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*Medicine: Cellular Pathology > Endocrine pathology > Flashcards

Endocrine pathology Flashcards

1
Q

Where does the pituitary gland sit?

A
  • in the sella turcica
  • of the sphenoid bone
  • attached to the hypothalamus
  • composed of two parts which are embryologically and functionally distinct
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2
Q

What hormones does the anterior pituitary secrete?

A

FLAG TP

  • Follicle stimulating hormone (FSH)
  • Luteinizing hormone (LH)
  • Adrenocroticotrophic hormone (ACTH)
  • Growth hormone (GH)
  • Thyroid stimulating hormone (TSH)
  • Prolactin

The secretion of all six anterior pit hormones is in turn regulated by hormones from the hypothalamus, which reach the pituitary through a portal system of blood vessels

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3
Q

What are the posterior pituitary hormones?

A
  • Antidiuretic hormone
  • Oxytocin

Both are synthesised in the hypothalamus and then pass down nerve fibres in the pituitary stalk to be secreted by the posterior pituitary.

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4
Q

What is the most common disease of the anterior pituitary?

A
  • pituitary adenomas
  • tumours derived from glandular tissue of ant pit
  • most cases are sporadic but may occur as part of the MEN-1 syndrome
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5
Q

What are the 2 main ways that pituitary adenomsa can cause clinical effects?

A
  1. Mass effects
  2. Endocrine effects
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6
Q

What are the mass effects?

A
  • bitemporal hemianopia (bc tumour causes compression of optic chiasm + thus affects optic nerves)
  • diplopia (tumour causes compression of cranial nerves III, IV or VI)
  • non-specific symptoms related to any intracranial mass eg. headache
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7
Q

What is the difference between a functional and non-functional adenoma?

A

With pit adenomas, you get mass effects and then you get endocrine effects too:

  • functional adenomas - produce symptoms related to XS hormone secretion (most commonly prolactin, GH, ACTH), bc of this, functional tumours are v small at presentation
  • non-functional adenomas - do not produce hormones, often larger at presentation bc they present via mass effects rather than endocrine dysfunction. Many non-functional adenomas remain tiny and never come to clinical attention bc they do not cause mass effects.
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8
Q

What is a common type of functional pituitary adenoma?

A
  • prolactinoma
  • produce excess prolactin
  • presentation depends on patient’s age + sex
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9
Q

How do prolactinomas present in women of reproductive age?

A

commonly present with either:

  • oligomenorrhoea (infrequent or v light menstruation - 4-9 periods/year)
  • or galactorrhoea (spontaneous flow of milk from breast unassociated w/ pregnancy or breast feeding)

These patients often have very small tumours and so present early

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10
Q

How do prolactinomas present in men and post-menopausal women?

A
  • usually present with mass effects such as headache or visual disturbance
  • may present with symptoms such as galactorrhoea
  • the tumours are typically larger at presentation
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11
Q

How do GH-secreting pituitary adenomas present?

A
  • acromegaly
  • rare clinical syndrome resulting from XS secretion of GH
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12
Q

Why does acromegaly result from XS GH?

A

somatic and metabolic effects of chronic GH hypersecretion are predominantly mediated by high levels of insulin like growth factor-1 (IGF-1), which is secreted by the liver in response to GH stimulating it.

IGF-1 then has a growth effect on tissues.

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13
Q

What are the specific tissue effects of IGF-1, in acromegaly - ie. what is the presentation?

A
  • Acromegalic facies (big nose, prognathia, course features)
  • Headaches + thickend calvaria
  • Left ventricular hypertrophy
  • Hypertension
  • Insulin resistance
  • Hepatomegaly
  • Impotence + loss of libido
  • Amenorrhoea in women
  • Large hands + thickened skin
  • Hyperostosis
  • Degenerative joint disease
  • Peripheral neuropathy
  • Large feet + heel pad
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14
Q

Acromegaly is a serious condition in which there is a doubling in mortality compared with normal populations, why is this?

A
  • mainly due to high incidence of cardiovascular disease due to left ventricular hypertrophy and hypertension
  • acromegaly is a diabetogenic state (ie. it causes insulin resistance), which is a strong risk factor for cadiovascular disease
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15
Q

What are the commonest causes of thyrotoxicosis?

A
  • Graves’ disease (80%)
  • toxic multinodular goitre (a nodule within a multinodular goitre whcih autonomously secreted thyroid hormones independently of TSH)
  • a functional thyroid adenoma (a follicular adenoma producing thyroid hormones)
  • other: drugs (amiodarone) + certain types of thyroiditis
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16
Q

Are TSH-secreting pituitary adenomas a common cause of thyrotoxicosis?

A

very rare cause of thyrotoxicosis

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17
Q

Where are the adrenal glands located?

A
  • in the retroperitoneum
  • superior to the kidneys
18
Q

What are the 2 functional parts of the adrenal gland?

A
  • cortex
  • medulla
19
Q

What is the function of the adrenal cortex?

A

composed of (from outermost to innermost) + produce:

  • zona glomerulosa -> mineralocorticoids (aldosterone)
  • zona fasciculata -> glucocorticoids (cortisol)
  • zona reticularis -> androgens
20
Q

What is the function of the adrenal medulla?

A

Produce catecholamines such as adrenaline and noradrenaline

21
Q

What is the HPA axis?

A
  • hypothalamus secretes CRH
  • stimulates anterior pituitary to secrete ACTH
  • this acts on adrenal cortex to stimulate release of cortisol
  • cortisol has a -ve feedback effect on hypothalamus + ant pit, so suppresses the secretion of CRH and ACTH respectively
22
Q

What syndrome do ACTH-secreting adenomas present as?

A

Cushing’s syndrome (see later cards for more detail)

23
Q

What are causes of Cushing’s syndrome?

A
  1. exogenous admin of glucocorticoids
  2. pituitary adenoma secreting ACTH
  3. adrenal cortical adenoma
  4. paraneoplastic syndrome
24
Q

Cushing’s syndrome is due to persistent XS circulating glucocorticoids (cortisol). What are common presenting symptoms and signs?

A
  • Weight gain (trunkal obesity, moon face, buffalo hump)
  • Mood change (lethargy, depression, irritability)
  • Proximal myopathy
  • Gonadal dysfunction (ED, irregular menses, hirsuitism)
  • Acne
  • Hypertension, DM, osteoporosis
  • Petechiae, striae, poor healing + bruising
  • Peripheral neuropathy
  • Bitemporal hemianopia
25
Q

What is the commonest cause of Cushing’s syndrome and how does it cause this?

A
  • exogenous admin of glucocorticoids (to treat other diseases)
  • adrenal cortices undergo atrophy bc of negative feedback effect of exogenous glucocorticoids on HPA axis
  • production of CRH + ACTH is suppressed
  • so adrenal cortices undergo atrophy
26
Q

The second most common cause of Cushing’s syndrome is a pituitary adenoma as mentioned before. What happens here to the adrenals?

A
  • pituitary adenoma secreting ACTH
  • Cushing’s syndrome due to ACTH-secreting pit adenoma = Cushing’s disease
  • adrenal cortices under go hyperplasia in response to effect of the circulating ACTH
27
Q

What is hyperplasia?

A
  • increase in the number of cells in an organ or tissue
  • resulting in an increased size
  • the cell proliferation ceases when causative stimulus removed
28
Q

Where does an adrenal cortical adenoma (secreting cortisol) arise from?

A
  • tumour arises from a cell in the zona fasciulata
29
Q

What is paraneoplastic syndrome and how do they give rise to Cushing’s syndrome?

A
  • rare disorders that are triggered by an altered immune system response to a neoplasm
  • defined as clinical syndromes involving nonmetastatic systemic effects that accompany malignant disease
  • the tumour cells of certain cancers (eg small cell lung cancer)
  • may produce ACTH -> inc secretion of cortisol by adrenal gland
  • -> cushing’s syndrome
30
Q

What is the equation for control of blood pressure?

A
  • BP = TPR x CO
  • TPR main determinant = calibre of arterioles
  • CO main determinant = determined by renal sodium handling
31
Q

In general, factors which cause an increase in sodium retention by the kidneys will tend to raise blood pressure. Why is this?

A
  • Na+ and water reabsorption by kidneys is coupled
  • ie. increase in Na+ reabsorption -> increase in water reabsorption
  • this leads to increase in circulatory volume
  • raising BP
  • (nb. CO = SV x HR)
32
Q

What is primary hyperaldosteronism?

A
  • XS aldosterone production
  • by adrenal cortex (zona glomerulosa)
33
Q

What is primary hyperaldosteronism (PA) caused by?

A
  • aldosterone-producing adrenal cortical adenoma (AKA Conn’s syndrome + accounts for 66% of PA cases)
  • or biltateral adrenal cortical hyplerplasia (~30% cases)
34
Q

What is the physiological function of aldosterone?

A
  • key component of RAAS
  • physiological fxn of RAAS is to regulate fluid balance + BP
  • if BP falls -> reduced BF in renal artery
  • -> stimulates release of renin by kidney
  • -> prod of Ang II, which helps raise BP by:
    • stimulates release of aldosterone from adrenal cortex
    • vasoconstriction of systemic arterioles
    • release of ADH by post pit
  • restoration of normal BP + BF through renal artery causes a reduction in secretion of renin + thus down-reg of RAAS (negative feedback)
35
Q

What is the effect of hyperaldosteronism?

A
  • there is a breakdown of the normal negative feedback loop so there is XS aldosterone circulating in blood
  • causes:
    • hypernatraemia
    • hypertension
    • hypokalaemia
36
Q

What is the physiology of a phaeochromocytoma?

A
  • neuroendocrine tumour of the adrenal medulla
  • secretes xs of catecholamines (usually adrenaline)
  • causes inc vasoconstriction + inc heart rate
  • -> inc TPR + inc CO
  • -> inc BP
37
Q

What are symptoms of phaeochromocytomas?

A
  • often asymptomatic
  • triad of symptoms related to episodic increases in circulating catecholamines
    • throbbing headache
    • sweating
    • palpitations
38
Q

Why is it important to identify phaeochromocytomas?

A
  • they are treatable cause of hypertension
  • pts BP returns to normal following surgical excision
39
Q

What is the investigation for phaeochromocytoma?

A
  • 24hr urine collection for catecholamine and meranephrine measurement
  • urinary VMAs also
40
Q

How many cases of phaeochromocytomas are familial?

A
  • historically about 10% were thought to occur as part of a familial syndrome eg. von hippel linday, neurofibromatosis t1, MEN t2
  • recent identification of familial cases associated w germline mutations in the subunits of the succinate dehydrogenase (SDHx) genes suggests that up to 30% are familial

*Medicine: Cellular Pathology (16 decks)

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