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endocrine system
network of various glands that synthesize & release hormones, which travel thru the bld to cells & organs for regulation
5 functions of the endocrine system
differentiation of reproductive & CNS of developing fetus
stim of sequential growth & development during childhood & adolescence
coordination of malee & female reproductive systems
maintenance of optimal intl environment thruought the lifespan
irritation of corrrective & adaptive responses when emergency demands occur
endocrine patholgoy may be due to ___ or ___ in the hypothalamus, pituitary, or other glands
inflammation; tumor
anatomic changes of the endocrine glands due to age
pituitary: decr weight by 80 y/o, decr bld flow
thyroid: gland shrinks, fibrosis
parathyroid: gland shrinks, fibrosis, no change in PTH levels
adrenals: fibrosis, no change in cortisol levels
reproductive glands: physiological effects on cardiovascular & skeletal systems
hormonal changes of the endocrine system due to age
menopause in women, decr GH
endocrine dysfunction NMS s/s
proximal muscle weakness, atrophy, myalgia, fatigue that doesn’t go away w/ rest, rheumatic-like s/s (joint pain), carpal tunnel, synovial fluid changes, DM, spondyloarthropathy, OA, osteoporosis, osteonecrosis, hand stiffness, pseudogout
endocrine dysfunction systemic s/s
excessive/delayed growth, polydipsia, polyuria, mental changes (nervousness, confusion, depression); changes in hair, skin pigmentation, body fat fistribution, VSs (elevated temp, pulse, BP); heart palpitations, incr perspiration, dehydration/excessive retention of body water, Kussmaul respirations (deep rpid breathing)
always be on alert for pts w/ bilat ___ ___, atypical ___, or adhesive capsulitis (DM)
carpal tunnel; RA
ant lobe of pituitary gland (adenohypophysis)
produces & releases hormones (GH, ACTH, TSH, FSH, LH, PRL); most affected by pituitary disorders
post lobe of pituitary gland (neurophypophysis)
stores & releases hormones (ADH, oxytocin from hypothalamus)
hyperpituitarism
oversecretion of 1+ hormones typically caused by benign tumors (pituitary adenoma) → excessive GH (acromegaly, gigantism), ACTH (Cushing disease), TSH (hyperthyroidism), PRL (amenorrhea/galactorrhea/gynecomstia)
pituitary tumors will also produce symptoms as they expand w/n the skull, such as…
visual field abnormalities, headaches, somnolence
hypopituitarism
undersecretion of 1+ hormones typically caused by hypophysectomy, nonsecreting pituitary tumors, postpartum hemorrhage, reversible functional disorders (starvation, anorexia, severe anemia, GI disorders) → insufficient GH (dwarfism), ACTH (hypoglycemia, anorexia, nausea, abdominal pain), TSH (fatigue, lethargy, cold sensitivity, menstrual disturbance), gonadal failure (2ndary amenorrhea, impotence, infertility, decr libido, absent 2ndary sex characteristics in children)
gigantism
enlarged tumor in normal tissue → hypersecr of GH → abrupt overgrowth of long bones before epiphyseal plates close → up to 9 ft height, incr IGF-1 & mortality, decr conscious/viscual acuitty, falling PR, rising BP, meningitis s/s
treatment: hypophysectomy, drugs, radiation, decr QOL, no coughing/sneezing/nose blowing
acromegaly
enlarged tumor in normal tissue → hypersecr of GH → slow incr bone thickness, soft tissue hypertrophy after epiphyseal plates close → coarse facial features & pronathism (thick ears, nose, tongue, hands), headache, diplopia, blindness, lethargy, myopathy, decr exercise tolerance, OA, chondrocalcinosis, CTS, backpain, incr mortality, weakness, change in ROM
treatment: decr QOL, hypophysectomy, drugs (statins for joint pain), radiation
orthopedic considerations of acromegaly
arthritis in hands & spine, osteophytes/bone spurs & incr joint space from thick cartilage, stenosis & chondrocalcinosis, bilat CTS, back pain (large osteophytes along ALL)
role of PT for acromegaly
joint mobilization, soft tissue ROM, muscle strengthening, functional skills & ADL training
thyroid gland
secretes hormones that act on nearly all body tissues, affecting multiple systems (nails, hair, skin, eyes, GI, respiratory, heart, bld vessels, nerves, bone, muscle; regulated by hypothalamus-pituitary feedback controls, intrinsic regulator
EX: thyroxine (T4), triiodothyronine (T3), calcitonin
hypothalamus-pituitary feedback
positive feedback where hypothalamus senses decr T3 & T4 → release TRH → tells pituitary to send TSH to thyroid → release more T3 & T4
negative feedback where hypothalamus senses incr T3 & T4 → tells ant pituitary to decr TSH & hypothalamus to decr TRH
hyperthyroidism
hypersec of thyroid hormones (thyrotoxicosis) → incr body metabolism → goiter → Grave’s disease → thyroid storm → CNS (tremors, hyperkinesis, nervousness, emotional lability, weakness/atrophy, incr DTR, fatigue), CV (tachycardia, palpitations, arrhythmias, weak respiratory muscles, low BP, HF), MS (weakness, fatigue, atrophy, chronic periarthritis, myasthenias gravis), integumentary (capillary dilation, heat intolerance, nail changes, hair loss), ocular (exophthalmos, eye muscle weakness, light sensitivity, lid tremor), GI (weight loss w/ incr appetite, incr peristalsis, N/V/D, dysphagia), GU (polyuria, amenorrhea, femaile infertility) s/s
treatment: antithyroid meds if under 18 y/o, radioactive iodine, surgery, prognosis is good but requires lifelong folowup after remission
goiter
lack of iodine → accumulation of thyroglobulin → enlargment of thyroid, inflammation, tumors → pressure on trachea, esophagus → dyspnea, dysphagia, hoarseness, carotid a. occlusion; usually in developping countries where iodine is deficient in diet but prevented w/ iodized salt in US/Canada
type 1 hyperthyroidism
hormone deficient
type 2 hyperthyroidism
homone resistant
Grave’s disease
hyperthyroidism autoimmune disease that incr T4 production; affects women more than men (4:1) b/n 20-40 y/o
thyroid storm
potentially fatal hyperthyroidism → high fever, severe tachycardia, delirium, dehydration, AMS
hypothyroidism
undersecr of thyroid hormones → slow body metabolism, pseudogout (early) → CNS (slow speech, hoarseness, slow mental functions, fatigue, headache, cerebellar ataxia, anxiety, depression), CV (bradycardia, CHF, poor peripheral circulation/pale/cold skin, cold intolerance, HTN, severe atherosclerosis, angina, incr BP, cardiomyopathy), MS (prox weakness, myalgia, trigger points, stiffness, CTS, decr DTR, edema, back pain, incr bone density, decr bone formation/resorption), integumentary (myxedema, thick/cool/dry/scaly skin, carotenosis, thin hair, cold intolerance, edema, poor healing), hematologic (anemia, easy bruising), GI (anorexia, constipation, weight gain, poor protein metabolism, delated glucose uptake), GU (infertility, menstrual irregularity, menorrhagia), respiratory (dyspnea, respiratory muscle weakness) systems s/s
treatment: synthetic thyroid hormone, good prognosis
type 1 hypothyroidism
hormone deficient, 95% of ppl, TSH elevated
type 2 hypothyroidism
hormone resistant; usually pituitary problem, low TSH
PT role in hypothyroidism
caution w/ manual techniques bc of fragile skin, poor exercise tolerance bc of cardiac s/s & thyroid hormone dosage (should start low & slow)
Hashimoto’s thyroiditis
genetic autoimmune disease → thyroid gland destruction bc of lymphocytes & antithyroid antibodies → TSH elevation → painless, symmetric/asymmetric goiter → pressure on surrounding structures; affects women 10x more frequently than men at 30-50 y/o
treatment: meds to suppress TSH
adrenal cortex & medulla are major players in the body’s response to ___
stress
adrenal cortex
outer adrenal glands that secrete mineralocorticoids (aldosterone), glucocorticoids (cortisol), androgens (sex hormones)
adrenal medulla
inner adrenal glands derived from neural tissue that secrete epinephrine & norepinephrine → vascular tone, heart, nervous system, glucose metabolism
adrenal primary insufficiency/Addison’s disease
acute/chronic disorder of insufficient cortisol & aldosterone → hypoglycemia, liver glycogen deficiency, anorexia, N/V, depression, bronzed/tanned skin (naturally light skin) or slate grey skin (naturally darker skin) on extensor surfaces, hypotension, dehydration, decr CO, arrhythmias & hypokalemia, cardiac arrest, poor coordination, poor exercise tolerance initially; uncommon but more in women more than men at 40-60 y/o, surgery, pergnancy, trauma, infection
treatment: replace fluids, electrolytes, glucose, cortisol; synthetic corticosteroids & mineralcorticoids; can be fatal if untreated
___ therapy is a contraindication for Addison’s disease/primary adrenal primary insufficiency due to…
aquatic; demand for cortisol (water affects diffusion of electrolytes), steroid-induced psychosis bc of synthetic meds
secondary adrenal insufficiency
hypothalamic/pituitary tumors, hypophysectomy, hypopituitarism, rapid corticosteroid w/drawal, long-term exogenous use of corticosteroids → insufficient cortisol & aldosterone → athralgias, myalgias, tendon calcification
treatment: synthetic corticosteroids & mineralocorticoids
adrenocortical hyperfunction
hypersecr of glucocorticoids, mineralocorticoids, androgens → persistent hyperglycemia (steroid diabetes), protein tissue wasting (weakness, fragile capillaries, osteoporosis), K+ depletion (hypokalemia, arrhythmias, renal disorders), Na/H2O retention (edema), HTN (L ventricular hypertrophy, CHF, CVA), abnormal fat distribution (moon face, Buffalo hump, stretch marks), incr infection risk & poor wound healing, incr androgen production (hirsutism, acne), mental changes (memory loss, poor concentration, depression,steroid psychosis)
EX: Cushing syndrome (excess gluco), Conn syndrome/aldosteronism (excess aldosterone), adrenal hyperplasia (androgenital syndrome)
treatment: restore hormone balance, pituitary irradiation, drug therapy, surgery, high-protein diet, lifelong glucosteroid replacement, prognosis dependent on cortisol levels control
obesity
multifactorial disease w/ complex interactions b/n lifestyle (sedentary, hyperglycemic diet), environment (hx of sexual abuse, socioeconomic status, EDs, lack of sleep, stress), and genetics (hypothyroidism, PCOS, Prader-Willi Syndrome) → imbalance b/n energy intake/expenditure → excessive accumulation of fat in the body → metabolic syndrome, type 2 DM, liver diseases, OA, sleep apnea, atherosclerosis, HTN, stroke, asthma, cancer, menstrual disorders, infertility, lymphedema, impair mobility, premature death; most significant contributor to ill health & preventable death, 2nd to smoking, numerous chronic diseases, early mortality, early morbidity
treatment: weight loss, meds, surgery, behavior/lifestyle changes, good prognosis w/ significant lifestyle changes
BMI & classification
current gold standard measurement for obesity but can be inaccurate; obesity measurement shifting towards waist circumference or waist-to-hip ratio
overweight, incr risk of death & disability BMI >/25
obese BMI >/ 30
adipose cell theory
some ppl have inherently excessive fat cells (hyperplasia) & larger fat cells (hypertrophy)
microbial theory
intestinal microorganisms → incr fat retention
metabolic syndrome
must have all characteristics
abdominal adiposity (waist >40 in men or >35 in women), high triglycerides (>150 mg/dL), low HDLs (<40 in men or <50 in women), high bld sugar (>100 mg/dL), high BP (>130/85 mmHg)
preventions for obesity
physical activity, nutrition education, positive social environments
PT role in treating obesity
primary prevention (appropriate energy balance to avoid weight gain), 2ndary prevention (decr severity/duration of existing conditions), and tertiary prevention (limit sequential chronic health conditions)
potential exercise consequences for pts w/ obesity
angina pectoris/MI, excessive incr in BP, aggravation of degenerative arthritis, ligamentous injuries, falls injury, excessive sweating, skin disorders, chafing, hypohydration, decr bld circulation, heat stroke/exhaustion
PT considerations for pts w/ obesity
pt education on body composition b/n adipose & muscle mass; back pain, joint pain (knee & hand); mobility/balance in single-leg stance, physical activity/ambulation difficulty, post-op complications (respiratory, integumentary, cardio), post-bariatric surgery (vitamin & mineral deficiencies → change in wound healing, neuro s/s)
diabetes mellitus (DM)
group of endocrine/metabolic diseases from defects in insulin secr, action, high cortisol/stress, lack of sleep, depression, FMHx → chronic systemic disorder of hyperglycemia → disruption of metabolism of carbs, fats, proteins → long-term damage to eyes, kidneys, nerves, heart, bld vessels; leading cause of blindness & renal failure in adults; common in non-white Americans (90% = type 2, 10% = type 1)
type 1 DM
hyperglycemic cell-mediated autoimmune destruction of beta cells → decr insulin, decr utilization of glucose, incr fat mobilization, impaired protein utilization → polyuria, polydipsia, polyphagia, weight loss, recurrent blurred vision, ketonuria, weakness, fatigue, dizziness; evidence of autoimmune process in the islet cells & genetic markers; prone to ketoacidosis; requires eogenous insulin; less common than type 2 DM
type 2 DM
hyperglycemic condition of difficulty utilizing insulin, meds preventing hyperglycemia, obesity, sedentarism, >45 y/o, hx of gestational diabetes, PCOS, hx of vascular disease, HTN, smoking → combo of cellular insulin resistance & inadequate insulin secr → polyuria, polydipsia, recurrent blurred vision, weakness, fatigue, dizziness; often asymptomatic; control w/ diet, exercise, oral hypoglycemic agents
glucose regulation glands
pancreas/islets of langerhand: glucagon, insulin, somatostatin, polypeptide
adrenal gland: epinephrine (stims glycogenolysis to incr bld glucose), glucocorticoids (incr bld glucose by sending AAs to liver)
ant pituitary: ACTH (incr bld glucose) & GH (limits fat storage, favors fat catabolism, incr glucose)
thyroid: T3 & T4 incr/decr bld glucose levels
hypoglycemia onset & mood
rapid; labile, irritable, nervous, weepy
hyperglycemia onset & mood
gradual; lethargic (slow, lacking energy)
complications of diabetes
hyperglycemia, fat accumulation, hyperostosis in spine, arthritis, osteoporosis, pressure injuries, cognitive decline, macrovascular (accelerated atherosclerosis), microvascular (retina blindness, glomerular kidney failure, vasa nervorum neuropathy)
diagnosis of diabetes
fasting plasma glucose test, oral glucose tolerance test, hemoglobin A1C test, s/s of hyperglycemia, blood/urine glucose, ketone abnormalities
casual [plasma glucose] >/ 200 mg/dL, fasting plasma glucose (FPG) >/126 mg/dL after no caloric intake for 8+ hours, 2-hour post-load glucose >/ 200 mg/dL during oral glucose tolerance test, A1C >/ 6.5%
PT considerations for pts w/ diabetes
glucose before & after exercise, high incidence of injuries, resistance exercise has the biggest effect on glycemic control, hypoglycemia s/s (pale, sweaty, goosebumps, tachycardic, palpitations, nervousness, weakness, sakiness, hunger, headache, blurred vision, slurred speech, numbness, confusion), worsening hyperglycemia, MI, arrhythmia, excessive rise in BP during exercise, post-exercise orthostasis, retinal hemorrhage or incr proteinuria, degenerative joint disease, orthopedic neuropathy injury
pts can have symptoms of hypoclycemia when glucose ___ quickly, even if the level is still elevated → keep easy administration of ___
drops; sugar
metabolism
physical & chemical processes that allow cells to utilize food to continually rebuild body cells & transform food into energy; anabolic (tissue-building) & catabolic (energy-producing) phases
osteoporosis
signs of decr bone density (osteopenia) → chronic, progressive disease characterized by low bone mass, impaired bone quality, decr bone strength, enhanced risk of fractures, loss of height, severe kyphosis, back pain, vertebral compression fx; common metabolic bone disease; incidence incr as life expectancy incr; common in postmenopausal women (estrogen deficiency), 50+ y/o, caucasion/asian, north european ancestry, prolonged inactivity/immobilization, depression, lactose intolerance, excess intake of alcohol/tobacco/caffeine, amenorrhea, testosterone deficiency, low BMI
treatment: exercises that optimally load the spine in neutral/ext postures (avoid flex)
primary osteoporosis
most common osteoporosis associated w/ age-related physiologic changes
secondary osteoporosis
loss of bone density due to diseases, medications, other conditions
bone strength depends on bone ___ & ___
density (how many bone cells p/mm2); quality (health of bone cells)
bone mineral density (BMD)
meshwork of Ca2+, PO4, minerals of bony tissue
peak bone mass is achieved in the ___ decade of life
3rd (if low peak, OP & fx are liekly)
disruption of osteoblastic & osteoblastic activity lead to bone ___
loss
___ stimuli may be the only stim capable of inducing modeling in mature bone
mechanical (muscle pulling on bone, activity is important)
paget disease/ostitis deformans
incr bone resorption by unrestrained osteoclasts, excessive & disorganized formation of new bone by osteoblasts → bone marrow replaced by vascular/fbrous tissue → weak, enlarged bones → deformity, fx, arthritis, pain, headache, myalgia, OA, femur pain, kyphoscoliosis, bowing, coxa varus, vertebral compression, incr CO, HF, confusion, fatigue, dizziness; 2nd most common metabolic bone disease after osteoporosis in older men
PT implications for paget disease
vague, diffuse aching pain, diffuse headaches, hearing loss/tinnitus, incontinence, diplopia, swallowing difficulties, dysarthria → comm findings to physician if undiagnosed; consider poor joint mechanics during multi-dimensional exercise (Ex-Rx: strengthing, strengthening, endurance, aerobics, balance, coordination), post-op complications (hemorrhage, infection, pathologic fx, delayed union); manage deformities via orthotics
upper GI
mouth → esophagus → stomach → duodenum; ingestion/digestion
lower GI
small intestine → large intestine; absorption of H2O & electrolytes
GI dysfunction s/s
N/V/D, anorexia, constipation, dysphagia, achalasia, heartburn, abdominal pain, GI bleeding (hematemesis, meena, hematochezia), fecal incontinence, malaise, fatigue, fever, night sweats, pallor, diaphoresis, dizziness; w/ strenuous exercise: cramps, belching, heartburn, N/V, diarrhea
age-related GI changes begin before ___ y/o
50 y/o
GI system oral changes due to aging
tooth enamel & dentin wear, tooth decay & loss, decr taste buds, decr sense of smell, depressed apetite, decr salivation
upper GI system changes due to aging
decr stomach acid → iron malabsorption, small bowel bacterial overgrowth, B12 deficiency; decr pancreatic secretions
lower GI system changes due to aging
prolonged transit time/decr neurotransmitters & receptors, constipation, less diverse microbiata, pro-inflammatory state
gastroesophageal reflux disease (GERD)
consequences from reflux of gastric contents into esophagus accompanied by failure of anatomic & physiologic mechanisms to protect the esophagus → esophagitis, strictures, barrett esophagus, gastric cancer, heartburn, belching, N/V, painful swallowing; common & chronic problem; can occur w/o visible damage to esophagus (non-erosive GERD); incr incidence w/ age, decr pressure of lower esophageal sphincter, or alteration in esophageal acid clearance
factors that incr GERD s/s
chocolate, peppermint, fatty foods, citrus, spicy foods, garlic, onions, coffee, carbonated drinks, alcohol, caffeine, obesity, smoking/nicotine, hiatal hernia, meds (morphine, diazepam, Ca2+ blockers, nitrates, aspirin, NSAIDs, dopamine, theophylline, tricyclic antidepressants, estrogen), nasogastric intubation, chronic diseases, 3rd trimester pregnancy
3 factors that keep the esophagus healthy
anatomic barriers b/n stomach & esophagus (LES impaired by low pressure or hiatal hernia), saliva & alkaline secr to clear acid, stomach acidity & acid volume
complications of GERD
esophagitis (necrosis of epithelial lining), strictures (narrow esophagus), barrett esophagus (precancerous change in cells), adenocarcinoma
GERD symptoms worsen w/ ___ ___, exercise (but still helpful)
lying down
PT implications for GERD
treatment usually includes meds & lifestyle mods; remain upright 3+ hours after meals; weight loss & elevation if obese pts; avoid meals before exercise; supine or incline positioning; prevent aspiration