Thyroid gland Disorders for BHMS Final Year Students

1. Thyroid Gland
Dr.Ravi Jain
M.D.(Hom.)
Assistant Professor
Department of Practice of Medicine
Jayoti Vidyapeet Women’s University,Jaipur

2.  Produces two hormones,
 Thyroxine (T4)
 Triiodothyronine (T3)
 Important Functions
 Cell differentiation during development.
 Help maintain thermogenic and metabolic homeostasis in
the adult.

3.  The thyroid derived from Greek word thyreos, shield, plus
eidos, form)
 It consists of two lobes connected by an isthmus.
 Located anterior to the trachea between the cricoid
cartilage and the suprasternal notch.

4.  Normal thyroid is :
 12–20 g in size
 Highly vascular
 Soft in consistency.
 The recurrent laryngeal nerves traverse the lateral borders of
the thyroid gland.
 The thyroid gland develops from the floor of the primitive
pharynx during the third week of gestation. The developing
gland migrates along the thyroglossal duct to reach its final
location in the neck.

5.  Autoimmune disorders of the thyroid gland can
stimulate:
 Overproduction of thyroid hormones (thyrotoxicosis)
 or
 Glandular destruction and hormone deficiency
(hypothyroidism).
 Benign nodules and various forms of thyroid cancer are
relatively common.

6. Hypothyroidism

7.  A common condition with various causes, but autoimmune
disease (Hashimoto’s thyroiditis) and thyroid failure
following I131
or surgical treatment of thyrotoxicosis
account for over 90% of cases.

8. Causes of Hypothyroidism
 Primary
 Transient
 Secondary

9. Primary
 Autoimmune hypothyroidism: Hashimoto’s thyroiditis,
atrophic thyroiditis.
 Iatrogenic : 131I treatment, subtotal or total thyroidectomy,
external irradiation of neck for lymphoma or cancer.
 Drugs : antithyroid drugs
 Congenital hypothyroidism: absent or ectopic thyroid gland,
dyshormonogenesis, TSH-R mutation.
 Iodine deficiency
 Infiltrative disorders: amyloidosis, sarcoidosis, scleroderma,
Riedel’s thyroiditis.

10. Transient
 Silent thyroiditis, including postpartum thyroiditis.
 Subacute thyroiditis.
 Withdrawal of thyroxine treatment in individuals with an
intact thyroid.
 After I131
treatment or subtotal thyroidectomy for Graves’
disease.

11. Secondary
 Hypopituitarism : tumors, pituitary surgery or irradiation,
infiltrative disorders,Sheehan’s syndrome, trauma.
 Hypothalamic disease : tumors, trauma, infiltrative
disorders, idiopathic.

12. Symptoms of Hypothyroidism
 Tiredness, weakness
 Dry skin
 Feeling cold
 Hair loss
 Difficulty concentrating and poor memory
 Constipation
 Weight gain with poor appetite

13.  Dyspnea
 Hoarse voice
 Menorrhagia (later oligomenorrhea or amenorrhea)
 Paresthesia
 Impaired hearing

14. Signs of Hypothyroidism
 Dry coarse skin
 Cool peripheral extremities
 Puffy face, hands, and feet (myxedema)
 Diffuse alopecia
 Bradycardia
 Peripheral edema
 Delayed tendon reflex relaxation
 Carpal tunnel syndrome
 Serous cavity effusions

15. Congenital Hypothyroidism
 Occurs in about 1 in 4000 newborns.
 Cause :
 Due to thyroid gland dysgenesis in 80–85%,
 Inborn errors of thyroid hormone synthesis in 10–15%,
 TSH-R antibody-mediated in 5%.
 Clinical Manifestations
 Majority of infants appear normal at birth.
 Prolonged jaundice, feeding problems, hypotonia, enlarged
tongue, delayed bone maturation, and umbilical hernia.

16. Congenital Hypothyroidism cont.
 Diagnosis : neonatal screening programs based on
measurement of TSH or T4 levels in heel-prick blood
specimens.
 Treatment : T4 is instituted at a dose of 10–15 μg/kg per
day.

17. Autoimmune Hypothyroidism
 Associated with :
 A goiter (Hashimoto’s, or goitrous thyroiditis)
 Minimal residual thyroid tissue (atrophic thyroiditis)
 Subclinical hypothyroidism
 Clinical hypothyroidism or overt hypothyroidism

18. Autoimmune Hypothyroidism cont.
 Prevalence :
 Incidence rate of autoimmune hypothyroidism is up to 4
per 1000 women and 1 per 1000 men.
 Common in Females 4 : 1
 Pathogenesis : marked lymphocytic infiltration of the
thyroid, atrophy of the thyroid follicles, absence of
colloid, and mild to moderate fibrosis.

19. Autoimmune Hypothyroidism cont.
 Clinical Manifestations :
 Onset is usually insidious.
 Goiter may not be large, but it is usually irregular and firm in
consistency.
 Skin is dry, decreased sweating, thinning of the epidermis, and
hyperkeratosis of the stratum corneum.
 Increased dermal glycosaminoglycan content traps water,
giving rise to skin thickening without pitting (myxedema).
 Puffy face with edematous eyelids and nonpitting pretibial
edema.

20. Autoimmune Hypothyroidism cont.
 Pallor, often with a yellow tinge to the skin due to carotene
accumulation.
 Nail growth is retarded, and hair is dry, brittle, difficult to
manage, and falls out easily.
 Thinning of the outer third of the eyebrows.
 Constipation
 Weight gain (despite a poor appetite).
 Libido is decreased in both sexes.
 Menorrhagia. Fertility is reduced, incidence of miscarriage is
increased.

21.  Myocardial contractility and pulse rate are reduced,
leading to a reduced stroke volume and bradycardia.
 Increased peripheral resistance with diastolic
hypertension.
 Blood flow is diverted from the skin, producing cool
extremities.
 Fluid may accumulate in other serous cavities and in the
middle ear, giving rise to conductive deafness.

22. Laboratory Evaluation
 TSH, T4 levels.
 Demonstration of TPO (Thyroid peroxidase) antibodies
present in >90%.
 FNA biopsy to confirm the presence of autoimmune
thyroiditis.
 Ultrasound
 Differential Diagnosis : An asymmetric goiter in
Hashimoto’s thyroiditis may be confused with a MNG
(multinodular groitre) or thyroid carcinoma.

23. Other Causes Of Hypothyroidism
 Iatrogenic hypothyroidism : In first 3–4 months after
radioiodine treatment, transient hypothyroidism may
occur due to reversible radiation damage.
 Because TSH levels are suppressed by hyperthyroidism,
unbound T4 levels are a better measure of thyroid
function.
 Iodine deficiency is responsible for endemic goiter and
cretinism.
 Secondary hypothyroidism : other anterior pituitary
hormone deficiencies. TSH levels may be low, normal, or
even slightly increased.
 The diagnosis is confirmed by detecting a low unbound T4
level.

24. Laboratory Evaluation
 Measurement of Thyroid Hormones : TSH assays
 Tests to Determine the Etiology of Thyroid Dysfunction :
circulating antibodies against TPO and Tg.
 Radioiodine Uptake and Thyroid Scanning : radioisotopes
of iodine (123
I, 125
I, 131
I) and 99
mTc
 Thyroid Ultrasound

25. Management
 Daily replacement dose of levothyroxine is usually 1.6
μg/kg body weight.
 Special consideration : Women with a history or high risk
of hypothyroidism should ensure that they are euthyroid
prior to conception and during early pregnancy because
maternal hypothyroidism may adversely affect fetal neural
development and cause preterm delivery.
 The presence of thyroid autoantibodies alone, in a
euthyroid patient, is also associated with miscarriage and
preterm delivery.

26. Thyrotoxicosis

27.  The state of thyroid hormone excess.
 Etiology of thyrotoxicosis :
 Hyperthyroidism caused by Graves’ disease, toxic MNG,
and toxic adenomas.
 1. Primary Hyperthyroidism
 2. Thyrotoxicosis Without Hyperthyroidism
 3. Secondary Hyperthyroidism

28. Primary Hyperthyroidism
 Graves’ disease
 Toxic multinodular goiter
 Toxic adenoma
 Struma ovarii
 Drugs: iodine excess (Jod-Basedow phenomenon)

29. Thyrotoxicosis Without
Hyperthyroidism
 Subacute thyroiditis
 Silent thyroiditis
 Other causes of thyroid destruction: radiation, infarction
of adenoma
 Ingestion of excess thyroid hormone (thyrotoxicosis
factitia) or thyroid tissue

30. Secondary Hyperthyroidism
 TSH-secreting pituitary adenoma.
 Thyroid hormone resistance syndrome: occasional patients
may have features of thyrotoxicosis.
 Chorionic gonadotropin-secreting tumors.
 Gestational thyrotoxicosis.

31. Clinical Features (Symptoms)
 Hyperactivity, irritability, dysphoria.
 Heat intolerance and sweating
 Palpitations
 Fatigue and weakness
 Weight loss with increased appetite
 Diarrhea
 Polyuria
 Oligomenorrhea,
 loss of libido

32. Clinical features (Signs)
 Tachycardia; atrial fibrillation in the elderly.
 Tremor.
 Goiter.
 Warm, moist skin.
 Muscle weakness, proximal myopathy.
 Lid retraction or lag.
 Gynecomastia.

33. Grave’s Disease
 It accounts for 60–80% of thyrotoxicosis.
 The prevalence varies among populations, reflecting
genetic factors and iodine intake.
 Occurs in up to 2% of women but is one-tenth as frequent
in men.
 Age : occurs between 20 and 50 years of age.

34. Predisposing factors
 Environmental and genetic factors.
 Stress
 Smoking
 Sudden increase in iodine intake.
 Postpartum period

35. Pathogenesis
 The hyperthyroidism of Graves’ disease is caused by TSI
(Thryoid Stimulating Immunoglobulin) that are synthesized
in the thyroid gland as well as in bone marrow and lymph
nodes.
 In the long term, spontaneous autoimmune hypothyroidism
may develop in up to 15% of patients with Graves’ disease.

36. Opthalmopathy reason :
 Cytokines appear to play a major role in thyroid-
associated ophthalmopathy.
 There is infiltration of the extraocular muscles by
activated T cells; the release of cytokines results in
fibroblast activation and increased synthesis of
glycosaminoglycans that trap water, thereby leading to
characteristic muscle swelling.
 Late in the disease, there is irreversible fibrosis of the
muscles.
 The increase in intraorbital pressure can lead to proptosis,
diplopia, and optic neuropathy.

37. Clinical Manifestations (Grave’s
Disease)
 Clinical presentation depends on the severity of
thyrotoxicosis, the duration of disease, individual
susceptibility to excess thyroid hormone, and the
patient’s age.
 Apathetic thyrotoxicosis : Occurs in elderly, present
mainly with fatigue and weight loss

38.  The thyroid is usually diffusely enlarged to two to three
times its normal size. The consistency is firm, but not
nodular.
 There may be a thrill or bruit, best detected at the
inferolateral margins of the thyroid lobes, due to the
increased vascularity of the gland and the hyperdynamic
circulation.

39. Graves’ Ophthalmopathy
 Sensation of grittiness, eye discomfort, and excess
tearing.
 Proptosis. proptosis may cause corneal exposure and
damage, especially if the lids fail to close during sleep.
 Periorbital edema, scleral injection, and chemosis are also
frequent.
 Muscle swelling results in diplopia.
 Most serious manifestation is compression of the optic
nerve.

40. “NO SPECS” scoring system to evaluate
ophthalmopathy
 0 = No signs or symptoms
 1 = Only signs (lid retraction or lag), no symptoms
 2 = Soft tissue involvement (periorbital edema)
 3 = Proptosis (>22 mm)
 4 = Extraocular muscle involvement (diplopia)
 5 = Corneal involvement
 6 = Sight loss

41.  Thyroid dermopathy : pretibial myxedema most frequent
over the anterior and lateral aspects of the lower leg. The
typical lesion is a noninflamed, indurated plaque with a
deep pink or purple color and an “orange skin”
appearance.
 Thyroid acropachy : Clubbing of fingers in <1%,

42. Laboratory Evaluation
 The TSH level is suppressed, and total and unbound
thyroid hormone levels are increased.
 Measurement of TPO antibodies.
 Diagnosis of Graves’ disease is straightforward in a patient
with biochemically confirmed thyrotoxicosis, diffuse
goiter on palpation, ophthalmopathy, and often a personal
or family history of autoimmune disorders.
 Diagnosis is generally established by a radionuclide
(99mTc, 123I, or 131I) scan and uptake of the thyroid.
 Scintigraphy is the preferred diagnostic test.

43. DD
 In secondary hyperthyroidism due to a TSH-secreting
pituitary tumor, there is also a diffuse goiter. The
presence of a nonsuppressed TSH level and the finding of
a pituitary tumor on CT or magnetic resonance scan (MRI)
scan suggest this diagnosis.
 Clinical features of thyrotoxicosis can mimic certain
aspects of other disorders, including panic attacks, mania,
pheochromocytoma, and weight loss associated with
malignancy.
 The diagnosis of thyrotoxicosis can be easily excluded if
the TSH and unbound T4 and T3 levels are normal.
 A normal TSH also excludes Graves’ disease as a cause of
diffuse goiter.

44. Treatment
 The hyperthyroidism of Graves’ disease is treated by :
 Reducing thyroid hormone synthesis, using antithyroid
drugs.
 Reducing the amount of thyroid tissue with radioiodine
(131
I) treatment or by thyroidectomy.

45. Thyroiditis

46. Causes of Thyroiditis
 Acute
 Subacute
 Chronic

47. Acute thyroiditis
 Bacterial infection: especially Staphylococcus,
Streptococcus, and Enterobacter.
 Fungal infection: Aspergillus, Candida, Coccidioides,
Histoplasma, and Pneumocystis.
 Radiation thyroiditis after 131I treatment

48. Subacute thyroiditis
 Viral (or granulomatous) thyroiditis
 Silent thyroiditis (including postpartum thyroiditis)
 Drug induced

49. Chronic thyroiditis
 Autoimmunity: focal thyroiditis, Hashimoto’s thyroiditis,
atrophic thyroiditis Riedel’s thyroiditis
 Parasitic thyroiditis: echinococcosis, strongyloidiasis,
cysticercosis
 Traumatic: after palpation

50. Acute Thyroiditis
 It is rare and due to suppurative infection of the thyroid.
 The patient presents with thyroid pain, often referred to
the throat or ears, and a small, tender goiter that may be
asymmetric.
 Fever, dysphagia, and erythema over the thyroid are
common with systemic symptoms of a febrile illness and
lymphadenopathy.
 The erythrocyte sedimentation rate (ESR) and white cell
count are usually increased, but thyroid function is
normal.

51. Subacute Thyroiditis (De Quervain’s
thyroiditis)
 De Quervain’s thyroiditis, granulomatous thyroiditis, or
viral thyroiditis.
 Caused by Viral infection (mumps, coxsackie, influenza,
adenoviruses, and echoviruses).
 The symptoms can mimic pharyngitis.
 The peak incidence occurs at 30–50 years.
 Women are affected three times more frequently than
men.

52. Pathophysiology of Subacute
Thyroiditis
 Characteristic patchy inflammatory infiltrate with
disruption of the thyroid follicles.
 During the initial phase of follicular destruction, there is
release of Tg and thyroid hormones, leading to increased
circulating T4 and T3 and suppression of TSH.
 During this destructive phase, radioactive iodine uptake is
low or undetectable.
 After several weeks, the thyroid is depleted of stored
thyroid hormone and a phase of hypothyroidism typically
occurs, with low unbound T4 (and sometimes T3) and
moderately increased TSH levels.

53.  Radioactive iodine uptake returns to normal or is even
increased as a result of the rise in TSH.
 Finally, thyroid hormone and TSH levels return to normal
as the disease subsides usually several months after onset.

54. Clinical Manifestations of Subacute
Thyroiditis
 Patient usually presents with a painful and enlarged
thyroid, sometimes accompanied by fever.
 There may be features of thyrotoxicosis or
hypothyroidism, depending on the phase of the illness.
 The patient typically complains of a sore throat, and
examination reveals a small goiter that is exquisitely
tender. Pain is often referred to the jaw or ear.
 Complete resolution is the usual outcome, but late onset
permanent hypothyroidism occurs in 15% of cases.

55. Laboratory Evaluation
 Thyroid function tests characteristically evolve through
three distinct phases over about 6 months:
 Thyrotoxic phase : T4 and T3 levels are increased, TSH is
suppressed. High ESR and low uptake of radioiodine. The
white blood cell count may be increased, and thyroid
antibodies are negative. FNA biopsy may be useful.
 Hypothyroid phase :
 Recovery phase :

56. Treatment of Subacute thyroiditis
 Large doses of aspirin or NSAIDs are sufficient to control
symptoms in many cases.
 Local or systemic symptoms, glucocorticoids should be
given.
 Thyroid function should be monitored every 2–4 weeks
using TSH and unbound T4 levels.
 Levothyroxine replacement may be needed if the
hypothyroid phase is prolonged

57. Silent Thyroiditis
 Painless thyroiditis, or silent thyroiditis.
 Patients with underlying autoimmune thyroid disease.
 Occurs in up to 5% of women 3–6 months after pregnancy
and is then termed postpartum thyroiditis.
 Thyrotoxicosis lasting 2–4 weeks, followed by
hypothyroidism for 4–12 weeks, and then resolution.
 Associated with the presence of TPO antibodies
antepartum.

58. Silent thyroiditis
 Silent thyroiditis can be distinguished from subacute
thyroiditis by a normal ESR and the presence of TPO
antibodies.
 Severe thyrotoxic symptoms can be managed with a brief
course of propranolol.
 Thyroxine replacement may be needed for the
hypothyroid phase but should be withdrawn after 6–9
months, as recovery is the rule.
 Annual follow-up thereafter is recommended.

59. Chronic Thyroiditis
 Associated with serologic evidence of autoimmunity,
particularly the presence of TPO antibodies.
 Hashimoto’s thyroiditis: an autoimmune disorder that
often presents as a firm or hard goiter of variable size.
 Riedel’s thyroiditis : a rare disorder that typically occurs
in middle-aged women.

60. Riedel’s thyroiditis
 Presents with insidious, painless goiter with local
symptoms due to compression of the esophagus, trachea,
neck veins, or recurrent laryngeal nerves.
 Dense fibrosis disrupts normal gland architecture and can
extend outside the thyroid capsule.
 Thyroid dysfunction is uncommon.
 The goiter is hard, nontender, often asymmetric, and
fixed, leading to suspicion of a malignancy.
 Diagnosis requires open biopsy.
 Treatment is directed to surgical relief of compressive
symptoms.

61. GOITER

62.  Goiter refers to an enlarged thyroid gland.
 Causes :
 Biosynthetic defects
 Iodine deficiency
 Autoimmune disease
 Nodular diseases

63.  Biosynthetic defects and iodine deficiency : are
associated with reduced efficiency of thyroid hormone
synthesis, leading to increased TSH, which stimulates
thyroid growth.
 In Graves’ disease, the goiter results from the TSH-R–
mediated effects of TSI.
 In Hashimoto’s thyroiditis it occurs because of acquired
defects in hormone synthesis, leading to elevated levels of
TSH and its consequent growth effects.
 Nodular disease is characterized by the disordered growth
of thyroid cells, often combined with the gradual
development of fibrosis.

64. DIFFUSE NONTOXIC (SIMPLE) GOITER
 Diffuse enlargement of the thyroid in absence of nodules
and hyperthyroidism.
 Most commonly caused by iodine deficiency.
 More common in women than men.
 TSH levels are usually normal or only slightly increased.
 Abnormalities at each step in hormone synthesis, iodide
transport , Tg synthesis, organification and coupling
(TPO), and the regeneration of iodide.

65. Clinical manifestations
 Thyroid function is preserved,
 Most goiters are asymptomatic.
 Examination of a diffuse goiter reveals a symmetrically
enlarged, nontender, generally soft gland without
palpable nodules.
 If the thyroid is markedly enlarged, it can cause tracheal
or esophageal compression.
 Substernal goiter may obstruct the thoracic inlet.

66. Pemberton’s sign
 Refers to symptoms of faintness with evidence of facial
congestion and external jugular venous obstruction when
the arms are raised above the head.
 It is used to evaluate venous obstruction in patients with
goiters. The sign is positive when bilateral arm elevation
causes facial plethora. It has been attributed to a “cork
effect” resulting from the thyroid obstructing the thoracic
inlet, thereby increasing pressure on the venous system.

67. Diagnosis and Treatment
 Low total T4, with normal T3 and TSH, reflecting
enhanced T4 T3 conversion.→
 Low urinary iodine levels (<50 μg/L) support a diagnosis of
iodine deficiency.
 Treatment
 Iodine replacement induces variable regression of goiter.
 Subtotal or near-total thyroidectomy for cosmetic reasons.
 Surgery should be followed by replacement with
levothyroxine

68. Multinodular Goiter
Non toxic multinodular goiter
Toxic multinodular goiter

69. Nontoxic Multinodular Goiter
 Occurs in up to 12% of adults.
 More common in women than men and increases in
prevalence with age.
 Pathogenesis includes multiple genetic, autoimmune, and
environmental influences.
 Histology reveals :hypercellular regions to cystic areas
filled with colloid. Fibrosis is often extensive, and areas of
hemorrhage or lymphocytic infiltration may be seen.
 TSH usually not elevated.

70. Clinical Manifestations
 Asymptomatic and euthyroid.
 Develops over many years and is detected on routine
physical examination, when an individual notices an
enlargement in the neck.
 If the goiter is large enough, it can lead to compressive
symptoms including difficulty swallowing, respiratory
distress (tracheal compression), or plethora (venous
congestion), but these symptoms are uncommon.
 Sudden pain in an MNG is usually caused by hemorrhage
into a nodule.
 Hoarseness, reflecting laryngeal nerve involvement, also
suggests malignancy

71. Diagnosis
 Thyroid architecture is distorted, and multiple nodules of
varying size are appreciated.
 Pemberton’s sign, characterized by facial suffusion when
the patient’s arms are elevated above the head, suggests
that the goiter has increased pressure in the thoracic
inlet.
 TSH level to exclude subclinical hyper- or hypothyroidism.
Thyroid function is usually normal.
 Tracheal deviation is common.
 Compression characteristically causes inspiratory stridor.

72.  CT or MRI to evaluate the anatomy of the goiter and the
extent of substernal extension or tracheal narrowing.
 Barium swallow reveal the extent of esophageal
compression.
 Ultrasonography to identify which nodules should be
biopsied based on sonographic features.

73. Treatment
 Dosage of 131
I Radioiodine is used with increasing frequency
because it can decrease goiter size and may selectively
ablate regions of autonomy.
 In acute compression occurs, glucocorticoid treatment or
surgery.

74. Toxic multinodular goiter
 Presence of functional autonomy is the cause. Molecular
basis for autonomy remains unknown.
 Genetic abnormalities known to confer functional
autonomy, such as activating TSH-R.
 Clinical Features includes subclinical hyperthyroidism or
mild thyrotoxicosis.
 The patient is usually elderly and may present with atrial
fibrillation or palpitations, tachycardia, nervousness,
tremor, or weight loss.

75. Diagnosis
 The TSH level is low. The uncombined T4 level may be
normal or minimally increased, T3 is often elevated to a
greater degree than T4.
 Thyroid scan shows heterogeneous uptake with multiple
regions of increased and decreased uptake.
 Ultrasound imaging to assess the presence of discrete
nodules corresponding to areas of decreased uptake.
 FNA may be indicated.

76. Treatment
 Antithyroid drugs normalize thyroid function.
 Radioiodine I131
is generally the treatment of choice.
 Surgery provides definitive treatment of underlying
thyrotoxicosis as well as goiter.

77. Hyperfunctioning Solitary Nodule
 Toxic adenoma : autonomously functioning thyroid
nodule.
 Cause : mutations that stimulate the TSH-R signaling
pathway.
 Clinical features : Thyrotoxicosis is usually mild. The
disorder is suggested by a subnormal TSH level.
 The presence of the thyroid nodule, which is generally
large enough to be palpable.
 Absence of clinical features suggestive of Graves’ disease
or other causes of thyrotoxicosis.

78. Diagnosis and Treatment
 Thyroid scan : provides a definitive diagnostic test,
demonstrating focal uptake in the hyperfunctioning nodule
and diminished uptake in the remainder of the gland.
 Treatment :
 Radioiodine ablation by 131
I.
 Antithyroid drugs and beta blockers can normalize thyroid
function.
 Ultrasound guidance, repeated ethanol injections and
percutaneous radiofrequency thermal ablation to ablate
hyperfunctioning nodules.

79. Thyrotoxic crisis (thyroid storm)
 It is rare and presents as a life threatening exacerbation
of hyperthyroidism, accompanied by :
 Fever,
 Delirium,
 Seizures,
 Coma,
 Vomiting,
 Diarrhea, and
 Jaundice.
 Even with treatment, The mortality rate is high 30%, due
to cardiac failure, arrhythmia, or hyperthermia.

80. Precipitated by
 Acute illness (e.g., stroke, infection, trauma, diabetic
ketoacidosis) with previously unrecognised or inadequately
treated thyrotoxicosis.
 Surgery : develop shortly after subtotal thyroidectomy.
 Radioiodine treatment : partially treated or untreated
hyperthyroidism with 131
I therapy when acute irradiation
damage may lead to a transient rise in serum thyroid
hormone levels.

81. Management
 Intensive monitoring and supportive care.
 Identification and treatment of the precipitating cause.
 Measures that reduce thyroid hormone synthesis.
 It includes :
 Rehydration
 Broadspectrum antibiotic
 Propranolol
 Sodium ipodate will restore serum T 3 levels to normal in
48–72 hours.
 Oral carbimazole to inhibit the synthesis of new thyroid
hormone.

82. Myxedema
 Primary hypothyroidism in juveniles and adults leads to
myxedema.
 Clinical features
 Depends upon the degree of impairment of thyroid
function and its duration.
 Insidious onset often unnoticed.
 Slow activities, lethargy, somnolence, constipation and
generalized disinterestedness.
 Weight gain, hairfall,Puffiness, thickening of skin.

83. Lab investigation
 T3 and T4 are low.
 TSH is very high.
 I131
uptake is low.
 Antibodies TPO are high.
 Serum cholesterol level raises above 300mg/dl.
 BMR is low.

84. Course and prognosis
 Slowly progressive with fluctuation in thyroid function.
 Delay in instituting treatment in children results in
permanent retardation of mental faculties.
 Treatment
 Replacement with thyroid hormone (levothyroxine)

85.  Myxedema coma : Coma results from a combination of
factors like heart failure, cerebral ischemia, hypothermia
and hypothyroidism.
 Treatment :
 Hospital admission with administration of tri-
iodothyronine IV 20 microgram every 4 hourly.
 Hydrocortisone to prevent hypoadrenal crisis.
 Dexamethasone.

86. Cretinism
 Results from hypofunction of the thyroid from birth.
 Iodine deficiency occuring in endemic goiter belts.
 Babies born to hypothyroid mothers or taking antithyroid
drugs during pregnancy.
 C/F
 Baby is lethargic by birth
 Growth retarded.
 Large protruding tongue.
 Broad flat nose
 Widely set eyes

87.  Sparse hair
 Dry skin
 Protuberant abdomen
 Umbilical hernia
 Abnormal persistence of physiological jaundice.
 Croaky voice
 Constipation
 Somnolense
 Feeding problems

88.  As baby grows older the retardation of growth and
milestones becomes evident.
 Neurological abnormalities like deafness, spastic limbs,
coma.
 Ossification delayed
 Treatment :
 Thyroid hormone replacement dose of 10-15
microgram/kg.
 Routine estimation of T3,T4,TSH