disease ch 2
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metabolic and nutritional disorders
physiological process that allows cells to transform food into energy and continually rebuild body cells
energy producing phase of metabolism, breaking down of large food, molecules into smaller ones
tissue building phase, body converts small molecules into larger ones
60% of an adult's body weight is water
Children and lean body types have higher water content since fat weighs more than water
the critical component of metabolism is
fluid and electrolyte balance
tests and treatment:
blood and urine test
epithelial tissue and rentinal function
normal metabolism, cell growth and blood formation
wound healing, burn healing, collagen and extracellular tissue that binds teeth, bones and capillaries
failure for normal bone calcification (rickets)
formation of red blood cells, assists with vitamin K, antioxidant, protects tissue from free radicals
prothrombin and clotting
bones, teeth, hair,skin, testes, lives, and muscles
body aches,muscle fatigues
excess of body fat, generally 20% above ideal weight
hypothalamus, genetic predisposition, abnormal absorption of nutrients, hormones, environmental factors, activity level, learned patterns of eating, stress, and emotional eating
poor prognosis for correction of obesity, less than 30% succeed in losing 20 lbs and only 50% of them maintain the loss over a long period of time
results from excessive calorie intake and inadequate expenditure of energy. There is a genetic/family/environment factors especially parent to child along with psychological factors such as stress which leads to over eating
children and adolescent obesity has doubled in the past 20 years
lifestyle management-reducing calories while increasing physical activity. Techniques include: behavior modifications, hypnosis, or bariatric surgery for morbid obesity (gastroplasty: lap band or gastric bypass)
chronic disease of absolute or relative insulin deficiency or resistance which disturbs carbohydrate, protein, and fat metabolism
syndrome characterized by hyperglycemia resulting from absolute or relative impairment in insulin secretion and or insulin reaction
leading cause of death by disease in the US.
contributes to 50% of myocardial infractions and 75% strokes, renal failure, and peripheral vascular disease.
leading cause of blindness.
DM affects 6% of the population in the US, half of which are undiagnosed.
greater occurrence in females and increases with age.
Type 2 DM accounts for 90% of all cases
accepted to be an autoimmune disease, triggered by a nonspecific viral infection that inflames the beta cells of the pancreas
affects an estimated 5% of the population
some cases is IDDM are viral in origin
heredity strongly influences most diabetics
diabetes type I
failure to release insulin and ineffectively transport through the body
usually higher in children then adults
unknown cause since most do not have any evidence of autoimmunity or failure to produce insulin
type 2-insulin is produced but ineffectively transported throughout the body to support body weight and chemical components
usually with ketoacidosis-fatigue, polyuria, dehydration, polydipsia, dry mucous membranes, poor skin tugor and unexplained weight loss.
long term effects: retinopathy, nephropathy, atherosclerosis(obesity, fat), peripheral and autonomic neuropathy(loss of feeling in hands, feet)
immune-mediated or idiopathic
children and adolescents with type I DM rapidly develop ketoacidosis while adults with type ! only experience modest hypoglycemia unless there is an infection or other stressors.
pancreas produces little or no insulin, therefore a person in dependent on insulin being added to their sustem.
neuropathy occursin 1/3 of patients.
can result in ESRD(end stage renal disease)
immune-mediated diabetes caused:
cell-mediated destruction of pancreatic beta-cells
no know cause
no evidence of autoimmunity
in the past this was referred to as juvenile-onset, ketotic, or brittle diabetres
usually occurs before age 30
patient is usually thin
requires exogenous(external source) insulin and dietary management
insulin is produced but has a problem attaching to things
related with obesity
lack of physical activity
history of gestational diabetes, hypertension, strong family history, older than 45, high cholesterol, and ethnicities: black, hispanic,pacific islander, asian american and native americans.
person is not dependent on insulin being added to their system and is treated with diest, exercise, and oral drugs
insulin is resistant but ketoacidosis is rare
neuropathy occurs in less the 1/3 of patients
can lead to ESRD
referred to as maturity-onset, nonketotic or stable diabetes
usually occurs in obese adults after age 40, now more in children
treat with diet/exercise
beta cells release insulin, but receptors are insulin-resistant and glucose transport is variable and ineffective
oral antidiabetic drugs stimulate endogenous insulin production and increase sensitivity
other specific types
- genetic defect
- endorinopathies, or exposure to certain drugs or chemicals
gestational diabetes mellitus
occurs during pregnancy and returns to normal after delivery of the child
effective treatment to normalize blood glucose and decrease complications through insulin use, diet and exercise.
long term complications include transplant or dialysis for renal failure aned vascular surgery for large-vessel disease(atherosclerosis)
autonomic neuropathy: postural hypotension, impotence, impaired bladder function, delayed gastric emptying, esophageal dysfunction, constipation, diarrhea, ESRD
large vessel disease leads to atherosclerosis
neuropathy leads to injury to nerves, demyelination(rate nerves react) and schwann cell degeneration
involves sensory and motor peripheral nerves & autonomic nervous system, hyperglycemia(high sugar), ketoacidosis
acidosis due to an excess of ketone bodies, due to break down of fat for energy ketoacidosis
diabetic ketoacidosis or diabetic coma-an acute life-treating complication of uncontrolled diabetes loss of water, potassium, ammonium, and sodium
a primary or secondary disease
diabetes problems occure in:
- cognitive and psychosocial due to: difficulty administering and regulating insulin, fatigue, weakness, weight loss
- loss or reflexes
- flexion contractures
- vision loss
- loss of touch
- decreased sense of pain
- difficulty with temperature
no cognitive imlpairments
- are due to this disorder except if associated with CVA
- aging process
usually involving the lower extremities that develops secondary to peripheral vascular disease
vascular, non-inflammatory retinal disorder that results from interference with the blood supply to the eye
control number of claories and amount of carbohydraes ingested, spacing carbohydrates throughout the day
oral and injectable insulin
control physical activities
facilitates transportation of glucose into cells
diabetic ketoacidosis(diabetic coma)
increased acidity in blood and ketones leads to diabetic coma
no natural insulin
- fruity odor to the breath
hypoglycemic shock caused by overdoes in insulin
decreased in take of food
- excessive exercise:
mrs. x is being seen by OT and PT for outpatient treatment. she has diabetes and finished an exercise session wiwth pt before starting her session with you. after completing (3 sets x 10) pulley exercises for shoulder flexion when you notoice she is sweating quite profusely and her skin is cold and clammy. she states she feels tremulous and nervous. you ask her if she had anything to eat or drink prior or during her pt session; she states that she took her insulin at 8.00 and had a glass of orange juice as she ran out the door because she was running.
these are sign/symptoms of:
diabetic ketoacidosis or insulin shock?
- what should you do?
- stop the exercise and tell the patient to take her insulin
- stop the exercise and ask her what she usually does? offer her some juice and or hard-candy
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