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Endocrine > Pituitary Disorders > Flashcards

Pituitary Disorders Flashcards

1
Q

This deck covers

A

Hypersecretion disorders:

  • Cushing’s Disease
  • Hyperprolactinaemia
  • Acromegaly

Hyposecretion disorders:

  • Craniopharyngioma
  • Infection
  • Sheehan’s syndrome
  • Cranial Diabetes Insipidus
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2
Q

What is Acromegaly?

A
  • Excess production of Growth Hormone after the long bones fuse (i.e. in adults)
  • Before long bones fuse is gigantism.
  • In acromegaly there is excess growth hormone secondary to a pituitary adenoma in over 95% of cases.
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3
Q

How does acromegaly present?
Symptoms [7]
Signs [6]

A

Symptoms

  • Rings and shoes no longer fitting
  • Headaches
  • Wonky bite
  • Sweating, snoring (OSAS)
  • Amenorrhea, reduced libido
  • Galactorrhea
  • Paresthesia

Signs

  • Coarse facial features
  • Increased growth of hands, jaw, feet
  • Macroglossia, puffy lips, eyelids
  • Scalp folds, skin darkening, acanthosis
  • Goitre
  • CTS

Remember features of a pituitary tumour: hypopituiraism, headaches, bitemporal hemianopia

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4
Q

What complications can arise from excess GH? [5]

What kind of follow up is required post-treatment of acromegaly? [5]

A
  • Chiasmal Compression
  • DM, Hypertension
  • Cardiomyopathy
  • Accelerated Osteoarthritis
  • Colonic Polyps & adenoma > CRC

Follow up:

  • Annual GH and IGF-1
  • OGTT
  • Visual field and vascular assessment
  • BMI
  • Photos
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5
Q

How would you test someone for Acromegaly? [4]

Treatment options [3]

A
  1. Visual Field Testing (chiasmal compression –> Bitemporal Hemianopia)
  2. Screen potential patients for IGF-1 Elevation - also used in monitoring of patients
  3. Confirm diagnosis with an OGTT if IGF-1 unequivocal. Acormegaly is diagnosed with GH suppressed.
  4. MRI for pituitary tumour

Treatment

  • Transphenoidal resection
  • Somatostatin analogues OCTREOTIDE monthly IM (inhibits GH)
  • GH receptor antagonist PEGVISOMANT, OD S/C.
  • Bromocriptine has been superceded.
  • External irradiation following failed surgical/medical tx in older patients.
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6
Q

What is Cushing’s Disease? [2]

A

Excessive Glucocorticoids [1] due to the excessive ACTH [1] release from pituitary

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7
Q

Presentation Cushing’s disease
Symptoms [6]
Signs [8]

A

Symptoms:

  • Easy bruising, Acne
  • Mood change
  • irregular periods
  • Recurrent Achilles tendon rupture
  • Increased hair growth
  • Swelling, weight gain

Signs:

  • DM
  • HTN, HF due to Na retention
  • Thin purpuric skin, pink striae
  • Proximal myopathy, atrophy
  • Osteopororsis
  • Facial mooning & plethora, pendulous breasts, abdomen
  • Edema, central obesity, supraclavicular fat, buffalo neck hump
  • Virilisation (masculinization)
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8
Q

What are the various causes of Cushing’s? [6]

A

ACTH dependant:

  • Pituitary Tumour ‘Cushings disease’
  • Ectopic ACTH (SCLC)

ACTH independent:

  • Adrenal adenoma 5-10% producing cortisol
  • Adrenal carcinoma is rare
  • CCS therapy
  • Carney complex
  • Micronodular adrenal dysplasia

Pseudo-Cushing’s: alcohol excess, severe depression

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9
Q

Cushing’s disease investigation algorithm

A

Tests to confirm Cushing’s syndrome:

  1. Overnight dexamethasone suppression test
    - 1mg oral at midnight then serum cortisol at 8am
  2. 24h urine cortisol

Localisation test
1. Paired morning & midnight ACTH-Cortisol
- If ACTH undetectable > ACTH-independent
- If ACTH detectable > ACTH dependent
2. High dose dexamethasone suppression test
8mg
- If cortisol is suppressed then pituitary adenoma
- If cortisol is not suppressed then ectopic ACTH likely

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10
Q

What can cause hyperprolactinaemia?

Split into 3 categories - give at least 2 eg of each

A

Physiological

  • Pregnancy
  • Lactation/stress
  • Stress

Pharmacological
* Dopamine antagonists or DA depleting
* Oestrogens (doesn’t include OCP)
* Antidepressants

Pathological
* Primary hypothyroidism
* Pituitary tumour

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11
Q

Give an example of each drug (DA depleting and DA antagonist) that causes hyperprolactinemia

How do we classify prolactinoma that also influences the treatment that it receives? [2]

A

Neuroleptics eg chlorpromazine
Anti-emetics eg metoclopramide

A microprolactinoma is <10mm
A macroprolactinoma is >10mm

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12
Q

How does hyperprolactinaemia present in women [3] and men [6]

A

Women:

  • Galactorrhoea
  • Menstrual irregularity
  • Infertility

Men:

  • Impotence
  • Visual field abnormalities
  • Headache
  • Extraocular muscle weakness
  • Other pituitary malfunction
  • Eventual galactorhea

Men present later due to less obvious early warning symptoms

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13
Q

Investigation [2]

How do you manage hyperprolactinaemia? [1]

A

Test Serum PRL
Elevated? –> Pituitary MRI
Treat with dopamine agonist Cabergoline

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14
Q

What is the primary management for all pituitary tumours?

Compare to this to the management of prolactinomas and give a reason for this difference [2]

A
  • Transphenoidal surgery to remove it +/- radiotherapy
  • Dopamine agonists - bromocriptine, cabergoline (1xweekly) can shrink prolactinomas.
  • Surgery is usually not indicated due to high response rate
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15
Q

What are the signs of hypopituitarism? [5]

What are 2 signs specific to hypopituitarism in children

A 
Tiredness, Weight gain, Depression
Lost libido, Impotence
Menstrual problems
Skin pallor
Reduced body hair

Children: reduced linear growth, delayed puberty

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16
Q

What is Cranial Diabetes Insipidus?

A
17
Q

How does CDI present? [2]

What are the dangerous sequelae? [2]

A

No vasopressin means huge amounts of urine [1] and consequent thirst [1]

Risk of dehydration [1] & hypokalemia [1]

18
Q

What causes CDI? [4]

A

Cranial DI - NO secretion of ADH
Nephrogenic - decreased sensitivity to ADH
Gestational DI - degradation of vasopressin by placental vasopressinase
Primary polydipsia - primary defect in osmoreg of thirst

19
Q

How do we test for CDI? [3]

A

Water deprivation test [1] - deprive fluids for 8h [1] then introduce desmopressin 2mcg [1]

  • Cranial DI: responds to ADH causing increase serum osmolality (kidneys are responsive)
  • Nephrogenic DI: unable to respond to ADH, kidneys dont respond. Urine osmolality stays low.
20
Q

What could a pituitary tumour press on? [2]

A
  • Optic chiasm

- Cavernous sinus nerves

21
Q

Causes of pituitary hypofunction [4]

A

Craniopharyngioma
Trauma
Infection - TB, sarcoidosis
Sheehan’s syndrome

22
Q

Management of cranial DI
Mild cases [1]
Main rx [1]
Monitoring [1]

Emergency management [5]

A

If mild, drinking water can do the trick [1]
Physiological replacement of desmoproressin [1]
Measure serum sodium 1-3 monthly for high Na

Emergency mx:

  • ABCDE
  • Urgent U&E, serum and urine osmolality, monitor urine output
  • Fluids: hypernatremic 0.9% saline with aim of reducing Na no more than 12 mmol/L per day
  • Desmopressin
23
Q

In testing for acromegaly, why is it not wise to rely on random testing of Growth Hormone?

A
  • GH: DO NOT rely on random testing as secretion is pulsatile and levels in acromegaly can overlap with normal pulsations and GH is also elevated in stress, sleep, puberty and pregnancy
24
Q 
Mx Cushing's disease:
Iatrogenic
Cushing's disease
Adrenal adenoma
Adrenal carcinoma [3]
Ectopic ACTH
Severe ACTH associated
A
  1. Stop CCS
  2. Cushing’s disease: transphenoidal excision of pituitary adenoma
  3. Adrenal adenoma: adrenalectomy
  4. Adrenal carcinoma: adrenalectomy, RT, adrenolytic drugs (mitotane)
  5. Ectopic ACTH: surgery
  6. Severe ACTH associated psychosis - intubation, mifepristone, etomidate
25
Q

Cushing’s disease vs syndrome [2]

A

Cushing’s Disease - pituitary source of ACTH

Cushing’s Syndrome - ACTH independent ie adrenal tumor or exogenous CCS

26
Q

What is the effect of pegvisomant on Acromegaly

A

very effective - decreases IGF-1 levels in 90% of patients to normal
doesn’t reduce tumour volume therefore surgery still needed if mass effect

27
Q

Hypopituitarism causes [5]

A
  • congenital empty sella
  • pressure from pituitary tumours
  • post-irradiation
  • post-surgery
  • pituitary infarction
28
Q

Hypopituitarism Investigations

A
  • Baseline bloods - 09.00 hours cortisol, LH/FSH, oestradiol, testosterone, TSH and fT4, prolactin
  • Insulin tolerance test ITT or glucagon test to confirm GH and ACTH reserve
  • Hypoglycaemia and glucagon should cause increase in cortisol and GH where pituitary is functioning
  • GnRH stimulation is rarely used to assess gonadotrophins.
29
Q

Management of hypopituitarism

A
  • Hormone replacement therapy is essential.
  • ACTH deficiency is treated with hydrocortisone replacement in a regime similar to that in adrenal insufficiency (e.g. 10 mg on waking, 5 mg at midday and 5 mg at 18.00 hours)
  • Similarly, the resulting secondary hypothyroidism is treated with levothyroxine and gonadotrophins with oestrogen or testosterone.
  • It is important to replace or confirm ACTH reserve before commencing thyroxine as the resulting increase in metabolism could otherwise precipitate an Addisonian crisis.
    690
  • In adults, replacement of GH (subcutaneously) will often relieve symptoms of low mood and fatigue.

Endocrine (25 decks)

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