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SBCP Pathology > Endocrine Pathology > Flashcards

Endocrine Pathology Flashcards

1
Q

What is Diabetes Mellitus?

A

A chronic disorder of carbohydrate, fat and protein metabolism. Defective or deficient insulin secretory response which results in impaired carbohydrate (glucose) use.

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2
Q

How can Primary Diabetes be divided?

A
  • Type 1
  • Type 2

Genetic defects of B cell function (including maturity onset diabetes of the young MODY)

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3
Q

What are the causes of secondary diabetes?

A
  • Chronic pancreatitis
  • Haemochromatosis
  • Infectious - congenital rubella, cytomegalovirus.
  • Endocrinopathies (adrenal, pituitary tumours)
  • Drugs (corticosteroids, pentamidine, Vacor)
  • Other genetic disorders e.g. Down’s Syndrome
  • Gestational Diabetes Mellitus
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4
Q

Why does chronic pancreatitis cause diabetes mellitus?

A
  • Alcohol/gallstones lead to inflammation of the pancreas
  • Loss of pancreatic tissue and replacement by fibrous tissue.
  • Therefore loss of both the exocrine (digestive enzymes) and endocrine (insulin, glucagon, pancreatic polypeptide) tissues.
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5
Q

Type 1 diabetes:

  • Describe clinically
  • Genetic link?
  • Explain pathogenesis
  • How islet cells are affected
A
  • Onset <20 years, normal weight, decreased blood insulin, anti-islet cell antibodies, ketoacidosis common.
  • 50% concordance in twins, HLA-D linked.
  • Autoimmunity, immunopathic mechanisms leading to severe insulin deficiency.
  • Insulitis early wth marked atrophy and fibrosis. B cell depletion.
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6
Q

Type 2 Diabetes:

  • Describe clinically
  • Genetic link?
  • Explain pathogenesis
  • How islet cells are affected
A
  • Onset >30 years of age, obese, normal or increased blood insulin, no anti-islet cell antibodies, ketoacidosis rare.
  • 90-100% concordance in twins, no HLA associated.
  • No insulitis. Focal atrophy and amyloid deposits and mild B cell depletion.
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7
Q

What is the normal effect of glucose on the islet cells?

A

Increasing levels of glucose in the blood are transported across the cell wall by GLUT-2 transporter. This causes increased synthesis of preproinsulin and proinsulin (stored in granules in the cell). This is then released from the cell and causes lowering of blood glucose level.

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8
Q

What is the normal effect of insulin on cells?

A

Insulin binds to the insulin tyrosine kinase receptor on the cell membrane, facilitating glucose uptake by the cell via GLUT-4 transporters.
Insulin also increases protein synthesis, DNA synthesis and has metabolic effects e.g. the transfer of glucose to lipids.

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9
Q

What causes type 1 Diabetes Mellitus?

A

Severe absolute lack of insulin (autoimmune destruction of B cells in the Islets of Langerhans of the pancreas).
Genetic predisposition + environmental insult (viral infection AND/OR damage to B cells) = autoimmune attack?

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10
Q

What genetic factors are involved in the development of Type 1 Diabetes Mellitus?

A
  • Northern European race
  • Familial 6% 1st degree relative
  • Identical twin 70%
  • Class II 6p21 (HLA-D)
  • 95% white people with DM have HLA-DR3/HLA-DR4 haplotype.
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11
Q

What auto-immune factors are involved in the development of Type 1 Diabetes?

A

Pre-clinical phase of islet destruction

  • Insulitis - CD8 CD9+ macrophages
  • Associated with increase in Class 1 MHC molecules and aberrant expression Class II MHC
  • 70-80% DM1 have islet cell autoantibodies
  • 10-20% have other autoimmune diseases.
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12
Q

What environmental factors are involved in the development of Type 1 DM?

A
  • Geographic location
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13
Q

Which viruses have a role in the development of T1DM?

A
  • ? mumps
  • Measles
  • Rubella
  • Coxsackie B - immune response cross reacts Beta cell protein
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14
Q

Describe the pathogenesis of Type 2 DM.

A

Genetic predisposition (multiple genetic defects) + environmental factors (obesity) cause a primary B cell defect with deranged insulin secretion and peripheral tissue insulin resistance with inadequate glucose utilisation. This leads to hyperglycaemia, to B cell exhaustion (reversible stage) and then type 2 diabetes.

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15
Q

Describe the stages of deranged insulin secretion in T2DM.

A
  • Initially there is loss of pulsatile, oscillating secretion of insulin
  • Abnormal response to hyperglycaemia
  • Later mild-moderate insulin deficiency
  • ? Genetic vulnerability to hyperglycaemia.
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16
Q

Describe insulin deficiency in T2DM.

A
  • Insulin deficiency is insufficient to explain clinical finding
  • Insulin resistance is seen with pregnancy and obesity
  • Reduction in synthesis and translocation of gluts in muscle and fat
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17
Q

What is the role of obesity in T2DM?

A
  • 80% of type 2 diabetics are obese
  • Patients have a relative insulin deficiency
  • Potentially reversal in early stages of disease with weight loss.
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18
Q

Why do complications arise from diabetes?

A
  • Non-enzymatic glycosylation: products of glucose become linked with protein. HbA1c and Advanced Glycosylation End products (AGE)
  • Intracellular hyperglycaemia: disturbances of polyol pathways and accumulation of sorbitol and fructose
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19
Q

What sites are involved in the complications of diabetes?

A
  • Brain: small vessel disease (microangiopathy), cerebral vascular infarcts and haemorrhage.
  • Eyes: retinopathy, cataracts, glaucoma.
  • Vessels: hypertension, atherosclerosis, peripheral vascular atherosclerosis leading to gangrene and infections.
  • Heart: MI
  • Nephrosclerosis: glomerulosclerosis, arteriosclerosis and pyelonephritis.
  • Nervous system: peripheral neuropathy, autonomic neuropathy.
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20
Q

What are the pancreatic complications of diabetes?

A

-More with Type 1 than Type 2
- Reduction in number and size of islets
Leucocytic infiltration of islets (insulitis)
- Beta cell degranulation
- Reduction in islet cell mass
- Amyloid deposition in type 2

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21
Q

What are the vascular complications of diabetes?

A
  • Accelerated atherosclerosis (esp aorta and coronary vessels)
  • Myocardial infarction (Male = female in diabetic subgroup) - need to revise heart lectures for gross and histological appearance of MI.
  • Gangrene in extremities (x100 more common than in population)
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22
Q

Why does diabetes cause vascular complications?

A
  • Elevated blood lipids
  • Low levels of HDL (protective lipids)
  • Increased thromboxane A2 activity & increased stickiness of platelets,
  • Hyaline arteriolosclerosis.
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23
Q

What are the renal complications of diabetes?

A
  • Large vessel disease - renal artery stenosis causes renal ischaemia and hypertension
  • Diabetic microangiopathy
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24
Q

What is diabetic microangiopathy?

A

Diffuse thickening of the basement membrane of small capillaries.

  • Glomerular lesions. Histologically uniform thickening due to increased deposition of glycogenated collagen proteins. Normal structure of internal lamina dense but external lamina rarae is lost. Diffuse and nodular patterns (Nodular = Kimmelstiel-Wilson lesion, typical of diabetic glomerulosclerosis). Increased mesangeal matrix in the centre of the glomerulus causing narrowing of the capillary loops due to deposition of abnormal collagen fibres.
  • Vascular lesions: hyaline arteriolosclerosis (deposition of hyaline materials in the vessels replacing the muscles of the tunica media) and arteriosclerosis (small and medium sized arteries are thickened). Lead to decrease in glomerular blood flow and the development of renal failure.
  • Pyelonephritis - inflammatory condition of the kidney due to ascending infection. On gross appearance the kidney has a mottled appearance with hyperaemic areas, inflammation and necrosis. Histologically tubules are filled with polymorphs and inflammatory debris.
  • Necrotising papillitis - due to inflammation of the kidney associated with ischaemia, can be seen with some analgesics. There is necrosis of the papilla and it moves into the ureter, and may cause obstruction. Sometimes passed into the bladder and voided externally.
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25
Q

What are the ocular complications of diabetes?

A
  • Microangiopathy
  • Visual impairment
  • Blindness
  • Retinopathy
  • Cataract Formation
  • Glaucoma
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26
Q

What are the neurological complications of diabetes?

A
  • Peripheral symmetrical neuropathy that involves sensory, motor or autonomic nerves (sympathetic nerves supplying the gut, leading to diarrhoea, constipation, or nerves to the badder)
  • CNS:
    > Microangiopathy
    > Cerebral haemorrhage
    > Cerebral infarction (primary due to involvement of vessels within the brain or secondary due to an embolus from an atherosclerotic neck vessel).
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27
Q

What are the skin complications of diabetes?

A
  • Recurrent infections- bacterial and fungal (can be first presentation of type 2 diabetes)
  • Necrobiosis lipoidica diabeticorum
  • Granuloma annulare
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28
Q

What are the pregnancy complications of diabetes?

A
  • Pre-eclamptic toxaemia
  • Large but immature babies
  • Neonatal hypoglycaemia
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29
Q

What is the embryologic origin of the thyroid gland?

A

Develops embryologically as a down growth from pharyngeal epithelium and descends in the neck (explains ectopic thyroid tissue at various sites in the neck along the midline).

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30
Q

Explain the role of cervical sympathetic nerves in innervation of the thyroid gland.

A

Cervical sympathetic nerves influence secretion from the thyroid by acting on blood vessels.

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31
Q

Describe normal thyroid histology.

A
  • Thyroid follicles of varying sizes lined by follicular epithelium
  • The centre of the follicle contains colloid - store for thyroid hormone.
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32
Q

Describe the physiology of release of hormone from the thyroid gland?

A
  • TSH released by pituitary after action of trophic factors from hypothalamus.
  • TSH acts on thyroid to release T4 (thyroxine) and lesser amounts of T3 (triiodothyronine).
  • T3 and T4 are released into the systemic circulation reversibly bound to thyroxine binding globulin TBG
  • T3 and T4 are maintained within narrow limits
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33
Q

What is hyperthyroidism?

A

A hypermetabolic state caused by excess levels of T3 and T4

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34
Q

What are the causes of hyperthyroidism?

A
  • Diffuse hyperplasia 85%
  • Ingestion of exogenous hormone (i.e. over-treatment of hypothyroidism)
  • Hyperfunction goitre
  • Thyroiditis
35
Q

Which diseases are associated with hyperthyroidism

A

Common:

  • Diffuse toxic hyperplasia i.e. GRAVE’s DISEASE
  • Toxic multi nodular goitre
  • Toxic adenoma

Uncommon:

  • Acute or subacute thyroiditis
  • Hyperfunctioning thyroid carcinoma
  • Choriocarcinoma or hydaditiform mole
  • Thyroid-stimulating hormone secreting pituitary adenoma
  • Neonatal thyrotoxicosis associated with maternal Grave’s Disease
  • Struma ovarii (ovarian teratomatous thyroid)
  • Iodine-induced hyperthyroidism
  • Iatrogenic (exogenous) hyperthyroidism
36
Q

What are the clinical features of hyperthyroidism?

A

OVERACTIVITY OF SYMPATHETIC NERVOUS SYSTEM
Cardiac manifestations: Increased CO, tachycardia, palpitations, caridomegaly, arrhythmias particularly AF, congestive heart failure
- Atrophy of musculoskeletal tissues - osteoporosis
- Neuromuscular: tremor, hyperactivity, emotional lability, anxiety
- Skin: warm and moist, increased sweating
- GI: increased appetite, weight loss, diarrhoea and crampy abdominal pain.

37
Q

How is hyperthyroidism diagnosed?

A
  • Increase in T4 levels (only measure T4 as T3 mimics T4)
  • TSH level after TRH injection NB** thyrotoxicosis caused by pituitary or hypothalamic factors may have a high TSH
  • Radioactive iodine uptake by the thyroid is an indication of activity within the gland.
  • TSH usually decreased or low in primary hyperthyroidism.
38
Q

What are the causes of hypothyroidism?

A
  • Insufficient thyroid parenchyma: developmental, radiation injury, surgical ablation, Hashimoto’s thyroiditis
  • Interference with thyroid hormone synthesis: idioapathic. hereditary biosynthetic defects, iodine deficiency, drugs, Hashimoto thyroiditis.
  • Suprathyroidal: pituitary lesion reducing the TSH secretion or hypothalamic lesions that reduce TRH delivery.
39
Q

What is cretinism?

A
  • Hypothyroidism developing in infancy
  • Endemic in iodine deficient areas
  • Poor development of skeleton and CNS along with severe mental retardation
  • T3 and T4 are able to cross the feto/maternal barrier before birth however following birth the baby is dependent on its own hormone secretion.
40
Q

What is myxoedema?

A
  • Adult hypothyroidism
  • Non-specific features
  • Decreased sweating
  • Constipation
  • Symptoms caused by accumulation of matrix substances in subcutaneous tissue:
    > Slowing of physical and mental activity
    > Fatigue, apathy, mental sluggishness
    > Speech and intellectual activity slowed
    > Listless, cold intolerant, overweight
    > CO decreased with SOB and decreased exercise tolerance.
41
Q

How is myxoedema diagnosed

A
  • Decreased T3 and T4
  • TSH elevated
  • –> Pituitary or hypothalamic causes of myxoedema may have a low TSH.
42
Q

What is thyroiditis?

A

A general term for an inflammatory condition of the thyroid gland and comes in several forms:

  • Hashimoto’s thyroiditis (most common and is auto-immune)
  • Granulomatous thyroiditis (may be associated with granulomatous disease elsewhere in the body)
  • Subacute lymphocytic thyroiditis (mild non-specific chronic inflammation)
  • Grave’s disease
  • Riedel’s thyroiditis (Associated with dense fibrosis which gives the thyroid gland a firm and hard feeling on palpation).
  • Palpation thyroiditis - rupture of some of the thyroid follicles causing a giant cell reaction.
43
Q

What is Hashimoto’s Thyroiditis?

A
  • Commonest cause of thyroiditis
  • Autoimmune disease caused by defect in T cells that involves both cellular and humeral immunity
  • Activation of thyroid specific CD4+ T cells and formation of CD8+ cytotoxic T cells
  • B cells secrete anti TSH factors
  • Genetic component to the disease - high prevalence of HLA DR3 and DR5.
44
Q

What are the clinical features of Hashimoto’s thyroiditis?

A
  • Female to male ratio 15:1
  • Typically aged 45-65
  • Painless thyroid enlargement
  • Gradual hypothyroidism after perhaps initial hyper phase
  • Increased incidence of B cell lymphoma of the thyroid.
  • Associated with other auto-immune diseases.
45
Q

Describe the gross appearance of the thyroid in Hashimoto’s thyroiditis.

A

In the early stages the gland is tender and enlarged due to inflammatory processes.
As disease progresses the inflammation decreases and the gland becomes fibrosed with loss of thyroid tissue. The gland becomes firm, pale and hard.

46
Q

Describe the histological appearance of thyroid tissue in Hashimoto’s thyroiditis.

A

Masses of lymphoid tissue and pink cell change of the epithelium.
At higher powers you can see an inflammatory infiltrate and germinal follicle.
Hürthle cells visible.

47
Q

What is Grave’s Disease?

A

Hyperthyroidism due to hyper functional diffuse enlargement of the thyroid.

Features include:

  • Infiltrative ophthalmology - exophthalmos
  • Dermopathy - pretibial myxoedema.
48
Q

What are the clinical features of Grave’s Disease?

A
  • It is a common condition affecting 1.5-2% females
  • Aged 20-40 years
  • Genetic features
  • HLA B8 & DR3
  • TSH-receptor antibodies bind to the TSH receptor and stimulate thyroid hormone production (i.e. mimic the effect of TSH) therefore free T3 and T4 are increased and TSH is decreased (due to negative feedback loop)
49
Q

Describe the histology of the thyroid in Grave’s Disease.

A

Considerable variation in the size of the follicles; some are small and contain little colloid and others are very large ad colloid is pale with scalloped border.
The lining follicular epithelium is columnar in appearance.

50
Q

What features are suggestive of a thyroid neoplasm?

A
  • Solitary nodule
  • Solid nodule
  • Nodule in a younger patient
  • Nodule in a male
  • Cold nodule that does not take up radioactive iodine.
51
Q

What is a thyroid adenoma?

A
  • A discrete solitary mass derived from follicular epithelium.
  • Shares architectural features with follicular carcinoma except has an intact surrounding capsule.
  • NOT precursors of follicular carcinoma.
  • May be difficult to differentiate from follicular cancer.
  • Range of histological subtypes
52
Q

Describe the gross and histological appearance of thyroid adenoma.

A

Gross appearance - well circumscribed lesion encapsulated in a fibrous border. Inside the lesion there is a reddish-brown appearance and some glistening material suggestive of colloid. Single nodule in an otherwise normal gland.

Histological - The tissue is made up of small follicles (smaller than those of normal thyroid tissue) and a capsule separating the adenoma from the adjacent thyroid tissue.

53
Q

Describe the pathogenesis of thyroid cancer.

A
  • Ionising radiation (treatment of thyroid disease or malignancies of the neck/brain)
  • Autoimmune thyroiditis
  • RET proto oncogene mutation
  • Multiple endocrine neoplasia syndrome II
54
Q

Name the types of thyroid cancer and their relative incidences.

A 
4 types: 
> Papillary Carcinoma - 75-85%
> Follicular Carcinoma - 10-20%
> Medullary Carcinoma - 5% 
> Anaplastic Carcinoma - <5%
55
Q

Papillary cancer:

  • Presentation
  • Diagnosis
  • Prognosis
A
  • Typically aged 20-40 with asymptomatic thyroid nodules.
  • Diagnosis based on papillary structure and nuclear cytology - radio nucleotide scan and FNA.
  • Prognosis: 10 year survival is 98%. 5-20% have local recurrence and 10-15% have metastases.
56
Q

Describe the histological appearance of papillary carcinoma.

A
  • Central fibrovascular core surrounded by a tall columnar type epithelium.
  • Nuclear features of the epithelium are very characteristic: overlapping nuclei, nuclear clearing (chromatin found at the periphery of the nucleus), prominent nucleoli and longitudinal grooves.
    ORPHAN ANNIE EYE appearance.
57
Q

How is follicular carcinoma different from papillary carcinoma?

A
  • Slightly worse prognosis
  • Nodules can be functional
  • Better differentiated lesions are TSH sensitive so patients are treated with thyroxine after surgery.
58
Q

Describe the distinct histological features of follicular carcinoma.

A
  1. Invasion of the fibrous capsule

2. Lymphovascular invasion outside the capsule

59
Q

What is medullary carcinoma of the thyroid gland?

A
  • Neuroendocrine carcinoma derived from parafollicular C cells
  • May secrete calcitonin
  • May produce amyloid stroma
  • Associated with MEN syndromes
  • Paraneoplastic syndromes
  • 5 year survival 50%
60
Q

Describe the histological appearance of medullary carcinoma.

A

Tumour cells form nest which are small and relatively regular.
Between the nests there is an eosinophilic material amyloid, which forms when fibrils (probably derived from calcitonin) form a ß pleated sheet and form fibrillary masses within the gland. This stains positively with Congo Red stain.

61
Q

Anaplastic carcinoma:

  • What is it?
  • Prognosis
  • Presentation
A
  • Poorly differentiated tumours. ? loss of p53 tumour suppressor gene
  • Mortality approaches 100%
  • Mean age 65, half patients have history of a multi nodular goitre and 20-30% have concurrent thyroid tumour.
62
Q

Describe the histological appearance of anaplasic carcinoma.

A

Tumour cells have spindle shaped appearance.
There is variation in nuclear size and detail and mitotic figures present.
No evidence of thyroid follicle formation within the tumour.

63
Q

Thyroid lymphoma?

A
  • Rare
  • May complicate thyroiditis (particularly Hashimoto’s)
  • Usually B cell and low grade but can be high grade and aggressive
64
Q

What is a carcinoid tumour?

From which tissues are they derived?

Where do they present?

When and how do they present?

A

A tumour arising from cells generating bioactive compounds. They synthesise a range of bioactive products and hormones e.g. insulin, 5-HT, calcitonin. Make up 2% colorectal tumours and 50% small intestine tumours.

Derived from epithelial stem cells but phenotypically resemble endocrine cells.

Cells present in many organs - pancreatic islets, lungs, biliary tract, liver, thyroid C cells, adrenal. Most commonly seen in GI tract.

Occur at any age (peal incidence 50-60)

65
Q

How do carcinoid tumours behave?

A
  • Potentially malignant tumours.
  • Aggressive behaviour correlates with the site of origin (appendiceal and rectal carcinoids are less aggressive than gastric or small intestine), depth of local penetration and size of tumour.
66
Q

Describe the gross and histological appearance of a carcinoid tumour.

A

Gross - small tumour.

Histological - bland and monotonous cells with little pleomorphism. Neurosecretory glands are present on EM and are characteristic of these tumours.

67
Q

What causes carcinoid syndrome?

Explain carcinoid syndromes according to the location of the tumour.

A

Elevated levels of 5-HT and 5-HIAA. Seen in 20% patients with metastatic carcinoid.

  • GI carcinoids: frequently asymptomatic and rarely produce local symptoms. Gastric, pancreatic carcinoids can produce gastrin causing Zollinger-Ellison syndrome
  • Lung carcinoids: Mass effect
68
Q

What is Cushing Syndrome?

A

Increased levels of cortisol in the blood.
Causes:
- Pituitary - increased ACTH secretion –> adrenal hyperplasia –> increase in cortisol secretion
- Adrenal - nodular hyperplasia or tumour
- Paraneoplastic - lung or other non endocrine cancer secreting ACTH –> adrenal hyperplasia –> increased cortisol
- Iatrogenic - steroids –> adrenal atrophy and Cushing syndrome.

69
Q

What are the causes of Cushing syndrome and their relative incidences?

A
  • PRIMARY hyper secretion of ACTH by the ANTERIOR PITUITARY - >50%
  • PRIMARY ADRENAL neoplasm 15-30%
  • Ectopic ACTH: small cell carcinoma of the lung, carcinoid tumours, medullary carcinoma of the thyroid - ?%
70
Q

List the features of Cushings Syndrome

A
  • Central obesity
  • Moon face
  • Weakness and fatiguability
  • Hirsutism
  • Hypertension
  • Plethora (high colour)
  • Glucose intolerance (diabetes)
  • Osteoporosis
  • Neuropsychiatric abnormalities
  • Menstrual abnormalities
  • Skin striae (sides of lower abdomen)
71
Q

What are the causes of primary adrenal insufficiency?

A

Loss of cortex because of:

  • Idiopathic (autoimmune)
  • Infection (mycobacteria, fungi)
  • AIDS, opportunistic microbes
  • Acute haemorrhagic necrosis (Waterhouse-Friderichsen syndrome)
  • Amyloidosis
  • Sarcoidosis
  • Haemochromatosis
  • Metastatic carcinoma
  • Metabolic hormone production failure
  • Congenital adrenal hypoplasia
  • Drug and steroid induced inhibition
72
Q

What are the causes of secondary adrenal insufficiency?

A

Hypothalamic pituitary disease:

  • Neoplasm
  • Inflammation (sarcoidosis, TB, pyogens, fungi)

Hypothalamic pituitary suppression

  • Long term steroid administration
  • Steroid-producing neoplasms
73
Q

Which tumours typically arise in the adrenal gland?

A

Cortex:

  • Adenoma
  • Carcinoma (rare)

Medulla

  • Phaeochromocytoma
  • Metastatic tumours

Multiple endocrine neoplasia.

74
Q

Describe the gross and histological appearance of an adrenal cortical adenoma.

A

Gross - large well defined well circumscribed nodule with characteristic yellow colour.

Histological - encapsulated lesions consisting of proliferation of adrenal cortical cells.

75
Q

Describe the gross and histological appearance of adrenal carcinoma.

A

Gross - large tumour replaces the adrenal gland. Has destroyed normal tissue and is invading into the surrounding structures. Invasion and size suggests a malignant tumour.

Histological - nests of cells bear some resemblance to normal adrenal cortex however there is mitotic activity and nuclear pleomorphism. Tumour invades the capsule of the gland.

76
Q

What is a phaeochromocytoma?

A
  • Tumour derived from cells of the sympathetic nervous system which arises in the adrenal medulla.
  • Produces excess catecholamines (adrenaline and noradrenaline) therefore causes symptoms of sweating, hypertension, tachycardia, anxiety, ‘feeling of impending doom’.
  • May behave in a malignant fashion (primarily are benign)
  • May be familial (MEN)
77
Q

Describe the gross and histological appearance of phaeochromocytoma.

A

Gross - tan appearance with rim of normal adrenal cortex. Tumour is well circumscribed and does not involve the surrounding fat.

Histological - nests of cells, may be considerable nuclear variability and mitotic activity.

78
Q

List the types of pituitary adenomas and their frequencies.

A
  • Prolactin cell adenoma 20-30%
  • Growth hormone cell adenomas 5%
  • Mixed growth hormone-prolactin adenomas 5%
  • ACTH cell adenomas 10-15%
  • Gonadotroph cell adenomas 10-15%
  • Null cell adenomas 20%
  • Thyroid stimulating hormone cell adenomas 1%
  • Other pleurihormonal adenomas 15%
79
Q

What are the effects of a pituitary adenoma?

A
  • Mass effect e.g. bitemporal hemianopia
  • Produce hormones e.g. prolactin
  • May be non functional
  • Present as mixture of functional effect and mass effect.
80
Q

What are the features of a pituitary adenoma?

A
  • They make up 10% intracranial neoplasms
  • Often incidental finding at autopsy
  • Present in adults aged 30-50
  • Usually isolated lesions
  • Almost always benign
  • If functional the effects are secondary to the hormone produced.
  • Can be associated with MEN1
81
Q

What are the pathological types of pituitary adenoma?

A

Normal gland composed of acidophils which produce GH, basophils which produce ACTH and chromophobes (may produce prolactin)
Therefore:
- Acidophil adenoma: GH excess
- Basophil adenoma: ACTH excess
- Chromophobe adenoma: no hormone effect but some may produce prolactin.
- Microadenoma: excess prolactin and causes infertility but no mechanical effect. Found only on histology.

82
Q

What are the clinical features of pituitary tumours?

A

ENDOCRINE ABNORMALITY + MASS EFFECT

  • Radiographic abnormality of the sella turcica.
  • Pressure on optic chasm and visual field abnormality of bitemporal hemianopia
  • Increased intracranial pressure: headache, nausea and vomiting.
  • May compromise adjacent non-neoplastic pituitary leading to hypopituitarism.
83
Q

What are the causes of hypopituitarism?

What are the symptoms?

A
  • Tumours and other mass lesions
  • Pituitary surgery/radiation
  • Rathke cleft cyst
  • Pituitary haemorrhage
  • Ischaemic necrosis/ Sheehan’s syndrome/ empty sella syndrome (arises due to haemorrhage in pregnancy, hypotension leads to inadequate blood supply and necrosis of gland).
  • Genetic?

Symptoms depend on the deficient hormones.

84
Q

Which syndromes originate from the posterior pituitary?

A
  • Diabetes insipidus

- Inappropriate ADH secretion hyponatraemia.

SBCP Pathology (4 decks)

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