Thyroid Gland

 Anatomy:

The thyroid gland is located in the front of the neck attached to the lower
part of the larynx and to the upper part of the trachea, so it moves with
swallowing. It has two lobes. These lobes are connected by isthmus. Each
lobe is about 4 cm long and 1 to 2 cm wide.

 Histology:

The thyroid is composed of spherical follicles that selectively absorb iodine

from the blood for production of thyroid hormones, and also for storage of
iodine in thyroglobulin. Twenty-five percent of the body's iodide ions are in
the thyroid gland.

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 Actions of thyroxin hormone:

1. Increases cardiac output and increases heart rate

2. Increases ventilation rate and oxygen consumption

3. Increases basal metabolic rate

4. potentiates the effects of catecholamine (i.e. increases sympathetic

activity)

5. Potentiates brain development

6. Thickens endometrium in females

7. Increases metabolism of proteins (i.e. they have a catabolic action).

8. Increases absorption and utilization of glucose

9. It lowers cholesterol.

Thyroid function tests:

1- TSH: (TSH, thyrotropin) is elevated in hypothyroidism and secondary

hyperthyroidism and decreased in hyperthyroidism and secondary
hypothyroidism. It is the most sensitive test for thyroid hormone function.

2- Total T4: rarely measured now, having been largely superseded by free
thyroxin tests, generally elevated in hyperthyroidism and decreased in
hypothyroidism. It is usually slightly elevated in pregnancy secondary to
increased levels of thyroid binding globulin (TBG).

3- Free T4: generally elevated in hyperthyroidism and decreased in

hypothyroidism. Reference ranges depend on the method of analysis.
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4- Estimation of T3: to diagnose T3 toxicosis.

5- T3 resin uptake: measures the free TBG, unoccupied sites og TBG.

Radioactive T3 added to patient serum, fixed to binding sites of TBG, the
remaining unabsorbed radioactive T3 is absorbed into a resin & its
radioactivity is measured. It decreased in hypothyroidism and increased in
hyperthyroidism.

6- Free thyroxine index: obtained by multiplying the total T4 with T3 resin

uptake. FTI is considered to be a more reliable indicator of thyroid status in
the presence of abnormalities in plasma protein binding.

7- TSH stimulation test: differentiate 1ry from 2ry hypothyroidism, we give

TSH to the patient;

-increase of thyroxin in 2ry hypothyroidism, but it will not be increased in

1ry hypothyroidism.

8- Calcitonin: Increased in medullary carcinoma.

9- Thyroid US : differentiate cystic from solid nodules and detect

retrosternal extension.

10- Thyroid scan: using radioactive iodine or Technetium uptake. High

uptake in hyperthyroidism or Iodine deficiency. Low uptake present in
hypothyroidism or thyroiditis. Differentiate functioning (hot) nodules from
non-functioning (cold) nodules.

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11- Fine needle biopsy: for pathological assessment.

12- Immunologic tests:

-Antithyroglobulin antimicrosomal antibodies in hashimoto thyroiditis.

-Thyroid stimulating immunoglobulin (TSI) marker of Graves' disease.

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GOITER

Definition

 A goiter is an enlarged thyroid gland, and it may be diffuse or

nodular. A goiter may extend into the retrosternal space, with or
without substantial anterior enlargement.
 Because of the anatomic relationship of the thyroid gland to the
trachea, larynx, superior and inferior laryngeal nerves, and esophagus,
abnormal growth may cause a variety of compressive syndromes.
 Thyroid function may be normal (nontoxic goiter), overactive (toxic
goiter), or underactive (hypothyroid goiter).

Types &causes of goiter:

Type of Goiter Cause Typical Symptoms and
Signs
Iodine deficiency (endemic Lack of sufficient dietary Thyroid gland enlargement
goiter) iodine intake (goiter)
Normal or underactive
thyroid (hypothyroidism)

Graves disease Autoimmune stimulation of Goiter

(diffuse toxic goiter) the thyroid gland Hyperthyroidism

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Autoimmune thyroiditis Persistent immune system Goiter
(Hashimoto, chronic inflammation of person's Hypothyroidism
lymphocytic) own thyroid
Subacute thyroiditis Viral infection Painful, tender and swollen
(painful, de Quervain) gland
Malaise, fever, chills, and
night sweats
Thyrotoxicosis, often
followed by
hypothyroidism

Toxic adenoma and toxic Benign thyroid tumor(s) Nodular goiter

multi-nodular goiter Hyperthyroidism

Goiter and thyroid Malignant thyroid tumors No symptoms

nodules suspicious for Local neck symptoms
malignancy Symptoms of tumor spread

Causes of goiter:
The different etiologic mechanisms that can cause a goiter include the
following:

 Iodine deficiency
 Autoimmune thyroiditis - Hashimoto or postpartum thyroiditis
 Excess iodine (Wolff-Chaikoff effect) or lithium ingestion, which decrease
release of thyroid hormone
 Goitrogens

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 Stimulation of TSH receptors by TSH from pituitary tumors, pituitary
thyroid hormone resistance, gonadotropins, and/or thyroid-stimulating
immunoglobulins
 Inborn errors of metabolism causing defects in biosynthesis of thyroid
hormones
 Exposure to radiation
 Deposition diseases
 Thyroid hormone resistance
 Subacute thyroiditis (de Quervain thyroiditis)
 Silent thyroiditis
 Riedel thyroiditis
 Infectious agents
 Acute suppurative - Bacterial
 Chronic - Mycobacteria, fungal, and parasitic
 Granulomatous disease
 Thyroid malignancy
 Low selenium levels: This may be associated with goiter prevalence.

NB
 Causes of Non toxic goiter:

1. Iodine deficiency
2. Dietary goitrogens
3. Hashimotos Thyroiditis
4. Subacute Thyroiditis

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5. Dyshormononogensis
6. Neoplasm : benign or malignant

 Iodine deficiency:

-Most common cause of endemic goiter.

-Daily allowance 150-300 ugm/day.
 Dietary goitrogens:

-Most common is iodide itself (especially in susceptible individuals

and hypothyroidism).
-Lithium carbonate
-Amiodarone
-Some vegetable foodstuffs: goitrogens found in certain roots and
seeds .Cyanogenic glycosides found in cassava and cabbage→ release
thiocyanates→goiter.
 Hashimoto Thyroiditis:

-Most common cause of goiter in developed countries.

-Subacute Thyroiditis: causes goiter and exquisite tenderness.

 Dyshormonogensis (familial goiter):

-Complete form: cretin with goiter

- Incomplete form: mild hypothyroidism with goiter.

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Thyrotoxicosis
Clinical syndrome that results when tissues are exposed to high levels of
circulating thyroid hormones.

Causes of thyrotoxicosis:

1. Diffuse toxic goiter (Graves disease)

2. Toxic adenoma (Plummer disease)

3. Toxic multi-nodular goiter

4. Subacute thyroiditis

5. Silent thyroiditis

6. Thyrotoxicosis factitia

7. Rare causes include: ovarian Struma, metastatic thyroid

carcinoma, hydatiform mole, TSH-Producing pituitary tumor

Graves’ disease

 Most common cause of thyrotoxicosis

 Female to male incidence 5:1

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 Peak incidence 20-40 years

 Consists of: thyrotoxicosis, goiter, ophthalmopathy, dermopathy.

 Etiology:

-Auto immune disease of unknown cause

-Strong familial predisposition.

-Environmental factors may trigger the process e.g. stress, tobacco

use, infection and iodine exposure.

 Pathogenesis

 T-lymphocytes are sensitized to antigen within the thyroid gland 

stimulate B lymphocytes  thyroid stimulating antibody (TSAB) or
thyroid- stimulating immunoglobulin (TSI)  stimulate thyroid
growth and function.

 Ophthalmopathy:

Cytotoxic lymphocytes and cytotoxic antibodies are sensitized to

antigens in orbital fibroblasts and muscles  ↑ cytokines 
proliferation of orbital fibroblasts and orbital tissue  ↑ amount of
orbital fat, glycosamino-glycans and inflammation of extraoccular
muscles  manifestations of ophthalmopathy.

 Dermopathy (pretibial myxedema)

Similar process lead to activation of dermal fibroblasts in the anterior

aspect of the legs.
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Clinical features:

1. General features:

 Weight loss associated with increased appetite

 Emotional lability

 Anxiety and difficult concentration

 Fatigue due to disturbed sleep

 Associated autoimmune diseases: Pernicious anemia, type I diabetes,

RA, myasthenia gravis, vitiligo, adrenal insufficiency

 Thyroid: Diffuse, painless and firm enlargement of the thyroid

2. Neurologic features

 Fine tremors in the hands

 Proximal muscle weakness  difficulty in climbing stairs, reach the

arm over the head, standing from the sitting position.

3. Dermatologic features:

 ↑ sweating, skin is worm, soft and smooth

 Heat intolerance

 Fingernails are separated from the nail bed (onycholysis)

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 Pretibial myxedema occurs in a small subset of patients with
Graves's disease. It is characterized by lymphocyte infiltration of
the dermis, accumulation of glycoaminoglycans, and edema. It
occurs in the anterolateral aspect of the shin. The skin is thickened,
indurated and non-pitting. It may be pruitic or painful

 Clubbing of fingers may occur (thyroid acropachy)

4. Ophthalmologic features

 Lid lag and stare look: due to ↑ sympath. tone  contraction of

the eyelid muscles (Muller muscle)

 Proptosis (exophthalmos): due to ↑ in volume of retro-bulbar

tissue

 Diplopia and limitation of eye movements at one or more gaze

due to involvement of extraoccular muscles

 Dry or gritty sensation of the eye and corneal ulceration due to

inability to fully close the eye lids.

 Other complications include peri-orbital edema, conjunctival

edema and hyperemia and photophobia.

5- Cardiovascular

 ↑ in heart rate, wide pulse pressure

 Flow murmur over precordium

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 Cardiac arrhythmia: atrial fibrillation, multiple premature beats

 CHF

 Anginal attacks

6- Gastrointestinal:

 Hyperphagia associated with weight loss

 ↑ gut motility  frequent defecation and/or diarrhea

 Obstructive dysphagia when large goiter is present

7- Reproductive system:

 Menstrual irregularities specially oligomenorrhea.

 Gynecomastia and sexual dysfunction: ↑ SHBG which has

higher affinity to androgens  ↓ level of free androgens
relative to estrogens. Also there is ↑ aromatization of
testosterone to estrogens in the peripheral tissues.

8- Bone:

 ↑ Thyroid hormone  ↑ loss of cortical and trabecular bone 

↑ risk of osteoporosis and bone fractures.

Laboratory findings:

 ↓ TSH concentration
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 ↑ free T4 and T3

 T3 level only may be ↑ in some cases (T3 toxicosis)

 ↑ in TSAb

 Hyperglycemia due to ↑ in catecholamine – induced

glycogenolysis.

 Hypercalcemia and ↑ in alkaline phosphatase due to ↑ bone

resorption.

Thyroid scintigraphy:

 Use technetium or iodine 123

 It shows diffuse uptake of radioisotope by thyroid.

Treatment of Graves Disease

A- Anti-thyroid drugs:

 Methimazole, carbimazole and propylthiouracil (PTU)

 They inhibit thyroid hormone synthesis

 PTU also prevent peripheral conversion of T4 to T3.

Recommendation

1. Thyroid function should be checked every 4-6 weeks and doses

are adjusted to achieve and maintain euthyroid state and avoid
hypothyroidism.

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2. Focus on free T3 and T4 level to assess thyroid state because
TSH may be suppressed for several months after peripheral
thyroid hormone levels are normalized.

Duration of therapy

 1-2 years to offer a chance for remission of hyperthyroid state.

 The chance of permanent remission after cassation of therapy is

35%-50%.

Dose and regimens:

 Start with large dose. When the patient becomes eurthryoid

after 4-12 weeks, maintenance therapy is achieved with lower
dose.

 For methimazole start with 10-20 mg/day and maintain with 5-

10 mg/day

 For PTU start with 300 – 400 mg/day and maintain with 50-200
mg/day.

 Another approach is to continue large loading dose and add

thyroid hormone (block and replace therapy)

Indications:

1. Mild disease and small goiter because they have high chance of
remission

2. Elderly or other comorbidities increasing surgical risk.

3. Limited life expectancy

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4. previous operation or irradiation to the neck

5. Lack of high-volume thyroid surgeon

Side effects

1. Skin rash, arthralgia, GI problems

2. Agranulocytosis: Potentially lethal adverse effect presents with

fever, sore throat which progress to sepsis. Any patient on
thionamide therapy who present with fever and sore throat
should have complete blood picture to exclude this condition.

3. Hepatic problems

 Methimazole may produce cholestasis

 PTU may produce hepatitis with elevated markers of

hepatocellular injury.

 Patients on thionamide therapy should have liver function

before starting therapy and during treatment with
antithyroid drugs.

B- Radio-active iodine

 Suitable for most patients with Graves' disease.

 It is effective, safe, and does not require hospitalzation.

 Given orally in a single dose in a capsule or liquid form.

 Very few side effects as no other tissue absorb RAI.

Precautions:

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Patients with severe hyperthyroidism, elderly patients or patients
with underlying heart disease should be pretreated with anti-thyroid
drugs and β-blockers to achieve an euthyroid state prior to radio-
active iodine.

Indication:

1. ↑ surgical risk due to associated comorbidities.

2. Previous operation or irradiation to the neck

3. Lack of access to high-volume thyroid surgeon

4. Contraindication for use of anti-thyroid drugs.

Disadvantages:

 Occurrence of permanent hypothyroidism

 Worsening of ophthalmopathy via unknown mechanism.

Contraindication:

 Pregnancy and lactation.

 Children

 Associated severe opthalmopathy

C- Thyroidectomy is indicated in:

 Failure of response to anti-thyroid drugs.

 Severe adverse reactions to anti-thyroid drugs.

 Patient refuses radioactive iodine treatment.

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 Huge goiter which cause pressure symptoms.

 Suspected malignancy in thyroid gland.

Preoperative preparation:

 Anti-thyroid drugs to reduce hyperfunction.

 β-blockers to control pulse rate below 80/min.

 Potassium iodide may be given for 2 weeks before surgery. It

reduce intraoperative blood loss.

Complications

A. Hypothyroidism.

B. Risk of hypoparathyroidsm.

C. Recurrent laryngeal nerve damage.

D. Complications of general anesthesia.

D-Adjuvant therapy (β-blockers)

Should be given to:

 All thyroid patients with resting heart rate >90/min.

 Elderly patients with symptomatic thyrotoxicosis.

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Toxic multi-nodular goiter

Etiology:

 Occur in patients with long-standing multi-nodular goiter.

 There is constitutive activation of TSH receptors in thyroid

nodules due to mutation in TSH receptor gene.

Clinical picture:

 Nodular thyroid enlargement.

 Manifestations of thyrotoxicosis.

 No opthalmopathy or dermopathy

Thyroid scintigraphy:

Heterogenous pattern with areas of hyperactivity (hot areas)

interspersed with hypoactive regions.

Treatment:

 Radioactive iodine

 Surgery (thyroidectomy) if the goiter is large and cause

pressure symptoms.

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Thyrotoxic Crisis

Definition: Thyrotoxic crisis also referred to as thyroid storm, is an acute, rare

life-threatening, hypermetabolic state induced by excessive release of thyroid
hormones in individuals with thyrotoxicosis. It is an endocrinal emergency.

Cause:
 Thyroid storm is precipitated by the following factors in individuals
with thyrotoxicosis:
 Stress
 Sepsis in untreated patients
 Surgery with lack of preoperative preparation
 Anesthesia induction
 Radioactive iodine (RAI) therapy
 Drugs : anticholinergic and adrenergic drugs such as pseudoephedrine,
salicylates; nonsteroidal anti-inflammatory drugs [NSAIDs],
chemotherapy and iodinated contrast agents
 Diabetic ketoacidosis
 Excessive thyroid hormone ingestion
 Withdrawal of or noncompliance with anti-thyroid medications
 Direct trauma to the thyroid gland
 Vigorous palpation of an enlarged thyroid
 Toxemia of pregnancy and labor in older adolescents; molar pregnancy

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Clinical picture:
 History: patients may have a known history of thyrotoxicosis.
 General symptoms: hyperpyrexia, sweating, weight loss and fatigue
 GIT :nausea, vomiting, diarrhea, Jaundice and aute abdominal pain
 CNS :anxiety altered behavior, seizures, coma, in old age apathy and
bulbar symptoms from myopathy
 CVS: tachycardia, Cardiac arrhythmia as supraventricular arrhythmias
are more common, but ventricular tachycardia may also occur, acute
high-output heart failure, hypertension with wide pulse pressure and
later hypotension
 Thyroid storm may be the initial presentation of thyrotoxicosis in
undiagnosed children, particularly in neonates.
 Clinical picture may be masked by B-blockers
Differential Diagnoses
 Heart Failure
 Arrhythmia
 Hypertension
 Pheochromocytoma
 Neurosis
Management: emergency
Patients with thyroid storm should be treated in an ICU setting for close
monitoring of vital signs and invasive monitoring and inotropic support.
a- Anti-thyroid:
 Propylthiouracil: 200-400 mg/8h. (orally,rectally or nasogstric).
 Propranolol in full dose is started immediately for tachyrrhthmias (160
mg/d orally or 1 mg/4h IV)
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 Na iodide or K iodide: 1 gm over 24h to ↓ release of thyroid hormones.
 Hydrocortisone: 100 mg/8h IV or IM to ↓ release of T4 & ↓
conversion of T4 to T3 and to correct hypotension
 Thyrotoxic crises →↑↑ cortisol metabolism →relative adrenal
insufficiency →refractory hypotension.

B- Symptomatic:
 Antipyretics : ice bags and acetaminophen
 IV fluids for dehydration:
 Digoxin and diuretics for AF& HF
 Nasogastric tube for bulbar palsy, nausea and vomiting

c- Ttt of cause & ppt factors: e.g. antibiotics for infection

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Hypothyroidism
Definition:

 It is a clinical and biochemical syndrome with manifestations of

thyroid hormone deficiency at target tissues.

Epidemiology:

 Prevalence is 4-8% of general population.

 Female to male ration is 3:1

Causes:

 Post Thyroiditis

 Post surgical

 Post radioiodine

 Congenital

Presentation according to age:

 Cretinism: onset at infancy

 Juvenile myxedema: onset before puberty

 Adult hypothyroidism ( myxedema): onset after puberty

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Hypothyroidism (myxoedema)

Causes:

A: Primary thyroid failure, thyroprevic:

 Idiopathic

 Thyroiditis:

 Post thyroidectomy

 Post radioiodine

 Goiterogens

B. Secondary thyroid failure (to pituitary failure) , thyrotrophic:

C. Tertiary thyroid failure: hypothalamic leions

 Sometimes , causes of pituitary and hypothalamic origin are

collectively termed " central hypothyroidism"

Clinical manifestations:

 Expressionless apathetic face, with puffy eyes and lost outer third of
eye brows hair.

 Malar flush

 Thickened lips and tongue

 Low body temperature with intolerance to cold weather.

 Skin is thick, dry, scaly, pale and coarse.

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 Carotenoderma.

 Weakness, fatigue arthralgia and musculoskeletal pains.

 Slow movements and weight gain.

Cardiovascular manifestations:

 Sinus bradycardia and heart block.

 Pericardial effusion (cholesterol pericarditis), less prone to produce

hemodynamic compromise.

 Enhanced atherosclerosis, affecting coronaries and peripheral arteries

( hypertension, atherogenic lipid profile, and hyperhomocystienemia)

 Myxoedematous heart disease of ischemic and metabolic

backgrounds.

 Hypertension especially diastolic due to invreased peripheral

resistance.

 Cardiomegaly and congestive heart failure.

 Rarely asymmetric septal hypertrophy (ASH).

 ECG changes: sinus bradycardia, prolonged P-R interval, low volt

QRS complexes, ST –T wave changes.

Neurologic manifestations:

 Poor cerebral performance, thinking, memory, and hypersomnia

 Hoarseness of voice, with slurred speech

 Suspended tendon jerks ( delayed muscle relaxation)

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 Peripheral neuropathy

 Entrapement neuropathy eg. carpal tunnel syndrome.

 Muscle hypertrophy involving gastrocnemius, back, and upper limbs

with EMG myopathic changes.

 Myxoedema madness with frank psychosis.

 Myxoedema coma.

Gastrointestinal manifestations:

 Atrophic gastritis with slow gastric motility.

 Atrophic intestinal villi with slow absorption, might lead to

steatorrhea.

 Constipation, megacolon and pseudo intestinal obstruction with ileus.

 Ascites.

Reproductive manifestations:

 Menstrual disturbances as menorrhagia or oligomenorrhea.

 Subfertility and anovulation.

 Amenorrhea- galactorrhea syndrome

 Spontaneous abortion

 Pregnancy induced hypertension.

 Gynecomastia in males.

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Urogenital:

 Reduced renal plasma flow and glomerular filtration rate.

 Increased total body water.

 Hyponatremia.

 Syndrome of inappropriate secretion of antidiuretic hormone

(SIADH).

Respiratory manifestations:

 Dyspnea: due to respiratory muscle weakness, cardiomyopathic,

pleural effusion, and pulmonary function abnormalities.

 Sleep apnea: obstructive due to macroglossia and enlarged pharyngeal

muscles, and central component due to reduced ventilatory drive.

 Sinusitis.

Metabolic manifestations:

 Slowing of metabolic processes which results in decreased energy

expenditure, oxygen consumption and use of substrate.

 Reduced thermogenesis, decreased appetite, with increased body fat.

 Hypercholesterolemia, high LDL, high lipoprotein (a) and high

oxidized LDL. Serum cholesterol can be used as a marker for tissue
hypothyroidism i.e. the higher the cholesterol the lower the thyroid
hormones.

 Normal triglycerides or modestly elevated.

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 Hyperhomocystienemia

Hematologic manifestations:

 Anemia: normocytic normochromic due to reduced erythropoietin

levels and low oxygen requirements may be iron deficiency due to
blood loss from menstrual troubles, or macrocytic hyperchromic of
associated pernicious anemia.

 Normal leucocytes and platelets.

 Bleeding tendency with prolonged bleeding time (thromboathenia and

low factor VIII).

Endocrinal manifestations:

 Decreased HGH secretion due to increased somatostatinergic tone

with resulting decrease of IGF-1.

 Moderate hyperprolactinemia due to high TRH (spill over).

 Wide pituitary fossa due to hyperplasia of pituitary thyrotrophs which

rarely cause distinct pituitary adenoma.

 Reduced bone turnover (decreased activity of osteoblasts and

osteoclasts).

 Decreased metabolic clearance and production of cortisol, with

normal serum cortisol.

Laboratory diagnosis:

 High TSH and low FT4 in primary hypothyroidism.

 Central hypothyroidism has low TSH and low FT4.

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 High TSH but normal FT4 diagnose subclinical hypothyroidism.

Treatment:

 Replacement therapy with oral levothyroxine sodium in a daily dose

of 1.6 ugm/kg/day. With average 100-200 ug/day.

 Start with a low dose and gradual titration up depending on severity

and duration of hypothyroid state, age of the patient, and presence of
heart disease.

Myxedema coma

 It is a rare, life- threatening clinical condition in patients with long

standing severe hypothyroidism.

Precipitating factors:

 Cold exposure.

 Infections.

 Drugs: diuretics, sedatives and tranquilizers.

 Trauma.

 Surgery.

 Stroke.

 Heart failure and acute MI.

 GIT bleeding.

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Clinical picture:

 The typical patient is elderly woman in winter season.

 Altered thermoregulation with hypothermia.

 Altered central nervous system with disorientation, lethargy,

psychosis and coma.

 Altered cardiovascular system: bradycardia and hypotension.

Laboratory diagnosis:

 Low FT4.

 TSH is usually high.

 CPK is high.

Treatment:

 Start with levothyroxine sodium 300-500 ugm IV, then 50-

100ugm/daily till oral therapy can be given.

 Hydrocortisone IV 100-200 mg daily in divided doses.

 Supportive measures:

-Hypothermia: blankets.

-Hypoventilation: mechanical ventilation.

-Hypotension: whole blood or saline cautiously.

-Hyponatremia: mild fluid restoration.

-Hypoglycemia: glucose IV.

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Thyroiditis
Definition: inflammation of the thyroid gland:

Causes and characteristics:

(1) Acute: suppurative or pyogenic thyroiditis, which is due to bacterial

infection

(2) Subacute: (de Quervain s) thyroiditis, which results from a viral

infection of the gland: multinuclear giant cells.

(3) Chronic (the commonest): autoimmune thyroiditis; Hashimoto s or

atrophic: grossly lymphocytic or fibrotic

(4) Others:

- Post- partum thyroiditis: lymphocytic.

- Drug- induced thyroiditis (amiodarone, interferon alpha)

- Radiation thyroiditis.

- Riedel s (chronic fibrosing) thyroiditis: extensive fibrosis.

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Forms of thyroiditis Clinical presentation Thyroid function

Acute: suppurative Painful, tender thyroid, Usually normal

fever
Subacute: (de Painful anterior neck, Early thyrotoxicosis,
Quervain s) preceding URTI, Occasionally late
arthralgia, generalized hypothyroidism.
fatigue.
Autoimmune Hashimoto s: goiter Usually hypothyroid
(painless) Sometimes euthyroid
Atrophic: no goiter Rarely early
thyrotoxicosis
High titres of
antithyroid antibodies
Post-partum Thyroid dysfunction Transient thyrotoxicosis
within the first six month or hypothyroidism
Riedel s Hard, woody consistency Usually normal
of thyroid

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Subacute Thyroiditis

(De Quervain, Acute viral Thyroiditis, Granulomatous Thyroiditis,

migrating Thyroiditis):

Definition: acute inflammatory condition due to viral infection.

E.g. Mumps, coxcakie, adenovirus
Pathology: inflammatory reaction involving the capsule, destruction of
thyroid parenchyma, phagocytes.
Clinical picture: fever, local pain in the neck radiating up .
Symptoms of thyrotoxicosis like sweats, palpitation.
On examination: -The gland is tender but no redness or
hotness ( to exclude abscess).
- Signs of thyrotoxicosis.

Investigation : -Initially toxic profile with low RAIU….then recovery

Or reach hypothyroid range.
- High ESR.
-Negative thyroid autoantibodies.

Treatment: -NSAID
-Short course of steroids 20 mg tds for a week.
Prognosis: -Complete resolution in weeks or months
-Hypothyroidism in 10% of cases

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Chronic Thyroiditis
Synonyms: Hashimoto Thyroiditis, chronic immune thyroiditis,
lymphocytic thyroiditis
Is considered the most common cause of hypothyroidism and goiter in
developed countries.

Pathology: immunologic inflammation with heavy lymphocyte infiltration.

Lymphoid follicles with germinal center may be found. Follicular epithelium
may be cytoplasm with basophilic cytoplasm (Hurthle cell).
Antibodies: -Anti- thyroglobulin
-Anti-thyroid peroxidase TPO
Clinical picture:
- Goiter
- Painless
-Hypothyroid manifestation
Investigations:
- Normal or hypothyroid profile.
-High titer of thyroid auto antibodies: anti TG, TPO.
-FINAC: lymphocyte infiltration with Hurthle cells.

Treatment of different types of thyroiditis :

Acute: suppurative: Antibiotic therapy and incision and drainage if fluctuant

area within the thyroid should occur.

Subacute: (de Quervain`s): non- steroidal anti-inflammatory agents and

paracetamol in mild cases.

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In severe cases, glucocorticoids can be effective. Propranolol can be used to
control associated thyrotoxicosis. T4 replacement is required if the patient is
hypothyroid.

Autoimmune thyroiditis: T4 replacement in hypothyroid patients.

Post- partum thyroiditis: most patients have a complete remission but

some may progress to permanent hypothyroidism and need for replacement.

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