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Adrenal Gland - SAWA

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Adrenal Gland - SAWA Powered By Docstoc
					Adrenal Gland

     Presented by:
Prof F. AMMARI FRCP
  JUST UNIVERSITY
      Synthesis of Adrenocortical
              Hormones


• Zona glomerulosa: aldosterone
• Zona fasciculata: glucocorticoids (cortisol)
• Zona reticularis: androgens (DHEA and
  androstenedione)
     Regulation of Adrenocortical
             Hormones
• Hypothalamus
  – CRH-containing neurons
    are stimulated
  – CRH delivered to anterior
    pituitary
  – CRH binds to receptors on
    corticotrophs, causing
    synthesis and secretion of
    ACTH
                   Cholesterol
 20,22 desmolase

5 Pregnolone        17 OH Pregnolone                  DHEA               Androstenediol




                                        desmolase
                                          17,20,
3 HSD               3 HSD                                3 HSD                 3 HSD


 Progesterone      17 OH Progesterone               Androstenedione          Testosterone




                                                       Oestrone              Oestrodiol

                                                                  5 Reductase

                                                                      Dihydrotestosteone




 Aldosterone               Cortisol
                 Actions of Cortisol
• Essential for response to stress
   – Stimulation of gluconeogenesis
       • Increases protein and lipid catabolism
       • Decreases glucose utilization
   – Anti-inflammatory effects
   – Suppression of immune response
       • Inhibits production of IL-2 and T lymphocytes
   – Maintenance of vascular responsiveness to cathecholamines
       • Required for vasoconstrictor effect of norepinephrine
            Actions of Aldosterone
• Helps maintain water and salt balance
   – Increases Na reabsorption
   – Increases K+ secretion
   – Increases H+ secretion
   – When aldosterone production falls too low, the kidneys are not
     able to regulate salt and water balance, causing blood volume
     and blood pressure to drop
                    Anatomy
• Paired retroperitoneal organs
  – Superior to kidney
• About 5 grams
  – Larger at birth (5-10g)
  – Susceptible to hemorrhage
  – Regresses over 6 weeks
• Up to 5 cm long, 3 cm wide
                       Anatomy
• Arterial supply (enters circumferentially)
   – Inferior phrenic (main)
   – Aorta and renal arteries
   – Gonadal (in fetus 60% of time)
• Venous return
   – Right: directly into posterior IVC
   – Left: to renal vein
      • Inferior phrenic vein
                   Anatomy
• Lymphatics
  – Paraaortic nodes


• Nerve supply
  – Mainly sympathetic from T10-L1
  – No cortex innervation
                     Histology
• Cortex
  – 90% of adult gland
  – Derived from mesoderm
     • Begins during 5th week of development
     • Mesothelial cell migration
  – Glomerulosa, fasciculata, reticularis
  – Zonation occurs until about 18 months of age
                     Histology
• Medulla
  – Derived from neuroectoderm
     • Neural crest cell migration
     • Begins during 7th week of development
     • Primitive medulla by 20th week
  – Continues growth until cortex atrophy (18 months)
                  Physiology
• Cortex
  – Cortisol
  – Aldosterone
  – DHEA, DHEAS, androstenedione
• Medulla
  – Epinephrine
  – Norepinephrine
  – Dopamine
               Aldosterone
• Stimulated by Angiotensin II
• Stimulated by hyperkalemia
• Suppressed by hypernatremia
• Sodium resorption in distal tubule
• Fluid absorption
• Potassium excretion
• Hydrogen Ion excretion
        Hyperaldosteronism
• Primary (Conn syndrome) or secondary
  – HTN, Low K+(<3.0), High Na+, Alkalosis
     • K+ normal in 20% of patients- usually bilateral adrenal
       hyperplasia
  – 1% of HTN patients
  – Symptoms: HA, muscle weakness, polyuria, cramps,
    visual disturbances, paralysis
     • Related to HTN and/or low K+ and/or excess fluid
     • Low K+ can cause baroreceptor paralysis and postural
       hypotension
        Hyperaldosteronism
• Mineralocorticoid escape
  – Due to breakdown of distal tubules ability to absorb
    sodium
     • Sodium retention decreases
     • Limits K+ loss
  – About 1.5kg of excess fluid absorption
     • No edema
     • Limits HTN
  – Worse with adenoma, better with hyperplasia
        Hyperaldosteronism
• Causes
  – Adenoma (most common)
     • F>M
     • 4th-5th decades of life
  – Bilateral adrenal hyperplasia
  – Adrenocortical carcinoma (rare)
  – Glucocorticoid remedial aldosteronism
     • Aldosterone producing adenoma
     • Responsive to renin
        Hyperaldosteronism
• Diagnosis
  – History, HTN, symptoms
  – Laboratory
     • Serum K+ (<3.0)
     • Serum aldosterone
        – Salt load patients (suppresses aldosterone)
        – Level >14 micrograms/d diagnostic of primary
          hyperaldosteronism
     • Serum renin
        – If >1.0 then unlikely primary hyperaldosteronism
        Hyperaldosteronism
• Localization
  – CT scan with thin cuts through adrenal
  – MRI (less sensitive)
  – Adrenal scintigraphy (less accurate)
  – Adrenal vein sampling
     • Gold standard
     • Measure selective aldosterone levels
        – Elevated on side of adenoma
        – Suppressed contralateral side
        Hyperaldosteronism
• Treatment
  – Medical: spironolactone, amiloride
     • Better for bilateral adrenal hyperplasia
     • Prepare for surgical treatment
     • Gynecomastia (spironolactone)
  – Surgical
     • Localize lesion
     • Control HTN with medicine; correct electrolytes
     • Removal of adenoma/carcinoma
     • 90% of patients have a decrease in HTN
           Cortex Hormones
• Fasciculata and Reticularis
  – Cortisol: glucocorticoid
     • Regulate carbohydrate and protein metabolism
  – Cogenital adrenal hyperplasia
     • Enzyme deficiency (11, 17, 21 hydroxylase)
  – Cushing’s Syndrome (excess)
  – Addison’s disease (deficiency)
       Cushing’s Syndrome
• Excess Cortisol
  – Protein catabolic state
  – Liberation of amino acids by muscle
  – AA are transformed into glucose and glycogen and
    then transformed into fat
  – Loss of calcium in urine
  – Weakened muscles and elastic tissues
                  Definitions
• Cushing’s Syndrome
  – Excess cortisol in the blood


• Cushing’s Disease
  – Excess cortisol in the blood due to an ACTH secreting
    pituitary tumour
             Epidemiology
• Incidence is 2/1 000 000 population


• 3-15:1 female : male


• Onset at 20-40 years old
             Actions of Cortisol

• Increases plasma glucose     • Proteins are catabolised
  levels                          – Releases Amino Acids
   – Inc gluconeogenesis       • Na+ and H2O Retention
   – Dec glucose utilisation      – Maintains BP
   – Increases glycogenesis
                               • Anti inflammatory
   – Inc glycogen storage
                               • Increased gastric acid
• Increases lipolysis
                                 production
   – Provides energy
       Cushing’s Syndrome
– Central obesity
– Moon face
– Buffalo hump               • changes in protein and
– Thin skin, easy bruising     fat metabolism
– Osteoporosis
– Diabetes


– Excess hair growth
                             • changes in sex hormones
– Irregular periods
– Problems conceiving
– Impotence
                             • salt and water retention
– High blood pressure
– Fluid retention
Cushing’s Syndrome
    The Investigation of
Cushing’s Disease is in Three
          Stages
• Screening


• Confirmation of the Diagnosis


• Differentiation of the Cause
 Screening and Confirmation
      of the Diagnosis
• Urinary free cortisol
• Diurnal Rhythm
• Over night dexamethasone suppression testing
Cortisol:Circadian Rhythm

    25



     0

    600




     0
          0800     2000   h
    Overnight Low Dose
Dexamethasone Suppression
           Test
• Cortisol is measured at 8am
• Dexamethasone 1mg is given at 11pm
• Cortisol is measured at 8am the next morning
• Cortisol suppression to <50nmol/l is normal
      Differential Diagnosis
• True Cushing’s Syndrome


• Pseudocushing’s Syndrome
  – Depression
  – Alcoholism


• Exogenous steroids
Dexamethasone Suppression
          Test
• LOW DOSE
  – 0.5 mg Dexamethasone six-hourly, 48 hrs


• Result
  – complete suppression in normal subject


  – If cortisol detectable then patient has CUSHING’S
    SYNDROME
  Differentiation of the Cause

• ACTH
• High dose Dexamethasone Suppression testing
• Localisation of the ACTH source
  – Imaging
  – IPSS
Dexamethasone Suppression
          Test
• HIGH DOSE
   – 2 mg Dexamethasone six-hourly for 48 hrs


• If cortisol suppresses to < 50% of baseline then the
  patient has Pituitary dependent Cushing’s Disease
• If the Cortisol does not suppress then the patient has
  ectopic ACTH production or an adrenal tumour
      Laboratory Features
• Hypokalaemia
• Metabolic Alkalosis
• Hyperglycaemia
• Increased Plasma LDH
• Very elevated plasma and urinary cortisol
• Non-suppression with dexamethosone
• Flat CRH response
• Very raised plasma ACTH (>110pmol/l)
       Cushing’s Syndrome
• Causes
  – Exogenous steroid use
     • PO or topical
     • Most common cause (overall)
  – Cushing’s Disease
     • Primary excretion of ACTH from pituitary
         – 95% have identifiable pituitary adenoma
         – Basophilic or chromophobe
     • Bilateral adrenocortical hyperplasia
     • 70% of endogenous cases
     • F>M (3:1)
       Cushing’s Syndrome
• Causes
  – Ectopic source
     • Produce ACTH or CRH
     • Small cell lung CA (most common), carcinoid tumors,
       medullary thyroid, pancreas, ovarian, pheochromocytoma,
       small-cell CA of prostate
     • 15% of endogenous causes
  – Adrenal adenomas (10%)
  – Adrenal carcinoma (5%)
     • Most common cause in children
       Cushing’s Syndrome
• Pseudo-Cushing’s disease
  – Mimic clinical signs and symptoms
  – Non-endocrine causes
     • Alcoholism
     • Major depression
     • Morbid obesity
     • Acute illness
       Cushing’s Syndrome
• Radiographic Localization
  – MRI of sella turcica
  – CT of chest/abdomen with 3mm cuts through adrenal
     • Adrenal hyperplasia
        – Thickening and elongation of adrenal rami bilaterally
        – Multinodularity of cortex bilaterally
       Cushing’s Syndrome
• Radiographic Localization
  – CT of adrenal glands
     • Adenomas- usually >2cm but <5cm
        – Low attenuation (lipid content)
        – Atrophy of opposite gland
     • Carcinoma- indistinguishable from adenomas
        – >5cm
        – Necrosis, calcifications, irregularity, invasion
  – MRI of adrenal- usually not needed
     • Signal intensity much higher than in spleen = carcinoma
     • Adjacent organ and/or vascular involvement
       Cushing’s Syndrome
• Treatment: Surgical
  – Cushing’s disease
     • Transphenoidal hypophysectomy
         – >90% cure rate 1st time, 50% salvage cure 2nd attempt
         – Exploration even if no obvious adenoma
         – Transient post-op diabetes insipidus, adrenal
           insufficiency, CSF rhinorrhea, meningitis
     • Tansphenoidal irradiation
         – High success rate in kids (80%)
         – Low success in adults (20%)
       Cushing’s Syndrome
• Treatment: Surgical
  – Cushing’s disease
     • Bilateral adrenalectomy
         – If failed pituitary surgery
         – Nelson’s syndrome (10-20%)
         – Life-long steroid replacement
  – Nelson’s syndrome
     • Rapid post-operative growth of ACTH-secreting pituitary
       adenomas that can be invasive
     • Hyperpigementation
     • Preoperative irradiation decreases incidence
       Cushing’s Syndrome
• Treatment: Surgical
  – Adrenal lesions/carcinoma
     • Removal of primary lesion
     • Survival based on underlying disease
  – Ectopic ACTH lesions
     • Remove lesion
     • Survival based on primary disease
     • May need bilateral adrenalectomy to control symptoms if
       primary tumor unresectable
       Cushing’s Syndrome
• Treatment: Medical
  – Used as prep for surgery or poor operative candidate
     • Metyrapone- inhibits conversion of deoxycortisol to cortisol
     • Aminoglutethimide-inhibits desmolase
         – Cholesterol to pregnenolone
         – Blocks synthesis of all 3 corticosteroids
         – Side effects: N/V, anorexia, lethargy
     • Ketoconazole- an imidazole that blocks cholesterol synthesis
     • Mitotane (O-P-DDD)-inhibits conversion to pregnenolone
         – Inhibits final step in cortisol synthesis
         – Destroys adrenocortical cells (spares glomerulosa cells)
ADRENAL INSUFFICIENCY
                 CLASSIFICATION

• Primary: destruction or impairment of the adrenal cortex
  (classic Addison’s disease)
   – Thomas Addison described this rare condition in his classical
     monograph published in 1855.
   – Incidence: 0.8 cases per 100,000
   – Prevalence: 4 to 11 cases per 100,000
   – Mean age of diagnosis: 40 years
• Secondary (Central): reduced ACTH secretion by the
  pituitary gland or failure of the hypothalamus to produce
  CRH (corticotrophin-releasing hormone)
ETIOLOGIES
   Etiologies – Primary Insufficiency

• Autoimmune
   – Autoimmune Polyglandular Syndrome
       • Type I: Addison's disease, chronic mucocutaneous candidiasis,
         hypoparathyroidism
       • Type II (Schmidt's syndrome): Addison's disease, primary
         hypothyroidism, primary hypogonadism, insulin-dependent diabetes

• Infection
   – Tuberculosis, HIV, Fungal
• Infiltrative
   – Amyloidosis, Sarcoidosis, Hemochromatosis,
     Adrenoleukodystrophy
  Etiologies – Primary Insufficiency

• Neoplasm
   – Adrenal metastases (lung and breast), Lymphoma
• Hemorrhage or infarct
   – Meningococcemia (Waterhouse-Friderichsen), DIC, Lupus
     (antiphospholipid antibody), Anticoagulation
• Iatrogenic
   – Bilateral adrenalectomy, Drugs that inhibit P-450 enzymes
     (ketoconazole, etomidate)
• Congenital adrenal hypoplasia
• ACTH resistance syndromes
Etiologies – Secondary Insufficiency

• Cessation of exogenous glucocorticoid therapy
   – Such therapy suppresses HPA axis with adrenal
     atrophy
   – Deficiency should be suspected if patient taking >
     30mg/d hydrocortisone (7.5mg/d prednisone or
     0.75mg/d dexamethasone) for >3 weeks
• Failure to give stress steroids
Etiologies – Secondary Insufficiency

• Inadequate ACTH production
  – Usually other pituitary hormones deficient, and
    patients present with partial or complete
    hypopituitarism
  – Isolated ACTH deficiency rare
     • Lymphocytic hypophysitis
     • Abnormal post-translational processing of POMC to ACTH

• Removal of ACTH-secreting pituitary adenoma
  – Function of ‘normal’ corticotrophs suppressed
CLINICAL FEATURES
       Manifestations of Adrenal
             Insufficiency
• Primary and Secondary Insufficiency
  – Weakness, fatigue, mental depression
  – Anorexia, weight loss
  – Nausea, vomiting, diarrhea
  – Postural dizziness, hypotension
  – Hyponatremia, hypoglycemia, mild normocytic
    anemia, lymphocytosis, eosinophilia
        Manifestations of Adrenal
              Insufficiency
• Primary Insufficiency
  – Hyperpigmentation
  – Vitiligo
  – Hyperkalemia, acidosis, elevated creatinine
  – Salt craving
  – Autoimmune thyroid disease
  – CNS symptoms in adrenomyeloneuropathy
Hyperpigmentation
Hyperpigmentation
        Manifestations of Adrenal
              Insufficiency
• Secondary insufficiency
  – Pallor without marked anemia
  – Amenorrhea, decreased libido
  – Scant axillary and pubic hair, small testicles
  – Secondary hypothyroidism
  – Prepubertal growth deficit, delayed puberty
  – Headaches, visual symptoms
  – Diabetes insipidus
         Manifestations of Adrenal
               Insufficiency
• Adrenal Crisis
   – Dehydration, hypotension, or shock out of proportion to severity
     of current illness
   – Nausea and vomiting with a history of weight loss and anorexia
   – Abdominal pain, so-called acute abdomen
   – Unexplained hypoglycemia and fever
   – Hyponatremia, hyperkalemia, azotemia, hypercalcemia, or
     eosinophilia
   – Hyperpigmentation or vitiligo
DIAGNOSIS
                    DIAGNOSIS

• Basal Cortisol Level
  – Avoid random level: low sensitivity
  – Check morning cortisol
     • Greater than 18 µg/dL indicates an intact axis
     • Less than 3 µg/dL strongly suggests insufficiency
     • No further tests
  – Intermediate values: perform cosyntropin stimulation
    test
                       DIAGNOSIS

• High-Dose Cosyntropin Stimulation Test
   – Intramuscular or intravenous administration of 250 µg of
     cosyntropin (exogenous ACTH)
   – Plasma cortisol levels are measured at 30 and 60 minutes
      • Normal response: peak plasma cortisol level > 18 µg/dL
      • Subnormal response: peak plasma cortisol level < 18 µg/dL
   – After positive test, primary adrenal insufficiency can be
     confirmed by an elevated ACTH level, whereas patients with
     secondary insufficiency typically have normal or low plasma
     ACTH levels
                       DIAGNOSIS

• High-Dose Cosyntropin Stimulation Test
   – Incremental responses (peak - basal values) are of no value
   – Response is unaffected by the time of day of the test
   – All glucocorticoid preparations except dexamethasone cross-
     react with cortisol assay; avoid within 24h of testing
                       DIAGNOSIS

• Low-Dose Cosyntropin Test
   – Cosyntropin doses as low as 0.5 to 1 ug will give a maximal
     response within 15 to 30 mins
   – Possibly superior to high-dose test for diagnosing secondary
     insufficiency because ACTH level closer to physiologic level
   – Normal response: peak plasma cortisol level > 18 µg/dL
   – Like high-dose test, low sensitivity when ruling out mild or recent
     secondary insufficiency; confirm with more sensitive tests
     (insulin tolerance, metyrapone)
                     DIAGNOSIS

• Insulin Tolerance Test
  – Hypoglycemia induced by the IV injection of reg
    insulin stimulates the entire HPA axis.
  – Plasma glucose and cortisol are measured after
    injection of insulin.
     • Normal response: cortisol increases to at least 18ug per dL

  – Expensive and contraindicated in patients with
    coronary heart disease or seizures
                       DIAGNOSIS

• Metyrapone Test
  – Metyrapone inhibits conversion of 11-deoxycortisol to cortisol
  – Give at midnight and measure the concentration of 11-
    deoxycortisol and cortisol at 8am
  – In normal subjects, the plasma 11-deoxycortisol concentration
    increases to at least 7ug per dL. In patients with adrenal
    insufficiency, the increase is smaller and is related to the severity
    of the corticotropin deficiency
                            DIAGNOSIS
• In acute settings, variability of cortisol and cosyntropin-stimulated
  cortisol is even greater
• Cutoff levels useful in outpatient setting cannot be projected to
  critical care setting
• Increment between basal and post-cosyntropin cortisol may be more
  useful indicator of adrenal insufficiency in acute setting (< 9ug/dl)
• Random cortisol levels:
     < 15ug/dl: insufficiency likely
     > 34ug/dl: insufficiency unlikely
     15-34ug/dl: perform Cosyntropin, increment <9 likely insufficient
TREATMENT
    ACUTE REPLACEMENT THERAPY
• IV hydrocortisone 100mg q6h
• Normal saline in the shocked patient
• Usually D5% because of possible hypoglycemia
• Clinical improvement should be seen in 4-6 hrs
• After the first 24 hours the dose of hydrocortisone can be
  reduced, usually to 50 mg IM q6h
• Then, if the patient can take it by mouth, to oral
  hydrocortisone, 40 mg in the morning and 20 mg at 6 PM
         CHRONIC REPLACEMENT
               THERAPY
• Aim: to mimic the normal cortisol secretion rate
• Most patients can cope with less than 30mg/d of
  hydrocortisone (usually 15 to 25 mg/day in divided
  doses)
   – Doses are usually given on wakening, with a smaller dose in the
     late afternoon
• Decisions about doses of replacement therapy are
  largely based on end points such as weight, well-being,
  and blood pressure
       CHRONIC REPLACEMENT
             THERAPY
• In primary adrenal failure, mineralocorticoid
  replacement is usually also required in the form
  of fludrocortisone at 0.05 to 0.2 mg/day.
• Adequacy of mineralocorticoid replacement
  should be assessed by measuring electrolytes,
  orthostatics, and plasma renin activity
• Mineralocorticoid replacement therapy is all too
  frequently neglected in patients with adrenal
  failure.
          CHRONIC REPLACEMENT
                THERAPY
• Patients should be advised to double the daily dose in the event of
  febrile illness, accident, or mental stress
• Surgery
    – Minor: 50 to 100 mg of hydrocortisone hemisuccinate with
      premedication
    – Major: As above, but followed by the same regimen as for acute adrenal
      insufficiency
• Pregnancy
    – Daily doses of hydrocortisone are usually increased modestly (5 to 10
      mg/day) in the last trimester
    – During labor, patients should be well hydrated with a saline drip and
      receive hydrocortisone at 50 mg intramuscularly every 6 hours until
      delivery
    – Thereafter, doses can be rapidly tapered off to usual maintenance
      regimens.
         CHRONIC REPLACEMENT
               THERAPY
• Adrenal androgen replacement therapy
   – DHEA at 25 to 50 mg/day in both primary and secondary
     insufficiency
   – To date, the reported benefit is principally confined to female
     patients and includes improvement in sexual function and well-
     being.
        Pheochromocytoma
• Originate from adrenal medulla or extraadrenal
  paraganglia cells
• Autopsy series: 1%
• Secrete norepinephrine, epinephrine, rarely
  dopamine and other neurohormones
        Pheochromocytoma
           “10% tumor”
• 10% bilateral
• 10% malignant
• 10% multifocal
• 10% extraadrenal
• 10% occur in children
• 10% familial (neuroectodermal disorders or
  MEN2)
• 10% normotensive
        Pheochromocytoma,
           Presentation
• Episodic headaches, tachycardia, diaphoresis
• HTN
   – Sustained HTN
   – Sustained HTN with paroxysm
   – Paroxysmal HTN with intermittent normotension
• Nausea/vomiting
• Flushing
• Raynaud’s phenomenom
• 10% present in “pheocrisis”
• 50% found as incidentaloma
         Pheochromocytoma,
             Diagnosis
• 24hr urinary catecholamines (NE, Epi, Dop) and
  metabolites (metanephrine, normetanephrine, VMA)
• Plasma catecholamine or metabolites during episode
• Elevated serum epinephrine suggests pheo in medulla or
  Organ of Zukerkandl
• NO FNA! (can precipitate hypertensive crisis)
      Pheochromocytoma,
          Diagnosis
• Localizing studies: CT, MRI, MIBG scan
  – Thin cut CT detects most lesions: 97%
    intraabdominal
  – MRI: 90% pheos bright on T2 weighted scan
  – MIBG: used for extraadrenal, recurrent, multifocal,
    malignant disease
• Malignant disease
  – Local invasion, disease outside of
    adrenal/paraganglionic tissue
  – No histological or clinical criteria can differentiate
    malignant disease
      Pheochromocytoma,
          Diagnosis
• Localizing studies: CT, MRI, MIBG scan
  – Thin cut CT detects most lesions: 97%
    intraabdominal
  – MRI: 90% pheos bright on T2 weighted scan
  – MIBG: used for extraadrenal, recurrent, multifocal,
    malignant disease
• Malignant disease
  – Local invasion, disease outside of
    adrenal/paraganglionic tissue
  – No histological or clinical criteria can differentiate
    malignant disease
       Pheochromocytoma,
           Treatment
• Treatment is surgery
• Must medically optimize prior to surgery
   – Treat HTN
   – Expand intravascular volume
   – Control cardiac arrhythmias
• Phenoxybenzamine (α-adrenergic antagonist)
   – most commonly given 1-3 wks prior to OR.
   – Other α-adrenergic antagonists, CCB, ACEI used
• PO salt and fluid repletion
• May need β-blocker as antiarrhythmic. Do not start
  until after pt α-blocked
• Metyrosine – decreases catecholamine synthesis
        Pheochromocytoma,
            Treatment
• Intraop- avoid anesthetic agents that precipitate
  catecholamine secretion.
  – Induce with thiopental/isoflurane
  – Phentolamine (short acting α-blocker)
  – Sodium nitroprusside for BP control
  – Norepinephrine if needed for hypotension
  – Lidocaine and esmolol to control arrhythmias.
• Medical options: chemo, high dose I131 MIBG,
  XRT – symptomatic relief
  Pheochromocytoma, follow
            up
• 6.5% of benign pheochromocytomas recur
• 50% of malignant dz have residual dz
• F/u with biochemical testing
• Imaging not routinely necessary

				
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