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Medicine block (Y3) > Week 5: Endocrine (1) > Flashcards

Week 5: Endocrine (1) Flashcards

1
Q

Common endocrine conditions

A
  • DM
  • Thyroid disorders
  • Menstrual disorders
  • Hirsutism, usually due to polycystic ovary syndrome
  • Subfertility
  • Osteoporosis and metabolic bone disease
  • Disorders of growth or puberty.
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2
Q

the pituitary

A
  • Pea sized and sits in pituitary fossa at the base of the brain
  • Anterior pituitary: derived from up growth of the gut
  • Posterior: primitive brain tissue
  • optic chiasm lies superior and cavernous sinuses laterally containing many CN
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3
Q

pituitary axis’

A

growth axis

adrenal axis

gonadal axis

thyroid axis

prolactin axis

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4
Q

Growth axis;

A

GH is secreted in a pulsatile manner with peak pulses during REM sleep.

  • GH acts on the liver to produce IGF-1, which is a marker of GH activity. GH acts directly on its receptor, as well as via IGF-1.
  • GH plays an important role in musculoskeletal growth in children, and has an important role in adults.
  • GH is under positive control by Growth Hormone Releasing Hormone (GHRH) and negative control by somatostatin.
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5
Q

Adrenal axis

A
  • ACTH has a circadian rhythm, with peak pulses early in the morning and lowest activity at midnight.
  • ACTH stimulates cortisol release by the adrenal gland
  • And is under positive control by CRH (hypothalamus)
  • . Cortisol has a negative feedback effect on ACTH.
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6
Q

Gonadal axis -

A

FSH leads to ovarian follicle development in women and sperm production in men.

  • In women, LH causes mid-cycle ovulation during the LH surge and formation of the corpus luteum.
  • In men, LH drives testosterone secretion from the Leydig cells of testes.
  • FSH and LH are stimulated by pulsatile GnRH.
  • Testosterone and oestrogen inhibit LH and FSH, and prolactin has a direct inhibitory effect on LH and FSH as well
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7
Q

Thyroid axis

A

TSH drives thyroxine release via stimulation of TSH receptors in the thyroid gland.

  • TRH (hypothalamus) stimulates TSH secretion, and is a weak stimulator of prolactin secretion. Thyroxine has a negative feedback effect on TSH.
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8
Q

Prolactin axis

A

- Prolactin causes lactation and has a direct inhibitory effect on LH and FSH.

  • It is under predominantly negative control by dopamine and weak stimulatory control by TRH. Anything that blocks dopamine will lead to an elevation prolactin.
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9
Q

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

A
  1. Mass effect of tumour on local structure- visual loss, headache
  2. Abnormality in pituitary function – hypo or hyper-secretion (rarer)
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10
Q

pituitary tumours

A

Most commonly caused by pituitary adenoma- a benign pituitary tumour.

  • Most tumours are non-functioning (do not produce any hormones), 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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11
Q

symptoms of non-functioning tumour

A
  • Headaches
  • Visual loss- bitemporal heminamoipa
  • Nausea and vomiting
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12
Q

functioning pituitary tumour

A
  • Rarer
  • Clinical symptoms dependent on which pituitary hormone they are over-secreting and its systemic effects
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13
Q

examples of fucntioning pit tumours

A
  • Acromegaly (GH)
  • Cushing’s (ACTH)
  • Prolactinoma (PRL)
  • TSHoma (TSH)
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14
Q

asessment of pit gland includes

A

clinical assessment and biochemical assessment

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15
Q

clinical assessment of the pit gland

A
  • Presentation related to compression of surrounding structures (e.g. optic chiasm- headaches, bitemporal hemianopia- do visual fields) or hormone excess
  • Functioning pit tumours
    • Acromegaly (GH)
    • Cushing’s (ACTH)
    • Prolactinoma (PRL)
    • TSHoma (TSH)
  • Look for symptoms and signs
  • Non-functioning tumours
    • Hypopituitarism or compression of local structures
    • In hypopituitism the only hormone that goes up is prolactin due to disinhibiting hyperprolactinaemia
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16
Q

biochemical asssessment: basal tests

A
  • Prolactin and TSH do not fluctuate so can be checked at any time
  • In women- LH and FSH should be measured within the 1st 5 days of the menstrual cycle
  • In men- LH and FSH and basal testosterone should be checked at 0900 in fasting state
  • Basal cortisol should be checked at 0900 when deficiency is suspected
  • IGF-1 is a marker of GH, low levels suggesting GH deficiency, high levels suggesting excess
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17
Q

biochemical assessment: dynamic tests

A
  • Synacthen test
    • Used to assess primary adrenal failure→ but also useful to assess pituitary ACTH reserve
  • Dexamethasone test
    • used to assess cushings syndrome
  • Insulin tolerance test (ITT)
    • Gold standard rest of ACTH and GH reserve
      • Should not be performed in patients with ischemic heart disease or epilepsy (risk of triggering coronary ischaemia and seizures)
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18
Q

imagining of pituitary

A

MRI pit

  • MRI modality of choice for pituitary
  • Decictated pituitary views with injection of contract highlights diff between tumour and normal gland
  • >1cm= macro-adenomas
  • <1cm = micro
  • CT may be required in those unable to have MRI
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19
Q

Pituitary deficiency

Hypothalamic control of the pituitary

A

When a tumour blocks the hypothalamic-pituitary access…

  • Hormones that decrease (due to being under positive control of hormones produced in the hypothalamus)
    • GH
    • LH/FSH
    • TSH
    • ACTH
  • 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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20
Q

Hypopituitarism

A

Cause:

  • Most commonly caused by a pituitary adenoma putting pressure on the pituitary glandular tissue.
    • Tumour could be blocking hypothalamic control of the pituitary
  • Progress loss of anterior pituitary function:
    • GH
    • LH
    • FSH
  • Posterior pituitary normally only affected if the tumour also affects hypothalamic function
    • Secretion of ADH and oxytocin normally unaffected
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21
Q

ADH deficiency

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

A
  • Symptoms
    • Dilute urine
    • Dehydration
    • Increased thirst
    • Diabetes insipidus
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22
Q

GH deficiency

A
  • Loss of GH
  • Can be hard to diagnose because GH is released in a pulsatile fashion
  • Symptoms
    • 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
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23
Q

treatment of GH deficiency

A

injected daily GH

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24
Q

Gonadotrophin (LH and FSH) deficiency

*

A
  • Loss of LH and FSH
  • Symptoms
    • Delayed puberty in children
    • Loss of secondary sexual characteristics in adult
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25
Q

Gonadotrophin (LH and FSH) deficiency in females

A
  • Reduced libido
  • Infertility
  • Oligomenorrhea- infrequent menstrual periods
  • Amenorrhea- absence of periods
  • Treatment- oestrogen ad progesterone
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26
Q

Gonadotrophin (LH and FSH) deficiency in males

A
  • Reduce libido
  • Impotence- inability to achieve erection of orgasm)
  • Treatment: testosterone
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27
Q

what are late features of pituitary tumours

A

TSH and Adrenocorticotropic hormone deficiency

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28
Q

TSH deficiency

A
  • Low thyroid hormones
  • Symptoms:
    • Cold, weight gain, tiredness, slow pulse, low T4 and non-elevated TSH
  • Treatment- thyroxine
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29
Q

ACTH deficiency

A
  • Low cortisol- addisons esk
  • Symptoms:
    • Tired, dizzy, low BP, low sodium
  • Treatment- hydrocortisone replacement – immediate increased energy and appetite
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30
Q

hyperprolactinoma

A
  • Common
  • Pregnancy should be excluded
  • Full medication history- dopamine antagonists such as antiemetics (metoclopramide) and anti-psychotics commonly cause high prolactin
  • Causes
    • Profound hypothyroidisms rare cause
    • PCOS
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31
Q

symptoms and signs of hyperprolactinoma

A
  • infertility.
  • irregular periods.
  • loss of libido.
  • lactation (galactorrhea)
  • pain in breasts.
  • vaginal dryness.
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32
Q

micro vs macro prolactinomas

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
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33
Q

treatment of prolactinoma

A
  • Dopamine (D2) agonists- cabergoline or bromocriptime
    • Cabergoline- given once or twice weekly (better tolerated than bromocriptine (given daily))
    • 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
34
Q

acromegaly

A

Caused by a GH-secreting pit tumour- long time till diagnosis

Symptoms and signs

  • Sweating
  • Headache
  • Coarsening of facial features
  • Increased hand and foot size
  • Menstrual cycle irregularity
  • Coarse oily thickened skin
  • Loss of libido
  • Sleep apnoea
  • Deepened voice
35
Q

investigations for acromegaly

A
  • Insulin-like Growth Factor 1 (IGF-1) is the initial screening test (raised)
  • Oral glucose tolerance test whilst measuring growth hormone (high glucose normally suppresses growth hormone)
  • MRI brain for the pituitary tumour
  • Refer to ophthalmology for formal visual field testing

Oral Glucose tolerance test-

  • Glucose suppresses GH release in normal individuals
  • Patients given glucose (glucose drink) and GH measured over different time frames
  • Failure to suppress hGH is diagnostic of acromegaly when coupled with elevated IGF1 and clinical signs of excess growth hormone.
  • MRI to look for pituitary tumour
  • Micro-adenomas may only be obvious with contrast
36
Q

acromegaly management

A
  • Surgical case
    • Pituitary tumours needs surgical resection (good chance of remission in micro)
  • Medicine
    • Somatostatin analogue (monthly injections)
    • GH receptor blcokers may control IGF-1 in patients with refractory acromegaly
    • Dopamine agonists in some patients
  • Stereotactic radiotherapy (take smany years to work and may cause hypopituitarism)
37
Q

cushings disease

A

Cushing’s Syndrome is used to refer to the signs and symptoms that develop after prolonged abnormal elevation of cortisol.

Cushing’s Disease is used to refer to the specific condition where a pituitary adenoma (tumour) secretes excessive ACTH.

Cushing’s Disease causes a Cushing’s syndrome, but Cushing’s Syndrome is not always caused by Cushing’s Disease.

Causes of Cushing’s Syndrome

  • Exogenous steroids (in patients on long term high dose steroid medications)
  • Cushing’s Disease (a pituitary adenoma releasing excessive ACTH)
  • Adrenal Adenoma (a hormone secreting adrenal tumour)
  • Paraneoplastic Cushing’s
38
Q

symptoms and signs of cushings disease

A

Round in the middle with thin limbs:

  • Round “moon” face
  • Central Obesity
  • Abdominal striae
  • Buffalo Hump (fat pad on upper back)
  • Proximal limb muscle wasting

High levels of stress hormone:

  • Hypertension
  • Cardiac hypertrophy
  • Hyperglycaemia (Type 2 Diabetes)
  • Depression
  • Insomnia

Extra effects:

  • Osteoporosis
  • Easy bruising and poor skin healing
39
Q

which conditions may look cushingoid

A

alcohol and severe depression

40
Q

investigations for cushings

A
  1. Dexamethasone suppression test
  • Low dose (1mg) to confirm cushings
  • High dose (8mg) to confirm source of cortisol (if low dose positive result)

or

  1. Urinary free cortisol - can be used as alternative to DST, but doesnt tell you source of cortisol

others

  • FBC (raised white cells) and electrolytes (potassium may be low if aldosterone is also secreted by an adrenal adenoma)
  • MRI brain for pituitary adenoma
  • Chest CT for small cell lung cancer
  • Abdominal CT for adrenal tumours
41
Q

differential diagnosis for cushings

A
  • Pituitary cause
    • More common than ectopic
    • ACTH high
    • Do an MRI to look for tumour
  • Adrenal
    • Significant and accelerated hirsutism
    • ACTH levels would be low due to negative feedback of ACTH by high cortisol levels
  • Ectopic ACTH
    • ACTH high
    • Hypokalaemia, smoking and weight loss suggestive of ACTH due to lung cancer and another malignancy
42
Q

management of cushings disease

A
  • Adrenal tumour will need a laparscopic adrenalectomy
  • If cushings disease e.g. pit tumour-→ transsphenoidal removal of adenoma indicated
  • Medical treatment metyrapone and ketoconazole
43
Q

hyponatraemia

A
  • Common in hospitals
  • Mild, mod, severe
  • Usually too much water, not too little salt
44
Q

presentation of hyponatraemia

A
  • Early: headache, nausea and vomiting and general malaise
  • Later: confusion, agitation and drowsiness
  • Acute severe: seizures, resp depression, coma and death
45
Q

investigations for hyponatraemia

A
  • Full history and exam
  • Drug history and hydrations tatus
  • Thiazide diuretics common cause
  • Biochemical investigations
    • Serum osmolaility
    • Urine osmolality
    • Urine sodium
    • Thyroid
    • Cortisol reserve (0900 cortisol or Synacthen)
46
Q

Syndrome of inappropriate ADH (SIADH)

A
  • Low serum osmolarity (not salty) due to water diluting
  • Only diagnosed after exclusion of hypothyroidism, total salt depletion and ACTH deficiency (appears identical to SIADH cause it reduces excretion of free water, since cortisol deficiency leads to increase ADH activity)
  • Could be caused by underlying malignancy e.g. lung cancer
  • Caused by anticonvulsants
  • Idiopathic SIADH is a diagnosis of exclusion
47
Q

management of hyponatraemia

A
  • Cause specific treatment
  • Appropriate fluid replacement in hypovolaemic hyponatraemia with saline
    • Special treatment for cirrhosis, nephrotic syndrome or CCF
48
Q

treatment of SIADH

A

fluid restriction (1-1.5L per day)- poorly tolerated. Drug treatment: demeclocycline and ADH antagonists

49
Q

SIADH

A

is a condition in which the body makes too much antidiuretic hormone (ADH). This hormone helps the kidneys control the amount of water your body loses through the urine. SIADH causes the body to retain too much water

50
Q

SIADH

A

is a condition in which the body makes too much antidiuretic hormone (ADH). This hormone helps the kidneys control the amount of water your body loses through the urine. SIADH causes the body to retain too much water

51
Q

Diabetes insipidus (DI)

A

Vasopressin deficiency (cranial) or resistance (nephrogenic)

52
Q

diagnosis of DI

A
  • High serum osmolarity
  • Low urine osmolality
  • High urine volume
53
Q

presentation of diabetes inspidus

A
  • Thirst
  • Colourless urine
  • Weak muscles
  • Hypernatremia
  • Dehydration
  • Death
54
Q

cranial DI

A
  • Cranial DI is usually seen in pituitary disease-→ vasopressin deficiency
  • A strong family history of CDI suggests a genetic cause.
55
Q

nephrogenic

A

Nephrogenic DI is usually caused by metabolic and electrolyte disturbance, renal disease and drugs affecting the kidney

Primary polydipsia is a behavioural condition leading to polydipsia, which drives polyuria. It is not associated with hypernatremia, and may in fact lead to dilutional hyponatraemia.

  • Some patients with primary polydipsia have an impaired ability to concentrate urine due to down-regulation of vasopressin release, and this can occasionally make it difficult to distinguish primary polydipsia from partial DI.
56
Q

diabetes inspidus investigations

A
  • Urine volume >3L in 24h
  • Highs serum osmolality and low urine osmolality
  • Water deprivation test
57
Q

water deprivation test

A
  • Patients with DI will have unacceptable thirst and lose significant weight
  • Synthetic vasopressin given
    • Cranial DI- reduced urine volume and increased urine osmolality
    • Nephrogenic- no response
58
Q

management of diabetes insipidus

A
  • Investigate for pit disease
  • Cranial DI- desmopressin can be given intra-nasally, orally, sublingually or parenterally
  • Nephrogenic- underlying cause should be reversed, if symptoms persist patient should drink according to thirst and keep with water loss
    • Low salt, low protein diet, thiazide diuretics and NSAIDS
59
Q

hypercalcaemia

A
  • Serum calcium >2.6 mmol/l
60
Q

causes of hypercalcaemia

A
  • Primary hyperparathyroidism - normal or high PTH
  • Malignancy - low PTH levels
  • Familial hypocalciuric hypercalcaemia- genetic defect in calcium sensing receptor

§

61
Q

presentation of hypercalcaemia

A
  • Often asymptomatic
  • Tiredness
  • Stones
  • Moans – psychiatric and pain (kidney stones)
  • Groans
  • Thrones
    • Polyuria and polydipsia due to nephrogenic DI
62
Q

investigations for hypercalcaemia

A
  • Primary hyperparathyroidism
    • Hypercalcemia with high or non-suppressed PTH
    • Low phosphate (PTH causes excretion of phosphate)
  • High ALP reflects increased bone turnover and is common in pt with vitamin D deficiency
  • Bone density recued (esp distal radius)
  • Nephrocalcinosis
  • Sub periosteal erosion of phalanges
63
Q

management of hypercalcaemia

A
  • Parathyroidectomy
  • Calcimimetic drugs (e.g. cinacalcet) effective at lowering calcium in primary hyperparathyroidism
64
Q

Hypercalcaemia with suppressed PTH – malignancy until proved otherwise

A
  • Malignancy must be excluded in all cases of hypercalcaemia where PTH is suppressed. (i.e. homestasis of calcium is still working because PTH is suppressed because calcium is high)
  • Hypercalcaemia with a low PTH may also be seen in benign granulomatous disease such as TB or sarcoidosis.
65
Q

Malignant causes of hypercalcaemia are usually associated with

A

squamous cell epithelial tumours due to the secretion of PTH-related peptide (PTH-rP).

  • Hypercalcaemia of malignancy occurs in large or advanced tumours, and bony metastases are not always present.
66
Q

Hypercalcaemia with non-suppressed PTH – primary hyper PTH until proved otherwise

A
  • When PTH is elevated or in the upper part of the normal range, malignancy is unlikely.
  • The usual cause is primary hyperparathyroidism which is most commonly due to a single parathyroid adenoma- US
    • US
    • SETAMIBI isotope scanning
67
Q

Parathyroid hyperplasia in more than one gland may suggest a

A
  • Genetic cause (e.g Multiple Endocrine Neoplasia). A very high serum calcium (>3.5 mmol/L) with a large parathyroid tumour may indicate parathyroid cancer but this is exceptionally rare.
  • Parathyroid cancer may occur rarely in association with jaw tumours (hyperparathyroidism-jaw tumour syndrome)
68
Q

Acute severe hypercalcaemia

A

Important point: This is a medical emergency and may present with profound dehydration and renal impairment, requiring urgent treatment and consideration of the cause

69
Q

hypocalcaemia

A
  • <1.9 mmol/L
70
Q

causes of hypocalcaemia

A
  • Post thyroidectomy
  • Post parathyroidectomy need long term follow up
  • Vitamin D deficiency
    • In neonates severe Vit D def may present with seizures and tetany
    • Phosphate low in Vit D def due to elevated PTH
    • Hypomagnesaemia
      • Functional hypoparthryoidism, with normal or low PTH levels
        • Causes: GI loss, alcohol and drugs (PPI)
71
Q

hypocalcaemia

A
  • Laryngospasm
  • Prolonged QT interval
  • Seizures
  • Muscle cramps
  • Carpo-pedal spasm
  • Peri-oral and peripheral paraesthesia
  • Neuropsychiatric symptoms
  • Chvosteks sign (facial spasm when cheek is tapped gently with finger)
  • Trousseau sign (carpo-pedal spasm induced after inflation of sphygmomanometer)
72
Q

hypocalcaemia

A
  • Calcium replacement e.g. oral Sandocal and adcal D3
  • Consider underlying cause reversal
  • Patients with severe vit D def should be given a loading dose of cholecalciferol
  • Magnesium def should also be replaced
73
Q

pseudohhypoparathyroidms

A
  • This rare condition is caused by a mutation in a G protein coupled to the PTH receptor and leads to PTH resistance.
  • It is characterised by hypocalcaemia and a high phosphate, which would normally suggest hypoparathyroidism, but the high PTH and normal vitamin D suggests PTH resistance rather than deficiency.
  • Patients may have a syndromic appearance with short stature, round face and short 4th and 5th metacarpals.
74
Q

when is a dexamethasone suppression tes used

A

to confirm cushings syndrome and the source of cortisol

75
Q

method of Dexamethasone suppression test

A

Dexamethasone given at 10pm

Cortisol measured at 9am

two parts

  • Low dose test (1mg)
  • High dose test (8mg)
76
Q

Low dose dexamethasone suppression test (1mg)

A

aim: does the patients have a normal response to dexamethasone - i.e. does the patients have Cushings syndrome

in normal patient: dexamethasone should suppress the hypothalamus (less CRH release) and the pituitary (less ACTH) causing reduced cortisol

in patient with cushings: 1mg of dexamethasone will not be a high enough dose to suppress hypothalamus or pituitary, due to normally high levels causing tolerance +ve dexamethasone suppression test

77
Q

High dose dexamethasone suppression test (8mg)

A

only done if low dose dexamethasone suppression test is +ve

aim: to elicit the source of cortisol (8mg should be enough to inhibit the hypothalamus and pit, therefore reducing cortisol

in patient with adenoma: 8mg should be enough to inhibit the hypothalamus and the pituitary adenoma → cortisol will decrease

in patient with adrenal gland adenoma: dexamethasone will have effect on the hypothalamus and the pituitary but not the adrenal gland, therefore cortisol is not suppressed (low ACTH, but high cortisol)

in patient with small cell lung cancer secreting ectopic ACTH: dex inhibits hypothalamus and pituitary, therefor only ACTH being produced is by the small cell lung cancer - therefore adrenal gland is stimulated and cortisol remains high

78
Q

Low cortisol can be split up into

A

Primary cortisol insufficiency- Addisons → damage to the adrenal gland

Secondary cortisol insufficiency - Damage directly to the pituitary (not enough ATCH)

79
Q

test for primary adrenal insufficiency (addisons)

A

Synacthen test

80
Q

Synacthen test

A
  1. give synacthen (artifical ACTH) first thing in the morning
  2. measure cortisol at 30 mins and then at 60 mins → cortisol should have doibled
  3. if it doesnt double this is a positive test suggesting damage to the adrenal gland itself

Medicine block (Y3) (38 decks)

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