Module 8: Endocrine Problems Flashcards by Jessica Rockowitz

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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

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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

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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

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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

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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)

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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

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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

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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

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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

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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

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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

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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

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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)

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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

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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