metabolic and endocrine systems Flashcards
1
Q
metabolic system
A
- governs chemical and physical changes that take place within body to enable growth and function
- catabolism: organic compounds breaking down
- anabolism: combining simple molecules for tissue growth
1
Q
inherited metabolic disorders
A
- diagnosed in utero via amniocentesis or chorionic villus sampling
- s/s tend to include lethargy, apnea, poor feeding, tachypnea, vomiting, hypoglycemia, urine changes, seizures
- more immediate symptoms = more dangerous disorder
2
Q
phenylketonuria
PKU - amino/organic acid metabolic disorder
A
- intellectual disability w/ behav and cog issues secondary to elevation of serum phenylalanine - excess primarily affects brain
- deficiency in enzyme ohenylalanine hydroxylase - normally converts excessive phenylalanine to tyrosine
- etiology: autosomal recessive, white people
- s/s: within few months of birth; gait disturbances, severe intellectual disability, hyperactivity, psychoses, lighter features, abnormal body odor
- treatment: dietary restriction of phenylalanine throughout lifetime can avoid all manifestations of disease
3
Q
tay-sachs disease
lysosomal storage disorder
A
- absence of deficiency of hexosaminidase A - produces acculmulation of gangliosides (GM2) within brain
- etiology: autosomal recessive, eastern european jewish
- s/s: at 6 MO, miss developmental milestones; continue to deteriorate in motor and cog skills; die by 5 YO
- treatment: no effective treatment; rec genetic testing in high risk populations
4
Q
mitochondrial disorders
A
- over 100 forms - each has different spectrum of disability
- etiology: genetically inherited or spont mutation in DNA -> impaired function of proteins in mitochondria
- s/s: vary depending on disorder; can include loss of muscle coordination, muscle weakness, visual and hearing problems, learning disability, heart, liver, kidney disease, GI disorders, dementia
- treatment: new diagnoses w/ varied treatment to alleviate symptoms and slow progression
5
Q
wilson’s disease
hepatolenticular degeneration
A
- inherited disorder in eastern europeans but can be any group, appears in people < 40 YO and can be in children 4-6 YO
- etiology: autosomal recessive; defect in body’s ability to metabolize copper -> accumulates in brain, liver, cornea, kidny
- s/s: kayser-fleischer rings around iris d/t copper deposits, basal ganglia degenerative changes, hepatitis, ataxic gait; emotional/behav changes, eventual MSK deformity, pathologic fracture, osteomalacia, muscle atrophy, contractures
- treatment: pharm intervention w/ B6 and D-penicillamine to excrete excess copper; prevent hepatic failure
6
Q
rehab for pts with inherited metabolic disorders
A
- awareness of dietary restrictions
- training to prevent deleterious effects from metabolic disease
- facilitate developmental milestones w/in pt tolerance
7
Q
acid-base metabolic disorders
A
- metab regulated by endocrine and NS
- if acid-base balance compromised, can alter metabolic function and cause s/s
8
Q
metabolic alkalosis
A
- increase in bicarbonate accumulation or loss of acids
- pH > 7.45
- etiology: after continuous vomitting, antacid ingestion, diuretic therapy; associated with hypokalemia or nasogastric suctioning
- s/s: nausea, diarrhea, prolonged vomiting, confusion, muscle fasciculations, muscle cramp, hyperexcitability, convulsions; if untreated, comatose, seizures, resp paralysis
- treatment: manage underlying cause, correct electrolyte imbalance, KCl administration
9
Q
metabolic acidosis
A
- accumulation of acids due to acid gain or bicarb loss
- pH < 7.35
- etiology: renal failure, lactic acidosis, starvation, diabetic or alcoholic ketoacidosis, diarrhea, toxins
- s/s: compensatory hyperventilation, vomiting, diarrhea, HA, malaise, hyperkalemia, cardiac arrhythmias; untreated can cause coma and death
- treatment: treat cause, correct imabalnce, administer sodium bicarb
10
Q
rehab considerations for pts with acid-base disorders
A
- recognize high risk populations - renal, CV, pulm disease; burns, fever, sepsis; mech vent; DM; vomiting, diarrhea, enteric drainage
- recognize signs of dehydration in a diabetic pt
- injury prevention during involuntary muscle contractions secondary to metabolic alkalosis
- pts w/ diuretic therapy may be at risk for potassium depletion
- trousseau’s sign during blood pressure - indicates calcium deficiency and early stages of tetany
11
Q
metabolic bone disease
A
- disruption in normal metab w/ skeletal system that houses calcium and phosphorus to continuously balance remodeling of cortical and trabecular bone to optimize structure of skeleton
- disruption of homeostasis - result in deformity, bone loss, frature, softening of bone, arthritis, pain
12
Q
osteomalacia
A
- metabolic condition where bones are soft secondary to calcium or phosphorous deficiency - adequat bone matrix but insufficient calcification in matrix d/t deficiency
- etiology: calcium lost d/t inadequate intestinal absorption and phosphorus lost d/t increase in renal excretion; can also be due to vit D deficiency
- s/s: aching, fatigue, weight loss; myopathy and sensory polyneuropathy w/ periarticular tenderness and pain, thoracic kyphosis deformity; bowing of LEs; struggle with trans and standing
- treatment: underlying etiology, increased nutrition, pharm intervention w/ vit D or phosphate supplements
13
Q
osteoporosis
A
- decrease in bone mass - increases risk of fracture; primarily affects trabecular and cortical bone where rate of bone resorption accelerates while rate of bone formation declines
- declining osteoblast function coupled with loss of calcium and phosphate salts will cause bones to becomes brittle
- etiology: primary - idiopathic, postmenopausal, involutional (senile); secondary - result of another primary conditoin or with meds
- s/s: compression and other spine fractures, low thoracic or lumbar pain, loss of lumbar lordosis, kyphosis, dowager’s hump
- treatment: vitamin and pharmacological intervention, nutrition, assistive and adaptive devices, some surgical intervention
14
Q
paget’s disease
A
- metabolic condition with heightened osteoclast activity - bone formation lacks true structural integrity
- bone appears enlarged but lacks strength d/t high turnover secondary to abnormal osteoclast proliferation
- etiology: genetic and geographical incidence, most common > 50 YO
- s/s: MSK pain w/ bony deformities; common with skull, clavicle, pelvis, femur, spine, and tibia; pain, HA, vertigo, hearing loss, mental deterioration, fatigue, increased cardiac output, HF
- treatment: pharmacological intervention using biphosphates to inhibit bone resporption and improve quality of involved bone; exercise, weight control, cardiac fitness
15
Q
rehab considerations for pts with metabolic bone disease
A
- awareness of signs of compression fracture
- resistance training and endurance training to build bone density and increase strength
- avoid treatments that exacerbate condition or placae pts at risk for fracture
16
Q
medical conditions that may cause low bone mass
A
- cushing’s syndrome
- osteomalacia
- hyperthyroidism
- hyperparathyroidism
- celiac
- RA
- renal failiure
- hypogonadism
- osteogenesis imperfecta
17
Q
osteopenia
A
- low bone mass not severe enough to qualify as osteoporosis
- may not have actual bone loss but naturally lower bone density than established norms
- t-score > -2.5 SD
18
Q
osteopetrosis
A
- conditions characterized by impaired osteoclast function causing bone to become thickened but fragile
- inherited condition
- s/s vary widely
19
Q
bone mineral density
A
- t-score: how many SDs above or below average young healthy adult norms in BMD is
- z-score: how many SDs above/below age and gender adjusted norms BMD is
- non-modifiable risk factors: age, early menopause, h/o fx, slender build, family history, female, Asian or white, sometimes glucotcorticoids
- modifiable: vitamin D and calcium intake, estrogen deficiency, smoking, drinking, caffeine, sedentary
- interventions for children/adolescents: nutrition, regular physical activity, avoid smoking/drinking
- interventions for adults: nutrition - vit D and calcium, regular WB exercises, avoid smoking and drinking, postural education and fall prevention
20
Q
osteoporosis
A
- t-score -2.5 SD or lower
- severe is -2.5 SD or lower w/ one or more related fractures
21
Q
endocrine system
A
- endocrine glands (specialized, ductless) secrete hormones in bloodstrem to travel to signal specific target cells throughout body
- work with NS to regulate metabolism, response to stress, sexual reproduction, BP, water and salt balance
22
Q
endocrine system vs NS
A
- endocrine system
- secreting cells send hormones through blood to signal specific target cells
- hormones diffuse into blood, travel long distances to virtually every area of body
- endocrine effectors consist of virtually all tissues
- regularoty effects slow and long lasting
- nervous system
- neurons secrete NTs to signal nearby cells that have appropriate receptor site
- NTs sent short distances across synapse
- nervous effectors limited to muscle and glandular tissue
- regulatory effects appear rapidly and are often short lived
23
Q
hypothalamus
A
- part of diencephalon below thalamus and cortex
- connects to pituitary gland through infundibular or pituitary stalk
- responsible for regulation of ANS - body temp, appetite, sweating, thirst, sexual behavior, rage, fear, BP, sleep
- affects other endocrine glands through impact on pituitary
24
Q
pituitary gland
A
- normally pea sized, located at base of brain just beneath hypothalamus
- two parts: adenohypophysis (anterior) and neurohypophysis (posteroir)
- considered most important part of endocrine system d/t it releasing hormones that regulate other endocrine glands
- “master gland” influenced by seasonal changes and emotional stress
- secretes endorphins that act on NS and reduce senstivity to pain
- controls ovulation, works as catalyst for testes and ovaries to create sex hormones
25
Q
thyroid gland
A
- on anterior and lateral surfaces of trachea immediately below larynx, shaped like bow tie or butterfly w/ 2 lobes (R and L) joined by an isthmus
- produces thyroxine and triiodothronine - control rate at which cells burn fuel from food
- increased thyroid hormones = increased rate of chemical reactions in body
26
Q
parathyroid glands
A
- 4 found on post surface of thyroid’s lateral lobes
- produce paraythyroid hormone - antagonist to calcitonin, important for maintenance of normal blood levels of calcium and phosphate
- PTH increases reabsorption of calcium and phosphate from bones to blood
- PTH secretion stimulated by hypocalcemia and inhibited by hypercalcemia
- normal calcium levels impacts neuromuscular excitability, normal clotting, and cell membrane permeability
27
Q
adrenal glands
A
- 2 adrenals on top of each kidney - out portion is adrenal cortex and inner is adrenal medulla, each secrete different hormones
- adrenal cortex: corticosteroids that regulate water and sodium balance, body’s response to stress, immune system, sexual development and function, metabolism
- adrenal medulla: epinephrine that increases HR and BP w/ stress
28
Q
pancreas
A
- in upper L quadrant of abdomen from duodenum to spleen
- has exocrine and endocrine tissues
- islets of langerhans: cells that produce hormones in pancreas
- alpha cells - glucagon
- beta cells - insulin
- [above] work in combo to ensure consistent level of glucose in bloodstrem and maintenance of energy stores within body
29
Q
ovaries
A
- provide estrogen and progesterone - contribute to regulation of menstrual cycle and pregnancy
- estrogen secreted by ovarian follicles - develop and maintain female sex characteristics (breast development, cycles)
- progesterone produced by corpus luteum - maintains lining of uterus at level necessary for pregnancy
30
Q
testes
A
- in scrotum btw upper thughs
- secrete androgens (including testosterone) - regulate changes associated with sexual development and support production of sperm
31
Q
steroid hormones
prostaglandins
A
- all cells create prostaglandins from phospholipids of cell membrane
- unique as they do not circulate in blood - instead exert effects only where they are produced
- capable of variety of effects - related to inflammation, pain mechanisms, vasodilation, vasoconstriction, nutrient metabolism, blood clotting
32
Q
amine hormones
catecholamines
A
- include epinephrine, norepinephrine, dopamine - synthesized from chromaffin cells within adrenal medulla
- SMS stimulation releases catecholamines into blood stream
- epi has one of largest effects on SNS - produces fight of flight response, targets CV and metabolic systems
- catecholamines also increase cardiac contraction, blood vessel constriction, activate glycogen breakdown, block insulin secretion, increase metabolic rate, dilation of airways in lungs
33
Q
peptide hormones
insulin
A
- insulin secreted by beta cells of islets of langerhans within pancreas
- released when there is elevation in blood glucose - insulin produces increase in cellular uptake of glucose for metabolism
- insulin stimulates skeletal muscle and liver to store glucose and increase amino acid transport across hepatic, muscle, and adipose tissues
- insulin release affects all body systems w/ primary goal to reduce blood glucose levels
34
Q
growth hormone-releasing hormone
A
- released by: hypothalamus
- target: pituitary gland
- function: increases release of GH
- regulation of secretion: CNS feedback, circulating levels of hormones
35
Q
growth hormone-inhibiting hormone
A
- released by: hypothalamus
- target: pituitary gland
- function: decreases release of GH
- regulation of secretion: CNS feedback, circulating levels of hormones
36
Q
gonadotropin-releasing hormone
A
- released by: hypothalamus
- target: pituitary gland
- function: increases release of luteinizing hormone and follicle-stimulating hormone
- regulation of secretion: CNS feedback, circulating levels of hormones
37
Q
thyrotropin-releasing hormone
A
- released by: hypothalamus
- target: pituitary gland
- function: increases release thyroid-stimulating hormone
- regulation of secretion: CNS feedback, circulating levels of hormones
38
Q
corticotropin-releasing hormone
A
- released by: hypothalamus
- target: pituitary gland
- function: increases release of adrenocorticotropic hormone
- regulation of secretion: CNS feedback, circulating levels of hormones
39
Q
prolactin-releasing hormone
A
- released by: hypothalamus
- target: pituitary gland
- function: stimulates release of prolactin
- regulation of secretion: CNS feedback, circulating levels of hormones
40
Q
prolactin-inhibitory factor; dopamine
A
- released by: hypothalamus
- target: pituitary gland
- function: decreases release of prolactin
- regulation of secretion: CNS feedback, circulating levels of hormones
41
Q
growth hormone
A
- released by: pituitary
- target: bone and muscle
- function: promote growth and development; increase rate of protein synthesis
- regulation of secretion: hypothalamus
42
Q
follicle-stimulating hormone
A
- released by: pituitary
- target: ovaries and testes
- function: promotes follicular development and estrogen creation in female; promotes spermatogenesis in males
- regulation of secretion: hypothalamus
43
Q
luteinizing hormone
A
- released by: pituitary
- target: ovaries and testes
- function: promote ovulation with estrogen/progesterone synthesis from corpus luteum in females; promotes testosterone synthesis in males
- regulation of secretion: hypothalamus
44
Q
thyroid-stimulating hormones
A
- released by: pituitary
- target: thyroid gland
- function: increases synthesis of thyroid hormones T3 and T4
- regulation of secretion: hypothalamus
45
Q
adrenocorticotropic hormone
A
- released by: pituitary
- target: adrenal cortex
- function: increase cortisol sythensis (adrenal steroids)
- regulation of secretion: hypothalamus
46
Q
prolactin
A
- released by: pituitary
- target: mammary glands
- function: allows for process of lactation
- regulation of secretion: hypothalamus
47
Q
oxytocin
A
- released by: pituitary
- target: uterus and mammary glands
- function: increases contraction of uterine muscles; promotes release of milk from mammary glands
- regulation of secretion: nerve impulses from hypothalamus, stretching of cervix, nipple stimulation
48
Q
antidiuretic hormone
A
- released by: pituitary
- target: kidneys
- function: increase water reabsoprtion, conserves water; increase BP through stimulating contraction of muscles in small arteries
- regulation of secretion: decreased water content
49
Q
androgen
A
- released by: adrenal cortex
- target: ovaries and testes
- function: increases masculinization, promotes growth of pubic hair in males and females
- regulation of secretion: influenced by hypothalamic production and release of GnRH and LH
50
Q
aldosterone (mineralocorticoid)
A
- released by: adrenal cortex
- target: kidneys
- function: increases reabsorption of sodium ions by kidneys to blood, increases potassium ion excretion by kidneys into urine
- regulation of secretion: low blood sodium level, high blood potassium level
51
Q
cortisol (glucocorticoid)
A
- released by: adrenal cortex
- target: GI system
- function: influences metabolism of food molecules; anti-inflammatory effect in large amounts
- regulation of secretion: adrenocorticotropic hormone
52
Q
epinephrine
A
- released by: adrenal medulla
- target: CV and metabolic systems
- function: increase HR and force of contraction; increases E production, vasodilation in skeletal muscles
- regulation of secretion: sympathetic impulses from hypothalamus in stress situations
53
Q
norepinephrine
A
- released by: adrenal medulla
- target: CV and metabolic systems
- function: vasoconstriction in skin, viscera, and skeletal muscles
- regulation of secretion: sympathetic impulses from hypothalamus in stress situations
54
Q
estrogen, progesterone
A
- released by: ovaries
- target: uterus and mammary glands
- function: involved in regultaion of female reproduction system and female sexual characteristics
- regulation of secretion: cyclical rise and fall of hormone levels
55
Q
glucagon
A
- released by: pancrease
- target: liver
- function: increases blood glucose by stimulating conversion of glycogen to glucose
- regulation of secretion: hypoglycemia
56
Q
insulin
A
- released by: pancreas
- target: all body systems
- function: decrease blood glucose and increase storage of fat, protein, carbs
- regulation of secretion: hyperglycemia
57
Q
parathormone
A
- released by: parathyroids
- target: bone, kidney, intestinal mucosa
- function: increase blood calcium
- regulation of secretion: hypocalcemia
58
Q
testosterone
A
- released by: testes
- target: pituitary gland
- function: involved in process of spermatogenesis and male sexual characteristics
- regulation of secretion: influenced by pituitary release of LH
59
Q
thyroxine (T4), triiodothyronine (T3)
A
- released by: thyroid
- target: all tissues
- function: involved with normal development, increases cellular level metabolism
- regulation of secretion: thryoid-stimulating hormone
60
Q
calcitonin
A
- released by: thyroid
- target: plasma
- function: increase calcium storage in bone, decreases blood calcium levels
- regulation of secretion: hypercalcemia
61
Q
endocrine system dysfunction general S/S
A
- neuromuscular: muscle weakness, periarthritis, myalgia, arthralgia, stiffness, OA, muscle atrophy, adhesive capsulitis
- systemic: polydipsia, growth dysfunction, skin pigmentation dysfunction, polyuria, increased VS, hair dysfunction, anxiety
62
Q
what causes endocrine system pathology
A
usually hypothalamus or pituitary gland affecting function of other endocrine glands
63
Q
endocrine gland hyperfunction
A
- usually secondary to overstimulation of pituitary gland
- can also occur d/t hyperplasia or neoplasia of gland itself
64
Q
hypofunction of endocrine gland
A
- usually secondary to understimulation of pituitary gland
- also from congenital or acquired disorders
65
Q
hypothalamus dysfunction d/t
A
- hypothalamus tumors (ependymomas)
- inflammatory processes (sarcoidosis)
- sugical transection
- trauma (skull fx)
66
Q
pituitary dysfunction d/t
A
- pituitary tumors (adenomas)
- ischemic necrosis or infarction of pituitary gland
- infiltrative disorders (hemochromatosis - too much iron)
- inflammatory processes (meningitis)
- iatrogenic (irradiation)
67
Q
hypopituitarism
A
- decreased or absent hormonal secretion from ant pituitary gland
- rare, s/s dependent on age and deficit hormones
- short stature (dwarfism), delayed growth and puberty, secual and repro disorders, diabetes insipidus
- treatment based on deficit hormones, usually includes pharm replacement therapy
68
Q
hyperpituitarism
A
- excessive secretion of hormones under pituitary control (usually GH that produces acromegaly)
- disorders and s/s dependent on hormones affected
- gigantism or acromegaly, hisutism, galactorrhea (abnormal lactation in males or female), amenorrhea, infertility, impotence
- treatment is hormone site dependent and can include tumor resection, surgery, radiation therapy, hormone suppression or replacement (if gland is dysfunctional after treatment)
69
Q
rehab considerations for pts with pituitary dysfunction
A
- amb/exercise encouraged within 24 hours of surgery (tumor/gland removal)
- awareness of signs of hypoglycemia
- bilat carpal tunnel syndrome, arthritis, osterophyte formation commeon with hyperpituitarism
- orthostatic hypotension may be present with hypopituitarism
- bilat hemianopsia can occur with hypopit
70
Q
addison’s disease
A
- adrenal dysfunction
- presents w/ hypofunction of adrenal coretx -> decrease in production of cortisol/glucocorticoid and aldosterone/mineralocorticoid
- etiology: adrenal cortex produces insufficient cortisol and aldosterone hormones
- s/s: widespread metabolic dysfunction s/t cortisol deficieny and fluid/electrolyte imbalances s/t aldosterone dysfunction; hypotension, weakness, anorexia, weight loss, altered pigementation; if untreated -> shock and death
- treatment: long-term pharm intervention using synthetic corticosteroids and mineralocorticoids
71
Q
cushing’s syndrome
A
- adrenal dysfunction
- presents w/ hyperfunction of adrenal gland, allowing for excessive cortisol/glucocorticoid production
- etiology: pituitary gland produces excessive adrenocorticotropic hormone (ACTH) w/ subsequent hypercortisolism
- s/s: evlove over years; persistent hyperglycemia, growth failure, truncal obesity, purple abdominal striae, moon face, buffalo hump, weakness, acne, HTN, male gynecomastia; depression, poor concentration, memory loss
- treatment: pharm intervention to block production of hormones, radiation therapy, chemotherapy, sx
72
Q
rehab considerations for pts with adrenal dysfunction
A
- recognize stress/exhaustion and avoid exacerbation
- notify physician w/ any signs of illness or increase intracranial pressure (papilledema) - meds need to be altered
- orthohypo common s/t long term cortisol therapy
- report sleep disturbances to MD
- increased incidence of osteroporosis, bone fx, degenerative myopathy, tendon ruptures, ataxia gait
- delayed wound healing may be common
73
Q
hypothyroidism
A
- decrease levels of thyroid hormones in blood, slowing metabolic processes in body
- s/s fatigue, weakness, decreased HR, weight gain, constipation, delayed puberty, slowed growth and development
- common causes - hashimoto’s thyroiditis, underdeveloped thyroid gland
- treatment: oral thyroid hormone replacement therapy
74
Q
hyperthyroidism
A
- excessive levels of thyroid hormones in blood
- s/s nervousness, excessive sweating, weight loss, increased BP, exopthalmos, myopathy, chronic periarthritis, enlarged thyroid gland
- treatments - pharm intervention, radioactive iodine, surgery
75
Q
graves’ disease
A
- thyroid dysfunction
- most specific cause of hyperthyroidism, most common in women > 20 YO, can also occur in men and any age
- etiology: autoimmune disease, certain antibodies stimulate thyroid gland -> becomes overactive
- s/s: hyperthyroid presentation; classic signs are enlargement of thyroid gland (goiter), heat intolerance, nervousness, weight loss, tremor, palpitations
- treatment: pharm intervention and/or removal of thyroid gland using radiation or surgical intervention
76
Q
postpartum thyroiditis
A
- painless inflammation of thyroid in some women after childbirth
- two phases: initially hyperthyroidism in first 1-4 months after birth, then hypothyroidism 4-8 months after delivery
77
Q
hypothyroidism vs hyperthyroidism
A
- hypo
- depression/anxiety, lethargy, fatiue, HA, slowed speech, slowed mental function, impaired STM
- proximal weakness, carpal tunnel, trigger points, myalgia, increased bone density, cold intolerance, paresthesias
- dyspnea, bradycardia, CHF, respiratory muscle weakness, decreased peripheral circulation, angina, cholesterol increase
- anorexia, constipation, weight gain, decreased absorption of food and glucose
- infertility, irregular menstrual cycle, increased menstrual bleeding
- hyper
- tremors, hyperkinesias, nervousness, increased DTRs, emotional lability, insomnia, weakness, atrophy
- chronic periarthritis, heat intolerance, flushed skin, hyperpigmentation, increased hair loss
- tachycardia, palpitations increased RR, increased BP, arrhythmias
- hypermetabolsim, increased appetite, N/V, diarrhea, dysphagia
- polyuria, infertility, increased first trimester miscarriage, amenorrhea
78
Q
rehab considerations for pts with thyroid dysfunction
A
- regonize exercise capacity and fatigue are typical
- acoid treatments that exacerbate condition - hot aquatic or gym d/t heat intolerance (Graves’)
- avoid CV stress to eliminate secondary complication from hypotension, goiter, graves’
- provide close monitoring of VS
- recognize effects of radioiodine therapy
- recognize rhabdomyolysis risk (hypothyroidism)
79
Q
hypoparathyroidism
A
- d/t hyposecretion or low-level production of parathyroid hormone by pt gland
- s/s hypocalcemia, seizuers, cog deficits, short stature, tetany, muscle pain, cramps
- treatment: elevation in serum calcium through IV calcium, LT includes pharm management and dietary modifications
- decreased bone resorption, hypocalcemia, elevated serum phosphate levels, shortened 4th and 5th metacarpals (psudohypoparathyroidism), compromised breathing d/t intercostal and diaphragm spasms, cardiac arrhythmias and potential HF, increased NM activity that can result in tetany
80
Q
hyperparathyroidism
A
- d/t excessive hormone production by parathyroid gland that leads to disruption of calcium, phosphate, and bone metabolism
- s/s: renal stones and kidney damage, ddepression, memory loss, muscle wasting, bone deformity, myopathy
- treatment: pharm for lowering of serum calcium w/ diuretics or antiresoptive meds, surgical intervention
- increased bone resorption, hypercalcemia, decreased serum phosphate levels, osteitis fibrosa, subperiosteal resorption, arthritis, bone deformity, nephrocalcinosis, renal HTN, renal damage, gout, decreased NM irritability
81
Q
rehab considerations for pts w/ parathyroid dysfunction
A
- be familiar w/ s/s
- recognize s/s of excess or inadequate pharm intervention
- recognize increased risk for fracture and effects for osteogenic synovitis - achilles, triceps, obturator tendons most affected
82
Q
type 1 diabetes mellitus (DM)
insulin-depenent or juvenile DM
A
- pancreas dysfunction - fails to produce enough or any insulin
- normally diagnosed in childhood but can occur at any age
- etiology: unknown, genetic predisposition in combo w/ exposure to viral or environmental trigger -> immune reaction that damages pancreas
- s/s: rapid onset of symptoms, polyphagia, weight loss, ketoacidosis, polyuria, polydipsia, blurred vision, dehydration, fatigue
- treatment: exogenous insulin, nutrition, insulin pumps, no cure, control blood glucose levels
83
Q
type 2 diabetes mellitus
A
- pancreas dysfunction - typically > 45 yo, increase in childhood cases s/t childhood obesity, retain ability to produce some endogenous insulin
- etiology: s/t array of dysfunctions resulting from combination of insulin resistance and inadequate insulin secretion; hyperglycemia when body cannot respond properly to insulin; obesity contributes by increasing insulin resistance
- s/s: relatively same as DM 1 but no ketoacidosis
- treatment: blood glucose control through diet, exercise, oral meds, insulin injections when necessary
84
Q
early signs of hyperglycemia
A
- blood glucose > 180-200 mg/dl
- increased thirst and frequent urination
- ketoacidosis - diabetic coma, ommon in DM 1, life-threatening -> dyspnea, fruity breath odor, dry mouth, nausea, vomiting, confusion, LOC
85
Q
hypoglycemia early symptoms
A
- blood glucose < 70 mg/dl
- hunger, sweating, shaking, dizziness, clumsiness, HA, LOC
- treated with glucose/carb-rich substance - sugar, honey, juice, crackers
86
Q
exercise response and DM
A
- physical/mental stressors elevate blood glucose
- exercise increases blood glucose uptake by muscles w/o impacting insulin levels
- if hypo concern, ingest carb snack before exercise to compensate for inc glucose demands and/or increased insulin absorption
87
Q
T1 vs T2 DM
A
- T1
- < 25 YO onset
- abrupt onset
- 5-10% all cases
- etiology: destruction of islets of langerhans cells s/t autoimmune or virus
- very little to no insulin production
- ketoacidosis can occur
- insulin injections, exercise, diet
- T2
- older than 45 onset
- gradual onset
- 90-95% all cases
- etiology: resistance at insulin receptor sites usually s/t obesity, ethnic prevalence
- variable insulin production
- ketoacidosis rare
- weight loss, oral insulin, exercise, diet
88
Q
rehab considerations for pts with DM
A
- risk for peripheral neuropathies, small vessel angiopathy, tissue ischemia and ulceration, impaired wound healing, tissue necrosis, amputation
- recognize acute metabolic changes
- recognize signs of sudden hypoglycemia and necessary treatment
- focus on management of insulin intake, diet, physical activty
- provide education for proper skin care, shoe eval, shoe wear
89
Q
gestational diabetes
A
- increase in insulin resistance and blood glucose levels w/ pregnancy in last trimester
- no known etiology but likely hormones that assist fetus growth and development lead to insulin resistance
- most return to normal glucose metabolism after pregnancy but if > 6 weeks after birth -> dif form of DM
- babies born after GD have increased glucose levels and increased risk for macrosomia (larger than average size) - difficult delivery and more dangerous; may also exp breathing difficulties, jaundice, hypoglycemia after birth
- children more likely to experience insulin resistance, obesity, behavior and health issues -> hyperactivity disorders, delays in gross and fine motor skills
90
Q
fasting plasma glucose
A
- blood glucose testing at least 8 hours after last food or drink
- (+) for DM if blodo glucose level is > 125 mg/dl
- normal is < 100 mg/dl
need 2 occasions of testing to confirm DM diagnosis
91
Q
oral glucose tolerance test
A
- 2 hours after ingestion of sugary drink
- (+) if BG is 200 mg/dl or greater
- normal < 140 mg/dl
92
Q
A1c testing
A
- blood test based on attachment of glucose to hemoglobin - measures average blood glucose level over last 2-3 months
- (+) if A1c is 6.5% or greater
- normal is < 5.7%
93
Q
in males, the hypothalamus produces
A
- hypothalamus produces gonadotropin-releasing hormone (GnRH) and pituitary responds by producing luteinizing hormone (LH) and follicle-stimulating hormone (FSH)
- leydig cells of testes respond and produce testosterone
- occurs daily
94
Q
in female, hypothalamus produces
A
- hypothalamus produces gonadotropin-releasing hormone (GnRH) and pituitary responds by producing luteinizing hormone (LH) and follicle-stimulating hormone (FSH)
- in ovaries, LH acts on theca and interstitial cells to produce progestins and androgens
- FSH acts on granulosa cells to stimulate precursor steroids to estrogen
95
Q
male hypogonadism
A
- primary hypogonadism: deficiency of testosterone s/t failure of testes to respond to LH and FSH (Kleinfelter’s syndrome)
- secondary hypogonadism: failure of hypothalamus or pituitary to produce hormones to stimulate production of testosterone ->
- before puberty: sparse body hair, underdeveloped skeletal muscles, long arms and legs s/t delay in closure of epiphyseal plates
- in adults: decreased libido, ED, infertiltiy, decreased cog skills, mood changes, sleep disturbances
- treatment: hormone replacemnt
96
Q
female hypogonadism
A
- primary hypogonadism: when gonad does not produce amount of sex steroid sufficient to suppress secretion of LH and FSH at normal levels (Turner syndrome)
- secondary hypogonadism: failure of hypothalamus or pituitary to produce hormones to stimulate production of estrogen ->
- before puberty: gonadal dysgenesis, short stature, failure to progress through puberty or primary amenorrhea, premature gonadal failure
- in adults: secondary amenorrhea
- treatment: hormone replacement therapy
97
Q
bone mineral regulating agents
endocrine management
A
- action: indications: enhance and maximize bone mass and prevent bone loss or rate of bone resoroption; estrogens, calcium and vit D, biphosphates, calcitonin, anabolic agents
- indications: paget’s disease, osteoporosis, hyperparathyroidism, rickets, hypoparathyroidism, osteomalacia
- side effects: agent dependent, GI distress, dysphagia, anorexia, bone pain, cardiac arrhythmias
- PT implications: risk for fracture and side effects from drug therapy; use amb and WB activities to stimulate bone formation
- examples: estrogens - premarin; calcium and vit D; tums, calderol; biphosphates; calcitonin
98
Q
hormone replacement agents
endocrine management
A
- actions: restore normal endocrine function when endogenous production of particular hormone is deficient or absent
- indications: decrease in endogenous hormone secretion
- side effects: vary by replacement used
- PT implications: s/s of hormone deficit and s/s of hormone therapy
99
Q
hyperfunction agents
endocrine management
A
- action: manage hyperactive endocrine function to allow for inhibition of hormone function; accomplished through (-) feedback loops or hormone antagonists
- indications: hyperactive or excessive endocrine function, excessive hormone levels
- side effects: variable
