Type 1 Diabetes
Type 1 Diabetes
¨Type 1 Diabetes
- cells that produce insulin are destroyed
- results in insulin dependence
- commonly detected before 30
Type 2 Diabetes
¨Type 2 Diabetes
- blood glucose levels rise due to
1) Lack of insulin production
2) Insufficient insulin action (resistant cells)
- commonly detected after 40
- effects > 90%
- eventually leads to β-cell failure
(resulting in insulin dependence)
Gestational Diabetes
Glucose intolerance during pregnancy
Placental hormones contributes to insulin resistance
High risk: glycosuria, family history, marked obesity
Native Americans, African Americans, Hispanics and Pacific Islanders
What is Diabetes?
a group of diseases characterized by high levels of blood glucose resulting from defects in insulin production, insulin action, or both.
¨Complications :
- Stroke
- Heart attack
- Kidney disease
- Eye Disease
- Nerve Damage
Body does not make or properly use insulin:
lno insulin production
linsufficient insulin production
lresistance to insulin’s effects
No insulin to move glucose from blood into cells:
lhigh blood glucose means:
hfuel loss. cells starve
hshort and long-term complications
Type 1 Diabetes
In the case of type 1 diabetes, insulin levels are grossly deficient. Thus type 1 diabetes is invariably treated with insulin
Genetic susceptibility
§Glycosuria
Fat breakdown
DKA
·auto immune disorder
·insulin-producing cells destroyed
·daily insulin replacement necessary
·age of onset:
usually childhood, young adulthood
·most prevalent type of diabetes in children and adolescents
ONSET:relatively quick
SYMPTOMS:
increased urination
tiredness
weight loss
increased thirst
hunger
blurred vision
CAUSE:
uncertain, likely both genetic and environmental factors
Type 2 Diabetes
Type 2 diabetes is frequently associated with obesity. Serum insulin levels are normal or elevated, so this is a disease of insulin resistance. A number of treatment options may be employed
§Resistance
Decreased production
Generally no fat breakdown
§HHNS
·Insulin resistance – first step
·Age at onset:
·Most common in adults
·Increasingly common in children
·overweight
.inactivity
Gestational Diabetes
Glucose intolerance during pregnancy
Placental hormones contributes to insulin resistance
High risk: glycosuria, family history, marked obesity
Native Americans, African Americans, Hispanics and Pacific Islanders
Women of average risk tested between 24-28 weeks of gestation
Goals for glucose levels during pregnancy are 105 or less before meals; 130 or less after meals
Will have greater risk of developing Type 2 DM later in life if weight not controlled
How Diabetes Occurs?
In a healthy individual,food that a body has digested is broken down into a type of sugar which is then converted into an energy source. This happens when the sugar enters the bloodstream and increases the amount of sugar in the blood. The body will then be alerted of the rise in sugar and send a signal to the pancreas, which in turn will release the chemical insulin. Insulin works by deceasing the level of sugar and allows the sugar to leave the blood and enter cells, which in turn acts as a fuel
Education
Almost a third of all diabetics do not know they have the disease until they are at a critical stage.
nType I symptoms can be instant and obvious, while the problem with Type II is that the symptoms can take a long while to appear.
nPeople who are at risk, such as those who are severely overweight or have a family history of diabetes, should be aware of the signs that coincide with diabetes.
nOnce people know what the warning symptoms are they can prevent or delay the onset of diabetes. Simple adjustments to a persons way of life,like diet and exercise,can make a huge difference.
Diabetic awareness,either preventative or after diagnoses care,can be achieved through educational booklets
ONSET:
in children variable timeframe
SYMPTOMS:( Clinical Manifestations)
Polyuria
Polydipsia
Polyphagia
Fatigue, tingling or numbness in hands, slow healing wounds and recurrent infections
some children show no symptoms at diagnosis
Diagnostic findings
Fasting plasma glucose—125 mg/dL
Random sugar >200mg/dL
According to text, OGTT and IV glucose tolerance test no longer used routinely—see latest guidelines
Diabetes is Managed,
But it Does Not Go Away.
GOAL:
To maintain target blood glucose
Diabetes Management
§Nutritional
§Exercise(30-45 minutes/day)
§Monitoring
§Pharmacologic
§Education
Dietary Management
§Carbohydrate 45-65% total daily calories
§Protein-15-20% total daily calories
§Fats—less than 30% total calories, saturated fats only 10% of total calories
§Fiber—(25-30 gm)lowers cholesterol; soluble—legumes, oats, fruits Insoluble—whole grain breads, cereals and some vegetables. Both increase satiety. Slowing absorption time seems to lower glycemic index.
§Consistent, well-balanced small meals several times per day
§Exchange system or counting carbohydrates
Exercise and Diabetes
§Exercise increases uptake of glucose by muscles and improves utilization, alters lipid levels, increases HDL and decreases TG and TC
§If on insulin, eat 15g snack before beginning
§Check BS before, during and after exercising if the exercise is prolonged
§Avoid trauma to the feet
§Avoid pounding activities that could cause vitreous hemorrhage
§Caution if CAD
§Baseline stress test may be indicated (especially in those older than 30 and with 2 or more risk factors for CAD)
Ketones
§Check in pregnancy
§During illness
§If BS >240
Acute Complications of
Diabetes
Hypoglycemia—50-60 or less
DKA
HHNS
Hypoglycemia
§Caused by too much insulin or oral agents, too little food or excessive physical activity
§Surge in epinephrine and norepinephrine results in sweating, tremors, tachycardia, palpitations, nervousness and hunger
CNS effects—inability to concentrate, headache, lightheadedness, confusion, memory problems, slurred speech, incoordination, double vision, seizures and even loss of consciousness
§Related to autonomic neuropathy
§Will not experience the sympathetic surge—with sweating, shakiness, HA, etc.
Treatment for hypoglycemia
§2-3 tsp. of sugar or honey
§6-10 hard candies
§4-6oz. of fruit juice or soda
§3-4 commercially prepared glucose tablets
§Recheck BS 15 minutes, same s/s, repeat treatment. After improvement, then cheese and crackers or milk.
§Extreme situations, give glucagon. (can cause n/v). D50W.
Diabetic Ketoacidosis
§Clinical features are:
1.Hyperglycemia
2.Dehydration and electrolyte loss
3.acidosis
§Three main causes: illness, undiagnosed and untreated and decreased insulin
§Other causes: patient error, intentional skipping of insulin
Presentation of DKA
§3 P’s
§Orthostatic hypotension
§Ketosis
§GI s/s
§Acetone breath
§hyperventilation
Long term complications of Diabetes
§Increasing numbers of deaths from cardiovascular and renal complications
§Renal (microvascular) disease is more common in type 1 diabetics
§Cardiovascular disease (macrovascular) complications are more common in type 2 diabetics
Microvascular complications-§Coronary artery disease
§Cerebrovascular disease
§Peripheral arterial disease
Management of Macrovascular Diseases-
§Modify/reduce risk factors
§Meds for hypertension and hyperlipidemia
§Smoking cessation
§Control of blood sugars which will help reduce TG
Microvascular Complications--Retinopathy-
§Diabetic retinopathy-leading cause of blindness in those 20-74
§Blood vessel changes—worst case scenario, proliferative retinopathy. Also an increased incidence of cataracts and glaucoma in diabetics.
§Need regular eye exams
§Control BP, control BS and cessation of smoking can help
Microvascular complications-Nephropathy-
§Accounts for 50% of patients with ESRD
§Earliest clinical sign of nephropathy is microalbuminuria.
§Warrants frequent periodic monitoring for microalbuminuria—if exceeds 30mg/24h on two consecutive random urines, need 24h urine sample
§Medical management: control BP (ACE or ARB)
§Tx of UTIs
§Avoid nephrotoxic agents, contrast dyes
§Low sodium diet
§Low protein diet
§Tight glycemic controle
Nephropathy-
§May require dialysis
§May have co-existent retinopathy
§Kidney transplantation—success now 75-80% for 5 years
§Pancreas transplantation may also be performed at time of kidney transplantation
Neuropathies-
§Group of diseases that affect all types of nerves.
§Includes peripheral, autonomic and spinal nerves.
§Prevalence increases with duration of the disease and degree of glycemic control
§Capillary basement membrane thickening and capillary closure may be present.
§May be demyelination of the nerves, nerve conduction is disrupted.
§Two most common types of neuropathy are: sensorimotor polyneuropathy and autonomic neuropathy.
Peripheral neuropathy-
§Manifestations:paresthesias, burning sensations, numbness, decrease in proprioception.
§Charcot foot can result from abnormal weight distribution on joints secondary to lack of proprioception
Autonomic Neuropathies-
§Cardiac, gastrointestinal and renal systems
§Cardiac—myocardial ischemia may be painless
§GI—delayed gastric emptying with early satiety, nausea, bloating, diarrhea or constipation
§Urinary retention—decreased sensation of bladder, neurogenic bladder
§No longer feel shakiness, sweating, nervousness and palpitations associated with hypoglycemia
§The inability to detect warning signs of hypoglycemia can place the patient at very high risk
The Guide is Focused on Doing!
Diabetes Management
Proactive> keep juggling the balls
Reactive>
Grains, Beans, Starchy Vegetables
•Milk/Yogurt
•Meat & Meat Alternates
•Plate Method Portions
1 slice of bread
•1/2 cup of cooked rice or pasta
•3/4 cup dry (unsweetened) cereal
•4 - 6 crackers
•Beans & Starchy Vegetables (1/2 cup)
•1/2 cup mashed potatoes
•1 small (3 oz.) potatoFruit (1/2 cup)
•1/2 cup canned fruit (light or juice syrup)
•1/4 cup dried fruit
8 oz. milk (cow's, soy or rice)
•6 - 8 oz. yogurt with low-calorie sweetenerVegetables (1/2 cup)
•1/2 cup cooked
•
•
•1-1/2 oz. cheese
•1/4 c. egg substitute
•4 oz. tofu
** equivalent to 1 oz. meat, fish, poultry
•10 peanuts
•2 Tablespoons reduced fat salad dressing
•th2 tsp. peanut butter
•2 Tablespoons reduced fat cream cheese
•1 Tablespoon sour cream
•1 strip bacon
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