Endocrinology - MTB Flashcards
Panhypotpituitarism: presentation
symptoms dependent of deficiency of a specific hormone
Panhypopituitarism
- caused by any condition that compression or damage to pituitary gland
- look for tumors (e.g. metastatic cancer, adenomas, Ranthke cleft cysts)
- look for conditions (e.g. hemachromatosis, sarcoidois)
Prolactin deficiency
- in women, prolactin deficiency inhibits lactation after childbirth
Deficiency of LH and FSH
- women are unable to menstruate (become anovulatory)
- men unable to produce sperm and have erectile dysfunction
- both men and women have decreased libido and decreased axillary, pubic, and body hair
Kellman syndrome
- decreased FSH and LH from decreased GnRH
- anosmia
- renal agenesis
Growth hormone deficiency
- children present with short stature and dwarfism
- adults have few symptoms b/c catecholamines, glucagon, and corticol act as stress hormones
Adult presentation of GH deficiency
- Central obesiry
- increased LDL and cholesterol levels
- reduced lean muscle mass
Growth hormone diagnostic tests
- Hyponatremia (2/2 hypothyroidism and isolated glucocorticoid underpoduction)
- potassium remains levels b/c aldosterone is not affected
- MRI detects compressing mass lesions
Low TSH and low thyroxine
confirm w/ decreased TSH response to TRH
decreased ACTH and decreased cortisol level
normal response to cosyntropin stimulation of adrenal, cortisol will rise in recent disease and cortisol is abnormal b/c of adrenal atrophy
Metyrapone
inhibits 11- B hydroxlase
- decreases output of adrenal gland
- should cause ACTH to rise b/c cortisol goes down
Insulin stimulation
- insulin decreases glucose levels so GH should rise
- failure to rise in response to insulin indicates pituitary insufficiency
Posterior pituitary
- produces ADH and oxytocin
- no deficiency disease for oxytocin
Oxytocin deficeiency
- aids with uterine contraction
- delivery still occurs even if active
Diabetes Inspidus
- decrease in amt of ADH from pituitary (central DI) or decease in response to ADH on collecting tubules (nephrogenic DI)
Central DI
any destruction of brain from stroke, tumor, trauma, hypoxia, or infiltration of gland from sarcoidosis or infection
Nephrogenic DI
Kidney diseases (e.g chronic pyelonephritis, amyloidosis, myeloma, and sickle cell disease) damaged kidney enough to inhibit effect of ADH
Electrolyte abnormalities that can cause nephrogenic DI
- Hypercalcemia
- Hypokalemia
DI: presentation
- presents with high volume urine and excessive thirst resulting in volume depletion and hypernatremia
- hypernatremia sx (condusion, disorientation, lethargy then later seizures, coma)
classic cause of nephrogenic DI
Lithium
- look for bipolar patients
Diabetes inspidus
- serum sodium is elevated
- decreased urine osmolality and urine sodium is decreased
Difference btwn central DI and nephrogenic DI
Response to vasopressin (desmopression(
Central DI: Treatment
- treated with long term vasopression
Nephrogenic DI: treatment
- correct underlying cuase (e.g. hypokalemia or hypercalcemia)
- treat with thiazides, amiloride, or prostiglandin inhibitors (NSAIDS)
Acromegaly
overproduction of growth hormone leading to soft tissue overgrowth
Acromegaly: Etiology
- often cuased by pituitary adenoma
- can be associated with MEN (e.g. parathyroid or pancreatic disorders)
- rarely caused by ectopic GH or GHrH production from lymphoma or bronchial carcinoid
Acromegaly: presentation
- increased hat, ring, and shoe size
- carpal tunnel syndrome and sleep apnea from enlarged soft tissues
- body odor from sweat gland hypertrophy
- coarsening facial features
- colonic polyps and skin tags
- arthralgias
- hypertension
- cardiomegaly and CHF
Best initial test for suspected acromegaly?
Insulin growth factor (IGF -1) levels
Acromegaly: lab testing
- Glucose interolerance and hyperlipidemia, which contribute to cardiac dysfunction
Most accurate test for acromegaly
Glucose suppression test
- normally glucose suppreses GH levels
When is the MRI done in diagnosis of acromegaly?
Only after lab identification of acromegaly
Acromegaly: Treatment
- Surgery: transphenoidal resection of pituitary
- Medications
- cabergoline
- octreotide or lanreotide
- pegvisomant - Radiotherapy
Cabergoline
dopamine will inhibit GH release
Octreotide or lanreotide
somatostatin inhibits GH release
Pegvisomant
Gh receptor antagonist, inhibits IGF release from the liver
Hyperprolactinoma
- prolactin can be cosecreted with GH and increase simply b/c of acromegaly
Physiologic cause of hyperprolactinoma
- Pregnancy
- Intense exercise
- Renal insufficiency
- Increased chest wall stimulation
Drug induced hyperprolactinoma
- Antipsychotic meds
- Methyldopa
- Metoclopromide
- Opioids
- TCAs
- Verapramil
Which the only CCB that raises prolactin levels?
Verapramil
Hyperprolactinoma: presentation
- women present with galactorrhea, amenorrhea, and infertility
- men experience erectile dysfunction and decreased libido
Hyperprolactinoma: Diagnostic tests
- Thyroid fxn tests
- Pregnancy tests
- BUN/Cr (kidney disease elevates prolactin)
- Liver fxn test (cirrhosis elevates prolactin)
When is the MRI done in diagnosis of hyperprolactinemia
- High prolactin level is confirmed
- Secondary causes such as meds are exclused
- Patient is not pregnant
Hyperprolactinemia: Treatment
- Dopamine agonitsts: cabergoline
- Transphenoidal surgery: when refractory to meds
- Radiation is rarely indicated
Hypothyroidism
- often of failure of thyroid gland from burn out (e.g Hashimoto thyroiditis)
Less common causes of hypothyroidism
- Dietary deficiency of iodine
- Amiodarone
Hypothyroidism: common sifns
- all bodily processes being slowed
- high TSH (2x upper limit) with T4
If patient has hypothyroidism and TSH is less than double normal, what’s next step?
- Get antithyroid peroxidase/antithyroidglobulin antibodies
- if antibodies are positive, replace thyroid hormone
Hypothyroid: presentaiton
- Bradycardia
- Constipation
- Weight gain
- Fatigue, lethargy, coma
- Cold intolerance’
- Hypothermia (hair loss, edema)
Hyperthyroidism
- Tachycardia, palpitations, arrhythmia
- Diarrhea
- Weight loss
- Anxiety, nervousness, restlessness
- Hyperreflexia
- Heat intolerance
- Fever
Best diagnostic test for suspected thyroid disorders
TSH levels
- if TSH is suppressed then meausre T4 levels
- if TSH is markedly elevated then gland has likely failed
Hypothyroidism: treatment
Thyroid hormone replacement
Pt has hyperthyroidism and presents with proptosis (eye drooping) and skin findings. Likely diagnosis?
Graves disease
Pt has hyperthyroidism and presents with a tender thyroid. What’s the most likely diagnosis?
Subacute thyroiditis
Patient has low TSH and high T4 but presents with nontender thyroid and normal exam results. Likely diagnosis?
Painless “silent” thyroiditis
Pt has high T4 levels and low TSH with an involuted gland that is not palpable. Likely diagnosis?
Exogenous thyroid hormone use
Patient has has T4 and high TSH. Likely diagnosis?
Pituitary adenoma
Graves disease: lab findings
- low TSH
- high RAIU
- positive antibody testing
Subacute thyroiditis: lab findings
- low TSH
- low RA iodine uptake
- confirm with tender thyroid
Painless “silent” thyroiditis: lab findings
- low TSH
- low radioactive iodine uptake
- no confirmatory testing
Exogenous thyroid hormone: lab findings
- low TSH
- low radioiodine uptake
- confirm with hx and involuted thyroid nonpalpable gland
Pituitary adenoma
- high TSh
- radioactive iodine uptake not dones
- confirm with MRI of head
Graves disease: treatment
Radioactive iodine
Subacute thyroiditis: treatment
Aspirin
Painless “silent” thyroiditis: treatment
None
Exogenous thyroid hormone: tx
Stop use
Pituitary adenoma: tx
Surgery
Thyroid Storm / Acute hyperthyroidism: Treatment
- Propranolol
- Thiourea drugs (methimazole and PTU)
- Iodinated contract material
- Steroids
- Radioactive iodine
Propranolol in thyroid storm
- blocks target organ effect, inhibits peripheral conversion of T4 to T3
Thiourea drugs: Methimazole and Propylthiouracil) in management of thyroid storm
- Blocks hormone production
Use of iodinated contrast material (iopanoic acid and ipodate) in thyroid storm mgmt
Blocks peripheral conversion of T4 to T3 (more active)
- blocks release of existing hormone
Graves Ophthalmopathy: Treatment
Steroids are best initial therapy
- radiation used when pt is unresponsive to steroids
Which is preferred in management of thyroid storm? Methimazole or PTU
Methimazole
Thyroid nodules
- extremely common
- 95 % benign (adenoma, colloid nodule, cyst)
- rarely associated with hyperfunctioning and hypofunction
46 y.o woman comes to the office b/c of small mass she found on palpation of her own thyroid. A small nodule is found in thyroid. No tenderness. Otherwise symptomatic and uses medications. Next step for management of this patient?
Check T4 and TSH levels
If patient has thyroid nodule > 1 cm and has normal thyroid fxn (T4/TSH). What’s the next step?
FNA
- no need for U/S or radionucleotide because they cannot exclude cancer
When patient has a nodule… next steps?
- Perform thyroid function tests (TSH and T4)
2. If tests are normal, biopsy the gland
46 y.o woman with thyroid nodule is found to have normal thyroid function testing. The FNA comes back as “indeterminant for follicular adenoma. What is the most appropriate next step?
Surgical removal (excisional biopsy)
Hypercalcemia
- most common cause in hyperparathyroidism
- most patients are asymptomatic
- symptomatic patients have high prevalence of cancer and hypermalignancy of malignancy
Other causes of hypercalcemia
- Vitamin D intoxication
- Sarcoidosis and other granulomatous disease
- Thiazide diuretics
- Hyperthyroidism
- Metastases to bone and multiple myeloma
Hypercalcemia: Presentation
- acute, symptomatic hypercalcemia presents with confusion, stupor, lethargy, and constipation
CV presentation: hypercalcemia
- short QT syndrome and hypertension
Hypercalcemia: Treatment
- Saline hydration at high volume
2. Bisphosphonate: pamidronate, zoledronic acid
75 y/o man with a hx of malignancy is admitted with lethargy, confusion, and abdominal pain. He is found to have a a markedly elevated calcium level. After 3 liters of normal saline and pamidronate, his calcium level is still markedly elevated the following day. What is the most appropriate next step in management?
Calcitonin
- inhibits osteoclasts
- onset of action of calcitonin is very rapidly
Hyperparathyroidism
- Solitary adenoma (** most common cause**)
- Hyperplasia of all 4 glands
- Parathyroid malignancy
Hyperparathyroid: presentation
- Asymptomatic elevation in calcium levels found on routine testing
Slower manifestations - osteoporosis
- nephrolithiasis and renal insufficiency
- muscle weakness, anoreia, nausea
- peptic ulcer disease
Hyperparathyroidism: diagnostic tests
- high calcium and high PTH
- low phosphate levels
- EKG shows short QT
- alkaline phosphotase may be elevated due to PTH effect on bone
Best test to determine PTH effect on bone
DEXA scan
Hyperparathyroidism: Treatment
Surgical removal of gland
- if surgeon is poor surgical candidate
Primary hypoparathyroidism
- often a complication of prior neck surgery (e.g. thyroidectomy)
Common causes of hypoparathyroidism
- prior neck surgery (most common)
- hypomagnesemia
- renal failure
Hypocalcemia 2/2 hypomagnesemia
Mg is necesssary for PTH to be released from gland
- low Mg levels also leads to increased urinary loss of calcium
Hypoparathyroidism 2/2 renal failure
Leads to hypocalcemia
- kidney converts 25 hydroxy vitamin D to 1,25 dihydroxy Vitamin D
Calcium correct with albumin levels
For every 1 point decrease in albumin, decrease calcium by 0.8
Discuss low albumin and low total calcium
Lab testing measures calcium bound to albumin thus less albumin means less calcium
Hypocalcemia: presentation
Signs of neural hyperexcitability in hypocalcemia:
- Chvostek sign (facial nerve hyprexcitability)
- Carpopedal spasm
- perioral numbess
- mental instability
- seizures
- tetany (Trousseau)
Hypocalcemia: treatment
Replace with vitamin D and calcium
- only done orally if symptoms are severe
Hypocalcemia: diagnostic testing
- Low Ca levels
- EKG shows prolonged QT that can cause arrhythmia
- slit lamp may show early cataracts
Low calcium: presentation
Twitchy and hyperexcitable
High calcium: presentation
Lethargic and slow
Diabetes Mellitus
- persistently high fasting glucose levels greater than 125 on at least 2 separate occasions
Type 1 DM
- onset in childhood
- insulin dependent from early age
- not related to obesity
- defined as insulin deficiency
Type 2 DM
- onset in adulthood
- directly related to obesity
- defined as insulin resistance
Diabetes Mellitus: presentation
- polyuria, polyphagia, and polydipsia
- type 1 diabetics usually thinner than type 2
- type 2 diabetics less likely to present with polyphagia
Diabetes Mellitus: Diagnostic Tests
- Two fasting blood glucose measurements > 125 mg/dL
- Single glucose level > 200 mg/dL with above symptoms
- Increased glcose level on oral glucose tolerance test
- Hemoglobin A1c > 6.5% is a diagnostic criterion and best to follow response to therapy for the past few months
Diabetes Mellitus: Treatment
- weight loss since less adipose tissue decreases insulin resistance
Best initial medical treatment for diabetes mellitus
Oral metformin
- blocks glucogenesis
Contraindications of metformin
In DM pts with renal dysfunction because it can accumulate and cause metabolic acidosis
Why aren’t sulfonyureas first line drugs for DM?
- Sulfonyureas increase insulin release from pancreas, thereby driving glucose intracellularly and increasing obesity
- goal of therapy < 7%
Thiazoledinediones (glitazones)
- provide no clear benefit over the other hypoglycemic conditions
- contraindicated in CHF because they increase fluid overload
Nateglinide and repaglinide
- stimulators of insulin release from pancrease
- don’t contain sufa
Alpha glucosidase inhibitors (e.g. acarbose, miglitol)
- block glucose absorption in the bowel
- add about 1/2 point decrease in HgA1c
- can cause flatus, diarrhea, and abdominal pain
- can be used with renal insuffiency
Incretins (exenatide, sitagliptin, saxagliptin, linagliptin)
- part of mechanism by which oral glucose normally produces rise in insulin and decreases glucagnon levels
- decreases gastrin motlity and help in weight loss, decreasing Type 2 diabetes
Exenatide: side effects
Pancreatitis
Pramlinitide
- analog of protein called amylin that is secreted normally with insulin
- amylin decrease gastric emptying
- decreases glucagon levels and decreases appetitie
Insulin use in Type 2 DM
used when oral hypoglycemics cannot control
Short acting insulin
- lispro
- aspart
- glulisine
- onset in 5 - 15 minutes
- peak action in 1 hr
- lasts for 3-4 hrsw
Regular insulin
- onset in 30 to 60 minutes
- peak action in 2 hrs
- duration of 6 - 8 hrs
NPH
- onset in 2 to 4 hrs
- peak action in 6 to 7 hrs
- lasts for 10 - 20 hrs
Glargine
- onset in 1 to 2 hrs
- peak action in 1 to 2 hrs
- lasts for 24 hrs
Diabetic ketoacidosis
- more common in type 1 diabetics
- Patients present w/
- hyperventilation
- possibly AMS
- metabolic acidosis w/ increased anion gap
- acetone odor on breath
- polydipsia and polyuria
- hyperkalemia in blood but decreased total body K
- increased anion gap on blood testing
- serum positive for ketones
- nonspecific abdominal pain
DKA: Treatment
Large volume saline and insulin replacement
- replace K when potassium level comes down to a level approaching normal
- correct underlying cause: meds, infection, pregnancy
57 y.o man is admitted to ICU with AMS, hyperventilation and markedly elevated glucose level. Which is the following is the most accurate measure of the severity of the condition?
Serum bicarbonate
- measure of anion gap acidosis
- the lower the bicarb, the more severe the acidosis
DM patients should receive the following for health maintenance:
- Pneumococcal vaccine
- Yearly eye exam for proliferative neuropathy
- statin meds if LDL > 100
- ACEis or ARBS if BP is > 130/80 mm Hg
- ACEis or ARBS if microalbuminuria is present
- Aspirin if diabetic patients > 50
- foot exam for neuropathy
Complications of DM
- CV risk
- Diabetic nephropathy
- Gastroparesis
- Retinopathy
- Neuropathy
CV complications of DM
- DM patients are at increased risk of MI
- CHF from premature atherosclerotic disease
- why BP goal is < 130/80
- target LDL goal < 100 mg/DL when initiating stain treatments
Diabetic Nephropathy
- DM can lead to microalbuminuria (30 - 300 mg per 24 hrs)
- should be screened annually for microalbuminuria
- if detected, DM pt should be started on ACEis and ARBs by decreasing intraglomerylar HRn and decreasing kidney damage
Gastroparesis
- immobility of bowels that leads to bloating, constupation and early satiety
- DM decreases ability of gut to sense the stretch of walls of bowel, important as stretch stimulates gastric motility
Gastroparesis: Treatment
Metoclopromide
Erythromycin
– increases gastric motility
Diabetic nonproliferative retinopathy
- DM affects nonproliferative retinopathy for tighter control of glucose
Diabetic proliferative retinopathy
- neovascularization and vitreous hemorrhages are present
- treat with laser photocoagulation, which markedly retards progression to blindness
Diabetic neuropathy
- damage to microvasculature damages vasonervorum that surrounds large peripheral nerves
- decreased sensation in the feet - main cause of skin ulcers
Diabetic neuropathy: treatment
- Preglabin
- Gabapentin
- Tricyclic antidepressants
Cushing syndrome
- aka hypercortisolism
- can be cased by prednisone or other glucocorticoid
Cushing disease
- pituitary overproduction of ACTH from carcinoid or cancer or from overproduction autonomously in the the adrenal gland
- can be caused by prednisone or other glucorticoids
Most common cause of hypercorticolism
Pituitary ACTH (Cushing disease)
Cushing syndrome: presentation
- Fat redistribution: “moon facies” , truncal obesity
- Skin: striae
- Osteoporosis
- Hypertension
- Menstrual disorders in women
- Erectile dysfunction in men
- Cognitive disturbance
- Polyuria
Best initial test for presence of hypercorticolism
24 hr urine cortisol
Test for hypercorticolism other than 24 hr urine cortisol
- 1mg overnight dexamethasone suppression test
** if suppression doesn’t occur, hypercorticolism can be excluded
More specific test of hypercorticolism
24 hr urine cortisol
Causes of false positive 1 mg dexamethasone suppression testing
- Depression
- Alcoholism
- Obesity
Best initial test to determine the cause (source) or location of hypercortisolism
ACTH testing
If ACTH level is high in someone with suspected hypercortisolism, the source could be from:
- Pituitary (suppresses w/ high dose dexamethsone)
- Ectopic production: lung cancer, carcinoid (dexamethasone doesn’t suppress)
If the ACTH level is elevated and doesn’t suppress with high dose dexamethasone
- Scan the brain MRI
If patient has suspected hypercortisolism and the MRI does not show pituitary lesion. What’s the next step?
Sample the inferior pretrosal sinus for ACTH, possible after the stimulating the patient with CRH
Why should the petrosal venous sinus must be sampled in cases of suspected hypercortisolism when head MRI is negative?
Some pituitary lesions are too small detected on RI
If patient has suspected hypercortisolism and the ACTH is levated and cannot find defect in pituitary either by MRI or petrosal sinus sampling, what’s the next step?
Scan chest for ectopic source of ACTH production
Patient has suspected hypercortisolism but low ACTH. Source of cortisol?
Adrenal srouce
Patient has suspected hypercortisolism but has high ACTH and has been given high dose dexamethasone. Source?
If dexamethasone test suppresses: pituitary source
If dexamethasone test does not suppress: ectopic + cancer
Effects of hypercortisolism
- Hyperglycemia
- Hyperlipidemia
- Hypokalemia
- Metabolic alkalosis
- Leukocytosis (from demargination of WBC cells)
Why does hypercortisolism cause hypokalemia and metabolic alkalosis?
Cortisol has an aldosterone-like effect on distal tubules in which potassium and hydrogen ions are excreted
Hypercortisolism: Treatment
Surgically remove the source of hypercortisolism
- transsphenoidal surgery is done for pituitary sources
- laparoscopic removal is adrenal sources
Evaluation of adrenal incidentaloma (unexpected, asymptomatic adrenal lesion found on CT)
- metanephrines of blood or urine to exclude pheochromocytoma
- renin and aldosterone levels to exclude hyperaldosternism
- 1 mg overnight dexamethasone suppression test
Adrenal source hypercortisolism: findings
- low ACTH
- petrosal sinus not does
- no suppression of high dose dexamethasone
Pituitary source hypercortisolism: findings
- high ACTH
- high ACTH found on petrosal sinus
- high dose dexamethasone suppresses ACTH
Ectopic source hypercortisolism findings
- high ACTH level
- low ACTH in petrosal sinus
- no suppression on high dose dexamethasone
Addison disease
- chronic hypoadrenalism
- caused by autoimmune destruction of the gland in more than 80% of causes
Most common cause of hypoadrenalism
Addison disease
Less common causes of hypoaldrenalism
- Infection (tuberculosis)
- Adrenoleukodystrophy
- Metastatic cancer to the adrenal gland
Acute adrenal crisis
- caused by hemorrhage, surgery, hypotension, or trauma that rapidly destroys the gland
- sudden remove of high dose prednisone (steroid) can precipitate episode
Hypoadrenalism: presentation
- weakness, fatigue, AMS
- hypotension
- hyponatremia
- hyperkalemia
- hyperpigmentation from chronic adrenal insufficiency
Acute adrenal crisis
- presents with profound hypotension, fever, confusion, and coma
Hypoadrenalism: diagnostic test
- Hypoglycemia
- Hyperkalemia
- Metabolic acidosis
- Hyponatremia
- High BUN
- Eosinophilia
Most specific test of adrenal function
Cosyntropin test
- cosyntropin is synthetic ACTCH
- measure the cortisol level before and after the administration of cosyn
Hypoadrenalism (acute adrenal crisis): treatment
- Replace steroids with hydrocortisone
- Fludrocortisone is steorid hormone that is particularly high in mineralicorticoid or aldosteroine-like effect
- fludrocortisone most useful in cases of postural instability
- mineralocorticoid supplements shoud be used in primary adrenal insufficiency
Patient is brought to the ED after a MVA in which he sustains severe abdominal trauma. On the 2nd hospital day, the patient necomes markedly hypotensive w/o evidence of bleeding. There is a fever, high eosinophil count, hyperkalemia, hyponatremia, and hypoglycemia. What is the most appropriate next step in management?
Draw cortisol level and administer hydrocortisone
- in suspected acute adrenal insufficiency, treatment is more important than diagnosis
Primary hyperaldosteronism
- autonomous overproduction of aldosterone despite high pressure with low renin activity
- 80% are from solitary adenoma
- other causes are from bilateral hyperplasia
Most common cause of primary hyperaldosteronism
Solitary adenoma
Risk factors for secondary hypertension
- under age 30 or after age 60
- not controlled by 2 anti-BP meds
- has characteristic finding on hx, physical, or labs
Primary hyperaldosteronism findings
- high blood pressure in association with low potassium level
- low K found on routine lab testing or b/c of symptoms of muscular weakness or diabetes insipidus from hypokalemia
Best test to measure primary hyperaldosteronism
Ratio of plasma aldosterone to plasma renin
- elevated plasma renin excludes primary aldosteronism
Most accurate test to confirm unilateral adenoma in primary hyperaldosteronism
- Sample of venous blood draining the adnreal
- it will show high aldosterone levels
Diagnostic order in suspected hyperaldosteronism
- ratio of plasma aldosterone to plasma renin
2. CT scan of adrenals (only AFTER biochemical confirmation of low K, high aldosteronism, low plasma renin)
High BP + hypokalemia =
Primary hyperaldosteronism
Hyperaldosteronism: Treatment
- Unilateral adenoma is resected by laparascopy
- Bilateral hyperpaslia is treated with eplerenone or spironolactone
Phemochromocytoma
- nonmalignant lesion of adrenal medulla autonomously overproducing catecholamines despite high BP
Pheochromocytoma: presentation
- Hypertension that is episodic in nature
- Headache
- Sweating
- Palpitations and tremor
Best initial test for pheochromocytoma
Plasma level of free metanephernes
Pheochromocytoma: diagnostic testing
- plasma level of free metanepherines
- confirmed with 24 hr urine collection for metanepherines
- imaging of adrenal glands w/ CT or MRI done after bio chemical testing
MIBG scanning
nuclear isotope scan that detects location of pheochromocytoma that originates outside of gland
Pheochromocytoma: treatment
- Phenoxybenzamine (alpha blocker) is best initial therapy
- CCBs and B-blockers are used afterwards
- Pheochromocytoma is removed surgically or by laparscopy
Spironolactone: side effects
- causes gynecomastia and decreased libido b/c it is antiadrenogenic
