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Flashcards in Hormones Deck (42)
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1
Q

What cells in the body produce adrenaline

A

chromaffin cells

2
Q

What is adrenaline

A

“catecholamine” hormone and neurotransmitter that stimulates the sympathetic nervous system and is responsible for the “fight or flight” response.

3
Q

What is Phaeochromocytoma

A

Tumour of the chromaffin cells that secretes unregulated and excessive amounts of adrenaline.

4
Q

What are the RF Phaeochromocytoma

A

25% familial

multiple endocrine neoplasia type 2 (MEN 2).

5
Q

What investigations should you carry out in patients with suspected phaeochromocytoma

A

24 hour urine catecholamines

Plasma free metanephrines

6
Q

Why measure urinary vs serum catecholamines

A
  • serum catecholamines: naturally fluctuate

- 24hr urine catecholamines: how much adrenaline is being secreted by the tumour over the 24 hour period.

7
Q

What are the symptoms of Phaeochromocytoma

A
  • Anxiety
  • Sweating
  • Headache
  • Hypertension
  • Palpitations, tachycardia and paroxysmal atrial fibrillation
8
Q

What is the management of Phaeochromocytoma

A
  • Alpha blockers (i.e. phenoxybenzamine)
  • Beta blockers once established on alpha blockers
  • Adrenalectomy to remove tumour is the definitive management
9
Q

What is acromegaly

A

clinical manifestation of excessive growth hormone (GH) by the anterior pituitary gland

10
Q

What is the most common cause of acromegaly

A
  • pituitary adenoma

- rarely lung and pancreatic cancer can secrete ectopic GH or GHRH

11
Q

What happens to te optic chiasm if a pituitary adenoma is allowed to grow

A
  • compresses optic chiasm

- leads to bi-temporal hemianopia

12
Q

What is bi-temporal hemianopia

A

Loss of outer vision of both eyes

13
Q

What are the main presentations of someone with acromegaly

A
  • SOL symptoms
  • overgrowth of tissues
  • organ dysfunction
  • profuse sweating
  • skin tags
14
Q

Which tissues often over grow in patients with acromegaly

A

Prominent forehead and brow (“frontal bossing”)
Large nose
Large tongue (“macroglossia”)
Large hands and feet
Large protruding jaw (”prognathism”)
Arthritis from imbalanced growth of joints

15
Q

What organ dysfunction can be caused by acromegaly

A

Hypertrophic heart
Hypertension
Type 2 diabetes
Colorectal cancer

16
Q

What are the investigations for someone with suspected acromegaly?

A
  • Insulin-like Growth Factor 1 (IGF-1): screening test (raised)
  • Oral glucose tolerance test whilst measuring growth hormone (high glucose normally suppresses growth hormone)
  • MRI brain for the pituitary tumour
  • Refer to ophthalmology for formal visual field testing
17
Q

why not measure GH in someone with suspected acromegaly

A

GH fluctuates throughout the day

18
Q

What is the management of acromegaly

A
  • Trans-sphenoidal removal of the pituitary tumour

- medications to block GH

19
Q

What medications can be used to block GH

A
  • Pegvisomant (GH antagonist)
  • Somatostatin analogues to block GH release (e.g. ocreotide)
  • Dopamine agonists to block GH release (e.g. bromocriptine)
20
Q

What is diabetes insipidus

A

Lack of ADH or lack of response to ADH preventing the kidneys from concentrating urine. Can be classified as nephrogenic or cranial

21
Q

What are the symptoms of diabetes insipidus

A
Polyuria 
Polydipsia 
Dehydration
Postural hypotension
Hypernatraemia
22
Q

What are the causes of nephrogenic diabetes insipidus

A
  • Drugs: lithium
  • Gene Mutations: AVPR2 gene (codes for the ADH R)
  • Intrinsic kidney disease
  • Electrolyte disturbance (hypokalaemia and hypercalcaemia)
23
Q

What are the causes of cranial diabetes insipidus

A
Brain tumours
Head injury
Brain malformations
Brain infections (meningitis, encephalitis and tuberculosis)
Brain surgery or radiotherapy
Idiopathic
24
Q

What is nephrogenic diabetes insipidus

A

collecting ducts of the kidneys do not respond to ADH

25
Q

What is cranial diabetes insipidus

A

hypothalamus does not produce ADH for the pituitary gland to secrete

26
Q

What are the investigations for diabetes insipidus

A

Low urine osmolality
High serum osmolality
Water deprivation test/desmopressin stimulation test

27
Q

How does the water deprivation/desmopressine test work?

A
  • No fluids for 8 hours: fluid deprivation
  • Urine osmolality is measured and synthetic ADH (desmopressin) is administered
  • 8 hours later urine osmolality is measured again.
28
Q

What would you expect to see in patients with cranial diabetes insipidus

A
  • Patient lacks ADH so urine osmolality remains low

- After synthetic ADH Kidneys resorb the water so urine osmolality increases

29
Q

What would you expect to see in patients with nephrogenic diabetes insipidus

A
  • Patient doesn’t respond to ADH so urine osmolality will be low
  • Following synthetic ADH, the kidneys still don’t respond to the urine osmolality will also remain low
30
Q

What would you expect to see in a patient with primary polydipsia

A

8 hours of water deprivation will cause the urine osmolality to be high even before the synthetic ADH is given

31
Q

What is the management of diabetes insipidus

A
  • treat underlying cause

- Desmopressin

32
Q

What is the role of ADH and where is it secreted

A

Anti-diurectic hormone (ADH) is produced in the hypothalamus and secreted by the posterior pituitary gland. It is also known as “vasopressin”. ADH stimulates water reabsorption from the collecting ducts in the kidneys

33
Q

What is SIADH

A

inappropriately large amounts of ADH are secreted

34
Q

What can cause SIADH

A

Post-operative from major surgery
Infection, particularly atypical pneumonia and lung abscesses
Head injury
Medications (thiazide diuretics, carbamazepine, vincristine, cyclophosphamide, antipsychotics, SSRIs, NSAIDSs,)
Malignancy, particularly small cell lung cancer
Meningitis

35
Q

What are the symptoms of SIADH

A
Headache
Fatigue
Muscle aches and cramps
Confusion
Severe hyponatraemia can cause seizures and reduced consciousness
36
Q

What would investigations in SIADH show

A
  • euvolaemic hyponatraemia
  • high urine osmolaity
  • high urinary sodium
37
Q

What are some other causes of hyponatraemia other than SIADH

A
  • Negative short synacthen test to exclude adrenal insufficiency
  • No history of diuretic use
  • No diarrhoea, vomiting, burns, fistula or excessive sweating
  • No excessive water intake
  • No chronic kidney disease or acute kidney injury
38
Q

What is the management of SIADH

A
  • treat the underlying cause
  • fluid restrictions
  • Tolvaptan. “Vaptans” are ADH receptor blockers: very powerful NEED ENDOCRINOLOGIST
39
Q

What is central pontine Myelinolysis/osmotic demyelination syndrome

A

complication of long term severe hyponatraemia (< 120 mmols/l) being treated too quickly (> 10 mmol/l increase over 24 hours).

40
Q

What is the first phase of central pontine Myelinolysis/osmotic demyelination syndrome

A

this is due to the electrolyte imbalance and the patient presents as encephalopathic and confused. They may have a headache or nausea and vomiting. These symptoms often resolve prior to the onset of the second phase.

41
Q

What is the second phase of central pontine Myelinolysis/osmotic demyelination syndrome

A

this is due to the demyelination of the neurones, particularly in the pons. This occurs a few days after the rapid correction of sodium. This may present as spastic quadriparesis, pseudobulbar palsy and cognitive and behavioural changes. There is a significant risk of death.

42
Q

What is the management of central pontine Myelinolysis/osmotic demyelination syndrome

A
  • Supportive

- some clinical improvement but most left with neurological deficits