Endocrine Disorders Flashcards

(46 cards)

1
Q

What is the anatomy of the pituitary?

A

o Anterior pituitary = epithelial cells

§ Blood supply from portal system

o Posterior pituitary = nerve cells

§ Nerves from supraoptic and paraventricular nuclei

§ Release ADH and oxytocin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the anterior pituitary made of?

A

o Composed of epithelial cells from the developing oral cavity

o Secrete hormones that are under the influence of control factors released by the hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the symptoms of pituitary disease?

A

o Hyperpituitarism

§ Excess secretion of trophic hormones

§ Usually due to a functional adenoma

o Hypopituitarism

§ Deficiency of hormones

o Local mass effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the adenoma growths?

A

o 30% prolactinoma, 15% ACTH-oma, 15% GH-oma

o 20% non-functioning adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How do we classify tumours?

A

Classified on basis of the hormones produced

o Detected by immunohistochemistry

o Prolactinoma most frequent

o N.B. “null cell” produces no hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the epidemiology of tumours?

A

o Pituitary adenomas = ~10% overt intracranial tumours

o Discovered incidentally in up to 25% of autopsies

o Age: 30-50 years

o Defined as a ‘microadenoma’ if <1 cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the clinical effects of the functioning pituitary adenomas?

A

o Prolactinomas

§ Amenorrhoea, galactorrhoea, loss of libido, infertility

§ Usually diagnosed quicker in females of reproductive age

o Growth Hormone Adenomas

§ Prepubertal children -> gigantism

§ Adult -> acromegaly

§ Diabetes, muscle weakness, hypertension, congestive cardiac failure

o Corticotroph Cell Adenomas

§ Cushing’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is hypopituitarism caused by?

A

Most cases are caused by:

o Non-secreting pituitary adenoma

o Ischaemic necrosis -> MOST COMMONLY post-partum (Sheehan syndrome)

§ This is because the pituitary enlarges during pregnancy and is more susceptible to ischaemia

§ If you get a post-partum haemorrhage (Sheehan syndrome) you may develop ischaemia

§ Other causes… DIC, sickle cell anaemia, elevated ICP, shock

o Iatrogenic: ablation of pituitary by surgery or irradiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the clinical features of hypopituitarism?

A

o Children – growth failure (pituitary dwarfism)

o Gonadotrophin deficiency

§ Amenorrhoea and infertility in women

§ Decreased libido and impotence in men

o TSH and ACTH deficiency – secondary hypothyroidism and secondary hypoadrenalism

o Prolactin deficiency – failure of post-partum lactation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the posterior pituitary syndromes?

A

Posterior pituitary syndromes = 2 peptides released by the posterior pituitary:

o ADH -> deficiency, insensitivity, excess -> DI or SIADH

o Oxytocin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the Local Mass Effect of Pituitary Tumours?

A

· Compression of optic chiasm gives rise to bitemporal hemianopia

· As the tumour gets larger, you may get features of raised ICP (e.g. headaches)

o In severe cases, you may get obstructive hydrocephalus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the thyroid gland?

A

· The follicles have a small amount of stromal tissue in between them

· Follicles lined by epithelial cells and have lots of colloid in the middle

· Parafollicular cells are found in between the follicles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the physiology of thyroid?

A

o In response to TSH, follicular epithelial cells pinocytose the colloid and convert thyroglobulin into T4 and T3

o T4 and T3 are released into the circulation and they increase basal metabolic rate

o Parafollicular cells (C cells) produce calcitonin which promotes the absorption of calcium by the skeletal system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is a non toxic goitre?

A

enlargement without overproduction of thyroid hormones

§ Common if there is impaired synthesis of thyroid hormones (most often due to iodine deficiency)

· There are certain parts of the world where iodine intake is low (developing countries)

§ May be seen during puberty in girls

§ Ingestion of some substances that interfere with thyroid hormone synthesis can cause it (e.g. brassicas)

§ May be due to hereditary enzyme deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is a multinodular goitre?

A

§ With time, simple thyroid enlargement may be transformed to multinodular pattern

§ May become massive and cause mechanical effects such as dysphagia and airway obstruction

§ A hyperfunctioning nodule may develop -> hyperthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the causes of thyrotoxicosis?

A

o Primary Causes

§ Graves’ disease Hyperfunctioning multinodular goitre

§ Hyperfunctioning adenoma Thyroiditis

o Secondary Causes

§ TSH secreting pituitary adenomas (RARE)

o Causes that are NOT associated with the thyroid gland

§ Struma ovarii (ovarian teratoma with ectopic thyroid)

§ Factitious thyrotoxicosis (exogenous thyroid intake)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is Graves’?

A

§ MOST COMMON cause of endogenous hyperthyroidism; mostly in FEMALES (7x)

§ Triad presentation: Thyrotoxicosis Exophthalmos Pretibial myxoedema

§ Autoimmune disorder associated with a variety of antibodies to the TSH-R and thyroglobulin

· They stimulate thyroid hormone release and increases proliferation of the epithelium

§ Associated with other AI diseases (SLE, pernicious anaemia, T1DM and Addison’s disease)

§ NOTE: autoimmune diseases of the thyroid gland are a SPECTRUM (from Graves to Hashimoto’s)

· Antibodies against thyroid antigens are common to both conditions but they differ in functio

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the causes of hypothyroidism?

A

o Primary Causes

§ Post-ablative (after surgery or radioiodine therapy) Autoimmune (Hashimoto’s)

§ Iodine deficiency Congenital biosynthetic defect

o Secondary Causes

§ Pituitary or hypothalamic failure (UNCOMMON)

o Hashimoto’s Thyroiditis (the opposite of AI disease from Graves’ disease)

§ Common; F>M; 45-65yo Anti-TG ABs

§ Painless enlargement Anti-TPO ABs

§ Histology à lot of lymphoid cells with germinal centres

· Hurthle cells = epithelial cells become large with lots of eosinophilic cytoplasm

· Lymphoid cells = chronic infection / A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the neoplasms of the thyroid gland?

A

· Adenomas – benign neoplasms of the follicular epithelium

· Carcinomas – uncommon and account for <1% of solitary thyroid nodules

20
Q

What are the features suggestive of neoplasia?

A

o Solitary rather than multiple

Solid rather than cystic

o Younger patients

M>F

o Nodules NOT take up radioiodine (cold nodule)

21
Q

What is required to give a definitive answer?

A

o FNA

o Histology

22
Q

What are adenomas of the thyroid like?

A

o Usually solitary

Well circumscribed and compress the surrounding parenchyma

o Well-formed capsule

Small proportion will be functional and cause thyrotoxicosis

o Important to examine the capsule for invasion to exclude follicular carcinoma

23
Q

What are the 4 types of thyroid cancer?

A

FOUR types – PFMA:

§ Papillary (80%) Psammoma bodies (calcifications), Orphan’s Annie Eyes (clear nuclei)

§ Follicular (15%)

§ Medullar (5%) Amyloid in thyroid (Congo red stain)

§ Anaplastic (< 5%)

24
Q

What are the RFs for thyroid cancer?

A

§ Genetic factors (e.g. MEN)

§ Ionising radiation (mainly papillary carcinoma)

25
Describe papillary carcinoma?
§ Can occur at any age § May have papillary architecture (central connective tissue stalk with surrounding epithelium) § Diagnosis is based on nuclear features: · Optically clear nuclei · Intranuclear inclusions · May have psammoma bodies (little foci of calcification) § Generally non-functional and present as a painless mass in the neck § May present with cervical lymph node metastasis § 10-year survival of 90%
26
What is follicular carcinoma?
§ Peak incidence in middle age § Follicular morphology § May be well demarcated or show invasion § Usually metastasise via the bloodstream to the lungs, bone and liver
27
What is medullary carcinoma?
§ Neuroendocrine neoplasm derived from parafollicular C-cells § 80% are sporadic (40-50-year-olds); 20% are familial (MEN - younger patients -\> 2A, 2B) § Characteristic feature: calcitonin produced by the tumour cells is broken down and deposited as amyloid within the thyroid -\> visualised using Congo Red and looking at it under polarised light
28
What is anaplastic carcinoma?
§ Occur in elderly patients § Very aggressive § Metastases are COMMON -\> most patients die within 1 year due to local invasion
29
What is parathyroid tissue?
Derive from developing pharyngeal pouches -\> 4 parathyroid glands [can be located in thymus or anterior mediastinum]
30
What is the physiology of parathyroid hormone?
Physiology = decreased calcium stimulates PTH release -\> PTH actions: o 1 alpha hydroxylase activation -\> calcidol to calcitriol -\> gut effects o Osteoclast activation-\> Ca2+ liberation o Direct renal calcium resorption o Direct renal phosphate excretion
31
What is normally hyperparathyroidism?
§ 80-90% are due to a solitary adenoma § 10-20% are due to hyperplasia of ALL four glands · Sporadic OR a component of MEN T1, 2a § \<1% are due to carcinoma
32
Clinical features of high PTH?
§ Hypercalcaemia · Most common case of incidentally discovered hypercalcaemia · PTH is high in comparison with the hypercalcaemia due to non-parathyroid disease · Bone resorption with thinning of the cortex and cyst formation (osteitis fibrosa cystica) o This can lead to fractures = BONES N.B. normal PTH with a high calcium § Renal stones and obstructive uropathy = STONES = hyperparathyroidism § GI disturbance (constipation, pancreatitis, gallstones) = GROANS § CNS alterations (depression, lethargy, seizures) = PSYCHIC MOANS § Neuromuscular abnormalities (weakness) § Polyuria and polydipsia
33
What is secondary hyperparathyroidism?
§ Caused by any condition (usually low vitamin D) -\> causes chronically low calcium § Vitamin D deficiency is the MOST COMMON cause (i.e. renal failure -\> low vitamin D) § The parathyroid glands become enlarged (may be asymmetrical) § Leads to bone changes (as in primary disease)
34
ye
35
What is hypoparathyroidism?
o Causes: § Surgical ablation § Congenital absence (DiGeorge syndrome) § Autoimmune o Clinical features: § Neuromuscular irritability (tingling, muscle spasms, tetany) § Cardiac arrhythmias § Fits § Cataracts o Mnemonic: CATS go numb (convulsions, arrhythmia, tetany, spasms, numbness)
36
What is MEN?
a group of inherited conditions resulting in proliferative lesions (hyperplasia, adenomas and carcinomas) of multiple endocrine organs · Tumours occur at a younger age than sporadic tumours · Arise in more than one endocrine organ or may be multifocal within one endocrine organ · Tumours are often preceded by hyperplasia · Tumours are usually more aggressive than sporadic tumours and harder to treat
37
What tumour exists of the adrenal medulla?
o Secretes catecholamines in response to signals from the CNS o Diseases: § Phaeochromocytoma = secretes catecholamines à 2nd HTN; rule of 10s · 10% associated with syndromes (MEN, vHL, Sturge-Weber) · 10% bilateral · 10% malignant occur outside the adrenal glands (paragangliomas) § Neuroblastoma
38
What is the anatomy of the adrenal medulla?
Anatomy – GFR-Medulla: o Glomerulosa -\> aldosterone [OUTER] o Fasciculata -\> glucocorticoids o Reticularis -\> androgens and glucocorticoids § Cortex = epithelial cells o Medulla -\> noradrenaline/adrenaline [INNER] § Medulla = neural cells
39
What are the facets of adrenal hyperfunction?
o Cushing’s syndrome – excess glucocorticoids o Hyperaldosteronism o Virilising syndromes – excess androgens
40
What are the features of cushing's syndrome?
§ HTN Weight gain Truncal obesity “Moon face” § “Buffalo hump” Cutaneous striae
41
What are the causes of Cushings syndrome?
§ Administration of glucocorticoids (adrenal glands are atrophic) = highest exogenous cause · Other exogenous cases due to ectopic ACTH (i.e. SCLC) · Adrenals show bilateral hyperplasia § Primary hypothalamic or pituitary disease with ­ inc. ACTH (Cushing's disease) = highest endogenous cause · 30% of cases of endogenous Cushing's syndrome are primary adrenal disorders · Most will be due to a solitary neoplasm (either adenoma or carcinoma) · It can sometimes be due to bilateral hyperplasia o Most of these are associated with an ACTH-producing pituitary adenoma o It can sometimes be caused by hyperplasia of the ACTH-secreting cells rather than a discrete adenoma § In these cases, the adrenal glands show nodular hyperplasia of the cortex
42
What is hyperaldosteronism?
o 35% due to an adenoma (Conn's syndrome) o 60% bilateral adrenal hyperplasia o Clinical features: § Hypertension – accounts for very small percentage of causes § Hypokalaemia
43
What is virilising syndromes?
o May be associated with neoplasms (more commonly carcinoma than adenoma) o Congenital Adrenal Hyperplasia – most common = 21-OH deficiency § Autosomal recessive § Caused by hereditary defects in enzymes involved in cortisol biosynthesis § Reduced cortisol production -\> increased ACTH, adrenal stimulation and increased androgen synthesis § More commonly presents in childhood (more obvious in females)
44
What are the types of adrenal insufficiency?
o Primary o Secondary to reduced ACTH § Non-functional pituitary adenoma § Another lesion of pituitary or hypothalamus (inc. infarction)
45
What is primary adrenal insufficiency?
o ACUTE § Sudden withdrawal of corticosteroid therapy § Haemorrhage (neonates) § Sepsis with DIC -\> haemorrhage into adrenals (Waterhouse-Friderichson syndrome) o CHRONIC (Addison's Disease) § Autoimmune (90%), TB, HIV § Metastatic tumour (in particular, lung and breast) § RARE: amyloidosis, fungal infections, haemochromatosis, sarcoidosis
46
What is adrenocorticol neoplasms?
o Adenomas § Mostly non-functional § May be associated with Cushing's syndrome or Conn's syndrome o Carcinomas § RARE; usually LARGE § Most commonly associated with virilising syndromes than adenomas