W.13: Distrubances of Adrenal Glands Flashcards
Name the layers and hormones produced by each layer.
Zona glomerulosa - Mineralocorticoids
Zona fasiculata - Glucocorticoids
Zona reticularis - Androgens
Which hormones are produced by adrenal medulla?
- Epinephrine (75- 80%)
- Norepinephrine (25- 30%)
Name the clinical features of acute adrenal crisis.
- 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
Name the clinical presenation of adrenal insufficiency.
- 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
Which are the primary causes pf adrenocortical insufficiency (Addison’s diease)?
- Autoimmune (90%)
- Degenerative (amyloid)
- Drugs (eg. ketoconazole)
- Infection (TB, HIV)
- Secondary (decrease ACTH, hypopituitarism)
- Other (eg. adrenal bleeding)
- Neoplasia (metastases)
What is the cause of secondary adrenocortical insufficiency?
Exogenous glucocorticoid therapy.
Which are the features of secondary adrenocortical insufficiency?
- Usually chronic
- No hyperpigmentation
- No volume depletion
- Dehydration electrolyte abnormalities
- Hypotension
Name the laboratory findings seen in secondary adrenocortical insuffiency.
- Anemia
- Lymphocytosis
- Eosinophilia
- Basal ACTH low or normal
- ACTH reserve impaired
- Stimulation test subnormal
Which are the features seen in Addisonian crisis?
- Severe shock - hypotension tachycardia
- Fever
- Abdominal pain
- Nausea
- Vomiting
Describe the management of Addisoninan crisis.
ABCDE assessment
- Correct volume depletion
- Replace glucocorticoids
- Correct metabolic abnormalities
- Treat underlying cause
Name some clinical features seen in Cushing’s syndrome.
- 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
Describe the two forms of Cushing’s syndrome.
ACTH dependent:
- Cushing’s disease
- Ectopic ACTH syndrome (10- 15%)
ACTH independent: (15- 20%)
- Adrenal adenoma
- Adrenal carcinoma
Androgen excess in woman cause what?
Hirsutism
Acne
Amenorrhea
Androgen excess in men cause what?
Decreased libido
Impotence
Name the pathophysiological manifestations of Cushing’s disease.
- 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
Clinical manifestations of ectopic ACTH syndrome?
- Random episodic secretion of ACTH
- Elevated serum ACTH
- Hyperpigmentation
- Totoal feedback failure
- Rapid onset
- Mineralocorticoid excess
(–> hypertension, hypokalemia)
Name the forms of adrenal tumors.
- Autonomous secretion
- Adrenal adenomas
- Adrenal carcinomas
Mechanism of autonomous secretion, adrenal tumours?
Random secretion. Unrespoinsive to the manipulation of hypothalamicpituitary axis.
What is the secretion diff. in adrenal adenomas vs. adrenal carcinomas?
Adrenal adenomas secrete one type of steorid, while Adrenal carcinomas secrete multiple adrenocortical steriods.
What is the etiology of primary mineralocorticoid excess (Conn’s syndrome)?
- Aldosterone- producing adenomas
- Aldosterone- producing carcinomas
- Hyperplasia
-Deoxycorticosterone excess
I. 17alfta- OHlase def.
II. 11beta- OHlase def.
Name the two forms of secondary mineralocorticoid excess.
Secondary mineralocorticoid excess with and without hypertension.
When can secondary mineralocorticoid excess with hypertension be seen?
- Renovascular disease (atherosclerosis, renal infarction etc.)
- Renin- secreting tumours
- Accelerated hypertension
- Estrogen therapy
When can secondary mineralocorticoid excess without hypertension be seen?
- Sodium- wasting syndrome
- Edematous states
I. Cirrhosis
II. Npehritic
III. Congestive heart failure - Baretter’s syndrome (hypokalemia, hyperreninemia, hyperaldosteronism)
Absence of side chain degrading enzymes, will lead to?
All corticoids will get blocked.
Absence of 3beta- OH- dehydrogenase and isomerase, will lead to?
Complete block, except for adrenal androgens.
21- hydroxylation deficiency leads to?
Partial or complete salt losing syndrome.
11- hydroxylation deficiency, will lead to?
Hypertensive syndrome
Name the causes of adrenogenital syndrome.
- Overactivity of adrenal cortex
- Hyperplasia of adrenal cortex
- Adenoma of adrenal cortex
- Carcinoma of adrenal cortex
21- hydroxylase deficiency will lead to…
- Excess sex steriods
I. Virilisation, hirsutism, premature adrenarche, infertility. - No aldosterone –> salt- losing crisis (hyperkalemia, hypotension)
11beta- hydroxylase deficiency will lead to…
- Excess sex steriods
I. Virilisation, hirsutism, premature adrenarche, infertility. - No aldosterone but high DOC, which is an agonist at MC receptors (hyperkalemia, hypotension)
Diff. btw 21- hydroxylase deficiency and 11beta- hydroxylase deficiency?
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.
Name the disorders of Adrenal medulla.
- Hypofunction
- Hyperfunction –> Pheochromocytoma
From which cells do the tumour arise from in pheochromocytoma?
From chromaffin cells in sympathetic neuron system.
Name the 4 locations/ types of pheochromocytoma that make up the “10% tumour”.
- Biltateral
- Extra- adrenal
- Familial
- Malignant
Name the clinical signs of pheochromocytoma during paroxysm.
- Hypertension
- Headache
- Sweating
- Palpitation
- Tremor
- Paleness
- Nausea, vomiting
Name the clinical signs of pheochromocytoma between the attacks.
- Cold hands and feet
- Weight loss
- Orthostaticus
- Hypotonia
- Fatigue
- Anciousness
- Panic
Which diagnostic tests and procedures are applied in diagnosis of pheochormocytoma?
- 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
Briefly describe the clonidin suppression test.
Cathecholamin- like effect –> decreases cathecolamin production normally.
What is chromogranin and where is it secreted?
Chomograning is a tumourmarker.
It is secreted in the adrenal medulla, the GI tract and in pancreas endocrine cells.
