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CP3 Medicine > Endocrinology 2 > Flashcards

Endocrinology 2 Flashcards

1
Q

What is hypothyroidism?

A

Clinical condition resulting In low levels of free T3/4

Much more common in females (10:1)

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2
Q

What are the causes of hypothyroidism?

A

Common causes:
Autoimmune: Hashimoto’s thyroiditis - associated with a goitre

Less common:

Drugs - amiodarone, iodine excess, lithium
iodine deficiency: most common cause worldwide
thyroiditis: often transient
Secondary - hypothalamic disorders,pituitary

Rare: Congenital Genesis, neoplastic infiltration

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3
Q

How does Hashimoto’s hypothyroidism come about?

A

T-cell destruction of the gland, plus B-cell secretion of TPO antibodies

Often initial hyperthyroid phase
symmetrical, bosselated goitre

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4
Q

What are the symptoms of hypothyroidism?

A 
Fatigue
Depression/psychosis
Cold intolerance
Weight gain
Constipation
menorrhagia
myxoedema coma
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5
Q

What are the signs of hypothyroidism?

A 
Hair loss
loss of outer 1/3 of eyebrow
anaemia
hoarse voice
goitre
bradycardia
dry skin
hyporeflexia
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6
Q

What investigations are done for hypothyroidism?

A

FBC: anaemia
Macrocytic if co-morbid pernicious anaemia
Microcytic if menorrhagia

TFTS: raised TSH, reduced free T4 in primary causes
low TSH in pituitary / hypothalamic disease, or ‘sick thyroid syndrome’ due to non-thyroidal illness

TPO antibodies: raised in Hashimoto’s

Cholesterol: can be raised due to hepatic hypothyroidism

CK: raised due to muscle hypothyroidism

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7
Q

What is the management for hypothyroidism?

A

Levo-thyroxine (L-T4)
low starting dose, titrated up to clinical effect
reassess every 4-6 weeks until TSH is in the lower half of the reference range in primary disease

TSH unreliable if secondary causes, titrate with free T4 levels and clinical symptoms

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8
Q

When does acute thyroiditis occur?

A

May follow an URTI

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9
Q

What is the presentation of acute thyroiditis?

A

Fever and malaise, plus thyroid swelling and tenderness - TENDER goitre

Initially there are thyrotoxic features as stored hormone is released. After this, the patient develops hypothyroidism which is usually transient but can occasionally be permanent.

There is classically low / absent uptake on technetium scanning

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10
Q

What is the treatment of acute thyroiditis?

A

Propanolol in the thyrotoxic phase, and then simple analgesia

Occasionally, prednisolone 30mg is used

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11
Q

What is the most common thyroid carcinoma?

A

Papillary carcinoma: 70%

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12
Q

What is the common age of papillary carcinoma?

A

40-50 years old

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13
Q

What are the risk factors for papillary carcinoma?

A

Previous neck irradiation

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14
Q

How does papillary carcinoma spread?

A

Locally, and metastasises to local nodes

can go to bone/lung but this is rare

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15
Q

How is papillary carcinoma cured?

A

By surgical resection, including metastases
Neck lymph node dissection if nodal involvement
Ablative radio-iodine therapy as an adjunct

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16
Q

What is the prognosis for papillary carcinoma?

A

GOOD

thyroglobulin can be used as a tumour marker following surgery

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17
Q

What % of thyroid carcinomas are follicular carcinomas?

A

20%

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18
Q

How does follicular thyroid carcinoma metastasise?

A

Via the bloodstream, classically to bone

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19
Q

How is follicular thyroid carcinoma treated?

A

Same as papillary carcinoma: surgical resection + lymph node dissection + radio ablative therapy

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20
Q

What % of thyroid cancers are medullary cancers?

A

5%

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21
Q

Who does medullary cancer tend to affect?

A

Older adults
Can affect children/young adults as part of multiple endocrine neoplasia syndrome: Men IIa/IIb
Exclude PCC prior to surgery in young patients

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22
Q

Where does Medullary cancer arise from?

A

Parafollicular ‘C’ cells
Secrete calcitonin, so plasma calcitonin levels are raised

They are slow growing and indolent, metastasising to local nodes, but the prognosis is poor

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23
Q

What % of thyroid cancer cases are anaplastic?

A

<5% cases

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24
Q

What population does anapaestic cancer arise in?

A

Elderly populations

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25
Q

How do anaplastic carcinomas spread?

A

Locally aggressive with rapid and extensive local invasion

Complications of tracheal/SVC

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26
Q

How is anaplastic carcinoma treated?

A

total thyroidectomy often not possible
External radiotherapy may give palliation

prognosis Is poor

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27
Q

What is the differential for thyroid malignancy?

A

Lymphoma

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28
Q

What is the presentation of thyroid malignancy?

A

Most present as asymptomatic thyroid nodules of lymph nodes

May be hoarseness / dysphagia

Thyroid dysfunction = rare

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29
Q

What is the approach to a solitary thyroid nodule?

A

History/examination
USS
Technetium scans: ‘Hot’ - ?adenoma
‘Cold’ - ?malignancy

FNA and cytology

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30
Q

What does the anterior pituitary synthesise and secrete?

A 
Growth hormone 
Prolactin 
Adrenocorticotrophic hormone (ACTH) 
Thyroid stimulating hormone (TSH) 
Gonadotrophin luteinising hormone (LH) 
Follicle stimulating hormone (FSH)
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31
Q

What does the posterior pituitary store and secrete?

A

ADH

Oxytocin

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32
Q

Where are ADH and oxytocin produced?

A

In the hypothalamus (connected by the pituitary stalk to the posterior pituitary)

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33
Q

What is a pituitary adenoma?

A

Benign tumour of the glandular tissue
Can be life threatening due to mass effects or secretory actions

Some are associated with MEN I / IIa syndromes

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34
Q

What is a micro adenoma / macro adenoma?

A

<1cm = microadenoma

> 1cm = macroadenoma

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35
Q

What is a ‘functioning’ vs ‘non-functioning’ adenoma?

A

Whether they are secretory or not

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36
Q

What Is the presentation of a non-functioning adenoma?

A

Bitemporal hemianopia: compression of the optic chiasm
Ocular palsy - compression of cranial nerves III, IV and VI
Hypopituitarism
Signs of raised ICP: headache

hypothalamic compression symptoms: altered appetite, thirst, sleep/wake cycle

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37
Q

What is the presentation of a functioning adenoma?

A

Acromegaly: excessive GH production
Hyperprolactinaemia: excessive prolactin production
Cushing’s syndrome: excessive ACTH production

These can cause any of the above mass effects

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38
Q

What dies prolactin do?

A

Stimulates milk production in the breast, and also inhibits GnRH and gonadotrophin production

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39
Q

What are the clinical features of hyperprolactinaemia?

A 
Galactorrhoea: in females, spontaneous / expressible 
Oligo/amenorrhoea
Decreased libido
Subfertility in males
Arrested puberty in younger patients

In the long term, osteoporosis may develop due to androgen/oestrogen deficiency

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40
Q

What are the other causes of hyperprolactinaemia?

A

Breast stimulation / stress (transient)
Drug-induced
Idiopathic

41
Q

How is diagnosis of hyperprolactinaemia done?

A

Pituitary MRI following raised serum prolactin

42
Q

How is a prolactinoma treated?

A

Dopamine agonists: dopamine inhibits prolactin release

Lifelong Ropinarole / Bromocriptine
Shrink tumours down without surgical risk.
Symptoms normally recur on stopping the drugs

43
Q

What are the side effects / long term effects of dopamine agonists?

A

S/E: nausea, vomiting, dizziness, syncope

Associated with pulmonary, cardiac and retroperitoneal fibrosis.
Monitor for with CXR and echo.

44
Q

What does GH do?

What does excess GH cause in children? Adults?

A

GH: stimulates skeletal ad soft-tissue growth

Excess GH causes gigantism in children (if prior to epiphyseal plate closure).

In adults - acromegaly.

Acromegaly: normally due to pituitary tumour. Rarely, neoplastic disease of GH/GH related proteins from non-pituitary tumours

45
Q

How is diagnosis of acromegaly done?

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

46
Q

What are the symptoms of acromegaly?

A

Space Occupying Lesion:
Headaches
Visual field defect (“bitemporal hemianopia”)
Overgrowth of tissues

Prominent forehead and brow (“frontal bossing”)
Large nose
Large tongue (“macroglossia”)
Large hands and feet
Large protruding jaw (”prognathism”)
Arthritis from imbalanced growth of joints
GH can cause organ dysfunction

Hypertrophic heart
Hypertension
Type 2 diabetes
Colorectal cancer
Symptoms suggesting active raised growth hormone

Development of new skin tags
Profuse sweating

47
Q

What are the signs of acromegaly?

A 
Protruding mandible
Prominent supraorbital ridge 
Interdental separation
Large tongues
Spade-line hands/feet 
Tight rings
Visual field defects 
Hypertension
48
Q

What is the management of acromegaly?

A

Somatastatin analogues may be used to shrink the tumour
Short term - prior to surgery
Long term if surgical removal not possible

Pegvisomant (GH antagonist given subcutaneously and daily)
Somatostatin analogues to block GH release (e.g. ocreotide)
Dopamine agonists to block GH release (e.g. bromocriptine

Surgical management: transphenoidal approach; look for scar beneath the upper lip

49
Q

What is Cushing’s syndrome?

A

Describes the symptoms of increased circulating glucocorticoid - cortisol

Occurs most commonly from exogenous administration of steroids
Spontaneous forms = rare

50
Q

What are the ACTH dependent causes of Cushing’s?

A

Cushing’s DISEASE: Increased ACTH from the pituitary (pituitary adenoma) (65%)

Ectopic ACTH - non-pituitary ACTH secreting tumour (10%). Classically small-cell lung cancer

ACTH independent causes: Excess adrenal cortisol production
Due to an adrenal tumour or nodular hyperplasia: 25%
Subsequent physiological ACTH suppression

51
Q

What are the symptoms of Cushing’s syndrome?

A 
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

52
Q

What are the signs of Cushing’s syndrome?

A 
Moon face
Frontal balding
Striae 
Hypertension
Pathological fractures
'Buffalo hump' - dorsal fat pad
Proximal myopathy

May be hypokalaemia due to the mineralocorticoid activity of cortisol.
A cushingoid appearance can also be caused by excess alcohol consumption

53
Q

How is the diagnosis of Cushing’s syndrome done?

A

Confirm raised cortisol
Overnight dexamethasone suppression test:

To perform the test the patient takes a dose of dexamethasone (a synthetic glucocorticoid steroid) at night (i.e. 10pm) and their cortisol and ACTH is measured in the morning (i.e. 9am). The intention is the find out whether the dexamethasone suppresses their normal morning spike of cortisol

54
Q

How is the dexamethasone suppression test done?

A

1mg oral dexamethasone given at midnight
Serum cortisol checked before and then at 8am

Normal –> negative feedback leads to cortisol level <50mmol/L

Cushings –> failure to suppress a cortisol secretion

55
Q

What are the screening tests to confirm Cushing’s syndrome?

A

48 hour dexamethasone test, 24 hour free cortisol or midnight cortisol.

If any are abnormal, localisation tests are required

56
Q

If you receive an abnormal low dose dexamethasone test, what is the next step?

A

HIGH DOSE Dexamethasone suppression test:
2mg/6h PO (total 8mg) for 2d to differentiate between pituitary and ectopic causes

Measure plasma and urinary cortisol at 0 and 48 Hours

Complete/partial suppression –> Cushing’s disease (pituitary) because the pituitary maintains some feedback control
MRI required

NO suppression indicates an ectopic source: do a CXR to find the primary tumour

57
Q

How does the CRH test work?

A

CRH is given and cortisol is measured at 2 hours

Raised with pituitary disease but not with ectopic sources

58
Q

What is the management for pituitary adenoma?

A

Transphenoidal surgery - apart from prolactinoma

Surgery should not be delayed, as prolonged disc optic chiasmal compression can lead to a permanent loss of vision

59
Q

What are the other causes of hypothalamic-pituitary disturbance?

A

Panhypopituitusm

Defective production of all pituitary hormones

60
Q

What is the presentation of panhypopituitism

What hormone does this suggest a deficiency of?

A

Fatigue, myalgia, hypotension: GH/corticotrophin deficiency

Diabetes insipidus: ADH deficiency

Hypothyroidism: TSH deficiency

61
Q

What are the causes of Panhypopituitusm?/

A

Pituitary causes:
Obliteration of pituitary by primary / metastatic tumour
Surgical removal / irradiation of the pituitary
Ischamic necrosis due to hypotensive shock

Hypothalamic causes: 
Destruction of the hypothalamus by: 
primary brain tumour: craniopharyngoma
infarction
Sarcoid
Infection
62
Q

How is diagnosis of Panhypopituitusm done?

A

pituitary hormones: low
effector gland hormones: low
Low response to stimulation tests
Imaging to localise the pathology

63
Q

How do diseases of the neurohypothesis occur?

A

mainly as a result of damage to the hypothalamus e.g. tumour invasion or infarction

failure of ADH production leads to diabetes insipidus, with polyuria and polydipsia

Excessive ADH production leads to SIADH

64
Q

What is pheochromocytoma (PCC)?

A

Catecholamine secreting tumours arising from sympathetic paraganglial cells, known as chromatin cells

65
Q

Where are PCCs found?

A

In the adrenal medulla

25% are familial and associated with multiple endocrine neoplasia type 2 (MEN 2).

There is a 10% rule to describe the patterns of tumour:

10% bilateral
10% cancerous
10% outside the adrenal gland

66
Q

What’s the presentation of PCC?

A

Severe/episodic Hypertension unresponsive to medical tx

General: sweating, heat intolerance , pallor or flushing
Neurological: Headaches, visual disturbances, seizures
CV: palpitations, chest tightness, dyspnoea, postural hypertension
GI: abdominal pain, nausea, constipation

Symptoms can be worsened by stress, alcohol and drugs
B-blockers can induce life threatening hypertensive episodes in patients without adequate alpha blockade. therefore, labetalol = treatment of choice

67
Q

How is diagnosis of PCC done?

A

3 x 24 hour urine collections for free met adrenaline and normetadrenaline
N.B. NICE now suggest metanepherines

MRI/CT/functional imaging to locate the tumour

68
Q

What is the management of PCC?

A

Alpha blockers (i.e. phenoxybenzamine)

Beta blockers once established on alpha blockers

Adrenalectomy to remove tumour is the definitive management

69
Q

What is Addison’s disease?

A

Primary adrenal insufficiency - autoimmune
Destruction of the ENTIRE adrenal cortex, leading to glucocorticoid (cortisol), mineralocorticoid (aldosterone) and sex-steroid deficiencies

70
Q

How does Addison’s disease differ from HPA disease?

A

HPA disease generally spares mineralocorticoid production, which is stimulated by ATII

Sex steroids are also largely independent of pituitary stimulation

71
Q

Describe the aetiology of Addison’s disease

A

80% autoimmune in UK
TB = most common worldwide

Sepsis
metastatic cancer: lung/breast
Lymphoma
Adrenal haemorrhage: Waterhouse-Friederichsen syndrome

72
Q

What are the symptoms of Addison’s disease?

A 
Fatigue
Nausea
Cramps
Abdominal pain
Reduced libido
Syncope 
Depression
73
Q

What are the signs of Addison’s disease?

A

Pigmentation, especially of new scars and palmar creases
Postural hypotension
Signs of dehydration
Loss of body hair (particularly axillary/pubic)

74
Q

What investigations should be done for Addison’s disease?

A

FBC: anaemia
U&Es: low sodium, high potassium, uraemia - due to mineralocorticoid insufficiency
Ca2+: raised
glucose: low due to lack of cortisol

ACTH / synacthen test

9AM ACTH/cortisol

adrenal autoantibodies

CT/MRI

75
Q

What is the short ACTH stimulation / synacthen test?

A

Give tetracosactide IM (ACTH analogue)
Measure plasma cortisol before and 30 minutes after

Synthetic ACTH should stimulate cortisol production in adrenals

Second value >550nmol/L excludes Addison’s

76
Q

Describe how the 9AM ACTH test is done?

A

Raised ACTH, low/normal cortisol confirms Addison’s

77
Q

What investigations can be done for the cause of Addison’s

A

21-hydroxylase adrenal autoantibodies: autoimmune disease
CXR: TB
Adrenal CT: to look for TB / metastatic disease if antibodies negative

78
Q

What is the management of Addison’s disease?

A

Long-term glucocorticoid cover
15-25mg hydrocortisone daily, in three divided doses
avoid giving late in day (can cause insomnia)

Long term mineralocorticoid cover: required if postural hypotension, low sodium or high potassium
Fludrocortisone 50-200 micrograms daily

79
Q

How should steroids be counselled / adjusted?

A

Steroids should never be abruptly stopped. Extra doses if strenuous exercise
Double dose for surgery, febrile illness or trauma

Carry a steroid card / bracelet and carry IM hydrocortisone in case of Addisonian crisis

80
Q

What is Addisonian crisis?

A

Severely inadequate levels of cortisol, occurring either as a first presentation of adrenal disease, or triggered by physiological stress

Presents with fever, nausea, vomiting, shock, hypoglycaemia, hyponatremia and hyperkalaemia

81
Q

What is the treatment for Addisonian crisis?

A

IV fluids and IV hydrocortisone

82
Q

What is CAH?

A

Congenital deficiency in 21-alpha-hydroxylase

This is necessary for the production of mineralocorticoids and glucocorticoids but NOT sex hormones

83
Q

What happens to hormone levels in CAH?

A

Aldosterone and cortisol levels decrease, with consequent ACTH rises
Precursors such as progesterone build up and go down the alternative pathway to form sex hormones

Testosterone levels are raised

84
Q

What are the clinical features of CAH?

A

Virilisation of the external genitalia in females: clitoral hypertrophy and variable fusion of the labia

Enlarged penis and pigmented scrotum is seen in teh male, yet this is rarely picked up
Salt-losing crisis in 80% males, at 1-3 weeks of age
in the non salt-losing males, presents as hypervirilisation

Early pubarche, adult body odour, muscular build

85
Q

What investigations are done for CAH?

A

17-alpha-hydroxyprogesterone levees: markedly raised

other features may be: low sodium, high potassium and metabolic acidosis in salt losers

86
Q

What is the management of CAH?

A

Steroid cover, as per Addison’s disease

Again, at risk of Addisonian crisis

87
Q

What is Conn’s syndrome?

A

Adrenal adenoma, leading to primary hyperaldosteronism

Responsible for hyperaldosteronism in 60% cases
Bilateral adrenal hyperplasia is the second most common cause for primary hyperaldosteronsim

LEADS TO SODIUM AND WATER RETENTION

88
Q

What is the presentation of Conn’s syndrome?

A

Mostly asymptomatic
HTN - resistant to treatment, may cause headaches

Features of hypokalaemia; may cause cramps, weakness, Tetany. may be polyuria

Biochemical features: hypokalaemia, with urinary potassium loss
Elevated plasma aldosterone:renin ratio

Plasma aldosterone levels will not be suppressed by fludrocortisone administration

89
Q

What further investigations can be done for Conn’s syndrome?

A

One primary hyperaldosterone is confirmed, adrenal CT is indicated to differentiate Conn’s from adrenal hyperplasia

can also do adrenal scintigraphy

90
Q

What is the management of Conn’s syndrome?

A

Laparoscopic adrenalectomy to remove adenoma

Spironolactone post-op to control hypertension/hypokalaemia (tx of choice for bilateral hyperplasia)

91
Q

Why is 40% of plasma calcium inactive?

A

Bound to albumin

92
Q

How does albumin affect measured calcium

A

Labs adjust for low/high serum albumin to give e measure of ionised calcium

If low albumin, non-adjusted calcium appears low

93
Q

How do acidotic/alkalotic states affect ionised calcium levels?

A

Acidotic states increase ionised calcium by decreasing albumin binding

Alkalotic states decrease ionised calcium by increasing albumin binding

94
Q

Where are the parathyroid glands?

How many are there?

A

4

Posterior to thyroid

95
Q

Which cells secrete PTH?

When is PTH secreted?

A

Chief cells

Secreted when plasma calcium levels are LOW
PTH can also be secreted in response to low vitamin D or high phosphate levels

96
Q

How does PTH increase plasma calcium levels?

A

Directly stimulating calcium reabsorption from bone
Directly increasing renal tubular calcium reabsorption
Indirectly stimulating increased GI calcium absorption: by increasing vitamin D activation in the kidney

PTH has a secondary effector increasing renal phosphate excretion

97
Q

How does Vitamin D sustain plasma calcium and phosphate levels?

A

Increasing inflow from GIT

98
Q

What is Vitamin D used for?

A

normal bone formation

CP3 Medicine (19 decks)

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