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Medicine Year 2 > Endocrine Topic 1 - General > Flashcards

Endocrine Topic 1 - General Flashcards

1
Q

How is acromegaly treated/managed?

A

Surgery (often not curative)

Medical - somatostatin to inhibit GH

Radiotherapy - risk of hypopituitarism

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2
Q

What is the difference between gigantism and acromegaly?

A

Gigantism - overproduction of growth hormone in childhood

Acromegaly - overproduction of growth hormone/IGF-1 in adulthood (after epiphyseal fusion)

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3
Q

List the functional cell types in the anterior pituitary and the hormones they produce

A
  • Somatotrophs (acidophils) - growth hormone, predominant cells type
  • Lactotrophs (acidophils) - prolactin
  • Corticotrophs (basophils) - adrenocorticotrophic hormone (ACTH), beta-lipotropin, alpha-melanocyte stimulating hormone, beta-endorphin
  • Thyrotrophs (basophils) - thyroid stimulating hormone (TSH)
  • Gonadotrophs (basophils) - FSH/LH
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4
Q

What is the action of ADH?

A

Binds to V2 receptor (G-protein coupled) on collecting tubules of the kidney, causes an increase in cAMP/PKA and therefore aquaporin 2 recruitment - increases water reabsorption

Also causes vasoconstriction to increase BP

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5
Q

From what are amine hormones derived?

A

Derived from amino acids

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6
Q

Define hyponatraemia

A

Serum Na+ below 135mmol/L

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7
Q

Define hypercalcaemia

A

High free calcium (45% of total)

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8
Q

What is the effect of a non-functioning pituitary adenoma?

A

Compresses surrounding structures e.g. optic chiasm, causing peripheral vision loss

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9
Q

List the causes of hyponatraemia

A
  • Water excess
  • Sodium and water excess
  • Excess ADH
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10
Q

What is the clinical consequence of hyponatraemia?

A

Brain oedema (water moves into cells)

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11
Q

How is the cause of hypercalcaemia diagnosed?

A
  • Measure PTH
    • If low malignancy likely
    • If normal/high - primary hyperparathyroidism
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12
Q

How is growth hormone release regulated?

A

Negative feedback - GH, IGF-1 or somatostatin

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13
Q

How is diabetes insipidus diagnosed?

A
  • 8 hour water deprivation, give synthetic ADH, measure osmolality of urine
  • Normal - 8hrs = >600, give ADH = >600
  • Cranial DI - 8hrs = <300, give ADH = >600
  • Nephrogenic DI - 8hrs = <300, give ADH = <300
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14
Q

What causes diabetes insipidus?

A
  • Cranial or nephrogenic causes
    • Cranial = ADH deficiency - idiopathic, genetic, trauma, tumours, infection
    • Nephrogenic = resistance to ADH - genetic (AVPR2 mutation), secondary to drugs (e.g. lithium), metabolic upset, renal disease
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15
Q

How is hypopituitarism treated?

A

Multiple hormone replacement (cortisol first if all affected)

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16
Q

Describe the structure of the parathyroid glands

A
  • Usually 4
  • 2 secretory cell types
    • Chief cells - most abundant, basophilic (stain purple)
    • Oxyphil cells - acidophilic (stain pink)
  • Often within thyroid capsule, if separate may have fine fibrous capsule surrounding
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17
Q

What causes water excess leading to hyponatraemia?

A
  • Glucocorticoid deficiency
  • Hypothyroid
  • Psychiatric
  • Drugs
  • Inappropriate ADH secretion
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18
Q

What causes hypopituitarism?

A
  • Tumours
  • Radiotherapy
  • Infarction - post-partum = Sheehan’s syndrome
  • Infiltrations - sarcoid
  • Trauma
  • Congenital
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19
Q

Describe the action of steroid hormones

A

Lipophilic - pass through plasma membrane, act on intracellular receptor

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20
Q

What causes hypernatraemia?

A

Mostly due to dehydration - insensible/sweat loss, GI loss, diabetes insipidus, osmotic diuresis due to hypoglycaemia

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21
Q

What are the consequences of hypopituitarism?

A
  • Can affect single axis (gonadotrophic most common) or all (panhypopituitarism)
  • Leads to secondary gonadal/thyroid/adrenal failure
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22
Q

How is hypernatraemia corrected?

A
  • Treat cause
  • Estimate total body water deficit
  • Avoid rapid correction (cerebral oedema)
  • Use IV 5% dextrose
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23
Q

How is hyponatraemia treated?

A
  • Severe/acute (unconscious/seizures) = hypertonic (8%) saline
  • Less severe/chronic = treat cause, usually need fluid restriction, increase slowly
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24
Q

How is hyponatraemia due to excess ADH diagnosed?

A
  • Osmolality of urine > plasma
  • Urine sodium >30mmol/L
  • Absence of adrenal/thyroid/pituitary/renal insufficiency
  • No recent diuretic use
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25
Q

From what are steroid hormones derived?

A

Cholesterol

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26
Q

What is the effect of growth hormone?

A

Multiple effects - direct or through IGF-1 production

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27
Q

What are the complications of acute hypocalcaemia?

A
  • Tetany
    • Peri-oral numbness, muscle cramps, tingling of hands/feet
    • Carpopedal spasm, laryngospasm, seizures
  • Cardiac complications
    • Dysrrhythmia, hypotension
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28
Q

Describe the embryonic origin of the pituitary gland

A
  • Anterior and posterior lobes
  • Anterior
    • Directly regulated by hypothalamus
    • From embryonic pharynx - oral ectoderm
  • Posterior
    • Down growth from diencephalon
    • Neuroectoderm
  • Fibroelastic capsule from primitive pia mater
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29
Q

How is acromegaly diagnosed?

A

Oral glucose tolerance test (no suppression of GH by high blood glucose concentration in acromegaly)

IGF-1 level (high in acromegaly) - longer half-life than GH

Pituitary MRI

30
Q

How is the lactotrope axis regulated?

A
  • Negative hypothalamic control - dopamine inhibits prolactin release from the pituitary
  • Oestrogen has positive effect, stimulates prolactin release
  • Stress stimulates
  • Only action is in pregnancy - lactation (none in males)
31
Q

Describe the clinical features of hypercalcaemia

A
  • Stones - nephrolithiasis, nephrocalcinosis, diabetes inspidis
  • Bones - bone pain, oesteoporosis, muscle weakness
  • Thrones - polyuria
  • Psychiatric overtones - depression, anxiety
  • ECG - shortened QTc, bradycardia
32
Q

What are the symptoms of diabetes insipidus?

A
  • Extreme thirst
  • Polyuria
  • Nocturia
  • No hyperglycaemia/hypercalcaemia
33
Q

List the hormones secreted by the posterior pituitary

A
  • Anti-diuretic hormone
  • Oxytocin
34
Q

How is hypocalcaemia treated?

A
  • IV Ca2+ replacement - if tetany or cardiac manifestations, +/- IV magnesium
  • Chronic management - Vitamin D supplement, oral calcium salts
  • Underlying cause
35
Q

How are the blood vessels of the pituitary functionally specialised?

A

Fenestrated

36
Q

Describe the anatomical location of the pituitary

A
  • Suspended from underside of brain by pituitary stalk (attached to hypothalamus)
  • In front of pons, behind nose and hypothalamus
  • Optic chiasm above
  • Sits in in sella turcica (Turkish saddle) of the sphenoid bone - in hypophyseal fossa
37
Q

List clinical disorders of the pituitary

A
  • Posterior pituitary - diabetes insipidus (low ADH)
  • Non-functioning pituitary tumours
  • Functioning pituitary tumours - high prolactin, GH, ACTH or TSH
  • Hypopituitarism
38
Q

List the types of hormones and give examples of each

A
  1. Amine e.g. catecholamines - adrenaline, noradrenaline, dopamine
  2. Peptide e.g. pituitary hormones, insulin, leptin, ghrelin
  3. Steroid e.g. glucocorticoids - cortisol, mineralocorticoids - aldosterone, androgens, progesterone
39
Q

What causes Na+ and water excess leading to hyponatraemia?

A
  • Nephrotic syndrome
  • Cardiac failure
  • Cirrhosis
  • Acute/chronic kidney disease
40
Q

What stimuli trigger growth hormone releasing hormone secretion?

A

Stress, exercise, sleep, hypoglycaemia

41
Q

From what are peptide hormones derived?

A

Amino acids

42
Q

What is the effect of parathyroid hormone?

A
  • Released in response to low serum calcium
  • Increases bone resorption
  • Increases kidney phosphate excretion and calcium reabsorption
  • Increases calcitriol formation (therefore increased GI absorption of calcium)
  • Net effect - increases serum calcium, phosphate same
43
Q

What is the effect of calcitriol?

A
  • Increased GI absorption
  • Increased bone resorption
  • Increased renal reabsorption
44
Q

What are the signs/symptoms of acromegaly?

A
  • Sweating
  • Headaches
  • Tiredness
  • Joint pain
  • Coarse facial features
  • Increased tongue/hand/foot size
  • Visual field loss
  • Hypertension
  • Impaired glucose tolerance
  • Increased bowel cancer risk
  • Heart failure
45
Q

How are prolactinomas managed?

A

Dopamine agonist (cabergoline), surgery

46
Q

What is the difference between an exocrine and endocrine gland?

A
  • Endocrine - secretes hormones directly into bloodsteam
    • Adrenal, thyroid, endocrine pancreas
  • Exocrine - secretes into a duct
    • Salivary, exocrine pancreas
47
Q

Describe the classification of hypercalcaemia

A
  • Mild < 3 mmol/L
  • Moderate 3-3.5mmol/L
  • Severe > 3.5 mmol/L
48
Q

What are the effects of functioning pituitary adenomas?

A
  • Corticotroph adenoma (ACTH secreting) - Cushing’s syndrome
  • Somatotroph adenoma (GH secreting) - acromegaly
  • Thyrotroph adenoma (TSH secreting) - hyperthyroidism
49
Q

What causes inappropriate ADH secretion leading to hyponatraemia?

A
  • Cancer - lung, lymphoma, leukaemia
  • Pneumonia
  • CNS infection/injury
  • Drugs - opiates, thiazides, proton pump inhibitors, anti-convulsants, anti-depressants
50
Q

What kind of receptors do amine hormones act on?

A

Mostly act on G-protein coupled receptors (or tyrosine kinase receptors)

51
Q

Describe the cell types which can be distuingished histologicall in the anterior pituitary

A
  • Chromophobes
    • Palely stained
    • Exhausted secretory cells
  • Chromophils
    • Strongly stained
    • Active secretory cells
    • Acidophils and basophils
      • Acidophils - pink, stained by eosin
      • Basophils - purple, stained by haematoxylin
52
Q

How is the hypothalamic-pituitary-thyroid axis regulated?

A

T3/4 has negative feedback effect on pituitary/hypothalamus

53
Q

Generally, what is the cause of hyponatraemia?

A

Usually due to a disorder of water balance e.g. renal impairment, diuretics (especially thiazide)

54
Q

What causes hypercalcaemia?

A
  • Primary hyperthyroidism (usually parathyroid adenoma)
  • Malignancy - breast, lung, myeloma, bone (direct osteolysis)
55
Q

What are the signs/symptoms of a prolactinoma?

A
  • Galactorrhoea - production of milk
  • Menstrual disturbance/subfertility in women
  • Low libido/erectile dysfunction in men
  • Low gonadotrophs
56
Q

How is the hypothalamic-pituitary-gonadal axis regulated?

A
  • Women - positive and negative feedback depending on time in cycle
    • Inhibin produced by granulosa cells of ovaries inhibit FSH secretion
  • Men - negative feedback through inhibin produced by Sertoli cells and androgens produced by Leydig cells
57
Q

What are the clinical features of hyponatraemia?

A
  • Asymptomatic
  • Confusion
  • Gait instability
  • Drowsiness
  • Seizures
58
Q

List the hormones released by the hypothalamus and the effect they have

A
  • Growth hormone releasing hormone - acts on the anterior pituitary to release growth hormone, leads to increased insulin-like growth factor 1 (IGF-1)
  • Gonadotrophin releasing hormone (GnRH) - acts on anterior pituitary to released FSH/LH
  • Corticotrophic releasing hormone - acts on anterior pituitary to release ACTH
  • Thyroid releasing hormone - acts on anterior pituitary to release TSH
  • Dopamine - acts on anterior pituitary to inhibit prolactin release
59
Q

What is the most common functioning pituitary adenoma?

A

Prolactinoma

60
Q

What is the action of oxytocin?

A

Needed for labour and breast feeding

61
Q

How is hypercalcaemia treated?

A
  • Dependent on severity, treat underlying cause
  • Rehydrate - isotone 0.9% saline
  • Bisphosphonate - osteoporosis, malignancy (Zoledronic acid)
  • Calcitonin
  • Glucocorticoids - inhibit Vitamin D production
  • Parathyroidectomy
62
Q

What causes hypocalcaemia?

A
  • Low PTH - surgery, autoimmune, hypoparathyroidism
  • Normal PTH - Vitamin D deficiency, chronic renal failure, calcium loss, drugs, hypomagnesaemia (PTH resistance)
63
Q

Which drugs affect prolactin secretion?

A
  • Any drug interacting with dopamine action can cause hyperprolactinaemia
    • Antipsychotics - typical and atypical
    • Antiemetics - metoclopramide, domperidone
    • Antidepressants - SSRIs, MOAI, TCA
    • Opiates
    • H2 receptor antagonists
64
Q

How is a prolactinoma diagnosed?

A
  • Confirmed on MRI screening
  • Microprolactinoma <1cm
  • Macroprolactinoma >1cm
65
Q

How are prolactinomas treated?

A
  • Medical treatment is first line
    • Dopamine (D2) agonists
      • Cabergoline - long half-life, once/twice weekly
      • Quinagolide
      • Bromocriptine - short half-life
66
Q

Describe the mechanism of action of ADH

A
  1. ADH (peptide hormone) secreted from posterior pituitary
  2. V1 receptors in vascular smooth muscle - vasoconstriction
  3. V2 receptors in distal tubule - aquaporin channel recruitment, reabsorption of water
67
Q

What causes ADH secretion?

A

Low plasma volume/increased serum osmolality

68
Q

Describe preparations of vasopressin (ADH)

A
  • Desmopressin (DDAVP) - synthetic analogue of vasopressin with no vasoconstrictor effects and longer half-life
69
Q

How is desmopressin administered in diabetes insipidus?

A
  • Maintenance therapy for cranial diabetes insipidus
    • Oral (bioavailability low)
    • Sublingual
    • Intranasal
  • Acute therapy
    • Subcutaneous
    • Intramuscular
    • Intravenous (variceal bleeding/shock)
70
Q

Describe the negative feedback loop involved in thyroid hormone production

A
  • Hypothalamus secretes thyrotropin releasing hormone (TRH)
  • TRH stimulates secretion of thyroid stimulating hormone (TSH) by the anterior pituitary
  • TSH stimulates the thyroid to secrete thyroxine (T4) and triiodothyronine (T3)
  • High T4 has negative feedback effect on the hypothalamus and pituitary
71
Q

Describe the absorption of levothyroxine

A

Incomplete gastric absorption, can be affected by other medication

Long half-life of 1 week in healthy patients, longer in myxoedema

72
Q
A

Medicine Year 2 (41 decks)

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