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Endocrine > Pituitary disease > Flashcards

Pituitary disease Flashcards

1
Q

What are the different causes for raised prolactin?

A

Physiological: breast feeding, pregnancy, stress, sleep

Drugs: dopamine antagonists (metoclopramide), antipsychotics, antidepressants (TCAs and SSRIs)

Pathological: hypothyroidism, pituitary stalk lesion, prolactinoma (prolactin producing pit. adenoma)

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2
Q

What are the clinical signs and symptoms for hyperprolactinaemia in males/females?

A

Males:

  • late presentation
  • galactorrhea <30%
  • visual field abnormality
  • headache
  • impotence
  • anterior pit. malfunction

Females:

  • early presentation
  • galactorrhea 30-80%
  • menstrual irregularity
  • amenorrhoea
  • infertility
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3
Q

What are the different investigations for prolactinoma?

A
  • prolactin concentration
  • MRI pituitary: pit. stalk, optic chiasm, microprolactinoma <1cm, macroprolactinoma >1cm
  • visual field: bitemporal hemianopia
  • pituitary function tests if other hormones affected
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4
Q

What is the medical treatment of prolactinoma?

A

Dopamine agonists:

  • bromocriptine 2x a day orally
  • quinagolide 1x a day orally
  • cabergoline 2x a week orally (less side effects)

Results: prolactin normalised/tumour shrinkage

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5
Q

What is acromegaly?

A

GH excess due to somatrophadenoma, which stimulates IGF1 = mediator of GH actions

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6
Q

What are the features of acromegaly?

A
  • giant if before epiphyseal fusion
  • thickened soft tissues (skin/jaw/hands)
  • HTN/cardiac failure
  • headaches
  • snoring/sleep disturbance
  • DM
  • local pituitary affects: visual field, hypopituitarism
  • early CV death
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7
Q

What investigations are involved in the diagnosis of acromegaly?

A
  • IGF1
  • GTT
  • visual field
  • CT/MRI pituitary
  • pituitary function tests
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8
Q

What is the treatment of acromegaly?

A

pituitary surgery than retest GTT and if still >11g/l needs dopamine agonists:
-carbegoline/ocreotide/pegvisomant

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9
Q

What is cushings syndrome? what is cushings disease?

A

Excess cortisol/mineralocorticoids/androgen

-cushings disease is specifically due to an excess of ACTH

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10
Q

What symptoms and signs are seen in cushings syndrome?

A

Excess cortisol:

  • protein loss = myopathy/wasting, osteoporosis, thin skin (bruising)
  • altered carb/lipid metabolism = DM/obesity
  • altered psyches = psychosis/depression

Excess mineralocorticoid = hypertension and oedema (conjunctival oedema)

Excess androgen = virilism, hirsutism, acne, oligo/amernorrhea (frontal balding in women)

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11
Q

How is cushings tested for?

A

Dexamethasone suppression test

Screening:

  • overnight 1mg DST = if cortisol <50nmol/l next morning is normal, if cortisol >100nmol/L is abnormal
  • urine free cortisol <250 = normal
  • cortisol/creatinine ratio <25 = normal
  • diurnal cortisol variation

measure ACTH to see whether it is a pituitary cause or ectopic (that produces ACTH)

Diagnosis: 2 day 2mg DST

  • <50nmol/L after last dose = normal
  • suppress an adenoma 50%
  • won’t suppress an ectopic
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12
Q

What is the epidemiology of cushings syndrome?

A

rare, commoner in women 20-40yrs

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13
Q

What are the different causes of cushings syndrome? split into 4 groups

A

Pituitary adenoma 80%+

Adenoma adrenal gland: benign/malignant

Ectopic: thymus, lung, pancreas (paraneoplastic secretes ACTH)

Pseudo: alcohol, depression, long term steroid medication (causes adrenal atrophy)

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14
Q

Describe the management of iatrogenic cushings syndrome?

A

Patients are unable to respond to stress and need extra doses if ill/surgery

  • can’t stop suddenly
  • gradual withdrawal steroid
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15
Q

Treatment of cushings syndrome if:

  • pituitary
  • adrenal
  • ectopic

What drug treatment is available?

A

Pituitary:
-hypophysectomy and if recurs external radiotherapy

Adrenal:
-adrenalectomy

Ectopic:
-remove source or bilateral adrenalectomy

Drug treatment:

  • metyrapone (if other treatments fail or whilst waiting for radiotherapy to work, S/E common)
  • ketoconazole
  • pasireotide (new somatostatin analogue)
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16
Q

What affects does pan-hypopituitarism cause due to the

  • anterior pituitary
  • posterior pituitary
A

Anterior pituitary:

  • growth failure
  • hypothyroid
  • hypogonadism
  • hypoadrenalism

Posterior pituitary:
-Diabetes insipidus

17
Q

List causes of pan-hypopituitarism

A

¥ Pituitary Tumours

¥ Secondary metastatic lesions
Ð lung, breast

¥ Local brain tumours
Ð Astrocytoma, meningioma, glioma

¥ Granulomatous diseases
Ð TB, Histiocytosis X, sarcoidosis

¥ Vascular diseases
Ð Polyarteritis

¥ Trauma
Ð road accidents, skull fractures

¥ Hypothalamic diseases
Ð Syphilis, meningitis

¥ Iatrogenic; surgery

¥ Autoimmune;Sheenan – post pregnancy
Infection; meningitis

18
Q

What are the symptoms and signs of pan-hypopituitarism?

A 
¥	Menstrual irregularities (F)
¥	Infertility, impotence
¥	Gynaecomastia (M)
¥	Abdominal obesity
¥	Loss of facial hair (M)
¥	Loss of axillary and pubic hair (M&amp;F)
¥	Dry skin and hair
¥	Hypothyroid faces
¥	growth retardation (children)
19
Q

How is pan-hypopituitarism tested for?

A 
Baseline pituitary function tests:
¥	fT4, TSH		
¥	Oestradiol/Testosterone,  LH FSH
¥	GH, IGF-1    
¥	Prolactin
20
Q

How is pan-hypopituitarism treated?

A

¥ Thyroxine 100-150mcg/day

¥ Hydrocortisone 10-25 mg/day (am/pm)

¥ ADH Desmospray (nasal) or tablets

¥ GH nightly sc

¥ Sex Steroids Oest/prog pill for F. Testosterone for males

Always give hydrocortison first before thyroxine otherwise adrenal crisis may precipitate

21
Q

How is testesterone replaced in pan-hypopituitarism? what are the risks?

A

¥ IM injection every 3-4 weeks (sustanon)
¥ Skin gel (testogel, tostram)
¥ Prolonged IM injection 10-14 wks (nebido)
¥ (Oral tablets (restandol))

Risks:
¥ Prostate Enlargement. Does NOT cause prostate cancer but may make it grow - monitor PR exam and PSA
¥ Polycythaemia- monitor FBC
¥ Hepatitis (only for oral tablets)- monitor LFTs

22
Q

what is cranial diabetes insipidus? what is nephrogenic?

A

Cranial - lack secretion ADH (vasopressin)

Nephrogenic - renal resistance to ADH

23
Q

what causes exist for cranial diabetes insipidus?

A

¥ Familial
Ð isolated in most cases
Ð DIDMOAD (DI, DM, optic atrophy, deaf)

¥ Acquired
Ð Idiopathic in 50%
Ð Trauma; road accidents, surgery, skull fracture

¥ RARE
Ð Tumour, sarcoid, ext irradiation, meningitis

24
Q

What is the treatment for cranial diabetes insipidus?

A

¥ Desmospray
Ð nasally; 10- 60 mcg/day

¥ Desmopressin oral tablets
Ð 100-1000mcg per day

¥ Desmopressin sublingual tablets
- 60 – 360 mcg per day

¥ Desmopressin injection
Ð 1-2mcg IM per day

25
Q

What is SIADH secretion?

A

ectopic production ADH - paraneoplastic syndrome

26
Q

Pituitary adenoma:

  • what two different types exist?
  • how are they classified?
A

sporadic or assoc. with MEN1

Classify by cell type/hormone produced:
-prolactin
-ACTH (bilateral adrenocortical hyperplasia)
-FSH/LH
-GH
-non-functional/hypo
(prolactinoma is most common functional tumour and growth hormone secretion is second most common)

27
Q

What clinical symptoms/signs do large adenomas produce?

A

Visual field defects
Pressure/atrophy of surrounding tissue
infarction could lead to pan-hypo

28
Q

Craniopharyngioma:

  • what is this derived from?
  • what is the pathology?
  • what is the incidence?
  • what clinical features are seen?
  • prognosis?
A

Derived from remnants rathke’s pouch
-slow growing, often cystic, may calcify

Bimodal incidence: 5-15yrs and 60-70yrs

Clinical features:
-headaches and visual disturbance - children may have growth retardation

Prognosis:
-good esp. if <5cm

Endocrine (18 decks)

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