Module 8: Endocrine Problems Flashcards
Hyperthyroidism
A sustained increase in synthesis and release of
thyroid hormones by thyroid gland
Occurs more often in women
Highest frequency between ages 20 to 40 years
Most common form
Graves’ disease
Other causes
Toxic nodular goiter
Thyroiditis
Excess iodine intake
Pituitary tumors
Thyroid cancer
Thyrotoxicosis
Physiologic effects/clinical syndrome of hypermetabolism
Results from increased circulating levels of T3, T4, or both
Hyperthyroidism and thyrotoxicosis usually occur together
Subclinical hyperthyroidism
Serum TSH level below 0.4 mIU/L
Normal T4 and T3 levels
Overt hyperthyroidism
Low or undetectable TSH
Increased T4 and T3 levels
Symptoms may or may not be present
Graves Disease Pathophysiology
Autoimmune disease
Diffuse thyroid enlargement
Excess thyroid hormone secretion
Risk factors may interact with genetic factors
Women are five times more likely than men to develop Graves’ disease
Graves Disease Clinical Manifestations
Related to effect of thyroid hormone excess
Increased metabolism
Increased tissue sensitivity to sympathetic nervous system stimulation
Goiter
Inspection
Auscultation: bruits
Ophthalmopathy
Abnormal eye appearance or function
Exophthalmos
Increased fat deposits and fluid
Eyeballs forced outward
Cardiovascular system
Systolic hypertension
Bounding, rapid pulse; palpitations
Increased cardiac output
Cardiac hypertrophy
Systolic murmurs
Dysrhythmias
Angina
Respiratory system
Dyspnea on mild exertion
Increased respiratory rate
GI system
Increased appetite, thirst
Weight loss
Diarrhea
Splenomegaly
Hepatomegaly
Skin
Warm, smooth, moist skin
Thin, brittle nails
Hair loss
Clubbing of fingers; palmar erythema
Fine, silky hair; premature graying in men
Diaphoresis
Vitiligo (patches of skin losing pigment)
Musculoskeletal system
Fatigue
Weakness
Proximal muscle wasting
Dependent edema
Osteoporosis
Nervous system
Hyperactive deep tendon reflexes
Nervousness, fine tremors
Insomnia , difficulty focusing eyes
Lability of mood, delirium
Lack of ability to concentrate
Stupor, coma
Reproductive system
Menstrual irregularities
Amenorrhea
Decreased libido
Decreased fertility
Impotence and gynecomastia in men
Intolerance to heat
Elevated basal temperature
Lid lag, stare
Eyelid retraction
Rapid speech
Acute Thyrotoxicosis
Thyrotoxic crisis (thyroid storm)
Excessive amounts hormones released
Life-threatening emergency
Death rare when treatment started early
Results from stressors
Thyroidectomy patients are at risk
Manifestations
Severe tachycardia, heart failure
Shock
Hyperthermia (up to 106° F [41.1° C])
Agitation
Seizures
Abdominal pain, vomiting, diarrhea
Delirium, coma
Decreased TSH (less than 0.4 mU/L)
Increased free thyroxine (free T4)
Total T3 and T4 (not definitive)
Radioactive iodine uptake (RAIU)
Distinguishes Graves’ disease from other forms of thyroiditis
Goals
Block adverse effects of thyroid hormones
Suppress hormone oversecretion
Prevent complications
Three primary treatment options
Antithyroid medications
Radioactive iodine therapy (RAI)
Surgery
Acute Thyrotoxicosis Drug Therapy
Useful in treatment of thyrotoxic states
Not considered curative
Antithyroid drugs
Iodine
β-Adrenergic blockers
Propylthiouracil and methimazole (Tapazole)
Inhibit thyroid hormone synthesis
Improvement in 1 to 2 weeks
Results usually seen within 4 to 8 weeks
Therapy for 6 to 15 months
Iodine
Potassium iodine (SSKI) and Lugol’s solution
Inhibit synthesis of T3 and T4 and block their release into circulation
Decreases vascularity of thyroid gland, making surgery safer and easier
Maximal effect within 1 to 2 weeks
Beta Adrenergic Blockers
Symptomatic relief of thyrotoxicosis
Block effects of sympathetic nervous stimulation
Decreases tachycardia, nervousness, irritability, tremors
Propranolol (Inderal)
Atenolol (Tenormin)
Radioactive Iodine therapy
Treatment of choice for most nonpregnant adults
Damages or destroys thyroid tissue
Delayed response of up to 3 months
Treated with antithyroid drugs and β-blocker before
and during first 3 months of RAI
Given on outpatient basis
Patient teaching
Frequent oral care for thyroiditis/parotiditis
Radiation precautions
Symptoms of hypothyroidism
Surgical Therapy
Indications
Large goiter causing tracheal compression
-Unresponsive to antithyroid therapy
-Thyroid cancer
-Not a candidate for RAI
Rapid reduction in T3 and T4 levels
Subtotal thyroidectomy
Preferred surgical procedure
Involves removal of 90% of thyroid
Can be done using minimally invasive procedures
* Endoscopic thyroidectomy
* Robotic surgery
Hyperthyroid Nutritional Therapy
High-calorie diet (4000 to 5000 cal/day)
6 full meals/day with snacks in between
Protein intake: 1 to 2 g/kg ideal body weight
Increased carbohydrate intake
Avoid highly seasoned and high-fiber foods, caffeine
Dietitian referral
Hypothyroidism
Deficiency of thyroid hormone
Causes general slowing metabolic rate
More common in women than in men
Subclinical hypothyroidism
TSH is greater than 4.5 mIU/L
T4 levels normal
Affects up to 10% of women over 60
Nonthyroidal illness syndrome (NTIS)
Critically ill patients
Low T3, T4, and TSH levels
Hypothyroidism Pathophysiology
Primary hypothyroidism
Caused by destruction of thyroid tissue or defective hormone synthesis
Secondary hypothyroidism
Caused by pituitary disease (decreased TSH) or
hypothalamic dysfunction or (decreased TRH)
Etiology
Iodine deficiency
Atrophy of the gland
Hashimoto’s thyroiditis
Graves’ disease
Treatment for hyperthyroidism
Drugs
Cretinism if occurs in infancy
Clinical Manifestations of Hypothyroidism
Systemic effects are characterized by slowing of body
processes
Manifestations vary depending on severity, duration of deficiency, age of onset
Slow onset unless occurs after thyroidectomy
Tired, lethargic, impaired memory, low initiative, weight gain
Cardiovascular system
CV problems may be significant in patients with history of cardiovascular disease
Decreased cardiac contractility and output
Increased serum cholesterol and triglycerides
Anemia
Respiratory system
Low exercise tolerance
Shortness of breath on exertion
Neurologic system
Fatigue and lethargy
Personality and mood changes
Impaired memory, slowed speech, decreased initiative, and somnolence
GI system
Decreased appetite
Nausea and vomiting
Weight gain
Constipation
Distended abdomen
Enlarged, scaly tongue
Celiac disease
Integumentary system
Dry, thick, inelastic, cold skin
Thick, brittle nails
Dry, sparse, coarse hair
Poor turgor of mucosa
Generalized interstitial edema
Puffy face
Decreased sweating
Pallor
Musculoskeletal system
Fatigue, weakness
Muscular aches and pains
Slow movements
Arthralgia
Reproductive system
Prolonged menstrual periods or amenorrhea
Decreased libido, infertility
Other
Increased susceptibility to infection
Increased sensitivity to opioids, barbiturates, anesthesia
Intolerance to cold
Decreased hearing
Sleepiness
Goiter
Hypothyroid Complications
Myxedema coma
Precipitated by infection, drugs, cold, trauma
Characterized by:
* Impaired consciousness or coma
* Subnormal temperature, hypotension, hypoventilation
* Cardiovascular collapse
Treated with IV thyroid hormone
Hypothyroid Diagnostic Studies
History and physical assessment
TSH and free T4
TSH increases with primary hypothyroidism
TSH decreases with secondary hypothyroidism
Thyroid antibodies
Autoimmune origin
High cholesterol
High triglycerides
High creatine kinase
Low RBCs (anemia)
Synthroid Medication
Levothyroxine (Synthroid)
Start with low dose
Monitor for chest pain, weight loss, nervousness, tremors, insomnia
Increase dose in 4- to 6-week intervals as needed based on TSH levels
Lifelong therapy
Cushing Syndrome and
Hyperaldosteronism - Pathophysiology
Caused by excess of corticosteroids
-Common causes:
Iatrogenic administration of exogenous corticosteroids
ACTH-secreting pituitary adenoma (Cushing Disease)
Adrenal tumors
Ectopic ACTH production by tumors
Clinical Manifestations
Excess glucocorticoids
Hyperglycemia related to glucose intolerance and increased gluconeogenesis
Muscle wasting causes weakness
Loss of bone matrix causes osteoporosis and back pain
Loss of collagen causes thin skin, easily bruises
Delay in wound healing
Mineralocorticoid excess may cause:
Hypokalemia
Hypertension
Adrenal androgen excess may cause:
Severe acne
Male characteristics in women
Feminization in men
Diagnostic Studies
Confirmation of increased plasma cortisol levels
Midnight or late-night salivary cortisol
Low-dose dexamethasone suppression test
24-hour urine cortisol
* Levels greater than 100 mcg/24 hr
Urine levels of 17-ketosteroids may be high
Plasma ACTH levels
High or normal with Cushing disease (pituitary etiology)
Low, normal, or high with Cushing syndrome
Hypokalemia and alkalosis
With ectopic ACTH syndrome and adrenal cancer
Treatment
Normalize hormone secretion
Treatment depends on cause
Surgical removal or irradiation of pituitary adenoma
Adrenalectomy for adrenal tumors or hyperplasia
Removal of ACTH-secreting tumors
If cause is prolonged, use of corticosteroids
Gradually discontinue therapy
Decrease dose
Convert to an alternate-day dosing
Dose must be tapered gradually
Addison’s Disease Pathophysiology
Primary
Addison’s disease
Reduction of glucocorticoids, mineralocorticoids, and
androgens
Secondary
Lack of pituitary ACTH
Lack of glucocorticoids and androgens
80% of cases caused by an autoimmune response
Autoimmune adrenalitis
Antibodies destroy adrenal cortex
Loss of
* Glucocorticoid
* Mineralocorticoid
* Adrenal androgen hormones
Autoimmune polyglandular syndrome
Co-occurring endocrine conditions
* Type 1 diabetes
* Autoimmune thyroid disease
* Pernicious anemia
* Celiac disease
Most common in white females
TB (not a common cause in United States)
Amyloidosis
Fungal infections
AIDS
Metastatic cancer
Iatrogenic Addison’s disease
Adrenal hemorrhage
Anticoagulant therapy
Chemotherapy
Ketoconazole therapy for AIDS
Bilateral adrenalectomy
Addison’s Disease Clinical Manifestations
Insidious onset
Anorexia
Nausea
Progressive weakness
Fatigue
Weight loss
Disease often advanced before diagnosed
Abdominal pain
Diarrhea
Headache
Orthostatic hypotension
Salt craving
Joint pain
Addison’s Disease Complications
Addisonian crisis
Acute adrenal insufficiency
Insufficient or sudden, sharp decrease in hormones
Life-threatening emergency
Various triggers
* Stress- infections, surgery
* Sudden withdrawal of corticosteroids
* Adrenal surgery
* Sudden pituitary gland destruction
Manifestations of glucocorticoid and mineralocorticoid
deficiencies
Hypotension, tachycardia
Dehydration
Decreased sodium, increased potassium, increased glucose
Fever, weakness, confusion
Severe vomiting, diarrhea, pain
Shock may cause circulatory collapse
Diagnostic Studies for Addison’s
ACTH stimulation test
Baseline levels of cortisol and ACTH
IV injection of synthetic ACTH (cosyntropin) given
Levels rechecked after 30 and 60 minutes
* Elevated blood cortisol level is normal
* Little or no increase in cortisol levels in Addison’s disease
* High ACTH level in primary adrenal insufficiency
CRH stimulation test
Abnormal ACTH test response
IV injection of synthetic CRH
Blood drawn after 30 and 60 minutes
* High ACTH levels with no cortisol indicates Addison’s disease
* Absence of ACTH or delayed response common in secondary adrenal insufficiency
High potassium
Low chloride, sodium, glucose
Anemia
Increased BUN
ECG changes
CT scan, MRI
Caring for Addison’s
Manage underlying cause
Lifelong hormone therapy
Hydrocortisone
* Increased during periods of stress
Fludrocortisone (Florinef)
Women need androgen replacement
Increase dietary salt intake
Corticosteroid Therapy
Effective in treating many diseases and disorders
Complications and side effects with long-term use
Potential benefits must be weighed against risks
Expected effects of corticosteroid therapy
Antiinflammatory action
Immunosuppression
Maintenance of normal BP
Side effects
Decreased potassium and calcium
Increased glucose and BP
Delayed healing
Susceptibility to infection
Suppressed immune response
Side effects
Peptic ulcer disease
Muscle atrophy/weakness
Mood and behavior changes
Moon facies, truncal obesity
Protein depletion
Risk for acute adrenal crisis if therapy is stopped abruptly
Hyperaldosteronism
Etiology and Pathophysiology
Conn’s syndrome
Excess aldosterone secretion
Sodium retention
Potassium and hydrogen ion excretion
Hypertension with hypokalemic alkalosis
Primary hyperaldosteronism
Solitary adrenocortical adenoma
Genetic link
Secondary hyperaldosteronism
Nonadrenal cause
* Renal artery stenosis
* Renin-secreting tumors
* Chronic kidney disease
Hyperaldosteronism
Clinical Manifestations
Increased aldosterone
Sodium retention
Potassium excretion
Sodium retention
Hypernatremia, hypertension, headache
No edema
Hypokalemia
Muscle weakness
Fatigue
Dysrhythmias
Glucose intolerance
Metabolic alkalosis → tetany
Primary aldosteronism
Increased plasma aldosterone levels
Increased sodium levels
Decreased potassium levels
Decreased plasma renin activity
CT scan or MRI
Plasma 18-hydroxycorticosterone level