Bone healing, or fracture healing, is a
proliferative physiological process in which the body facilitates
the repair of a bone fracture.
Generally bone fracture treatment consists of a doctor
reducing (pushing) dislocated bones back into place via
relocation with or without anaesthetic, stabilizing their position,
and then waiting for the bone's natural healing process to
occur.
PATHOPHYSIOLOGY
• thyroid hormone secretion leads to
hyperthyroidism
• What you see in this is called: thyrotoxicosis
WHAT DO THYROID HORMONES
AFFECT?
• Metabolism in all body organs
• Stimulate the heart
– heart rate
– stroke volume
– cardiac output
– blood flow
HYPERTHYROIDISM
INCREASED THYROID HORMONES:
• Hypermetabolism
• sympathetic nervous system activity
• Effects protein, lipid and carbohydrate
metabolism
EFFECTS ON PROTEIN METABOLISM
• Protein synthesis and degradation
• More breakdown than buildup
• Leads to loss of protein
• Called negative nitrogen balance
EFFECTS ON GLUCOSE
• Glucose tolerance decreased
• Leads to hyperglycemia
EFFECTS ON FAT METABOLISM
• fat metabolism
• body fat
• appetite
• food intake; food intake does not meet energy
demands
• weight
• nutritional deficiencies with prolonged disease
CAUSES
GRAVES DISEASE:
• Client has a goiter (enlarged thyroid gland (p1484)
• Autoimmune problem
• Antibodies attach to gland causing it to enlarge
• SYMPTOMS:
– exophthalmos (protrusion of the eyes) p1484)
– Pretibial myxedema (dry, waxy swelling of the frontal
surfaces of the lower legs)
•
ADDITIONAL CAUSES OF
HYPERTHYROIDISM
1. TOXIC MULTINODULAR GOITER: multiple thyroid
nodules, milder disease
2. EXOGENOUS HYPERTHYROIDISM: excessive use of
thyroid replacement hormones
3. THYROID STORM: untreated or poorly controlled
hyperthyroidism; life threatening
WHO GETS IT
• Most often women between 20-40 yrs
ASSESSMENT
• Recent wgt loss
• Increased appetite
• Increase in # BM/day
• ****heat intolerance
• Diaphoresis even when temperatures comfortable
for others
• Palpitations/chest pain
• Dyspnea with or without exertion
ASSESSMENT
VISUAL PROBLEMS MAY BE EARLIEST PROBLEM:
• Infiltrative Exophthalmopathy (abnormal eye
appearance or function)
• Blurring/double vision/tiring of eyes
• Increased tears
• Photophobia
• Eyelid retraction(eyelid lag) (p1483)
• Globe lag (eyeball lag) (p1483)
GOITER
• Thyroid gland may be 4 X normal
• Bruits (turbulence from increased blood flow)
heard with stethoscope
CARDIAC PROBLEMS
• systolic BP
• tachycardia
• dysrhythmia
FURTHER SYMPTOMS
• Fine, soft, silky hair
• Smooth, moist skin
• Muscle weakness
• Hyperactive deep tendon reflexes
• Tremors of hands
• Restless, irritable, mood swings
• Decreased attention span
• Fatigued, inability to sleep
LABORATORY ASSESSMENT
IN HYPERTHYROIDISM:
• T3
• T4
• TSH in Graves disease
• Radioactive Thyroid Scan
• Ultrasonography: used to determine goiter or
nodules
• EKG: note tachycardia
DRUG THERAPY
• ***antithyroid drugs: thioamides
– propylthiouracil (PTU)
– methimazole (Tapazole)
– carbimazole (Neo-Mercazole)
• ACTION: blocks thyroid hormone production; takes
time
Need to control cardiac manifestations (tachycardia,
palpitations, diaphoresis, anxiety) until hormone
production reduced: use beta-adrenergic blocking
drugs: propranolol (Inderal, Detensol)
DRUG THERAPY
Iodine preparations:
• Lugol’s Solution
• SSKI (saturated solution of potassium iodide)
• Potassium iodide tablets, solution, and syrup
ACTION:
– decreases blood flow through the thyroid gland
– This reduces the production and release of thyroid
hormone
– Takes about 2 wks for improvement
– Leads to hypothyroidism
DRUG THERAPY
• Lithium Carbonate
• ACTION: inhibits thyroid hormone release
• NOT USED OFTEN BECAUSE OF SIDE EFFECTS:
depressions, diabetes insipidus, tremors, N&V
DRUG THERAPY
RADIOACTIVE IODINE THERAPY:
• Receives RAI in form of oral iodine
• Takes 6-8 Weeks for symptomatic relief
• Additional drug therapy used during this type
of treatment
• Not used on pregnant women
SURGICAL MANAGEMENT
Why use surgery?
• Used to remove large goiter causing tracheal or
esophageal compression
• Used for pts who do not have good response to
antithyroid drugs
TWO TYPES OF SURGERIES:
1. Total thyroidectomy (must take lifelong thyroid
hormone replacement)
2. Subtotal thyroidectomy
PREOPERATIVE CARE
Low weight:
• Hi protein, hi CHO diet for days/weeks before
surgery
PRE-OPERATIVE CARE
1. Antithyroid drugs to suppress function of the
thyroid
2. Iodine prep (Lugols or K iodide solution) to
decrease size and vascularity of gland to minimize
risk of hemorrhage, reduces risk of thyroid storm
during surgery
3. Tachycardia, BP, dysrhythmias must be controlled
preop
PREOPERATIVE TEACHING
• Teach C&DB
• Teach support neck when C&DB
• Support neck when moving reduces strain on
suture line
• Expect hoarseness for few days (endotracheal
tube)
POST-OP THYROIDECTOMY NURSING
CARE
1. VS, I&O, IV
2. Semifowlers
3. Support head
4. Avoid tension on sutures
5. Pain meds, analgesic lozengers
POSTOP THYROIDECTOMY NURSING CARE
• Humidified oxygen, suction
• First fluids: cold/ice, tolerated best, then soft
diet
• Limited talking , hoarseness common
• Assess for voice changes: injury to the
recurrent laryngeal nerve
POSTOP THYROIDECTOMY NURSING CARE
• CHECK FOR
HEMORRHAGE 1st 24 hrs:
• Look behind neck and
sides of neck
• Check for c/o pressure or
fullness at incision site
• Check drain
• REPORT TO MD
• CHECK FOR RESPIRATORY
DISTRESS
• Laryngeal stridor (harsh hi
pitched resp sounds)
• Result of edema of glottis,
hematoma,or tetany
• Trach set/airway/ O2,
suction
• CALL MD for extreme
hoarseness
TETANY
• accidental removal of the parathyroid gland during
surgery can happen
• This disturbs the Ca metabolism
• low blood calcium: see hyper-irritability of the
nerves, spasms of the hands and feet, muscle
twitchings occur, tingling, around
mouth/toes/fingers
• RISK: laryngospasm, airway obstruction
• TREAT: IV calcium gluconate or calcium chloride
POSTOP NURSING CARE
CHECK FOR THYROID STORM: 25% mortality rate
• result of release of TH during surgery
• Observe for fever, tachycardia, systolic hypertension,
agitation leading to seizures, delirium and coma, heart
failure and shock
TREAT:
• Patent airway, cardiac monitor
• Antithyroid drugs IV: PTU, propyl-Thyracil, Tapazole,
sodium iodide solution
• Inderal, Detensol for cardiac symptoms
• Glucocorticoids (hydrocortisone IV)
• Antipyretics and cooling blanket for fever
HYPOTHYROIDISM
Decreased levels
of
Thyroid Hormone
CAUSES
• Cells damaged; no longer function
• Cells might be normal, person doesn’t ingest
enough iodide & tyrosine needed to make
thyroid hormones
SYMPTOMS
• Blood levels of thyroid hormones are low
• Decreased metabolic rate
• Hypothalamus and anterior pituitary gland
make stimulatory hormones (TSH) as
compensation
• Thyroid gland enlarges forming goiter
MYXEDEMA DEVELOPS
• With low metabolism metabolites build up inside the
cells which increases mucous and water leading to
cellular edema
• Edema changes client’s appearance
• Nonpitting edema appears everywhere especially
around the eyes, hands, feet, between shoulder
blades
• Tongue thickens, edema forms in larynx, voice husky
INCIDENCE OF HYPOTHYROIDISM
• 30-60 yrs of age
• Mostly women
ASSESSMENT
• Increased sleeping (14-16 hours daily)
• Generalized weakness
• Anorexia
• Muscle aches
• Paresthesias
• Constipation
• Cold intolerance
• Decreased libido, woman:difficulty becoming
pregnant, changes in menses;men/impotence
ASSESSMENT
• Coarse features
• Edema around eyes and face
• Blank expression
• Thick tongue
• Overall muscle movement is slow
• Lethargic, apathetic, drowsy, poor attention
span, poor memory
LABORATORY ASSESSMENT
• T3
• T4
• TSH
DRUGS THAT IMPAIR THYROID
FUNCTION
• lithium carbonate (Lithane)
• Aminoglutethimide
• Sodium or potassium perchlorate
• Thiocyanates
• cobalt
NURSING DIAGNOSES
NURSING INTERVENTIONS
• EXPECTED OUTCOMES:
– Maintains HR greater than 60/min
– Maintains BP within normal limits
– No dysrhythmia, peripheral edema, neck vein
distension
TREATMENT
LIFELONG THYROID HORMONE REPLACEMENT
• levothyroxine sodium (Synthroid, T4, Eltroxin)
• IMPORTANT: start at low does, to avoid
hypertension, heart failure and MI
• Teach about S&S of hyperthyroidism with
replacement therapy
MYEXEDEMA COMA
• Rare serious complication of untreated
hypothyroidism
• Decreased metabolism causes the heart muscle
to become flabby
• Leads to decreased cardiac output
• Leads to decreased perfusion to brain and other
vital organs
• Leads to tissue and organ failure
• LIFE THREATENING EMERGENCY WITH HIGH
MORTALITY RATE
PROBLEMS SEEN WITH MYXEDEMA
COMA
• Coma
• Respiratory failure
• Hypotension
• Hyponatremia
• Hypothermia
• hypoglycemia
TREATMENT OF MYEXEDEMA COMA
• Patent airway
• Replace fluids with IV NSSS
• Give levothyroxine sodium IV
• Give glucose IV
• Give corticosteroids
• Check temp, BP hourly
• Monitor changes LOC hourly
• Aspiration precautions, keep warm
PARATHYROID DISORDERS
HYPERPARATHYROIDISM
HYPOPARATHYROIDISM
RESPONSIBILITY OF GLANDS
• Maintain calcium and phosphate balance
INCREASED PTH
EFFECTS ON KIDNEY
• acts directly on the kidney causing increased
kidney reabsorption of calcium and increased
phosphate excretion
• Leads to hypercalcemia and
hypophosphatemia
INCREASED PTH
EFFECTS ON BONE
• Increase bone resorption (bone loss of
calcium)
• by decreasing osteoblastic (bone production)
activity and increasing osteoclastic (bone
destruction activity)
• This process releases Ca and phosphate into
the blood and reduces bone density
CHRONIC CALCIUM EXCESS
• Calcium is deposited in soft tissues
CAUSES OF HYPERPARATHYROIDISM
• Tumors
• Trauma
• Radiation
• Vit D deficiency
• Chronic renal failure with hypocalcemia
ASSESSMENT
High levels of PTH:
• Cause renal calculi
• Pathologic fractures
• Osteoporosis
High levels of Calcium:
• Anorexia, N/V, constipation, wgt loss, peptic
ulcers
• Fatigue/lethargy
• Mental confusion, psychosis, coma, death if
serum Ca greater than 12 mg/dL
LABORATORY ASSESSMENT
Serum calcium elevated:
• normal range: 9-10.5mg/dL
Serum phosphate decreased:
• Normal 3.0-4.5mg/dL
Serum parathyroid hormone increased:
• Normal 50-330 pg/ml
NONSURGICAL MANAGEMENT
GOAL: reduce serum calcium levels
• Hydration: IV saline in large volumes
promotes renal excretion of calcium
• Diuretics: furosemide (Lasix, Uritol) - increases
kidney excretion of calcium
INTERVENTIONS
• Assess cardiac function and I&O q2-4 hrs
during hydration therapy
• Continuous cardiac monitoring
• Close monitoring of serum calcium levels
reporting precipitous drops to MD
• Sudden drops may lead to tingling/numbness
in muscles
DRUG THERAPY
PHOSPHATES:
• oral phosphates inhibit bone resorption and
interfere with calcium absorption
• IV only used when serum calcium levels need
rapid lowering
DRUG THERAPY
CALCITONIN:
• Decreases the release of calcium and
increases the kidney excretion of calcium
• Best effect when combined with
glucocorticoids
DRUG THERAPY
CALCIUM CHELATORS:
• Lower calcium levels by binding (chelating) calcium which
reduces the levels of free calcium
FIRST EXAMPLE: mithramycin (cytotoxic agent), one IV dose
can lower serum calcium in 48 hrs
• DANGER: THROMBOCYTOPENIA, increased tendency to
bleed, kidney and liver toxicity
SECOND CALCIUM CHELATOR: penicillamine (Cuprimine,
Pendramine)
SURGICAL REMOVAL OF
PARATHYROID GLAND
• Used to manage hyperparathyroidism
• Surgery similar to that of removal of thyroid
gland
HYPOPARATHYROIDISM
PATHO
• Rare disorder
• Parathyroid function decreased
• Either lack of PTH secretion or lack of
effectiveness of PTH secretion
• End Result: hypocalcemia
Caused by:
• removal of glands during thyroidectomy,
• or hypomagnesemia (seen in alcoholics or chronic
renal disease, or malnutrition); causes
impairment of PTH secretion
ASSESSMENT
• Mild tingling and numbness due to tetany
• Tingling and numbness around the mouth or in the
hands and feet reflect mild to moderate
hypocalcemia
• Severe muscle cramps, carpopedal spasms, and
seizures (with no loss of consciousness or
incontinence), mental changes from irritability to
psychosis reflect a more severe hypocalcemia)
ASSESSMENT
• Positive signs indicating potential tetany
CHVOSTEK’S SIGN: sharp tapping over facial
nerve causes twitching of mouth, nose and
eye
TROUSSEAU’S SIGN: carpopedal spasm induced
by application of BP cuff
LABORATORY ASSESSMENT
• EEG
• CT scan (shows brain cacifications from
chronic hypocalcemia)
• Serum calcium:
• Serum phosphate:
• Serum magnesium:
• Serum vitamin D:
INTERVENTIONS
• CORRECT HYPOCALCEMIA: IV calcium with 10%
solution of calcium chloride or calcium gluconate
over 10-15 minutes;
• then long term oral therapy Calcium 0.5-2G daily
• Oral calcium: OSCAL
Calcium gluconate
Calcium lactate
Calcium carbonate
INTERVENTIONS
CORRECT VITAMIN D DEFICIENCY: large doses of vit D
to increase absorption of Calcium; acute treated with
calcitriol (Rocaltrol)
CORRECT HYPOMAGNESEMIA: acute is treated with
50% magnesium sulfate either IM or IV
• Then long term is treated with 50,000 to 400,000
Units of ergocalciferol daily
INTERVENTIONS
• DIET: high in calcium, low in phosphorus
• Avoid milk, yogurt and processed cheeses because of
high phosphorus content
• aluminun hydroxide (Amphogel) with or before
meals to decrease phosphate levels
• THERAPY FOR HYPOCALCEMIA IS LIFELONG
• WEAR MEDIC ALERT

wound and bone healing.ppt WOUND HEALING

  • 2.
    Bone healing, orfracture healing, is a proliferative physiological process in which the body facilitates the repair of a bone fracture. Generally bone fracture treatment consists of a doctor reducing (pushing) dislocated bones back into place via relocation with or without anaesthetic, stabilizing their position, and then waiting for the bone's natural healing process to occur.
  • 15.
    PATHOPHYSIOLOGY • thyroid hormonesecretion leads to hyperthyroidism • What you see in this is called: thyrotoxicosis
  • 16.
    WHAT DO THYROIDHORMONES AFFECT? • Metabolism in all body organs • Stimulate the heart – heart rate – stroke volume – cardiac output – blood flow
  • 17.
    HYPERTHYROIDISM INCREASED THYROID HORMONES: •Hypermetabolism • sympathetic nervous system activity • Effects protein, lipid and carbohydrate metabolism
  • 18.
    EFFECTS ON PROTEINMETABOLISM • Protein synthesis and degradation • More breakdown than buildup • Leads to loss of protein • Called negative nitrogen balance
  • 19.
    EFFECTS ON GLUCOSE •Glucose tolerance decreased • Leads to hyperglycemia
  • 20.
    EFFECTS ON FATMETABOLISM • fat metabolism • body fat • appetite • food intake; food intake does not meet energy demands • weight • nutritional deficiencies with prolonged disease
  • 21.
    CAUSES GRAVES DISEASE: • Clienthas a goiter (enlarged thyroid gland (p1484) • Autoimmune problem • Antibodies attach to gland causing it to enlarge • SYMPTOMS: – exophthalmos (protrusion of the eyes) p1484) – Pretibial myxedema (dry, waxy swelling of the frontal surfaces of the lower legs) •
  • 22.
    ADDITIONAL CAUSES OF HYPERTHYROIDISM 1.TOXIC MULTINODULAR GOITER: multiple thyroid nodules, milder disease 2. EXOGENOUS HYPERTHYROIDISM: excessive use of thyroid replacement hormones 3. THYROID STORM: untreated or poorly controlled hyperthyroidism; life threatening
  • 23.
    WHO GETS IT •Most often women between 20-40 yrs
  • 24.
    ASSESSMENT • Recent wgtloss • Increased appetite • Increase in # BM/day • ****heat intolerance • Diaphoresis even when temperatures comfortable for others • Palpitations/chest pain • Dyspnea with or without exertion
  • 25.
    ASSESSMENT VISUAL PROBLEMS MAYBE EARLIEST PROBLEM: • Infiltrative Exophthalmopathy (abnormal eye appearance or function) • Blurring/double vision/tiring of eyes • Increased tears • Photophobia • Eyelid retraction(eyelid lag) (p1483) • Globe lag (eyeball lag) (p1483)
  • 26.
    GOITER • Thyroid glandmay be 4 X normal • Bruits (turbulence from increased blood flow) heard with stethoscope
  • 27.
    CARDIAC PROBLEMS • systolicBP • tachycardia • dysrhythmia
  • 28.
    FURTHER SYMPTOMS • Fine,soft, silky hair • Smooth, moist skin • Muscle weakness • Hyperactive deep tendon reflexes • Tremors of hands • Restless, irritable, mood swings • Decreased attention span • Fatigued, inability to sleep
  • 29.
    LABORATORY ASSESSMENT IN HYPERTHYROIDISM: •T3 • T4 • TSH in Graves disease • Radioactive Thyroid Scan • Ultrasonography: used to determine goiter or nodules • EKG: note tachycardia
  • 30.
    DRUG THERAPY • ***antithyroiddrugs: thioamides – propylthiouracil (PTU) – methimazole (Tapazole) – carbimazole (Neo-Mercazole) • ACTION: blocks thyroid hormone production; takes time Need to control cardiac manifestations (tachycardia, palpitations, diaphoresis, anxiety) until hormone production reduced: use beta-adrenergic blocking drugs: propranolol (Inderal, Detensol)
  • 31.
    DRUG THERAPY Iodine preparations: •Lugol’s Solution • SSKI (saturated solution of potassium iodide) • Potassium iodide tablets, solution, and syrup ACTION: – decreases blood flow through the thyroid gland – This reduces the production and release of thyroid hormone – Takes about 2 wks for improvement – Leads to hypothyroidism
  • 32.
    DRUG THERAPY • LithiumCarbonate • ACTION: inhibits thyroid hormone release • NOT USED OFTEN BECAUSE OF SIDE EFFECTS: depressions, diabetes insipidus, tremors, N&V
  • 33.
    DRUG THERAPY RADIOACTIVE IODINETHERAPY: • Receives RAI in form of oral iodine • Takes 6-8 Weeks for symptomatic relief • Additional drug therapy used during this type of treatment • Not used on pregnant women
  • 34.
    SURGICAL MANAGEMENT Why usesurgery? • Used to remove large goiter causing tracheal or esophageal compression • Used for pts who do not have good response to antithyroid drugs TWO TYPES OF SURGERIES: 1. Total thyroidectomy (must take lifelong thyroid hormone replacement) 2. Subtotal thyroidectomy
  • 35.
    PREOPERATIVE CARE Low weight: •Hi protein, hi CHO diet for days/weeks before surgery
  • 36.
    PRE-OPERATIVE CARE 1. Antithyroiddrugs to suppress function of the thyroid 2. Iodine prep (Lugols or K iodide solution) to decrease size and vascularity of gland to minimize risk of hemorrhage, reduces risk of thyroid storm during surgery 3. Tachycardia, BP, dysrhythmias must be controlled preop
  • 37.
    PREOPERATIVE TEACHING • TeachC&DB • Teach support neck when C&DB • Support neck when moving reduces strain on suture line • Expect hoarseness for few days (endotracheal tube)
  • 38.
    POST-OP THYROIDECTOMY NURSING CARE 1.VS, I&O, IV 2. Semifowlers 3. Support head 4. Avoid tension on sutures 5. Pain meds, analgesic lozengers
  • 39.
    POSTOP THYROIDECTOMY NURSINGCARE • Humidified oxygen, suction • First fluids: cold/ice, tolerated best, then soft diet • Limited talking , hoarseness common • Assess for voice changes: injury to the recurrent laryngeal nerve
  • 40.
    POSTOP THYROIDECTOMY NURSINGCARE • CHECK FOR HEMORRHAGE 1st 24 hrs: • Look behind neck and sides of neck • Check for c/o pressure or fullness at incision site • Check drain • REPORT TO MD • CHECK FOR RESPIRATORY DISTRESS • Laryngeal stridor (harsh hi pitched resp sounds) • Result of edema of glottis, hematoma,or tetany • Trach set/airway/ O2, suction • CALL MD for extreme hoarseness
  • 41.
    TETANY • accidental removalof the parathyroid gland during surgery can happen • This disturbs the Ca metabolism • low blood calcium: see hyper-irritability of the nerves, spasms of the hands and feet, muscle twitchings occur, tingling, around mouth/toes/fingers • RISK: laryngospasm, airway obstruction • TREAT: IV calcium gluconate or calcium chloride
  • 42.
    POSTOP NURSING CARE CHECKFOR THYROID STORM: 25% mortality rate • result of release of TH during surgery • Observe for fever, tachycardia, systolic hypertension, agitation leading to seizures, delirium and coma, heart failure and shock TREAT: • Patent airway, cardiac monitor • Antithyroid drugs IV: PTU, propyl-Thyracil, Tapazole, sodium iodide solution • Inderal, Detensol for cardiac symptoms • Glucocorticoids (hydrocortisone IV) • Antipyretics and cooling blanket for fever
  • 43.
  • 44.
    CAUSES • Cells damaged;no longer function • Cells might be normal, person doesn’t ingest enough iodide & tyrosine needed to make thyroid hormones
  • 45.
    SYMPTOMS • Blood levelsof thyroid hormones are low • Decreased metabolic rate • Hypothalamus and anterior pituitary gland make stimulatory hormones (TSH) as compensation • Thyroid gland enlarges forming goiter
  • 46.
    MYXEDEMA DEVELOPS • Withlow metabolism metabolites build up inside the cells which increases mucous and water leading to cellular edema • Edema changes client’s appearance • Nonpitting edema appears everywhere especially around the eyes, hands, feet, between shoulder blades • Tongue thickens, edema forms in larynx, voice husky
  • 47.
    INCIDENCE OF HYPOTHYROIDISM •30-60 yrs of age • Mostly women
  • 48.
    ASSESSMENT • Increased sleeping(14-16 hours daily) • Generalized weakness • Anorexia • Muscle aches • Paresthesias • Constipation • Cold intolerance • Decreased libido, woman:difficulty becoming pregnant, changes in menses;men/impotence
  • 49.
    ASSESSMENT • Coarse features •Edema around eyes and face • Blank expression • Thick tongue • Overall muscle movement is slow • Lethargic, apathetic, drowsy, poor attention span, poor memory
  • 50.
  • 51.
    DRUGS THAT IMPAIRTHYROID FUNCTION • lithium carbonate (Lithane) • Aminoglutethimide • Sodium or potassium perchlorate • Thiocyanates • cobalt
  • 52.
  • 53.
    NURSING INTERVENTIONS • EXPECTEDOUTCOMES: – Maintains HR greater than 60/min – Maintains BP within normal limits – No dysrhythmia, peripheral edema, neck vein distension
  • 54.
    TREATMENT LIFELONG THYROID HORMONEREPLACEMENT • levothyroxine sodium (Synthroid, T4, Eltroxin) • IMPORTANT: start at low does, to avoid hypertension, heart failure and MI • Teach about S&S of hyperthyroidism with replacement therapy
  • 55.
    MYEXEDEMA COMA • Rareserious complication of untreated hypothyroidism • Decreased metabolism causes the heart muscle to become flabby • Leads to decreased cardiac output • Leads to decreased perfusion to brain and other vital organs • Leads to tissue and organ failure • LIFE THREATENING EMERGENCY WITH HIGH MORTALITY RATE
  • 56.
    PROBLEMS SEEN WITHMYXEDEMA COMA • Coma • Respiratory failure • Hypotension • Hyponatremia • Hypothermia • hypoglycemia
  • 57.
    TREATMENT OF MYEXEDEMACOMA • Patent airway • Replace fluids with IV NSSS • Give levothyroxine sodium IV • Give glucose IV • Give corticosteroids • Check temp, BP hourly • Monitor changes LOC hourly • Aspiration precautions, keep warm
  • 58.
  • 59.
    RESPONSIBILITY OF GLANDS •Maintain calcium and phosphate balance
  • 60.
    INCREASED PTH EFFECTS ONKIDNEY • acts directly on the kidney causing increased kidney reabsorption of calcium and increased phosphate excretion • Leads to hypercalcemia and hypophosphatemia
  • 61.
    INCREASED PTH EFFECTS ONBONE • Increase bone resorption (bone loss of calcium) • by decreasing osteoblastic (bone production) activity and increasing osteoclastic (bone destruction activity) • This process releases Ca and phosphate into the blood and reduces bone density
  • 62.
    CHRONIC CALCIUM EXCESS •Calcium is deposited in soft tissues
  • 63.
    CAUSES OF HYPERPARATHYROIDISM •Tumors • Trauma • Radiation • Vit D deficiency • Chronic renal failure with hypocalcemia
  • 64.
    ASSESSMENT High levels ofPTH: • Cause renal calculi • Pathologic fractures • Osteoporosis High levels of Calcium: • Anorexia, N/V, constipation, wgt loss, peptic ulcers • Fatigue/lethargy • Mental confusion, psychosis, coma, death if serum Ca greater than 12 mg/dL
  • 65.
    LABORATORY ASSESSMENT Serum calciumelevated: • normal range: 9-10.5mg/dL Serum phosphate decreased: • Normal 3.0-4.5mg/dL Serum parathyroid hormone increased: • Normal 50-330 pg/ml
  • 66.
    NONSURGICAL MANAGEMENT GOAL: reduceserum calcium levels • Hydration: IV saline in large volumes promotes renal excretion of calcium • Diuretics: furosemide (Lasix, Uritol) - increases kidney excretion of calcium
  • 67.
    INTERVENTIONS • Assess cardiacfunction and I&O q2-4 hrs during hydration therapy • Continuous cardiac monitoring • Close monitoring of serum calcium levels reporting precipitous drops to MD • Sudden drops may lead to tingling/numbness in muscles
  • 68.
    DRUG THERAPY PHOSPHATES: • oralphosphates inhibit bone resorption and interfere with calcium absorption • IV only used when serum calcium levels need rapid lowering
  • 69.
    DRUG THERAPY CALCITONIN: • Decreasesthe release of calcium and increases the kidney excretion of calcium • Best effect when combined with glucocorticoids
  • 70.
    DRUG THERAPY CALCIUM CHELATORS: •Lower calcium levels by binding (chelating) calcium which reduces the levels of free calcium FIRST EXAMPLE: mithramycin (cytotoxic agent), one IV dose can lower serum calcium in 48 hrs • DANGER: THROMBOCYTOPENIA, increased tendency to bleed, kidney and liver toxicity SECOND CALCIUM CHELATOR: penicillamine (Cuprimine, Pendramine)
  • 71.
    SURGICAL REMOVAL OF PARATHYROIDGLAND • Used to manage hyperparathyroidism • Surgery similar to that of removal of thyroid gland
  • 72.
  • 73.
    PATHO • Rare disorder •Parathyroid function decreased • Either lack of PTH secretion or lack of effectiveness of PTH secretion • End Result: hypocalcemia Caused by: • removal of glands during thyroidectomy, • or hypomagnesemia (seen in alcoholics or chronic renal disease, or malnutrition); causes impairment of PTH secretion
  • 74.
    ASSESSMENT • Mild tinglingand numbness due to tetany • Tingling and numbness around the mouth or in the hands and feet reflect mild to moderate hypocalcemia • Severe muscle cramps, carpopedal spasms, and seizures (with no loss of consciousness or incontinence), mental changes from irritability to psychosis reflect a more severe hypocalcemia)
  • 75.
    ASSESSMENT • Positive signsindicating potential tetany CHVOSTEK’S SIGN: sharp tapping over facial nerve causes twitching of mouth, nose and eye TROUSSEAU’S SIGN: carpopedal spasm induced by application of BP cuff
  • 76.
    LABORATORY ASSESSMENT • EEG •CT scan (shows brain cacifications from chronic hypocalcemia) • Serum calcium: • Serum phosphate: • Serum magnesium: • Serum vitamin D:
  • 77.
    INTERVENTIONS • CORRECT HYPOCALCEMIA:IV calcium with 10% solution of calcium chloride or calcium gluconate over 10-15 minutes; • then long term oral therapy Calcium 0.5-2G daily • Oral calcium: OSCAL Calcium gluconate Calcium lactate Calcium carbonate
  • 78.
    INTERVENTIONS CORRECT VITAMIN DDEFICIENCY: large doses of vit D to increase absorption of Calcium; acute treated with calcitriol (Rocaltrol) CORRECT HYPOMAGNESEMIA: acute is treated with 50% magnesium sulfate either IM or IV • Then long term is treated with 50,000 to 400,000 Units of ergocalciferol daily
  • 79.
    INTERVENTIONS • DIET: highin calcium, low in phosphorus • Avoid milk, yogurt and processed cheeses because of high phosphorus content • aluminun hydroxide (Amphogel) with or before meals to decrease phosphate levels • THERAPY FOR HYPOCALCEMIA IS LIFELONG • WEAR MEDIC ALERT

Editor's Notes

  • #18 Degradation (breakdown)
  • #25 Infiltrative Exophthalmopathy (abnormal eye appearance or function): the wide-eyed or startle look is due to edema in the extraocular muscles and increased fatty tissue behind the eye which pushes the eyeball forward. Pressure on the optic nerve may impair vision Swelling and shortening of the muscles may cause problems with focusing Corneal ulcers or infection: if eyelid fails to close completely leaving eye unprotected Eyelid retraction(eyelid lag) (p1483): upper eyelid fails to descend when the client gazes slowly downward Globe lag (eyeball lag) (p1483: upper eyelid pulls back faster than the eyeball when the client gazes upward To assess: ask client to look down and then look up and document the response
  • #40 Check every 30-60 min for extreme hoarseness (S&S) of respiratory distress
  • #52 Decreased cardiac output RT altered heart rate and rhythm as a result of decreased myocardial metabolism Ineffective Breathing pattern RT to decreased energy, obesity and fatigue Disturbed thought processes RT to impaired brain metabolism and edema Imbalanced nutrition More than body requirements RT to excessive intake in relation to metabolic needs Hypothermia RT to decreased metabolic rate Constipation RT to decreased motility of the GI tract Disturbed body image RT to illness Deficient knowledge of condition, diagnosis and TX RT to cognitive limitation