Transcript ENDOCRINE SYSTEM 10

ENDOCRINE SYSTEM
THYROID GLAND
Thyroid hormones affect nearly all body
tissues
 Dysfunctions cause profound effects
 Three hormones:
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– T3 ; T4 ; calcitonin
Thyroid hormone’s main component is
iodine
 Minimum daily requirement of I= 80 mcg;
more like 500mcg (contained in bread,
water, and iodized salt)
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THYROID
 Thyroid
gland can store large
quantities for months
 S/S may not appear for months
 Works on negative feedback system;
TRH signals TSH which stimulates
thyroid gland
 Most hormone is bound to protein
THYROID
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Functions:
– Metabolism: increase rate, accelerate food utilization for
energy, excites mental processes
– Growth: in children accelerates growth
– Carbohydrate: stimulates metabolism, including insulin
secretion
– Fat: enhances fat metabolism
– Body wt: production relates inversely to body wt (does
not stimulate appetite)
– CV: causes vasodilation, increased cardiac output and
heart rate, increased systolic B/P by 10-20 mm but
diastolic may drop the same
– Respiration: increases O2 use, rate, and depth
– GI: increases appetitie, absorption,motility
– CNS: speeds mental processes
THYROID
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Assessments:
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Swallowing
Skin changes
Tolerance to heat or cold
Weight changes
Palpitations
Drugs
Radiation to neck or surgery
Head trauma
Alcohol
Growth rate
Appetite
Menstrual periods
BEGIN WITH INSPECTION, LOOKING FOR LUMPS, PUFFINESS,
FACIAL EXPRESSIONS, ENLARGED TONGUE, VOICE, HAIR,
VISION, NAILS, AND MUSCLE ACHES.
THYROID
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Diagnostic tests:
– Thyroid panel: T3 & T4; free and bound;
– RAIU: radioactive iodine uptake; uses
radioactive iodine and scan thyroid as it uses
iodine. Given PO, IV, or liquid; only use small
amt. no risk, do before scan with contrast
– Stimulation tests
– Scans
– Ultasound
– Biopsy
THYROID
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Hyperthyroidism:
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Involves excessive hormone production
Leads to hypermetabolism
Signs and symptoms: thyrotoxicosis
Stimulates heart, protein synthesis,
breakdown>buildup leading to negative
nitrogen balance (degradation);
hyperglycemia; increased fat metabolism
– Caused by two etiologies:
 Increased
iodine uptake (Grave’s, goiter, adenoma
 Low iodine uptake (subacute and silent)
THYROID
Grave’s disease: toxic diffuse goiter
 Most common
 Strikes women, 20-30.
 Multisystem syndrome, affecting eyes,
skin, bones
 Increased thyroid hormone as well as
goiter
 No sure cause: autoimmune disorder
 Generally emotional upset precedes
symptoms
 Has heredity component
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THYROID
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Assessment:
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Increase appetite but slight wt loss
Dyspnea
Decreased heat tolerance
Menstruation may decrease or stop
Increased bowel movements or diarrhea
Nervous, irritable, restless
Speak rapidly; laugh inappropriately
Exopthalamus (BUG-EYE)
Moist skin, thinning hair, elbows red; clubbing of nails
(Plummer’s nails), hyperpigmentation (vitiligo- milk-white
patches)
Tremors, weakness
Tachycardia, atrial fibrillation; widened pulse pressure
Fine, soft hair; moist skin
Hyperactive deep tendon reflexes
THYROID
 Diagnostic
tests:
– Elevated T3, T4
– RAIU
– No response to TRH
– Below normal TSH
– Thyroid scan
THYROID
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Interventions:
– Record vital signs
– Rest, frequent linen changes, cool environment
– Drugs to reduce hormone: can cause thyroid storm
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PTU
Tapezole
Iodine-radioactive; cells are destroyed
Lithium
Inderal: not used on clients with asthma or heart disease
– Watch for agranulocytosis: fever, sore throat, rash
– Treatment does not correct infiltrative opthalopathy; use
tears, elevate head, diuretics for edema; prednisone
THYROID
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Surgical intervention:
May perform total or subtotal
Treat with drugs to return to near normal thyroid
function prior to surgery
– Give Lugol’s solution or SSKI (saturated solution of
potassium iodide) prior to OR to firm thyroid, reduce
vascularity which can reduce bleeding
– Give in milk, OJ, sip thru straw so as not to discolor
teeth
– Watch for toxicity: buccal mucosal swelling, excessive
salivation, skin reactions
– May receive Inderal to reduce cardiac problems
– Teach T,C, & DB; support head, explain about risk for
hoarseness and soreness
THYROID
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After surgical assess:
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Vital signs
Voice-may be hoarse; usually temporary
Neuromuscular functioning
Expect moderate drainage; check back of neck
Respiratory distress- use humidified air
Laryngeal stridor, paralysis, tetany
Keep in semi-Fowler’s
Avoid strain on suture line- avoid neck extension
Keep emergency drugs:
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O2, suction, trach tray, calcium gluconate
Monitor for transient hypothyroidism, damage to voice,
nerves, hypocalcemia, and tetany
THYROID
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Thyroid storm:
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Crisis situation- usually caused by Grave’s
Life-threatening
Uncontrolled hyperthyroidism
Develops quickly and triggered by stress;
over-palpation of gland
– Fever, tachycardia, systolic hypertension, GI,
restlessness, confused, psychotic
– Even with treatment, 25% mortality rate
THYROID
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Hypothyroidism:
– Deficiency in thyroid hormone
– Leads to low metabolism with build-up of
metabolites
– Metabolites with water accumulate within cells,
cause edema, called myxedema
– Myxedema coma: rare but can occur; heart
becomes flabby, chambers increase in size, CO
decreases; life threatening; high mortality rate
THYROID
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3 TYPES:
– HYPOTHYROIDISM: adult onset; tissue
destruction is most probable cause
– CRETINISM:
 Profound
hypothyroidism in infants
 All developmental aspects are retarded
 Severe brain damage can occur
 If caught early, can prevent retardation
– JUVENILE HYPOTHYROIDISM:
 Begins
during childhood, Hashimoto’s disease, caused
by drugs, autoimmune
 Affects growth and sexual maturation
THYROID
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Assessments:
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Changed sleeping habits (increased)
Lethargy,
HA, wt gain
Cold intolerance
Dyspnea
Constipation
Menorrhagia
Muscle aches
Anorexia
Lack of expression
Cool, dry, skin, yellow tint, rough, thick, scaly
Dry hair, coarse, lusterless
Enlarged tongue
Speech slow and deliberate with hoarse voice
Impotence and infertility
Decreased blood pressure; bradycardia; dysrhythmias; decreased
urinary output
THYROID
 Diagnostic
tests:
– Below-normal T3 & T4
– Above-normal TSH
– Above-normal TRF
– Above-normal creatinine phosphokinase
– Anemia
THYROID
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Interventions:
– Requires life-long replacement hormone
– Synthetic usually used T4 (Levothyroid,
Synthroid, Noroxine)
– Start with lowest dose possible and work way
up every 1-3 weeks
– With known cardiac problems, always use
lowest dose possible
– T3 (Cytomel) has more rapid effect.
– Euthroid (Liotrix)– combined T3 & T4
– Make sure client knows to continue with meds
even if he feels better
– Avoid sedation if possible
THYROIDITIS
Inflammation of thyroid
 Three types:
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– Acute: bacterial; pain, malaise, fever,
dysphagia; treat with antibiotics
– Subacute: viral infection; fever, chills,
dysphagia, pain, hard & enlarged gland; treat
symptoms; antivirals
– Chronic: (Hashimoto’s)- auto immune, invade
thyroid with antibodies and lymphocytes
causing tissue destruction; treat with thyroid
hormone
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Administer thyroid hormones; surgery;
promote comfort and teaching
THYROID CANCER
4
types
 Surgery is treatment- total
 Suppressive doses of thyroid for 3
months after surgery
 Ablation- laser destruction of tissue
 chemotherapy
PARATHYROIDS
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Parathyroid hormone corrects calcium deficiency by
promoting calcium conservation by kidneys, stimulating
calcium release by bone, enhance calcium absorption from
GI, & reduce serum phosphate levels.
Works on negative feedback control
In kidneys, causes calcium to be reabsorbed with release of
phosphorus
Stimulates kidneys to convert Vit D to a metabolite that
allows for PTH to work on bone
In bone, helps convert osteoblasts to osteoclasts,
promoting bone breakdown and release of calcium.
Acts on GI to stimulate absorption of calcium (must have
calcitriol).
Calcitonin from thyroid causes inhibition of Ca++ release
from bones
PARATHYROID
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Hyperparathyroidism:
– Primary:
 Faulty
PTH regulation; adenoma, genetics, CA,
radiation, hyperplasia; occurs more commonly in
women, 35-65
– Secondary:
 Compensatory
response to defective homeostasis,
chronic renal failure, malabsorption disorders
– Tertiary:
 Compensates
for secondary malfunction to primary,
leading to overgrowth of gland and overproduction
and secretion
PARATHYROID
 All
three lead to increased calcium
and decreased phosphorus
PARATHYROID
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Assessments:
– Urine calcium increase and kidneys fail to
concentrate urine
– Phosphorus excretion increases
– Enhances sodium, potassium, amino acids,
bicarbonate (acidosis leading to excretion of
Ca++
– Polyuria
– Renal calculi
– Bone demineralization (breakdown):
 Bone
pain
 Pathologic fractures
 Cystic bone disease
PARATHYROID
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Other assessments:
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Weakness, wt. loss, fatigue
HA, depression
Renal colic pain, back pain,
Hematuria, renal calculi, cholelithiasis
Anorexia, vomiting, constipation
Peptic ulcer (stimulates gastric HCL)
Increase heart contractility; decreased automaticity
Increased sensitivity to digitalis
Hypertension
Depressed reflexes- hyporeflexia
Confusion, irritability, mood swings
PARATHYROID
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Diagnostic tests:
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Serum PTH: elevated
Calcium: elevated (>10.5mg/dl; 5.2mEq/L
Kidney stones
Phosphorus: decreased
X-rays; CT; MRI: look at bone density and
demineralization
– PTH infusion test: (Ellsworth-Howard excretion
test); give IV PTH, hourly urine samples
looking for phosphorus
– Calcitonin stimulation test: if cancer
suspected; use calcium gluconate
PARATHYROID
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Interventions:
– Surgery (usually remove only three)
– Stabilize calcium levels prior to surgery
 Hemorrhage
 Laryngeal
paralysis
 Difficulty swallowing
 Respiratory distress
 Transient hypoparathyroidism
 Tetany
 Muscle cramps
 Hyperactive tendon reflexes
 Prolonged QT on EKG
 Positive Chvostek’s and Trousseau’s signs
PARATHYROID
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Interventions:
– Medical treatment:
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Rehydration with isotonic fluids
Diuresis
Mobilization
Restrict intake of calcium (thyazides and Vit D.
Monitor EKG
Drugs:
– Phosphates: Neutra-phos
– Calcitonin: IV; IM- decrease release from skeletal areas;
increased excretion by kidneys
– Calcium chelators ( bind calcium) Plicamycin: mithramycin;
cytotoxic agents; watch for thrombocytopenia
– Steroids: inhibit Vit D
– Estrogen
– Alpha & beta blockers
– cimetidine
PARATHYROID
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Hypoparathyroidism
– Too little PTH leading to decreased calcium and
increase phosphorus
– 3 types
 Iatrogenic:
– Most common, resulting from surgery of neck removing
glands, radiation, or other trauma
 Idiopathic:
– Early onset and late onset; autoimmune; genetic
causes of absent glands, pernicious anemia, ovarian
failure
 Functional:
– Long term hypomagnesemia causes this (alcohol,
malabsorption)
PARATHYROID
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Assessments:
– Neuromuscular problems, increased excitability, tetany,
muscle cramps, tingling, numbness, hyperreflexia
– Tetany leads to anxiety; leads to hyperventilation; leads
to hypocapnia and alkalosis, which worsens
hypocalcemia
– Seizures, laryngeal spasms
– Personality changes
– Increased ICP
– Nausea, vomiting
– Dysrhythmias, decreased contractility, reduced CO
– Cataracts, dry skin, scaly, coarse
– Alopecia
– Bands or pits on teeth
PARATHYROID
 Diagnostic
tests:
– Serum calcium: low
– Serum phosphorus: high
– Serum magnesium: normal to low
– Serum PTH: low
– Urinary creatinine: low
– Urinary excretion of calcium: high
– X-ray; MRI; CAT scans
PARATHYROID
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Interventions:
– Treatment focuses on preventing tetany and
correcting hypocalcemia
 IV
calcium gluconate or calcium gluconate
– Do not use saline, promotes calcium and sodium
excretion
– Avoid bicarbonate, cause precipitation
 Vit
D and calcium supplements
– Ergocalciferol (Vit D2 ); Rocaltrol; may use combined
therapy of oral and IV initially
– Need 1 gram of calcium daily if using Vit D
– Life-long therapy
– Emergency airway if laryngeal spasms occur
– Foods high in calcium but low in phosphorus- milk,
yogurt, processed cheese.
ADRENAL GLANDS
 Widespread
effects, confusing clinical
picture
 S/S mimic many other disorders
 Survival depends upon prompt
diagnosis and treatment
ADRENAL GLANDS
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Cortex secretes glucocorticoids and
mineralocorticoids
ACTH from anterior pituitary is controlled by CRF
Other factors controlling release include stress,
circadian rhythms
ACTH peaks at 6am, Cortisol at 8am; lowest level
at midnight
With decreasing cortisol, ACTH is stimulated and
released
Stress prompts release of glucocorticoids to
promote metabolism of proteins, amino acids,
fatty acids, and glucose
ADRENAL GLANDS
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Mineralocorticoids, aldosterone, is controlled by
renin-agiontension system
Renin is increased by blood volume, blood
pressure, and Na+
Renin lead to angiotension II production and
aldosterone formation
K+ & Na+ directly affect aldosterone release
Increased K+ increases aldosterone and Na+
decreases aldosterone
Epinephrine and norephinephrine are produced,
but because brain produces we can survive
without adrenal medulla
ADRENAL GLAND
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Assessments:
– Most disorders have slow, gradual onset and
progression
– Changes early are subtle, hard to detect
– Weight changes
– Fatigue
– Apathy
– Depressed or neurotic
– Worsens with increased stress
– Physical appearance may be a clue
ADRENAL GLAND
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Physical assessment:
– Responds appropriately, but facial expressions
do not match
– Normal weight
– Increased secondary sex characteristics
– Fat distribution abnormal
– Poor skin turgor
– Purplish striae on abdomen
– Pitting edema
– Hyperpigmentation
– Hair distribution is abnormal
– Muscle weakness
ADRENAL GLANDS
 Diagnostic
tests:
– Secreted in minute amounts, therefore
most sensitive tests are RAI
– Remember: if anxious, will affect
results of some tests
– Samples must be timed!!
ADRENAL GLANDS
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Cushing’s syndrome: hypercortisolism
Cortisol excess
Affects more women than men
Primary:
– Usually a neoplasm
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Secondary:
– Pituitary or hypothalamus disorder causing increased
ACTH; adrenal hyperplasia
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Iatrogenic:
– Excessive use of steroids (prednisone)
– Artifically increases cortisol, suppresses ACTH, causing
adrenal atropy
– S/S are of hyperfunction
ADRENAL GLAND Cushing’s
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Assessments:
– Fatigue, muscle wasting
– Frequent infections, slow wound healing
– Suppressed immune response ( can mask S/S); kill
lymphocytes
– Truncal obesity, buffalo hump, moon-shaped face, scrawny
arms and legs (PICKLE WITH LEGS)
– Fragile skin, purplish striae on abdomen, buttocks, breasts,
bruises
– Masculinization in women, hirsutism (increased hair growth),
acne
– Hypertension
– Osteoporosis
– Labile emotions
– Abnormal sleep patterns
– Nitrogen, carbohydrate, and mineral metabolism
– Elevated blood glucose
ADRENAL GLANDS CUSHING’S
 Diagnostic
tests:
– Cortisol: high with no circadian variation
– Urinary levels of steroid metabolites:
high
– RBC and granulocytes: high
– X-rays, MRI, CAT scans
– Dexamethasone suppression test: give
1 mg at night, test at 8am; high level
ADRENAL GLAND CUSHING’S
 Interventions:
– Treat underlying cause; stop steroids
– Remove tumors of pituitary or
adrenalectomy ( uni or bi lateral)
– Drugs:
 Mitotane
to inhibit cortisol synthesis ( watch
for adrenal crisis!!
 Cyproheptadine: ACTH inhibitor
 Aldactone: mineralocorticoid antagonist to
relieve hypertension and hypokalemia
ADRENAL GLAND CUSHING’S
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Complications:
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Fluid and e-lyte imbalances
Hypertension: Na+ and water retention
CHF: excess volume in compromised heart
Hypokalemia
Ventricular dysrhythmias: due to CHF and
hypokalemia
– Increased risk for infections & fractures
– Skin breakdown
ADRENAL GLAND
INSUFFICIENCY: ADDISON’S
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Suppressed adrenocortical function and
hormones
May precipitate “adrenal crisis”: life-threatening
Primary:
– Addison’s- rare, chronic disorder
– 90% gland usually destroyed before symptoms appear
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Secondary:
– Reduced ACTH secretion caused by pituitary disease or
exogenous steroid administration; more common
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Impairs stress response by reducing cortisol,
aldosterone, and androgens
ADRENAL GLAND ADDISON’S
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Assessments:
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Muscle weakness and fatigue (especially during stress)
Nausea, vomiting, diarrhea, abdominal pain
Salt craving
Anxiety, restlessness, irritability, and confusion
Orthostatic hypotension
HYPOGLYCEMIA & HYPERKALEMIA
Hyperpigmentation (ONLY PRIMARY DISEASE HAS
THIS)
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Knees, elbows, nipples, palm creases, scars( bronzed,
“dirty tan”)
Small black freckles on neck, face; bluish splotches on
mucous membranes
ADRENAL GLANDS ADDISON’S
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Diagnostic tests:
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Serum cortisol: low
Urinary metabolites: low
ACTH:
ACTH stimulation: elevated
cortisol=Addision’s; low cortisol=secondary
disease
Hyperkalemia
Hyponatremia
Hpochloremia
Fasting hypoglycemia
BUN elevated; hematocrit HCT elevated
ADRENAL GLANDS ADDISON’S
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Interventions:
– Lifelong therapy with replacement
– Drugs:
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Cortisone: twice daily, increase dose for stressful times
Florinef: aldosterone replacement
Salt food liberally
Avoid fasting
Eat high carbs and proteins
Always wear medic alert identification
Carry emergency kit with 100mg hydrocortisone for
injection
– Prevent acute exacerbations
– Avoid salt and fluid restriction with diuretics; may lead
to crisis
ADRENAL GLANDS
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Complications:
– Adrenal crisis: due to insufficiency; can occur
gradually or abruptly (acute adrenal
insufficiency)
– Potentially lethal
– Occurs in individuals who don’t respond to
therapy; increased stress without increased
meds; abrupt corticosteroid withdrawal
– ALWAYS WITHDRAW STEROIDS THERAPY
GRADUALLY
ADRENAL GLANDS ADRENAL
CRISIS
 Treatment:
– Restore volume with D5NS
– Be sure to assess fluid status frequently
– Cortisol q 6 hr. (Solu-Cortef IV): if given
with saline, proves adequate to replace
Aldosterone
– Do not give methyleprednisolone (SoluMedrol: lack mineralocorticoid effects)
– Reduce anxiety
ADRENAL GLANDS
PHEOCHROMOCYTOMA
 Rare,
benign tumor; arises in
medulla
 Results in hypersecretion of
epinephrine and norepinephrine
 Tumors appear more commonly on
right side; middle-aged women
 Can occur with thyroidal cancer and
hyperparathyroidism-Sipple’s
syndrome
PHEOCHROMOCYTOMA
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Assessment:
– Exaggerated flight or fight reaction
– High blood pressure (Hallmark sign) 200/150
– End-organ damage; CVA, heart disease, kidney
damage
– Orthostatic hypotension
– Attack occurs with sporadic release of
catecholamines
– Pounding heart beat, deep breathing, HA
– Peripheral vasoconstriction
– Hyperglycemia
– anxiety
PHEOCHROMOCYTOMA
 Attacks
may occur frequently or
seldom
 May last minutes to hours
 May result from exercise, lifting,
emotional distress, exposure to cold,
food, alcohol, sex, etc.
PHEOCHROMOCYTOMA
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Diagnostic tests:
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Must rule out all other disorders
Hyperglycemia
Elevated hematocrit
240 urine for catecholamines and their
metabolites (metanephrine(catecholamine) is
more conclusive than vanillylmandelic
acid(epinephrine)
– EKG changes
– CAT scan shows tumor
– Diagnostic tests may precipitate a crisis!!!
PHEOCHROMOCYTOMA
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Interventions:
– Surgical removal
– Prior to surgery, drugs to reduce the excessive
adrenergic action (2 weeks)
– Receive plasma volume expanders
– During surgery, receive Regitine, alpha-adrenergic
blocker to prevent hypertensive crisis
– If unable to have surgery, may order drug, Demser,
inhibits an enzyme promoting norepinephrine synthesis
– Avoid drugs like opiates, histamines, OTC cold
medications
– During attack, maintain bedrest, HOB elevated to at 300
to reduce orthostatic hypotension
PHEOCHROMOCYTOMA
 Complications:
– Severe hypotension
– CVA
– Heart problems
– If left untreated, always leads to
death
ALDOSTERONISM
Excessive secretion of mineralocorticoids,
especially aldosterone
 Primary:
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– Called Conn’s syndrome, usually benign
Aldosterone producing adenoma
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Secondary:
– Excess renin-angiotension stimulation;
stimulation occurs with conditions involving
low circulating blood volume: pregnancy,
hypvolemia, CHF, cirrhosis, oral contraceptives,
chronic renal failure
ALDOSTERONISM
 Assessment:
– Sodium and water retention, increased
fluid volume, hypertension
– HA, visual disturbances
– Hypokalemia
– Metabolic alkalosis: finger tingling and
paresthesia
– Increased urine output
ALDOSTERONISM
 Diagnostic
tests:
– Decreased potassium
– Elevated aldosterone
– Urinary potassium elevated >30mEq/L
– X-rays, CAT scans, MRI
ALDOSTERONISM
 Interventions:
– Reduce B/P, correct hypokalemia
– Surgical removal of tumor
– Administer Aldactone
– Potassium supplements
– Sodium restriction
ALDOSTERONISM
 Complications:
– Hypertension and hypokalemia possibly
leading to neurologic impairment
– CHF
– Lethal dysrhythmias
– Profound muscle weakness