Adrenal disorders
By Dr Osman Sadig Bukhari
Adrenal gland
1- Cortex
- Mineralocorticoids (aldosterone)
Na retention
and K excretion
- Glucocorticoids (Cortisol) hyperglycemia,
anti inflammatory & immunosuppressive
- Androgens
2- Medulla
- Catecholamines (Nor adrenalin &
adrenalin)
Cushing’s syndrome
(Hypercortisolism)
It refers to manifestations of excessive C/S
Causes:
1- exogenous glucocorticoids
2- ACTH secreting pituitary adenoma
(Cushing’s
disease)
3- Ectopic ACTH secreting tumors e.g small
cell Ca of the lungs
4- Adrenal tumors: adenomas & Ca
Clinical features: (symptoms & signs)
-Central obesity & protuberant abdomen and
thin limbs
- Plethoric moon face
-Bufallo hump & supra clavicular fat pads
-Oligomenorrhea or amenorrhea
-Impotence
-Headache, proximal muscle weakness &
wasting
-Osteoporosis & backache & back tenderness
-Avascular necrosis of neck of femur
- Acne & purple striae
- Thin skin, easy bruising, impaired wound
healing and hirsutism
- Susceptibility to infection
- Thirst & polyuria
- Hypertension
-Glucoma, cataract
-Gynaecomastia
-Mental symptoms
Lab features:
-Impaired glucose tolerance
-Leucocytosis & lymphopenia
-Hypokalemia
- Increased serum cortisol & 24h urinary
cortisol
- Dexamethasone suppression test
- Plasma ACTH
- MRI pituitary
- CT chest & abdomen
Complications:
- HTN
-MD
-Increased susceptibility to infections
-Compression # of the osteoporotic spine and
aseptic necrosis of the femoral head
- Psychosis
- Nephrolithiasis
- Nelson’s syndrome following bilateral
adrenalectomy
Treatment:
-Selective trans nasal resection for pituitary
adenoma for Cushing’s disease. If no
response
bilateral adrenalectomy
-Pituitary irradiation
-Ketoconazole in patients not candidate for
surgery
- Resection of adrenal tumors
- Metyrapoe & ketoconazole in metastatic
adrenal
Ca
-Resection of ectopic ACTH secreting tumors.
If this can not be done Ketoconazole
and metyrapone (suppress ACTH secretion)
Acute adrenocortical insufficiency
(Adrenal crisis)
Medical emergency caused by insufficient
Cortisol
It occurs in the course of chronic
adrenocortical
Insufficiency & is more commonly seen in Pry
Adrenal insufficiency (Addison’s Addison’s dis).
It is precipitated following:
-Stress
-Sudden withdrawal C/S
- Bilateral adrenalectomy
- Thyroxin therapy in patients with Sheehan’s.
- Injury to both adrenals by trauma, hage, infect
Clinical features (symptoms & signs)
-Headache, lassitude, abd pain, nausea,
vomiting & often diarrhea.
-Dehydration
-Hypotension
-Skin hyper pigmentation
-Hyponatremia
-Hyerkalemia
-Hypoglycemia
- Hypercalcemia
- Eosinophilia
- Look for source of infection as a precipitating
cause
-Failure to respond to ACTH stimulation
-Markedly elevated plasma ACTH
Management
-Blood sample for cortisol and start:
-Hydrocortisone 200mg & NS immediately
(without waiting the results) 6 hourly for 24h
then 8 hourly next day
- Correct hypoglycemia & monitor serum
electrolytes, urea & creatinine
-Broad spectrum antibiotic
-When patient able to take orally start
maintenance dose of hydrocortisone
(20mg morning & 10mg evening) +/-
mineralocoeticoids.
-Early recognition & rapid treatment is life
saving
Chronic adrenocortical insufficiency
(Addison’s disease)
- Caused by destruction or dysfn of the adrenal
cortices
-Characterized by chronic deficiency of cortisol,
aldosterone & adrenal androgens and causes
skin pigmentation. Volume & Na depletion
and K excess eventually occur except in
if secondary to pituitary disease
Causes:
- Autoimmune, TB
- Sudden withdrawal of C/S
- Bilateral adrenaline hage
- Adrenal leukodystrophy
- Lymphoma, metastatic Ca, amyloidosis,
haemochromatosis, fungal infections.
Clinical features:
-Weakness, fatigability, myalgia, arthralgia
-Anorexia, nausea, vomiting, WT loss
-Skin hyperpigmentation (also mucus
membranes)
-Emotional changes
-Hypoglycemic symptoms
- Hypotension
- Small heart
- Scanty axillary & pubic hair
- Hyperplasia of lymphoid tissues
- Manifestation of other AI disorders
- Features of underlying cause
- Neutropenia, lymphocytosis, eosinophilia
- Low Na, high K
- Low FBS
- Hypercalcemia
- Low plasma cortisol & elevated ACTH
- ACTH stimulation test
- CXR
- CT abd
Complications
- Susceptibility to infection
-Associated AI diseases
-Adrenocortical crisis
Management:
-Replacement therapy with hydrocortisone and
mineralocoeticoids (fludrocortisone). In mild cases
hydrocortisone alone is adequate
- Treat all infections & raise dose of hydrocortison
- Increase dose of hydrocortisone in any stress
- Medical alert bracelet
Conn’s syndrome
- It is due to an adenoma of adrenal gland
secreting aldosterone. It could also be due to
bilateral hyperplasia of the zona glomerulosa
-It results in hyperaldosteronism:
- Increased plasma Na
- Reduced plasma K
- Increased serum bicarbonate
- Alkalosis
- Reduced urinary Na & increased K
- All patients are hypertensive
- Treated by aldosterone antagonist
spironolactone in high doses. ACE- I are
effective antihypertensive
-Surgery is the definite TR for adrenal
adenoma
Phaeochromocytoma
-Usually due to benign tumor of chromaffin
tissues of the adrenal medulla that secretes
principally
Nor adrenaline
-Causes HTN which can paroxysmal
-May present with headache, pallor, sweating,
palpitation, tremors, apprehension & anxiety or
-Complications of HTN
-May be associated with MEA
-Raised 24h urinary VMA
-24h urinary metanephrines++
- 24h urinary free catecholamines
- CT abd to localize the tumor
-Treatment is by surgery
-Long term TR with both alpha and beta
blockers if surgery is not feasible

Adrenal disorders in human beingssss.pptx

  • 1.
    Adrenal disorders By DrOsman Sadig Bukhari
  • 2.
    Adrenal gland 1- Cortex -Mineralocorticoids (aldosterone) Na retention and K excretion - Glucocorticoids (Cortisol) hyperglycemia, anti inflammatory & immunosuppressive - Androgens 2- Medulla - Catecholamines (Nor adrenalin & adrenalin)
  • 3.
    Cushing’s syndrome (Hypercortisolism) It refersto manifestations of excessive C/S Causes: 1- exogenous glucocorticoids 2- ACTH secreting pituitary adenoma (Cushing’s disease) 3- Ectopic ACTH secreting tumors e.g small cell Ca of the lungs 4- Adrenal tumors: adenomas & Ca
  • 4.
    Clinical features: (symptoms& signs) -Central obesity & protuberant abdomen and thin limbs - Plethoric moon face -Bufallo hump & supra clavicular fat pads -Oligomenorrhea or amenorrhea -Impotence -Headache, proximal muscle weakness & wasting -Osteoporosis & backache & back tenderness -Avascular necrosis of neck of femur - Acne & purple striae
  • 5.
    - Thin skin,easy bruising, impaired wound healing and hirsutism - Susceptibility to infection - Thirst & polyuria - Hypertension -Glucoma, cataract -Gynaecomastia -Mental symptoms Lab features: -Impaired glucose tolerance -Leucocytosis & lymphopenia -Hypokalemia
  • 6.
    - Increased serumcortisol & 24h urinary cortisol - Dexamethasone suppression test - Plasma ACTH - MRI pituitary - CT chest & abdomen Complications: - HTN -MD -Increased susceptibility to infections -Compression # of the osteoporotic spine and aseptic necrosis of the femoral head
  • 7.
    - Psychosis - Nephrolithiasis -Nelson’s syndrome following bilateral adrenalectomy Treatment: -Selective trans nasal resection for pituitary adenoma for Cushing’s disease. If no response bilateral adrenalectomy -Pituitary irradiation -Ketoconazole in patients not candidate for surgery
  • 8.
    - Resection ofadrenal tumors - Metyrapoe & ketoconazole in metastatic adrenal Ca -Resection of ectopic ACTH secreting tumors. If this can not be done Ketoconazole and metyrapone (suppress ACTH secretion)
  • 9.
    Acute adrenocortical insufficiency (Adrenalcrisis) Medical emergency caused by insufficient Cortisol It occurs in the course of chronic adrenocortical Insufficiency & is more commonly seen in Pry Adrenal insufficiency (Addison’s Addison’s dis). It is precipitated following: -Stress -Sudden withdrawal C/S - Bilateral adrenalectomy
  • 10.
    - Thyroxin therapyin patients with Sheehan’s. - Injury to both adrenals by trauma, hage, infect Clinical features (symptoms & signs) -Headache, lassitude, abd pain, nausea, vomiting & often diarrhea. -Dehydration -Hypotension -Skin hyper pigmentation -Hyponatremia -Hyerkalemia -Hypoglycemia
  • 11.
    - Hypercalcemia - Eosinophilia -Look for source of infection as a precipitating cause -Failure to respond to ACTH stimulation -Markedly elevated plasma ACTH Management -Blood sample for cortisol and start: -Hydrocortisone 200mg & NS immediately (without waiting the results) 6 hourly for 24h then 8 hourly next day
  • 12.
    - Correct hypoglycemia& monitor serum electrolytes, urea & creatinine -Broad spectrum antibiotic -When patient able to take orally start maintenance dose of hydrocortisone (20mg morning & 10mg evening) +/- mineralocoeticoids. -Early recognition & rapid treatment is life saving
  • 13.
    Chronic adrenocortical insufficiency (Addison’sdisease) - Caused by destruction or dysfn of the adrenal cortices -Characterized by chronic deficiency of cortisol, aldosterone & adrenal androgens and causes skin pigmentation. Volume & Na depletion and K excess eventually occur except in if secondary to pituitary disease Causes: - Autoimmune, TB
  • 14.
    - Sudden withdrawalof C/S - Bilateral adrenaline hage - Adrenal leukodystrophy - Lymphoma, metastatic Ca, amyloidosis, haemochromatosis, fungal infections. Clinical features: -Weakness, fatigability, myalgia, arthralgia -Anorexia, nausea, vomiting, WT loss -Skin hyperpigmentation (also mucus membranes) -Emotional changes -Hypoglycemic symptoms
  • 15.
    - Hypotension - Smallheart - Scanty axillary & pubic hair - Hyperplasia of lymphoid tissues - Manifestation of other AI disorders - Features of underlying cause - Neutropenia, lymphocytosis, eosinophilia - Low Na, high K - Low FBS - Hypercalcemia - Low plasma cortisol & elevated ACTH - ACTH stimulation test
  • 16.
    - CXR - CTabd Complications - Susceptibility to infection -Associated AI diseases -Adrenocortical crisis Management: -Replacement therapy with hydrocortisone and mineralocoeticoids (fludrocortisone). In mild cases hydrocortisone alone is adequate - Treat all infections & raise dose of hydrocortison
  • 17.
    - Increase doseof hydrocortisone in any stress - Medical alert bracelet
  • 18.
    Conn’s syndrome - Itis due to an adenoma of adrenal gland secreting aldosterone. It could also be due to bilateral hyperplasia of the zona glomerulosa -It results in hyperaldosteronism: - Increased plasma Na - Reduced plasma K - Increased serum bicarbonate - Alkalosis - Reduced urinary Na & increased K - All patients are hypertensive
  • 19.
    - Treated byaldosterone antagonist spironolactone in high doses. ACE- I are effective antihypertensive -Surgery is the definite TR for adrenal adenoma
  • 20.
    Phaeochromocytoma -Usually due tobenign tumor of chromaffin tissues of the adrenal medulla that secretes principally Nor adrenaline -Causes HTN which can paroxysmal -May present with headache, pallor, sweating, palpitation, tremors, apprehension & anxiety or -Complications of HTN -May be associated with MEA -Raised 24h urinary VMA -24h urinary metanephrines++
  • 21.
    - 24h urinaryfree catecholamines - CT abd to localize the tumor -Treatment is by surgery -Long term TR with both alpha and beta blockers if surgery is not feasible