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Medicine (Year 5) > Endocrine (Pituitary disorders) > Flashcards

Endocrine (Pituitary disorders) Flashcards

1
Q

pituitary disorders

A

Disorders of the pituitary are rare, and can manifest themselves as either an over or under secretion of pituitary hormone.

Clinical presentation of pituitary tumours
1. Mass effect of tumour on local structure- visual loss, headache
2. Abnormality in pituitary function – hypo or hyper-secretion

Most commonly caused by pituitary adenoma- a benign pituitary tumour

  • Most tumours are non-functioning (do not produce any homrones), but cause inadequate production of one or more pituitary hormone due to the physical pressure of the growing tumour on the glandular tissue.
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2
Q

symptoms of pituitary tumour

A

Symptoms of mass movement:
- Headaches
- Visual loss- bitemopar heminamopia
- Nausea and vomiting

Functioning tumour (hyper-secreting)
- Rarer
- Clinical symptoms dependent on which pituitary hormone they are over-secreting and its systemic effects

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3
Q

When a tumour blocks the hypothalamic-pituitary access…

A

1) Hormones that decrease (due to being under positive control of hormones produced in the hypothalamus)

  • GH
  • LH/FSH
  • TSH
  • ACTH

2) Hormones that will increase (due to be under under negative control of hormones produced in the hypothalamus)

  • Prolactin (positive control by dopamine)
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4
Q

Acromegaly

A

excess growth hormone prduced by the pituitary after closure of growth plate. Leads to:
- overgrowth of all organ systems: bones, joints, soft tissue

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5
Q

Gigantism

A

is where excess GH release occurs before the end of puberty and growth plate closure, leading to excess height.

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6
Q

pathophysiology of acromegaly

A
  • Excess GH secretion from pit adenoma or ectopic neuroendorcrine tumours e.g. GI tumour
  • GH stimulates the production of insulin-like growth factor 1 (IGF-1) which plays an important role in growth.
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7
Q

presentation acromegaly

A

features sdue to excess GH/IGF-1

Facial

  • frontal bossing
  • enlarged nose
  • prognathism
  • maxillary widening
  • macroglossia

Skin, soft tissue and bone

  • increased sweating and oily skin
  • thicker skin
  • increased foot and hand size
  • osteoarthritis

CVD

  • HTN
  • hypertrophic caediomyoparthy

Endocrine

  • impaired glucose tolerance
  • DM
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8
Q

GH can be co-secreted with

A

prolactin

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9
Q

Features due to prolactin co-secretion

A

Prolactin co-secretion is seen in 1/3 of patients:

  • Galactorrhoea
  • Decreased libido
  • Erectile dysfunction
  • Oligomenorrhoea/amenorrhoea
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10
Q

acromegaly: Features due to tumour mass effects

A
  • Visual field defects – classically a bitemporal hemianopia
  • Headaches
  • Hypopituitarism if other parts of the pituitary gland are compressed
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11
Q

investigations for acromegaly

A

1) Serum insulin-like growth factor 1 (IGF-1)
- initial screen
- IGF-1 rises with GH

2) OGYY + measure GH

  • done aftewr initial IGF-1 screen to confirm diagnosis
  • GH is supressed agfter consuming glucose in unaffected patinets, in acromegaly there is a failure of suppression
  • GH is not suppressed to <1ug/L after OGTT

3) Pituitary MRI

  • may demonstrate adenoma- can be missed if very small
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12
Q

OGTT and GH

A

GH levels will not be suppressed after consuming glucose
- GH >1 ug/L after OGTT

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13
Q

management of acromeg

A

First line: trans-sphenoidal surgery

Second line:
- Somatostatin analogue e.g. Octreotide - most effective drug.
- GH receptor antagonists e..g Pegvisomant -> prevents dimerisation of GH receptor
- Dopamine agonists e.g. bromocriptine (first effective therapy for acro, but now not used as much as somatostatin analogue)

Third line:
- radiotherapy can be considered if surgery is unsuitable

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14
Q

Somatostatin analogues

A

(e.g. octreotide):
1. Directly inhibits GH release
1. Used in preference to the other options

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15
Q

complications of acromegaly

A

Complications

  • Hypertension
  • Hypertrophic cardiomyopathy
  • Arrhythmia
  • Sleep apnoea
  • Osteoarthritis
  • Diabetes mellitus
  • Carpal tunnel syndrome
  • Colorectal cancer
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16
Q

Hypopituitarism

A

Hypopituitarism describes the decreased secretion of one or more of the hormones secreted by the pituitary gland. If there is a deficiency of most or all of the pituitary hormones, the term panhypopituitarism is used.

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17
Q

hypopituitarism pathophysiology

A
  • Pituitary tumours (e.g. pituitary adenoma) – most common
  • Craniopharyngioma:
  • May affect the hypothalamus which in turn can affect the pituitary gland
  • Subarachnoid haemorrhage
  • Sheehan’s syndrome
  • Pituitary apoplexy
  • Iatrogenic (e.g. irradiation/surgery)
  • Head injury
  • Infiltrative causes (e.g. sarcoidosis, haemochromatosis)
  • Idiopathic
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18
Q

presentation of hypopituitarism depends on

A

which hormone is affected

  • Adrenocorticotropic deficiency- adrenal isnufficiency
  • Thyroid stimulating hormone deficiency - hypothyroidism
  • Growth hormone deficiency
  • Antidiuretic hormone deficiency - Diabetes insipidus
  • Gonadotropin deficiency
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19
Q

Adrenocorticotropic deficiency

A

see Adrenal Insufficiency:

  • Fatigue
  • Dizziness
  • Nausea
  • Postural hypotension
  • Hypoglycaemia
  • Hyponatraemia

Background
- Low cortisol- addisons esk
- Treatment- hydrocortisone replacement – immediate increased energy and appetite

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20
Q

Thyroid-stimulating hormone deficiency

A

See Hypothyroidism:

  • Fatigue
  • Cold intolerance
  • Constipation
  • Dry skin
  • Hair loss
  • Weight gain
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21
Q

Growth hormone deficiency

A
  • Loss of GH
  • Can be hard to diagnose because GH is released in a pulsatile fashion

Symptoms

1) Adults (adenoma)

  • Decreased exercise tolerance
  • Decreased muscle tone
  • Increased body fat
  • Reduced sense of wellbeing

Children (idiopathic- specific mutations and autoimmune may be linked)
- Short stature in children- can be treated with GH manufactured by recombinant DNA technology

Treatment- injected daily GH (subcut)

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22
Q

Antidiuretic hormone deficiency

A

see Diabetes Insipidus:
May occur from a hypothalamic tumour or pituitary tumour that has ended up in the hypothalamus.

  • Polyuria
  • Polydipsia
  • Hypernatraemia
23
Q

Gonadotropin deficiency:

A

In women:

  • Oligomenorrhoea
  • Infertility
  • Reduced libido

Treatment: O+ P

In men:

  • Impaired sexual function- impotence
  • Loss of facial, pubic, and body hair
  • Reduced libido

Treatment: T

24
Q

Investigations for hypopituitarism

A

Hormone profile testing:

  • These are tests according to what deficiencies are suspected (e.g. thyroid function tests, cortisol testing etc.)

MRI pituitary gland:

  • Assesses the presence of a pituitary adenoma
  • Ideally, blood tests should be performed first as incidental pituitary masses (‘incidentalomas’) may be present, potentially incorrectly suggesting a pituitary mass is a cause
25
Q

management of hypopituitarism

A

1st-line: manage underlying cause (e.g. surgery) + replace deficient hormones

  • Early diagnosis and intervention are associated with a better prognosis
  • The presence of complications is associated with a poorer prognosis
26
Q

diabetes insipidus

A

is characterised by increased thirst and the production of large amounts of dilute urine as a result of inadequate antidiuretic hormone (ADH, also known as vasopressin) function.

DI can be associated with hypernatraemia.

27
Q

Antidiuretic hormone

A

Also known as vasopressin, antidiuretic hormone (ADH) is a hormone secreted from the posterior pituitary gland in response to increased blood osmolality. It promotes water reabsorption in the kidney’s collecting ducts through the insertion of aquaporin-2 channels. It also constricts arterioles, increasing peripheral vascular resistance and hence, arterial blood pressure.

28
Q

Types of diabetes insipidus

A
  • Cranial DI - decreased secretion of ADH by PP
  • Nephrogenic DI - kidneys do not respond to ADH effectively e.g. lithium
  • Gestational DI- only during prgenancy, palcenta produces an enzymes called vasopressinase that breaks down ADH
  • **Dipsogenic DI **(primary polydipsia)- due to increased intake of fluids without impaired ADH function- can be due to dmaage to thirst mechaism in the hypothalamus or psychiatric illness
29
Q

Risk Factors: Cranial DI

A
  • Idiopathic
  • Head trauma/surgery
  • Pituitary tumours
  • Pituitary surgery
  • Craniopharyngioma
  • Sarcoidosis
  • Haemochromatosis
  • Meningitis/encephalitis – usually seen in late disease
  • Subarachnoid haemorrhage
30
Q

Nephrogenic DI

A

Genetic mutations:

  • Most are mutations in the ADH receptor
  • Others can be mutations coding for aquaporin 2 channels

Drugs:

  • Lithium
  • Demeclocycline
  • Gentamicin
  • Rifampicin

Other:

  • Hypercalcaemia
  • Hypokalaemia
  • Chronic kidney disease
31
Q

presentation of diabetes insipidus

A

The presentation of DI can be vague and insidious. Features are:

  • Polyuria
  • Polydipsia
  • Nocturia

Signs of hypernatraemia:

  • Irritability
  • Lethargy
  • Spasticity
  • Hyperreflexia
32
Q

Psychogenic polydipsia

A
  • Patients may have an underlying psychiatric condition
  • Waking at night with the need to drink water rather than pass urine is more suggestive of primary polydipsia
  • Water deprivation tests are normal
33
Q

investigations for DI

A

U&Es and calcium:

  • Sodium: may be normal/elevated
  • An elevated sodium + low urine osmolality is strongly suggestive of DI
  • Potassium: may be normal or low in nephrogenic DI
  • Calcium: may be normal or high in nephrogenic DI

Serum glucose:

  • Normal – done to exclude diabetes mellitus

Serum osmolality:

  • Normal or elevated

Urine osmolality:

  • Reduced (<300 mOsm/kg)

Special tests

  • Water deprivation test:
  • Desmopressin stimulation test:
34
Q

Water deprivation test

A

Patients have their urine osmolality measured, are deprived of fluids for 8 hours, and then have it measured again

35
Q

Desmopressin stimulation test:

A

Patients are given desmopressin and the urine osmolality is measured.
See interpretation of results below

36
Q

findings if: Cranial DI

A
  • High plasma osmolality
  • Low urine osmolality after fluid deprivation
  • Urine osmility icnreases after desmopressin
37
Q

Findings if: Nephrogenic DI

A
  • High plasma osmolality
  • Low urine osmolality after fluid deprivation
  • Urine osmility stays the same after desmopressin
38
Q

Findings if: primary polydipsia

A
  • Low plasma osmolality
  • High urine osmolality after fluid deprivation
  • High osmility icnreases after desmopressin
39
Q

findings if: without DI

A
  • Normal plasma osmolality
  • > 600 urine osmolality after fluid deprivation
  • > 600 osmolality after desmopressin
40
Q

management of DI

A

treat underlying cause e.g. lithium toxicity

Central DI - desmopressin (sublingual, intranasal, subcut, IV or IM divided into daily doses and adjusted according to response

Nephrogenic:

  • thiazide diuretic - decrease urine volume
  • high dose desmopressin
  • NSAIDs
41
Q

complications of DI

A

Complications

Hypernatraemia:

  • Can occur if patients do not drink water while feeling thirsty due to DI

Iatrogenic hyponatraemia:

  • Replacement desmopressin can lead to hyponatraemia

Bladder dysfunction and/or hydronephrosis:

  • In cases of nephrogenic DI
42
Q

Syndrome of inappropriate antidiuretic hormone secretion (SIADH)

A

is characterised by excess antidiuretic hormone (ADH) in the blood either from the posterior pituitary gland or from an ectopic source.

43
Q

pathophysiology of SIADH

A

The increased ADH secretion causes an excess amount of water reabsorption which leads to dilution of the solutes in the blood, and a reduced osmolality. A common finding is that patients have euvolaemic hyponatraemia. At the same time, cells can swell which can lead to complications according to the site affected (e.g. the brain cells swelling leading to seizures and comas).

44
Q

causes of SIADH

A

Malignant:

  • Small cell lung cancer
  • Pancreatic cancer
  • Prostate cancer
  • Lymphoma

Neurological causes:

  • Stroke
  • Subarachnoid haemorrhage
  • Meningitis
  • Encephalitis
  • Brain abscess
  • Infection:
  • Pneumonia
  • Tuberculosis

Drugs:

  • SSRIs
  • Tricyclic antidepressants
  • Carbamazepine
  • Sulfonylureas
  • NSAIDs
45
Q

Presentation SIADH

A

Features may be:

  • Asymptomatic
  • Features of brain swelling:
  • Nausea
  • Vomiting
  • Headache
  • Seizures
  • Changes to consciousness
  • Coma
46
Q

investigations for SIADH

A

U&Es:

  • Shows hyponatraemia
  • Urea may be low due to dilution

Serum osmolality:

  • Reduced

Urine osmolality:

  • Increased (>100 mOsm/kg H2O)

Urine sodium:
* Increased (>30 mmol/L)

47
Q

diagnosing SIADH

A

SIADH can be diagnosed if there is a:

  • reduced serum osmolality
  • increased urine osmolality, and
  • increased urinary sodium so long as the patient is euvolaemic, has no orthostasis, no features of dehydration or hypervolaemia, has normal thyroid and adrenal function, and there has been no recent diuretic use.
48
Q

management of SIADH

A
  • The sodium must be corrected slowly to reduce the risk of central pontine myelinolysis
  • 1st-line: fluid restriction + treat the underlying cause
  • Other options are vasopressin receptor antagonists (e.g. tolvaptan)
49
Q

Complications of SIADH

A
  • Features of brain swelling (mentioned above)
  • Central pontine myelinolysis if hyponatraemia is corrected too quickly
50
Q

hyperprolactinoma

A

Hyperprolactinaemia

  • Common
  • Pregnancy should be excluded
  • Full medication history- dopamine antagonists such as antiemetics (metoclopramide) and anti-psychotics commonly cause high prolactin
  • Causes
    o Profound hypothyroidisms rare cause
    o PCOS
51
Q

hyperprolactinoma presentation

A

Symptoms and signs

  • infertility.
  • irregular periods.
  • change in menstrual flow.
  • pause in menstrual cycle.
  • loss of libido.
  • lactation (galactorrhea)
  • pain in breasts.
  • vaginal dryness.
52
Q

macro vs microprolactinoma

A

Micro

  • <1cm
  • Women >men
  • Menstrual disturbance (or hypogonadism in men)
  • Galactorrhoea
  • PCOS distinguished from prolactinoma by presence of androgenic symptoms and less elevated prolactin and no pituitary lesion on MRI

Macro

  • > 1cm
  • Men>women
  • Prolactin >5000 miU
53
Q

management of prolactinomas

A
  • Dopamine (D2) agonists- cabergoline or bromocriptime
    o Cabergoline- given once or twice weekly (better tolerated than bromocriptine (given daily))
    o Side effect nausea and postural hypotension, psychiatric disturbance
  • Macro-prolactinomas are treated medically even if very larger
  • In 15% of macro-prolactinomas, CSF leak occurs due to rapid reduction in size of lesion–> risk of meningitis

Medicine (Year 5) (34 decks)

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