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Hypothyroidism. By: Elias S. Hypothyroidism. A common disorder associated with thyroid hormone deficiency resulting from a defect anywhere in the hypothalamic-pituitary-thyroid axis Majority  primary thyroid D. Less common TSH , TRH Prevalence U.S. NHANES III on 17353 persons

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hypothyroidism

Hypothyroidism

By: Elias S.

hypothyroidism1
Hypothyroidism
  • A common disorder associated with thyroid hormone deficiency resulting from a defect anywhere in the hypothalamic-pituitary-thyroid axis
    • Majority  primary thyroid D.
    • Less common TSH , TRH
  • Prevalence
    • U.S. NHANES III on 17353 persons

hypothyroidism… 4.6%

(subclinical 4.3%, overt 0.3%)

  • international

2-5% ( to 15% by the age of 75)

  • Autoimmune Hypothyroidism

annual incidence: 4/1000 women, 1/1000 men

prevalence cont
Prevalence cont…….
  • Age: … with age
    • More prevalent in elderly
    • Autoimmune hypoth.- Mean age at Dx- 60.
  • sex: women >(5-8x) Men

Framingham study in adults>60yrs

5.9%-women 2.4%- men

Race: more common-Japanese

NHASESIII, U.S

whites(5.1%)>Hispanic A.(4.1%)>African A(1.7%)

causes
causes
  • Worldwide:
    • iodine deficiency most common cause
  • In areas of iodine sufficiency
    • Autoimmune thyroiditis (Hashimoto’s)
    • Iatrogenic causes
  • Hypothyroidism

- Primary H.

- Central (secondary/tertiary)

  • Primary hypothyroidism – 2 forms

Subclinical  Overt( clinical)

(TSH, N FT4,N FT3) (TSH, FT4,FT3)

autoimmune hypothyroidism
Autoimmune hypothyroidism
  • Ch. Autoimmune thyroiditis

(Hashimoto’s thyroiditis)

    • Caused by cell-and Ab mediatd destruction of thyroid tissue
    • Both humoral and cellular factors contribute
    • Cytotxic T cells
    • Auto Abs.. TPO 95%, Tg 60%,

TSH-R bloking Ab 20%, TBII 10-20%

    • Two formsHashimoto’s(goitrous)thyroiditis

Atrophic thyroiditis

slide7
Hashimotos

(goitruos)thyroiditis

Marked lymph.infiltration

Atrophy of thyroid

follicles with absence of colloid

Mild to moderate fibrosis

Present with goiter

Minimal or no Sx

Atrophic thyroiditis

 fibrosis

Less lymph. infiltration

Thyroid follicles completely absent

Late stage of Hashimotos thyroiditis

Minimal residual thyroid tissue

Overt symptoms

risk factors
Risk factors
  • Genetic suseptibility
    • Polymorphism in: HLA DR3,-DR4,-DR5
    • CTLA-4(a T-cell regulating gene)
    •  in down’s S., Turners S.
  • Env. Factors
    • High iodine intake
    • infection:

congenital rubella s. - autoimmune H.

    • Cigarette smoking
iatrogenic causes
Iatrogenic causes
  • Thyroidectomy
    • 1-4wks after total thyroidectomy
    • In the 1st yr in the majority of subtotal t.

 If euthyroid at one year, 0.5-1% chance of hypothyroidism each year

  • Radioiodine(I-131)therapy
    • Months to yrs later
    • Dose dependant
  • External neck/Total body irradiations
  • Anti-thyroid drugs (over Rx of Hyperth.)
other causes
Other causes
  • Iodine deficiency
  • Iodine excess (the wolf-chaikoff effect)
  • Drugs – Ethanolamine, Lithium,

Amiodarone, INF-alpha, IL2

    • In Hypothyroid P’ts taking T4:

Chlestyramine,Iron salts - T4 absorption

Rifampin, Phenytoin,Carbamazepin- clearance

Amiodarone, glucocotricoids

- conversion of T4T3

other causes cont
Other causes cont…
  • Infiltrative diseases – rare
    • Fibrous thyroiditis(reidel’s th.),hemochromatosis,scleroderma,

leukemia,amyloidosis

    • Infections: Tbc., P.carini
  • Subacut thyroiditis

(De-quervain’s,granulomatous)

  • Silent(painless)thyroiditis –postpartum th.

ESR

-ve TPOAB

Normal ESR, +TPOAb

secondary tertiary hypothyroidism central
Secondary/tertiary Hypothyroidism(Central)
  • <1%
  • TSH or TRH
    • Dx – inappropriatly low(low or N. TSH)

low T4 and T3

  • Causes
    • Hypopituitarism(tumor,surgery irradiation,sheehan’s s.,hypophysitis)
    • Mutations in TSH/TSH-R gene
    • Hypothalamic Damage (tumor,trauma,radiation,inf. D.)
    • Mutations in TRH-R gene
    • Drugs – Dopamine, lithium
  • Dx - MRI
congenital hypothyroidism
Congenital hypothyroidism
  • 1:4000 newborns
    • Thyroid g. agenesis 80-85%
    • Inborn errors of thyroid H. synthesis

10-15%

    • TSH-R Ab mediated(Moinfant) 5%
    • Anti-thyroid (Moinfant)
  • Majority – appear normal at birth
    • <10% - prolonged jaundice,feeding problem,hypotonia,enlarged tongue,delayed bone maturation, unblical H., cong.Malf.
  • Permanent neurologeic D. – if Rx is delayed
neurologic manifestations
Neurologic manifestations
  • Mental state, poor concentration
  • Poor memory , emotional lability
  • Carpal tunnel S. (25-30%)
  • Cerebellar ataxia (10-30%)
  • Peripheral neuropathy
  • Proximal muscle weakness
  • Hashimoto’s encephalopathy
  • Myxedema coma
metabolic abnormalities
Metabolic Abnormalities
  • Hyponatremia
  • Hyperlipidemia (LDL, cholesterol)
  • Hyperuricemia (Gout)
  • serum creatinin
  • carotenemia
  •  drug clearance

drug toxicity

disorders that affect tsh
High TSH

1° hypothyroidism

Non-thyroidal illness(5%)

Drugs:

Dopamin antagonists,

Amiodarone, cholecystographic dyes

TSH-producing pit. Adenoma

Adrenal insufficiency

Thyroid homone

resistance S.

Low TSH

1° Hyperthyroidism

Incomplete recovery

from Hyperthyroidism

Non-thyroidal illness

(10%)

High HCG (early pregnancy, molar P.,

choriocarcinoma)

Central hypothyroidism

Drugs:

Dopamin,

Glucocorticoids

Somatostatin analogues

Phenytoin

disorders that affect TSH
other investigations
Other investigations
  • CBC, ESR
  • OFT, Electrolytes
  • Lipid profile
  • Uric acid
  • FNA
  • Central hypothyroidism
    • Imaging studies(sellar/supracellar)
    • Other hormonal profiles (pituitary)
treatment
Treatment
  • Most P’ts …. Require lifelong Rx
  • The Goals

Restoration of euthyroid State

Reversion of Sx &Sns

Reduction of gotre

  • Rx thyroid hormone replacement
    • Synthetic thyroxin(T4)
    • A pro-hormone, 80% absorbed
    • Active hormone production controlled

by the patient’s own physiologic Mech.

    • Long half-life(7days)
    • Once daily when steady state is reached
    • Should be taken in an empty stomach
replacement dose
Replacement dose
  • Adults <60 with out evidence of Heart D.
    • 1.6 mcg/kg/day (50-150)
  • Older p’ts , p’ts with CHD
    • 1/2-1/4 of the dose(25-50mcg)
  • P’t evaluation every 3-6wks
    • Measure T4(early phase), TSH
    • Dose adjustment by 12.5-25 ( or )
  • Once steady state is reached
    • Maintenance dose, yearly evaluation with TSH
additional adjustment
Additionaladjustment
  • dose: Pregnancy

Estrogen Rx

Nephrotic syndrom

coadministration of drugs

that clearance orabsorbtion

  • dose: elderly

marked w’t loss

androgen therapy

t3 t3 t4
?T3 ?T3+T4
  • Not recommended
    • Wide fluctuations of serum T3 conc.
    • Multiple daily doses
    • Serum T4 remains low
  • T3+T4 therapy
    • For some hypothyroid p’ts who remain symptomatic despite Rx + normal TSH
    • Meta-analysis of 11 trials  No benefit
central hypothyroidism
Central Hypothyroidism
  • Think of other hormonal deficiencies
    • T4 Rx to p’ts with untreard 2° adrenal

insuficiency acut adrenal crisis!

  • Glucocorticoid with T4 Rx if adr. Insuff.
  • Need less T4 than 1°hypothyroidism
  • Rx monitoring by- FT4 (TSH – no value)