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Endocrine > Pituitary > Flashcards

Pituitary Flashcards

1
Q

What is the hypophysis?

A

Another name for the pituitary gland

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2
Q

What is the neurohypophysis?

A

Another name for the posterior pituitary gland

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3
Q

What is the adenophysis?

A

Another name for the anterior pituitary gland

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4
Q

What is the infundibulum?

A

Another name for the pituitary stalk connecting the hypothalamus to the pituitary gland

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5
Q

Give two problems that pituitary pathology can cause on the surrounding structures

A
  1. Compression of the optic chiasm e.g. bitemporal hemianopia
  2. Compression of structures in the cavernous sinuses e.g. damage to cranial nerves III, IV,V1 (opth), V2 (max), VI
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6
Q

What are hypophysiotropic hormones?

A

Hormones which are released into the anterior pituitary gland to cause the release of anterior pituitary hormones

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7
Q

Name the 5 hypophysiotropic hormones and what they do

A
  1. Corticotrophin-releasing hormone (CRH) - Stimulates the release of ACTH
  2. Growth hormone-releasing hormone (GHRH) - Stimulates the release of GH but GHRH release is inhibited by somatostatin (SST)
  3. Thyrotropin-releasing hormone (TRH) - Stimulates the release of TSH
  4. Gonadotropin-releasing hormone (GnRH) - Stimulates the release of LH & FSH
  5. Dopamine (DA) - Inhibits the release of prolactin (PRL)
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8
Q

What does the abbreviation CRH stand for?

A

Corticotrophin-releasing hormone

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9
Q

What does the abbreviation ACTH stand for?

A

Adrenocorticotropic hormone

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10
Q

What does the abbreviation GHRH stand for?

A

Growth hormone-releasing hormone

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11
Q

What does the abbreviation GH stand for?

A

Growth hormone

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12
Q

What does the abbreviation SST stand for?

A

Somatostatin

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13
Q

What does the abbreviation TRH stand for?

A

Thyrotropin-releasing hormone

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14
Q

What does the abbreviation TSH stand for?

A

Thyroid stimulating hormone

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15
Q

What does the abbreviation GnRH stand for?

A

Gonadotropin-releasing hormone

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16
Q

What does the abbreviation LH stand for?

A

Luteinising hormone

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17
Q

What does the abbreviation FSH stand for?

A

Follicle stimulating hormone

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18
Q

What does the abbreviation DA stand for?

A

Dopamine

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19
Q

What does the abbreviation PRL stand for?

A

Prolactin

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20
Q

What type of hormones does the anterior pituitary produce?

A

Peptide hormones

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21
Q

Name the 6 hormones produced by the anterior pituitary and which cells produce them

A
  1. Follicle-stimulating hormone (FSH) - gonadotrophs
  2. Luteinizing hormone (LH) - gonadotrophs
  3. Adrenocorticotropic hormone (ACTH) (aka corticotropin) - cortiocotrophs
  4. Thyroid-stimulating hormone (TSH) (aka thyrotropin) - thyrotrophs
  5. Prolactin (PRL) - lactotrophs
  6. Growth hormone (GH) (aka somatotropin) - somatotrophs
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22
Q

Which hormone causes FSH and LH to be released from the anterior pituitary?

A

Gonadotropin-releasing hormone (GnRH)

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23
Q

Which organs do LH and FSH target?

A

The gonads

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24
Q

What does LH and FSH do in the ovaries?

A
  • LH acts on the theca cells to convert cholesterol to testosterone
  • FSH converts testosterone to oestrogen in the granulosa cell via the aromatase enzyme
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25
Q

What does LH and FSH do in the testes?

A
  • LH acts on the Leydig cells to produce testosterone

* FSH acts on the Sertoli cells to initiate sperm production

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26
Q

What are the roles of oestrogen and progesterone in the control of FSH and LH?

A
  • FSH stimulates oestrogen release
  • Oestrogen inhibits FSH (+ve feedback) and causes a surge in LH
  • LH causes the egg to release which stimulates the release of progesterone to thicken the uterine wall
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27
Q

Which hormones cause and inhibit the release of GH?

A
  • Growth-hormone releasing hormone (GHRH) causes its release

* Growth-hormone inhibiting hormone aka somatostatin (GHIH/SST) inhibits release

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28
Q

State and describe the 3 actions of GH

A
  1. Increases blood glucose - stimulates gluconeogenesis and inhibits insulin
  2. Breaks down fat - works on adipose tissue
  3. Indirectly stimulates growth and protein synthesis - acts on the liver to increase protein synthesis and stimulate IGF-1 production
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29
Q

What does IGF-1 do and how is it related to GH?

A
  • It acts on the skeleton to increase cartilage proliferation.
  • It is stimulated by GH and it is the substance measured to reflect GH levels
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30
Q

Which hormone stimulates ACTH release?

A

Corticotrophin-releasing hormone (CRH)

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31
Q

Which organs does ACTH act on?

A

The adrenal glands

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32
Q

Which hormones does ACTH stimulate the release of and where from?

A
  1. Cortisol and other steroid hormones - zona fasciculata in the adrenal cortex
  2. Androgens - zona reticularis in the adrenal cortex
  3. Adrenaline - adrenal medulla
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33
Q

What are some of the major roles of cortisol?

A
  1. Regulates and breaks down proteins, fats and carbohydrates
  2. Has an anti-inflammatory effect – lowers immune response (but this can be bad if prolonged)
  3. Helps the body overcome stress
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34
Q

Which hormones cause and inhibit the release of TSH?

A
  • Thyrotropin-releasing hormone (TRH) stimulates release

* Growth-hormone inhibiting hormone aka somatostatin (GHIH/SST) inhibits release

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35
Q

What does TSH stimulate the release of?

A

Thyroid hormones

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36
Q

Give some actions of the thyroid hormones

A
  • Control rate of metabolic reactions
  • Accelerate food metabolism
  • Increase protein synthesis
  • Stimulate carbohydrate metabolism
  • Enhance fat metabolism
  • Increases ventilation rate
  • Increases cardiac output & heart rate
  • Brain development during foetal life and postnatal development
  • Growth rate acceleration
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37
Q

How does dopamine affect prolactin?

A

Dopamine inhibits prolactin

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38
Q

What is the action of prolactin?

A

Stimulates the breasts to produce milk and helps with breast development

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39
Q

What are the type of receptors that all pituitary and hypothalamic hormones act on?

A

G-protein coupled receptors

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40
Q

What does ADH stand for and what is another commonly used name for it?

A

Anti-diuretic hormone - aka vasopressin

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41
Q

Which hypothalamic neurones are responsible for oxytocin and vasopressin synthesis?

A
  • Paraventricular nucleus - oxytocin synthesis

* Supraoptic nucleus - vasopressin synthesis

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42
Q

What are the names of the 2 hormones related to the posterior pituitary?

A
  1. Oxytocin

2. Vasopressin/ADH

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43
Q

What type of hormones are oxytocin and vasopressin?

A

Peptide hormones

44
Q

What 2 main functions does vasopressin do?

A
  1. Increases blood volume

2. Increases blood pressure

45
Q

How does vasopressin work?

A
  • Hypovolaemia causes vasopressin secretion which binds to aquaporin channels in the collecting duct of the nephrons which allow more water to be reabsorbed
  • Acts on the smooth muscle cells around blood vessels to cause vasoconstriction to increase blood pressure
  • Stimulates ACTH release from the anterior pituitary to increase aldosterone release to increase fluid retention
46
Q

Give 6 stimuli which cause the release of vasopressin

A
  1. Decreased blood volume
  2. Trauma
  3. Stress
  4. Increase blood CO2
  5. Decreased blood O2
  6. Increased osmotic pressure of blood
47
Q

Are they half-lives of oxytocin and vasopressin long or short?

A

They are both very short

48
Q

What is the impact of the half-life length of oxytocin and vasopressin?

A

They are regulated frequently once they are released on a minute-to-minute basis

49
Q

When do the 2 main functions of oxytocin occur?

A

In pregnancy and breast feeding

50
Q

What are the 2 main functions of oxytocin?

A
  1. Stimulating cervical dilatation in the onset of labour and uterine smooth muscle contraction until the baby is born
  2. The ejection of milk during breast feeding - mammary gland stimulation causes the release of oxytocin which stimulates the release of milk
51
Q

Give 5 conditions of the pituitary

A
  1. Benign pituitary adenoma
  2. Craniopharyngioma
  3. Trauma
  4. Apoplexy/Sheehan’s syndrome
  5. Sarcoidosis/TB
52
Q

What 3 key problems do pituitary tumours cause?

A
  1. Pressure on local structures
  2. Pressure on normal pituitary (hypopituitarism)
  3. Functioning tumour (hyperpituitarism)
53
Q

Describe the presentation of hypopituitarism

A

• Can be fatal – particularly if it causes cortisol deficiency
• In males:
- Pale, no body hair (takes 9 months to occur), central obesity
- Effeminate skin
• In females
- Loose body hair
- Sallow complexion

54
Q

State the 3 major presentations of hyperpituitarism

A
  • Prolactinoma – increased prolactin
  • Acromegaly – increased GH
  • Cushing’s – increased CTH
55
Q

Describe the key presentations of prolactinomas

A
  • Common in young women
  • Galactorrhoea
  • Reduced fertility
  • Amenorrhoea = menstruation stops
  • Treated using a dopamine agonist which will inhibit prolactin release e.g. cabergoline
56
Q

What is Cushing’s syndrome?

A

Chronic, excessive and inappropriate elevated levels of cortisol

57
Q

Give some clinical features of Cushing’s syndrome

A 
•  Obesity
•  Red and round face
•  Protein catabolic (breakdown) effects
   - Thin skin that bruises easily
   - Muscle atrophy -> proximal weakness
   - Purple striae on the abdomen, breasts and thighs
•  Acne
•  Increased BP
•  Gonadal dysfunction (menstrual irregularity, erectile dysfunction etc) and decreased libido
•  Decreased linear growth
•  Hirsutism
•  Hyperglycaemia – glucose intolerance
•  Osteopenia/osteoporosis
•  Increased susceptibility to infection
58
Q

What are the causes of Cushing’s syndrome?

A

• ACTH dependent:
- Excessive ACTH from the pituitary = Cushing’s disease
- Ectopic ACTH producing tumours
- Excess ACTH administration e.g. asthma treatment
• Non-ACTH dependent:
- Adrenal adenomas/carcinomas
- Excessive glucocorticoid administration e.g. prednisolone

59
Q

What is the differential diagnosis for Cushing’s syndrome?

A

Pseudo-Cushing’s syndrome due to alcohol excess – resolves after 1-3 weeks of alcohol abstinence

60
Q

How would you diagnose Cushing’s syndrome?

A
  • Take a careful drug history
  • Random plasma cortisol
  • Overnight dexamethasone suppression test
  • CT adrenals
  • MRI pituitary and CRH test
61
Q

What is the management and treatment for Cushing’s syndrome?

A

• Medical
- Adrenal blockade in preparation for surgery (not usually a long-term solution)
- Stop any steroids
• Surgical
- Cushing’s disease = Trans-sphenoidal surgery or bilateral adrenalectomy
- Ectopic = Remove source -> bilateral adrenalectomy
- Adrenal adenoma/carcinoma or PPNAD = Adrenalectomy
- AIMAH = Adrenalectomy or block aberrant receptors
• Radiotherapy
- As adjuvant therapy in Cushing’s disease

62
Q

What is the difference between acromegaly and gigantism?

A
  • Acromegaly = excess GH in adults

* Gigantism = excessive GH production in children BEFORE the fusion of the epiphyses of the long bones

63
Q

What are the causes of acromegaly?

A
  • Majority = benign GH-producing pituitary tumour

* In rare cases = hyperplasia e.g. ectopic GHRH from a carcinoid tumour

64
Q

Give some clinical features of acromegaly

A
  • Overgrowth of all organ systems, bones, joints, and soft tissues
  • Increased height
  • Excessive sweating
  • Mild hirsutism (particularly in women)
  • Headaches
  • Visual field defects
  • Hypogonadal symptoms
65
Q

Give 6 associated co-morbidities of acromegaly

A
  1. Impaired glucose tolerance
  2. Diabetes mellitus
  3. Sleep apnea
  4. CVD and hypertension
  5. Colon cancer
  6. Arthritis
66
Q

How would you diagnose acromegaly?

A

• High glucose, Ca2+ and phosphate
• Plasma GH levels
- Non-diagnostic but can exclude if undetectable
• Glucose-tolerance test (GTT)
• IGF1
- Diagnostic
• Visual field examination
• MRI of pituitary fossa
• ECHO of the heart to look for cardiomyopathy
• Old photos (if possible) to compare changes

67
Q

What is the treatment for acromegaly?

A 
• Trans-sphenoid surgery
• If surgery fails:
   - Somatostatin analogues 
   - GH receptor antagonists
   - Dopamine agonist
• Radiotherapy
• Stereotactic radiotherapy
• Gamma knife, LINAC or proton beam
68
Q

What is a prolactinoma?

A

A lactotroph cell tumour of the pituitary causing excessive prolactin secretion

69
Q

Give some clinical features of hyperprolactinemia

A
  • Galactorrhoea
  • Menstrual irregularity/amenorrhoea
  • Infertility
  • Low libido
  • Low testosterone in men
  • Headache
  • Visual field defects
  • CNS leak (rare)
70
Q

What are the causes of hyperprolactinemia?

A

• Prolactinoma (can be micro or macro)
• Pituitary stalk damage
- Results in less dopamine so less PRL inhibition
- Can be due to pituitary adenomas, surgery, or trauma
• Drugs
- Most common cause e.g. metoclopramide or ecstasy
- Don’t measure PRL levels in patients on anti-dopaminergic drugs
• Physiological
- Pregnancy, breast feeding, stress

71
Q

How would you diagnose hyperprolactinemia?

A

Measure the basal prolactin level - it will be very high

72
Q

How would you treat hyperprolactinemia?

A

Use dopamine agonists, e.g. oral cabergoline, as they cause massive tumour shrinkage

73
Q

How is water homeostasis in the body controlled?

A
  1. Efferent neurones project from the osmoreceptor to the PVN and SON
  2. Baroreceptors are stimulate the nuclei
  3. The thirst centre triggers feelings of thirst in response to dehydration
  4. Vasopressin binds to G-protein coupled 7 transmembrane domain receptors
74
Q

Where are the baroreceptors which detect water levels located?

A

In the great vessels (carotid sinus and aortic arch) and in the brainstem

75
Q

Name the 3 key receptors which vasopressin binds to and thier location

A
  1. V1a = vasculature (vasoconstriction in the presence of vasopressin)
  2. V2 = renal collecting tubules (allows reabsorption of water)
  3. V1b = pituitary (vasopressin causes the release of ACTH on the anterior pituitary)
76
Q

What condition does a lack of vasopressin lead to?

A

Cranial diabetes insipidus

77
Q

What condition does a resistance to vasopressin lead to?

A

Nephrogenic diabetes insipidus

78
Q

What does SIADH stand for?

A

Syndrome of inappropriate antidiuretic hormone secretion

79
Q

Give the 4 ways of classifying hyponatraemia

A
  1. Biochemical
  2. Symptoms
  3. Aetiology
  4. Acuity of onset
80
Q

Give the ranges for the biochemical classification of hyponatraemia

A
  • Mild: 130-135mmol/L
  • Moderate: 125-129mmol/L
  • Severe: <125mmol/L
81
Q

What are the 3 stages of symptomatic classification of hyponatraemia?

A

Mild, moderate and severe

82
Q

What are the 3 areas of aetiological classification of hyponatraemia?

A

Hypovolaemic, euvolaemic, hypervolaemic

83
Q

What is the division of acuity of onset classification of hyponatraemia?

A
  • Acute: <48hrs

* Chronic: >48hrs

84
Q

State some mild/moderate symptoms of hyponatraemia

A
  • Headache
  • Irritability
  • Nausea and vomiting
  • Mental slowing
  • Unstable gait/falls
  • Confusion/delirium
  • Disorientation
85
Q

State some severe symptoms of hyponatraemia

A
  • Stupor/coma
  • Convulsions
  • Respiratory arrest
86
Q

How would you test for and manage hyponatraemia?

A
  • Stop hypotonic fluids
  • Review drug card – many drugs may cause this e.g. PPIs
  • Measure plasma and urine osmolality
  • Measure urinary sodium
  • Check glucose level – to exclude hyperglycaemia
  • TFTs
  • Assess cortisol
  • Assessment of underlying cause e.g. CXR, imaging
87
Q

What is the cause off 25% of all hyponatraemia cases?

A

SIADH

88
Q

How does SIADH affect the body?

A
  • There is continued ADH secretion despite dilute plasma levels
  • Excess aquaporin 2 channels are inserted in the collecting duct leading to excess water retention
  • This results in hyponatraemia as Na+ is less concentrated
89
Q

Give 5 causes of SIADH

A
  • Tumours
  • CNS causes e.g. meningitis, head injury, SLE
  • Pulmonary lesions e.g. pneumonia, TB, asthma, cystic fibrosis
  • Drugs e.g. SSRIs, vincristine (chemo), carbamazepine (snit-convulsant),
  • Metabolic causes e.g. alcohol withdrawal
90
Q

What is the clinical presentation of SIADH?

A
  • Symptoms as a result of hyponatraemia
  • Varied and generic
  • Anorexia/nausea and malaise
  • Weakness and aches
  • Reduction in GCS and confusion with drowsiness
  • Fits and coma (occurs later)
91
Q

How would you diagnose SIADH?

A
  • Low serum Na+ but euvolaemia
  • High urine Na+ >30mmol/L
  • No response to 1-2L 0.9% saline unlike in common hyponatraemia
  • Normal renal, adrenal and thyroid function
92
Q

How would you treat SIADH?

A

• Treat underlying cause where possible
• Restrict fluid intake
• Give hypotonic saline if very symptomatic
• Drugs e.g.
- Oral demeclocycline – induces nephrogenic DI
- Vasopressin antagonist e.g. oral tolvaptan – V2 blocker
- Salt and loop diuretic e.g. oral furosemide

93
Q

How would you test for functional tumours causing Cushing’s?

A
  • Dexamethasone suppression testing

* CRH stimulation

94
Q

How would you test for functional tumours causing Acromegaly?

A

Oral glucose GH suppression test

95
Q

How would you test for a functional TSHoma?

A

TRH stimulation

96
Q

How would you test for functional tumours causing gonadotropin deficiency?

A

GnRH stimulation

97
Q

How would you test for functional tumours causing GH or ACTH deficiency?

A
  • Insulin-induced hypoglycaemia (for both)

* Glucagon test (for GH deficiency)

98
Q

Give 5 non-functioning tumours/pituitary mass lesions

A
  1. Craniopharyngioma
  2. Rathke’s cyst
  3. Meningioma
  4. Lymphocytic hypophysitis
  5. Non-functioning pituitary adenoma (NFPA)
99
Q

What are craniopharyngiomas derived from?

A

Squamous epithelial remnants of Rathke’s pouch

100
Q

What are the peak ages for presenting with a craniopharyngioma?

A

5-14yrs, 50-74yrs

101
Q

What are Rathke’s cysts derived from?

A

Remnants of cuboidal epithelium from Rathke’s pouch

102
Q

What is lymphocytic hypophysitis and who is it most common in?

A
  • Inflammation of the pituitary gland due to an autoimmune reaction
  • More common in women, usually during or after pregnancy
103
Q

What are the steps in the negative feedback loop of cortisol level control?

A
  1. Low serum cortisol causes CRH to be secreted from the hypothalamus
  2. CRH binds to pituitary receptors to stimulate the production of ACTH
  3. ACTH travels in the blood and binds to the specific receptors in the adrenal cortex
  4. The adrenal cortex releases cortisol into the blood
  5. Increased serum cortisol inhibits CRH and ACTH secretion
104
Q

What external factor triggers changes in the circadian rhythm?

A

The quantity and quality of light

105
Q

When do cortisol levels usually peak?

A

Typically within the first hour of waking up

106
Q

What are the 3 main functions of cortisol?

A
  1. Promoting gluconeogenesis to increase blood glucose levels
  2. Supressing the immune system
  3. Aiding metabolism of fat, protein and carbohydrates

Endocrine (7 decks)

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