What are the two main parts of the adrenal gland and what is the secretory product of each part
The adrenal cortex and the adrenal medulla make up the adrenal gland. The cortex secretes aldosterone, cortisol, and sex hormones and the medulla secretes the catecholamines including epinephrine and norepinephrine.
What is the function of aldosterone
Kidney resorption of sodium and secretion of potassium and hydrogen ions
What is Addison disease
Primary adrenal insufficiency caused by the destruction of the adrenal cortex leading to
deficiency in both mineralocorticoids as well as glucocorticoids
What is secondary adrenal insufficiency
Decreased secretion of ACTH by the pituitary gland; the adrenal gland is functional
What is the cause of tertiary adrenal insufficiency
Decreased hypothalamic function
What is the most likely etiology of Addison disease
Autoimmune destruction of the adrenal gland
What are some other causes of Addison disease
TB, amyloidosis, sarcoidosis, HIV, adrenal hemorrhage secondary to DIC or trauma,
Waterhouse-Friderichsen syndrome, congenital adrenal hyperplasia, metastasis to the adrenals
What is Waterhouse-Friderichsen syndrome
Endotoxin-mediated adrenal hemorrhage usually caused by meningococcemia
What is the most likely cause of secondary adrenal insufficiency
Hypothalamic-pituitary axis disturbance, usually by sudden cessation of exogenous corticosteroids, which leads to decreased ACTH secretion
What are some other causes of secondary adrenal insufficiency
Pituitary infarction, Sheehan syndrome, pituitary adenoma
What are some signs and symptoms of Addison disease
Because of low aldosterone and cortisol there are hyponatremia, hyperkalemia, pica (craving for salt), weakness, anorexia, hypotension, nausea, vomiting, hyperpigmentation
What are the diagnostic findings in primary adrenal insufficiency
Hyperpigmentation,? ACTH, ? cortisol and aldosterone response to ACTH challenge
What is the test used to diagnose adrenal insufficiency
ACTH (Cortrosyn) test in which a dose of ACTH is given to the patient and then serum cortisol levels as well as serum ACTH levels are measured.
Primary adrenal insufficiency: ?cortisollevels in response to ACTH and ?aldosteronelevels
Secondary adrenal insufficiency: ?cortisollevels in response to ACTH andnormal
aldosterone levels
How is the diagnosis of secondary adrenal insufficiency distinguished from primary adrenal insufficiency
No hyperpigmentation,?cortisol response, ?ACTH
What kind of metabolic disturbance is seen in primary adrenal insufficiency
Metabolic acidosis due to aldosterone and cortisol deficiency and, therefore, lack of secretion of H ions
What is the treatment for adrenal insufficiency
Glucocorticoid replacement. Extra glucocorticoids should be given in times of physical stress such as infection. You should instruct patients to taper off this extra replacement slowly as to prevent an adrenal crisis.
What is Cushing syndrome
A term used to describe the symptoms caused by hypercortisolism
How is Cushing syndrome different from Cushing disease
Cushing disease refers to a type of Cushing syndrome caused specifically by ACTH hypersecretion by the pituitary
What are the different causes of hypercortisolism
1. Exogenous glucocorticoids
2. Pituitary hypersecretion of ACTH
3. Hypersecretion of cortisol due to adrenal hyperplasia/neoplasm
4. Ectopic ACTH production such as with small cell lung carcinoma
What is the most common cause of Cushing syndrome
Exogenous corticosteroids
What is the most common cause of endogenous hypercortisolism
Cushing disease (pituitary hypersecretion of ACTH)
What are the signs and symptoms of Cushing syndrome
Buffalo hump,moon facies, truncal obesity, striae, virilization/menstrual disorders, hyperglycemia, hypertension, hypokalemia, immune suppression, osteoporosis, hirsutism, acne
What tests are used to diagnose hypercortisolism
24-hour urine-free cortisol and the dexamethasone suppression tests, ACTH level, diurnal cortisol variation
What is the dexamethasone suppression test
First a low dose of dexamethasone is given and cortisol is measured. If cortisol is not elevated then Cushing is ruled out;if it is elevated then a high-dose dexamethasone suppression test is done and ACTH is measured. If ACTH is decreased then the pituitary
has good feedback and, therefore, it must be an adrenal etiology. However, if the ACTH is high or normal then it is probably ectopic ACTH; and if it is only partially suppressed, then the pituitary is the etiology.
Dexamethasone ? ? ACTH (ectopic/pituitary)
?ACTH (adrenal)
What are some other studies to consider to localize the lesion in hypercortisolism
A CT scan can look for an adrenal mass and an MRI can look for a pituitary mass.
What is the treatment for hypercortisolism
Treat the underlying cause. If it is a resectable tumor, tumor resection with postoperative
glucocorticoids. In nonresectible tumors, medical therapy with ketoconazole, mitotane, metyrapone, aminoglutethimide. If the etiology is exogenous glucocorticoids, taper off the glucocorticoids and eventually stop
What is Conn syndrome
Primary hyperaldosteronism
What is the etiology of Conn syndrome
Either hyperplasia of the zona glomerulosa or aldosterone-producing adenoma
What are the signs and symptoms of Conn syndrome
Hypertension, muscle cramps, palpitations, polyuria, polydipsia, hypokalemia
What percent of hypertensive patients have Conn syndrome
1%–2%
What are some of the laboratory findings in Conn syndrome
?Na, ?Cl, ?K (muscle cramps, palpitations), ?renin-angiotensin feedback, metabolic
alkalosis
How is Conn syndrome diagnosed
Captopril stimulation test: captopril ( ACE inhibitor) is administered and then serum renin and aldosterone levels are measured. ?aldosterone and ?renin confirm the diagnosis
What is the renin level in Conn syndrome
Low renin
What other study can help in the diagnosis of Conn syndrome
CT demonstrating an adrenal nodule or hyperplasia
What is the treatment for Conn syndrome
Adrenal adenoma: resection of tumor; unilateral adrenal hyperplasia: unilateral adrenalectomy; bilateral adrenal hyperplasia: spironolactone (potassium-sparing diuretic) or ACE inhibitor to control blood pressure
What is secondary hyperaldosteronism
Elevated aldosterone levels due to elevated renin levels secondary to renal ischemia in CHF, renal artery stenosis, shock, renal tumor.
How is secondary hyperaldosteronism diagnosed
?Renin
What can be measured to differentiate primary from secondary hyperaldosteronism
Renin(this is very important)
What is treatment for 2ry hyperaldosteronism
Treat the hypertension with a potassium-sparing diuretic, a beta-blocker, and treat the underlying cause
What is a pheochromocytoma
Tumor of the adrenal medulla that produces excess catecholamines
What percentage of people with hypertension have a pheochromocytoma
0.5%
What are the possible etiologies for a pheochromocytoma
MEN 2 or 3, von Hippel-Lindau disease, Recklinghausen disease, neurofibromatosis
What are the five P’s of pheochromocytoma
1. Pain (headache)
2. Pressure
3. Perspiration
4. Palpitation
5. Pallor and hypertension
What is the most common sign of a pheochromocytoma
Hypertension
What is the diagnostic test for pheochromocytoma
Urine screen for elevated VMA (vanillyl mandelic acid), a urine catecholamine; as well elevated urine and serum epinephrine and norepinephrine levels
What other test can be done to localize a pheochromocytoma
A CT scan can identify asuprarenal mass (adrenal mass).
What are some other laboratory findings in a pheochromocytoma
Hyperglycemia, hypercalcemia, polycythemia
What is the “rule of 10’s” for a pheochromocytoma
10% malignant
10% bilateral
10% extrarenal
10% familial
10% in kids
10% multiple tumors
10% calcified
What must be ruled out in a patient with a pheochromocytoma
MEN type II or III
What is the treatment for a pheochromocytoma
In operative cases preoperative alpha-blockers and beta-blockers, then surgical resection
In inoperable cases phe noxybenzamineor phe ntolamine
Why treat with preoperative alpha-blockers and beta-blockers
To prevent unopposed vasoconstriction and thus, volume depletion
التوقيع
اللهم إنك عفو كريم تحب العفو فاعف عنى
خللى بالكم يا شباب سادسة من الجرعات دى مهمة جدااااااااااااااااااااا فى النسا
Mg Sulfate as anticonvulsant in ttt of PET
IV 4-6 gm slowly (over 15-20 min) then 1-2 gm/hr by drip
,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,, ,,,,,,,,,, Oxytocin as ecbolic
most commonly used in (saline , dextrose , lactated ringer)
start by small dose at slow rate then gradualy increase
.5 - 2 mIU /min then increase by 1-2 mIU/30-60min
,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,, دكتور أبو عمار
Increased secretion of parathyroid hormone (PTH)
What is the most common cause of primary hyperparathyroidism
Adenoma is the most common cause; however, other etiologies include hyperplasia, carcinoma, MEN 2 or 3
What does elevated PTH cause
There is an ultimate increase in serum calcium (hypercalcemia) because PTH leads to increased vitamin D hydroxylation and, therefore, increased calcium resorption as well as decreased resorption of phosphate (hypophosphatemia). Calcium levels are also increased because of increased osteoclastic activity(osteoporosis) .
What are the signs and symptoms of hyperparathyroidism
Same as those for hypercalcemia. “Stones, maons, groans, and psychiatric overtones.” Because of the osteoclastic activity it can also lead to osteoporosis.
What EKG finding could you expect with hyperparathyroidism
Shortened QT, because of hypercalcemia
How is hyperparathyroidism diagnosed
Hypercalcemia, hypophosphatemia, hypercalciuria, and PTH level
What other differential diagnoses should be considered with hypercalcemia
Neoplasm, sarcoidosis, thiazide diuretic treatment, Paget disease, vitamin D intoxication, milk alkali syndrome, myeloma
What is the acute medical treatment for hyperparathyroidism
Asymptomatic patients with calcium levels below 13 should just be watched. However,
symptomatic patients or those with higher calcium levels should be treated with furosemide and bisphosphonates to decrease bone resorption and prevent osteoporosis. Calcitonin can be used as well.
What long-term treatment must be considered in hyperparathyroidism
Surgical treatment. Adenomas should be removed. In hyperplasia, all four parathyroids are removed and a small piece is placed usually near the sternocleidomastoid for functionality.
What are the most common complications of parathyroidectomy
Hoarseness because of damage of the recurrent laryngeal nerve and hypocalcemia
What is secondary hyperparathyroidism
Increased PTH secretion secondary to chronic renal failure or vitamin D deficiency
What is hypoparathyroidism
Decreased PTH
What are the causes of hypoparathyroidism
Idiopathic, secondary to surgery or neck irradiation, DiGeorge syndrome, hypomagnesemia
Why does hypomagnesemia lead to hypoparathyroidism
Because magnesium is necessary for parathyroid to secrete PTH
In what conditions is low magnesium seen
Syndrome of inappropriate secretion of antidiuretic hormone (SIADH), pancreatitis,alcoholism
How is hypoparathyroidism diagnosed
Hypocalcemia, hyperphosphatemia, low PTH
What are the signs and symptoms of hypoparathyroidism
Same as that for hypocalcemia: perioral paresthesias, tetany, seizures, Trousseau sign,
Chvostek sign, anxiety
What EKG findings could you expect in hypoparathyroidism
Prolonged QT interval because of the hypocalcemia
What is Trousseau sign
Carpal spasm with arterial occlusion with BP cuff
What is Chvostek sign
Spasm of the facial nerve upon tapping
How is hypoparathyroidism treated
Emergently treat with IV calcium, then treat with vitamin D and oral calcium for maintenance TTT
التوقيع
اللهم إنك عفو كريم تحب العفو فاعف عنى
خللى بالكم يا شباب سادسة من الجرعات دى مهمة جدااااااااااااااااااااا فى النسا
Mg Sulfate as anticonvulsant in ttt of PET
IV 4-6 gm slowly (over 15-20 min) then 1-2 gm/hr by drip
,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,, ,,,,,,,,,, Oxytocin as ecbolic
most commonly used in (saline , dextrose , lactated ringer)
start by small dose at slow rate then gradualy increase
.5 - 2 mIU /min then increase by 1-2 mIU/30-60min
,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,, دكتور أبو عمار
اللهم إنك عفو كريم تحب العفو فاعف عنى
خللى بالكم يا شباب سادسة من الجرعات دى مهمة جدااااااااااااااااااااا فى النسا
Mg Sulfate as anticonvulsant in ttt of PET
IV 4-6 gm slowly (over 15-20 min) then 1-2 gm/hr by drip
,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,, ,,,,,,,,,, Oxytocin as ecbolic
most commonly used in (saline , dextrose , lactated ringer)
start by small dose at slow rate then gradualy increase
.5 - 2 mIU /min then increase by 1-2 mIU/30-60min
,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,, دكتور أبو عمار
اللهم إنك عفو كريم تحب العفو فاعف عنى
خللى بالكم يا شباب سادسة من الجرعات دى مهمة جدااااااااااااااااااااا فى النسا
Mg Sulfate as anticonvulsant in ttt of PET
IV 4-6 gm slowly (over 15-20 min) then 1-2 gm/hr by drip
,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,, ,,,,,,,,,, Oxytocin as ecbolic
most commonly used in (saline , dextrose , lactated ringer)
start by small dose at slow rate then gradualy increase
.5 - 2 mIU /min then increase by 1-2 mIU/30-60min
,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,, دكتور أبو عمار
اللهم إنك عفو كريم تحب العفو فاعف عنى
خللى بالكم يا شباب سادسة من الجرعات دى مهمة جدااااااااااااااااااااا فى النسا
Mg Sulfate as anticonvulsant in ttt of PET
IV 4-6 gm slowly (over 15-20 min) then 1-2 gm/hr by drip
,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,, ,,,,,,,,,, Oxytocin as ecbolic
most commonly used in (saline , dextrose , lactated ringer)
start by small dose at slow rate then gradualy increase
.5 - 2 mIU /min then increase by 1-2 mIU/30-60min
,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,, دكتور أبو عمار
اللهم إنك عفو كريم تحب العفو فاعف عنى
خللى بالكم يا شباب سادسة من الجرعات دى مهمة جدااااااااااااااااااااا فى النسا
Mg Sulfate as anticonvulsant in ttt of PET
IV 4-6 gm slowly (over 15-20 min) then 1-2 gm/hr by drip
,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,, ,,,,,,,,,, Oxytocin as ecbolic
most commonly used in (saline , dextrose , lactated ringer)
start by small dose at slow rate then gradualy increase
.5 - 2 mIU /min then increase by 1-2 mIU/30-60min
,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,, دكتور أبو عمار
اللهم إنك عفو كريم تحب العفو فاعف عنى
خللى بالكم يا شباب سادسة من الجرعات دى مهمة جدااااااااااااااااااااا فى النسا
Mg Sulfate as anticonvulsant in ttt of PET
IV 4-6 gm slowly (over 15-20 min) then 1-2 gm/hr by drip
,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,, ,,,,,,,,,, Oxytocin as ecbolic
most commonly used in (saline , dextrose , lactated ringer)
start by small dose at slow rate then gradualy increase
.5 - 2 mIU /min then increase by 1-2 mIU/30-60min
,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,, دكتور أبو عمار
اللهم إنك عفو كريم تحب العفو فاعف عنى
خللى بالكم يا شباب سادسة من الجرعات دى مهمة جدااااااااااااااااااااا فى النسا
Mg Sulfate as anticonvulsant in ttt of PET
IV 4-6 gm slowly (over 15-20 min) then 1-2 gm/hr by drip
,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,, ,,,,,,,,,, Oxytocin as ecbolic
most commonly used in (saline , dextrose , lactated ringer)
start by small dose at slow rate then gradualy increase
.5 - 2 mIU /min then increase by 1-2 mIU/30-60min
,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,, دكتور أبو عمار
اللهم إنك عفو كريم تحب العفو فاعف عنى
خللى بالكم يا شباب سادسة من الجرعات دى مهمة جدااااااااااااااااااااا فى النسا
Mg Sulfate as anticonvulsant in ttt of PET
IV 4-6 gm slowly (over 15-20 min) then 1-2 gm/hr by drip
,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,, ,,,,,,,,,, Oxytocin as ecbolic
most commonly used in (saline , dextrose , lactated ringer)
start by small dose at slow rate then gradualy increase
.5 - 2 mIU /min then increase by 1-2 mIU/30-60min
,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,, دكتور أبو عمار
اللهم إنك عفو كريم تحب العفو فاعف عنى
خللى بالكم يا شباب سادسة من الجرعات دى مهمة جدااااااااااااااااااااا فى النسا
Mg Sulfate as anticonvulsant in ttt of PET
IV 4-6 gm slowly (over 15-20 min) then 1-2 gm/hr by drip
,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,, ,,,,,,,,,, Oxytocin as ecbolic
most commonly used in (saline , dextrose , lactated ringer)
start by small dose at slow rate then gradualy increase
.5 - 2 mIU /min then increase by 1-2 mIU/30-60min
,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,, دكتور أبو عمار
دكتور أبو عمار 
العرض العادي
