Download Diabetes - Disorder metabolism characterized by hyperglycemia

Diabetes
- Disorder metabolism characterized by hyperglycemia
- Polyuria, polydipsia, polyphasia
- Cardinal signs/symptoms: polyuria, polydipsia, polyphasia, weight loss, fatigue and general weakness,
ketoacidosis, increased visual blurring, neuropathic complications, tendency to infection, poor wound healing
- Screening:
 Elevated waist circumference (40 in/102cm MALE, >35 in/88 cm FEMALE),
 triglyercides >150, HDL male < 40mg/dL <50 female,
 HTN SBP > 120 and/or DBP > 85,
 elevated resting glucose level > 100mg/dL and/or pharmacological treatment,
 history interview,
 HTN, dyslipidemia, obesity,
 history impaired glucose tolerance,
 history vascular disease,
 polycysctic ovarian syndrome,
 delivery of baby greater than 9lbs,
 sedentary lifestyle,
 gestational diabetes,
 ethnic origin (African American, Latinos, Native American, Asian American, pacific islander)
- Diagnostic assessment:
 blood glucose stick (self monitoring),
 fasting blood sugar,
 glucose tolerance test,
 glycosylated hemoglobin (A1C—average of the individual fasting glucose over 3 month period/glucose
control),
 urine ketone levels
Type 1:
 IDDM, juvenile onset
 Hyperglycemia caused by absolute deficiency of insulin production, secretion beta cells, normal is 70110mg/dL
 Prone to ketoacidosis and metabolic derangements
 Cell mediated autoimmune destruction, slow or rapid at any age and genetic
 Risk factors: presence of type 1 and first degree relative
 Managing: take insulin to survive, dosage varies depending on age/level of compliance/severity (how
brittle diabetes is)
Type 2:
 NIDDM, adult onset
 Endogenous insulin present, but cellular resistance to insulin action
 Abnormal secretory response by insulin, relative insulin deficiency, obesity, controlled with diet, exercise
and oral hypoglycemic agents
 Risk factors: family history, ethnic origin, obesity over 45, history of gestational diabetes, impaired
glucose tolerance test, hypertension greater than 140/90, HDL <35mg/dL, triglycerides >250mg/dL
 Managing: beings with diet and daily exercise, oral med may be prescribed, insulin may be added or
substituted if oral meds don’t work effectively
Pathogensis
 Insulin function impaired because circulating glucose is not taken up or removed and accumulates in the
blood
 Adipose tissue, skeletal and cardiac muscle are affected.
 3 major problems without insulin:
o decrease utilization of glucose: new glucose has not be deposited in liver, liver synthesis more
glucose and releases into general circulation increasing already elevated glucose level),
o increase fat mobilization: formation of ketones, ketones are measured in blood and urine to indicate
presence of DM, interfere with acid/base balance by producing hydrogen ions, person can develop
metabolic acidosis from low pH),
o impaired protein utilization: transport of amino acids cell requires insulin, increase in protein
catabolism, protein loss hampers inflammatory process which leads to poor wound healing)
- In an attempt to restore balance:
 kidney excretes excess glucose resulting in glucosuria
 ketones excreted excess fluid loss
 sodium eliminated, depletion for further acidosis
- Fat primary source of energy:
 body lipid level can rise to 5x normal amount which can promote vessel diseases
 can lead to artherosclerosis and cardiovascular complications
- Micro angioplasty
1. long standing diabetes
2. glycosylation of proteins
3. protein deposits in basement membrane
4. thickened leaky blood vessels
5. exudation and ischemia
6. organ damage
Control:
- Control regulation blood glucose based on balance of insulin food and activity
 Blood glucose monitoring, appropriate use meds, regular physical activity, meal planning,
attention to relevant medical and psychosocial factors
- Family and patient education
- Diet; foods for both fast and slow glucose conversion
- Insulin injection is timed so it works when it has the most glucose it can handle
- Weight reduction will increase sensitivity of receptors
- Skipped meals may result in hypoglycemia
- Reckless ingestion result in hyperglycemia
- Exercise:
 begins once patient is in good control,
 promote weight loss/relax/decreases stress,
 improve insulin receptor sensitivity,
 improves glucose tolerance,
 decreases risk for heart and PVD,
 thins capillary membranes,
 emphasis on duration aerobic activities/stretching
- Prescription: best determined using signs and symptoms
- General criteria:
 Aerobic: Karvonen’s formula, duration 20-30 minutes with 5-10 warm up cool down, frequency
4-7 days a week or every other day
 Resistance: 8-10 rep max weight, 1 set to 3 sets
Exercise precautions: exercise takes up glucose without aid of insulin, hypoglycemia danger
- Type: proceed with CHO ingestion, work out with a friend, carry hard candy/juice or glucagon tablets,
pay attention to symptoms
Absolute contraindications to exercise:
- ingesting alcohol 3 hours prior to exercise
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hypoglycemia (symptoms include: <70, shakiness, pale skin, dizziness, behavior changes, sweating,
clumsy jerking movement, hunger, seizure, headache, tingling sensation around mouth)
hyperglycemia (>300 with ketones—ketones with one or more symptoms require immediate treatment—
SOB, nausea and vomiting, fruity breath, very dry mouth)
Long-term effects
- Precautions to exercise:
 blindness,
 kidney disease (diabetic neuropathy is most common cause of ESRD),
 heart disease and stroke,
 nerve disease and amputations,
 impotence,
 neuromuscular skeletal problems,
 syndrome of limited joint mobility
- frequently with T1
- painless/stiffness of finger joints
- flexion contractures
- severity correlated to duration of disease
- paraesthesias
- vascular insufficiency
- flexor tenosynovitis
 adhesive capsulitis
 chronic progressive degeneration
- sharocot arthroplasty (tarsal/TMT most commonly involved)
 spine
- diffuse idiopathic skeletal hyperostosis (DISH)
 osteoporosis develops within first 5 years of onset: more common IDDM
 ulceration
- changes in pressure and gait
- fat atrophy, muscle weakness
- diabetic foot ulcers
- more common on heel and metatarsal heads
 infection
 CRPS
 Vascular dysfunction
 Arthrosclerosis
 Neuropathy (motor and peripheral)
- avoid weight lifting, breath holding, high aerobic intensity exercise
Prevention
- applies to foot/skin care
- inspect feet daily
- inspect for deformities: sharcot or claw toes
- dry scaly skin
- hygiene: oral, eye evaluation, MD visit
- foot hygiene:
 wash in temped water
 thoroughly dry
 nail and callus care by podiatrist
 select comfortable shoes
Prognosis
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depends on proper interaction between:
 food
 insulin to lower blood glucose
 activity/ exercise
can be fatal or can cause permanent disabilities
Endocrine System
- endocrine cells
- granular secretory cells that release secretion into extracellular fluid
- chemicals released may only affect close/adjacent cells or cells throughout the body
- 5 general functions:
 Differentiation - reproductive and CNS of fetus
 Coordination - male and female reproductive systems
 stimulation of sequential growth - growth and development in childhood and adolescence
 maintenance - optimal internal environment through life span
 initiation - corrective and adaptive responses in emergency demands occur
- hypothalamus controls:
 function of endocrine organs by neural and hormonal pathways
 integrates nervous and endocrine system
 exerts hormonal control
- 3 methods of hypothalamic control
 secretion of regulatory hormones to control anterior pituitary
 control of sympathetic output to adrenal medulla
 production of ADH and oxytocin
Anterior pituitary (adenohypophysis)
- hypothalamic control by RH and IH
 trophic (stimulating hormones):
- ACTH
- TSH
- LH
- FSH
 effector hormones
- GH
- PRL
 affect adrenal cortex, thyroid and gonads
Posterior pituitary (neurohypophysis)
- provoke secretion of two effector hormones:
 ADH (vasopressin)
- stimulus is rise in electrolyte (osmolality) in blood
- fall in BP
- controls body fluids, decrease amount of water loss at kidneys
- causes vasoconstriction of peripheral blood vessels raising BP
 Oxytocin
Thyroid gland
- secretes iodinated thyroid hormones
 T3, T4
- necessary for normal growth and development
- elevate oxygen and energy consumption
- increase heart rate and contractility
- increase sensitivity to sympathetic stimulation
- stimulation of RBCs
- accelerate turn over of mineral and bone
Parathyroid gland (secretes PTH)
- regulates calcium and phosphate metabolism
- stimulate calcium reabsorption and phosphate from bone
- reabsorption calcium and excretion of phosphate by kidneys
- combined action with vitD
Endocrine pancreas
- produce glucagon from alpha cells: releases stored glucose to raise blood sugar
- produce insulin from beta cells: facilitates glucose transport, storage, protein synthesis and free fatty acid
uptake
Adrenal cortex
- mineralocorticoids
 aldosterone: regulates Na reabsorption and K secretion to regulate BP
 stimulated by angiotensin II
- glucocorticoids
 cortisol: accelerates glucose synthesis and glycogen formation, anti-inflammatory effect
- sex steroids
 androgens converts to estrogens
Adrenal medulla
- produce epinephrine and norepinephrine
- mobilize glycogen reserves and breakdown glucose
- stored fats broken down
- glycogen break down in liver
- heart rate and contractility increase
Signs and symptoms of endocrine disease
- develops as a result of dysfunction of releasing trophic or effector hormones or when defects occur in
target tissue
Specific endocrine disorders
- pituitary gland
 anterior lobe:
1. hyperpituitarism (tumors)
- gigantism: overgrowth of long bones, children
- acromegaly: increase both thickness, adults
- management: removal, drugs, radiation
2. hypopituitarism (panhypopituitarism)
- short stature, delayed growth & puberty, ACTH deficiency,
sexual/reproductive disorders
- management: removal of causative factor, replacement
 posterior lobe:
1. hypersecretion
- excessive release of ADH: water intoxication from fluid retention, hyponutrimia, CNS
dysfunction from brain swelling
- management: correct Na imbalance and underlying cause
2. hyposecretion
- diabetes insipidus: ADH deficiency,
- kidney fail to reabsorb water
- large amounts of dilute urine
- polydipsia, dehydration, constipation
- management: exogenous replacement of ADH
- thyroid gland
1. hypothyroidism
- congenital (cretinism) abnormal growth/development
- myxedema (adults) slow body metabolism, lethargy, subacute swelling, dry skin, weak,
bradycardia
- management: correct deficiency, manage symptoms
2. hyperthyroidism
- thyrotoxicosis (graves disease T4): tachycardia, restless, excitable, weight loss,
exophthalmos, goiter, periarticular arthritis, myopathy
- management: drugs, radioactive iodine, surgery
- parathyroid gland
1. hypoparathyroidism
- increased bone resorption= bone damage
- hypercalcemia
- kidney damage= nephrocalcinosis
- management: removal, drugs
2. hyperparathyroidism
- decreased bone resorption
- hypokalcemia: neuromuscular irritability
- management: elevate calcium levels pharmacologically
- adrenal gland
1. hypo function of the adrenal cortex- Addison’s disease
- decrease cortisol= decrease in gluconeogenesis= weakness, exhaustion, anorexia, weight loss,
dehydration
- decrease aldosterone= increase Na excretion, dehydration, hypotension and decrease CO
- management: drugs
2. hyper function of the adrenal cortex- Cushing’s disease
- hypercortisolism, excessive breakdown of protein and lipid reserve, impaired glucose
metabolism
- weakness, buffalo hump, round face, osteoporosis, excessive hairiness
- management: correct imbalance
Neuroendocrine theory of aging
- changes that may be associated with aging
1. altered biological activity of hormones
2. altered circulating level of hormones
3. altered secretory responses of endocrine glands
4. altered metabolism of hormones
5. loss of circadian control of hormone release
Metabolic System
- metabolic rate can be increased by: exercise, increased digestive action following food ingestion, elevated
body temperature
- homeostasis
o maintaining the body’s chemical and physical balance
- metabolic disorders
- functions of bone
o rigid internal support for trunk and extremities
o attachment sites for soft tissue structures
o protect nervous system and visceral organs
o primary storage – calcium, phosphate, sodium, and magnesium
o hosts – hemopoietic bone marrow
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primary influences on bone remodeling
o primary influences on process
 parathyroid hormone, calcitonin, cortisol, GH, TH, and sex hormones
metabolic bone disease
o Paget’s disease
Osteoporosis
o A group of disorders which result in a reduction of bone mass per unit of bone volume
o Most common metabolic bone disease
o Primary risk factors (female, heredity, hormonal status, sedentary, smoking, meds, ETOH,
nutrition, ethnicity)
o Primary osteoporosis – postmenopausal osteoporosis (most common); senile or involutional
osteoporosis (associated with aging); idiopathic osteoporosis
o Secondary osteoporosis – associated with other disorders (Malabsorption syndrome)
o Clinical manifestations: LBP and Fx; Postural changes (thoracic kyphosis)
o Dx: thinning or cortical bone and reduction in the number and size of the trabeculae of cancellous
(trabecular) bone; DEXA (dual-emission X-ray absorptiometry is gold standard)
o Tx: best Tx is prevention – no cure
Osteomalacia
o A generalized bone condition in which insufficient mineralization results
o Softening of bone without loss of bone matrix
o Sometimes referred to as adult form of rickets
o Two primary causes: insufficient intestinal calcium absorption and increased renal phosphorus
losses
o Risk factors: old age, residence in cold geographic area, vit D deficiency, long-term use of meds,
gastrectomy or intestinal malabsorption
o Pathogenesis:
 Low calcium and phosphate (ossification does not proceed normally)
 Vitamin D deficiency (disrupts mineralization)
 Pseudofracture occur (concave side of long bones, ischial and pubic rami, ribs and scapula)
 Mechanical stress points allowing true fractures to develop
Cardiovascular System
- Consists of heart, arterial system, venous system, capillaries
- Low pressure pulmonary circuit and high pressure systemic circulation
- Closed system (output of right and left heart must be equal overtime for effective functioning)
- Cardinal signs and symptoms:
o Chest, neck, arm, and/or jaw pain
o Palpitations (irregular heartbeats)
o Dyspnea (SOB)
o Cardiac syncope (fainting and light-headedness)
o Fatigue (provoked by minimal exertion)
o Cough (typically associated with pulmonary conditions)
o Cyanosis
 Bluish lips, nail beds, fingers, toes
 Inadequate oxygenation levels
o Peripheral edema (hallmark of right ventricular failure)
o Claudication
 Leg pain and cramping
 PVD, CAD
 Pitting edema and claudication = vascular disease
- Aging
o Arterial walls stiffen
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o Aorta dilated and elongated (aneurysms become more frequent)
o Changes in functional capacity with exercise (oxygen uptake, HR, CO)
Cardiac diseases
o Ischemic heart disease
 Coronary arteries carry oxygen to the myocardium
 When these arteries are narrowed or blocked the heart muscle supplied by that artery
becomes ischemic, injured, and infarction may result
 Major disorders:
 Ischemic heart disease (IHD)
 Coronary heart disease (CHD)
 Coronary artery disease (CAD)
Arteriosclerosis
o A group of diseases that cause thickening and loss of elasticity of the arterial walls (“hardening of
the arteries”)
o Arteriosclerosis can be divided into three types:
 Atherosclerosis
 Plaques of fatty deposits form in the intima
 Monckeberg’s arteriosclerosis
 Involving the middle layer of the arteries
 Destructions of muscle and elastic fibers and formation of calcium deposits
 Arteriolosclerosis
 Thickening of the walls of the small arteries (arterioles)
Pathogenesis
o Injury permits the infiltration of macromolecules (especially cholesterol) from blood through the
damaged endothelium to the underlying smooth muscle cells
o Naked collagen acts like fly-paper for platelets, causing them to aggregate at the site of the injury
and plug up the wound
o Once they adhere, platelets release chemicals that alter the structure of the blood vessel wall
 A small erosion in the wall can end up a swollen mound of platelets, muscle cells, and
fibrous clots (coronary thrombosis)
o Obstructs the flow of blood through the vessel
Types of Angina
o Chronic stable angina
 Also known as exertional angina
 Occurs at a predictable level of physical activity or emotional stress
 Ceases with rest or nitroglycerin
o Unstable angina
 Unpredictable and not related to the usual demand for myocardial oxygen
 It is a symptom of disease progression
o Prinzmetal’s or vasospastic angina is due to coronary artery spasm and is likely to occur in the first
few hours of rising
 Occurs at rest and is often relieved with minor activity
Myocardial infarction
o The zone of infarction is the area of myocardium that was completely deprived of oxygen resulting
in cell death
o The zone of hypoxic injury immediately surrounds the area of infarction and will recover if blood
flow is restored quickly
o The adjacent zone of ischemia is usually reversible
Right heart failure
o Edema is early sign but heart failure can be present without edema
o Fluid is retained
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Pressoceptors of the body detect decreased volume because heart is failing
Kidney then retains fluid so a greater volume can be ejected to peripheral tissues
(compounds problems)
 Fluid accumulates leading to dependent edema, can back up into lunges and venous system
 JVD
 Hepatomegaly
Left heart failure
o Causes of pulmonary edema
o Dyspnea
 Exertional
 Paroxysmal nocturnal dyspnea – awakening with feeling of suffocation
 Orthopnea – sleeping in a lazyboy
o Inadequate CO leads to decreased peripheral blood flow to skeletal mm (hypoxia, fatigue)
o Sleep and rest disturbance aggravates fatigue
o Muscle atrophy
o Daytime upright posture decreases blood flow to kidney resulting in oliguria
 Na+ and water are retained adding to load
 Kidney secretes renin which indirectly increases aldosterone from adrenal cortex
 Aldosterone acts on the kidney
o Nocturia
Cardiomyopathy classifications and clinical manifestations
o Dilated – fatigue and weakness with normal or low BP
o Hypertrophic – frequently asymptomatic, with sudden death being a presenting sign, dyspnea is
common
o Restrictive – decreased CO leading to high intravascular pressure and signs of CHF