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metabolic and endocrine systems Flashcards

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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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16
Q

medical conditions that may cause low bone mass

A
  • cushing’s syndrome
  • osteomalacia
  • hyperthyroidism
  • hyperparathyroidism
  • celiac
  • RA
  • renal failiure
  • hypogonadism
  • osteogenesis imperfecta
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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
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18
Q

osteopetrosis

A
  • conditions characterized by impaired osteoclast function causing bone to become thickened but fragile
  • inherited condition
  • s/s vary widely
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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
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20
Q

osteoporosis

A
  • t-score -2.5 SD or lower
  • severe is -2.5 SD or lower w/ one or more related fractures
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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
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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
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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
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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
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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
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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
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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
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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
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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
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30
Q

testes

A
  • in scrotum btw upper thughs
  • secrete androgens (including testosterone) - regulate changes associated with sexual development and support production of sperm
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
100
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

NPTE (32 decks)

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