Diabetes

what is type 1 diabetes?

autoimmune disorder in which the body develops antibodies against insulin and/or the pancreatic beta cells that produce insuline

what is the main problem with insulin in type 1 diabetes?

not enough insulin for a person to survive

what causes 80-90% reduction of normal function before hyperglycemia and other manifestations occur>

autoantibodies to the islet cells

what are factors that may contribute to the pathogenesis of immune-related type 1 diabetes?

genetic predisposition and exposure to a virus

what is type 2 diabetes?

the pancreases does not produce enough insulin or does not use it effectively or both

type 2 diabetes: insulin receptors

unresponsive to the action of insulin and/or insufficient in number

what happens when there is a decrease in ability of pancreas to produce insulin?

beta cells become fatigued from compensatory overproduction of insulin or when beta cells mass is lost

what happens with glucose production in type 2 diabetes?

inappropriate production by the liver

what does adipose tissue do in type 2 diabetes?

alter production of hormones and cytokines

type 1 DM

- more common in young adults or pediatrics

- abrupt onset

- accounts for 5-10%

- virus, toxins

- thin, normal or obese

- require exogenous insulin

type 2 DM

- usually > 35

- may be undiagnosed for years

- 90-95%

- obesity, lack of exercise

- frequently overweight, larger waist circumference

- may require lifestyle mod, oral agents, and potentially exogenous insulin

what are individuals with metabolic syndrome at an increased risk for?

development of type 2 diabetes

how can overweight individuals with metabolic syndrome reduce their risk for diabetes?

through a program of weight loss and regular physical activity

metabolic syndrome

1. waist circumference > 40 in men; > 35 in women

2. triglycerides: > 150

3. HDL cholesterol: < 40 in men; < 50 in women

4. BP: > 130/ > 85

5. fasting blood glucose: > 110

prediabetes

intermediate stage between normal glucose homeostasis and diabetes where the blood glucose levels are elevated but not high enough to meet diagnostic criteria for diabetes

what is impaired in prediabetes?

glucose tolerance, fasting glucose or both

s/s of prediabetes

- impaired fasting glucose: 100-125 and A1C of 5.7-6.4%

- no symptoms

considerations for prediabetes

- important to screen

- monitor A1C and glucose

- weight loss, exercise, and eating healthy can reduce risk of developing diabetes

gestational diabetes

develops during pregnancy and usually returns to normal 6 weeks post partum

when are women at high risk for gestational diabetes screened?

- first prenatal visit

- others = 24-28 week

what are women with gestational diabetes are at higher risk of?

- needing cesarean delivery

- babies have increased risk for perinatal death

- birth injury

- neonatal complications

classic signs of DM

- polyphagia

- polydipsia

- polyuria

s/s of type 1 DM

- usually acute polyuria, polydipsia, polyphagia

- weight loss

- fatigue and then ketoacidosis

s/s of type 2 DM

- nonspecific

- fatigue

- recurrent infections & profound wound healing

- visual changes

diabetic dermopathy

- reddish brown, round or oval patches

- initially scaly then flatten out and indented

- appear on shins but may appear elsewhere

acanthosis nigricans

`brown to black skin thickening on flexures, axillae and neck

necrobiosis lipoidica diabeticorum

red lesions with blood vessels

Diagnosis Glycosylated Hgb (HbA1C)

- blood glucose bound to hgb

- indicates glucose control over several months

- values are expressed in percentage of total hgb

- fasting is not required

what is HbA1C goal for patients with diabetes?

7% or lower (controlled = 4-6%)

diagnosis for diabetes

1. hemoglobin A1C level or 6.5% or higher

2. fasting plasma glucose level of 126 or higher

3. two-hour plasma glucose level of 200 or higher during OGTT, with a glucose load of 75 g

4. classic symptoms + random plasma glucose level of 200 or higher

when is repeat testing for diabetes not necessary?

if a patient presents with a hyperglycemic crisis or clear symptoms (polyuria, polydipsia, polyphagia) with a random plasma glucose level of 200 or higher

how does a fasting plasma glucose tolerance test work?

- no food or drink 8-12 hours prior to test

- blood is drawn & tested

- if > 200 = potential diabetes

how does a oral glucose tolerance test work?

- no food or drink 8-12 hours prior to test

- drink glucose

- blood is tested two hours later

- if > 200 = potential diabetes

angiopathy

disease of blood vessels

how does diabetes result in angiopathy?

- damage to blood vessels secondary to chronic hyperglycemia

- leading cause of diabetes-related death

- tight glucose levels can prevent or minimize complications

microvascular complications of diabetes

- thickening of vessel membranes in capillaries and arterioles

- retinopathy (eyes)

- nephropathy (kidneys)

- neuropathy (nerves)

- dermopathy

- appears 10-20 years after diagnosis

macrovascular complications of diabetes

- diseases of the large and medium-sized blood vessels

- greater frequency and earlier onset in pt’s with diabetes:

• cerebrovascular (stroke, TIA)

• cardiovascular (MI)

• PVD

what are risk factors for macrovascular complications of diabetes?

- obesity

- smoking

- hypertension

- high fat intake

- sedentary lifestyle

- screen for and treat hyperlipidemia

sensory neuropathy

- loss of sensation, pain, abnormal sensation or paresthesia to hands and feet:

• foot injury and ulcerations

• glucose control only treatment

• medications to control symptoms

autonomic neuropathy

- affects all body systems:

• bowel incontinence

• urinary retention

• gastroparesis

• postural hypotension

• silent MI

• ED

neuropathy lower extremities

High risk for foot ulcerations & lower extremity amputations

PAD

decreased blood flow leads to decreased oxygen, white blood cells and nutrients are not available to tissues

s/s of PAD

- intermittent claudication

- pain at rest

- cold feet

- loss of hair

- delayed cap refill

neuropathy: feet

- foot injury and ulcerations can occur w/o patient ever having pain

- paresthesias may be associated with tingling, burning and itching sensations

- complete or partial loss of sensitivity to touch and temperature is common

what may diabetes patients experience with paresthesia?

- pt. may report a feeling of walking on pillows or numb feet

- at times, skin becomes so sensitive (hyperesthesia) that even light pressure from bed sheets cannot be tolerated

monofilament test

- predicts the risk of future for ulcers in the foot.

- use in patients with diabetic neuropathy

foot care for diabetics

1. wash feet daily with mild soap & warm water

2. pat feet dry, gently especially between toes

3. inspect feetDAILY for cuts, swelling, blisters, red areas

4. use lanolin to prevent dry skin & cracking but do not put between toes

5. mild foot powder on sweaty feet

6. do not use commercial remedies to remove calluses or corns

7. cleans cuts with mild soap & water and don't use iodine, alcohol or adhesives

8. Report skin infections or nonhealing sores.

9. Trim nails after shower or bath and cutevenly with rounded contours.

10. Separate overlapping toes with cotton

11. Do not go barefoot, wear open-toe, open-heel or plastic shoes. Only shoes with soles and shake out shoes before wearing.

12. Clean, absorbent socks

13. No hot water bottles

wound healing deficit

- delayed wound healing may be a sign you need to consider a DM diagnosis

- may mean better control is needed for wound to heal

- complication r/t hyperglycemia

infection risk

- reccuring or persistent infections such as candida albicans as well as boils and furuncles

- loss of sensation may delay detection of an infection

what can persistent glycosuria do?

- may predispose patient to bladder infections, especially in patients with a neurogenic bladder.

- decreased circulation resulting fromangiopathy can prevent or delay the immuneresponse.

what has prevented infection from being a major cause of death among patients with diabetes?

antibiotic therapy

how is diabetes infection treated?

promptly and vigorously

cornerstones of DM care

- if type 2, lifestyle modification

- drug therapy: insulins, oral, noninsulin injectable

- nutritional therapy

- exercise

- monitoring blood glucose

goals of DM care

- reduce symptoms

- promote well-being

- prevent acute complications of hyperglycemia and hypoglycemia

- prevent or delay onset and progression of long term complications

when is insulin normally secreted?

in response to glucose (meal times)

nursing care: insulin

- simulates body's own normal insulin output

- combine "basal" insulin with "mealtime" insulin

- use rapid and short acting (bolus) before meals

- use background insulin once a day

- commonly prescribed as 4 injections a day

how does 4 injections a day of insulin work?

- lantus or levemir at bedtime: basal

- novolog or regular before each meal: bolus

nursing considerations: insulin

- first, always check current glucose level

- second, check diet order and patients oral intake tolerance

- what is onset of action of insulin

- type of insulin

- peak

- how will i know if my pt. develops hypoglycemia?

- is pt. NPO?

- nursing interventions for hypoglycemia

insulin: high alert medication

always have another nurse double check your insulin (type and dose) before administering

what kind of needle to administer insulin?

only use insulin syringe: 50 units or 100 units

what is important about injection sites?

- rotate to prevent lipodystrophy

- fastest absorption is from abdomen, to arm, thigh and buttock

nursing peals r/t to insulin administration

- insulin is a protein and thus affected by extremes in temperature. avoid temp extremes.

- room temperature OK for vial that is currently in use

- store extra insulin in the refrigerator

- gently roll prefilled syringes before administering

timing is crucial for insulin

- rapid-acting has onset of 15 min and should be given 0-15 min before meals (lispro, novolog)

- short-acting has onset of 30-60 min and should be given 30-45 min before meals (regular)

basal insulin

- no peak

- levemir & lantus

- often given at bedtime

why do type 1 DM pt's use long-acting basal or intermediate-acting (background) insulin?

to maintain blood glucose levels in b/w meals & overnight

what happens w/o 24-hour background insulin for ppl with type 1 DM?

more prone to developing diabetic ketoacidosis

what do you do for patients who want to use only one or two injections per day?

short- or rapid-acting insulin is mixed with intermediate-acting insulin in the same syringe

what to remember when mixing insulins

- wash hands

- gently rotate NPH bottle

- wipe tops of both vials with alcohol, draw air into syringe for TOTAL dose of insulin

- inject air for NPH dose into NPH vial first and remove syringe from vial

- inject air equal to regular insulin dose in regular insulin vial

- withdraw regular insulin dose

- then withdraw NPH dose adding to the regular insulin already in the syringe

complications of insulin

1. allergy

2. lipodystrophy

3. hypoglycemia

allergy to insulin

- a true insulin allergy is rare

- it is manifested by a systemic response with urticaria and possibly anaphylactic shock.

- zinc or protamine, used as preservatives in the insulin, and the latex or rubber stoppers on the vials have been implicated in allergic reactions`

lipodystrophy

- abnormal distribution of fat

- local inflammatory reactions to insulin may occur, such as itching, erythema, and burning sensation around the injection site

- rotate injection sites

hypoglycemia

- < 70

- caused by too much insulin or not eating after insulin

- ANS activated

clinical manifestations of hypoglycemia

- confusion

- irritability

- diaphoresis

- tremors

- hunger

- weakness

- visual disturbances

- difficulty speaking

- palpitations/anxiety

- pallor

- loss of consciousness, coma, death

nursing actions for hypoglycemia

- symptoms in DM client? Check a blood sugar

- if monitoring equipment not available, treatment should be initiated

hypoglycemia treatment

- finger stick blood sugar

- rule of 15

- FSBS in 15 min; then eat regular meal

- if still < 70, repeat and when glucose stable give additional food

Rule of 15 (hypoglycemia)

- 15g simple CHO (juice, soda, 3 glucose tabs)

- avoid sugars w/ fat (candy bar; delays absorption)

- 15 gms of CHO increase BS 50 mg/dL

what do you do if hypoglycemic pt. is unresponsive or unable to swallow?r

- iM glucagon

- D50 IV push

dawn phenomenon

- hyperglycemia upon awakening

- very common in growing years

- predawn (2-3 am) blood glucose = high

dawn phenomenon treatment

- increase bedtime insulin or adjust timing of insulin

- pt. eating high glycemic snack before bed and needs to find something else

somogyi effect

- hyperglycemia upon awakening

- rebound effect r/t too much insulin on board at night

- predawn (2-3 am) blood glucose = < 70

somogyi effect treatment

- eat a snack before bed

- decrease nighttime insulin

diabetes: exercise

- doesn't have to be vigorous

- properly fitting footwear

- make adjustments in insulin dose and food intake to compensate for extensive planned and spontaneous activity after glucose monitoring

when is the best timing for exercise?

after meals when blood glucose is rising

what to do if before exercise, glucose is < 100 ?

- eat 10-15 g CHO snack and retest in 15-30 min

- do not exercise if < 100

what to do if before exercise, glucose is > 250?

vigorous activity should be avoided, especially in type 1 and if ketones present

hyperglycemia

- emotional and physical stress can result in hyperglycemia

- stressors may evoke counterregulatory hormone response including minor illnesses such as flu and URI

- body requires extra energy to deal with illness- intake and meds IMPORTANT

what to do if decreased intake of glucose?

continue oral hypoglycemics and/or insulin and supplement food with CHO-containing fluids such as soup, juices, regular decaf soft drinks

hyperglycemia complications

- diabetic ketoacidosis (DKA)

- HHNS

DKA causes

- infection

- illness

- inadequate insulin dose

- undiagnosed type 1 diabetes

- poor self management

- neglect

DKA clinical manifestations

- dehydration

- poor skin turgor

- dry mucous membranes

- tachycardia

- orthostatic hypotension

- skin dry and loose; eyes soft and sunken

- abdominal pain, anorexia, N/V

- lethargy, weakness early

- kussmaul respirations

- sweet, fruit breath odor

DKA labs

- BG level > 250

- blood pH < 7.3

- serum bicarbonate level < 16

- moderate to high ketone levels in urine or serum

DKA treatment and nursing action

- ensure patent airway: O2 as needed

- monitor

- establish IV access; begin fluid resuscitation

- continuous regular insulin drip 0.1 U/kg/hr and titrate as needed

- K+ replace as needed

what do you need to monitor with DKA?

- IV fluids

- insulin drip

- VS

- LOC,

- cardiac rhythm

- urine output

- breath sounds

- glucose and K+

what do you give IV for DKA?

- NaCl 0.45 or 0.9%

- add 5-10% dextrose when BG level approaches 250

why is it important to prevent rapid drops in serum glucose?

- avoid cerebral edema

- a blood glucose reduction of 36 to 54 mg/dL (2 to 3 mmol/L) per hour will avoid complications

K+ replacement for DKA

insulin allows water and potassium to enter the cell along with glucose and can lead to a depletion of vascular volume and hypokalemia; therefore, monitor the patient's fluid balance and potassium levels

HHNS causes

- acute illness or new diagnosis type II DM

- massive hyperglycemia

- fewer symptoms lead to higher glucose levels (>600 mg/dL)

HHNS

hyperosmolar hyperglycemic nonketotic syndrome

HHNS clinical manifestations

• higher blood glucose levels increase serum osmolality

• produce more severe neurologic manifestations, such as somnolence, coma, seizures, hemiparesis, and aphasia

• ketone bodies are absent or minimal in both blood and urine

why is HHNS dangerous?

because HHS produces fewer symptoms in the earlier stages, blood glucose levels can climb quite high before the problem is recognized