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imed3004 > Endocrine pathology: Adrenal and Putuitary Gland > Flashcards

Endocrine pathology: Adrenal and Putuitary Gland Flashcards

1
Q

What are the core concepts of endocrine pathology?

A

Feedback loops involving multiple organ systems = normal endocrine function

Disruption of feedback loops = disease states

Scenarios where there is an increase or decrease in hormone production, release or function result in endocrine disease

All endocrine organs may be involved by the usual range of diseases that can affect any tissue.

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2
Q

How to think about endocrine pathology:

A

The potential effects, signs, and symptoms of deficiency and excess of each hormone.

Potential causes:

By site: Local, distant (or primary vs secondary)

By time course: Acute vs chronic

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3
Q

Where is the pituitary gland located and what structures are located around it?

A

In the sella turcica of the sphenoid bone surrounded by dura. The sellar diaphragm covers the sella turcica.

Laterally the internal carotid artery, cavernous sinus, and cranial nerves III, IV, V, VI

Superiorly the optic chiasm, hypothalamus, and third ventricle

Blood supply from superior and inferior hypophysial arteries via portal vessels arising in capillaries of hypothalamus and posterior pituitary (therefore vulnerable to ischaemia)

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4
Q

What is a portal system?

A

Capillary bed -> venous bed -> another capillary bed

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5
Q

Where does the anterior lobe of the pituitary come from embryologically and what does this mean?

A

Anterior lobe is derived from Rathke’s pouch in the pharynx which is an epithelial structure.

Embryological abnormalities can occur in this structure (eg Rathke’s cleft cyst which is benign and can resemble a cancerous tumour)

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6
Q

Where does the posterior pituitary arise from embryologically?

A

From the floor of the 3rd ventricle (connection persists as pituitary stalk) It is a direct anatomical connection to the brain and is basically a part of the brain.

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7
Q

What makes up the histology of the anterior pituitary?

A

Nests, cords and small acini of secretory epithelial cells

Supported by reticulin framework and intervening capillary network

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8
Q

What makes up the histology of the posterior pituitary?

A

Modified glial cells known as pituicytes and nerve fibers extending from the hypothalamus.

These fibers contain secretory granules of stored hormones such as ADH and oxytocin, produced in the hypothalamus

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9
Q

What are the main hormones produced by the anterior and posterior pituitary?

A

Anterior:

ACTH

FSH

LH

GH

TSH

Prolactin

Posterior:

ADH and oxytocin

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10
Q

What are the clinical consequences of a pituitary lesion?

A

Mechanical due to mass effect:

Raised intracranial pressure

Bony erosion

Local pressure on third ventricle, hypothalamus, optic chiasm, or cranial nerves III, IV, V, and VI

These effects can be with or without altered hormonal secretion (anterior, posterior or both):

Hyperpituitarism

Hypopituitarism

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11
Q

What are the clinical features of pituitary disease?

A

Often subtle:

Can be detected from hormone assays, imaging, or biopsies/resection

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12
Q

What is an excess of growth hormone called?

A

Acromegaly (if after puberty)

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13
Q

How commonly is pituitary hyperfucntion a cause of hyperthyroidism?

A

It is a rare cause

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14
Q

What causes hypopituitarism?

A

Inadequate functional tissue: Absence or destruction of pituitary tissue

Lack of stimulus driving secretion: eg. Hypothalamic disease.

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15
Q

What can trigger hypofunction of pituitary products if there is hypersecretion of other products?

A

‘Pressure’ atrophy and pituitary hypofunction leads to secondary hypofunction of pituitary dependent endocrine glands.

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16
Q

What are some possible causes of hyperpituitarism?

A

Pituitary adenoma

Secondary hyperplasia

Pituitary carcinoma

Secretion of hormones by non-pituitary tumours

Hypothalamic disorders

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17
Q

What is the most common cause of hyperpituitarism?

A

Pituitary adenoma

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18
Q

What ages is pituitary adenoma most common in?

A

30 - 50 (incidence is 20%)

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19
Q

What is the difference between micro and macroadenoma?

A

<1cm = micro >1cm = macro

20
Q

How are pituitary adenomas pathologically classified?

A

3 ways:

Immunohistochemical phenotype

H&E cell type

Ultrastructural phenotype based on size and morphology of granules.

21
Q

Do all pituitary adenomas have endocrine effects?

A

They may be functional or non-functional.

The endocrine effects may be subtle and diagnosis is often delayed.

22
Q

What types of hormones are produced by functional pituitary adenomas?

A

Lactotroph/prolactinomas (30%)

Somatotroph (GH causing gigantism or acromegaly)

Corticotroph (cushing’s disease)

Plurihormonal

Gonadotroph

Thyrotroph (only 1%)

23
Q

What percentage of pituitary adenomas are non-functional?

A

20 - 30%, these usually still express hormonal markers by immunohistochemistry

24
Q

Are pituitary carcinomas functional?

A

No they are rare and non-functional. They are diagnosed based on aggressive behaviour and poor-correlation with histology

25
Q

What are the features of people with acromegaly/gigantism?

A

Enlargement of hands, thickening of skin, skullbones, macroglossia, wide spaced teeth, hyperpigmentation, and seborrhoaea.

Severe headaches, arthritis, cardiomegaly, hepatofibrosis, insulin resistance, and renal failure.

26
Q

What causes craniopharyngioma?

A

Mostly in childhood or early adulthood it is derived from Rathke’s pouch remnants. It is often large and calcified.

27
Q

What do craniopharyngiomas look like histologically?

A

Enamel organ of tooth embedded in fibrous stroma. Usually benign but can be locally invasice and difficult to treat

28
Q

What are the most common posterior pituitary neoplasms?

A

Gliomas

Least common pituitcytoma

29
Q

Where are secondary neoplasms most common?

A

More common in posterior pituitary, may present as diabetes insipidus

30
Q

Do clinical symptoms of hyperpituitarism only occur in pituitary adenomas? If no, what else causes them?

A

No it can occur due to physiological hyperplasia, head trauma, mass effect.

Cushing syndrome has many non-pituitary causes

Most hyperthyoidism is non-pituitary in origin

Some malignant tumours have paraneoplastic syndromes

31
Q

What is pituitary apoplexy?

A

Caused by sudden haemorrhage into the pituitary, often into an adenoma

32
Q

What is diabetes insipidus?

A

Passage of large volumes of dilute urine.

33
Q

What are the symptoms of diabetes insipidus?

A

Kidney is unable to resorb water from urine = dilute urine

Serum sodium and osmolality increased

Thirst and polydipsia

Higher risk of dehydration

34
Q

What are the 2 main types of diabetes insipidus? What are they?

A

Central and nephrogenic.

Central = decreased secretion of ADH from pituitary (due to mass effect, inflammation, trauma, surgery, or even idiopathic)

Nephrogenic = decreased ability of kidney to concentrate urine due to ADH resistance in the kidney

35
Q

What is SIADH?

A

A posterior pituitary syndrome where there is excess production of ADH (Syndrome of Inappropriate ADH)

36
Q

What are the symptoms of SIADH?

A

Resorption of excessive amounts of water

Hyponatremia, cerebral oedema (key defining feature)

Blood volume normal, no peripheral oedema (key defining feature)

Usually caused by ectopic ADH secretion (Not from pituitary itself but more commonly a paraneoplastic syndrome of cancers like small cell carcinoma of the lung)

37
Q

What are the important actions of glucocorticoids?

A

Weak mineralocorticoid action

Metabolic regulation:

Inhibit protein synthesis

Increase protein breakdown

Increase gluconeogenesis

Inhibit glucose uptake by cells

Redistribution of fat

Modulation of innate and adaptive immune response

38
Q

What controls production of glucocorticoids?

A

Under pituitary control

39
Q

What are the common disorders that result from hyperadrenalism?

A

Cushing syndrome (Cortisol)

Conn syndrome (Aldosterone)

Adrenogenital or virilising syndrome (androgens)

40
Q

What are the common disorders that result from hypoadrenalism?

A

Primary acute adrenal insufficiency (adrenal crisis)

Primary chronic adrenal insufficiency (Addison disease)

Secondary adrenocortical insufficiency (deficiency of ACTH)

41
Q

What is cushing syndrome?

A

Too much glucocorticoid production. (hypercortisolism)

42
Q

What causes hypercortisolism?

A

Exogenous due to steroid use as antiinflammatory drugs.

Endogenous causes can be ACTH dependent (eg cushing or ectopic ACTH syndrome (paraneoplastic)) or independent.(Adrenal cortical adenoma, carcinoma, or hyperplasia)

43
Q

What is cushing’s disease? How is it different to cushing syndrome?

A

ACTH dependant hypercortisolism. It is one cause of cushing syndrome.

Syndrome is the set of features caused by hypercortisolism (characterized by the CUSHINGOID pneumonic)

44
Q

What are the conditions caused by primary cortical hyperplasia?

A

Sporadic condition in adults

McCune Albright syndrome (GNAS mutation)

45
Q

What are the clinical features of cushing syndrome?

A

CUSHINGOID

Cataracts
Ulcers
Striae, skin thinning
Hypertension, Hirsutism
Immunosuppression
Necrosis of femoral heads
Glucose elevation
Osteoporosis, Obesity
Impaired wound healing
Depression/mood changes

Moon Face and Buffalo hump

46
Q

What happens to the adrenals in cushing syndrome?

A

In iatrogenic: Bilateral cortical atrophy

In ACTH-dependent: Diffuse bilateral hyperplasia

In ACTH independent: Neoplasm or nodular hyperplasia

imed3004 (50 decks)

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