HYPOTHYROIDISM Flashcards
What is hypothyroidism?
Clinical syndrome resulting from a deficiency of thyroid hormone → to generalised slowing of metabolic process
Epidemiology of hypothyroidism
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
How is hypothyroidism classified?
Primary
Secondary
Tertiary
Peripheral resistance to action of thyroid hormone
Goitrous or non goitrous
Spontaneous and iatrogenic
What are primary causes of hypothyroidism?
- 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
What are causes of Transient hypothyroidism (temporary low thyroid hormone levels)?
- Sub acute lymphocytic thyroiditis
- Sub acute granulomatous thyroiditis
- Postpartum thyroiditis
- After 131I treatment or subtotal thyroidectomy for Graves’ disease
Secondary hypothyroidism can be due to what?
- Pituitary disease e.g hypopitutarism
- Pituitary resistance syndromes-rare
Tertiary hypothyroidism can be due to what?
Hypothalamic disease
What is CHRONIC AUTOIMMUNE THYROIDITIS? How common is it and amongst which people? What are the stages? What causes it?
- 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
Generalized thyroid hormone resistance (rare disorder)
- 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
Progression of Hashimoto’s thyroiditis?
Marked lymphocytic infiltration CD4+, CD8+ & B cells of thyroid gland
Atrophic:
More fibrosis, less lymphocytic infiltration
Represents end stage of Hashimoto thyroiditis
Clinical features of hypothyroidism in adults
Symptoms in adults often non-specific:
Fatigue
cold intolerance
weight gain
constipation
myalgia (muscle pain)
menstrual irregularities
Slow movement and speech
Clinical features of hypothyroidism in older children
- Short stature due to linear growth retardation
- Retarded secondary sexual characteristics
- Delayed onset of puberty
- Poor school performance
- Bradycardia
- 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
- Overt muscle weakness
- Entrapment neuropathy of median nerve producing paresthesia & weakness of hands
- Obstructive sleep apnea
- Cardiomegaly: dilation of the heart; pericardial effusion
- Neuropsychiatric manifestations
- A dynamic ileus leading to mega colon & functional intestinal obstruction delayed relaxation of deep tendon reflexes
Investigation of hypothyroidism by measuring TSH, T3 and T4
- 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
Investigations; testing for conditions associated with hyperthyroidism
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
Treatment if hypothyroidism
- 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
Therapeutic goal of treatment and processes to undergo
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
INTERFERENCE WITH THYROXINE METAB
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
Complications
Myxedema coma
Ischaemic heart disease
Dyslipidemia
Poor obstetric history
