13.1 - Thyroid Gland Dysfunction Flashcards
Basic anatomy of the thyroid
- 2 lobes joined by isthmus
- Bow tie shape
- Lies against and around front larynx and trachea
- Below thyroid cartilage and above cricoid cartilage
- Located near C7 of spine
Thyroid embryology
- First endocrine gland to develop
- At 3-4 weeks gestation, appears as an epithelial proliferation in base of tongue
- Takes several weeks to migrate to final position
- First descends as diverticulum through thyroglossal duct and migrates downwards
- During migration it remains connected to tongue by thyroglossal duct, which subsequently degenerates
- If migration doesn’t occur as normal, thyroid gland will be located in a different place
Normal stimulation of production of thyroid hormones (recap)
Low blood levels of thyroid hormone detected by hypothalamus → hypothalamus releases TRH into the hypophyseal portal system → stimulates anterior pituitary to produce more TSH → stimulates thyroid gland → more T3 + T4 produced
What is hypothyroidism and primary/secondary (brief)
- Endocrine condition where too little thyroid hormones are produced
- Two main causes of hypothyroidism: primary and secondary (in more detail on sep cards)
- primary is where the thyroid gland is the problem ☞ not making enough T3 + T4
- secondary aka central hypothyroidism where the body doesn’t produce enough TSH
- Both types result in decreased thyroid hormone and reduced BMR
Primary hypothyroidism (causes + features, symptoms on different card)
Thyroid gland problem, where it’s not making enough thyroid hormone. Increased TSH due to negative feedback. Causes include:
iodine deficiency as follicular cells don’t have enough iodine to produce T3 + T4. This is most common in countries that don’t fortify foods with iodine
hashimoto’s thyroiditis (autoimmune disorder) where T-cells and autoantibodies infiltrate the thyroid → thyroid responds to autoimmune damage by hypertrophy + hyperplasia (causes goitre) → this compensation is short lived → eventually autoantibodies cause so much follicular cell damage → destroy thyroid function altogether
treatment for hyperthyroidism ie surgery (removes thyroid tissue) or radioiodine therapy (damages too many follicular cells)
congenital hypothyroidism newborn’s thyroid gland not working properly (gland can be absent, underdeveloped, in wrong location or defective). Either sporadic (at random) or inherited gene cause.
Secondary hypothyroidism
aka ‘central hypothyroidism where body doesn’t produce enough TSH. Two main causes:
- Damage to hypothalamus ie from tumours or trauma, decreasing TRH production
- Tumor in anterior pituitary: compresses gland → prevents TRH production
Symptoms of hypothyroidism (congenital on different card)
- myxedema (swelling in soft tissues and skin, eg eyes and tongue). Due to increased TSH (due to negative feedback trying to stimulate the gland) → stimulates fibroblasts in skin and soft tissues → start depositing glycosaminoglycans in the interstitium
- goiter mainly in hashimoto’s thyroiditis (due to the initial hyperplasia + hypertrophy)
- weight gain despite decreased appetite (due to decreased BMR)
- sensitivity to cold as body is producing less heat
- bradycardia, mental slowness, constipation, lethargy due to decreased effects of thyroid hormone on sympathetic NS
- Other general symptoms: obesity, dry skin, alopecia, hoarse voice, constipation and slow reflexes
Symptoms of congenital hypothyroidism
mainly due to decreased BMR ie excessive sleeping, however if it goes on undetected long enough, can cause:
- Mental retardation
- Intellectual disabilities
- Delayed physical growth
- Shortened height
- Poor bone development
- Slow pulse
- Muscle weaknesses
- GI disturbances
= cretinism
How is diagnosis of hypothyroidism made (and how to differentiate between primary and secondary causes)
- Will have decreased T3 + T4
- Elevated TSH if primary
- Normal or decreased TSH if secondary
- In congenital hypothyroidism, screening programme in all newborns in NHS
What is the main treatment for hypothyroidism
Hormone replacement therapy using thyroid hormones (most commonly synthetic T4)
What is myxedema coma
- Severe and life-threatening hypothyroidism
- Complication in poorly managed cases of hypothyroidism who undergo stress, eg serious infection or surgery
- All normal symptoms of hypothyroidism are elevated eg:
☞ severe bradycardia
☞ altered consciousness
☞ confusion
☞ hypothermia
What is hyperthyroidism (in general, causes and symptoms on separate card)
- Condition where excess thyroid hormones
- Aka thyrotoxicosis
- Can happen in a few different ways (causes on separate card)
- All of causes result in too much thyroid hormone
- Leads to a hypermetabolic state
Causes of hyperthyroidism
graves disease in more detail on another card. Primary cause. Autoimmune disorder → B cells produce antibodies against thyroid proteins → autoantibodies can stimulate FSH → results in growth of thyroid gland + stimulates follicular cells to produce more thyroid hormones
toxic nodular goiter where one or more follicles start generating lots of THs. This could be due to a mutated TSH receptor that keeps the follicular cells inappropriately active. Primary cause
hyperfunctioning thyroid adenoma where follicular cells start proliferating. Forms a benign tumour and makes excess thyroid hormones. primary cause
inflammation or trauma to thyroid causes a large release of pre-formed thyroid hormones. Primary cause
Jod-Basedow syndrome ie iodine – induced thyrotoxicosis. Occurs after an iodine deficient person receives a large dose of iodine. primary cause
neonatal hyperthyroidism occurs in newborns who have mothers with Grave’s Disease → thyroid stimulating immunoglobulins crosses the placenta → received by baby → causes baby to generate too much THs. primary cause
pituitary tumor where a TSH secreting tumor in anterior pituitary → healthy thyroid starts generating too much thyroid hormone. secondary cause
General symptoms of hyperthyroidism
- weight loss despite decreased appetite due to increased BMR
- heat intolerance as body producing excess heat
- tachycardia, sweating, hyperactivity, anxiety, insomnia due to the effect of THs on sympathetic NS
-
exophthalmos ie eye bulging due to sympathetic over-stimulation of muscles controlling eye movement
☞ longer term risk of developing congestive heart failure and osteoporosis
Mechanism of Grave’s Disease
B cells produce antibodies against thyroid proteins → produces thyroid-stimulating immunoglobulin (TSI) → binds to TSH receptors on thyroid follicle cells, imitating TSH → greater production of T3 + T4
Additionally, TSI can also stimulate thyroid hypertrophy + hyperplasia → more follicular cells → goitre
