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Medicine, Year 3, Metabolic Medicine > Clinical Topic 6: Pituitary, Adrenal, Thyroid Disease > Flashcards

Clinical Topic 6: Pituitary, Adrenal, Thyroid Disease Flashcards

1
Q

What hormones are released by the anterior pituitary gland?

A
  • FSH
  • LH
  • Growth hormone
  • Prolactin
  • ACTH
  • TSH
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2
Q

What hormones are released by the posterior pituitary gland?

A
  • Oxytocin

- ADH

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3
Q

What hormones are released at each level of the HPA axis?

A

Hypothalamus: Corticotropic releasing hormone (CRH)
Pituitary gland: Adrenocorticotropic releasing hormone (ACTH)
Adrenal: Glucocorticoids

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4
Q

What hormones are released at each level of the HPT axis?

A

Hypothalamus: Thyroid releasing hormone (TRH)
Pituitary gland: Thyroid stimulating hormone (TSH)
Thyroid gland: T3 and T4

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5
Q

What hormones are released by the Thyroid gland?

A

T3, T4

Calcitonin

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6
Q

What is the role of Calcitonin?

A

Opposes the action of Parathyroid hormone, thus decreasing serum calcium

Inhibits osteoclast activity (bone breaking)
Activates osteoblast activity (bone building)
Inhibits GIT absorption of calcium
Inhibits reabsorption of calcium from kidney tubules

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7
Q

What cells release T3, T4 and Calcitonin in the Thyroid?

A

T3 and T4: Follicular cells

Calcitonin: Parafollicular cells (C cells)

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8
Q

What is the most common and second most common form of Hyperthyroidism?

A
  • Graves disease (most common)

- Toxic nodular goitre

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9
Q

How does Graves disease cause hyperthyroidism?

A

TSH antibodies stimulate thyroid follicular cells to secrete T3 and T4

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10
Q

How does a Toxic multi-nodular / single nodular goitre cause hyperthyroidism?

A

The nodules themselves secrete T3 and T4

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11
Q

How does Thyroiditis cause hyperthyroidism?

A

Inflammation of the thyroid gland causes release of preformed hormones from follicular cells

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12
Q

Give examples of drugs which can cause Hyperthyroidism / Hypothyroidism (TAIL)

A

Thyroxine
Amiodarone
Iodine
Lithium

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13
Q

What is the difference between primary and secondary hyperthyroidism?

A

Primary -> within thyroid gland

Secondary -> within pituitary gland

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14
Q

How does pregnancy cause hyperthyroidism?

A

Gestional hyperthyroidism is caused by beta-hCG stimulation of follicular cells to release T3/T4

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15
Q

How does a pituitary adenoma cause hyperthyroidism?

A

Excess TSH release causing T3/T4 release

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16
Q

What are the classical findings unique to Graves disease which other hyperthyroidism conditions do not have? 3 examples

A
  • Pre-tibial myxoedema
  • Thyroid eye disease
  • Thyroid acropatchy
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17
Q

In primary hyperthyroidism, what are the TSH, T3, T4 levels?

A

TSH - Low (due to feedback)

T3/T4 - High

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18
Q

In secondary hyperthyroidism, what are the TSH, T3, T4 levels?

A

TSH - High (due to impaired feedback)

T3/T4 - High

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19
Q

In subclinical hyperthyroidism, what are the TSH, T3, T4 levels?

A

TSH - Low (due to feedback)

T3/T4 - Normal

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20
Q

What are the uptake patterns in a radionuclide scan in a:

  • Graves disease patient
  • Toxic single nodule patient
  • Toxic multinodular patient
  • Thyroiditis patient
A
  • Graves disease patient - diffuse uptake
  • Toxic single nodule patient - single area of uptake
  • Toxic multinodular patient - patchy uptake
  • Thyroiditis patient - reduced / absent uptake
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21
Q

What is the best advice to give a Grave’s disease patient to limit their chance of developing Thyroid eye disease?

A

Stop smoking

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22
Q

What non-specific treatment can be offered to all Hyperthyroidism patients, regardless of the cause?

A

Beta blockers

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23
Q

What are the treatment options for Graves disease?

A

Beta blockers +

Anti-thyroid drugs, thyroidectomy or radio-iodine

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24
Q

What are the treatment options for a toxic nodular goitre?

A

Beta blockers +

Due to relapse from anti-thyroid drugs, radio-iodine is preferred or thyroidectomy

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25
Q

What are the treatment options for thyroiditis?

A

Beta blockers +

Resolve on their own

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26
Q

Give three examples of anti-thyroid drugs. What is their MoA?

A

Carbimazole, Methimazole
Propylthiouracil

They inhibit thyroid peroxidase

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27
Q

Out of Carbimazole, Methimazole and Propylthiouracil. Which are preferred?

A

Carbimazole and Methimazole > Propylthiouracil*

However, Prophythiouracil is preferred during pregnancy

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28
Q

What are the adverse side-effects associated with Anti-thyroid drugs? Are there any specific side-effects

A

Skin rash, itchiness, joint pain, agranulocytosis

In Carbi / Methamizole -> Cholestatic liver disease
In Prophylthiouracil -> Fulminant hepatic failure

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29
Q

What are the two dosing regimens for Anti-thyroid drugs?

A
  • Titration regimen -> Dose of drug based on TFTs to partially block T4 secretion
  • Block-and-replace regimen -> High dose of Anti-thyroid drug + Levothyroxine
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30
Q

State two side-effects of Radio-iodine therapy for hyperthyroidism

A
  • Hypothyroidism

- Worsening of eye-disease

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31
Q

What is the most common hypothyroidism disorder in the developed world? In the developing world?

A

Developed world: Auto-immune thyroiditis (Hashimoto’s)

Developing world: Iodine deficiency

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32
Q

What are some complications of thyroidectomy surgery?

A

Vocal cord paralysis

Hypoparathyroidism (hypocalcaemia)

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33
Q

How are periods affected in Hyperthyroidism and Hypothyroidism?

A

Hyperthyroidism: Oligomenorrhoea, amenorrhoea
Hypothyroidism: Menorrhagia

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34
Q

Myxoeodema coma is associated with Hyperthyroidism or Hypothyroidism?

A

Hypothyroidism

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35
Q

What two findings on blood tests are common in patients with untreated Hypothyroidism?

A

Hyponatraemia

Hypercholesterolaemia

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36
Q

Failure to comply with Thyroxine treatment in Hypothyroidism patients results in what affect on TSH and free T4?

A

High TSH

Low free T4

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37
Q

Primary hypothyroidism is denoted by what levels of T4 and TSH?

A

Low free T4

High TSH

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38
Q

Secondary hypothyroidism is denoted by what levels of T4 and TSH?

A

Low free T4

Low or normal TSH

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39
Q

Subclinical hypothyroidism is denoted by what levels of T4 and TSH?

A

Normal T4

High TSH

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40
Q

What is the main treatment for Hypothyroidism?

A

Lifelong Levothyroxine

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41
Q

What antibodies can be tested to diagnose Hashimoto’s?

A

Thyroid peroxidase antibodies

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42
Q

What is the characteristic finding on palpating Subacute (de Quervain’s) thyroiditis?

In the history for Subacute Thyroiditis, what may be found?

A

Tender thyroid gland

A previous viral infection

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43
Q

What is Pemberton’s sign?

A

When a patient presents with facial flushing on raising their arms. Caused by compression of vascular structures in thoracic inlet

Due to a goitre

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44
Q

When might a euthyroid goitre be excised?

A
  • Due to malignancy
  • If patient has symptoms of tracheal obstruction
  • When goitre is rapidly growing / cosmetic problem
45
Q

What are the investigations of choice for a goitre?

A

TFTs
TSH and TPO antibodies
Ultrasound

46
Q

State the four main types of thyroid cancer

A
  • Papillary
  • Follicular
  • Anaplastic
  • Medullary
47
Q

Which of the thyroid cancer subtypes are derived from Follicular cells?

A

Papillary, follicular, anaplastic

48
Q

Which of the thyroid cancer subtypes are derived from Parafollicular cells?

A

Medullary

49
Q

Which is the most common thyroid cancer? What is second most common?

A

Papillary - most common

Follicular - 2nd most common

50
Q

Which of the thyroid cancer subtypes are “differentiated”?

A

Papillary

Follicular

51
Q

Which of the thyroid cancer subtypes are “undifferentiated”?

A

Anaplastic

52
Q

Which of the thyroid cancer subtypes have the best prognosis and worst prognosis?

A

Papillary - best prognosis

Anaplastic - worst prognosis

53
Q

Which of the thyroid cancer subtypes are use Calcitonin as a tumour marker?

A

Medullary

54
Q

Which of the thyroid cancer subtypes are use Thyroglobulin has a tumour marker?

A

Papillary

Follicular

55
Q

Which of the thyroid cancer subtypes are common in young females?

A

Papillary

56
Q

Which of the thyroid cancer subtypes are common in older women?

A

Anaplastic

57
Q

Which of the thyroid cancer subtypes are associated with MEN2 syndrome?

A

Medullary

58
Q

Which of the thyroid cancer subtypes are associated with the RET oncogene?

A

Medullary

59
Q

What is the diagnostic instrument of choice for thyroid cancer?

A

Fine needle aspiration

60
Q

Vitiligo is associated with which, Hypo or hyperthyroidism?

A

Hypothyroidism

61
Q

Thyrotoxic storm is treated how?

A

Beta blockers, propylthiouracil and hydrocortisone

62
Q

ACROMEGALY

  1. What is it?
  2. What is the pathophysiology of Acromegaly?
  3. What are some symptoms associated with Acromegaly?
A
  1. A multisystem disorder characterised by excessive growth hormone from the anterior pituitary gland
    • Somatotroph adenoma of pituitary gland or..
    • Ectopic secretion in lungs / pancreas of..

Pulsatile secretion of growth hormone -> acts on Insulin-like growth factor 1 which regulates cell division / cell apoptosis

    • Large hands and feet
    • Parasthesia (due to carpal tunnel syndrome)
    • Macroglossia / Interdental septation / Strong jaw
    • Obstructive sleep apnoea
    • Polyuria / polydypsia (diabetes)
    • Visual defects (bitemporal hemianopia)
    • Frontal bossing, headaches
    • Polyarthalgia
63
Q

What is the childhood version of Acromegaly?

A

Giantism

64
Q

5% of Acromegaly are associated with which genetic condition?

A

MEN1 syndrome

65
Q

What is the first-line diagnostic test for Acromegaly? What are other tests?

A
  • Insulin-like growth factor 1 - first line

Other tests:

  • GH measurements after glucose tolerance (should normally decrease)
  • Serum prolactin (may increase in 20% cases)
  • MRI pituitary gland
  • 12-Lead ECG for cardiomyopathy
  • Visual field testing
66
Q

What are the treatments for Acromegaly?

A
  • Transphenoidal surgery (first-line)
  • Dopa agonists i.e. Cabergoline, Bromocriptine
  • Somatostatin analogue i.e. Octreotide
  • GH receptor antagonist i.e. Pegvisomant
67
Q

Addison’s disease is also known as..?

What are the features?

A

Primary adrenal insufficiency

Lethargy, weakness, anorexia, nausea, vomiting, weight loss, salt craving, hyperpigmentation, vitiligo, postural hypotension

68
Q

What is the most common cause of Addison’s disease in the developed world? In the developing world?

A

Developed world: Auto-immune

Developing world: Tuberculosis

69
Q

What would be found on U&Es and on an ABG in patients with Addison’s disease?

A

Hyponatraemia
Hyperkalaemia
Metabolic acidosis

70
Q

What do different regions of the Adrenal Cortex produce?

A

Zona Glomerulosa: Aldosterone
Zona Fasciculata: Cortisol + other Glucocorticoids
Zona Recticularis: Androgens

71
Q

What findings would be present in patients where the Zona Glomerula were affected in Addison’s disease?

A

Loss of aldosterone, hence hyponatraemia, hyperkalaemia, metabolic acidosis. Hypovolaemia (postural hypotension) could also occur

72
Q

What findings would be present in patients where the Zona Fasciculata were affected in Addison’s disease?

A

Loss of cortisol, hence hypoglycaemia. Upregulation of POMC and CRH hence occurs, producing more ACTH and MSH leading to hyperpigmentation

73
Q

What findings would be present in patients where the Zona Recticularis were affected in Addison’s disease?

A

Little effect in men, however women may lose pubic hair and their sex drive

74
Q

What things may trigger an Addisonian crises?

A

Infection, surgery, stress, abruptly stopped steroids

75
Q

What are symptoms of an Addisonian crisis?

A

Vomiting and diarrhoea
Low blood pressure
Sudden pain in back, knees, legs

76
Q

How do you treat an Addisonian crises?

A

High dose corticosteroids

IV saline

77
Q

On X-ray, what finding may be present in a patient with Addison’s?

A

Calcification of the adrenal glands

78
Q
  1. What are some investigations used to investigate Addison’s disease?
A
  • U&Es, hyponatraemia, hyperkalemia
  • ABG - Metabolic acidosis
  • Short Synacthen test = Cortisol fails to increase after 30mins
  • Morning Serum Cortisol, will be low in < 100 = abnormal
  • Plasma Aldosterone levels = Low
  • Plasma Renin = High
  • Endogenous ACTH measurements = High
  • Anti-adrenal antibodies i.e. 21-hydroxylase antibodies
79
Q

What is the first-line diagnostic test for Addison’s disease? How is it performed, what results could you expect?

A

Short Synacthen test

Administer IM Synacthen, then measure Cortisol 30 mins after. If Cortisol fails to increase -> Addison’s

80
Q

What findings for Cortisol and ACTH would you expect in Primary adrenal insufficiency?

A

Cortisol - Low

ACTH - High

81
Q

What findings for Cortisol and ACTH would you expect in Secondary adrenal insufficiency?

A

Cortisol - Low

ACTH - Normal / Low

82
Q

In Secondary adrenal insufficiency, why do you not see hyperpigmentation?

A

Secondary adrenal insufficiency is characterised by low / normal levels of ACTH. A lack of ACTH production means that there is also a lack of POMC, and hence a lack of MSH which causes hyperpigmentation

In primary adrenal insufficiency the low Cortisol sends a feedback mechanism to upregulate ACTH which does so by increasing POMC (its pre-cursor) to synthesis both ACTH and MSH

83
Q
  1. What is the treatment for Addison’s disease?
  2. During acute illness, what changes?
  3. What does hydrocortisone and Fludrocortisone replace?
A
  1. Hydrocortisone + Fludrocortisone
  2. Double hydrocortisone, keep Fludrocortisone the same
  3. Hydrocortisone replaces cortisol, Fludrocortisone replaces Aldosterone
84
Q

What is the treatment for Myxoedemic coma?

A

Levothyroxine + Hydrocortisone

85
Q

If an Addison’s disease patient is systemically unwell, how would you change their treatment regime of Hydrocortisone and Fludrocortisone?

A

Double hydrocortisone only

86
Q

In Sick Euthyroid syndrome, what are the expected T3, T4 and TSH levels?

A

T3 - Low
T4 - Low
TSH - Low / Normal

87
Q

What is Phaeochromocytoma?

A

Tumour of adrenal medulla, which secretes excessive catecholamines i.e. Adrenaline and Noradrenaline

88
Q

What are the symptoms of Phaeochromocytoma?

A

Headaches, sweating, palpitations - classic

Anxiety, hypertension, tachycardia, pallor

89
Q

How do you diagnose Phaeochromocytoma?

A

24-hour urine Metacholamines

90
Q

What is the initial treatment for Phaeochromocytoma? What may be considered after?

A

Alpha blockers: Phenoxybenzyamine, Doxasozin
Beta blockers: Propanolol / Bisoprolol

ALWAYS GIVE ALPHA BLOCKERS FIRST to avoid hypertensive crises / massive vasoconstriction

Surgery later

91
Q

Which drug can be used as both an Alpha and Beta blocker for Phaeochromocytoma?

A

Labetalol

92
Q

What four conditions are associated with Phaeochromocytoma?

A

MEN2a Syndrome
MEN2b Syndrome
Von Hippel Lindau Syndrome
Neurofibromatosis Type 1

93
Q

Cushing’s syndrome is associated with which condition?

A

MEN1 syndrome

94
Q

What is the most common cause of Cushing syndrome?

A

Exogenous steroid use

95
Q

What is the first-line diagnostic test for Cushing’s?

A

Overnight Dexomethasone Supression test

96
Q
  1. What does it mean if on a Overnight Dexamethasone Suppression test there is low cortisol when giving 1mg Dexamethasone?
  2. What does it mean if on a Overnight Dexamethasone Suppression test there is high cortisol when giving 1mg Dexamethasone?
  3. What does it mean if on a Overnight Dexamethasone Suppression test there is low cortisol when giving 8mg Dexamethasone?
  4. What does it mean if on a Overnight Dexamethasone Suppression test there is high cortisol when giving 8mg Dexamethasone?
  5. What does it mean if on a Overnight Dexamethasone Suppression test there is high cortisol and low ACTH when giving 8mg Dexamethasone?
  6. What does it mean if on a Overnight Dexamethasone Suppression test there is high cortisol and high ACTH when giving 8mg Dexamethasone?
A
  1. This is NORMAL
  2. Cushing SYNDROME
  3. Cushing’s Disease i.e. Pituitary adenoma
  4. Either Adrenal Cushing’s or Ectopic ACTH (need to look at ACTH)
  5. Adrenal Cushing’s
  6. Ectopic ACTH i.e. small cell lung cancer
97
Q

What would be found on U&Es and on an ABG in patients with Cushing’s syndrome?

A

Hypokalaemia

Metabolic alkalosis

98
Q

What is Conn’s also known as?

A

Primary hyperaldosteronism

99
Q

Conn’s is caused by what two conditions?

A

Bilateral adrenal hyperplasia

Unilateral benign adenoma

100
Q

What would be found on U&Es and on an ABG in patients with Conn’s syndrome?

A

Hypokalaemia

Metabolic alkalosis

101
Q

What is the first-line investigation for Conn’s?

A

Aldosterone/Renin ratio

102
Q

What is the treatment for Conn’s syndrome?

A

Bilateral adrenal hyperplasia -> Spirinolactone to increase K+

Unilateral benign adenoma -> Surgery

103
Q

What is the main symptom of Conn’s?

A

Hypertension

104
Q

What is Waterhouse-Friederich syndrome?

A

Bleeding of adrenal gland due to meningitis

105
Q

What is Nelson’s syndrome?

A

ACTH producing adenoma that occurs after the removal of both adrenal glands (bilateral adrenalectomy) which is an operation used for Cushing’s syndrome

106
Q

THYROID STORM

  1. What is it?
  2. What may it be caused by?
  3. What are the features?
  4. What is the management?
A
  1. A life-threatening complication of thyrotoxicosis
  2. May be caused by thyroid surgery, non-thyroid surgery, trauma, infection
  3. Fever, hypertension, tachycardia, nausea, vomiting, confusion, agitation
4.
Treat the underlying cause
Analgesia i.e. Paracetamol
Beta-blockers i.e. Propranolol
Anti-thyroid drugs i.e. Methimazole, Propylthiouracil
Lugol's Iodine
Dexamethasone
107
Q

MYXOEDEMA COMA

  1. What is it?
  2. What are the two main features?
  3. What is the management?
A
  1. A severe form of hypothyroidism
  2. Hypothermia and confusion
  3. IV fluids, IV thyroid replacement, IV steroids, rewarming
108
Q

SIADH

  1. What is the normal function of ADH?
  2. What is SIADH?
  3. What are some cases of SIADH?
  4. What is the main serum electrolyte finding on U&Es?
  5. What is the urine findings for SIADH?
  6. SIADH is a diagnosis of exclusion - what investigations can you do to help rule in / rule it out?
  7. What is a complication of rapid correction of SIADH?
  8. What is the management of SIADH?
A
  1. ADH normally stimulates water reabsorption from the collecting duct in the kidneys
  2. SIADH refers to high levels of ADH and high water reabsorption
  3. Malignancy: Small cell lung cancer, pancreatic cancer, prostate cancer

Neurological: SAH, stroke, encephalitis, meningitis, subdural haemorrhage

Infective: TB, pneumoniae

Drugs: Sulfonylurea, SSRIs, TCAs, cyclophosphamide, Carbamazepine

Other: PEEP, Porphyrias

  1. Euvolemic hyponatremia
  2. High urine osmolality, high urinary sodium
  3. Must exclude other causes of hyponatraemia, i.e. Addison’s disease via Short Synacthen Test, perform CXR to rule out malignancy or chest infection

Ensure patient has not been using diuretics, no diarrhoea / vomiting, no increased water intake, no CKD/AKI

  1. Central pontine myelinolysis
  2. Fluid restriction, ADH receptor antagonists

Medicine, Year 3, Metabolic Medicine (9 decks)

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