THYROID DISEASE
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Transcript of THYROID DISEASE
THYROID DISEASEBy: Dr Ismah
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Contents
1. Physiology and development
2. Epidemiology
3. Hyperthyroidism
4. Hypothyroidism
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1. Physiology and development
Thyroid glands descend to ant lower neck by the end of 1st trimester
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Hypothalamic-pituitary-thyroid axis becomes functional in 2nd trimester
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Peripheral metabolism of thyroid hormones matures in 3rd trimester
T3, T4, TSH do not cross placenta in significant amount
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Functions of thyroid hormones
Target tissue Mechanism
Nervous system Promote normal brain development
Heart • Increase number, affinity of beta adrenergic receptors• Enhance responses to circulating catecholamine
Muscle Increase protein breakdown
Bone Promote normal growth and skeletal development
Gut Associated with carbohydrate absorption
Adipose tissue Stimulate lipolysis
Lipoprotein Stimulate formation of LDL receptors
Other • Stimulate oxygen consumption by metabolically active tissues
• Increase metabolic rates• Promote development of reproductive system • Maturation of fetal lungs
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Normal level of thyroid hormones
Age TSH (mIU/L) Free T4 (pmol/L)
Birth-D3 OL <21 26-65
D4-D30 0.51-10.8 12-30
D31-1yr 0.39-7 9-16.1
≥ 1 yr 0.4-6 13.2-22.2
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2. Epidemiology
Hypothyroidism:
Incidence of congenital hypothyroidism worldwide is 1:2500 - 4000 live births
In Malaysia, it is reported as 1:3666
It is the commonest preventable cause of mental retardation in children
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Hyperthyroidism:
Study in US (2008) concluded that the incidence among individuals aged 0-11 years was 0.44 cases per 1000 population
The incidence among individuals aged 12-17 years was 0.59 cases per 1000 population.
Thus, the incidence increases throughout childhood, with a peak incidence in children aged 10-15 years
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3. Hypothyroidism
Decreased free T4, increased TSH
Primary, secondary or tertiary
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A. Congenital hypothyroidism
Causes
Maldescent thyroid, athyrosis
Dyshormonogenesis
Iodine deficiency
TSH deficiency
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Clinical features
FTT
Feeding problem
Prolonged jaundice
Constipation
Pale, cold, mottled skin
Quiet baby
Coarse face
Large tongue
Hoarse cry
Goiter
Umbilical hernia
Delayed development
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MOSTLY , ASYMPTOMATIC AT BIRTH
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CORD TSH
Treatment
Timing Should begin immediately after diagnosis is
established
If features of hypothyroidism are present, treatment is started urgently.
Duration Treatment is life long
Except in children suspected of having transient hypothyroidism where re-evaluation is done at 3 years of age.
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Preparation
L-thyroxine tablets
The L-thyroxine tablet should be crushed, mixed with breast milk, formula, or water and fed to the infant.
Tablets should not be mixed with soy formulas or any preparation containing iron (formulas or vitamins), both of which reduce the absorption of T4.
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19Pediatric Protocol 3rd ed
Goal of therapy
To restore the euthyroid state
Serum FT4 level usually normalise within 1-2 weeks, and then TSH usually become normal after 1 month of treatment.
Some infants continue to have high serum TSH concentration (10 - 20 mU/L) despite normal serum FT4 values due to resetting of the pituitary-thyroid feedback threshold.
Compliance to medication has to be reassessed and emphasised.
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21Pediatric Protocol 3rd ed
Follow up
Monitor growth parameters and developmental assessment.
Imaging studies
If the FT4 is low and the TSH value is elevated, permanent hypothyroidism is confirmed and life-long L-thyroxine therapy is needed.
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Measurement schedule (FT4, TSH)
The recommended by American Academy of Pediatrics
At 2 and 4 weeks after initiation of T4 treatment.
Every 1 to 2 months during the first 6 months of life.
Every 3 to 4 months between 6 months and 3 years of age.
Every 6 to 12 months thereafter until growth is completed.
After 4 weeks if medication is adjusted.
At more frequent interval when compliance is questioned or abnormal values are obtained.
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Re-evaluation of patients likely having transient hypothyroidism
Can be due to factors primarily affecting the thyroid-like iodine deficiency or excess, maternal TSHR antibodies, maternal use of anti thyroid drugs
This is best done at age 3 years when thyroid dependent brain growth is completed at this age.
Stop L-thyroxine for 4 weeks then repeat thyroid function test: FT4, TSH.
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B. Acquired hypothyroidism
The commonest cause autoimmune thyroiditis i.e. Hashimoto thyroiditis
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Clinical features
Short stature
Cold intolerance
Dry skin
Cold peripheries
Bradycardia
Thin, dry hair
Goiter
Slow relaxing reflexes
Constipation
Delayed puberty
Obesity
Slipped upper femoral epiphysis
Learning difficulties
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Hashimoto thyroiditis
In older children, adolescence
+ve family h/o thyroid disease in 25-35% of patient
Autoimmune process targeted the thyroid gland thus resulting in fibrosis and atrophy of thyroid glands
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Firm, non tender, diffuse goiter
Onset after 6 years old
Associated with DM type 1, adrenal insufficiency and hypoparathyroidism, down syndrome, turner syndrome
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Diagnosis
Clinically
Confirmed by serum antithyroid peroxidase and antithyroid globulin antibodies
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Treatment
L thyroxine
Monitor TSH, FT4 6-12 monthly
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4. Hyperthyroidism
Increased T4, T3 & decreased TSH
Clinical features
Systemic
Anxiety
Restlessness
Sweating
Diarrhea
Weight loss
Rapid growth in ht
Tremor
Tachycardia
Warm peripheries
Learning difficulty
Behavior problems
Psychosis
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Eye signs (not common in children)
Exophthalmos
Ophthalmoplegia
Lid retraction
Lid lag
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Lid retraction
Exophthalmos
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Opthalmoplegia
Lid lag means delay in moving the eyelid as the eye moves downwards
A. Graves’ disease
Autonomous functioning of thyroid caused by thyroid stimulating immunoglobulins (TSIs)
Increased thyroid hormones production and peripheral conversion
Firm, diffuse goiter
Common in girls, in adolescence
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TREATMENT
1.
Drugs
2.
Surgery
3.
Radioactive iodine
Drugs
Block thyroid hormones synthesis
Carbimazole
PTU
- Side effect: rash, fever, arthralgia, agranulocytosis, liver damage, lupus like syndrome
Beta blockers e.g. propranolol
- To control cardiac manifestation
- Contraindicated in asthmatic pt
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Surgery
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Thyroidectomy
Indications:
- Failed medical treatment
- Large goiters, especially with pressure effects
- Severe progressive ophthalmopathy
B. Thyroid storm
Medical emergency. The mortality is 20 - 30 %.
Exacerbation of the hyperthyroid state with evidence of decompensation in one or more organ systems
Precipitated by stress including concurrent infections, surgery
Clinical diagnosis with features of severe thyrotoxicosis, hyperpyrexia and neuro-psychiatric manifestations such as delirium
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Management
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Rehydration
Treat hyperpyrexia (use fans, tepid sponging and oral paracetamol)
Do NOT use aspirin or NSAIDs
Beta sympathetic blocking agentsOral propanolol 40 mg qid, or I/V 1-2 mg 4-6hourly
Iodide
Oral saturated solution of potassium iodide (SSKI) 5 drops 6-hourly
or I/V Sodium Iodide 500 mg 8 hourly
or oral Lugol's iodine 5-10 drops, 6-hourly
Antithyroid Drugs
Carbimazole 15-20 mg 6-hourly
or propylthiouracil 150-200 mg 6-hourly
Corticosteroids
I/V dexamethasone 2 mg 6-hourly
or I/V hydrocortisone 200 mg 6-hourly
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C. Other causes (rare)
McCune-Albright syndrome
Thyroid neoplasm
TSH hypersecretion
Subacute thyroiditis
Excessive iodine or thyroid hormone ingestion
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D. Neonatal hyperthyroidism
Associated with infant of mother with Graves’ disease
Transient placenta transfers of thyroid stimulating immunoglobulins (TSIs)
Potentially fatal
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Clinical features
Irritability
Tachycardia
Polycythemia
Craniosynthesis
Poor feeding
FTT
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Treatment
Minimally affected: observation
Severe:
Oral propranolol
PTU
Spontaneous resolution because of TSIs usually in 2-3 months of age
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Take home message
Important to understood the physiology of thyroid hormone
Congenital hypothyroidism – screening, treat to prevent MR
Patient education and compliance to treatment/follow up
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50American Association of Clinical Endocrinologists (AACE)
References:
1. Nelson Essential of Pediatrics 6th ed
2. Illustrated Textbook of Pediatrics 3rd ed
3. Pediatric Protocol 3rd ed
4. Practice Guidelines for Thyroid Disorders The Malaysian Consensus 2000
Thank You
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