Thyroid Disease Flashcards

1
Q

What is the general pathway for stimulating thyroid hormone release?

A

Release of TRH by Hypothalamus

Triggers release of TSH by Anterior Pituitary

Triggers release of T3 and T4 from Thyroid

**Iodine dependent

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2
Q

What is cretinism?

Epidemiological features?

A

Congenitally severely stuntend physical and mental development secondary to untreated fetal thyroid hormone deficiency, secondary to maternal hypothyroidism

100,000 born every year

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3
Q

Epidemiology of Iodine Deficiency

A

Affects 50 million children worldwide
1.6 billion people at risk

Tasmanians are at risk of iodine deficiency - our soils are iodine poor

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4
Q

RDI of iodine:

A

Children: 90-120ug/day
Adults: 150ug/day
Pregnancy: 250ug/day

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5
Q

Where is dietary iodine derived from?

A

Derived from iodine in soil and water, thus present in:

  • Milk
  • Seafood
  • Seaweed
  • Drinking water
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6
Q

Consequences of iodine deficiency

A
Goitre
Reduced fertility
High risk of miscarriage
Growth retardation
Hearing and speech impairments
mental retardation
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7
Q

Iodine Prophylaxis

A

ID considered inexcusable due to ease with which iodine can be supplemented - and very cheaply

Best way = iodinised salt

  • Cheap and easy to make
  • Universally and readily consumed

Other methods to supplement:

  • Iodine tablets
  • Iodinised milk and bread and oil
  • Iodinised water
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8
Q

Cellular mechanisms of TSH

What problems can occur with TSH binding and causing T3 and T4 secretion?

A

Released from Ant. Pit.

Binds to G Protein-coupled TSH-receptors (TSH-R) in thyroid gland cells

Stimulates T3 and T4 secretion

Problems:

  1. Autoantibodies against TSH-R = TSH-RAb
    - These may be stimulatory or blocking
  2. Mutations of TSH-R
    - Can produce a variety of clinical syndromes
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9
Q

How are T3 and T4 carried in circulation?

A

Mainly protein-bound >99%

Bound to:

  • Albumin
  • TBPA (thyroid binding pre-albumin)
  • TBG (thyroid binding globulin)

Relatively more free T3 than T4

FT3 and FT4 are the ones measured in TFTs, along with TSH levels

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10
Q

TFT Interpretation: Normal values, and what is measured and when

A

Normally, TSH levels are measured:

Euthyroid = normal TSH levels: 0.4-4.0

Hypothyroid = high TSH levels: >5.0

Hyperthyroid = low TSH levels: <0.05

FT3 and FT4 are usually only measured when making a diagnosis of abnormal thyroid function
Or, if HPA axis is impaired

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11
Q

What are the forms of ‘subclinical’ Thyroid dysfunction

A

Can sometimes still represent clinically significant conditions, that can be missed

Subclinical Hypothyroidism: (aka ‘compensating’ or ‘prehypothyroidism’)
- High TSH (>5.0) but T3 and T4 are normal

Subclinical Hyperthyroidism:
- Low TSH (<0.05) but normal T3 and T4

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12
Q

Grave’s Disease: Autoimmune Hyperthyroidism

A

Hyperthyroidism.

Incidence: 0.05-0.5%
Risk Factors: Females and FHx
Clinically: Symptoms typical of hyperthyroidism, eye signs, goiter
Diagnosis: Low TSH, presence of TRAB (>70%), with Tc Scan

*TRAB stimulatory antibody

Treatment: Two options

  1. Temporary - Antithyroids
  2. Definitive - Resection and Radioactive Iodine

Prognosis: Most (75%) return to Euthyroid within 2 years of diagnosis

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13
Q

Postpartum Thyroid Thyroiditis

A

Presents with Hypothyroidism, Hyperthyroidism, or Hyperthyroidism->Hypothyroidism sequale

Incidence: 5-9% women post-partum
Typically occurs 6 weeks to 6 months post-partum
Risk Factors: IDDM, increased ATPO/TRAB, Prior PPTD, FHx
Clinically: Symptoms of Hyper or Hypothyroidism, depression
Presentation:
- Hypothyroidism (50% cases) -> persists in ~1/4
- Hyperthyroidism-> Hypothyroidism (30%)
- Hypothyroidism (20%)

Treatment: Nil, or temporary Antithyroids or Thyroid replacement, depending on presentation. Note that long-term Hypothyroidism will occur in ~20%

Prognosis: Recurrance in 70%

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14
Q

Hashimoto’s Disease

A

Autoimmune Hypothyroidism

Incidence: 0.5-2%
Risk Factors: Females, FHx
Clinically: Symptoms of hypothyroidism, +/- Goitre
Diagnosis: Based on clinical presentation, high TSH and low T3, T4, and presence of ATPO (>80%)
Treatment: Thyroid replacement - Thyroxine
Prognosis: Usually life-long replacement

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15
Q

What is TPO?

A

Thyroid Peroxidase

Enzyme present mainly in the thyroid which liberates iodine, enabling T3 and T4 production

ATPO - autoantibody against thyroid peroxidase is a risk marker for hypothyroidism

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16
Q

What are the goals of thyroxine therapy?

A

Dose adjusted to keep TSH within idealt herapeutic range: 0.05-2 (which is only valid if pituitary functioning normally, of course)

TSH regulation is the main goal - even if T4 ends up being high. *Remember also that the exogenous T4 is replacing the endogenous T3 as well, so will probably read higher.

E.g. TSH = 0.10 with FT4 of 26 (9-20) = satisfactory

Must reduce Thyroxine dose if TSH low, even if FT4 is in normal range.

E.g. TSH = 0.02 with FT4 of 15 (9-20) = unsatisfactory

17
Q

Classification of Thyroid Nodules:

Considerations?

A

May be:

  • Symptomatic
  • Palpable incidental finding
  • Impalpable indicental finding (i.e. on US)

Most pressing concern = risk of malignancy

Most are benign:

  • colloid nodules in MNG
  • cysts
  • adenomas
18
Q

Prevalence of Thyroid Nodules: General and in TAS

A

Generally, Thyroid nodules discovered as incidental findings at autopsy have been reported at rates as high as 30-60%

In Tasmania, quite high rates of thyroid nodules - higher for women

Incidence increases with age

(males have a bit of a peak which subsides again, before steadily rising with age again. This peak occurs at ~40-50 years of age)

19
Q

Protocol for Investigations and Management of Thyroid Nodules

A
  1. Thyroid Nodule Discovered
  2. Measure TSH

3a. If TSH is LOW ( Treat
- If Tc Scan = COld -> Need to conduct FIne Needle Aspirate Biopsy (FNAB)

3b. If TSH is NORMAL (0.4-4.0), need to conduct FNAB
Outcomes:
- 15% of FNABs are non-diagnostic and thus requires repeat FNAB
- 70% are BENIGN -> Management involves OBSERVATION
- 5% are MALIGNANT and 10% are SUSPICIOUS -> Both require COMPLETE RESECTION

*Risks not taken with suspicious nodules, because FNAB takes such a small sample, cannot guaruntee no malignancy exists

20
Q

Thyroid Carcinomas: General Stats

A

TCs = most common endocrine malignancy

Papillary Thyroid Carcinomas (PTC) = most common, accounting for 65-80%

Follicular Thyroid Carcinomas (FTC) = 15-30%

Medullary Thyroid Carcinomas (MTC) = 5%

Others account for remaining 2-5%

21
Q

Prognosis of Thyroid Carcinomas:

A

Papillary (65-80% TCs) and Follicular (15-30% TCs) TCs have generally good prognosis if appropriate management occurs

PTCs have 10-year survival rate of >90%

22
Q

Incidences of PTC

A

Papillary Thyroid Carcinomas

Generally rising in incidence.

  • Due to iodine nutrition?
  • Due to iodinising radiation?

400% increase in TAS over last 30 years

23
Q

General management of PTC

A
  1. Complete Thyroid Resection
  2. Radioiodine (PTC, FTC)
  3. Ongoing T4 replacement - thyroxine drug therapy
24
Q

Describe ‘occult’ Thyroid Carcinomas: General Stats

A

Occult TCs = Asymptomatic, Impalpable TCs that are 90%

Overall, occult papillary thyroid carcinomas are believed to have very little risk of progression