hyperthyroidism prevalence women 2% men 0.2% 15% of cases occur in patients older than 60 years of...
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HYPERTHYROIDISM
Prevalence
Women 2%Men 0.2%15% of cases occur in
patients older than 60 years of age
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Clinical Symptoms
Depends on Age of patient Magnitude of hormonal excess Presence of co-morbid condition
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Mechanism of Clinical Symptoms
1. Catabolism2. Enhancement of sensitivity to
catecholamines
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Clinical Symptoms
Clinical manifestations of hyperthyroidism are largely independent of its cause.
However, causing disorder may have other effects.
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Clinical Symptoms
Older patient presents with lack of clinical signs and symptoms, which makes diagnosis more difficult
Thyroid storm is a rare presentation, occurs after stressful illness in under treated or untreated patient.
Characteristics -Delirium -Dehydration -Severe tachycardia -Vomiting -Fever -Diarrhea
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Clinical symptoms
Skin -Warm
-May be erythematous (due to increased blood flow)
-Smooth- due to decrease in keratin-Sweaty and heat intolerance-Onycholysis –softening of nails and
loosening of nail beds
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Clinical symptoms
Hyperpigmentation -Due the patient increase ACTH secretion
Pruritis -mainly in graves disease
Thinning of hair Vitilago and alopecia areata
-mainly due to autoimmune disease Infilterative dermopathy
-Graves disease, most common on shins
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Clinical symptoms
Eyes Stare Lid lag
*Due to sympathetic over activity *Only Grave’s disease has ophthalmopathy
-Inflammation of extraocular muscles, orbital fat and connective tissue.
-This results in exopthalmos -More common in smokers
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Clinical symptoms
Eyes Impaired eye muscle function (Diplopia) Periorbital and conjunctival edema Gritty feeling or pain in the eyes Corneal ulceration due to lid lag and proptosis Optic neuritis and even blindness
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Clinical symptoms
Cardiovascular System
Increased cardiac output (due to increased oxygen demand and increased cardiac contractibility.
Tachycardia Widened pulse pressure High output – heart failure
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Clinical symptoms
Cardiovascular System
Atrial fibrillation, 10-20% of patients. More common in elderly
Atrial ectopy 60% of A-fib will convert to normal sinus
rhythm with treatment (4-months of becoming euthyroid)
Mitral valve problems LVH and cardiomyopathy
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Serum Lipids
Low total cholesterol Low HDL Low total cholesterol/HDL ratio
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Respiratory System Dyspnea on rest and with exertion Oxygen consumpation and CO2 production
increases. Hypoxemia and hypercapnea, which
stimulates ventilation Respiratory muscle weakness Decreased exercise capacity Tracheal obstruction May exacerbate asthma Increased pulmonary arterial pressure
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Clinical symptoms
GI System -Weight loss due to increased calorigenesis -Hyperdefecation
-Malabsorption-Steatorrhea-Celiac Disease (in Grave’s Disease)-Hyperphagia (weight gain in younger patient)-Anorexia- weight loss in elderly-Dysphagia-Abnormal LFT especially phosphate
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Clinical symptoms
Hematological System Normochromic normocytic anemia Serum ferritin may be high Grave’s disese
ITP Pernicious anemia Anti-neutrophiliac antibody
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Clinical symptoms
GU System Urinary frequency and nocturia Enuresis is common in children
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Clinical symptoms
GU SystemWomen Increased SHBG High serum estradiol Low free estradiol High LH Reduce mid-cycle LH surge Oligomenorrhea and amenorrhea Anovulatory infertility
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Clinical symptoms
GU SystemMen High SHBG High total testosterone Low free testosterone High serum LH High serum estradiol Gynecomastia Decreased libido Erectile dysfunction Decreased or abnormal sperm
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Clinical symptoms
Skeletal System Bone resorption Increased porosity of cortical bone Reduced volume of trabecular bone Serum alkaline phosphate is increased Increased osteoblasts Inhibit PTH secretions Decreased calcium absorption and increased
excretion Osteoporosis, Fractures
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Clinical symptoms
Skeletal SystemGrave’s disease is associated with thyroid
acropathy-Clubbing of nails-Periosteal bone formation in metacarpal bone or phalanges
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Clinical symptoms
Neuromuscular System
Tremors-outstretched hand and tongue Hyperactive tendon reflexes
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Clinical symptoms
Psychiatric Hyperactivity Emotional lability Anxiety Decreased concentration Insomnia
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Clinical symptoms
Muscle Weakness
Proximal muscle weakness in 50% pts. Decreased muscle mass and strength May take up to six months after euthyroid
state to gain strength Hypokelemic periodic paralysis especially in
Asian men (cause is not known) Myesthenia Gravis, especially in Grave’s
disease.
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Clinical symptoms
Endocrine Increased sensitivity of pancreatic beta cells to
glucose Increased insulin secretion Antagonism to peripheral action of insulin Latter effects usually predominate leading to
intolerance.
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Etiology
1 Grave’s disease Autoimmune disease caused by antibodies to
TSH receptors Can be familial and associated with other
autoimmune diseases2 Toxic multi-nodular goiter 5% of all cases 10 times more common in iodine deficient
area Typically occurs in older than 40 with long
standing goiter
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Etiology
3 Toxic adenoma More common in young patients Autonomically functioning nodule
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Etiology
4 ThyroiditisSubacute Abrupt onset due to leakage of hormones Follows viral infection Resolves within eight months Can re-occurLymphatic and postpartum Transient inflammation Postpartum can occur in 5-10% cases in the
first 3-6 months Transient hypothyroidism occurs before
resolution
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Etiology
5 Treatment Induced HyperthyroidismIodine Induced Excess iodine indirect Exposure to radiographic contrast media Medication Excess iodine increases synthesis and release of
thyroid hormone in iodine deficient and older patients with pre-existing goiters
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Etiology
Amiodarone Induced Thyroiditis Up to 12% of patients, especially in iodine
deficient cases Most common cause of iodine excess in US. Two types: *Type I - due to excess iodine Amiodarone
contains 37% iodine. *Type II –– occurs in normal thyroid
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Etiology
Thyroid Hormone Induced Factitious hyperthyroidism in accidental or
intentional ingestion to lose weight Tumors -Metastatic thyroid cancer -Ovarian tumor that produces thyriod
hormone (struma ovarii) -Trophoblastic tumor -TSH secreting tumor
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Signs and symptoms of hyperthyroid
TSH level
Low TSHHigh TSH (rare)
Measure T4
High
Secondary hyperthyroidism
Image pituitary gland
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Low TSH
Measure Free T4 Level
Normal High
Measure Free T3 Level
Normal High
-Subclinical hyperthyroidism
-Resolving Hyperthyroidism
-Medication
-Pregnancy
-New thyroid illness
T3 Toxicosis
Primary hyperthyroidism
Thyroid uptake
Low High
Measure thyroglobulin
decreased Increased
Exogenous ThyroiditisIodide exposureExrtraglandular production
DIffuse Nodular
hormone
Graves disease
Multiple areas
One “hot” area
Toxic multinodular goiter
Toxic adenoma
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Etiology
Hyperthyroidism with high RIU - Grave’s disease - Toxic adenoma - Toxic multinodular goiter - TSH- producing pituitary adenoma - Hyperemesis gravidarum - Trophoblastic disease
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Etiology
Hyperthyroidism with low RIU - Subacute thyroiditis - Exogenous harmone intake - Ectopic ovarii - Metastatic follicular thyroid CA - Radiation thyroiditis - palpation thyroiditis - Amiodarone induced
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Treatment
Treatment depends upon -Cause and severity of disease -Patients age -Goiter size -Comorbid condition -Treatment desired
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Treatment
The goal of therapy is to correct hyper-metabaolic
state with fewest side effects and lowest incidence of hypothyroidism.
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Options Anti-thyroid drugs Radioactive iodine Surgery Beta-blocker and iodides are adjuncts to above
treatment
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Beta Blockers
Prompt relief of adrenergic symptoms Propranolol widely used Any beta blocker can be used, but non-
selectives have more direct effect on hyper-metabolism
Start with 10-20 mg q6h Increase progressively until symptoms are
controlled Most cases 80-320 mg qd is sufficient CCB can be used if beta blocker not tolerated
or contraindicated
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Iodides
Iodide blocks peripheral conversion of T4 to T3 and inhibits hormone release. These are used as adjunct therapy
• Before emergency non-thyroid surgery• Beta blockers cannot curtail symptoms• Decrease vascularity before surgery for
Grave’s disease
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Iodides
Iodides are not used for routine treatment because of paradoxical increase of hormone release with prolonged use
Commonly used: Radiograph contrast agents -Iopanoic acid -Ipodate sodium Potassium iodide Dose 1 gram/ 12 weeks
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Anti-thyroid Drugs
They interfere with organification of iodine—suppress thyroid hormone levels
Two agents: -Tapazole (methimazole) -PTU (propylthiauracil)
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Anti-thyroid Drugs
Remission rate: 60% when therapy continued for two years
Relapse in 50% of cases. Relapse more common in -smokers -elevated TS antibodies at end of therapy
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Anti-thyroid Drugs
Methimazole
Drug of choice for non-pregnant patients because of :
Low cost Long half life Lower incidence of side effects Can be given in conjunction with beta-blocker Beta-blockers can be tapered off after 4-8
weeks of therapyDose 15-30 mg/day
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Anti-thyroid Drugs
Methimazole Monthly Free T4 or T3 until euthyroid Maintenance dose 5-10 mg/day TSH levels may remain undetectable for months
after euthyroid and not to be used to monitor the therapy
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Anti-thyroid Drugs
Methimazole At one year if patient is clinically and
biochemically euthyroid and TS antibodies are not detectable, therapy can be discontinued
Monitor every three months for first year then annually
Relapses are more common in the first year but can occur years later
If relapse occurs, iodide or surgery although anti-thyroid drugs can be restarted
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Anti-thyroid Drugs
PTU Prefered for pregnant patients Methimazole is associated with rare genetic
abnormalities Dose 100 mg t.i.d Maintenance 100-200 mg/day Goal: Keep Free T4 at upper level of normal
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Anti-thyroid Drugs
Complications Agranulocytosis up to 0.5% High with PTU Can occur suddenly Mostly reversible with supportive Tx Routine WBC monitoring controversial Some people monitor WBC every two weeks
for first month then monthly Advised to stop drug if they develop sudden
fever or sore throat
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Radioactive Iodine
Treatment of choice for Grave’s disease and toxic nodular goiter
Inexpensive Highly effective Easy to administer Safe Dose depends on estimated weight of gland Higher dose increases success rate but higher
chance of hypothyroidism Some studies have shown increase of
hypothyroidism irrespective of dose
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Radioactive Iodine
Higher dose is favored in older patient Cardiac disease Other group needs prompt control Toxic nodular goiter or toxic adenoma
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Radioactive Iodine
Side effects 50% of Grave’s ophthalmology can develop or
worsen by use of radioactive iodine Use 40-50 mg Prednisone for at least three
months can prevent or improve severe eye disease in 2/3 of patients
Use lower dose in ophthalmology because post Tx hypothyroidism may be associated with exacerbation of eye disease
Smoking makes ophthalmopathy worse.
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Radioactive Iodine
Use of anti-thyroid drugs with iodine is not recommended in most cases
May improve safety for severe or complicated cases
Withdraw three days before iodine Tx Beta blockers used to control symptoms before
radioactive iodine and can be combined throughout Tx
Iodine containing meds need to be stopped several weeks before therapy
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Radioactive Iodine
Safety Most radioactive iodine is eliminated in the
urine, saliva and feces in 4-8 weeks. Have double flushing of toilet and frequent
hand washing for several weeks No close contact with children and pregnant
patients for 48-72 hours Additional Tx may be needed after three
months if indicated
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Surgery
Radioactive iodine has replaced surgery for Tx of hyperthyroidism
Subtotal thyroidectomy is most common This limits incidence of hypothyroidism to 25% Total thyroidectomy in large goiter or severe
disease
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New Treatment
Endoscopic subtotal thyroidectomy Embolization of thyroid arteries Plasmaphoresis Percutaneous ethanol injection into toxic
nodule L-Carnitine supplementation may improve
symptoms and may prevent bone loss