HYPERTHYROIDISM

Dr RAJESHWAR REDDY
Normal Thyroid State
 Synthesis and release of thyroid hormone is
controlled by TSH released from the anterior
pituitary
 TSH is controlled by the release of thyroid
releasing hormone (TRH) from the
hypothalmus and a negative feedback loop to
the pituitary
 Thyroid hormone production is dependent on
adequate adequate iodine intake
Normal Thyroid State
 Thyroid hormone is reversible bound to
various proteins including thyroxine-binding
globulin (TBG)
 Free unbound portions are biologically active
 T4 is the predominant circulating hormone
 T4 is deiodinated to t3
 T3 is biologically more active than T4 but has

a shorter half-life
Hyperthyroidism
 Occurs in in all ages
◦ Uncommon under the age of 15
 10 x’s more common in women
 Graves disease is the most common

etiology
 Toxic multinodular and toxic nodular

goiters are the next most common

etiologies
Clinical features of thyrotoxicosis
 Neuromuscular:
 Nervousness,irritability,emotional
liability,psychosis
 Tremor
 Hyperreflexia,ill sustained clonus
 Muscle weakness,proximal myopathy,bulbar
myopathy
 Reproductive:Amenorrhoea,Oligomenorrhoe
a
Infertility,impotence
Thryotoxicosis..
 Gastrointestinal:
 Weight loss despite increased appetite
 Hyperdefecation
 Diarrhoea and steatorrhoea
 Vomiting
 Cardiorespiratory:
 Palpitations,Sinus tachycardia,Atrial fibrillation
 Increased pulse pressure
 Dyspnea on exertion
 Angina,cardiomyopathy and heart failure
Thyrotoxicosis..
 Others:
 Heat intolerance
 Increased sweating
 Fatigue
 Gynaecomastia
 Palmar erythema, Onycholysis
Nuclear thyroid scintigraphy iodine 123
(I-123) uptake and scan:
Radioactive iodine
Common Forms (85-90% of cases)
uptake over neck
Diffuse toxic goiter (Graves disease) Increased
Toxic multinodular goiter (Plummer disease) Increased
Thyrotoxic phase of subacute thyroiditis Decreased
Toxic adenoma Increased
Less Common Forms
Iodide-induced thyrotoxicosis Variable
Excess human chorionic gonadotropin (molar
Decreased
pregnancy/choriocarcinoma)
Thyrotoxicosis factitia Decreased

14
15
Hyperthyroidism
Graves’ disease
 Also known as Parry’s or Basedow’s disease.
 Graves’ disease is a disorder with three

major manifestations:
 1)Hyperthyroidism with diffuse goitre
 2)Ophthalmopathy and
 3)Dermopathy.
 These three manifestations may not appear

together.
Incidence and prevalence
 Relatively common disease that can occur at
any age
 More common in the 3rd and 4th decade
 Disease is more frequent in women(7:1)
 Genetic factors play a important role
 An overlap exsists with other autoimmune

diseases suggesting Graves is also a

autoimmune thyroid disease
Etiology and Pathogenesis
 Cause of Graves’ is unknown
 No single factor is responsible for the entire
syndrome
 With respect to hyperthyroidism,the central
disorder is a disruption of homeostatic
mechanisms that normally control hormone
[Link] disruption results from the
presence in the plasma of thyroid
stimulating immunoglobulins(TSI’s) of IgG
class and inhibition of the binding of TSH to
its receptors(TBII’s).These factors represent
TRAb’s.
Pathology
 Thyroid gland is diffusely enlarged,soft
and vascular.
 There is parenchymatous hyperplasia and
hypertrophy with lymphocytic infilteration.
 The ophthalmopathy is characterized by
an inflammatory infilterate of the orbital
contents,with lymphocytes,mast cells and
plasma cells
 The dermopathy of Graves’ disease is
characterized by thickening of the
dermis,which is infilterated by
lymphocytes and mucopolysaccharides
Clinical features
 The clinical manifestations include those
that reflect the associated thyrotoxicosis
and those specifically related to Graves’
disease
Clinical features of thyrotoxicosis
 Neuromuscular:
 Nervousness,irritability,emotional
liability,psychosis
 Tremor
 Hyperreflexia,ill sustained clonus
 Muscle weakness,proximal myopathy,bulbar
myopathy
 Reproductive:Amenorrhoea,Oligomenorrhoe
a
Infertility,impotence
Thryotoxicosis..
 Gastrointestinal:
 Weight loss despite increased appetite
 Hyperdefecation
 Diarrhoea and steatorrhoea
 Vomiting
 Cardiorespiratory:
 Palpitations,Sinus tachycardia,Atrial fibrillation
 Increased pulse pressure
 Dyspnea on exertion
 Angina,cardiomyopathy and heart failure
Thyrotoxicosis..
 Others:
 Heat intolerance
 Increased sweating
 Fatigue
 Gynaecomastia
 Palmar erythema, Onycholysis
Manifestations of Graves’ disease
 The distinctive manifestations-diffuse
hyperfunctioning goiter,ophthalmopathy,and
dermopathy-appear in varying
combinations,and in varying
frequencies,goiter being the most common.
 Premature greying of hair and patchy vitiligo

are non specific features of Graves’s

Goiter
 Is diffuse and toxic and maybe asymetric and
lobular.
 There may be presence of bruit over the

goiter
Ophthalmopathy
 Signs of Graves’s ophthalmopathy are
divided into two components:
 1) Spastic: Stare, lid lag and lid retraction
which account for the “frightened” facies.
 2) Mechanical: Proptosis of varying
degrees,ophthalmoplegia,and congestive
occulopathy characterized by
chemosis,conjunctivitis,periorbital swelling
and the potential complications of corneal
ulceration,optic neuritis and optic atrophy.
Dermopathy
 Usually occurs over the dorsum of the legs or
feet and is termed localized or pretibial
myxedema.
 It is usually a late phenomenon
 The affected area is usually demarcated from
the normal skin by being raised andthickened
and having a peau d’ orange appearance;it
may be pruritic and hyperpigmented.
 The most common presentation is non pitting
oedema,but lesions maybe plaque
like,nodular or polypoid.
 Clubbing of the fingers and toes accompanies
and is termed thyroid acropachy
Toxic multinodular goiter
 Toxic multinodular goiter causes 5 percent
of the cases of hyperthyroidism.
 It typically occurs in patients older than 40

years with a long-standing goiter.

Toxic adenoma
 Toxic adenomas are autonomously
functioning nodules that are found most
commonly in younger patients and in
iodine-deficient areas.

33
Subacute thyroiditis

 Soreness in the neck.

 It often follows a viral illness.
 Symptoms usually resolve within one year.
 This condition can be recurrent in some

patients.
 ESR is markedly elevated.

34
Subacute thyroiditis

Time course of changes in thyroid function

tests in patients with Subacute thyroiditis.

35
Amiodarone-induced
 Amiodarone- (Cordarone-) induced
hyperthyroidism can be found in up to 12
percent of treated patients.
 Type I - Because amiodarone contains 37
percent iodine, is an iodine induced
hyperthyroidism.
 Type II is a thyroiditis that occurs in
patients with normal thyroid glands.
 Medications such as interferon and
interleukin-2 also can cause type II.

36
Thyroid hormone-induced

 Factitial hyperthyroidism is caused by the

intentional or accidental ingestion of excess
amounts of thyroid hormone.
 Some patients may take thyroid

preparations to achieve weight loss.

37
Thyroid Storm
 A life threatening hypermetabolic state due
to hyperthyroidism
 Mortality rate is high (10-75%) despite

treatment
 Usually occurs as a result of previously

unrecognized or poorly treated

hyperthyroidism
 Thyroid hormone levels do not help to

differentiate between uncomplicated

hyperthyroidism and thyroid storm
Thyroid Storm
 Preciptatnts of Thyroid Storm (tabel 215-4)

Infection Trauma

DKA MI

CVA PE

Surgery Withdrawal of thyroid

med
Iodine administration Palpation of thyroid
gland
Ingestion of thyroid Unknown etiology (20-
hormone 25%)
Thyroid Storm
 Clinical features
◦ The most common signs are fever, tachycardia out
of proportion to the fever, altered mental status,
and diaphoresis
◦ Clues include a history of hyperthyroidism,
exophthalmoses, widened pulse pressure and a
palpable goiter
◦ Patients may present with signs of CHF
Thyroid Storm
 Clinical features cont.
◦ Common GI symptoms include diarrhea and
hyperdefecation
◦ Apathetic thyrotoxicosis is a distinct presentation
seen in the elderly
 Characteristic symptoms include lethargy, slowed
mentation, and apathetic facies
 Goiter, weight loss , and proximal muscle weakness
also present
Thyroid Storm
 Diagnosis
◦ Thyroid storm is a clinical diagnosis based upon
suspicion and treated empirically
◦ Lab work is non specific and may include
Leukocytosis, hyperglycemia, elevated transaminase
and elevated bilirubin
Thyroid Storm
 Treatment
◦ Initial stabilization includes airway protection,
oxygenation, fluids and cardiac monitoring
◦ Treatment can then be divided into 5 areas:
 General supportive care
 Inhibition of thyroid hormone synthesis
 Retardation of thyroid hormone release
 Blockade of peripheral thyroid hormone effects
 Identification and treatment of precipitating events
Thyroid Storm
 Drug Treatment of Thyroid Storm (table 216-6)
◦ Decrease de novo synthesis:
 Porpythiouracil 600-1000mg PO initially, followed by 200-250 mg q 4
hrs
 Methimazole 40 mg PO initial dose, then 25 mg PO q6h
◦ Prevent releases of hormone (after synthesis blockade intiated)
 Iodine Iaponoric acid (Telepaque) 1 gm IV q8h for the first
24 h, then 500 mg bid or Potassium iodide (SSKI) 5 drops PO
q6h or Lugol solution 8-10 drops PO q6h
 Lithuim 800-1200 mg PO every day
◦ Prevent peripheral effects:
 B-Blocker Propanolol (IV) titrate 1-2 mg q 5min prn (may need
240-480mg PO q day) or Esmolol (IV) 500 mcg/kg IV bolus, then
50-200 mcg/kg per min maintenance
 Guanethidine 30-40 mg PO q 6 h
 Reserpine 2.5-5 mg IM q4-6h
 Other consideration:
 Corticosteroids Hydrocortisone 100 mg IV q 8 h or
dexamethosone 2 mg IV q 6 hr
 Antipyretics Cooling blanket
acteaminophen 650 mg PO q 4-6h
Thyroid Storm
 Treatment cont
◦ Propranolol has the additional effects of blocking
peripheral conversion of T4-T3
◦ Avoid Salicylates because it may displace T4
from TBG
◦ If the patient continues to deteriorate despite
appropriate therapy circulating thyroid hormone
may be removed by plasma transfusion,
plasmapheresis, charchoal plasmaperfusion
◦ Remember you must not administer iodine until
the synthetic pathway has been blocked
HYPERTHYROIDISM IN
PREGNANCY
Physiologic
Changes in Pregnancy
 Free thyroxine levels remain within the
normal range during pregnancy (though total
thyroxine levels are increased secondary to
increased TBG.)
 TSH decreases slightly in first trimester.
 The thyroid gland increases slightly

in size during pregnancy.

Hyperthyroidism
 95% of hyperthyroidism in pregnancy
is secondary to Graves’ Disease.
 A good pregnancy outcome can be

expected in patients with good control.

Hyperthyroidism
 Untreated hyperthyroidism is associated
with decreased fertility, an increased rate
of miscarriage, intrauterine growth
retardation (IUGR), premature labor, and
perinatal mortality.
 Poorly controlled thyrotoxicosis is associated

with thyroid storm especially at labor and

delivery.
DIAGNOSIS
 The diagnosis of hyperthyroidism in pregnant
women should be based primarily on a serum TSH
value <0.01 mU/L and also a high serum free T4
value. Free T3 measurements may be useful in
women with suppressed serum TSH concentrations
and normal or minimally elevated free T4 values.
 High serum hCG concentrations during early

pregnancy, found in women with hyperemesis

gravidarum or multiple pregnancies, may result in
transient subclinical or rarely overt
hyperthyroidism