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Tiredness & Thyroid Disorders Flashcards

1
Q

What are the possible cardiac, respiratory and endocrine differentials for fatigue?

A

Cardiac:

  • heart failure
  • atrial fibrillation
  • myocardial infarction

Respiratory:

  • COPD
  • tuberculosis
  • obstructive sleep apnoea

Endocrine:

  • diabetes
  • hypothyroidism
  • Addison’s disease
  • Vitamin D deficiency
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2
Q

What are the neurological, infectious and GI differentials for fatigue?

A

Neurological:

  • stroke
  • multiple sclerosis
  • Parkinson’s disease

Infectious:

  • COVID-19
  • glandular fever
  • HIV

GI:

  • coeliac disease
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3
Q

What are the haematological, neoplastic and mental health possible differentials for fatigue?

A

Haematological:

  • anaemia

Neoplastic:

  • any cancer, including lymphoma and leukaemia

Mental health:

  • depression
  • anxiety
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4
Q

What are other possible differentials for fatigue?

A
  • poor sleep hygiene
  • drugs / alcohol
  • fibromyalgia
  • chronic fatigue syndrome
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5
Q

What bedside investigations would be performed in someone presenting with fatigue?

A
  • examination - resp / cardiac / GI / thyroid
  • urine dip to check for UTI
  • baseline observations
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6
Q

What blood tests might be performed in someone presenting with fatigue?

A
  • FBC to check for anaemia
  • haematinics (iron, B12, folate) to assess for anaemia
  • U&Es to check baseline kidney function for CKD
  • LFTs to assess for underlying liver disease
  • CRP / ESR to check for underlying inflammation
  • TFTs to assess thyroid function
  • HbA1c to assess for possible diabetes
  • IgA tissue transglutaminase to assess for coeliac disease
  • consider bone biochemistry / myeloma screen
  • vitamin D
  • HIV / hepatitis if at risk
  • Monospot test for glandular fever
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7
Q

What imaging / interventional tests may be considered in someone presenting with fatigue?

A

Imaging:

  • consider CXR to screen for malignancy / TB
  • consider CT if high concerns for malignancy

Interventional:

  • consider OGD / colonoscopy if evidence of anaemia with an unclear cause
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8
Q

What is the main function of the thyroid gland?

What can high levels of thyroid hormones cause?

A
  • the thyroid gland is a regulator of metabolism
  • T3 and T4 act via nuclear receptors in target tissues to initiate a variety of metabolic pathways
  • high levels of T3 and T4 cause the processes to occur faster and more frequently
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9
Q

What are the main metabolic processes that are increased by thyroid hormones?

A
  • basal metabolic rate
  • gluconeogenesis (making new glucose)
  • glycogenolysis (breaking down glycogen into glucose)
  • protein synthesis
  • lipogenesis
  • thermogenesis
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10
Q

In what ways can T3 and T4 increase the rates of metabolic processes?

A
  • increasing the size and number of mitochondria within cells
  • increasing Na-K pump activity
  • increasing the presence of B-adrenergic receptors in tissues such as cardiac muscle
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11
Q

How is the thyroid involved in bone metabolism?

A
  • it secretes calcitonin in response to hypercalcaemia
  • this inhibits osteoclasts to slow down bone breakdown and decrease calcium levels
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12
Q

What are the 2 components of thyroid function tests and why are they tested for?

A
  • T4

this is a marker of what the thyroid function is actually doing (producing or not producing hormones) and what will produce the symptoms

  • TSH

this is marker to work out if the problem is in the thyroid itself or higher up the HPT axis

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13
Q

What are the different components involved in the hypothalamic-pituitary-thyroid axis and what do they produce?

A
  • the paraventricular nuclei in the hypothalamus release thyroid-releasing hormone (TRH)
  • this causes thyrotrope cells in the anterior pituitary to release thyroid-stimulating hormone (TSH)
  • the thyroid responds to TSH by releasing T3 and T4
  • T4 inhibits the pituitary and hypothalamus in a negative feedback loop
    • this is the “brake system” which aims to maintain a state of homeostasis
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14
Q

What are the 2 stages in deciding what type of hyper/hypo thyroidism is present?

A
  • look at the T4 - is it high, low or normal?
  • look at the TSH - is it compensating for or causing the change in T4?
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15
Q

What are the levels of T4 and TSH like in secondary hyperthyroidism?

What usually causes this?

A

there is high T4 and high TSH (or normal TSH)

  • normally due to a TSH secreting pituitary adenoma
    • the tumour does not respond to the inhibiting effects of T4
  • can also be caused by excessive pituitary stimulation from the hypothalamus
    • ​this is sometimes called tertiary hyperthyroidism
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16
Q

What are the levels of T4 and TSH like in primary hyperthyroidism?

What is the most common cause of this?

A

high T4 and low TSH

  • 75% of cases are Graves’ disease
  • this is an autoimmune condition against the thyroid where the binding of IgG autoantibodies to activate TSH receptors causes overproduction of thyroid hormones
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17
Q

What are other less common causes of primary hyperthyroidism?

A
  • toxic multi-nodular goitre
  • toxic adenoma
  • iodine-induced
  • trophoblastic tumour
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18
Q

What are the levels of T4 and TSH in secondary hypothyroidism?

What are the causes of this?

A

low T4 and low TSH (or normal TSH)

  • most common cause is a non-secreting pituitary adenoma
  • can also be caused by pituitary surgery or damage
  • can be caused by hypothalamic tumour or damage
    • this is sometimes called tertiary hypothyroidism
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19
Q

What are the levels of TSH and T4 like in primary hypothyroidism?

What is the most common cause of this?

A

there is low T4 and high TSH

  • 50% of cases are due to autoimmune thyroiditis (Hashimoto’s)
  • this results in lymphocyte infiltration and fibrosis of the thyroid gland
20
Q

What are other causes of primary hypothyroidism?

A
  • iodine deficiency
  • thyroidectomy
  • radiotherapy
21
Q

What is subclinical hyperthyroidism?

A

there are normal T4 levels but lowered TSH

22
Q

What is subclinical hypothyroidism?

What condition / situation is this commonly seen in?

A

this is normal T4 levels with raised TSH

this is seen in hypothyroidism with poor adherence to levothyroxine

(i.e. people start taking their tablets in the week leading up to a TFT)

23
Q

What are all the possible causes of primary hypothyroidism?

A
  • iodine deficiency
  • autoimmune thyroiditis
    • if this is with a goitre then it is Hashimoto’s thyroiditis
    • if there is no goitre then it is atrophic thyroiditis
  • can be caused by medication - such as carbimazole used to treat hyperthyroidism
  • surgery / injury to the thyroid
  • transiently can be caused secondary to viral infections or post-partum
24
Q

What is the epidemiology of primary hypothyroidism like?

A
  • prevalence of 1-2% in the UK
  • 10x more common in women than men
  • 95% of hypothyroidism is primary
25
What are the risk factors for primary hypothyroidism?
* **_female_** gender * age **_\>60_** * **TPO autoantibodies** * **pregnancy** * having other **autoimmune** diseases
26
What are the symptoms of primary hypothyroidism?
* fatigue / lethargy * cold intolerance * weight gain * constipation * non-specific weakness * menstrual abnormalities * dry skin / hair loss * hoarse voice * neck swelling
27
What are the signs of primary hypothyroidism?
* bradycardia * delayed reflexes * paraesthesia / peripheral neuropathy
28
What are the investigations and treatments for primary hypothyroidism?
***_Investigations:_*** ``` * thyroid function tests (TFTs) TPO autoantibodies (only done once) ``` ***_Treatment:_*** * regular **TSH monitoring** + **replacement of T4** with **_levothyroxine_**
29
What is the epidemiology of primary hyperthyroidism like?
* prevalence of **0.5-2%** in the UK * **women** are **10x** more likely to have this than men
30
What are the 3 most common causes of primary hyperthyroidism?
* the most common is **_Graves' disease_** (80%) * then **_toxic multinodular goitre_** * this involves at least 2 autonomously functioning thyroid nodules * then **_toxic thyroid nodule_** * ​this is a single nodule producing hormones autonomously
31
What are other possible but less common causes of primary hyperthyroidism?
* **medications** - **_iodine_** & **_amiodarone_** * during **pregnancy** * **thyroiditis** can also cause hyperthyroidism as already made T4 is released * this is thyroid toxicosis rather than hyperthyroidism
32
What are risk factors for primary hyperthyroidism?
* **female** gender * **smoking** * having other **autoimmune** diseases
33
What are the symptoms of primary hyperthyroidism?
* agitation * emotional lability / irritability * insomnia * anxiety * palpitations * heat intolerance / increased sweating * increased appetite * diarrhoea * polyuria
34
What are the signs of primary hyperthyroidism?
* tremor * sinus tachycardia * atrial fibrillation * thyroid enlargement * hyperreflexia * in Graves' disease there is **eyelid retraction, lid lag & proptosis**
35
What investigations and treatments are there for primary hyperthyroidism?
***_Investigations:_*** * TFTs * TSH-receptor antibodies * neck USS ***_Treatments:_*** * **_carbimazole_** * radioactive iodine * surgery
36
What mnemonic is used to remember the 6 steps involved in the synthesis of thyroid hormone?
**_ATE ICE:_** * A - active transport * T - thyroglobulin * E - exocytosis * I - iodination * C - coupling * E - endocytosis
37
What is involved in the active transport phase of thyroid hormone synthesis?
* active transport of **_iodide_** into the **follicular cell** via the **_sodium-iodide symporter (NIS)_** * this is **_secondary_ active transport** and the sodium gradient driving it is maintained by a **sodium-potassium ATPase**
38
What is involved in the thyroglobulin stage of thyroid hormone synthesis?
* thyroglobulin (Tg) is a **large protein** that is rich in **_tyrosine_** * it is formed in **follicular ribosomes** and placed into **_secretory vesicles_**
39
What is involved in the exocytosis stage of thyroid hormone synthesis?
* **_exocytosis of thyroglobulin_** into the **follicle lumen**, where it is stored as **_colloid_** * thyroglobulin is the **scaffold** upon which thyroid hormone is synthesised
40
What is involved in the iodination stage of thyroid hormone synthesis?
* **_iodination of thyroglobulin_** * iodide is made **reactive** by the enzyme **_thyroid peroxidase_** * iodide binds to the **benzene ring** on **tyrosine residues** of thyroglobulin, forming **_monoiodotyrosine_** (MIT) then **_diiodotyrosine_** (DIT)
41
What is involved in the coupling stage of thyroid hormone synthesis?
* coupling of **_MIT and DIT_** gives **_triiodothyronine (T3) hormone_** * coupling of **_DIT and DIT_** gives **_tetraiodothyronine (T4) hormone_**, also known as **thyroxine**
42
What is involved in the endocytosis stage of thyroid hormone synthesis?
* endocytosis of **_iodinated thyroglobulin_** back into the **follicular cell** * thyroglobulin undergoes **proteolysis in lysosomes** to **_cleave the iodinated tyrosine residues_** from the larger protein * **_free T3 or T4_** is then released and the **thyroglobulin scaffold is recycled**
43
How are T3 and T4 carried in the blood?
they are **fat soluble** and mostly carried by **plasma proteins** these are **_Thyronine Binding Globulin_** and **_albumin_**
44
What is the more potent form of thyroid hormone? What is its half-life like relative to the other thyroid hormone?
* **_T3_** is the more potent form * it has a **shorter half-life** due to its **low affinity** for the binding proteins * less than 1% of T3 and T4 is unbound free hormone * at the peripheries, **_T4 is deiodinated_** to the **more active T3**
45
How are T3 and T4 deactivated?
* T3 and T4 are deactivated by **_removing iodine_** * this happens in the liver and kidney
46
Which thyroid hormone is used in the treatment of hypothyroidism and why?
* T4 is used as it has a longer half-life * its plasma concentrations are also easier to manage
47

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