Hypothyroidism can be primary, meaning it is caused by a problem in the thyroid gland itself, or secondary, caused by a lack of TSH from the pituitary gland. Primary causes include congenital defects, iodine deficiency, autoimmune disorders like Hashimoto's thyroiditis, and surgery or radiation treatment of the thyroid. Secondary hypothyroidism is caused by problems of the pituitary gland or peripheral resistance to thyroid hormone. Diagnosis is made through blood tests showing low T3 and T4 and high TSH for primary hypothyroidism. Treatment is lifelong thyroid hormone replacement, usually levothyroxine. Dosage depends on age, severity, and other factors.

1. HYPOTHYROIDISM

2. CLASSIFICATION
ETIOLOGICAL
PRIMARY
TRANSIENTSECONDARY

3. pathogenesis

4. Causes
PRIMARY
1) Congenital
 Agenesis
 Ectopic thyroid remnants
2) Defects of hormone synthesis
 Iodine deficiency
 Dyshormonogenesis
 Drugs -Antithyroid drugs, lithium,
amiodarone, interferon)
3)Autoimmune
 Atrophic thyroiditis
 Hashimoto's thyroiditis
 Postpartum thyroiditis
4) Infective
 Post-subacute thyroiditis
5) Post-surgery
6) Post-irradiation
 Radioactive iodine therapy
 External neck irradiation
7) Infiltration
 Tumour
SECONDARY
1) Hypopituitarism
2) Isolated TSH deficiency
3) Peripheral resistance to thyroid hormone
 Hypothyroidism may be due to primary disease of the thyroid gland(primary) or due to lack of
pituitary TSH(secondary)

5. Clinical features

6. EVALUATION OF HYPOTHYROIDISM

7. investigations
 Classical findings of primary hypothyroidism are reduced levels of
T3 and T4 and increased levels of TSH.
 Secondary hypothyroidism T3, T4, TSH all are reduced, along with
other pituitary hormones.
 Other abnormal investigations are
 Anemia –macrocytic or microcytic (mennoraghia).
 ECG-- bradycardia, low voltage complexes.
 Increase in CK from muscle.
 Hypercholesterolemia.
 Antibodies to thyroid peroxidase are positive in spontaneous
atrophic thyroiditis and hashimoto’s thyroiditis.

8. treatment
• DRUG OF CHOICE: thyroxine
• Drug should be taken 30 minutes before a meal
• Dose depends on:
a) severity of deficiency
b) Age of patient
c) Fitness of patient

9. • INITIATION OF THERAPY:
 Based on age
 Young and middle aged adults:100
mcg daily
 Healthy elderly: 50 mcg daily
 With cardiac disease: 25-50 mcg daily

10.  Based on severity of disease
 Clinical hypothyroidism
i. No residual thyroid function: 100-150
mcg/d
ii. Underlying autonomous function of gland
is present: 75-125mcg/d
 Subclinical hypothyroidism:

11. • This term is used when TSH is elevated
(>10microUnits per litre) and T3, T4 are normal
with vague symptoms.
• This condition should be treated only if there are
• High titers of antibodies
• Lipid abnormalities
• Associated with goiter
• If above indications are not present then patient
should be followed up with TSH andT3, T4 every
3-6 months.
 DOSE: 25-50 microgram/d
Subclinical hypothyroidism

12. • DOSE ADUSTMENT AND FOLLOW-UP
 Primary hypothyroidism:
 GOAL-maintain plasma TSH within normal
range
 Plasma TSH is measured 6-8 weeks after
initiation of therapy
 Dose is adjusted in 12-25 mcg increments at 6-
8 week intervals till plasma TSH is normal
 Annual TSH measurement is adequate
thereafter
 Overcorrection of TSH levels will increase the
risk of atrial fibrillation and osteoporosis

13.  Secondary hypothyroidism
 GOAL: maintain plasma free T4 levels near the
upper limit of the reference range
 Dose is adjusted in 12-25 mcg increments a 6-8
week intervals till plasma TSH is normal
 Annual TSH measurement is adequate
thereafter
 Subclinical hypothyroidism
 Goal:normalise TSH
 Annual evaluation if not treated

14. MYXOEDEMA COMA
 Myxedema coma is a medical emergency.
 Commonly seen in elderly patients with longstanding
hypothyroidism.
 Common precipitating factors are sedatives , anaesthetics,
pneumonia,CCF, MI, GI bleed, CVA
 Mortality rates are 50%

15.  Clinical manifestations:
 Hypothermia
 Altered consciousness- result of delayed cerebration .
 Hypoventilation -
 Bradycardia
 Hypoglycemia and SIADH.

16. Management
 Levothyroxine (T4)
loading dose.:500mcg I.V. bolus
continued at a dose of 50 to 100 mcg/d.
.
 alternative :
liothyronine (T3) :10 to 25 mcg every 8 to
12h .
 Inj. Hydrocortisone 50mg I.V 6hrly should be
given and can be stopped if cortisol levels are
normal.

17.  Other measures include:
---Oxygen and gradual rewarming.
---Glucose and sodium correction.
---Ventilatory support if required.
• Medication blood levels should be monitored, when
avavilable, to guide dosage.

18. THYROIDITIS
 Thyroiditis most often results from an infective or
autoimmune process
Classification of thyroiditis
 Acute thyroiditis - Bacterial, viral,
 Subacute thyroiditis - de Quervain's thyroiditis
 Chronic thyroiditis - Autoimmune - Hashimoto’s
(chronic lymphocytic), Riedel thyroiditis

19. HASHIMOTO’S THYROIDITIS
 It is autoimmune thyroiditis.
 Common in middle aged females.
 Histologically, there is marked lymphocytic
infiltration to the extent of formation of
germinal centers. Askanazy cells are present.
 Gland is diffusely enlarged and is firm.
 Patient may be euthyroid or hypothyroid.
 AntiTPO Ab is positive and thyroid scan
uptake is low.
 Treatment is required only if there is
hypothyroidism or goiter.

20. Non thyroidal illnesses
T4 to T3 and binding to TBG
TFT: low T3
Normal T4
Normal TSH
THE SICK EUTHYROID SYNDROME