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Flashcards in ENDOCRINE: Thyroid Deck (43)
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1
Q

What are the physiological effects of thyroid hormone?

A
Increase HR and CO 
Increase bone resorption 
increases gut motility 
Increases gluconeogenesis 
Maintains normal hypoxic and hypercapnic drive
2
Q

Outline the normal thyroid hormone axis?

A

TRH released from hypothalamus–> TSH secreted from ant pit–> thyroid to release T3 and T4

3
Q

What is Graves disease?

A

A type of HYPERthryoidism where TSH-receptor stimulating antibodies cause excess T3/T4

4
Q

Apart from Graves disease, outline another autoimmune cause of thyrotoxicosis?

A

Nodular, either toxic nodule on the thyroid or a multiple nodules, secreting T3/T4

5
Q

What is thyroiditis?

A

Inflammation of the thyroid gland causing release of thyroxine (T4)

6
Q

What can cause thyroiditis?

A

Viral infection, medication (amiodarone) or following pregnancy

7
Q

What are the symptoms of hypothyroidism?

A
dry thick skin 
brittle hair 
macroglossia 
puffy face 
loss of lateral 1/3 eyebrow 
weight gain 
carpal tunnel syndrome 
peripheral neuropathy 
bradycardia
8
Q

What is a thyroid storm?

A

Severe form of thyroid disease.

Can occur in thyroxic patients who experience an acute stressor e.g. illness, trauma, surgery

9
Q

How do you treat a thyroid storm?

A
symptomatic treatment e.g. paracetamol
treatment of underlying precipitating event
HDU 
Strong dose of anti-thyroid medication e.g methimazole or propylthiouracil
Beta blockers (IV propranolol) 
Potassium iodide aka Lugol's iodine (to inhibit production of anymore thyroid hormone) 
High dose steroids: dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3

Propylthiouracil, B blocker and hydrocortisone/ steroids

10
Q

A 10 week pregnant patient comes in with heat intolerance and palpitation, upon further investigations it is found she has hyperthyroidism, what drug would you prescribe here?

A

Propylthiouracil as carbimazole crosses the placenta, therefore unable to use in first trimester of pregnancy

11
Q

Levothryroxine side effects?

A
  • hyperthyroidism: due to over treatment
  • reduced bone mineral density
  • worsening of angina
  • atrial fibrillation
12
Q

What is myxoedema coma?

A

extreme form of hypothyroidism
high mortality

13
Q

Clinical features of myxoedema coma?

A
  • CVS: non-pitting oedema of hands and feet, bradycardia, hypotension refractory to vasopressors, reduced contractility, pericardial effusion
  • RESP: respiratory depression, impaired respiratory muscle function, hypoxia and hypercapnia
  • RENAL: bladder atony, urinary retention, urinary Na+ normal or high
  • ELECTROLYTES: hyponatraemia from increased H2O reabsorption from high levels of ADH
  • GI: macroglossia, anorexia, abdominal pain, constipation, ileus
  • CNS: delayed tendon reflexes, slow mentation, depression -> psychosis, seizures

stupor
hypothermia
respiratory failure
confusion
coma
dry skin
sparse hair
hoarse voice
periorbital oedema

14
Q

Risk factors for myxoedema coma?

A
  • hypothermia
  • CVACHF
  • infections
  • drugs: anaesthetics, sedatives, narcotics, amiodarone, lithium
  • GIH
  • trauma
  • electrolytes: hypoglycaemia, hyponatraemia
  • acidosis
  • hypoxaemia
  • hypercapnia
15
Q

Inv and suspected findings in myxodema coma?

A
  • TSH: markedly elevated in 95% of cases, 5% are caused by central TSH failure
  • low free T4
  • low T3
  • hyponatraemia
  • hypoglycaemia
  • anaemia
  • hypercholesterolaemia
  • high LDH
  • high CK
16
Q

Management for myxoedema coma?

A

RESUSCITATION
* admit to ICU because if high mortality and multi-faceted therapy
* may require intubation for various reasons (respiratory failure, airway obstruction from macroglossia, coma)
* ventilation may be required for several days -> weeks
* IV fluid resuscitation and vasoactive agents until thyroid hormone action begins
* warm patient and pre-empt vasodilation and hypotension

Acid-base and Electrolytes
* supportive care
* glucose
* hyponatraemia: cautious correction over time (<10mmol/L day)

Specific Therapy
* hydrocortisone 100mg Q 6hourly if adrenal or pituitary insufficiency suspected
* replacement of thyroid hormones (T4 or T3 is controversial):
* (1) T4 – loading dose = 500mcg IV -> 50-100mcg OD IV or orally
* (2) T3 – loading dose = 10mcg IV -> 10mcg Q4 hrly for 24 hours then every 6 hours

Underlying Cause
treat precipitant (withdraw drugs, treat infection…)

17
Q

Features of thyroid storm?

A

fever > 38.5ºC
tachycardia
confusion and agitation
nausea and vomiting
hypertension
heart failure
abnormal liver function test - jaundice may be seen clinically

18
Q

Causes of HYPOthryoidism?

A

Primary:
* Hashimotos Thyroiditis
* Subacute Thyroiditis
* Riedel Thyroiditis
* Post- thyroidectomy
* Drug therapy e.g. lithium, amiodarone
* Dietary iodine deficiency

Secondary:
* due to Pit failure
* associated conditions: Downs syndrome, Turners syndrome and coeliac disease

19
Q

What is Hashimotos Thryoiditis?

A
  • most common cause of hypothyroid
  • autoimmune disease
  • may cause transient thyrotoxicosis in the acute phase
  • 5-10 time more common in women
20
Q

What other diseases is Hashimotos associated with?

A
  • IDDM
  • Addisons
  • Pernicious anaemia
21
Q

Inv for ?hypothyroid

A
  • Bedside: ECG, BM
  • Bloods: FBC (anaemia), WCC (infection), CRP (infection), Vit D (deficiency), U&Es (rule out any electrolyte abnormalities), LFTs (if yellowish tinge to skin)
  • Other: change in bowel habit consider stool sample
22
Q

Management of hypothyroidism?

A
  • patients should be started on a dose of 50-100mcg od
  • patients with cardiac disease, severe hypothyroidism or patients over 50 years the initial starting dose should be 25mcg od with dose slowly titrated.
  • following a change in thyroxine dose thyroid function tests should be checked after 8-12 weeks
  • the therapeutic goal is ‘normalisation’ of the thyroid stimulating hormone (TSH) level
  • TSH aim: 0.5-2.5 mU/l
  • women with established hypothyroidism who become pregnant should have their dose increased ‘by at least 25-50 micrograms levothyroxine’ due to the increased demands of pregnancy. The TSH should be monitored carefully, aiming for a low-normal value
23
Q

What is subclinical hypothyroidism?

A
  • elevated TSH
  • Normal T4
24
Q

How does subclinical hypothryoidism present?

A
  • usually asymptomatic
  • mild symptoms incl fatigue, weight gain and cold intolerance
25
Q

Managaement of subclinical hypothyroidism?

A
  • TSH is > 10mU/L and the free thyroxine level is within the normal range:
    consider offering levothyroxine if the TSH level is > 10 mU/L on 2 separate occasions 3 months apart
  • TSH is between 5.5 - 10mU/L and the free thyroxine level is within the normal range:
    if < 65 years consider offering a 6-month trial of levothyroxine if:
    the TSH level is 5.5 - 10mU/L on 2 separate occasions 3 months apart,
    and
    there are symptoms of hypothyroidism

in older people (especially those aged over 80 years) follow a ‘watch and wait’ strategy is often used

if asymptomatic people, observe and repeat thyroid function in 6 months

26
Q

What is De Quervain’s thyroiditis?

A
  • post viral infection
  • typically presents with hyperthyroidism
27
Q

Phase of De Quervain’s thyroiditis?

A

There are typically 4 phases;
* phase 1 (lasts 3-6 weeks): hyperthyroidism, painful goitre, raised ESR
* phase 2 (1-3 weeks): euthyroid
* phase 3 (weeks - months): hypothyroidism
* phase 4: thyroid structure and function goes back to normal

28
Q

Inv for ?De Quervain’s thyroiditis?

A
  • Thyroid scintigraphy: globally reduced uptake of iodine- 131
29
Q

Management for De Quervains?

A
  • self limiting- usually no treatment
  • thyroid pain may respond to aspirin or other NSAIDs
  • more severe cases esp if hypothryoid is present- steroids
30
Q

What other manifestations of Graves disease may patients have?

A

30% of pts will have extrathyroidal manifestations
* orbitopathy
* acropachy
* pretibial myxoedema

31
Q

RF for Graves disease?

A
  • +ve fhx
  • Female
  • Smoking (tobacco increases risk of orbitopathy)
32
Q

Associations of Graves disease?

A
  • T1DM
  • Addisons disease
  • Pernicious anaemia
33
Q

Clinical features of Graves disease?

A

General hyperthyroidism signs and symptoms:
* Metabolic:
Heat intolerance: due to increased metabolism leading to higher body temperature.
Weight loss: caused by higher metabolic rate and accelerated metabolism.
Increased appetite: in 90% this is in the absence of weight gain.
Excessive sweating: must be differentiated from ‘hot flushes’ due to oestrogen deficiency in post-menopausal women.
* Cardiac:
Palpitations: this includes atrial fibrillation (20%) or other supraventricular tachycardias, especially in older patients.
Tachycardia
Atrial fibrillation: a cause of palpitations, especially in older patients.
Hypertension
Heart failure: thyrotoxic cardiomyopathy, especially in the elderly.
* Excessive nervous stimulation:
Anxiety: a feeling of nervousness and trembling.
Tremor: usually fine.
* Other:
Palpable thyroid: smooth, diffusely and uniformly enlarged thyrotoxic (excess production of thyroid hormone) goitre.
Oligomenorrhoea

Extrathyroidal manifestations specific to Graves’ disease:
* Eye disease (30%): upper eyelid retraction, exophthalmos, ophthalmoplegia, eye pain, tearing, diplopia, photophobia, blurred vision.
* Pretibial myxoedema (3%): waxy, discoloured induration of the skin on the anterior aspect of the lower legs.
* Thyroid acropachy (1%): clubbing of fingers and toes with soft tissue swelling due to sub-periosteal formation of new bone.

34
Q

Inv for ?Graves disease?

A

Thyroid dysfunction:
* TSH
* fT4
* fT3
Specific tests for Graves:
* TSH receptor antibodies- present in graves
* Technetium scan of thyroid gland- consider if receptor antibodies are negative

35
Q

A pt has confirmed Graves disease, what further inv would you like to do?

A

If there is a discrete thryoid nodule
* USS- assess size, vascularity and presence of nodules. In graves an englarged hypervascular thyroid is seen w nodules in 15% of graves pts
* Radioactive iodine scane- uneven uptake indicates presence of nodule, diffuse and high uptake suggests graves , low uptake suggests thyroiditis

36
Q

What does a radioactive iodine scan show?

A
  • uneven uptake indicates presence of nodule
  • diffude and high uptake: Graves
  • low uptake: thyroiditis
37
Q

How to assess for thyroid eye disease?

A
  • Examine visual fields, acuity and eye movement s
  • MRI or CT scans can confirm the diagnosis esp if subclinical
38
Q

TFT results in Graves disease?

A
  • TSH: low
  • fT4: high
  • fT3: high
39
Q

Ddx for Graves disease?

A

Toxic nodular goitre
* Similarities: hyperthyroidism.
* Differences: palpable nodular goitre, absence of extrathyroidal manifestations and thyroid receptor antibodies.
Subacute thyroiditis (de Quervain)
* Initial transient hyperthyroidism followed by hypothyroidism, usually resolving in a few months.
* Similarities: hyperthyroidism.
* Differences: systemic febrile illness, painful thyroid, raised C-reactive protein, absence of thyroid receptor antibodies.
Gestational hyperthyroidism
* During the first trimester, high levels of hCG stimulate the TSH receptor.
* Similarities: hyperthyroidism.
* Differences: usually subclinical but can be overt (more likely if hyperemesis gravidarum), absence of thyroid receptor antibodies.
TSH-producing pituitary adenoma
* Similarities: hyperthyroidism.
* Differences: MRI shows pituitary tumour, absence of thyroid receptor antibodies, normal or raised TSH.
Iodine-induced hyperthyroidism
* Following iodine exposure (e.g. radiographic contrast, amiodarone).
* Similarities: hyperthyroidism.
* Differences: history of iodine exposure, absence of thyroid receptor antibodies.
Inflammatory eye conditions, myasthenia gravis
* Similarities: proptosis, ophthalmoplegia, photophobia, diplopia.
* Differences: clinically euthyroid, often unilateral eye signs.
Postnatal thyroiditis
* An initial transient hyperthyroid period usually followed by a transient hypothyroid period.
* Similarities: hyperthyroidism (in the initial phase).
* Differences: absence of thyroid receptor antibodies.
Thyrotoxicosis factitia
* Ingestion of exogenous thyroid hormone (mistaken ingestion of excess, or a symptom of Munchausen syndrome).
* Similarities: hyperthyroidism.
* Differences: goitre usually absent, no thyroid receptor antibodies.

40
Q

Managment of Graves diease?

A

Beta blockers
* for rapid control of symtpoms incl tachycardia, palpitations, anxiety and heat intolerance
Radioactive iodine
* first line definitve treatment
* unsuitable in pregancy, attempting to conceive in next 4-6 months, presence of active eye disease, concerns about compression or malignancy
* pts often become hypothryoid and need replacement
Antithyroid drugs
* Offer a 12-18 month course as first-line definitive treatment if it is likely to achieve remission, or if radioactive iodine and surgery are unsuitable.
* Examples include carbimazole (first-line) and propylthiouracil.
Surgery
* Total thyroidectomy if concerns of compression or malignancy or radioactive iodine or antithryoid drugs are unsuitable
* If antithyroid drugs have been tried but hyperthyroidism has replapsed
* Risk: recurrent laryngeal nerve samage, hypoparathryoidism
* become hypothyroid and need replacement

41
Q

Where should Graves disease pts be managed?

A
  • Secondary care with primary care starting antithyroid durgs and B blockers whilst waiting
42
Q

early complications of Graves?

A

Early complications include:
* Atrial fibrillation
More likely over 40 years and may be the presenting feature of hyperthyroidism.
Can result in thromboembolic events and stroke.
* Pregnancy-related issues
These include miscarriage, pre-term birth, thyroid dysfunction in the foetus, poor foetal growth, pre-eclampsia and maternal heart failure.
* Sight-threatening orbitopathy
Problems include corneal ulcers and optic neuropathy.
Rare and usually occurs within one year of diagnosis.

43
Q

Later complications of Graves?

A
  • Osteoporosis
    The degree of bone mineral loss is proportional to the duration in which the hypothyroidism is left untreated.
  • Congestive heart failure
    Occurs more frequently in the elderly.
    High-output failure can occur due to thyrotoxic cardiomyopathy.

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