T5-L3: Investigating the Endocrine System Flashcards

1
Q

What are the 3 types of hormones?

A
  • Peptide hormones e.g. insulin
  • Steriod hormones e.g. oestrodiol
  • Tyrosine-based hormones - e.g. T4 and T3
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2
Q

Why do patients with hypothyroidism develop hyperprolactinaemia?

A

TRH stimulates prolactin.

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3
Q

What is a likely cause of a patient having a high TSH and high T4?

A

Interference - other hormones could have been picked up.

This can be seen in the neonatal peoriod.

Other causes include thyroid hormone resistance, TSH tumour or a patient is not taking their medication but has taken it just before testing.

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4
Q

Why may a normal TSH indicate further testing is required?

A

If not you may miss causes of secondary hypothyroidism where most patents have normal TSH and low T4.

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5
Q

What is PanHypoPit? What can this lead to?

A

Panhypopituitarism. ACTH deficiency can lead to inadequate cortisol and an adrenal crisis.

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6
Q

What are the 2 main types of adrenal medullary tumours?

A

There are 2 types of adrenal medullary tumours
• Pheochromocytoma (adults)
•Neuroblastoma (children)

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7
Q

Why are Pheochromocytoma said to follow a 10 percent rule?

A
  • 10% in extra-adrenal neuroendocrine cells
    • 10% malignant
    • 10% familial
    • 10% found in children
    • 10% Bilateral
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8
Q

What are the clinical features of Pheochromocytoma?

A

The features are all to do with excess catecholamines:

  • Hypertension
  • Sweating, pallor
  • Panic attacks
  • Headaches
  • abdominal Pain

However some are asymptomatic.

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9
Q

How do we diagnose Pheochromocytoma?

A

This can be difficult as false negative and false positives are not uncommon Catecholamines are fluctuant even in pheochromocytomas We measure plasma metanephrines. These are metabolites of catecholamines and are more constantly high.

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10
Q

What follow up tests can be used after plasma metanephrines in the diagnosis of Pheochromocytoma?

A
  • Clonidine suppression test - Useful in patients with suspected pheochromocytoma and borderline changes in catecholamines or Metanephrines
    • Plasma Chromogranin A
    • MRI or CT of adrenals
    • MIBG scan (nuclear scan test), especially to detect extra-adrenal pheochromocytomas or metastases
    • Genetic counselling and screening for MEN mutations in young patients, or those with a family history
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11
Q

What forms Whipple’s Triad?

A
  • Signs and symptoms of hypoglycaemia
  • Resolution of Symptoms once glucose levels rise
  • low plasma glucose level (less than 3mmol/L)
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12
Q

What does our body do in response to hypoglycaemia?

A
  • Increase Glucagon, switch off insulin, to break down glycogen to increase blood glucose
  • Increase GH, cortisol and adrenaline to increase blood glucose

This leads to activation of fight to flight mode from the adrenaline. We also get neuroglycopenic syndromes due to cognition and lack fo glucose in the brain.

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13
Q

What are signs and symptoms of hypoglycaemia?

A

Symptoms:

  • Hunger
  • Sweating
  • Anxiety
  • Paresthesias
  • palpation
  • Tremurs

Neuroglycopenic symptoms include weakness/fatigue, dizziness, headache, confusion, behavioural change, blurred vision and cognition dysfunction.

Signs:

  • Pallor
  • Tachycardia
  • Widened Pulse

Neuroglycopenic signs include cortical blindness, hypothermia, seizures and coma.

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14
Q

What is an insulinoma?

A

Insulinoma is the most common tumour arising from the islets of Langerhans - has increased production of insulin. It has its highest incidence between 40-60 years. It is most common in females.

Diagnosis is through a simple fasting blood test. The patient would have a low blood sugar, high insulin and high levels of C peptide.

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15
Q

How would be differentiate between ketonic and non; ketonic hypoglycaemia?

A

Measure beta hyddroxybutyrate.

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16
Q

How do we distinguish between exogenous and endogenous hyperglycaemia?

A
  • C peptide helps to differentiate between exogenous and endogenous - if high insulin and low C-peptide this would be consistent with exogenous insulin production. If we administer insulin exogenously it would not have the C-peptide with it
17
Q

What are features of Cushing’s Syndrome?

A
  • Purple Striate
  • Hirsutism
  • Central obesity
  • Thin arms and Legs
  • Glucose intolerance - cortisol is a counter regulator in hypoglycaemia. Cushing’s can therefore lead to abnormally high glucose levels.
  • Moon face
  • Fat pads of the shoulders
  • Obesity due to glucocorticoids, cortisol affects the metabolism
  • HTN - due to cortisol having mineralocorticoid function
  • Bain pain due to osteoporosis
  • Psychiatric disturbances - depression and psychoses
18
Q

What are the 4 causes fo Cushing’s syndrome?

A
  1. Excess cortisol producing a ACTH secreting tumour (Cushing’s disease).
  2. Adrenal adenoma/carcinoma that produces cortisol. there is suppression of ACTH so we get atrophy of the contralateral pituitary. This is a primary cortisol excess.
  3. Secondary Hyperadrenalism via an ectopic ACTH producing tumour. ACTH would be high, often much higher than an ACTH producing tumour.
  4. Iatrogenic causes through uses of steroids
19
Q

What is an ectopic ACTH producing tumour most commonly associated with?

A
▪ Benign carcinoid tumours of the lung
	▪ Small cell tumours of the lung
	▪ Islet cell tumours of the pancreas
	▪ Medullary carcinoma of the thyroid
	▪Tumours of the thymus gland