740 likes | 1.27k Views
PATHOPHYSIOLOGY. thyroid hormone secretion leads to hyperthyroidismWhat you see in this is called: thyrotoxicosis. . WHAT DO THYROID HORMONES AFFECT?. Metabolism in all body organsStimulate the heart heart rate stroke volume cardiac output blood flow. . . . . HYPERTHYROIDISM. I
                
                E N D
1. THYROID DISORDERS	 HYPERTHYROIDISM
HYPOTHYROIDISM 
2. PATHOPHYSIOLOGY   thyroid hormone secretion leads to hyperthyroidism
What you see in this is called: thyrotoxicosis 
3. WHAT DO THYROID HORMONES AFFECT? Metabolism in all body organs
Stimulate the heart 
    heart rate
    stroke volume
    cardiac output
     blood flow 
4. HYPERTHYROIDISM INCREASED THYROID HORMONES:
Hypermetabolism
   sympathetic nervous system activity
Effects protein, lipid and carbohydrate metabolism
 
5. EFFECTS ON PROTEIN METABOLISM    Protein synthesis and degradation
More breakdown than buildup
Leads to loss of protein
Called negative nitrogen balance Degradation (breakdown)Degradation (breakdown) 
6. EFFECTS ON GLUCOSE Glucose tolerance decreased
Leads to hyperglycemia 
7. EFFECTS ON FAT METABOLISM    fat metabolism
   body fat
    appetite
    food intake; food intake does not meet energy demands
    weight
    nutritional deficiencies with prolonged disease     
8. 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)
   
9. ADDITIONAL CAUSES OF HYPERTHYROIDISM TOXIC MULTINODULAR GOITER: multiple thyroid nodules, milder disease
EXOGENOUS HYPERTHYROIDISM: excessive use of thyroid replacement hormones
THYROID STORM: untreated or poorly controlled hyperthyroidism; life threatening	 
10. WHO GETS IT Most often women between 20-40 yrs 
11. 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 
12. 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)
 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
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
 
13. GOITER Thyroid gland may be 4 X normal
Bruits (turbulence from increased blood flow) heard with stethoscope 
14. CARDIAC PROBLEMS    systolic BP
   tachycardia
   dysrhythmia 
15. 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 
16. LABORATORY ASSESSMENT IN HYPERTHYROIDISM: 
   T3
   T4
   TSH in Graves disease
    Radioactive Thyroid Scan
Ultrasonography: used to determine goiter or nodules
EKG: note tachycardia  
17. 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)
 
18. 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
 
19. DRUG THERAPY Lithium Carbonate
ACTION: inhibits thyroid hormone release
NOT USED OFTEN BECAUSE OF SIDE EFFECTS: depressions, diabetes insipidus, tremors, N&V 
20. 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 
21. 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: 
Total thyroidectomy (must take lifelong thyroid hormone replacement)
Subtotal thyroidectomy
 
22. PREOPERATIVE CARE Low weight:
Hi protein, hi CHO diet for days/weeks before surgery
 
23. PRE-OPERATIVE CARE 
Antithyroid drugs to suppress function of the thyroid
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
Tachycardia,  BP, dysrhythmias must be controlled preop 
24. 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) 
25. POST-OP THYROIDECTOMY NURSING CARE VS, I&O, IV
Semifowlers
Support head
Avoid tension on sutures
5.  Pain meds, analgesic lozengers 
26. 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 
27. 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  Check every 30-60 min for extreme hoarseness (S&S) of respiratory distressCheck every 30-60 min for extreme hoarseness (S&S) of respiratory distress 
28. 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
 
29. 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
 
30. HYPOTHYROIDISM  Decreased levels 
of 
Thyroid Hormone 
31. CAUSES	 Cells damaged; no longer function
Cells might be normal, person doesn’t ingest enough iodide & tyrosine needed to make thyroid hormones 
32. 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 
33. 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 
34. INCIDENCE OF HYPOTHYROIDISM 30-60 yrs of age
Mostly women 
35. 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 
36. 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 
37. LABORATORY ASSESSMENT   T3
  T4
  TSH 
38. DRUGS THAT IMPAIR THYROID FUNCTION lithium carbonate (Lithane)
Aminoglutethimide
Sodium or potassium perchlorate
Thiocyanates
cobalt 
39. NURSING DIAGNOSES 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 limitationDecreased 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 
40. NURSING INTERVENTIONS EXPECTED OUTCOMES:
Maintains HR greater than 60/min
Maintains BP within normal limits
No dysrhythmia, peripheral edema, neck vein distension 
41. 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
 
42. 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
 
43. PROBLEMS SEEN WITH MYXEDEMA COMA Coma
Respiratory failure
Hypotension
Hyponatremia
Hypothermia
hypoglycemia 
44. 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 
45. PARATHYROID DISORDERS HYPERPARATHYROIDISM
HYPOPARATHYROIDISM 
46. RESPONSIBILITY OF GLANDS Maintain calcium and phosphate balance 
47. 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  
48. 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 
49. CHRONIC CALCIUM EXCESS Calcium is deposited in soft tissues 
50. CAUSES OF HYPERPARATHYROIDISM Tumors
Trauma
Radiation
Vit D deficiency
Chronic renal failure with hypocalcemia 
51. 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
 
52. 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 
53. 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
 
54. 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 
55. DRUG THERAPY PHOSPHATES:  
oral phosphates inhibit bone resorption and interfere with calcium absorption
IV only used when serum calcium levels need rapid lowering 
56. DRUG THERAPY CALCITONIN:
Decreases the release of calcium and increases the kidney excretion of calcium
Best effect when combined with glucocorticoids 
57. 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) 
 
58. SURGICAL REMOVAL OF PARATHYROID GLAND Used to manage hyperparathyroidism
Surgery similar to that of removal of thyroid gland
 
59. HYPOPARATHYROIDISM 
60. 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 
61. 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) 
62. 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 
63. LABORATORY ASSESSMENT EEG
CT scan (shows brain cacifications from chronic hypocalcemia)
Serum calcium:
Serum phosphate:
Serum magnesium:
Serum vitamin D: 
64. 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
 
65. 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 
66. 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