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Adrenal Gland
Adrenal Gland
Plasma Cortisol Description This is direct measure of the primary secretory product of the adrenal cortex by radioimmunoassay technique. Serum concentration varies with circadian cycle so normal values vary with time of day and stress level of patient (8 a.m. levels typically double that of 8 p.m. levels). Useful as an initial step to assess adrenal dysfunction, but further workup is usually necessary.
Nursing and Patient Care Considerations A fasting sample is preferred. Blood specimens should coincide with circadian rhythm with draw time indicated on laboratory slip.
24-Hour Urinary Free Cortisol Test Description Test measures cortisol production during a 24-hour period. Useful to establish diagnosis of hypercortisolism. Less influenced by diurnal variations in cortisol.
Nursing and Patient Care Considerations Instruct patient in appropriate collection technique. Collection jug should be kept on ice and sent to laboratory promptly when collection completed. Interfering factors:
Elevated values pregnancy, oral contraceptives, spironolactone, stress. Recent radioisotope scans can interfere with test results.
Dexamethasone Suppression Test Description The dexamethasone suppression test (DST) is a valuable method to evaluate adrenal hyperfunction. Adrenal production and secretion of cortisol is stimulated by adrenocorticotropic hormone (ACTH, corticotropin) from the pituitary gland.
Dexamethasone is a synthetic steroid effective in suppressing corticotropin secretion. In a healthy patient, the administration of dexamethasone will inhibit corticotropin secretion and will cause cortisol levels to fall below normal.
Nursing and Patient Care Considerations Explain the procedure to the patient.
Overnight 1 mg DST (used primarily to identify those without Cushing's syndrome). Administer dexamethasone 1 mg orally at 11 p.m. Draw cortisol level at 8 a.m. before patient rises. Expect suppressed cortisol levels (less than 5 mcg/dL).
High-dose overnight DST (helpful to distinguish Cushing's disease from other forms of Cushing's syndrome). Give patient dexamethasone 8 mg orally at 11 p.m. Draw cortisol level at 8 a.m. before patient rises. Suppressed cortisol levels (less than 50% of baseline value) indicative of patient with corticotropin-secreting pituitary adenoma (Cushing's disease). Unsuppressed cortisol levels are associated with ectopic corticotropin secretion (malignancy) or adrenal tumors.
Adrenocorticotropic Stimulation Test Description ACTH stimulates the production and secretion of cortisol by the adrenal cortex. Demonstrates the ability of the adrenal cortex to respond appropriately to ACTH. This is an important test to evaluate adrenal insufficiency, but may not distinguish primary insufficiency from secondary insufficiency.
Nursing and Patient Care Considerations Obtain baseline cortisol level. Administer 0.25 mg ACTH (cosyntropin [Cortrosyn] I.V. or I.M.). Collect cortisol levels at times ordered (usually at 30 and 60 minutes). Interpretation of test results:
Range of normal responses may vary; however, typically a rise in cortisol of double baseline value is considered normal.
Diminished response adrenal insufficiency with low cortisol values, adrenal tumor with high cortisol values, prolonged glucocorticoid therapy. Exaggerated response adrenal hyperplasia with high cortisol values.
Corticotropin Releasing Hormone Stimulation Test Description Test measures responsiveness of pituitary gland to corticotropin-releasing hormone (CRH), a hypothalamic hormone that regulates pituitary secretion of ACTH. Useful to differentiate the cause of excess cortisol secretion when ectopic source of ACTH is suspected. In general, CRH will stimulate ACTH secretion in the pituitary, but not in nonpituitary corticotropin-secreting tissues.
Patient is given CRH (1 mcg/kg or 100 mcg) I.V. Catheters are advanced through the femoral veins to areas near the adrenal glands, so sampling can take place near ACTH secretion. Blood samples for ACTH test are collected at 2, 5, 10, and 15 minutes.
Cushing syndrome
Definition
Cushing syndrome is a spectrum of clinical abnormalities caused by an excess of corticosteroids, particularly glucocorticoids.
Classification
ACTH
Dependent
Pituitary dependent bilateral adrenal hyperplasia Ectopic ACTH syndrome (bronchial carcinoid, small cell lung carcinoma) Iatrogenic (ACTH therapy)
Pseudo-Cushing syndrome is cortisol excess as a part of another illness. Alcohol excess Major depressive illness Primary obesity
Etiology
Adrenal hyperplasia Secondary to pituitary ACTH over production Pituitary hypothalamic dysfunction Pituitary ACTH or CRH producing micro and macro adenoma
Secondary to ACTH or CRH producing endocrine tumors (bronchiogenic carcinoma, carcinoid of the thymus, pancreatic carcinoma, bronchial adenoma) Adrenal macro nodular hyperplasia Adrenal micro nodular hyperplasia Sporadic Familial Primary adrenal neoplasms such as adrenal adenoma and carcinoma and
primary cortical hyperplasia Exogenous and iatrogenic causes Prolonged use of glucocorticoids Prolonged use of ACTH
Pathophysiology
Due to etiological factors Normal feedback mechanism of mechanisms that control the function of adrenal cortex is disturbed
CLINICAL MANIFESTATIONS
Insidious in onset. Muscle weakness and fatigability due to mobilization of peripheral supportive tissue. Hypertension and weight gain due to sodium and water retention. centripetal distribution of adipose tissue with truncal obesity moon face accumulation of fat in the posterior neck and back.
Selective atrophy of fast twitch myofibres with resultant decreased muscle mass. Glucocorticoid induce gluconeogenesis with resultant hyperglycemia and polydipsia mimicking diabetes mellitus. Skin is thin fragile and easily bruised, cutaneous strior in the abdomen due to catabolic effect of protien causing loss of collagen Bone resorption result in development of fracture.
Increased risk for infection. Hirsutism and mineralized abnormalities like oligomenorrhea or amenorrhea due to increased adrenal androgens. Emotional changes may be profound, ranging from irritability to severe depression confusion or even frank psychosis. thinning of scalp hair. Posterior sub capsular cataract.
Truncal obesity Moon face Fat deposits supraclavicular fossa and posterior neck- buffalo hump HTN Hirsutism Amenorrhea or impotence Depression Thin skin Easy bruising Purplish abdominal striae Proximal muscle weakness Osteoporosis Diabetes Mellitus Avascular necrosis Wound healing impaired Pysch symptoms Hyperpigmentation Hypokalemic alkalosis
DIAGNOSTIC EVALUATION Urine cortisol. Overnight Dexamethasone test. Diurnal rhythm of plasma cortisol. Insulin tolerance test. High dose dexamethasone suppression test. Corticotropin releasing harmone test
Screening Test
Overnight dexamethasone suppression test (1 mg at 11 pm, cortisol measured at 8 am) normal <2 micrograms/dL Or 24 hour urine free cortisol (>140 nmol/day)
Confirmatory Test
Low dose dexamethasone suppression test Dexamethasone 0.5 mg q 6 x 48 hours Measure urine cortisol during the last 24 hours (urine free cortisol >20 micrograms/dL or urine 17-hydroxycorticosteroid >4.5 mg/d) Or plasma cortisol (failure to fall to <5 micrograms/dL)
Confirmatory Test
Low dose dexamethasone suppression test Dexamethasone 0.5 mg q 6 x 48 hours Measure urine cortisol during the last 24 hours (urine free cortisol >20 micrograms/dL or urine 17-hydroxycorticosteroid >4.5 mg/d) Or plasma cortisol (failure to fall to <5 micrograms/dL)
Treatment
Cushings Disease: Transphenoidal resection of pituitary adenoma Adrenal neoplasms: resection Ectopic ACTH: resection if possible Bilateral adrenal hyperplasia: may need adrenalectomies (lifelong glucocorticoid and mineralcorticoid replacement)
Medical Adrenalectomy
Medications that inhibit steroidogenesis Ketoconazole (600 to 1200 mg/day) metyrapone (exacerbates female virilization) (23 g/day) Mitotane(2-3 G/day)- slow onset Aminoglutethinide (1g/day) Ocreotide can work in 1/3 of patients. Major side affect is adrenal insufficiency, therefore start at lowest dose and titrate
Drug Name:Metyrapone (Metopirone) Description:Inhibitor of endogenous adrenal corticosteroid synthesis. Inhibits 11-B-hydroxylation reaction in the adrenal cortex .Adult Dose:1 g/d PO divided qid; increase gradually, not to exceed 4.5 g/d
Drug Name:Ketoconazole (Nizoral) Description:Imidazole broad-spectrum antifungal agent that acts on several of the P450 enzymes, including the first step in cortisol synthesis, cholesterol side-chain cleavage, and conversion of 11deoxycortisol to cortisol. Adult Dose200-400 mg PO bid/tid
Drug Name;Aminoglutethimide (Cytadren) Description:Inhibits conversion of cholesterol to delta-5-pregnenolone, which, in turn, reduces the production of adrenal glucocorticoids, mineralocorticoids, aldosterone, estrogens, and androgens. Adult Dose:250 mg PO bid initially; increase to 2 g qid
Prognosis
Benign adrenal adenoma- 95% 5 year survival, 90% 10 year Cushings disease (pituitary adenoma) same survival, but 10-20% transphenoidal resection failure rate over 10 years. Ectopic ACTH survival depends on malignancy Unknown cause of elevated ACTH- 65% 5 year survival, 55% 10 year survival Adrenal carcinoma- median survival 7 months
Hyperaldosteronism
Definition
Classification
Primary aldosteronism Cause lie within the adrenal gland May be due to a adrenal leision which is benign It produce hypokalemia, hypernatremia and secondary hypertension.
Secondary Aldosteronism Stimulus is extra adrenal Condition include sodium wasting renal disease, excessive laxative and diuretic use, dehydration , cirrhosis with ascities, heart failure.
Primary aldosteronism
Definition Primary aldosteronism indicate a primary autonomous overproduction of aldosterone with resultant suppression of renin angiotensin system and decreased plasma renin activity
Etiology
aldosterone producing adrenal adenoma. Bilateral cortical nodular hyperplasia Rarely adenocarcinoma
Pathophysiology
Due to hypersecretion of aldosterone Increased renal tubular exchange of intratubular sodium for secreted potassium and hydrogen ions
Hypernatremia hypokalemia hypovolemia Hypertension muscle weakness hypertension Cerebral infarct, renal damage
Clinical manifestation
Usually asymptomatic But findings include Hypernatremia hypokalemia and hypertension. Large urinary output leads to polydipsia Hypokalemia leads to metabolic alkalosis metabolic alkalosis causes adecrease in ionized calcium levels which can result in tetany and respiratory suppression.
Diagnostic evaluation
Serum potassium decreased Urine PH- NEUTRAL TO ALKALINE Serum sodium increased Metabolic alkalosis Test for mineralocorticoid suppressibility Radionuclide scanning technique to visualize tumors.
Management
Adrenalectomy Dietary sodium restriction Aldosterone antagonist
Secondary Aldosteronism
Definition Secondary aldosteronism refers to an appropriately increased production of aldosterone in response to activationof renin angiotensin system.
Etiology
Occurs in association with accelerated phase of hypertension or on the basis of an underlying edema disorder like cirrhosis or nephrotic syndrome. Narrowing of major renal arteries by atherosclerosis Profound renal vasoconstriction. Renin producing tumors
Pathophysiology
Due to etiological factors Narrowing of renal arteries Decrease in renal blood flow
Overproduction of renin
Hypokalemia, alkalosis, hypertension, increased aldosterone.
Incidence
Usually rare , but may occur at any age and affect both sexes equally.
Tuberculosis Fungal-histoplasma capsulatum Viral Haemorrhage Invasion:metastasis from the lung,breast,Gi tract Metabolic failure in hormone production Congenital adrenal hyperplasia Enzyme inhibitirs(metyrapone,ketoconazole) Cytotoxic agent ACTH blocking antibiotics
Mutation in ACTH receptor gene Adrenal hypoplasia congenita RISK FACTORS a history of other endocrine disorders Taking glucocorticoid for more than 3 weeks withsudden cessation Taking glucocorticoid more than once every other day
Pathophysiology
Clinical features
Insidious onset of fatigability,weakness,pigmentation of skin,weight loss,anorexia,nausea,vomiting,hypotension ,pigmentation of mucus membrane,abdominal pain,salt craving,diarrhea,constipation,syncope and occassional hypoglycemia
Asthenia is a cardinal symptom.early it may be sporadic -More evident at the time of stress -As adrenal function become more impaiired the patient is continuously fatigued Hyperpigmentation appears as diffuse brown or bronze darkening of elbows,creases of the hand
-Bluish black patches may appear on mucus membrane -Tanning following sun exposure -Arterial hypotension 80/50 or less Abnormalities of gi function Mild anorexia with weight loss to fulminating nausea,vomitting,diarrhea and abdominal pain
Excessive irritability and restlessness Axillary's and pubic hair decreased in women due to loss of adrenal adrogens
Diagnostic tests
Serum sodium,chloride, and bicarbonate decreased Serum pottasium level elevated Low cortisol level Low aldosterone level ACTH stimulation test :plasma ACTH will be more Blood count to assess anemia Blood glucose X ray,CT,MRI
Management
Medical: -all patients should receive specific hormone replacement -Glucocorticoid-hydrocortisone(cortiso) is the mainstay treatment 20-30mg/day -To stimulate normal diurnal rhythm 2/3rd is taken in morning and 1/3rd evening
Side effects -Insomnia,irritability,mental excitement Minerelocorticoid-fludeocortisone 0.050.1mg/day orally -Maintain ample intake of Na -Measure blood pressure or serum electrolyte Androgen:DHEA 25-50mg/day orally
pathophysiology
Due to etiological factors Loss of adrenalresponsiveness to ACTH and failure of pituitary ACTH release Adrenal atropy and prolonged pituitary adrenal insufficiency
Clinical features
Weakness,fatigability Severe dehydration Hyponatremia Hyperkalemia GI disturbances include anorexia,nausea vomitting,weight loss,diarrhea
Diagnostic test
treatment
Glucocorticoid therapy
causes
Sepsis Surgical stress Acute haemorrhagic destruction of both glands Septicemia with pseudomonas and meningococcemia Congenital adrenalhyperplasia Drugs which inhibits steroids synthesis(ketoconazole )
Clinical features
Manifestations are related to degree of hormones deficiency and electrolyte imbalance and include Suddenpenetrating pain at back ,abdomen and legs Depressed or changed mentation Volume depletion
management
Replace steroids -hydrocortisone at 100mg iv bolus followed by 100mg every 8hrs for 24hrs Replacement of Na and water deficits-an isotonic solution usually correct the volume depletion,salt depletion and hypotension
Vasoconstrictive agent dopamine as adjuant to volume depletion Sodium polysterene sulfonate orally or as enema in combination with sorbital.it is a resin that releases Na ions in exchange of K ions Hypoglycemia corrected with 5% dextrose
Adrenal steroids glucocorticoids Evaluating patient prior to initiating steroid therapy 1. Chronic infection-if TB is present steroid therapy should be given in conjunction in antitubercular drug 2. Diabetes mellitus 3. Prolonged therapy may aggravate DM
Osteoporosis with vertebral fracture or comcompression is a high risk complication Peptic ulcer,gastric hypersecretion,esophagitis Hypertension or cardiovascular diseases Psychological difficulties-sleeplessness is common
hypoaldosteronism
Isolated aldosterone deficiency accompanied by normal cortisol production occurs in association with hyporeninism as an inherited biosynthetic defect postoperatively following removal of aldosterone secreting adenoma,during protracted heparin or heparinoid administration
features
Unexplained hyperkalemia Severe cases,urine sodium wastage occurs at a normal salt intake.In milder forms,excessive loss of urine sodium occurs only with salt restriction
pathophysiology
Due to renal disease,autonomic neuropathy extracellular fluid volume expansion Plasma renin fail to rise following Na restriction and K changes Failure of aldosterone level to rise
Diagnostic test
Serum K level ACTH stimulation test Renin and aldosterone levels
management
Replace mineralocorticoid 0.05-0.15mg fludrocortisones daily orally Patients with hyporeninic hypoaldosteronism may require higher doses Potential risk in patient with hypertension,mild renal insufficiency and CCF Reduce salt intake and administer frusemide
pheochromocytoma
Definition Pheochromocytoma is a catecholamine secreting tumor of the chromaffin cells of the sympathetic nervous system that is usually found in the adrenal medulla
pathophysiology
The pathophysiology of the pheochromocytoma is best appreciated with an understanding of catecholamine biochemistry. The following is an abbreviated version of the important steps in the biosynthesis and metabolism of catecholamines.
Tyrosine
Dihydroxyphenylalanine (DOPA) Dopamine (DA) Norepinephrine + Epinephrine
an alteration in the regulation of the catecholamine biosynthesis possibly suggests an alteration in the feedback inhibition of tyrosine hydroxylase, the key enzyme in the production of catecholamines.
Extraadrenal tumors
Weigh 20-40gm and are less than 5cm diameter Located in abdomen,urinary bladder(10%) less than 3% seen in neck within the sympathetic ganglia
Clinical features
Hypertension - common manifestation -40% B>P elevation occur during attack -often severe and not treated with antihypertensives Paroxysm/crisis: -Occur in half of patients -May be frequent or sporadic
Sudden onset Last from a few mnts to several hours or longer Headache,profuse sweating,palpitations Apprehensions are common Pain in chest and abdomen Nausea and vomiting pallor
B.P elevated with tachycardia Paroxyms may be precipitated by any activity that displaces abdominal content.smoking,micturation may stimulate paroxysms Activities that displaces abdominal content include bending,exercising,straining,vigorous palpations of abdomen in pregnancy
Cardiac manifestations-sinus bradycardia,arrythmias,angina,MI,cardiom yopathy Carbohydrate intolerence Hypercalcemia Fever Polyuria Urinary bladder pheochromocytomasproduce typical paroxysms in relation to micturation,hematuria
diagnosis
History and p/E Lab test -elevated haematocrit due to diminished plasma volume -increased ESR due to production of interleukin Assay of urinary catecholamines
Assay of urinary VMA levels -performed on 24hr urine specimen -advice client to avoid tea,coffee,chocolate,vannilla for atleast 2 days before the test -normal less than 7mg in 24 hrs
Direct assay of catecholamines -normal epinephrine-0.02-0.2mg/L norepinephrine-0.1-0.5mg/L X-ray imaging,CT,MRI Pheochromocytomas of urinary bladdercystoscopy
complications
Cardiomyopathy Multisystem organ failure Acute pancreatitis Renal failure
management
Drug Name :Phenoxybenzamine (Dibenzyline) Adult Dose:10 mg PO bid initially; increase dose by 10-mg increments every other day until an optimal dosage is obtained; usual dosage range is 20-40 mg PO bid/tid
Adult Dose:Prevention or control of hypertension in pheochromocytomas: 5 mg IV/IM 1-2 h before surgery; repeat prn; administer 5 mg IV during surgery as indicated to control paroxysms of hypertension, tachycardia, respiratory depression, or seizures
Adult Dose: 1 mg PO bid/tid initially; increase prn; not to exceed 20 mg/d PO divided bid/tid
blocking agents
These agents are used as adjunctive therapy for cardiac effects. The agents inhibit chronotropic, inotropic, and vasodilatory responses to beta-adrenergic stimulation.
Adult Dose: Hypertension: 40 mg/dose PO bid; may increase 10-20 mg/dose q35d; not to exceed 640 mg/d Pheochromocytoma preoperatively: 60 mg/d PO for 3 d in divided doses; inoperable tumor, 30 mg/d PO in divided doses
Adult Dose: Incremental doses starting at 20-40 mg IV; a response should be obtained within 5 min and a maximum effect at 10 min; IV dose can be doubled q30-60min until target BP is achieved; not to exceed 300 mg total dose
Drug Category: Nitrates These agents provide peripheral and coronary vasodilation. Drug Name: Sodium nitroprusside (Nipride, Nitropress) Adult Dose0.3-0.5 mcg/kg/min IV continuous IV infusion initially, titrate upward by 0.5 mcg/kg/min increments to effect; usual dose is 3-4 mcg/kg/min; infusion rates >10 mcg/kg/min may lead to cyanide toxicity
agents
These agents alter the electrophysiologic mechanisms responsible for arrhythmia. Drug Name: Amiodarone (Cordarone) Adult DoseRapid loading: 5 mg/kg IV; not to exceed 450 mg; mixed in D5W infused over 10-30 min; not to exceed 50 mg/kg
Drug Name:Lidocaine (Xylocaine) Adult Dose0.7-1.4 mg/kg IV push, repeat in 5 min; not to exceed 300 mg/h; follow with an infusion of 2-4 mg/kg/min
Surgical management
Adrenalectomy It is the surgical removal of one or both adrenal glands depending on tumors whether it is unilateral or bilateral Techniques Standard transabdominal Thoraco abdominal Retroperitoneal laproscopic
CARE OF THE PATIENT UNDERGOING ADRENALECTOMY Adrenalectomy may be unilateral or bilateral to treat adrenal tumors, Cushing's syndrome, or hyperaldosteronism. It is accomplished through abdominal or flank incision. Careful manipulation of the gland is necessary if surgery is for pheochromocytoma to prevent excessive release of epinephrine causing hypertensive crisis
Preoperative Management BP and fluid volume are optimized. Surgery and nursing care are explained to patient. Patient is shown where adrenal glands lie on top of kidneys and where incision may be on abdomen or loin area. BP will be checked frequently before and after surgery and glucocorticoids will be given to cover period of stress (surgery) because at least one adrenal gland will be removed. Patient is prepared as for major abdominal surgery
Postoperative Management Usual postoperative care for abdominal surgery includes frequent check of vital signs; assessment for hemorrhage; turning, coughing, and deep breathing; early ambulation; slow progression of diet when bowel sounds return; and control of pain with scheduled opioid administration or patient-controlled analgesia I.V. hydrocortisone (Solu-Cortef) is given as directed to prevent adrenal crisis
Nonstressful environment is maintained, rest is promoted, and meticulous care is given to protect the patient from infection and from other complications that could cause adrenal crisis. Serum sodium, potassium, and glucose are monitored for abnormality.
Sodium and potassium may normalize, or potassium may become elevated (because of transient adrenal insufficiency after surgery). Electrolyte imbalances may persist for 4 to 18 months after surgery.
Hydrocortisone treatment causes glucose to rise and worsens control in patients with diabetes; may require additional treatment Complications Hemorrhage, adrenal crisis
Providing Patient Education Teach patient with bilateral adrenalectomy that glucocorticoid and mineralocorticoid replacement is necessary for rest of life. Administer additional doses I.M. in times of stress. Administer oral glucocorticoids after unilateral adrenalectomy and teach patient that this treatment will be needed for 6 months to 2 years after surgery until remaining adrenal gland can compensate.
Encourage wearing or carrying this information at all times, so that proper treatment can be instituted if patient becomes unconscious. Encourage follow-up to monitor for signs of adrenal insufficiency