-126 mg/dl

OGTT(casual bg) 140-200 mg/dl

if obese--weight loss

frequent screenings for DM

nutritional therapy

abnormality of glucose tolerance

fasting BG 100-125

OGTT 140-199

strong family history of DM

obesity

frequent screenings

if obese-weight loss and nutritional therapy**

exercise**

**may prevent or delay DM

corticosteroids

estrogen--birth control pills, hormone replacement therapy

monitoring BG

pharmacologic therapy

nutritional therapy

exercise

education

hypoglycemia

mild

moderate

severe low

low blood glucose

mild<50-70

moderate <30-50

severe low <30

sulfonylureas

biguanides

alpha-glucosidase inhibitors

thiazolidinediones

meglitinides

incretin mimetics

types of insulin

rapid acting

short acting

intermediate acting

long acting or basal insulins

combination insulin

humalog

lispro

novolog

aprida

humulin R

Novalin R

Velosulin BR

humulin N

Iletin NPH

Lente insulin

**look for N or NPH on label

ultra lente

lantus (glargine)

detremir (levemir)

humulin 70/30-70NPH/30Reg

humulin 50/50

maintain blood glucose as close to normal as possible

**balancing food choices, taking meds and maintaining activity

maintain near normal blood glucose

achieve optimal lipid levels

achieve optimal blood pressure control

prevent and treat complications

improve overall health through optimal nutrition and exercise

diet history

eating habits

cultural/religious/ethnic influences

**any special dietary requirements

Consistent Carbohydrate diabetic meal plan

focuses on maintaining similar amounts of carbs at each meal to stabilize postprandial(after meal) blood glucose levels

1 unit

regular, humalog, or lispro is used

hypoglycemic

**alcohol may interfere with antidiabetic meds and insulin

consumed with food and added to daily exchange(bc it is considered a fat exchange)

light beer is the only recommended alcoholic drink

**avoid or limit--sweet wines, wine coolers, sweet mixers

likes and dislikes

who prepares the food

age changes affecting taste

dental health

transportation to buy food

income to buy food

assess and monitor nutritional status

know patients nutritional perscription

reinforce nutritional teaching with pt and family

answer questions about nutritional therapy

increases glucose uptake by muscle

improves insulin utilization

reduces need for meds

reduces cholesterol and triglycerides

improves circulation

decreases cardiovascular complication

can decrease insulin resistance in type 2

monitor BG closely

avoid if BG is over 250 or positive ketones in urine

avoid if really hot/cold out

wear proper shoes

inspect feet daily

hyper/hypoglycemia

DKA

HHNS

dawn phenomena

somogyi effect

still increases even if not eating

**pt should take meds, monitor BG more frequently

monitor BG at least 4/day

keep taking meds

8-12 oz fluid hourly

call dr if not eating for 24 hours or vomit/diarrhea for 6 hours

prevent dehydration

prevent hyperglycemia and DKA

provide nutrition to promote recovery

insufficient insulin

(sick diabetic--infection or acute illness)

**requires hospitalization to correct

usually type 1

sudden

infection

stress

inadequate insulin

polyuria, polyphagia, polydipsia

elevated ketones

ab cramps, N/V

fatigue

dehydration

weight loss

headache

tachycardia

hypotension

fruity breath

kussmal respirations

BG with DKA

serum ketones with DKA

urine ketones with DKA

over 300-800 mg/dl

positive

positive

serum pH with DKA

serum HCO3 with DKA

serum K+ with DKA

BUN

6.8-7.3

0-15 mEq/L

low in severe DKA

increased >20 mg/dl due to dehydration

BG Q1H

IV drip or subq insulin

IV NS 500cc/hr with potassium---after 2-3 hrs or when BP normalizes--->.45 NS at 200-300 cc/hr with K+

dextrose is added when BG gets to 250 to prevent drop(cerebral edema)

ICU-monitored bed-cardiac dysrhythmias from electrolyte imbalance

monitor acidosis levels

(hyperosmolar nonketotic coma)

usually in type 2

**severe dehydration that causes

inadequate circulating blood volume

decreased renal function

lactic acidosis

increasingly viscose blood that further decreases perfusion

more severe than DKA-mort rate of 10-40%

pts with poorly controlled type 2

newly diagnosed type 2

elderly pts

stress

infection

cardiac events, MI

CVA

inability to drink fluids

lack of antibiotics or insulin

usually type 2

gradual

severe osmotic diuresis

dehydration

poor skin turgor

tachycardia

hypotension

electrolyte loss--NA, K+, phosphorus

neurologic s/s

lethargy

change in loc

seizures

coma

hyperosmolality with HHNS

blood glucose with HHNS

serum ketones

urine ketones

>350 mOsm/L--due to profound dehydration

over 600-1200 mg/dl

negative

negative

HHNS---serum pH

HCO3

serum K+

serum NA

BUN

<7.4

<20

normal to low

normal to low

elevated due to dehydration

check BG at 2 and 4 am-if high=DP

adjust insulin dosage or increase bedtime insulin

wide differences in early morning(low) and fasting(high) glucose levels before breakfast

-BG drops below normal due to too much insulin at bedtime--counter regulatory response to night time low

**hypoglycemia in the middle of the night

check B at 2 and 4 am--low BG and check morning fasting before breakfast

more dietary intake if less than 60 or give less insulin in the evening

why are cardiovascular complications of diabetes related to macrovascular changes

and what are they

 due to alterations in lipid metabolism (increased triglycerides and cholesterol)

CAD

cerebrovascular disease--lead to CVA

atherosclerosis--2x more MI/CVA in pts with diabetes

HTN

peripheral vascular disease

monitor and correct BP

exercise

monitor lipids

low saturated fat meal plan

statin drugs

daily aspirin

nephropathy

retinopathy

neuropathy

gradual decrease in renal function due to inadequate BG control

reduces blood flow to kidneys

urine albumin increases

proteinuria

HTN

changes in urine output

24 hour urine

serum BUN-increased

serum creatinine-increased

prevention

low protein meal plan

control HTN

reduces renal fuction-decrease meds

retinal edema

vision changes--red/black lines or spots

retinal detachment

tests--opthalmic examination

mgmt--

prevent

BG control

HTN control

aspirin therapy

laser photocoag

autonomic-affect multiple systems cause hypoglycemic unawareness

GU- neurogenic bladder, incontinence

GI-gastroparesis, N/V, anorexia, GERD, diarrhea, constipation

cardio- postural hypotension,tachycardia, asymptomatic MI

reproductive-sexual dysfunction, male ed, female decreased libido

promote prevention of complications of DM

screening for macrovascular complications like:

increasing BP

lipid levels

increasing BG

compliance with meal plan

pt education concerning foot care and skin care

imbalanced nutrition

ineffective tissue perfusion

risk for infection

risk for impaired skin integrity

risk for injury

deficient knowledge