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Yr 3 - December lectures 2018 > Therapeutics of endocrine disease > Flashcards

Therapeutics of endocrine disease Flashcards

1
Q

What are the two parts of the pituitary gland?

A

adenohypophysis (anterior) and neurohypophysis (posterior) = connected to the hypothalamus via the H-H tract

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2
Q

What are the different cell types of the anterior lobe of the pituitary and what hormones are released and what hypothalamic hormones act on it?

A

ACIDOPHILS
Somatotrophs - GHRH/Somatostatin (inhibitory) => somatotrophin
Lactotrophs - TRH/dopamine (inhibitory) => prolactin
BASOPHILS
Corticotrophs - CRH =>ACTH
Gonadotrophs - GnRH => FSH/LH
Thyrotrophs - TRH =>TSH

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3
Q

What are the hormones released from the posterior lobe?

A

ADH and oxytocin - they are produced in the hypothalamus

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4
Q

What are the different types of pituitary disease?

A

hyper-secretion - usually due to a pituitary tumour or rarely hypothalamic disease or ectopic release of hormone
if macroadenoma hypersecretion of one hormone may be associated with hyposecretion of others (mass effects)
hyposecretion

Also important to be aware of local effects e.g. optic chiasm compression

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5
Q

Are there differences between malignant and benign tumours?

A

malignant pituitary tumours are very rare but are difficult to distinguish from benign ones

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6
Q

What pituitary disease is associated with ACTH?

A

cushing’s- raised cortisol

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7
Q

What pituitary disease is associated with GH?

A

Acromegaly - raised GH and IGF-1

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8
Q

What pituitary disease is associated with LH/FSH?

A

Gonadotrophisome - raised oestrogen / testosterone

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9
Q

What pituitary disease is associated with TSH?

A

TSH-oma - thyrotoxicosis

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10
Q

What pituitary disease is associated with prolactin?

A

prolactinoma - galactorhoea, amenorrhoea, headache

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11
Q

What is acromegaly and what are the symptoms?

A

excess of GH and therefore IGF-1
Main symptoms: abnormally large hands and feet, large prominent facial features, enlarged tongue, abnormally tall height (gigantism before puberty)

other symptoms: headaches, joint pain

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12
Q

What are the signs for acromegaly?

A

coarse facial features
macroglossia
nerve entrapment - carpal tunnel syndrome (compression of nerve in the wrist causing numbness and weakness of the hands)

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13
Q

What is Cushing’s disease and what are the signs?

A

caused by a pituitary adenoma secreting ACTH causing excess cortisol
Signs:
- round, plethoric face
- weight gain - very rapid and leads to striae
- striae - >1cm broad, pruple and red trans-abdominal
- thin skin, easy bruising
- mood disturbances
- hypertension
- diabetes
- infections

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14
Q

Which pts can cushing’s pts be confused with?

A

obese pts just on examination

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15
Q

What is the treatment for cushing’s pts?

A

usually pituitary surgery - esp if seen on CT
medical treatment to reduce cortisol production = metyrapone or ketoconazole (inhibit adrenal enzymes)
may also try somatostatin analogues
need to monitor cortisol levels
can be difficult to get the right balance
if untreated prognosis is the same as a malignant disease

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16
Q

How do you treat prolactinomas?

A

treat medically rather than surgically
- dopamine agonists e.g. bromocriptine (SA) or cabergoline (LA) highly effective = restore fertility, tumour shrinkage
some may be able to come off treatment

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17
Q

What are the side effects of treatment for prolactinomas?

A

nausea and occasionally psychosis or movement disorders
by being careful when these medications are taken we can control these SEs (same as in PD)
small theoretical risk of cardiac valve problems - need regular echocardiography

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18
Q

What are the treatments for pituitary tumours?

A

pituitary surgery
- trans-sphenoidal or trans-frotnal craniotomy (if too big for TSS) - done if tumour is growing or giving mass effects

Radiotherapy
- effect is delayed but it causes shrinkage - risk of inducing hypopituitarism and potentially a risk of inducing malignancy

drug therapy

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19
Q

What are non-functional tumours?

A

those that do not secrete a pituitary hormone that leads to a clinical syndrome
most pituitary tumours are non-functional

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20
Q

What are the conditions associated with hypopituitarism ?

A

LH/FSH deficiency - hypogonadism, infertility = HRT/OCP, testosterone, assisted conception
TSH deficiency - hypothyroidism = levothyroxine
ACTH deficiency - adrenal insufficiency = hydrocortisone
GH deficiency - reduced growth in children - Growth hormone subcut - dont tend to give to adults, unless specific need (mental health)
ADH deficiency - diabetes inspidus = desmopressin

21
Q

What does ADH do?

A

ADH secreted in response to increases in plasma osmolality (also important for vol regulation)
Acts on collecting ducts - (intrinsically impermeable to water), therefore ADH stimulates production of AQPs and their incorporation into the walls of collecting ducts
Allows reabsorption of “free” water from tubular fluid

ADH levels rise in water deprivation

22
Q

What is diabetes insipidus?

A

can be secondary to generalised pituitary disease or isolated/idiopathic

23
Q

What do you get with diabetes insipidus ?

A

polyuria e.g.>3L/day and polydipsia

hypernatraemia and increased serum osmolality - occurs if you aren’t replenishing what’s lost

24
Q

How is diabetes insipidus diagnosed?

A 
having a dilute urine in the context of a concentrated plasma 
needs specialist (and dangerous) test to diagnose - have to water deprive and measure urine osmolality
25
Q

How is diabetes insipidus treated?

A

oral or intranasal desmopressin (ADH analogues) if the cause is central
overuse can lead to hyponatraemia

26
Q

What is SIADH and what does it cause?

A

syndrome of inappropriate ADH release = make too much ADH
- common cause of hyponatraemia = excessive water retention relative to sodium => low serum sodium in the absence of volume depletion

  • inappropriately high urinary sodium loss and urine osmolality greater than serum as they are concentrating urine too much
27
Q

What is the treatment for SIADH?

A

water restriction, not a normal saline infusion
significant risks if hyponatraemia is corrected too rapidly and therefore we should not >8mmol/L per 24 hours correction of sodium

28
Q

What happens if you do correct sodium levels too quickly?

A

risk of pontine demyelination - risk is increased if the patient has a poor diet or liver disease

29
Q

What are the causes of SIADH?

A 
Medication 
- diuretics
- anti-epileptics
- anti-depressants 
- MDMA
Tumours 
- lung cancer (small cell)
Infection 
- meningitis
- pneumonia
Trauma 
- head injury
30
Q

What are the treatments for SIADH?

A

treat underlying problem e.g. stopping offending medication and treat underlying infections
water restrictions 0.8-1.5L/24hours

demeclocycline (induces nephrogenic diabetes inspidus) - used if DI is more severe - give 600-1200mg / day - danger of hypernatraemia

Vasopressin antagonsts (vaptans) specific antagonists given orally and are very expensive - reduce hypernatraemia

31
Q

What are the common causes of thyrotoxicosis?

A

excessive production of thyroid hormone

  • auto-immune disease (TSH R stimulating autoantibodies) - more common in F
  • toxic nodular disease - single or multiple= autonomous functioning nodules are more common as age increases
  • drugs - amiodarone can cause hypo or hyperthyroidism
32
Q

What does thyrotoxicosis cause?

A

1) increased metabolic rate
- weight loss, increased appetite, tiredness, heat intolerance, weakness, loose bowels
2) increased sympathetic drive
- sweating, tachycardia, tremor, lid retraction
3) goitre
4) ophthalmopathy

33
Q

If patients have severe thyrotoxicosis causing tachycardia and hyperthermia what treatment is used?

A

beta-blockers - decrease sympathetic activity (control tachycardia and tremor) (contraindicated in asthma)
carbimazole or propylthiouracil - block formation of thyroid hormones - used in a reducing dosage for 12-18 months - check thyroid function every few weeks

chance the drugs may cure the patients

34
Q

What are the side effects of carbimazole?

A

minor reactions - skin rashes, arthralgia
major side effects - agranulocytosis - 1:500 incidence, therefore need FBC checked immediately if devlop sore throats or infections

35
Q

What treatments are available if the initial drug treatments aren’t effective ?

A

radioiodine - I-131 = reduces the capacity of the thyroid to generate thyroxine. Effective long-term and used in nodular disease or relapses of graves disease BUT high rate of induced hypothyroidism

36
Q

What are the side effects of radioiodine and contraindications?

A

exacerbate thyroid eye disease and we would cover this by giving steroids
contraindicated in pregnancy - to be avoided for at least 6 months - not even recommended for patients in contact with young children /(little evidence to support an increased risk of cancer)

Surgery - high recurrence rate with subtotal op- rarely used except in pregnancy - laryngeal nerve and parathyroid glands may get damaged

37
Q

What causes hypothyroidism?

A

thyroxine deficiency - usually autoimmune but may be iatrogenic (from surgery, drugs or radioiodine)
iodine deficiency is less common in UK
can be congenital/developmental issues (severe disease)
pituitary disease
incidence rises with age

38
Q

What are the symptoms of hypothyroidism ?

A 
tiredness 
cold intolerance
weight gain 
dry skin and hair 
hoarse voice
bradycardia
puffy face
hypothermia
deafness (in children)
growth arrest in children)
39
Q

How is hypothyroidism treated?

A

levothyroxine (T4) 50-150mcg per day orally - take after fasting - first thing in the morning
- main problem is overtreatment - occurs in 10-20% - diagnosed by suppressed TSH =>increased risk of cardiac and CNS death (AF) and osteoporotic fracture

40
Q

When is TSH suppression deliberate?

A

in thyroid cancer as TSH is a tumour growth factor - TSH should not be allowed to become detectable in this setting

41
Q

What does the adrenal gland produce?

A

glucocorticoids (cortisol) and mineralocorticoids (aldosterone - needed for salt homeostasis adn regulated via RAAS)

42
Q

What causes cushings and conn’s disease?

A

excess adrenal hormones

43
Q

What are the causes of primary adrenal disease?

A 
autoimmune disease (addison's disease)
tuberculosis 
rapid withdrawal of long term steroid therapy
44
Q

What is different between primary and secondary disease of the adrenal glands?

A

in primary disease mineralocorticoids and glucocorticoids deficient
in secondary mineralocorticoids intact as RAAS system is unchanged

45
Q

When do cortisol levels peak?

A

diurnal variation - steroids peak in early morning and reach lowest point by midnight

46
Q

How is adrenal insufficiency treated?

A

hydrocortisone (e.g. 20mg AM and 10mg Pm) - increase dose when pt gets stressed
fludrocortisone - 50-100mcg /OD if primary AI (aldosterone replacement) - dose calculated by BP and plasma electrolyte concentration

main side effects: excessive action - cushing’s or hyperaldosteronism

47
Q

What are the signs and symptoms of addisonian crisis?

A 
hypotension (shock)
tachycardia
anorexia
nausea
vomiting 
hypoglycaemia 
electrolyte disturbance - hyponatraemia, hyperkalaemia 
needs urgent treatment with IV hydrocortisone and IV fluids
48
Q

What can precipitate addisonian crisis?

A

surgery, trauma or infection if not receiving steroids - this can occur if they don’t receive a stress dose when needed

Yr 3 - December lectures 2018 (15 decks)

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