HYPOTHYROIDISM Flashcards

1
Q

What is hypothyroidism?

A

Clinical syndrome resulting from a deficiency of thyroid hormone → to generalised slowing of metabolic process

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2
Q

Epidemiology of hypothyroidism

A

13.6% in women & 5.7% in men > 60 yrs in Framingham study

Half as common in African-Americans compared to Caucasians

Prevalence in Nigeria-not known

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3
Q

How is hypothyroidism classified?

A

Primary
Secondary
Tertiary
Peripheral resistance to action of thyroid hormone
Goitrous or non goitrous
Spontaneous and iatrogenic

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3
Q

What are primary causes of hypothyroidism?

A
  • Chronic autoimmune thyroiditis
  • Iodine deficiency – endemic goitre
  • Post ablative
  • Drugs blocking synthesis: Thionamides, lithium, iodides
  • Goitrogens in food stuffs
    *Infiltrative diseases; Sarcoidosis, haemochromatosis, amyloidosis,
  • Congenital thyroid agenesis, dysgenesis or biosynthetic defects
  • Transient Post-thyroiditis
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4
Q

What are causes of Transient hypothyroidism (temporary low thyroid hormone levels)?

A
  • Sub acute lymphocytic thyroiditis
  • Sub acute granulomatous thyroiditis
  • Postpartum thyroiditis
  • After 131I treatment or subtotal thyroidectomy for Graves’ disease
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5
Q

Secondary hypothyroidism can be due to what?

A
  • Pituitary disease e.g hypopitutarism
  • Pituitary resistance syndromes-rare
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6
Q

Tertiary hypothyroidism can be due to what?

A

Hypothalamic disease

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6
Q

What is CHRONIC AUTOIMMUNE THYROIDITIS? How common is it and amongst which people? What are the stages? What causes it?

A
  • Commonest cause of hypothyroidism in iodine-sufficient areas of the world
  • Commoner in older women
  • cellular & antibody-mediated destruction of thyroid tissue

Stages:
1. Goitrous
2. Atrophic

differ in extent of lymphocytic infiltration, fibrosis, & follicular cell hyperplasia of thyroid, but not in pathophysiology

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6
Q

Generalized thyroid hormone resistance (rare disorder)

A
  • autosomal recessive trait
  • mutations in the gene for the T3 nuclear receptor
  • results in a decreased affinity for T3
  • can also inhibit action of normal receptors
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7
Q

Progression of Hashimoto’s thyroiditis?

A

Marked lymphocytic infiltration CD4+, CD8+ & B cells of thyroid gland

Atrophic:
More fibrosis, less lymphocytic infiltration
Represents end stage of Hashimoto thyroiditis

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8
Q

Clinical features of hypothyroidism in adults

A

Symptoms in adults often non-specific:
Fatigue
cold intolerance
weight gain
constipation
myalgia (muscle pain)
menstrual irregularities
Slow movement and speech

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9
Q

Clinical features of hypothyroidism in older children

A
  1. Short stature due to linear growth retardation
  2. Retarded secondary sexual characteristics
  3. Delayed onset of puberty
  4. Poor school performance
  5. Bradycardia
  6. Coarse hair and skin, puffy facies, loss of eyebrows, enlargement of the tongue, voice hoarseness due to accumulation of matrix substances e.g glycosaminoglycans in interstitial space of tissues
  7. Overt muscle weakness
  8. Entrapment neuropathy of median nerve producing paresthesia & weakness of hands
  9. Obstructive sleep apnea
  10. Cardiomegaly: dilation of the heart; pericardial effusion
  11. Neuropsychiatric manifestations
  12. A dynamic ileus leading to mega colon & functional intestinal obstruction delayed relaxation of deep tendon reflexes
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10
Q

Investigation of hypothyroidism by measuring TSH, T3 and T4

A
  • Primary hypothyroidsm – low or normal serum T4 with elevated TSH
  • Secondary hypothyroidsm – low serum T4 + low or inappropriately normal TSH
  • Subclinical hypothyroidsm – normal serum T4 & elevated serum TSH (no symptoms or signs usually)
    T3 levels may remain normal because increased TSH levels may increase relative secretion of T3
  • Raised TSH, normal free T4 or T3
    Recovery phase of non thyroidal illness
    Intermittent thyroxine therapy in hypothyroidism
    Interfering antibodies
    Drugs-cholestyramine, sertraline
  • Congenital
    TSH receptor defects
    TSH resistance syndromes
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10
Q

Investigations; testing for conditions associated with hyperthyroidism

A

Hyperlipidaemia – occurs with increased frequency in hypothyroidism

Hyponatraemia – often resulting from inappropriate ADH secretion
Elevated muscle enzymes (CPK, AST. LDH)

Anaemia normochronic, normocytic

E.C.G. changes- bradycardia, low amplitude QRS complexes, evidence of ischaemic heart disease

Thyroid autoantibodies (antithyroglobulin antibody, thyroid peroxidase antibody)

Imaging studies of sellar and suprasellar region

Evaluate for other hormone deficiencies

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11
Q

Treatment if hypothyroidism

A
  • If no residual thyroid function, daily replacement of levothyroxine @~1.6µg/kg
  • Elderly (> 50-60) years & no evidence of heart disease, stat 50 µg daily
  • Those who have history of CHD initiate at 25 µg /day, dose can be increased by 25 mcg/day every 3 to 6 wks until replacement is complete
  • Gradual increase, as rapid increase in dose may tax coronary or cardiac reserve
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11
Q

Therapeutic goal of treatment and processes to undergo

A

Therapeutic goal: alleviation of clinical syndrome & normalization of TSH in primary hypothyroidism

After initiation of T4 therapy, reevaluate

Serum T4 & TSH measured in 3 to 6 wks (depending upon patient’s symptoms) & dose adjusted accordingly

process of increasing dose of T4 should continue, based upon periodic measurements of serum TSH (& free T4 if therapeutic goals have not been achieved)

Once desired T4 dose is established, annual evaluation
Changing requirements
Altered absorption
Compliance issues

Monitor for signs of overtreatment
Life long therapy in majority

Surgical therapy for huge goiters with compressive symptoms

Subclinical hypothyroidism: Treat if there is goitre, suggestive symptoms, low T3, drugs which may potentiate, uncertain follow up, cholesterol

12
Q

INTERFERENCE WITH THYROXINE METAB

A

decrease T4 absorption
cholestyramine, iron salts, AL(OH)2

increase clearance
phenytoin, carbamazepine, Rifampicin

Inhibition of thyroid hormone synthesis/and or release
amiodarone

Pregnancy
estrogen-induced rise in serum TBG; increased T4 clearance & transfer of T4 to the fetus contribute to need for more T4

13
Q

Complications

A

Myxedema coma
Ischaemic heart disease
Dyslipidemia
Poor obstetric history