PREPARED BY MOSES KAZEVU JR

THYROID GLAND

THYROID
DEVELOPMENT
• The thyroid gland is the first endocrine gland to develop at the 24th day of
gestation.
• It develops from a median down growth of a column of cells from the pharyngeal
floor between the first and second pharyngeal pouches (subsequently marked by
the foramen caecum of the tongue).
• The canalized column becomes the thyroglossal duct which is displaces forward
by the developing hyoid bone and then below the hyoid (C3), lies slightly to one
side, more commonly to the left.
• The duct bifurcates to form the thyroid lobes and a portion of the duct forms the
pyramidal lobe.

Figure 1: The thyroid gland

 Figure 2: Development of the thyroid gland

ANATOMY
• The gland weighs about 15-20g and is located in the anterior triangle of the neck
(muscular triangle).
• It originates in early embryonic life from the foregut endoderm.
• The parafollicular cell or C-cells are derived from the neural crest (ectoderm).
• It consists of a right and left lobe that are connected by an isthmus which extends
from the 2nd to the 4th tracheal rings.
• Each lobe is 5 x 3 x 1.5 cm in size and extends from the middle of the thyroid
cartilage to the 6th tracheal ring.
• The thyroid also has a pyramidal lobe which is an upward extension as fibrous
strands or muscular strands from the junction of the isthmus and left lateral lobe.
• The gland is covered by pretracheal fascia which is attached to the larynx thus
causing the thyroid to move on swallowing. This important clinical finding helps
to discriminate thyroid swellings from other swellings in the neck.
• Berry’s ligament is a strong condensed vascular connective tissue between the
lateral lobe and cricoid cartilage on each side.
• Blood supply:
➢ Arterial
 o Superior thyroid artery: 1st branch of external carotid artery, enters at the
superior pole of the gland and bifurcates into a larger anterior superficial
branch and a smaller posterior branch.
o Inferior thyroid artery: a branch of thyrocervical trunk of subclavian
artery. It passes behind the carotid sheath running medially reaching the
posterolateral aspect of the gland.
o Thyroidea ima artery: a branch of aorta or brachiocephalic artery enters
the isthmus or lower pole of one of the lateral lobes (10%).
o Tracheal and esophageal branches serve blood supply to retained thyroid
gland after thyroidectomy.
➢ Venous
o Superior thyroid vein: drains in the internal jugular.
o Middle thyroid vein: short and drains into the internal jugular. It is first to
be ligated in thyroidectomy.
o Inferior thyroid veins are many in number. Drain into brachiocephalic
vein.
o Kocher’s vein may be present which drains lower or middle thyroid.

Figure 3: Venous drainage of the thyroid

• Lymphatic drainage
➢ Primary:
o Tracheao-esophageal nodes.
o Pre-laryngeal nodes (Delphian nodes). Formerly purpose of these lymph
nodes were uncertain hence the name.
- Delphi is a place in Greece where Pythia, snake women after
sulphurous fume inhalation uttered meaningless jargon purpose of it
was unclear.
o Mediastinal nodes.
➢ Secondary:
o Deep cervical nodes
o Supraclavicular nodes
o Occipital nodes

Figure 4: Lymphatic drainage of the thyroid

• Important Relations
➢ Recurrent laryngeal nerve lies in the tracheooesophageal groove in relation to
Berry’s ligament. It supplies the intrinsic muscles of the larynx and vocal
cords
➢ Superior laryngeal nerve which gives a branch, external laryngeal nerve
supplies cricothyroid muscle (A tensor/adductor of vocal cords). It
accompanies superior thyroid artery.
➢ Parathyroid glands- four in number, 2 on each side embedded in thyroid.
PHYSIOLOGY
• Thyroid gland contains 2 secretory cells:
➢ Follicular cells: secrete thyroxine (T4) and tri-iodothyronine (T3)
➢ Parafollicular cells (“C” cells)- secrete calcitonin
• 90% of body iodide uptake is in the thyroid gland, whose uptake into the
follicular cells is regulated by TSH and follicular iodide content.
• Iodothyronins (MIT, DIT) are formed in follicular cells by coupling of inorganic
iodide with tyrosine under the control of the enzyme thyroid peroxidase.
• These are biologically inert molecules. T4 is formed by coupling 2 DIT
molecules and T3 by coupling 1 MIT and 1 DIT molecule. Both are bound to
thyroglobin which is the primary component of colloid matrix.
• The hypothalamus-pituitary-thyroid axis regulates thyroid hormone production
and releases in a classic feedback system.
• TRH is a regulatory hormone from hypothalamus and TSH is a regulatory
hormone from the anterior pituitary.
HYPERTHYROIDISM
• Thyrotoxicosis is a symptom complex due to raised levels of thyroid hormones.
• It refers to biochemical and physiological manifestations (e.g. hyperthermia) of
excessive thyroid hormone.
➢ Thyrotoxicosis= Excessive thyroid hormone release in blood + Clinical
manifestations
• Hyperthyroidism is the term used to refer to overproduction of the thyroid
hormones.
• Hyperthyroidism is divided into:
➢ Primary thyrotoxicosis (pathology is in the thyroid gland)
o Puberty, pregnancy, emotion and infection are the precipitating factors for
primary thyrotoxicosis.
➢ Secondary thyrotoxicosis (pathology not in thyroid gland)

Figure 5: Primary thyrotoxicosis vs Secondary thyrotoxicosis

TYPES
• Diffuse toxic goiter (Primary thyrotoxicosis)
➢ Graves’ disease
➢ Basedow’s disease
• Toxic multinodular goiter (Secondary thyrotoxicosis): Plummer disease
• Toxic nodule (Goetsch’s disease)
• Other causes of thyrotoxicosis without hyperthyroidism include:
➢ Ectopic function thyroid
➢ Struma ovarii
 ➢ Functioning metastatic follicular carcinoma
➢ Trophoblastic tumors
➢ Thyrotoxicosis factitia- drug induced due to intake of L-thyroxine more than
normal
GRAVES DISEASE
• This is an autoimmune thyrotoxicosis that is caused by an antibody against the
TSH receptor (TSH receptor antibody).
• Graves’ disease has genetic predisposition and it affects most females (8:1).
• Due to the stimulating TSH receptor antibodies, the acinar of the thyroid undergo
hypertrophy and hyperplasia with absence of normal colloid in the tall columnar
epithelium (normal is flat epithelium
with colloid). As the cells are empty
they look vacuolated. Tissues are
highly vascular.
• Clinical features are those of
thyrotoxicosis. It is also associated with
vitiligo. Exophthalmos producing
substance causes Graves
ophthalmopathy (manifested by lower
eyelid retraction, lid lag, periorbital
Figure 6: Patient with exophthalmos
edema, chemosis or if severe proptosis
and exophthalmos).
• Diffuse goiter, thyrotoxicosis and autoimmune manifestations (infiltrative
ophthalmopathy, dermopathy, myopathy) are essential components of Graves’
disease. Thyroid stimulating antibodies produced against thyroid antigen in
Graves’ disease which is directed to TSH receptor acting as TSH receptor
antibody. TSH receptor antibody is observed only in Graves’ disease.
• Examination reveals a moderate firm goiter which in severe thyrotoxicosis may
have a vascular thrill and bruit.
• Investigations:
➢ Suppressed TSH with raised free T4 and/or T3
➢ 90% of patients have raised TSH antibodies
➢ 70% of patients will have raised thyroid peroxidase antibodies.
• Treatment:
➢ Medical
o Thyroid uptake blocking drugs to render the patient euthyroid
 - Carbimazole
▪ Important side-effects: neutropenia (which presents as sore throat),
profuse diarrhea or hepatocellular failure (which initially presents
as jaundice), skin rash, nausea and joint pain
- Propylthiouracil
o Beta-blockers (Propranolol) can be used if the patient is symptomatic with
sweating, tremor or tachycardia
o Control of thyrotoxicosis usually takes about 6 weeks but maintenance is
required for at least 18 months before cessation of carbimazole.
Alternatively, higher doses of carbimazole can be taken in conjunction
with thyroxine for about 12 months (block and replace).
o If the patient relapses after this then definitive long term treatment is
required either radioactive iodine or if inappropriate (e.g. young children
at home) surgery can be performed.
➢ Surgical
o Patient has to be rendered euthyroid before surgery.
o If surgery is the preferred option, then previously a subtotal
thyroidectomy was performed to render the patient ‘euthyroid’ however
10% of these patients developed recurrent thyrotoxicosis and 70%
develop hypothyroidism in the long run.
o Total thyroidectomy and long term thyroxine postoperative can be done.
TOXIC MULTINODULAR GOITER
• While the majority of multinodular goiters are non-toxic, over a period the
presence of large functioning nodules may render the patient hyperthyroid
leading to toxic multinodular goiter (Plummer’s disease).
• The large goiter may extend retrosternally and cause tracheal deviation and
compression occasionally leading to stridor (a low-pitched crowding noise on
inspiration caused by narrowing of the trachea).
• Examination will reveal multiple nodules either bilaterally or unilaterally.
• If there is a dominant nodule within the gland then this should be investigated as
for solitary thyroid nodule as the risk of malignancy in this nodule is about 10%.
• Elevation of the patient’s arms may lead to venous congestion and stridor if there
is retrosternal extension of the goiter (Pemberton’s sign). The position of the
trachea should be checked for possible tracheal deviation.
• Thyroid ophthalmopathy is not associated with multinodular goiter.
• Investigations:
 ➢ TSH: reduced if toxic multinodular goiter.
➢ Fine-needle aspiration of dominant nodule, if present
➢ Ultrasound may confirm multiple nodules
➢ X-ray of thoracic inlet and CT will delineate the extent of retrosternal
extension and the degree of tracheal deviation and compression
• Treatment:
➢ Total thyroidectomy should be performed for non-toxic multinodular goiter if
there is retrosternal extension of the goiter, tracheal compression or if the
patient finds the goiter cosmetically unacceptable.
➢ Toxic multinodular goiter: treat with carbimazole initially and then either total
thyroidectomy or radioiodine depending on the suitability of the patient.
SOLITARY TOXIC ADENOMA
• Occasionally, a single thyroid adenoma may be active
enough to render the patient hyperthyroid.
• The patient normally presents with a solitary thyroid
nodule and should be investigated as such in order to
exclude malignancy.
• In patients with solitary toxic adenoma, TSH is
suppressed and a 99mTcO4 thyroid isotope scan will
show a solitary ‘hot’ nodule.
• Treatment is initially with carbimazole followed by
either thyroid lobectomy or radioactive iodine
depending on preference. Figure 7: 'Hot' nodule on thyroid
isotope scan
CLINICAL FEATURES OF THYROTOXICOSIS
• It is 8 times more common in females.
• Occurs in any age group.
➢ Primary type is seen in younger group.
➢ Secondary type is common in older age group.
• Note: Graves’ disease often presents without any obvious thyroid swelling in the
neck. Whenever there are unexplained behavioral problems, insomnia,
myopathy, unexplained diarrhea or loss of weight, tachycardia, Graves’ disease
should be suspected and evaluated
SYMPTOMS
SYSTEM SYMPTOMS
CENTRAL NERVOUS • Irritability
SYSTEM • Nervousness
• Insomnia
• Fine tremor (Due to diffuse irritability of grey
matter)
• Heightened emotions
CARDIOVASCULAR • Palpitations (thyroid hormones increase
SYSTEM expression of Beta 1 adrenergic receptors)
• Shortness of breath at rest or on minimal exertion
• Angina
• Irregularity of heart rate (Arrhythmias)
• Cardiac failure in the elderly
• Undue fatigue and muscle weakness
GASTROINTESTINAL • Weight loss in spite of increased appetite
SYSTEM • Diarrhea (due to increased activity at ganglionic
level) and malabsorption
GENITOURINARY • Oligo or amenorrhea
SYSTEM • Occasional urinary frequency
SKELETAL SYSTEM • Increase in linear growth in children
• Bone resorption and hypercalcemia
• Decreased muscle mass with weakness
INTEGUMENTARY • Hair loss, gynecomastia
SYSTEM • Pruritus
• Palmar erythema
METABOLIC • Increase in basal metabolic rate (increase in the
SYSTEM synthesis of sodium-potassium ATPase)
• Hypocholesterolemia
• Hyperglycemia (due gluconeogenesis and
glycogenolysis)
• Sympathetic over activity causes dyspnea, palpation, heat intolerance, sweating,
nervousness, increased appetite and decrease in weight.
• Because of the increased catabolism they have increased appetite, decreased
weight and so also increased creatinine level which signifies myopathy (Due to
more muscle catabolism).
• Fine tremor is due to diffuse irritability of grey matter.
SIGNS OF HYPERTHYROIDISM/ TOXICOSIS
EYE SIGNS IN TOXIC GOITRE
• Common in primary thyrotoxicosis.
• Lid lag, lid spasm can occur in secondary thyrotoxicosis also.
• Eye signs include:
➢ Lid retraction: the upper eyelid is higher than normal and lower eyelid is in
normal position with visible sclera adjacent to upper eyelid. It is due to
sympathetic over activity causing spasm of involuntary smooth muscle of the
levator palpebrae superioris. It is a sign of thyrotoxicosis not a sign of
exophthalmos.
➢ Lid Lag sign: it is inability of the upper eyelid to keep pace with the eyeball
when it looks downwards to follow the examiners finger.
➢ Staring gaze (absence of normal
blinking)
➢ Exophthalmos: this is proptosis of
the eye, it is caused by infiltration
of retrobulbar tissue with fluids and
round cells with lid spasm of upper
eyelid.
o It is seen with Grave’s disease
and is believed that fibroblast
have TSH receptors and in
response to TSH like antibodies
e.g. Grave’s disease fibroblast
Figure 8: Eye signs in
produce mxyoid substances e.g.
hyperthyroidism/Thyrotoxicosis
glycosaminoglycans (GAGs)
which deposit in the retro-orbital tissues.
o Remember: antithyroid drugs may worsen exophthalmos and the patient
should be observed once antithyroid drugs are started as steroid
supplementation may be required.
CARDIAC MANIFESTATIONS
• Tachycardia (common), take sleeping pulse rate for 3 consecutive nights and
average is taken as the value
➢ Grade 1 <90b/m
➢ Grade 2: 90-110b/min
➢ Grade 3: >110 b/min
• Ectopic heart beats
• Multiple extrasystoles
• Paroxysmal atrial tachycardia & fibrillation
• Persistent atrial fibrillation (not responsive to digoxin)
• Pulsus paradoxus
• Wide pulse pressure
MYOPATHY
• Weakness of proximal muscles occurs i.e. front thigh muscle, arm muscles.
• Weakness is more when muscle contracts isometrically either while getting down
steps or lifting a full bucket.
• Often when it is severe it resembles myasthenia gravis. Once hyperthyroidism is
controlled recovery occurs.
PRETIBIAL MYXEDEMA
• This is a misnomer.
• It is often a feature of primary thyrotoxicosis.
• It is due to deposition of myxomatous tissue (mucin like deposits) in skin and
subcutaneous plane. Glycosaminoglycans (hyaluronic acid) deposition occurs-
same as exophthalmos.
• It is usually bilateral, symmetrical, shiny, red thickened dry skin with coarse hair
in the feet and ankles.
• In severe cases skin of entire leg below the knee with involvement of foot and
ankle can occur.
• It might or might not regress completely after treatment for toxicity.
• Skin becomes cyanotic when cold. Skin changes in toxicosis are called as thyroid
dermopathy. They include- pretibial myxoedema, pruritus, palmar erythema, hair
thinning, Dupuytren’s contracture.
THYROID ACROPACHY
• Thyroid acropachy is clubbing of fingers and toes in primary thyrotoxicosis.
• Hypertrophic pulmonary osteoathropathy can develop.
OTHERS
• Thrill is felt in the upper pole of thyroid and also bruit on auscultation. It is
because in upper pole, superior thyroid artery enters the gland superficially and
so thrill and bruit can easily be felt. In lower pole inferior thyroid artery enters
the gland from deeper plane and so thrill cannot be felt.
• Hepatosplenomegaly.
INVESTIGATIONS
• Thyroid function tests: Increased T3, T4 and low TSH. Sometimes T3 is the only
thing elevated (T3 toxicosis)
➢ Normal Free T3= 3-9 pmol/L
➢ Normal Free T4= 8-26pmol/L
• Thyroglobulin antibodies
➢ Raised in pregnancy, cirrhosis, hyperestrogenism
➢ Decreased in high androgen levels, hypoproteinemia, acromegaly
• Thyroid antibody estimation- antithyroglobulin and TSH receptor antibody
• Radioisotope study (I-123 or 99mTc-technetium 99m) for hot nodules
➢ I-131 is used for radioactive iodine therapy (beta rays are used)
➢ I-123 is used for diagnostic studies (gamma rays are used)
• ECG- to look for cardiac involvement
• FBC- total count and neutrophil count are very essential base line investigations
before starting antithyroid drugs (as it may cause agranulocytosis)
MANAGEMENT
• Medical (anti-thyroid drugs)
➢ Indications:
o Toxicity in pregnant women (propylthiouracil is preferred)
o Toxicity in children and young adults
o Before subtotal thyroidectomy to make the patient euthyroid. Note:
antithyroid drugs should be continued during and after surgery for 7-10
days.
o Soon after starting radioactive I-131 therapy for 6 to 12 weeks (effects of
radiotherapy start only in 6 to 12 weeks)
➢ Carbimazole:
o Blocks thyroid hormone synthesis. It also suppresses the autoimmune
process in Graves’ disease
o Dose: 5-10mg exactly 8 hourly/TID (as half-life of carbimazole is 8
hours). Each table is 5mg. It is usually given for 12-18 months.
o Often Tri-iodothyronine 20micrograms QID or thyroxine 0.1 mg daily are
given in combination with antithyroid drugs to prevent iatrogenic thyroid
insufficiency or to prevent increase in size of goiter.
o Side effects: fever, rashes, arthralgia, myalgia, neuritis, lymph node
enlargement, liver cell dysfunction, psychosis, agranulocytosis
➢ Methimazole: like carbimazole. Dose is 5 to 20 mg daily long acting, once a
day dose.
➢ Propylthiouracil:
o Blocks thyroid hormone synthesis and peripheral conversion of T4 to T3
o It also decreases the thyroid autoanibody levels.
o Can be given for hyperthyroidism in children, pregnancy and lactation.
o Dose: 200mg 8 hourly (TID)
o Side effects: dose unrelated hepatotoxicity, agranulocytosis,
antineutrophilic cytoplasmic antibody (20% of patients on long term use)
➢ Propranolol
o Dose: 40mg TID
o It reduces the cardiac problems as well as blocks peripheral conversion of
T4 to T3.
o Contraindications: bronchial asthma, heart block, cardiac failure.
o Long acting nadolol
➢ Lugol’s iodine (5% iodine + 10% potassium iodide): decreases the vascularity
of the gland and makes it more firm and easier to handle during surgery. Dose
 is 10-30 drops/day (minims) for 10 days prior to surgery. Potassium iodide
tablets 60mg TID also can be given instead of Lugol’s iodine. But its use at
present is disqualified. (1 minim =1 drop. 1ml= 16 drops)
o Note: Lugo’s iodine prevents the release of hormone from the gland
(thyroid constipation). After 2 weeks, effects of Lugol’s iodine is lost
causing thyroid escape from iodine control.
• Surgical
➢ Indications:
o Failed medical treatment in primary thyrotoxicosis in young patients
o Autonomous toxic nodule
o Nodular toxic goiter
o When malignancy cannot be ruled out
o Graves’ disease in children, Graves with nodules
o Need for antithyroid drugs for more than 2 years
o Large goiter, substernal/intrathoracic goiter
o Pressure symptoms, Graves ophthalmopathy
o Amiodarone induced thyrotoxicity
➢ Procedures done:
o Subtotal thyroidectomy: both lobes with isthmus are remove and a tissue
equivalent to pulp of finger is retained at the lower pole of the gland on
both side (5-8g)
o Hemithyroidectomy: this is done in an autonomous nodule. The entire
lateral lobe with the whole of isthmus is removed.
o Total thyroidectomy: this is the better option in Graves disease to achieve
the lowest relapse rate and successful stabilization of thyroid
ophthalmopathy as it clears the antigenic focus in thyroid completely.
➢ Complications of thyroid surgery:
o Damage to the recurrent laryngeal nerve leading to palsy (2% of
thyroidectomies) and causes hoarseness.
o Damage to the external branch of the superior laryngeal nerve, leading to
palsy and causing hoarseness.
o Hypocalcemia due to damaged parathyroid (5% of thyroidectomies)
o Hemorrhage, potentially causing laryngeal edema and respiratory
compromise.
• Radioiodine therapy
➢ Indications:
o Primary thyrotoxicosis after 45 years of age
o Autonomous toxic nodule
o Recurrent thyrotoxicosis
➢ Radioiodine destroys the cells and causes the complete ablation of thyroid
gland. It is given only after the age of 45 years as the chances of genetic
mutation (Damage), leukemia, carcinomas are high in younger individuals.
➢ Usual dose is 5 to 10 millicurie or 160 microcurie/g of thyroid.
➢ The patient is made euthyroid using antihyroid drugs, drug is discontinued for
5 days, I-131 300-600 MBq is given orally, antithyroid drugs are started after
7 days and are continued for 8 weeks. In 30% of patients additional 2 or 3
doses may be required.
➢ It takes 3 months to get full responses and so until then, the patient has to take
antithyroid drugs. Often additional 1 or 2 doses of radioiodine are required to
have complete ablation. Eventually they go for hypothyroidism and so require
maintenance dose of L-thyroxine 0.1 mg daily.
➢ To give therapeutic dose, patient should be admitted and isolated for 7 days
(half-life) to prevent irradiation. It is given orally soon after getting from the
manufacturer without much delay to have optimal efficacy.

Figure 9: Choice of therapies

HYPOTHYROIDISM
• This is characterized by low thyroid hormones.
• It is common among females (10:1).
CLASSIFICATION
• It may be classified as:
➢ Primary- due to thyroid disease or removal of the thyroid.
➢ Secondary- due to hypopituitarism
➢ Tertiary- due to hypothalamic disease
ETIOLOGY
• Classified as:
➢ Congenital:
o Agenesis or dysgenesis of the thyroid
o Enzyme deficiency (Dyshormonogenetic goiter: peroxidase enzyme
deficiency)
➢ Acquired:
o Iodine deficiency (commonest cause in developing countries)
o Hashimoto’s thyroiditis (commonest cause in developed countries):
antibodies raised against the enzyme thyroid peroxidase and
thyroglobulin (anti-thyroglobulin antibodies)
o Radioiodine
o Drugs: lithium, amiodarone
o After thyroidectomy (common cause)
CRETINISM MYXEDEMA
• This is hypothyroidism in younger • This is hypothyroidism in adults
children. • Causes:
• It is due to inadequate thyroid ➢ Iodine deficiency
hormone production during fetal and ➢ Hashimoto thyroiditis
neonatal period. (commonest cause of
• Cause: hypothyroidism where iodine is
➢ Thyroid agenesis sufficient)
➢ Inborn error of thyroid ➢ Drug e.g. lithium
metabolism ➢ Surgical removal or radioablation
➢ Dyshormonogenetic goiter: of thyroid
peroxidase enzyme deficiency • Clinical features:
➢ Maternal hypothyroidism during ➢ General: Tiredness, weight gain,
early pregnancy cold intolerance, goiter,
➢ Iodine deficiency (endemic) hyperlipidemia,
• Clinical features: hypercholesterolemia
➢ Mental disability (thyroid ➢ Cardiovascular: bradycardia with
hormones required for normal decreased cardiac output
brain development- formation of (Shortness of breath and fatigue),
neuronal synapses) angina, cardiac failure,
➢ Short stature with skeletal pericardial effusion
abnormalities ➢ Hematological: anemia
➢ Delayed puberty ➢ Gastrointestinal: constipation,
➢ Coarse facial features ileus
➢ Enlarged tongue ➢ Reproductive: infertility,
➢ Typical hoarse cry menorrhagia, galactorrhea
➢ Thickened skin ➢ Dermatological: dry skin,
➢ Umbilical hernia vitiligo, alopecia, erythema
• It is treated with L-thyroxine OD in ➢ Others: Carpal tunnel syndrome,
the morning myalgia, hoarseness, deafness,
ataxia, depression, psychosis
(myxedema madness)
• Treatment is with L-
thyroxine/Levothyronine,
Glucocorticoids, and antibiotics
• Examination will usually reveal a small firm goiter. If a nodule is present, then
this should be investigated as for a solitary thyroid nodule in order to exclude
malignancy.
• Thyroid lymphoma usually develops on a background of autoimmune
hypothyroidism.
• Extreme hypothyroidism can present as myxedema madness with confusion
leading to coma.
• Note: myxedema is severe thyroid failure
INVESTIGATIONS
• TSH: elevated in hypothyroidism with decreased free T4 and/or T3
• Antibodies: Thyroid peroxidase and antithyroglobulin
TREATMENT
• Patients are rendered euthyroid by treatment with Levothyroxine (L-thyroxine).
• In the elderly patients with ischemic heart disease, L-thyroxine should be
introduced cautiously starting at 25-50 g and increasing the dose every fortnight
in order to avoid precipitating tachyarrhythmias and cardiac failure.
• Normal thyroxine dose= 75-150 g.
• Patients should have their TSH checked every 12-18 months thereafter to ensure
correct thyroxine dosage.
• For some patients, liothyronine (T3) is an alternative. Initial rapid response can
be achieved by giving L- iodothyronine 20 g TID.
• Myxedema coma is characterized by:
➢ Hypothermia (precipitated by cold)- Drug of choice- T3 (levothyroinin) 10 g
IV QID
➢ Hypotension (precipitated by infection or trauma)- Levothyroxine 300 g IV/
1000 g orally (large dose)
➢ Hyponatremia- give glucocorticoids
➢ Hypoventilation- give antibiotics
➢ Hypoglycemia- slow warming
➢ Bradycardia- electrolyte management
➢ Skin that is cold like a todd
➢ Coma