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Endocrinology > Thyroid Disorders > Flashcards

Thyroid Disorders Flashcards

1
Q

What is primary, secondary, tertiary hyperthyroidism?

A
  1. primary = thyroid problems
  2. secondary = pituitary problems but healthy thyroid. Overproduction of TH in response to a TSH-secreting tumour in anterior pituitary
  3. tertiary = hypothalamus problem
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2
Q

What causes primary hyperthyroidism?

A
  1. Graves Disease (most common
  2. Toxic multinodular goitre
  3. Toxic adenoma
  4. Damage/inflammation of thyroid
  5. Iodine-induced thyrotoxicosis/Jod-Basedow syndrome
  6. Neonatal hyperthyroidism
  7. Drug induced hyperthyroidism (Iodine, Amiodarone, Lithium, Radiocontrast agents)
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3
Q

Symptoms of hyperthyroidism (6), risks (for chronic) and complications associated

A
  1. Hyperphagia and Weight loss
  2. Heat intolerance
  3. Amenorrhoea, gynaecomastia (men) infertility, reduced libido
  4. Fatigue
  5. Tachycardia
  6. Goitre, Pretibial myxoedema, Ophthalmopathy in Graves
  7. Chronic = risk of congestive HF and osteoporosis
  8. Severe = thyroid storm
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4
Q

How do you diagnose hyperthyroidism?

A
  1. TFT
    - Low TSH, high T3, 4 = primary
    - High TSH, high T3, 4 = pituitary tumour
  2. Autoantibodies: TSHR-AB in graves
  3. Imaging: US or RAI + thyroid uptake scan
    - if malignancy suspected or aetiology uncertain
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5
Q

What is RAI uptake test? What does it show for: Graves disease, Thyroiditis, Nodule presence?

A

Once hyperthyroidism is confirmed, help determine the specific cause of the disorder.

  • This is used to test for iodine in blood absorbed thyroid gland
  • High uptake suggests Graves Disease
  • Low uptake indicates hyperthyroidism is caused by inflammation/destruction of TG (thyroiditis)
  • Uneven uptake indicates presence of nodule
  • NOTE: pt eating high iodine foods (diary, seafood) will impact results
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6
Q

Treatment and Management (5)

A
  1. Bb or CCB: treat adrenergic sx
  2. Thioamides/Anti-thyroid drug (ATD) e.g. carbimazole, methimazole, PTU
    - Pregnancy = PTU for 1st, methimazole for 2nd, 3rd trimester
    - ‘Block and Replace’ Regime: ATD + levothyroxine
    - Titration Regime: ATD adjusted to achieve euthyroid
  3. Radioiodine therapy
    - Partially or completely destroy thyroid function, followed by replacement hormone therapy.
    - 1st line for relapse graves
  4. Surgery of thyroid
    - if malignancy suspected, compressive goitre or RAI/ATD are unsuitable.
    - complications: hypocalcaemia, recurrent laryngeal n. injury.
  5. Steroids for Graves’ ophthalmopathy
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7
Q

What is Grave’s disease? and it’s RF?

A
  1. Autoimmune disorder that affects the TG to cause HYPERthyroidism. Commonest cause of primary hyperthyroidism
  2. RF = women, aged 30-50yrs, Fx, Hx of autoimmune disorders
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8
Q

Describe the pathophysiology of Graves and how it may cause ophthalmopathy

A
  1. B-cells produces thyroid-stimulating Ig that mimics TSH and binds to TG’s follicular cells as a result releases more T3 and T4
  2. This causes thyroid hypertrophy and hyperplasia
  3. Fibroblasts around the eyes and skin are also stimulated by antibodies and causes ophthalmopathy
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9
Q

Investigations for Graves (5)

A
  1. TFT: High T3 and T4, low TSH
  2. Thyroid stimulating receptor autoantibodies (TSHR-AB)
  3. RAI uptake scan: uptake will be high and diffuse in GD
  4. Ultrasound of neck
  5. Biopsy/aspirate if goiter is suspicious of malignancy.
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10
Q

What is primary hypothyroidism? And what causes it (6)?

A
  1. Iodine deficiency
    - Common in low income countries
  2. Hashimoto thyroiditis (most common)
  3. Amiodarone-induced hypothyroidism
  4. Postpartum thyroiditis (typically a transient change that occurs 6m after birth)
  5. Iatrogenic
    - surgery or radioiodine therapy
  6. Congenital defects
    - Absence or abnormality of TG
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11
Q

What is secondary hypothyroidism? And what causes it (5)?

A
  1. Tumour compressing hypothalamus or pituitary dec TRH or TSH production
  2. Radiation therapy to brain
  3. Sheehan syndrome
    - Loss of blood during childbirth, resulting in severe low BP and body deprived of oxygen.
    - Lack of oxygen causes damage to pituitary.
  4. Central congenital hypothyroidism - TRH resistance
  5. Lymphocytic hypophysitis
    - pituitary gland becomes infiltrated by lymphocytes, resulting in pituitary enlargement and impaired function
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12
Q

Signs and Symptoms of hypothyroidism (6).

A
  1. Dec appetite & weight gain
  2. Cold intolerance
  3. Slowing of ANS: dec sweating, bradycardia, mental slowness, lethargy, constipation
  4. Myxoedema
    - Puffy face, hands and feet
    - High TSH levels stimulate fibroblasts in skin and soft tissues
    - Fibroblasts start depositing ECM proteins in the interstitium
  5. Galactorrhea, menorrhea
    - elevated TRH causes elevated PL + TSH
  6. Dry coarse skin, thinning hair
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13
Q

What is Myxoedema Coma? Signs (4) + Mx?

A
  1. Rare but fatal outcome of hypothyroidism
  2. It is a medical emergency
  3. Usually occurs if hypothyroidism is poorly managed or individual undergoes stressful situation - serious infection or surgery.
  4. Sx of hypothyroidism becomes exaggerated
    - Bradycardia
    - Cognitive decline
    - Hypotensive
    - Hypothermic
  5. Mx = IV levothyroxine, correct electrolyte imbalances and hypothermia
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14
Q

Investigations for hypothyroidism (3)

A
  1. TFT
    - Primary (hasimoto) = Raised TSH, Low T3, T4
    - Secondary = Low/normal TSH, Low T3, T4
  2. TPOAbs
    - anti-TPO or anti-thyroglobulin found in 90-95% of patients
  3. Thyroid US U
    - If pt has an asymmetrical goitre to rule out neoplastic lesions
    - Assess thyroid size, if nodules are present
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15
Q

Treatment and Management of hypothyroidism (3)

A
  1. Endocrinology referral for following:
    - cardiac, endocrine conditions
    - Goitre, nodule changes (2ww if malignancy suspected)
    - After Tx adverse effects/not responding
    - Female planning pregnancy
    - Atypical TFTs
  2. Levothyroxine (T4) monotherapy
    - 1.6ug = <50yr no Hx of CVD
    - 25ug = >50yrs, CVD, severe hypothyroidism
    - Monitor TFT and adjust dose accordingly
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16
Q

What is Hashimoto’s Thyroiditis?

A
  1. AI destruction of thyroid gland causing progressive fibrosis.
  2. Thyroid hormones dec -> hypothalamus + pituitary respond to this by inc TRH + TSH
  3. Inc in TSH, leads to thyroid enlargement
    - Initially pts may show symptoms of hyperthyroidism
  4. This compensation is short-lived and eventually the autoantibodies cause so much follicular cell damage that they destroy thyroid function altogether.
  5. When enough destruction occurs, pts exhibit symptoms of hypothyroidism
17
Q

Signs and symptoms of Hashimoto’s Thyroiditis (7).

A
  1. Weight gain
  2. Dry, coarse skin and hair
  3. Fatigue, exertional dyspnea, and exercise intolerance
    - Due to limited pulmonary and cardiac reserve and increased muscle fatigue
  4. Slowing ANS
    - bradycardia, cold intolerance, dec sweating, memory loss, muscle cramps, joint pain, constipation
  5. Heavy period and galactorrhoea
  6. Goitre related Sx
    - voice hoarseness, difficulty swallowing
  7. Myxoedema (severe cases)
18
Q

Treatment and Management of Hashimoto’s Thyroiditis

A
  1. PO Levothyroxine titrated
    - Taken in the morning on an empty stomach for optimum absorption
    - Not be given with iron, Ca supps, PPI to avoid suboptimal absorption
    - <50years = 1.6ug/kg
    - >50years, CVD = 25ug/day. Revaluated in 6-8w
    - Pregnancy, short-bowel syndrome = Inc dose to maintain euthyroid state
  2. Surgical Removal
    - If goitre compressing on surrounding organs, suspected lymphoma
19
Q

Impact of thyroid disease on fetus and mother (untreated hypo and hyper [7,7] )

A

Untreated hypothyroidism

  1. Gestational hypertension and pre-eclampsia
  2. Placental abruption
  3. Post-partum haemorrhage
  4. Low birth weight
  5. Preterm delivery
  6. Neonatal goitre
  7. Neonatal respiratory distress

Untreated hyperthryoidism

  1. intrauterine growth restriction, IUGR
  2. Low birth weight
  3. Pre-eclampsia
  4. Preterm delivery
  5. Risk of stillbirth
  6. Risk of miscarriage
  7. Fetal malformation
20
Q

What drugs (5) can cause thyroid dysfunction

A
  1. Amiodarone
    - Causes Hypo and hyper.
    - HIGH iodine has a toxic effect on thyroid (Note: low levels of iodine is ok)
  2. Lithium
  3. Interferone
  4. Immune therapies
  5. Dopamine decreases TSH secretion
21
Q

What is thyrotoxicosis?

A
  1. Medical condition caused by an excessive amount of thyroid hormones in the bloodstream
  2. Hyperthyroidism is the main cause
22
Q

Why may TFT differ in pregnancy? What is appropriately low in the 1st trimester?

A
  1. Thyroid function is altered in pregnancy due to INC METABOLIC REQUIREMENTS.
  2. HCG is released in 1st trimester and stimulates TSH-receptor, which leads to a fall in TSH in the 1st trimester.
  3. Low TSH levels would be seen and this is appropiate
23
Q

What is Transient gestational thyrotoxicosis

A
  1. hCG mediated hyperthyroidism
  2. Elevated hCG levels in 1st Trimester and stimulates TSH-R.
  3. Leading to an increase in T4 and T3 levels. Their levels peak by week 16 and remain high until delivery.
24
Q

Why may you give 250mcg of iodine during pregnancy?

A
  1. There is an increase in iodine requirement during pregnancy due:
    - increase in maternal thyroid hormone production
    - increase in renal iodine clearance,
    - fetal iodine requirement
  2. Dietary iodine requirements are higher during pregnancy
  3. Maternal iodine deficiency has adverse effects on the fetus including poor neurological and cognitive development
25
Q

Both Graves and transient gestational thyrotoxicosis show dec TSH and inc T3, T4. How would you differentiate between these?

A
  1. Low TSH levels in transient gestational thyrotoxicosis is due to hCG mediated stimulation of TSH-R.
  2. Low TSH levels in Graves is due to Ig stimulation of TSH-R
  3. Serology test - looking at TSH receptor antibodies elevated in blood test can be used to differentiate between the two conditions.
26
Q

How would you treat hyper and hypothyroidism in pregnancy? And what is the goal of this treatment?

A

Hyper

  • Low dose of antithyroid drug
  • Goals is to maintain mild maternal hyperthyroidism while avoiding fetal hypothyroidism.

Hypo

  • Thyroid hormone replacement
  • Goal is to keep TSH level in trimester specific range
27
Q

Treatment and Management of Graves during pregnancy (3).

A
  1. ATD
    - 1st trimester = PTU
    - 2nd trimester = Methimazole used due to hepatotoxicity risk associated with PTU
  2. Bblocker
    - Short-term use for Sx control.
    - Avoid long-term due to the risk of intrauterine fetal growth retardation
  3. Thyroidectomy
    - Only reserved for patients who cannot tolerate ATDs due to severe SE or when euthyroidism cannot be achieved
  4. Radioactive iodine ablation is CI during pregnancy.
28
Q

What is thyroid storm/thyrotoxic crisis? Signs (6), Mx?

A
  • Medical emergency as a result of uncontrolled/untreated hyperthyroidism
  • Signs = hyperthermia, tachycardia, arrhythmia, N+V, seizure, cognitive decline
  • Mx: Bblockers, ATD, Steroids, Correct electrolyte imbalances, HF, hyperthemia, monitor BGL
  • Dialysis and plasma exchange may be required

Endocrinology (9 decks)

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