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Yr3 Medicine- Endocrinology > Thyroid > Flashcards

Thyroid Flashcards

1
Q

Explain the difference between hyperthyroidism and thyrotoxicosis

A
  • Hyperthyroidism: overproduction of thyroid hormones by thyroid gland
  • Thyrotoxicosis: excessive quantity of thyroid hormone in the body
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2
Q

Explain the difference between primary and secondary hyperthyroidism

A
  • Primary: due to thyroid pathology
  • Secondary: thyroid is producing excess thyroid hormones as it is being overstimulated by TSH; the pathology is in the hypothalamus or pituitary
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3
Q

Remind yourself of the structure and location of thyroid gland

A
  • Two lobes joined by isthmus
  • Lies in fro of the lower larynx and upper trachea below thyroid cartialge (Adam’s apple). Isthmus extends from 2nd to 3rd rings of trachea
  • Spans between C5 and T1
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4
Q

State some potential causes of hyperthyroidism

A
  • Grave’s disease
  • Toxic multinodular goitre
  • Solitary toxic thyroid nodule
  • Thyroiditis e.g. De Quervain’s, Hashimotos, post-partum, drug induced thyroiditis
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5
Q

What is the most common cause of hyperthyroidism?

A

Grave’s disease

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6
Q

Discuss the pathophysiology of Grave’s disease

A
  • Autoimmune condition where body produces TSH receptor antibodies
  • These antibodies mimic TSH and stimulate TSH receptors on the thyroid (and other places such as periorbital fat)
  • This causes thyroid gland to enlarge and to produce more thyroid hormones
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7
Q

State some risk factors for developing Grave’s disease

A
  • Family history autoimmune thyroid disease
  • Female sex
  • Tobacco use
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8
Q

What conditions are associated with Grave’s disease?

A
  • T1DM
  • Addison’s disease
  • Myasthenia gravis
  • Coeliac disease
  • Pernicious anaemia
  • Vitiligo
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9
Q

Toxic multinodular goitre is also known as..?

Discuss the pathophysiology of toxic multinodular goitre

A
  • Also known as Plummer’s disease
  • Nodules develop on thyroid and act independently of the normal feedback system; hence, they continuoulsy produce excessive thyroid hormone
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10
Q

Discuss the pathophysiology of solitary toxic thyroid nodules

A
  • There is a single, abnormal thyroid nodule acting alone to release thyroid hormone (indepent of the negative feedback sysytem)
  • Nodules are usually benign adenomas
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11
Q

Discuss the pathophysiology of De Quervain’s thyroiditis

A
  • Pt presetns with a viral infection with fever, neck pain & tenderness, dysphagia and features of hyperthyroidism
  • Acute inflammation of thyroid gland which causes an initial hyperthyroid phase
  • As TSH levels fall, due to negative feedback, a hypothyroid phase follows
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12
Q

State some symptoms of hyperthyroidism/thyrotoxicosis

A
  • Irritability
  • Anxiety
  • Sweating
  • Heat intolerances
  • Frequent loose stools
  • Sexual dysfunction
  • Weight loss
  • Palpitations
  • Tremor
  • Oligomenorrhea
  • Fatigue
  • Thirst & polydipsia
  • Dyspnoea
  • Pruritis
  • Infertility
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13
Q

Briefly outline why a pt gets most of the symptoms of hyperthyroidism

A

Thought that thyroid hormones, when in excess, overstimulate metabolism and exacerbate effects of sympathetic nervous system

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14
Q

State what you might find on clinical examination of a pt with hyperthyroidism WHO DOESN’T HAVE GRAVE’s

A
  • Onycholysis
  • Warm moist skin
  • Palmar erythema
  • Tachycardia (pule may also be irregular)
  • Thin hair
  • Lid lag
  • Lid retraction
  • Hyperkinesia
  • Hyperreflexia
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15
Q

Lid lag (also known as V_on Graefe’s sign_) is seen in hyperthyroidism; why is it thought that a pt has lid lag?

A

Thought that it is due to increased sympathetic activity seen in hyperthyroidism

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16
Q

State some signs & symptoms which are specific to Grave’s disease

A
  • Diffuse goitre (without nodules)
  • Graves Eye disease
    • Lid retraction
    • Chemosis
    • Corneal ulceration
    • Los of colour vision
    • Bilateral exomphalmos
    • Opthalmoplegia
  • Pretibial myxoedema
  • Thyroid acropachy
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17
Q

What is meant by Grave’s eye disease?

A

Pts with hyperthyroidism can have ‘eye signs’ such as lid retraction and lid lag. If pt has other eye signs such as exomphalamos, chemosis or optic neuropathy then it is indicative of Grave’s disease

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18
Q

Discuss why pts with Grave’s disease get Grave’s eye disease

A
  • TSH receptors are expressed on the fibroblasts of retro-orbital and dermal tissues
  • TSH autoantibodies bind and stimulate fibroblasts to secrete GAGs (which increases interstitual fluid content), differentiate into adipocytes
  • Increased interstitital fluid content along with infiltaration of inflammatory cells causes swelling of orbital tissues
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19
Q

Explain why pretibial myxoedema occurs in Grave’s disease

A
  • TSH receptors found on fibroblasts in dermis
  • TSH autoantibodies bind to TSH recpetors and cause fibroblasts to secrete GAGs and differentiate into adiposcytes
  • Get mucin deposition
  • Gives discoloured, waxy, oedematous appearance to skin in pre-tibial area
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20
Q

What is thyroid acropachy?

A

Triad of:

  • Clubbing
  • Soft tissue swelling
  • Periosteal reaction (only seen on imaging. Periosteal reaction= formation of new bone in response to injury or other stimuli of the perisoteum)
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21
Q

What investigations would you do if you suspect a pt has hyperthyroidism, include:

  • Bedside
  • Bloods
  • Imaging

*Where appropriate, justify why

A

Bedside​

No specific ones to do to help diagnose hyperthyroidisms

Bloods

  • FBC: may be mild normocytic anaemia, mild neutropenia in Grave’s
  • U&E
  • LFTs
  • TFTs: T3, T4, TSH, thyroid binding globulin
  • Thyroid autoantibodies
  • CRP: check for inflammation
  • ESR: check for inflammation- raised in De Quervain’s thyroiditis

Imaging

  • Thyroid ultrasound: look for nodules
  • Isotope scan/scintiscanning (using radioactive iodine or Technetium 99): look for uptake- uptake high or low? Is uptake diffuse or nodular?
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22
Q

What thyroid autoantibodies can you test for?

Discuss how common it is for each antibody to be present in:

  • Grave’s disease
  • Hashimoto’s disease
A
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23
Q

Hyperthyroidism is managed differently dependent on the cause; discuss the management of hyperthyroidism caused by:

  • Solitary toxic thyroid nodule
  • Toxic multinodular goitre
  • De Quervain’s thyroiditis
    *
A

Solitary toxic thyroid nodule

  • Surgical removal of nodule

Toxic multinodular goitre

  • If goitre is obstructing breathing or swallowing do complete thyroidectomy. Pt would need levothyroxine for life.
  • If goitre not obstructing breathing or swallowing manage:
    • Radioactive iodine if not pregnant or breast feeding
    • Anti-thyroid drugs (thionamides) e.g. carbimazole or propylthiouracil if not pregnant or breast feeding
    • Beta blockers e.g. propanolol to treat sympathetic symptoms

De Quervain’s thyroiditis

  • Self limiting condition manged with supporitve treatment:
    • NSAIDs for pain & inflammation
    • Beta blockers e.g. propanolol to treat sympathetic symptoms
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24
Q

Hyperthyroidism is managed differently dependent on the cause; discuss the management of hyperthyroidism caused by:

  • Grave’s disease
A
  • Antithyroid drugs (thionamides)
    • First line= carbimazole
    • Second line= propylthiouracil
  • Radioactive iodine
  • Surgery
  • Beta blockers (e.g. propanolol for relief of sympathetic symptoms)
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25
Q

For the anti-thyroid drug carbimazole:

  • Describe the mechanism of action
  • State how long it usually takes for thyroid function to return to normal
  • Options/different aims of maintenance carbimazole
  • State how long it usually takes for complete remission to occur- in which pt can stop taking carbimazole
A
  • Carbimazole is a pro-drug which is converted into methimazole which prevents thyroid peroxidase from coupling and iodinating tyrosine residues
  • Thyroid function return to normal in 4-8 weeks
  • Once pt has normal thyroid levels they continue on maintenace carbimazole and either:
    • Dose is titrated to maintain normal levels (titration block)
    • Dose is sufficient to block all productionof thyroid hormones and pt takes levothyroxine to replace (block and replace)
  • Complete remission, and ability to stop taking carbimazole, usually achieved within 18 months
26
Q

For the antithyroid drug propylthiouracil:

  • Describe the mechanism of action
  • Explain why it is second line
A
  • Similar to carbimazole, inhibits actions of thyroid peroxidase
  • Second line due to ADRs such as: samll risk of severe hepatic reactions (including death)
27
Q

Discuss the use of radioactive iodine as at treatment for hyperthyroidism, include:

  • How it works
  • How long it takes for remission to occur
  • Potential consequences
  • Rules/criteria for use of radioactive iodine
A
  • Drink single dose of radioactive iodine; this is taken up by thyroid gland and the emitted radiation destroys portion of thyroid cells. Reduction in functioning cells results in decrease in thyroid function and thus remission from hyperthyroidism
  • Remission ~ 6months
  • Pt may end up hypothyroid afterwards and need levothyroxine
  • Rules/criteria:
    • Must not be pregnant and are not allowed to get pregnant within next 6 months
    • Must avoid close contact with children and pregnant women for 3 weeks (depending on dose)
    • Limit contact with anyone for several days after receiving dose
28
Q

If you do a complete thyroidectomy what will the pt require for life?

A

Levothyroxine

29
Q

State some potential complications of hyperthyroidism

A
  • Mass effect (if goitre)
  • Atrial fibrillation
  • Surgery related recurrent laryngeal nerve damage
  • Surgery related hypopararthyroidism
  • Bone mineral loss leading to osteoporosis (if hyperthyroidism been going on long time)

Grave’s specific

  • Congestive high output cardiac failure
  • Sight threatening complications of Grave’s opthalmology
30
Q

What is a hyperthyroid crisis/thyrotoxic storm?

A
  • Rare but life-threatening exacerbation of the manifestations of thyrotoxicosis
31
Q

State the signs & symptoms of a hyperthyroid crisis/thyrotoxic storm?

A
  • Altered mental status/confused
  • Agitation
  • Fever
  • Tachycardia
  • Tachyarrhythmias e.g. AF
  • Vomitting, jaundice, diarrhoea
  • Severe clincial signs of hyperthyroidism
  • Multisystem decompensation: cardiac failure, resp distress, congestive hepatomegaly, dehyddration, renal failure
32
Q

State some potential precipitants of a thyroid storm/hyperthyroid crisis

A
  • Recent thyroid surgery
  • Recent radioiodine
  • Infection
  • MI
  • Trauma
33
Q

Discuss the management of a thyrotoxic storm/hyperthyroid crisis

A
  • Supportive
    • Fluids if dehydrated
    • NG tube if vomitting
    • Sedate if necessary
  • Beta blockers to manage tachycardia, tremors and other adrenergic symptoms
  • Antiarrhythmic drugs e.g. digoxin
  • Antithyroid drugs e.g. carbimazole in large doses
  • High doses of glucocorticoids to block T4 to T3 conversion
  • Potassium iodide/Lugols’ solution to block thyroids uptake of iodine
  • Treat any suspected infection with broad spectrum antibiotics
34
Q

What is hypothyroidism?

A

Inadequete production of thyroid hormones from the thyroid gland

35
Q

What is the most common cause of hypothyroidism in the developed world?

What is the most common cause of hypothyroidism in the developing world?

A
  • Developed world: Hashimoto’s
  • Developing world: iodine deficiency
36
Q

Explain the difference between primary hypothyroidism and secondary hypothyroidism

A
  • Primary: pathology with thyroid
  • Secondary: pathology with pituitary or hypothalamus
37
Q

State some risk factors for developing hypothyroidism

A
  • Family history autoimmune thyroid disease
  • Other autoimmune disorders
  • Female
  • Radiotherapy
  • Amiodarone & lithium use
  • Post partum (leading to post-partum thyroiditis)
38
Q

State some potential causes of hypothyroidism

A
  • Hashimoto’s thyroiditis
  • Primary atrophic hypothyroidism
  • Iodine deficiency
  • Secondary to treatment of hyperthyroidism
  • Secondary to medications such as lithium and amiodarone
  • Central/secondary causes e.g. tumours, infection, vascular (e.g. Sheehan syndrome), radiation
  • Subacute thyroiditis (temporary hypothyroid phase following hyperthyroid phase)
39
Q

Lithium and amiodarone can cause hypothyroidism; which drug can cause thyrotoxicosis aswell as hypothyroidism?

A

Amiodarone; it usaully causes hypothyroidism but it can also cause thyrotoxicosis

40
Q

Discuss the pathophysiology of primary atrophic hypothyroidism

A
  • Diffuse lymphocyte infiltration of thyroid leading to atrophy (hence these pts have no goitre)
41
Q

Discuss the pathophysiology of Hashimoto’s thyroiditis

A

Autoimmune condition in which body produces anti-thyroid peroxidase (anti-TPO antibodies) and antithyroglobulin antibodies. Initially causes goitre after which there is atrophy of gland.

42
Q

State some symptoms of hypothyroidism

A
  • Fatigue
  • Weight gain
  • Dry skin
  • Coarse hair and hair loss
  • Fluid retention (oedema, pleural effusion, ascites)
  • Heavy or irregular periods
  • Constipation
  • Cold intolerance
  • Slowing of intellectual & motor activities
  • Decreased visual acuity
  • Hoarse voice
  • Cramps
  • Weakness
43
Q

State what you might find on clinical examination of someone with hypothyroidism

A
  • General: Deep hoarse voice, mental and physical sluggishness, dry skin
  • Face: Puffy eyes, thinning of scalp hair, tongue swelling, xanthelasma, peaches & cream complexion
  • Thyroid: +/- Goitre
  • Cardiovascular: Hypertension, bradycardia, small volume pulse, pleural effusion
  • Neurological: proximal muscle weakness, hyporeflexia (slow tendon reflex), carpal tunnel syndrome (bilateral)
44
Q

Disucss what investigations you would do if you suspect a pt has hypothyroidism, include:

  • Bedside
  • Bloods
  • Imaging

*Justify each where appropriate

A

Bedside

No specific ones

Bloods

  • FBCs
  • U&Es
  • LFTs
  • TFTs: T3, T4, TSH, thyroxine binding globulin
  • Serum cholesterol: often elevated and often improves as hypothyroidism is treated
  • Blood glucose: primary hypothyroidism associated with T1DM
  • Autoantibodies: antithyroid peroxidisase, anti-thyroglobulin, TSH antibodies

Imaging

No specific imaging indicated

45
Q

Discuss the treatment of hypothyroidism

A
  • Replacement of thyroid hormones with oral levothyroxine (a synthetic T4 which is metabolised to T3 in body)
  • Dose is titrated until TSH levels are normal
  • Monitor TSH levels monthly until stable then can monitor less frequently

NOTE: if TSH level too high, means dose is too low. If TSH level too low, means dose is too high

46
Q

State some potential complications of hypothyroidism

A
  • Angina
  • Resistance hypothyroidism
  • Atrial fibrillation
  • Osteoporosis
  • Myxoedema crisis (coma)
  • Complications in pregnancy
47
Q

If you are concerned about posible thyroid disease you can use TSH alone as a screening test; true or false?

A

True; then if TSH is abnormal you can measure T3 and T4 for more informatino

48
Q

Discuss what you expect the TSH, T3&T4 levels to be in hypothyroidism and hyperthyroidism

*Think of any exceptions to generic rules

A

Hypothyroidism

  • TSH= high, T3 & T4= low
  • Unless it is a pituitary or hypothalamic cause of hypothyroidism (secondary hypothyroidism) in which case TSH will be low

Hyperthyroidism

  • TSH= low, T3 & T4= high
  • Unless it is a pituitary adenoma that secretes TSH in which case TSH will be high
49
Q

For each of the thyroid antibodies, state which diseases they are present in:

  • Anti-thyroid peroxidase antibodies
  • Anti-thyroglobulin antibodies
  • TSH receptor antibodies
A
  • Anti-thyroid peroxidase antibodies: Hashimoto’s thyroiditis & Grave’s
  • Anti-thyroglobulin antibodies: Hashimoto’s, Graves & thyroid cancer
  • TSH receptor autoantibodies: Grave’s disease
50
Q

If you do a radioisotope scan, what would the following results indicate:

  • Diffuse uptake
  • Focal high uptake
  • Cold areas (abnormally low uptake)
A
  • Diffuse uptake: Grave’s
  • Focal high uptake: toxic multinodular goitre or adenomas
  • Cold areas: thyroid cancer
51
Q

What is a myxoedema crisis/coma?

A

Emergency due to sevre untreated hypothyroidism. Typcially presents with impaired consciousness, hypoventilation and hypothermia

52
Q

State some potential precipitants of a myxoedema crisis/coma

A
  • Infection
  • MI
  • Trauma
  • Stroke
53
Q

State the symptoms & signs of a myxoedema crisis/coma

A
  • Bradycardia
  • Hypothermia
  • Hypoventilation
  • Hyporeflexia
  • Hypotension (cardiogenic shock)
  • Cyanosis
  • Cold hands
  • Seizures
  • Psychosis
  • Coma
  • Other usual signs of hypothyroidism
54
Q

Discuss what investigations you would do for myxoedema crisis/coma

A

Bedside​

  • ABG: PO2 & PCO2 if hypoventilating
  • VBG: glucose, electrolytes

Bloods

  • TFTs: T2, T4, TSH, thyroxine binding globulin
  • FBC
  • U&Es
  • Blood cultures
  • Cortisol
55
Q

Discuss the treatment for myxoedema crisis/coma

A
  • Oxygen if cynaosed
  • IV liothyronine (T3)
  • IV hydrocortisone
  • IV fluids- rehydrate as needed but watch for cardiac dysfunction
  • If infection suspected give IV antibiotics
  • Correct any hypoglycaemia
  • Active warming
56
Q

Autoimmune causes of hyperthyroidism usually present at an earlier age than nodular hyperthyroidism; true or false?

A

True

Autoimmune: 30-50yrs

57
Q

What is apathetic hyperthyroidism?

A

Overactivity of the thyroid gland, presenting as heart failure, arrhythmias (such as atrial fibrillation), weight loss, fatigue or psychological withdrawal. This is more often a presentation of hyperthyroidism in older than in younger patients

58
Q

What is T3-toxicosis?

A

Elevated free T3 with normal free T4 and supressed TSH

59
Q

What is subclinical hyperthyroidism?

A

Normal free T3 & T4 but supresses TSH

60
Q

What rare side effect can thionamides cause?

What should you inform pts?

A
  • Thionamides can cause agranulocytosis (bone marrow does’t make enough white cells)
  • Pts should be warned of this before commencing treatment. They should also be advised that if they get an unexplained fever or sore throat they must seek medical attention
    • Pt will need urgent FBC to exclude pancytopenia and drug should be stopped if neutrophil count is low
  • A more common side effect is a genrealised rash which disappears after cessation of drug
61
Q

Hypothyroidism commonly presents with subtle symptoms and is often diagnosed incidentally during routine blood tests; true or false?

A

True

62
Q

What is subclinical hypothyroidism?

Do you treat it?

A
  • Normal free T3 & T4 with elevated TSH
  • Guidelines reccomend sarring thyroxine if TSH >10miU/L even if pts asymptomatic due to high likelihood of progression to frank hypothyroidism. Treatment should also be considered at lower levels of TSH if woman is planning pregnancy, symptomaic or if pt has significant dyslipidaemia

Yr3 Medicine- Endocrinology (9 decks)

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