Adrenal Gland Pathology Flashcards

1
Q

Recap: State the location and hormones produced in adrenal gland.

A

ADRENAL GLAND:

Adrenal cortex - zona glomerulosa - aldosterone

Adrenal cortex - zona fasciculata + reticularis - cortisol + sex hormones

Adrenal medulla - norepinephrine, epinephrine

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2
Q

Recap: State the condition related to
1. hypercortisolism
2. hyperaldosteronism
3. hypocortisolism + hypoaldosteronism
4. overproduction of epinephrine and norepinephrine

A

hypercortisolism - cushing’s syndrome

hyperaldosteronism - conn’s disease

hypocortisolism + hypoaldosteronism - addison’s disease

overproduction of epinephrine and norepinephrine - pheochromocytoma

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3
Q

State some common diseases associated with HYPERCORTISOLISM (CUSHING’S SYNDROME).

A
  1. cushing’s disease = pituitary tumour (hyperactive anterior pituitary)
  2. ectopic ACTH
  3. adrenal adenoma
  4. adrenal carcinoma
  5. iatrogenic cushing’s syndrome due to inappropriate use of exogenous glucocorticoids
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4
Q

State the common presentation of cushing’s syndrome. (10)

A
  1. central obesity
  2. htn
  3. glucose intolerance
  4. plethoric facies (moon face)
  5. purple striae
  6. hirsutism
  7. menstrual dysfunction (amenorrhoea)
  8. muscle weakness
  9. osteoporosis
  10. bruising
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5
Q

Explain how hypercortisolism (cushing’s syndrome) can lead to osteoporosis.

A

HYPERCORTISOLISM –> OSTEOPOROSIS

  1. inhibition of bone formation - cortisol inhibits the production and activity of osteoblasts –> weakened bone structure
  2. increased bone resorption - cortisol promotes actiivty of osteoclasts –> bone resorption outpaces bone formation –> net loss of bone density
  3. decreased serum calcium levels - cortisol decreases calcium absorption from intestines AND increases calcium excretion by kidneys
  4. decreases GH levels (minor)

However, raised cortisol levels reduces activation of vitamin D which acts by
- promoting bone resorption to maintain calcium levels
- increase calcium reabsorption at small intestine

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6
Q

Explain how hypercortisolism (cushing’s syndrome) results in amenorrhoea.

A

HYPERCORTISOLISM –> AMENORRHOEA

elevated levels of cortisol from adrenal gland –> inhibit secretion of GnRH from hypothalamus –> decreased stimulus of anterior pituitary to secrete LH and FSH –> decreased stimulus of ovaries to produce oestrogen –> irregular menorrhoea or amneorrhoea

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7
Q

Recap: State the test used to confirm hypercortisolism (cushing’s syndrome).

A

LOW-DOSE DEXAMETHASONE TEST
- dexamethasone suppresses cortisol –> physiologically, cortisol levels should decrease while ACTH increases slightly
- if cortisol levels remain high –> primary adrenal disorder, normal acth production

HIGH-DOSE DEXAMETHASONE TEST
- used to differentiate between secondary pathology and ectopic acth production
- only used after ruling out primary adrenal pathologies (tumours)

URINARY-FREE CORTISOL
- measure conjugated amount of cortisol excreted in urine

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8
Q

State the common presentation of conn’s syndrome.

A
  1. hypertension
  2. metabolic alkalosis
  3. hypokalaemia
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9
Q

State the common conditions resulting in conn’s syndrome.

A
  1. adrenal aldosterone producing adenoma (APA)
  2. idiopathic hyperaldosteronism with bilateral adrenal hyperplasia (BAH)
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10
Q

State some conditions that cause addison’s disease. (6+5)

A

PRIMARY CAUSES
1. idiopathic adrenal atrophy
2. granulomatous diseases (TB, sarcoidosis, histoplasmosis)
3. neoplastic infiltration
4. haemochromatosis (abnormal accumulation of iron)
5. amyloidosis (abnormal accumulation of amyloid deposits in body)
6. post bilateral adrenalectomy

SECONDARY CAUSES
1. tumours
2. pituitary infarction and haemorrhage
3. granulomatous diseases
4. post hypophysectomy (removal of pituitary gland)
5. prolonged exogenous steroid administration

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11
Q

State the presentation of addison’s disease

A

GLUCOCORTICOID DEFICIENCY (HYPOCORTISOLISM)
- weakness
- hypoglycaemia
- weight loss
- GI discomfort

MINERALCORTICOID INSUFFICIENCY (HYPOALDOSTERONISM)
- if primary adrenal –> sodium wasting, postural hypotension, hypovolaemia, hyperkalaemia, dark skin
- if secondary pituitary –> NO SYMTPOMS OF ALDOSTERONE INSUFFICIENCY instead HYPOGONADISM + HYPOTHYROIDISM symptoms + pale skin

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12
Q

State the tests used to determine addison’s disease

A

SHORT SYNACTHEN TEST
- to differentiate between primary and secondary pathologies

LONG SYNACTHEN TEST
- to differentiate between normal and hypocortisolism

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13
Q

State the condition associated with overproduction of epinephrine and norepinephrine.

Describe some features of this condition (hint: rule of 10%)

A

Hypercortisolism + Hyperaldosteronism = Pheochromocytoma (adrenal medullary tumour)

  • 10% familial
  • 10% recurrent
  • 10% bilateral
  • 10% malignant
  • 10% extra-adrenal
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14
Q

State some presentations of pheochromocytoma. (5)

A
  1. htn - sympathetic overdrive –> vasoconstriction of blood vessels to pool in muscles and major organs + increased HR –> increase BP
  2. headache
  3. sweating (excessive catecholamines activates sweat glands+ increased metabolic activity –> increased production of sweat to compensate for higher body temperatures)
  4. palpitations
  5. tachycardia
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15
Q

State the tests used to confirm pheochromocytoma.

A

SERUM
- free catecholamine level
- presence of metanephrines (broken down epinephrine)
- chromogranins A, B and C
- pancreastatin (inhibits insulin secretion - continuous supply of glucose to support metabolic processes)
- neuropeptide Y (stimulates hypothalamus for food intake)

URINE
- free catacholamine level
- presence of metanephrines
- VMA or HMMA
- HVA, DHPG

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