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My MRCP > Thyroid Disorders > Flashcards

Thyroid Disorders Flashcards

1
Q

How does hypothyroidism present? [8]

Severe cases [4]so

A
  • Weight Gain
  • Cold intolerance
  • Brittle nails, thin/dry skin & hair
  • Hyporeflexia, slow speech
  • Lethargy & low mood
  • Constipation
  • Bradycardia
  • Heavy periods

Severe cases can cause puffy face, large tongue, hoarseness and coma

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2
Q

How does hyperthyroidism present? [9]

A
  • Weight loss
  • Heat intolerance
  • Hyperreflexia
  • Bowel frequency
  • Palpitations
  • Light periods
  • Sweaty palms
  • Thyroid eye symptoms (bulging)
  • Anxiety/irritibility
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3
Q

How does gender affect thyroid disease?

A

Both hyper and hypothyroidism are much more common in women

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4
Q

What are the types of Hypothyroidism? [3]

A

Primary
Subclinical
Secondary

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5
Q

What causes congenital Hypothyroidism? [2]

A
  • developmental problems e.g. agenesis

- Dyshormogenensis (autosomal recessive condition preventing TH production)

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6
Q

What causes acquired Primary Hypothyroidism? [4]

A
  • Autoimmune (hashimoto’s) thyroiditis
  • Iatrogenic
  • Chronic Iodine Deficiency
  • Post-subacute thyroiditis
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7
Q

What can cause secondary or tertiary hypothyroidism? [4]

A
  • Pituitary tumours
  • Craniopharyngioma
  • Pituitary surgery/radiotherapy
  • Sheehan’s Syndrome
  • Isolated TRH deficiency
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8
Q

What is Sheehan’s Syndrome? [2]

A

Post-partum ischaemic necrosis [1] of the pituitary due to blood loss/hypovolaemic shock of childbirth [1]

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9
Q

List some iatrogenic causes of primary hypothyroidism? [4]

A

Post op
Radioactive Iodine or Anti-Thyroids
Amiodarone (Sub-acute thyroiditis)
RT for H/N cancer

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10
Q

What tests would you run for suspected hypothyroidism? What are the expected results? [7]

A
  • TFTs i.e. TSH & fT4
  • Thyroid Peroxidase Antibodies
  • FBC (MCV inc)
  • Lipids (inc)
  • Hyponatremia
  • Elevated Muscle enzymes, ALT & CK
  • Prolactin (inc)
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11
Q

Explain the results of the test for:
Lipids [1]
Hyponatremia [1]
Hyperprolactinemia [1]

A

Hypercholesterolaemia - decreased LDL receptors in liver
Na+ - Hyponatremia due to excess ADH from hypothyroidism
Hyperprolactinaemia - Increase TRH levels also stimulates an increase in prolactin levels

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12
Q

How will TFT’s (TSH, FT4) appear for each class of Hypothyroidism for:
Primary
Secondary
Subclinical

A

Primary - Low fT4 but high TSH
Secondary - Low fT4 & low or normal TSH
Subclinical - Normal fT4 & High TSH

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13
Q

What do we use to manage hypothyroidism? [4]

A

Levothyroxine (T4) tablets
Initial dose 50-100 mcg/day
Adjusted in steps of 25-50 mcg every 3-4w
Maintenance dose 100-200 mcg OD
Keep increasing until their TSH (primary disease) or fT4 (Secondary Disease) is normal.

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14
Q

What special cases affect how you use Levothyroxine? [4]

A
  • IHD needs to be started lower and titrated slowly as it can trigger Angina
  • Pregnant women need more T4
  • Myxedema Coma needs IV T3
  • Post-partum Thyroiditis needs to have the meds removed for 6 weeks and TFTs measured to see when it abates
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15
Q

What level is subclinical hypothyroidism [4]

A

Only if:

  • TSH >10
  • > 5 + Antibodies
  • TSH elevated + symptoms (temporary trial therapy for symptom improvement)
  • Pregnant or planning pregnancy
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16
Q

What are the risks of levothyroxine? [3]

Interactions [1]

A
  • Thyrotoxicosis
  • AF
  • Osteopenia

Interactions: iron reduces absorption so give 2h apart

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17
Q

How does Goitre occur in hypothyroidism? [4]

A

No fT4
No -ve feedback
Excess TSH
Hyperstimulation -> Hyperplasia of Thyroid gland

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18
Q

What are the causes for Primary hyperthyroidism? [4]

A

Graves Disease - 70%
Toxic Multinodular Goitre - 20%
Thyroid Adenoma
Thyrotoxic phase of thyroiditis (eventual hypothyroidism)

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19
Q

What is Grave’s Disease? [2]

A

Autoimmune condition, TSH receptor antibodies [1] continuously stimulate the thyroid [1] causing Primary hyperthyroidism

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20
Q

What is Toxic Multinodular goitre?
Most common cause [1] and its pathogenesis [2]
Presentation [4]

A 
Multinodular Goitre producing excess thyroid hormones
Dietary iodine deficiency
Rise in TSH to compensate
Hypertrophy and hyperplasia of thyroid follicular cells
Presentation:
Cosmetic problem
Airway obstruction
Dysphagia
SVC syndrome
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21
Q

Whats the main cause of secondary hyperthyroidism? [1]

A

Pituitary Adenoma producing TSH

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22
Q

What is Thyrotoxicosis without hyperthyroidism?

Name 2 causes

A

Where you get excess thyroid hormone without hyperthyroidism [1]

Due to exogenous thyroxine [1] or destructive thyroiditis causing stores of thyroid hormones to be released [1]

23
Q

What causes destructive thyroiditis? [2]

A

Post-partum

Amiodarone induced

24
Q

How do you diagnose Hyperthyroidism? [3]

Clinical features - associated conditions of Graves’ disease [2]

A

Clinical dx, TFT test, TSH receptor antibody test

Associated conditions:

  • Thyroid eye disease
  • Pre-tibial myxoedema
25
Q

How will TFT’s (TSH, FT4) appear for each class of Hyperthyroidism for:
Primary
Secondary
Subclinical

A

Primary - High fT4 & low TSH

Secondary - High fT4 & High TSH

Subclinical - Normal fT4 & low TSH

26
Q

How is Hyperthyroidism treated? [3]

A

1st) Anti-thyroid Drugs (ATDs)
2nd) Radioiodine

Resection of thyroid or pituitary adenoma

27
Q

What are anti-thyroid drugs used? [2]

A

Carbimazole

Propylthiouracil

28
Q

When would we treat Subclinical hyperthyroidism? [3]

A

If:

  • Elderly
  • Persistant subclinical hyperthyroidism
  • High cardiac risk patient
29
Q

Risks of Hyperthyroidism treatments? [2]

A

Carbimazole causes agranulocytosis

Radioiodine makes ~70% of patients hypothyroid and can cause eye disease

30
Q

How would you investigate a thyroid lump? [5]

A
  • TFTs
  • Technetium 99 Isotope scan
  • US (solid or cystic)
  • FNAC
  • CXR (retrosternal extension, mets)

IF you suspect cancer a serum calcitonin to rule out MEdullary Thyroid Cancer

31
Q

What are the main types of thyroid cancer? [6]

A

Differentiated thyroid carcinoma: papillary, follicular ca

Anaplastic, Lymphoma and medullary thyroid cancer.

32
Q

What is medullary thyroid cancer? [2]
What gene mutation is associated? [1]
Treatment [2]

A

Cancer of C cells in the thyroid gland [1]
Produces calcitonin [1]
Associated with MEN 2 gene mutation
Tx: total thyroidectomy, nodal clearance, no role for radio iodine

33
Q

Treatments for Thyroid cancers?

A

High Dose radioiodine
Long-Term levothyroxine to suppress the tumour

Lymphoma - External RT/chemo

Anaplastic - Can be delayed with external RT

Thyroidectomy - Only treatment that works on medullary thyroid cancer

34
Q

When would we stop Levothyroxine for Thyroid cancer?

A

Withdraw from the thyroxine for 2 weeks as a trial and do a full body radioisotope scan to see if its all gone

35
Q 
Subacute thyroiditis (de Quervain's) hypothyroidism
Trigger [2]
Symptoms [4]
Ix and result [1]
Prognosis [1]
Rx [2]
A

Viral trigger: enterovirus, coxsackie
Symptoms: painful goitre, fever, myalgia
ESR increased
Self limiting, 6-8w
Short term steroids 40mg OD weaned over 4 week period, NSAIDs, symptomatic control with B-blockers

36
Q 
Toxic adenoma
Define [1]
Presentation [2]
Pathogenesis: explain what is meant by thyroid autonomy [2]
Diagnosis [1]
A

Benign tumor that produces excess thyroid hormones
Painless solitary nodule + thyrotoxicosis sx
Patho: somatic mutation > follicular cells secrete thyroid hormone independent of stimulation (thyroid autonomy)
Diagnosis: biopsy

37
Q

Differentiated thyroid carcinomas
Follicular ca - what common mutations are found in patients? [2]
Describe prognosis of follicular [1]
Ix [3]

A

Papillary - associated with good prognosis
Follicular ca - BRAF mutation, RET/PTC gene re-arrangement
Prognosis:
- Good prognosis if resectable
Ix: TFT, US, FNA

38
Q

Differentiated thyroid carcinoma

Poor prognostic factors [4]

A

Age <16, >45
Tumour size
Spread outside thyroid capsule
Metastases

39
Q

Management of Differentiated thyroid carcinoma

A

Near total thyroidectomy
High dose radio iodine
Long term thyroxine

40
Q

Other types of thyroid cancer

Anaplastic - describe progression of disease, response to treatment, recommended tx

A

Anaplastic - aggressive, locally invasive, not responsive to radio iodine, try external RT

41
Q

Struma ovarii
Define [1]
Treatment [2]

A

Ovary has differentiated in thyroid cells

Tx: thyroidectomy > RAI

42
Q

Thyroid eye disease
Ax
RF
Px [2]

A

Ax: any form of thyroid disease (can be hypo, hyper or euthyroid)
RF: smoking
Px: autoimmunity leads to inflammatory response and periorbital oedema

43
Q

Thyroid eye disease
Symptoms [3]
Signs [5]

A

Sy:

  • eye discomfort, grittiness
  • increased tear production
  • diplopia, reduced acuity

Signs:

  • exophthalmos (appearance of protruding eyes)
  • proptosis (eyes protrude beyond orbit (look above in same plane as forehead))
  • conjunctival oedema, corneal ulceration, papilledema
  • loss of colour vision
  • afferent pupillary defect (optic nerve compression = URGENT expert advice rqd)
44
Q

Thyroid eye disease mx

  • Mild [3]
  • Severe [4]
A
  • Mild:
  • artificial tears, sunglasses, avoid dust
  • elevate head when sleeping to reduce periorbital oedema
  • Fresnel prism on one lense of glasses for diplopia
  • Severe:
  • IV METHYLPREDNISLONE
  • if gross oedema or opthalmoplegia, surgical decompression with inferior approach using spaces of paranasal sinuses for severe sight threatening disease or cosmetic reasons
  • eyelid surgery for cosmetic and function
  • orbital RT (improves opthalmoplegia but little effect on proptosis)
45
Q

Amiodarone effects on thyroid gland

A large proportion of amiodarone is comprised of iodine (37% by weight)

A

Amiodarone induced thyrotoxicosis
* Type 1 AIT
* Type 2 AIT
Amiodarone induced hypothyroidism

46
Q

How does amiodarone cause thyrotoxicosis and hypothyroidism?

A
  • structurally similar to thyroxine or T4 AND high iodine content > excess thyroid hormone synthesis
  • amiodarone inhibits deiodination, reducing peripheral conversion of T4 to T3 so T4 levels rise by 20-40% in first month
  • hypothyroidism - The Wolff Chaikoff effect describes the phenomenon whereby a large iodine load prevents iodine organification necessary for thyroid hormone synthesis. Hence, amiodarone, with its large iodine content, inhibits thyroid hormone synthesis and can result in hypothyroidism.
47
Q

Differentiate the presentation of Type 1 amiodarone induced thyrotoxicosis and Type 2

A

Type 1 AIT
* pre-existing thyroid dysfunction
* goitre
* radioiodine uptake scan normal
* same treatment as Graves disease thyrotoxicosis

Type 2 AIT
* Destructive thyroiditis, damage to follicular cells results in release of thyroid hormone
* radioiodine uptake scan reduced
* treated with steroids to reduce conversion of T4 to T3.

48
Q

What is Riedel’s thyroiditis

A

Riedel’s thyroiditis is rare and caused by a chronic fibrosing process, leading to a characteristic ‘woody’ sen- sation on palpation of the thyroid gland. It is associated with fibrosis of other structures including salivary glands and bile ducts (sclerosing cholangitis) and retroperitoneal fibrosis. Patients are euthyroid. Surgery may be required for symptomatic management.

49
Q

Thyroid storm

A

Thyroid storm is a rare but life-threatening complication of thyrotoxicosis. It is typically seen in patients with established thyrotoxicosis and is rarely seen as the presenting feature. Iatrogenic thyroxine excess does not usually result in thyroid storm.

50
Q

Thyroid storm
Precipitating events

A

thyroid or non-thyroidal surgery
trauma
infection
acute iodine load e.g. CT contrast media

51
Q

Thyroid storm
Clinical features include

A

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

52
Q

Thyroid storm management

A

symptomatic treatment e.g. paracetamol
treatment of underlying precipitating event
beta-blockers: typically IV propranolol
anti-thyroid drugs: e.g. methimazole or propylthiouracil
Lugol’s iodine
dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3

53
Q

Thyroid nodule

Investigation

A

Work up for thyroid nodules is as follows:

  1. Check TSH
  2. TSH suppressed → Thyroid uptake scan → Cold/iso nodule → FNA cytology
  3. TSH suppressed → Thyroid uptake scan →Hot nodule → No FNA required
  4. TSH normal/elevated → Thyroid USS → Suspicious features → FNA cytology

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