Hypothyroidismfinalppt

Hypothyroidism
Dr.Vitrag Shah
Second Year Resident
MD, Medicine
GMC,Surat
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Introduction
 According to a projection from various studies on thyroid
disease, it has been estimated that about 42 million people in
India suffer from thyroid diseases.
 Congenital hypothyroidism is common in India, the disease
occurring in 1 out of 2640 neonates.
 The prevalence of hypothyroidism was 3.9%
 Second only to DM as most common endocrine disorder.
 Incidence increases with age.
 More common in females.
 2-3% of older women.
 The term myxedema, formerly used as a synonym for
hypothyroidism, refers to the appearance of the skin and
subcutaneous tissues in the patient who is in a severely
hypothyroid state.
Thyroid Regulation
HYPOTHALAMUS - TRH
ANT. PITUITARY - TSH

TSH -R
THYROID T4 and T3
PLASMA T4 + FT4
PLASMA T3 + FT3
TISSUES FT4 to FT3, rT3

In the Thyroid Gland
There the following 5 steps in the hormonogenesis

1. Trapping of inorganic Iodine from dietary Iodides
2. Activation of Iodine to high valance I2
3. Incorporation of I2 into Tyrosine of Thyroid Globulin
4. Coupling of formed MIT and DIT to form T4 & T3
5. Proteolysis of Thyroglobulin to release T4 & T3
Thyroid hormone biosynthesis
Thyroid hormone synthesis includes the following steps: (1) iodide (I -) trapping by the thyroid
follicular cells; (2) diffusion of iodide to the apex of the cells; (3) transport of iodide into the
colloid; (4) oxidation of inorganic iodide to iodine and incorporation of iodine into tyrosine residues
within thyroglobulin molecules in the colloid; (5) combination of two diiodotyrosine (DIT)
molecules to form tetraiodothyronine (thyroxine, T4) or of monoiodotyrosine (MIT) with DIT to
form triiodothyronine (T3); (6) uptake of thyroglobulin from the colloid into the follicular cell by
endocytosis, fusion of the thyroglobulin with a lysosome, and proteolysis and release of T4, T3,
DIT, and MIT; (7) release of T4 and T3 into the circulation; and (8) deiodination of DIT and MIT to
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tyrosine. T3 is also formed from monodeiodination of T4 in the thyroid and in peripheral
tissues. Modified from Scientific American Medicine, Scientific American, New York, 1995.
The Thyronines
Mono Iodo Tyrosine – MIT
Di Iodo Tyrosine – DIT
Tri Iodo Thyronine – T3 – half life 6 hours
Tetra Iodo Thyronine – T4 half life 7 days
Reverse T3 - metabolically inactive
T4 is 99.9% protein bound to TBG, TPA, TA
T3 is 99.5% protein bound to TBG, TPA, TA
Bound hormones are inactive – should not be measured
Only Free T4 and Free T3 are metabolically active
The Thyroxines
Tri Iodo Thyronine – T3

- 10% is from thyroid gland
- 90% derived from conversion of T4 to T3
Tetra Iodo Thyronine – T4
- Is exclusively from thyroid gland
From the thyroid gland
- 80% of hormone secreted is T4
- 20% of hormone secreted is T3
Classification of Hypothyroidism
 Primary hypothyroidism(90%) is characterized by a high
serum thyrotropin (TSH) concentration and a low serum free
thyroxine (T4) concentration.
 Subclinical hypothyroidism is defined biochemically as a
normal free T4 concentration in the presence of an elevated TSH
concentration. Other terms for this condition are mild
hypothyroidism, early thyroid failure, preclinical hypothyroidism,
and decreased thyroid reserve.
 Secondary (central) hypothyroidism is characterized by a low
serum T4 concentration and a serum TSH concentration that is
not appropriately elevated.
 Transient or temporary hypothyroidism can be observed as a
phase of subacute thyroiditis.
 Consumptive hypothyroidism, identified in an increasing
number of clinical settings, is the result of accelerated
inactivation of thyroid hormone by the type 3 iodothyronine
deiodinase (D3).
GOITROGENS
DRUGS
Anti-thyroid
Cough medicines
Sulfonamides
Lithium
Phenylbutazone
PAS
Oral hypoglycemic agents
GOITROGENS
FOOD
Soybeans
Millet
Cassava
Cabbage
Congenital Hypothyroidism
 The majority of infants appear normal at birth, and
<10% are diagnosed based on clinical features, which
include prolonged jaundice, feeding problems,
hypotonia, enlarged tongue, delayed bone maturation,
and umbilical hernia.
 Importantly, permanent neurologic damage results if
treatment is delayed.
 Typical features of adult hypothyroidism may also be
present.
 Other congenital malformations, especially cardiac,
are four times more common in congenital
hypothyroidism.
Congenital Hypothyroidism
Diagnosis & Treatment
 Because of the severe neurologic consequences of untreated
congenital hypothyroidism, neonatal screening programs
have been established based on measurement of TSH or T4
levels in heel-prick blood specimens.
 When the diagnosis is confirmed, T4 is instituted at a dose of
10–15 µg/kg per day, and the dose is adjusted by close
monitoring of TSH levels.
 T4 requirements are relatively great during the first year of
life, and a high circulating T4 level is usually needed to
normalize TSH.
 Early treatment with T4 results in normal IQ levels, but
subtle neurodevelopmental abnormalities may occur in
those with the most severe hypothyroidism at diagnosis or
when treatment is delayed or suboptimal.
Autoimmune Hypothyroidism
 Autoimmune hypothyroidism may be associated with a
goiter (Hashimoto's, or goitrous thyroiditis) or, at the
later stages of the disease, minimal residual thyroid
tissue (atrophic thyroiditis).
 Because the autoimmune process gradually reduces
thyroid function, there is a phase of compensation when
normal thyroid hormone levels are maintained by a rise
in TSH. Though some patients may have minor
symptoms, this state is called subclinical
hypothyroidism.
 Later, unbound T4 levels fall and TSH levels rise further;
symptoms become more readily apparent at this stage
(usually TSH >10 mIU/L), which is referred to as clinical
hypothyroidism or overt hypothyroidism.
Epidemiology
 The mean age at diagnosis is 60 years, and the
prevalence of overt hypothyroidism increases with
age.
 Iodine deficiency is most common cause of

hypothyroidism worldwide while Autoimmune
hypothyroidism is most common cause in iodine
sufficient regions.
Pathogenesis
 In Hashimoto's thyroiditis, there is a marked
lymphocytic infiltration of the thyroid with germinal
center formation, atrophy of the thyroid follicles
accompanied by oxyphil metaplasia, absence of colloid,
and mild to moderate fibrosis.
 In atrophic thyroiditis, the fibrosis is much more
extensive, lymphocyte infiltration is less pronounced, and
thyroid follicles are almost completely absent. Atrophic
thyroiditis likely represents the end stage of Hashimoto's
thyroiditis rather than a distinct disorder.
 Genetic Associations: HLA-DR (3,4,5) & CTLA-4
(Cytotoxic T Lymphocyte associated antigen 4)
polymorphism
 Modifying Environmental Factor : Chronic exposure to
high iodine diet
 No role of infection except Congenital Rubella
Syndrome
Associated conditions
 Other Autoimmune disorders: (MC)
Type 1 diabetes mellitus
Addison's disease
Pernicious anemia
Vitiligo
Alopecia areata
Celiac disease
Dermatitis Herpatiformis
Chronic Active Hepatitis
RA, SLE, Sjogren syndrome
Thyroid associated ophthalmopathy( in 5% of pt)
 Turner syndrome, Down’s syndrome
 Type 1 or 2 polyglandular autoimmune syndrome
Other causes of hypothyroidism
 Iatrogenic hypothyroidism is a common cause of
hypothyroidism.
 In the first 3–4 months after radioiodine treatment,
transient hypothyroidism may occur due to
reversible radiation damage. Low-dose thyroxine
treatment can be withdrawn if recovery occurs.
 Because TSH levels are suppressed by
hyperthyroidism, unbound T4 levels are a better
measure of thyroid function than TSH in the
months following radioiodine treatment.
 Mild hypothyroidism after subtotal thyroidectomy
may also resolve after several months, as the gland
remnant is stimulated by increased TSH levels.
 Iodine deficiency is responsible for endemic goiter and
cretinism but is an uncommon cause of adult
hypothyroidism unless the iodine intake is very low or
there are complicating factors, such as the consumption
of thiocyanates in cassava or selenium deficiency.
 Paradoxically, chronic iodine excess (Rx with
amiodarone, lithium) can also induce goiter and
hypothyroidism, individuals with autoimmune thyroiditis
are especially susceptible.
 Secondary hypothyroidism is usually diagnosed in the
context of other anterior pituitary hormone deficiencies;
isolated TSH deficiency is very rare. TSH levels may be
low, normal, or even slightly increased in secondary
hypothyroidism; the latter is due to secretion of
immunoactive but bioinactive forms of TSH. The
diagnosis is confirmed by detecting a low unbound T4
level.
Clinical Manifestations
 The onset is usually insidious, and the patient may become aware
of symptoms only when euthyroidism is restored.
 Patients with Hashimoto's thyroiditis may present because of
goiter rather than symptoms of hypothyroidism. The goiter may
not be large, but it is usually irregular and firm in consistency.
 Hypothyroidism is less prominent clinically and better tolerated
when there is a gradual loss of thyroid function (as in most cases of
primary hypothyroidism) than when it develops acutely after
thyroidectomy or abrupt withdrawal of exogenous thyroid
hormone.
 The symptoms of central hypothyroidism are usually milder &
less obvious than in primary hypothyroidism because of
concurrent symptoms of coexisting hormone deficiencies. i.e. hot
flashes due to hypogonadism may mask the cold intolerance of
hypothyroidism.
 When hypothyroidism follows treatment of Graves'
hyperthyroidism, some manifestations of Graves' disease, such as
ophthalmopathy and vitiligo, may persist throughout the patient's
life.
Differentian between Primary &
secondary hypothyroidism
Features Primary Secondary
Skin Thick, without wrinkles Thin with fine wrinkles
Hair Coarse Fine
Menstrual disturbances Menorrhagia Amenorrhea
Secondary sexual Normal Poor
characteristics
Heart size May be enlarged Normal
Goiter May be present Absent
Soft tissue edema Marked Absent
BP Normal/High Low
Cholesterol Increased Normal
TSH High Low
Plasma Cortisol Normal Low
TRH stimulation test Exaggerated response No response
Thyroid Autoantibodies May be present Absent
CLINICAL MANIFESTATIONS
 Many of the manifestations of hypothyroidism reflect one
of two changes induced by lack of thyroid hormone:
 A generalized slowing of metabolic processes. This can
lead to abnormalities such as fatigue, slow movement and
slow speech, cold intolerance, constipation, weight gain
(but not morbid obesity), delayed relaxation of deep
tendon reflexes, and bradycardia.
 Accumulation of matrix glycosaminoglycans in the
interstitial spaces of many tissues. This can lead to coarse
hair and skin, puffy facies, enlargement of the tongue, and
hoarseness. These changes are often more easily
recognized in young patients, and they may be attributed
to aging in older patients.
Skin
 The skin is cool and pale in patients with hypothyroidism
because of decreased blood flow.
 The epidermis has an atrophied cellular layer and hyperkeratosis
that results in the characteristic dry roughness of the skin.
 Sweating is decreased because of decreases in calorigenesis
and acinar gland secretion.
 A yellowish tinge may be present if the patient has carotenemia,
while hyperpigmentation may be seen when primary
hypothyroidism is associated with primary adrenal failure
 Hair may be coarse, hair loss is common, and the nails become
brittle.
 Nonpitting edema (myxedema) occurs in severe
hypothyroidism and may be generalized. It results from
infiltration of the skin with glycosaminoglycans with associated
water retention.
 Vitiligo and alopecia areata may be present in patients with
hypothyroidism after treatment of Graves‘ hyperthyroidism.
Myxoedema with Carotineamia
Eyes
 Periorbital edema
 Thinning of outer third of eyebrows (Madarosis)
 Graves' ophthalmopathy may persist when
hypothyroidism develops after treatment of Graves'
hyperthyroidism
Hematologic
 Decrease in red blood cell mass
 Normochromic, normocytic hypoproliferative anemia
 Pernicious anemia occurs in 10 percent of patients
with hypothyroidism caused by chronic autoimmune
thyroiditis : macrocytic anemia with marrow
megaloblastosis
 Women in the childbearing years may develop iron
deficiency anemia, secondary to menorrhagia. In
patients with IDA and hypothyroidism, combined
therapy with levothyroxine and oral iron supplements
results in correction of the anemia, which may be
refractory to treatment with iron alone
Cardiovascular system
 Decrease in cardiac output that is mediated by reductions in
heart rate and contractility
 Thyroid hormoneregulation of genes coding for specific
myocardial enzymes involved in myocardial contractility and
relaxation is responsible for the decrease in contractility.
 Reduced cardiac output probably contributes to decreased
exercise capacity and shortness of breath during exercise.
 Pericardial effusion
 Hypercholesterolemia, which is caused by a decrease in the
rate of cholesterol metabolism
 Hyperhomocystemia
 Diastolic Hypertension, because of an increase in peripheral
vascular resistance. In normotensive patients, blood pressure
increases are small (<150/100).
 ECG : Low voltage, sinus bradycardia, non-specific ST-T
changes
Respiratory system
 Fatigue, shortness of breath on exertion, rhinitis,
and decreased exercise capacity
 Hypoventilation occurs because of respiratory
muscle weakness and reduced pulmonary
responses to hypoxia and hypercapnia
 Sleep apnea occurs in some patients with
hypothyroidism, mostly as a result of macroglossia.
Gastrointestinal disorders
 Decreased gut motility results in constipation
 Decreased taste sensation.
 Gastric atrophy due to the presence of antiparietal
cell antibodies
 Celiac disease is four times more common in
hypothyroid patients
 Modest weight gain (despite poor appetite)due to
decreased metabolic rate and accumulation of fluid
 Ascites is a rare finding
Reproductive abnormalities
 Decreased fertility
 Early abortion
 Hypermenorrhea-menorrhagia (More common). Or
oligo- or amenorrhea (later stage)
 Low serum sex hormone-binding globulin
concentration
 Hyperprolactinemia may occur, and is occasionally
sufficiently severe to cause amenorrhea or
galactorrhea
 Decreased libido, erectile dysfunction
Neurological dysfunction
 Affects both CNS & PNS
 Slow growth and delayed facial maturation, delayed
appearance of permanent teeth
 Myopathy, with muscle swelling, is more common in
children than in adults.
 In most cases, puberty is delayed, but precocious
puberty sometimes occurs
 Intellectual impairment if the onset is before 3 years
and the hormone deficiency is severe.
 Carpal tunnel and other entrapment syndromes
 Slow relaxation of tendon reflexes and pseudomyotonia
 Memory and concentration are impaired, Bradylalia
 Rare neurologic problems include reversible cerebellar
ataxia,
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Hashimoto's encephalopathy
 Hashimoto's encephalopathy has been defined as a
steroid-responsive syndrome associated with TPO
antibodies, myoclonus, and slow-wave activity on
electroencephalography.
 Hashimoto's encephalopathy is believed to be an
immune-mediated disorder rather than
representing the direct effect of an altered thyroid
state on the central nervous system.
Musculoskeletal symptoms
 Joint pains, aches, and stiffness
 Increased prevalence of hyperuricemia and gout
 Elevated AST, CK, LDH
Metabolic abnormalities
 Hyponatremia may result from a reduction in free
water clearance. Hypothyroidism must be excluded
in any hyponatremic patient before making the
diagnosis of the syndrome of inappropriate
antidiuretic hormone secretion.
 Reversible increases in serum creatinine
 Hypercholesterolemia and hypertriglyceridemia
 Hyperhomocysteinemia
Drug clearance
 The clearance of many drugs, including
antiepileptic, anticoagulant, hypnotic and opioid
drugs, is decreased in hypothyroidism
Myxedema coma
 Myxedema coma is defined as severe hypothyroidism leading to
decreased mental status, hypothermia, and other symptoms related to
slowing of function in multiple organs.
 It is a medical emergency with a high mortality rate.
 There may be a history of treated hypothyroidism with poor
compliance, or the patient may be previously undiagnosed.
 Myxedema coma almost always occurs in the elderly and is usually
precipitated by factors that impair respiration, such as drugs
(especially sedatives, anesthetics, antidepressants), pneumonia,
congestive heart failure, myocardial infarction, gastrointestinal
bleeding, or cerebrovascular accidents, sepsis.
 Hypoventilation leading to hypoxia and hypercapnia, plays a major
role in pathogenesis;
 Exposure to cold, Hypoglycemia and dilutional hyponatremia also
contribute to the development of myxedema coma.
 The diagnosis should be considered in any patient with coma or
depressed mental status who also has hypothermia, hyponatremia,
and/or hypercapnia. Additional clues to the possible presence of
myxedema coma in a poorly responsive patient are the presence of a
thyroidectomy scar or a history of I-131 therapy or hypothyroidism.
Lab Evaluation
Thyroid Function Tests
 Total T4 (thyroxine), Total T3 (triiodothyronine)

 Free T4 , Free T3
 TSH
 T3 -Uptake
 Free T4 Index, Free T3 Index
 Anti-Thyroid Antibodies
 Nuclear Scintigraphy
 FNAC of nodule
Thyroid Antibodies
 Anti Microsomal (TM ) Antibodies
 Anti Thyroglobulin (TG) Antibodies
 Anti Thyroperoxidase (TPO) Ab
 Anti Thyroxine antibodies
 Thyroid Stimulating (TSA) Antibodies
 High titres TPO Ab in Hashimoto’s & Reidle’s thyroiditis
 Anti thyroxine Ab in peripheral resistance to Thyroxine
 TSA (TSI) in Graves’ Hyperthyroidism
Tests of thyroid function
Test Reference Ranges*
TSH 0.3- 4.0 mU/ L
Free T4 0.7- 2.1 ng/ dL
T4 4- 11 μg/ dL
T3 75- 175 ng/ dl
Laboratory tests of thyroid function can be abnormal in 70% of

hospitalized patients and in up to 90% of critically ill patients.
In most cases, the abnormality represents an adaptive response to non-
thyroidal (systemic) illness and is not a sign of pathologic thyroid
disease.
Adopted from:
Stockigt JR . In : Werner and Ingbar’s The Thyroid , 7th ed . 1996: 399
*Reference ranges may vary according to laboratory Tests
Thyroxine (T4) and Triiodothyronine (T3)
 Thyroxine (T4) is the principal hormone secreted by the
thyroid gland, but the active form is triiodothyronine
(T3), which is formed by deiodination of thyroxine in
extrathyroidal tissues.
 Both T3 and T4 are extensively (.99%) bound to plasma
proteins, especially thyroxine-binding globulin.
 Approximately 0.2% of the total T3 is in the unbound or
physiologically active form.
 Because of the minor representation of unbound T3 and
T4 in plasma, and the potential for plasma protein
concentrations to vary in ICU patients, only
measurements of free T3 and T4 should be performed in
ICU patients.
What tests should I order ?
As per the Guidelines of the AACE and ATA, ITS

1. TSH alone if Hypothyroidism is suspected
2. TSH and Free T4 only if Hyperthyroidism is
suspected or for routine evaluation
3. Free T3 if T3 toxicosis is suspected
4. For follow-up of treatment only TSH
5. Don’t order for Total T4 or Total T3
6. Never order RIU in pregnancy or lactation
Which Lab to choose ?
1. Depends on the method of estimation of hormones
2. Equilibrium Dialysis is the gold Standard for TSH
3. Radio-immuno assay - 3rd or 4th gen. RIA is the best
4. Reliability of ELISA is not adequate
5. Chemiluminescence immuno assay - CIA is the gold
standard for FT4 but expensive and less widely
available
Choose a lab which offers
vitrag24 - www.medicalgeek.com 3 rd or 4th generation RIA method
Indications to test for hypothyroidism
Clinical symptoms and signs
Fatigue Laboratory test abnormalities
Cold intolerance
Constipation
Hypercholesterolaemia
Impaired memory
Slowed mental processing Hyponatraemia
Depression
Hyperprolactinaemia
Nerve entrapment syndromes
Ataxia Hyperhomocysteinaemia
Muscle weakness
Anemia
Muscle cramps
Menstrual disturbance Creatine phosphokinase
Infertility elevation
Bradycardia
Radiological abnormalities
Diastolic hypertension
Hoarseness
Pericardial and pleural effusions
Goitre
Periorbital oedema
Pituitary gland enlargement
Weight gain
Galactorrhoea
Indications to test for hypothyroidism
Risk factors for hypothyroidism
Autoimmune thyroiditis Previous thyroid injury
Established serological or tissue Thyroidectomy or other neck surgery
diagnosis Radioactive iodine therapy
Diffuse goitre External radiotherapy
Previous Graves' disease, de Quervain's Exposure to polybrominated and
thyroiditis, or painless (postpartum) polychlorinated biphenyls, and resorcinol
thyroiditis
Postpartum status
Family history of autoimmune thyroid Drugs impairing thyroid function
disease
Lithium carbonate
Down's syndrome
Amiodarone
Personal or family history of associated Aminoglutethimide
autoimmune disorders (eg, vitiligo,
pernicious anaemia, adrenal Interferon α
insufficiency, diabetes mellitus type 1, Thalidomide
ovarian failure, coeliac disease,
Sjögren's syndrome) Betaroxine
Stavudine
Primary pulmonary hypertension
Hypothalamic disorders
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Sclerosis
Pituitary disorders
How to interpret results ?
The Nine Square Game

To evaluate our Thyroid patient
As per the AACE and ITS Guidelines
BASIC THYROID EVALUATION
FREE THYROXINE or FT4
LOW NORMAL HIGH
THYROID STIMULATING HORMONE - TSH

EUTHYROID
LOW NORMAL HIGH

PRIMARY
HYPOTHYROID
LOW NORMAL HIGH

PRIMARY
HYPERTHYROID
LOW NORMAL HIGH

SECONDARY
HYPOTHYROID
LOW NORMAL HIGH

SECONDARY
HYPERTHYROID
LOW NORMAL HIGH

SUB-CLINICAL
HYPERTHYROID
LOW NORMAL HIGH

SUB-CLINICAL
HYPOTHYROID
LOW NORMAL HIGH

NON THYROID
ILLNESS or NTI
LOW NORMAL HIGH

NTI or Pt.
on ELTROXIN
LOW NORMAL HIGH

PRIMARY NTI or Pt. SECONDARY

HYPERTHYROID on ELTROXIN HYPERTHYROID
SUB-CLINICAL SUB-CLINICAL
HYPERTHYROID
EUTHYROID HYPOTHYROID
SECONDARY NON THYROID PRIMARY

HYPOTHYROID ILLNESS - NTI HYPOTHYROID
LOW NORMAL HIGH

Common Patterns of Thyroid Function
Tests in Critically Ill Patients
Non-Thyroidal Ilness Free T4 Free T3 TSH
Early systemic illness Normal ↓ Normal
Early critical illness ↓ ↓ Normal
Chronic critical illness ↓ ↓ Normal/↓

(>2 days)
Sick Euthyroid Syndrome

Euthyroid sick syndrome, sick euthyroid syndrome, non-thyroidal
illness syndrome or low T3 low T4 syndrome is a state of adaptation
or dysregulation of thyrotropic feedback control where the levels of T3
and/or T4 are at unusual levels, but the thyroid gland does not appear
to be dysfunctional. This condition is often seen in starvation, critical
illness
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T.F.T. in Progressive Hypothyroidism
TSH
Mild Moderate Severe
Normal Range
Free T3
Free T4
Algorithm for Hypothyroidism
Measure TSH
Elevated TSH Normal TSH
Measure FT4 Considering Pituitary
Normal Low No Yes
Sub-clinical hypo Primary hypothyroid No tests Measure FT4
TPO + TPO - TPO + TPO - Low Normal
T4 repl Annual FU Hashimoto Evaluate Pituitary

Sick Euthyroid No tests
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Treatment
 Goal : Normalize TSH level regardless of cause of
hypothyroidism
 Treatment of choice is thyroxine

 Brand consistency recommended
 Not recommended for routine use :
 Desiccated thyroid hormone
 Combination of thyroid hormones
 T3
 TSH should be measured at 6 to 8 weeks after any

change in L-thyroxine brand or dose
Determinants of Thyroxine
Requirements
 Age
 Severity and duration of hypothyroidism
 Weight
 Malabsorption
 Pregnancy
 Presence of cardiac disease
 Concomitant drug therapy
Treatment : Outline
 Goal : normalize TSH level, , ideally in the lower half of
the reference range.
 Single daily dose of levothyroxine as half life is 7 days.
 Always take on empty stomach
 Starting dose for healthy patients <50 years should be
at 1.6 μg/kg/day
 Starting dose for healthy patients >50 years should be
<50 μg/day. Dose should be increased by 12.5-25
μg/day, if needed, at 6 to 8 weeks intervals. (Start low
and go slow)
 Starting dose for patients with heart disease should
be 12.5 to 25 μg/day and increase by 12.5 to 25 μg/day,
if needed, at 6 to 8 weeks intervals
Treatment : Clinical Hypothyroidism
 If there is no residual thyroid function, the daily replacement dose
of levothyroxine is usually 1.6 µg/kg body weight (typically 100–
150 µg). In many patients, however, lower doses suffice until
residual thyroid tissue is destroyed.
 In patients who develop hypothyroidism after the treatment of
Graves' disease, there is often underlying autonomous function,
necessitating lower replacement doses (typically 75–125 µg/d).
 TSH responses are gradual and should be measured about two
months after instituting treatment or after any subsequent
change in levothyroxine dosage.
 The clinical effects of levothyroxine replacement are slow to
appear. Patients may not experience full relief from symptoms
until 3–6 months after normal TSH levels are restored.
 Adjustment of levothyroxine dosage is made in 12.5- or 25 µg
increments if the TSH is high; decrements of the same magnitude
should be made if the TSH is suppressed.
 Once full replacement is achieved and TSH levels are stable,
follow-up measurement of TSH is recommended at annual
intervals and may be extended to every 2–3 years if a normal
TSH is -maintained
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Follow-up After 6 to 8 Weeks of
Thyroxine Therapy
If Repeat TSH is Then
> 4.0 mU/L Increase daily thyroxine dose by 12.5-
25 μg/d & repeat TSH in 6 to 8 week
0.3 to 4.0 mU/L Continue dose; repeat TSH in 6

months and then annually or if
symptomatic
If TSH remain normal for several
years, then monitor every 2-3 years
<0.4 mU/L Decrease daily thyroxine dose by 12.5

to 25 μg/d and repeat in 6 to 8 weeks
 There is no place for liothyronine alone as long-term
replacement, because the short half-life necessitates three
or four daily doses and is associated with fluctuating T3
levels.
 It is important to ensure ongoing adherence, however, as
patients do not feel any symptomatic difference after
missing a few doses of levothyroxine, and this sometimes
leads to self-discontinuation.
 In patients of normal body weight who are taking 200 µg
of levothyroxine per day, an elevated TSH level is often a
sign of poor adherence to treatment. Such patients often
have normal or high unbound T4 levels, despite an
elevated TSH, because they remember to take medication
for a few days before testing; this is sufficient to normalize
T4, but not TSH levels.
 Because T4 has a long half-life (7 days), patients who miss
a dose can be advised to take two doses of the skipped
tablets at once.
Over - and Under-Replacement Risks
 Over-replacement Risks
 Reduced bone density/osteoporosis
 Tachycardia, arrhythmia : Atrial fibrillation
 In elderly or patients with heart disease, angina,
arrhythmia, or myocardial infarction
 Under-replacement Risks
 Continued hypothyroid state
 Long-term end-organ effects of hypothyroidism
 Increased risk of hyperlipidemia
Recovery after L-Thyroxine
Recovery after L-Thyroxine
Treatment : Subclinical Hypothyroidism
 By definition, subclinical hypothyroidism refers to
biochemical evidence of thyroid hormone deficiency in
patients who have few or no apparent clinical features
of hypothyroidism.
 Routine treatment not recommended when TSH levels
are below 10 mU/L.
 Any elevation of TSH must be sustained over a 3-month
period before treatment is given.
 Treatment is administered by starting with a low dose
of levothyroxine (25–50 µg/d) with the goal of
normalizing TSH. If thyroxine is not given, thyroid
function should be evaluated annually.
 There is a risk that patients will progress to overt
hypothyroidism, particularly when the TSH level is
elevated and TPO antibodies are present.
Special Treatment Considerations
 Women with a history or high risk of hypothyroidism should
ensure that they are euthyroid prior to conception and during
early pregnancy as maternal hypothyroidism may adversely affect
fetal neural development and cause preterm delivery.
 Thyroid function should be evaluated immediately after
pregnancy is confirmed and at the beginning of the second and
third trimesters. The dose of levothyroxine may need to be
increased by 50% during pregnancy and returned to previous
levels after delivery.
 Elderly patients may require 20% less thyroxine than younger
patients. In the elderly, especially patients with known coronary
artery disease, the starting dose of levothyroxine is 12.5–25 µg/d
with similar increments every 2–3 months until TSH is
normalized. In some patients, it may be impossible to achieve full
replacement despite optimal antianginal treatment.
 Emergency surgery is generally safe in patients with untreated
hypothyroidism, although routine surgery in a hypothyroid
patient should be deferred until euthyroidism is achieved.
Treatment : Myxedema coma
 Levothyroxine can initially be administered as a single IV
bolus of 500 µg, which serves as a loading dose. Although
further levothyroxine is not strictly necessary for several days,
it is usually continued at a dose of 50–100 µg/d.
 If suitable IV preparation is not available, the same initial dose
of levothyroxine can be given by nasogastric tube (though
absorption may be impaired in myxedema).
 An alternative is to give liothyronine (T3) intravenously or via
nasogastric tube, in doses ranging from 10 to 25 µg every 8–
12 h. This treatment has been advocated because T4 to T3
conversion is impaired in myxedema coma. However, excess
liothyronine has the potential to provoke arrhythmias.
 Another option is to combine levothyroxine (200 µg) and
liothyronine (25 µg) as a single, initial IV bolus followed by
daily treatment with levothyroxine (50–100 µg/d) and
liothyronine (10 µg every 8 h).
 Recovery within 24 hours is usual.
Supportive Treatment : Myxedema coma
 External warming is indicated only if the temperature is <30°C,
as it can result in cardiovascular collapse. Space blankets should
be used to prevent further heat loss.
 Parenteral hydrocortisone (50 mg every 6 h) should be
administered, because there is impaired adrenal reserve in
profound hypothyroidism.
 Any precipitating factors should be treated, including the early
use of broad-spectrum antibiotics, pending the exclusion of
infection.
 Ventilatory support with regular blood gas analysis is usually
needed during the first 48 hours.
 Hypertonic saline or IV glucose may be needed if there is
severe hyponatremia or hypoglycemia; hypotonic IV fluids
should be avoided because they may exacerbate water retention
secondary to reduced renal perfusion and inappropriate
vasopressin secretion.
 The metabolism of most medications is impaired, and sedatives
should be avoided if possible or used in reduced doses.
Medication blood levels should be monitored, when available,
tovitrag24
guide- www.medicalgeek.com
dosage.
Diet in Iodine deficiency
 Iodized salt
 Selenium supplementation
 Avoid Cassava
 Avoid cabbage (goitrogens)
 Avoid formula milk
 Fish, meat, milk & eggs
References
 Williams Textbook of Endocrinology – 12th Edition
 Harrison’s Principles of internal medicine – 18th Edition
 AFP journal
 UpToDate 19.3
 eMedicine
 Publications from the American Thyroid
Association, American Association of Clinical
Endocrinologists, and the Endocrine Society
 The ICU Book, 3rd Edition - Paul L. Marino

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Hypothyroidism

ANT. PITUITARY - TSH

TISSUES FT4 to FT3, rT3

There the following 5 steps in the hormonogenesis

Tri Iodo Thyronine – T3

 Iodine deficiency is most common cause of

 Total T4 (thyroxine), Total T3 (triiodothyronine)

Laboratory tests of thyroid function can be abnormal in 70% of

As per the Guidelines of the AACE and ATA, ITS

The Nine Square Game

As per the AACE and ITS Guidelines

LOW NORMAL HIGH

THYROID STIMULATING HORMONE - TSH

LOW NORMAL HIGH

THYROID STIMULATING HORMONE - TSH

LOW NORMAL HIGH

THYROID STIMULATING HORMONE - TSH

LOW NORMAL HIGH

THYROID STIMULATING HORMONE - TSH

LOW NORMAL HIGH

THYROID STIMULATING HORMONE - TSH

LOW NORMAL HIGH

THYROID STIMULATING HORMONE - TSH

LOW NORMAL HIGH

THYROID STIMULATING HORMONE - TSH

LOW NORMAL HIGH

THYROID STIMULATING HORMONE - TSH

LOW NORMAL HIGH

THYROID STIMULATING HORMONE - TSH

LOW NORMAL HIGH

THYROID STIMULATING HORMONE - TSH

PRIMARY NTI or Pt. SECONDARY

SECONDARY NON THYROID PRIMARY

LOW NORMAL HIGH

THYROID STIMULATING HORMONE - TSH

Non-Thyroidal Ilness Free T4 Free T3 TSH

Early systemic illness Normal ↓ Normal

Early critical illness ↓ ↓ Normal

Chronic critical illness ↓ ↓ Normal/↓

Sick Euthyroid Syndrome

Mild Moderate Severe

Elevated TSH Normal TSH

Measure FT4 Considering Pituitary

Normal Low No Yes

Sub-clinical hypo Primary hypothyroid No tests Measure FT4

TPO + TPO - TPO + TPO - Low Normal

T4 repl Annual FU Hashimoto Evaluate Pituitary

 Treatment of choice is thyroxine

 TSH should be measured at 6 to 8 weeks after any

0.3 to 4.0 mU/L Continue dose; repeat TSH in 6

<0.4 mU/L Decrease daily thyroxine dose by 12.5

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