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Pathophysiology > W.13: Distrubances of Adrenal Glands > Flashcards

W.13: Distrubances of Adrenal Glands Flashcards

1
Q

Name the layers and hormones produced by each layer.

A

Zona glomerulosa - Mineralocorticoids

Zona fasiculata - Glucocorticoids

Zona reticularis - Androgens

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2
Q

Which hormones are produced by adrenal medulla?

A
  • Epinephrine (75- 80%)

- Norepinephrine (25- 30%)

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3
Q

Name the clinical features of acute adrenal crisis.

A
  • Hypotension and shock
  • Fever
  • Dehydration
  • Nausea, vomitng, anorexia
  • Weakness, apathy, depressed mentation
  • Hypoglycemia
  • Vascular collapse (decreased BP)
  • Decrease of Na+ serum
  • Increase of K+ serum
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4
Q

Name the clinical presenation of adrenal insufficiency.

A
  • Bronze pigmentation of skin AND bucal mucosa and gums
  • Changes in distibution of body hair
  • Hypoglycemia
  • Postural hypotension
  • Weight loss
  • GI disturbances (diarrhea, abdominal pain)
  • Weakness
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5
Q

Which are the primary causes pf adrenocortical insufficiency (Addison’s diease)?

A
  • Autoimmune (90%)
  • Degenerative (amyloid)
  • Drugs (eg. ketoconazole)
  • Infection (TB, HIV)
  • Secondary (decrease ACTH, hypopituitarism)
  • Other (eg. adrenal bleeding)
  • Neoplasia (metastases)
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6
Q

What is the cause of secondary adrenocortical insufficiency?

A

Exogenous glucocorticoid therapy.

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7
Q

Which are the features of secondary adrenocortical insufficiency?

A
  • Usually chronic
  • No hyperpigmentation
  • No volume depletion
  • Dehydration electrolyte abnormalities
  • Hypotension
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8
Q

Name the laboratory findings seen in secondary adrenocortical insuffiency.

A
  • Anemia
  • Lymphocytosis
  • Eosinophilia
  • Basal ACTH low or normal
  • ACTH reserve impaired
  • Stimulation test subnormal
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9
Q

Which are the features seen in Addisonian crisis?

A
  • Severe shock - hypotension tachycardia
  • Fever
  • Abdominal pain
  • Nausea
  • Vomiting
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10
Q

Describe the management of Addisoninan crisis.

A

ABCDE assessment

  • Correct volume depletion
  • Replace glucocorticoids
  • Correct metabolic abnormalities
  • Treat underlying cause
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11
Q

Name some clinical features seen in Cushing’s syndrome.

A
  • Moon facies
  • Cardiac hypertrophy (hypertension)
  • Gastric ulcer
  • Obesoty
  • Abdominal striae
  • Amenorrhea
  • Muscle weekness
  • Purpura
  • Skin ulcers (poor wound healing)
  • Emotional disturbances
  • Osteoporosis
  • Buffalo hump
  • Glucose intolerance
  • Andreal tumor or hyperplasia
  • Thin, wrinkled skin
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12
Q

Describe the two forms of Cushing’s syndrome.

A

ACTH dependent:

  • Cushing’s disease
  • Ectopic ACTH syndrome (10- 15%)

ACTH independent: (15- 20%)

  • Adrenal adenoma
  • Adrenal carcinoma
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13
Q

Androgen excess in woman cause what?

A

Hirsutism
Acne
Amenorrhea

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14
Q

Androgen excess in men cause what?

A

Decreased libido

Impotence

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15
Q

Name the pathophysiological manifestations of Cushing’s disease.

A
  • Random ACTH secretion
  • Abscence of normal diurnal rhytm
  • Failure in physiological feedback
  • Increased glucocorticoid secretion
  • No hyperpigmentation
  • Decreased secretion of TSH, GH, LH and FSH
  • Androgen excess
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16
Q

Clinical manifestations of ectopic ACTH syndrome?

A
  • Random episodic secretion of ACTH
  • Elevated serum ACTH
  • Hyperpigmentation
  • Totoal feedback failure
  • Rapid onset
  • Mineralocorticoid excess
    (–> hypertension, hypokalemia)
17
Q

Name the forms of adrenal tumors.

A
  • Autonomous secretion
  • Adrenal adenomas
  • Adrenal carcinomas
18
Q

Mechanism of autonomous secretion, adrenal tumours?

A

Random secretion. Unrespoinsive to the manipulation of hypothalamicpituitary axis.

19
Q

What is the secretion diff. in adrenal adenomas vs. adrenal carcinomas?

A

Adrenal adenomas secrete one type of steorid, while Adrenal carcinomas secrete multiple adrenocortical steriods.

20
Q

What is the etiology of primary mineralocorticoid excess (Conn’s syndrome)?

A
  • Aldosterone- producing adenomas
  • Aldosterone- producing carcinomas
  • Hyperplasia
    -Deoxycorticosterone excess
    I. 17alfta- OHlase def.
    II. 11beta- OHlase def.
21
Q

Name the two forms of secondary mineralocorticoid excess.

A

Secondary mineralocorticoid excess with and without hypertension.

22
Q

When can secondary mineralocorticoid excess with hypertension be seen?

A
  • Renovascular disease (atherosclerosis, renal infarction etc.)
  • Renin- secreting tumours
  • Accelerated hypertension
  • Estrogen therapy
23
Q

When can secondary mineralocorticoid excess without hypertension be seen?

A
  • Sodium- wasting syndrome
  • Edematous states
    I. Cirrhosis
    II. Npehritic
    III. Congestive heart failure
  • Baretter’s syndrome (hypokalemia, hyperreninemia, hyperaldosteronism)
24
Q

Absence of side chain degrading enzymes, will lead to?

A

All corticoids will get blocked.

25
Q

Absence of 3beta- OH- dehydrogenase and isomerase, will lead to?

A

Complete block, except for adrenal androgens.

26
Q

21- hydroxylation deficiency leads to?

A

Partial or complete salt losing syndrome.

27
Q

11- hydroxylation deficiency, will lead to?

A

Hypertensive syndrome

28
Q

Name the causes of adrenogenital syndrome.

A
  • Overactivity of adrenal cortex
  • Hyperplasia of adrenal cortex
  • Adenoma of adrenal cortex
  • Carcinoma of adrenal cortex
29
Q

21- hydroxylase deficiency will lead to…

A
  • Excess sex steriods
    I. Virilisation, hirsutism, premature adrenarche, infertility.
  • No aldosterone –> salt- losing crisis (hyperkalemia, hypotension)
30
Q

11beta- hydroxylase deficiency will lead to…

A
  • Excess sex steriods
    I. Virilisation, hirsutism, premature adrenarche, infertility.
  • No aldosterone but high DOC, which is an agonist at MC receptors (hyperkalemia, hypotension)
31
Q

Diff. btw 21- hydroxylase deficiency and 11beta- hydroxylase deficiency?

A

No aldosterone is seen in either of the deficiencies, but in 11beta- hydroxylase deficiency there is high [DOC] which is an agonist at MC receptors.

32
Q

Name the disorders of Adrenal medulla.

A
  • Hypofunction

- Hyperfunction –> Pheochromocytoma

33
Q

From which cells do the tumour arise from in pheochromocytoma?

A

From chromaffin cells in sympathetic neuron system.

34
Q

Name the 4 locations/ types of pheochromocytoma that make up the “10% tumour”.

A
  • Biltateral
  • Extra- adrenal
  • Familial
  • Malignant
35
Q

Name the clinical signs of pheochromocytoma during paroxysm.

A
  • Hypertension
  • Headache
  • Sweating
  • Palpitation
  • Tremor
  • Paleness
  • Nausea, vomiting
36
Q

Name the clinical signs of pheochromocytoma between the attacks.

A
  • Cold hands and feet
  • Weight loss
  • Orthostaticus
  • Hypotonia
  • Fatigue
  • Anciousness
  • Panic
37
Q

Which diagnostic tests and procedures are applied in diagnosis of pheochormocytoma?

A
  • Hormone assays (plasma or urine=
    I. Urin: adrenalin, noradrenalin, dopamin, metanephrin, normetanephrin, VMA
    II. Serum: Chromogranin A
  • Clonidin supression test
  • Imagning
    I. UH, MRI, CT, 131I. MIBG uptake
38
Q

Briefly describe the clonidin suppression test.

A

Cathecholamin- like effect –> decreases cathecolamin production normally.

39
Q

What is chromogranin and where is it secreted?

A

Chomograning is a tumourmarker.

It is secreted in the adrenal medulla, the GI tract and in pancreas endocrine cells.

Pathophysiology (14 decks)

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