Adrenocortical hyperfunction
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Transcript of Adrenocortical hyperfunction
Adrenal disorders Adrenal disorders
Adrenal Gland Adrenal Gland
Adrenal Gland Adrenal Gland
TESTS OF ADRENAL FUNCTIONTESTS OF ADRENAL FUNCTION
Plasma CortisolPlasma Cortisol DescriptionDescription This is direct measure of the primary This is direct measure of the primary
secretory product of the adrenal cortex by secretory product of the adrenal cortex by radioimmunoassay technique.radioimmunoassay technique.
Serum concentration varies with circadian Serum concentration varies with circadian cycle so normal values vary with time of cycle so normal values vary with time of day and stress level of patient (8 a.m. day and stress level of patient (8 a.m. levels typically double that of 8 p.m. levels typically double that of 8 p.m. levels).levels).
Useful as an initial step to assess adrenal Useful as an initial step to assess adrenal dysfunction, but further workup is usually dysfunction, but further workup is usually necessary.necessary.
Nursing and Patient Care Nursing and Patient Care ConsiderationsConsiderations
A fasting sample is preferred.A fasting sample is preferred. Blood specimens should coincide Blood specimens should coincide
with circadian rhythm with draw time with circadian rhythm with draw time indicated on laboratory slip.indicated on laboratory slip.
Interpretation of test results:Interpretation of test results:– Decreased values seen in: adrenal Decreased values seen in: adrenal
hyperplasia, Addison's disease, anterior hyperplasia, Addison's disease, anterior pituitary hyposecretion, secondary pituitary hyposecretion, secondary hypothyroidism, hepatitis, and cirrhosis.hypothyroidism, hepatitis, and cirrhosis.
– Increased values seen in: Increased values seen in: hyperthyroidism, stress (eg, trauma, hyperthyroidism, stress (eg, trauma, surgery), carcinoma, Cushing's surgery), carcinoma, Cushing's syndrome, hypersecretion of syndrome, hypersecretion of corticotropin by tumors (oat cell cancer), corticotropin by tumors (oat cell cancer), adrenal adenoma, and obesity.adrenal adenoma, and obesity.
24-Hour Urinary Free Cortisol 24-Hour Urinary Free Cortisol TestTest
DescriptionDescription Test measures cortisol production Test measures cortisol production
during a 24-hour period.during a 24-hour period. Useful to establish diagnosis of Useful to establish diagnosis of
hypercortisolism.hypercortisolism. Less influenced by diurnal variations Less influenced by diurnal variations
in cortisol.in cortisol.
Nursing and Patient Care Nursing and Patient Care ConsiderationsConsiderations
Instruct patient in appropriate Instruct patient in appropriate collection technique.collection technique.
Collection jug should be kept on ice Collection jug should be kept on ice and sent to laboratory promptly when and sent to laboratory promptly when collection completed.collection completed.
Interfering factors:Interfering factors:– Elevated values pregnancy, oral Elevated values pregnancy, oral
contraceptives, spironolactone, stress.contraceptives, spironolactone, stress.– Recent radioisotope scans can interfere Recent radioisotope scans can interfere
with test results.with test results.
Dexamethasone Suppression Dexamethasone Suppression TestTest
DescriptionDescription The dexamethasone suppression test The dexamethasone suppression test
(DST) is a valuable method to (DST) is a valuable method to evaluate adrenal hyperfunction.evaluate adrenal hyperfunction.
Adrenal production and secretion of Adrenal production and secretion of cortisol is stimulated by cortisol is stimulated by adrenocorticotropic hormone (ACTH, adrenocorticotropic hormone (ACTH, corticotropin) from the pituitary corticotropin) from the pituitary gland.gland.
Dexamethasone is a synthetic Dexamethasone is a synthetic steroid effective in suppressing steroid effective in suppressing corticotropin secretion.corticotropin secretion.
In a healthy patient, the In a healthy patient, the administration of dexamethasone will administration of dexamethasone will inhibit corticotropin secretion and will inhibit corticotropin secretion and will cause cortisol levels to fall below cause cortisol levels to fall below normal.normal.
Nursing and Patient Care Nursing and Patient Care ConsiderationsConsiderations
Explain the procedure to the patient.Explain the procedure to the patient.– Overnight 1 mg DST (used primarily to Overnight 1 mg DST (used primarily to
identify those without Cushing's identify those without Cushing's syndrome).syndrome). Administer dexamethasone 1 mg Administer dexamethasone 1 mg
orally at 11 p.m.orally at 11 p.m. Draw cortisol level at 8 a.m. before Draw cortisol level at 8 a.m. before
patient rises.patient rises. Expect suppressed cortisol levels (less Expect suppressed cortisol levels (less
than 5 mcg/dL).than 5 mcg/dL).
– High-dose overnight DST (helpful to High-dose overnight DST (helpful to distinguish Cushing's disease from other distinguish Cushing's disease from other forms of Cushing's syndrome).forms of Cushing's syndrome). Give patient dexamethasone 8 mg Give patient dexamethasone 8 mg
orally at 11 p.m.orally at 11 p.m. Draw cortisol level at 8 a.m. before Draw cortisol level at 8 a.m. before
patient rises.patient rises. Suppressed cortisol levels (less than Suppressed cortisol levels (less than
50% of baseline value) indicative of 50% of baseline value) indicative of patient with corticotropin-secreting patient with corticotropin-secreting pituitary adenoma (Cushing's disease).pituitary adenoma (Cushing's disease).
Unsuppressed cortisol levels are Unsuppressed cortisol levels are associated with ectopic corticotropin associated with ectopic corticotropin secretion (malignancy) or adrenal secretion (malignancy) or adrenal tumors.tumors.
Adrenocorticotropic Stimulation Adrenocorticotropic Stimulation TestTest
DescriptionDescription ACTH stimulates the production and ACTH stimulates the production and
secretion of cortisol by the adrenal secretion of cortisol by the adrenal cortex.cortex.
Demonstrates the ability of the adrenal Demonstrates the ability of the adrenal cortex to respond appropriately to ACTH.cortex to respond appropriately to ACTH.
This is an important test to evaluate This is an important test to evaluate adrenal insufficiency, but may not adrenal insufficiency, but may not distinguish primary insufficiency from distinguish primary insufficiency from secondary insufficiency.secondary insufficiency.
Nursing and Patient Care Nursing and Patient Care ConsiderationsConsiderations
Obtain baseline cortisol level.Obtain baseline cortisol level. Administer 0.25 mg ACTH Administer 0.25 mg ACTH
(cosyntropin [Cortrosyn] I.V. or I.M.).(cosyntropin [Cortrosyn] I.V. or I.M.). Collect cortisol levels at times ordered Collect cortisol levels at times ordered
(usually at 30 and 60 minutes).(usually at 30 and 60 minutes). Interpretation of test results:Interpretation of test results:
– Range of normal responses may vary; Range of normal responses may vary; however, typically a rise in cortisol of however, typically a rise in cortisol of double baseline value is considered double baseline value is considered normal.normal.
– Diminished response adrenal Diminished response adrenal insufficiency with low cortisol values, insufficiency with low cortisol values, adrenal tumor with high cortisol values, adrenal tumor with high cortisol values, prolonged glucocorticoid therapy.prolonged glucocorticoid therapy.
– Exaggerated response adrenal Exaggerated response adrenal hyperplasia with high cortisol values.hyperplasia with high cortisol values.
Corticotropin Releasing Hormone Corticotropin Releasing Hormone Stimulation TestStimulation Test
DescriptionDescription Test measures responsiveness of Test measures responsiveness of
pituitary gland to corticotropin-pituitary gland to corticotropin-releasing hormone (CRH), a releasing hormone (CRH), a hypothalamic hormone that hypothalamic hormone that regulates pituitary secretion of ACTH.regulates pituitary secretion of ACTH.
Useful to differentiate the cause of Useful to differentiate the cause of excess cortisol secretion when excess cortisol secretion when ectopic source of ACTH is suspected.ectopic source of ACTH is suspected.
In general, CRH will stimulate ACTH In general, CRH will stimulate ACTH secretion in the pituitary, but not in secretion in the pituitary, but not in nonpituitary corticotropin-secreting nonpituitary corticotropin-secreting tissues.tissues.
Nursing and Patient Care ConsiderationsNursing and Patient Care Considerations Describe procedure to patient.Describe procedure to patient.
– Patient is given CRH (1 mcg/kg or 100 mcg) Patient is given CRH (1 mcg/kg or 100 mcg) I.V.I.V.
– Catheters are advanced through the femoral Catheters are advanced through the femoral veins to areas near the adrenal glands, so veins to areas near the adrenal glands, so sampling can take place near ACTH sampling can take place near ACTH secretion.secretion.
– Blood samples for ACTH test are collected at Blood samples for ACTH test are collected at 2, 5, 10, and 15 minutes.2, 5, 10, and 15 minutes.
Normal response is a rise in ACTH to at Normal response is a rise in ACTH to at least double the baseline value.least double the baseline value.
Interpretation of test results:Interpretation of test results:– Brisk rise in ACTH double baseline value Brisk rise in ACTH double baseline value
Cushing's disease.Cushing's disease.– No response in ACTH corticotropin-No response in ACTH corticotropin-
independent Cushing's syndrome independent Cushing's syndrome (adrenal tumor) or ectopic source of (adrenal tumor) or ectopic source of corticotropin secretion (ectopic tumor).corticotropin secretion (ectopic tumor).
– Test can produce false-negative Test can produce false-negative response.response.
Cushing syndromeCushing syndrome
Definition Definition
Cushing syndrome is a spectrum of Cushing syndrome is a spectrum of clinical abnormalities caused by an clinical abnormalities caused by an excess of corticosteroids, particularly excess of corticosteroids, particularly glucocorticoids. glucocorticoids.
Classification Classification
ACTH DependentACTH Dependent Pituitary dependent bilateral adrenal Pituitary dependent bilateral adrenal
hyperplasiahyperplasia Ectopic ACTH syndrome (bronchial Ectopic ACTH syndrome (bronchial
carcinoid, small cell lung carcinoma)carcinoid, small cell lung carcinoma) Iatrogenic (ACTH therapy)Iatrogenic (ACTH therapy)
Non ACTH dependentNon ACTH dependent
Iatrogenic (chronic glucocorticoid Iatrogenic (chronic glucocorticoid therapy)therapy)
Adrenal adenomaAdrenal adenoma Adrenal carcinomaAdrenal carcinoma
Pseudo-Cushing syndrome is cortisol Pseudo-Cushing syndrome is cortisol excess as a part of another illness.excess as a part of another illness.
Alcohol excessAlcohol excess Major depressive illnessMajor depressive illness Primary obesityPrimary obesity
Etiology Etiology
Adrenal hyperplasiaAdrenal hyperplasia
Secondary to pituitary ACTH over Secondary to pituitary ACTH over productionproduction
Pituitary hypothalamic dysfunctionPituitary hypothalamic dysfunction
Pituitary ACTH or CRH producing micro Pituitary ACTH or CRH producing micro and macro adenomaand macro adenoma
Secondary to ACTH or CRH producing Secondary to ACTH or CRH producing endocrine tumors (bronchiogenic endocrine tumors (bronchiogenic carcinoma, carcinoid of the thymus, carcinoma, carcinoid of the thymus, pancreatic carcinoma, bronchial pancreatic carcinoma, bronchial adenoma)adenoma)
Adrenal macro nodular hyperplasiaAdrenal macro nodular hyperplasia Adrenal micro nodular hyperplasiaAdrenal micro nodular hyperplasia SporadicSporadic FamilialFamilial Primary adrenal neoplasms such as Primary adrenal neoplasms such as
adrenal adenoma and carcinoma and adrenal adenoma and carcinoma and
primary cortical hyperplasiaprimary cortical hyperplasia
Exogenous and iatrogenic causesExogenous and iatrogenic causes
Prolonged use of glucocorticoidsProlonged use of glucocorticoids
Prolonged use of ACTHProlonged use of ACTH
Pathophysiology Pathophysiology
Due to etiological factorsDue to etiological factors
Normal feedback mechanism of Normal feedback mechanism of mechanisms that control the function mechanisms that control the function of adrenal cortex is disturbed of adrenal cortex is disturbed
Overproduction of endogenous Overproduction of endogenous corticosteroidscorticosteroids
Signs and symptoms of Cushing Signs and symptoms of Cushing syndromesyndrome
CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS
Insidious in onset.Insidious in onset. Muscle weakness and fatigability due to Muscle weakness and fatigability due to
mobilization of peripheral supportive mobilization of peripheral supportive tissue.tissue.
Hypertension and weight gain due to Hypertension and weight gain due to sodium and water retention. sodium and water retention.
centripetal distribution of adipose tissue centripetal distribution of adipose tissue with truncal obesity moon face with truncal obesity moon face accumulation of fat in the posterior neck accumulation of fat in the posterior neck and back. and back.
Selective atrophy of fast twitch Selective atrophy of fast twitch myofibres with resultant decreased myofibres with resultant decreased muscle mass.muscle mass.
Glucocorticoid induce gluconeogenesis Glucocorticoid induce gluconeogenesis with resultant hyperglycemia and with resultant hyperglycemia and polydipsia mimicking diabetes mellitus.polydipsia mimicking diabetes mellitus.
Skin is thin fragile and easily bruised, Skin is thin fragile and easily bruised, cutaneous strior in the abdomen due to cutaneous strior in the abdomen due to catabolic effect of protien causing loss catabolic effect of protien causing loss of collagenof collagen
Bone resorption result in development Bone resorption result in development of fracture. of fracture.
Increased risk for infection.Increased risk for infection. Hirsutism and mineralized Hirsutism and mineralized
abnormalities like oligomenorrhea or abnormalities like oligomenorrhea or amenorrhea due to increased amenorrhea due to increased adrenal androgens.adrenal androgens.
Emotional changes may be profound, Emotional changes may be profound, ranging from irritability to severe ranging from irritability to severe depression confusion or even frank depression confusion or even frank psychosis.psychosis.
thinning of scalp hair.thinning of scalp hair. Posterior sub capsular cataract. Posterior sub capsular cataract.
Extra adrenal Cushing syndrome Extra adrenal Cushing syndrome caused by pituitary or ectopic ACTH caused by pituitary or ectopic ACTH secretion.secretion.
Symptoms of Excess CortisolSymptoms of Excess Cortisol Truncal obesityTruncal obesity Moon faceMoon face Fat deposits supraclavicular Fat deposits supraclavicular
fossa and posterior neck- fossa and posterior neck- buffalo humpbuffalo hump
HTNHTN HirsutismHirsutism Amenorrhea or impotenceAmenorrhea or impotence DepressionDepression Thin skinThin skin Easy bruisingEasy bruising Purplish abdominal striaePurplish abdominal striae Proximal muscle weaknessProximal muscle weakness OsteoporosisOsteoporosis Diabetes MellitusDiabetes Mellitus Avascular necrosisAvascular necrosis Wound healing impairedWound healing impaired Pysch symptomsPysch symptoms HyperpigmentationHyperpigmentation Hypokalemic alkalosisHypokalemic alkalosis
DIAGNOSTIC EVALUATIONDIAGNOSTIC EVALUATION Urine cortisol.Urine cortisol. Overnight Dexamethasone test.Overnight Dexamethasone test. Diurnal rhythm of plasma cortisol.Diurnal rhythm of plasma cortisol. Insulin tolerance test.Insulin tolerance test. High dose dexamethasone High dose dexamethasone
suppression test.suppression test. Corticotropin releasing harmone test Corticotropin releasing harmone test
Screening TestScreening Test
Overnight dexamethasone Overnight dexamethasone suppression testsuppression test (1 mg at 11 pm, (1 mg at 11 pm, cortisol measured at 8 am) – normal cortisol measured at 8 am) – normal <2 micrograms/dL<2 micrograms/dL
OrOr 24 hour urine free cortisol (>140 24 hour urine free cortisol (>140
nmol/day)nmol/day)
Confirmatory TestConfirmatory Test
Low dose dexamethasone suppression testLow dose dexamethasone suppression test Dexamethasone 0.5 mg q 6 x 48 hoursDexamethasone 0.5 mg q 6 x 48 hours Measure urine cortisol during the last 24 Measure urine cortisol during the last 24
hours (urine free cortisol >20 hours (urine free cortisol >20 micrograms/dL or urine 17-micrograms/dL or urine 17-hydroxycorticosteroid >4.5 mg/d)hydroxycorticosteroid >4.5 mg/d)
OrOr plasma cortisol (failure to fall to <5 plasma cortisol (failure to fall to <5
micrograms/dL)micrograms/dL)
Confirmatory TestConfirmatory Test
Low dose dexamethasone suppression testLow dose dexamethasone suppression test Dexamethasone 0.5 mg q 6 x 48 hoursDexamethasone 0.5 mg q 6 x 48 hours Measure urine cortisol during the last 24 Measure urine cortisol during the last 24
hours (urine free cortisol >20 hours (urine free cortisol >20 micrograms/dL or urine 17-micrograms/dL or urine 17-hydroxycorticosteroid >4.5 mg/d)hydroxycorticosteroid >4.5 mg/d)
OrOr plasma cortisol (failure to fall to <5 plasma cortisol (failure to fall to <5
micrograms/dL)micrograms/dL)
TreatmentTreatment
Cushing’s DiseaseCushing’s Disease: Transphenoidal : Transphenoidal resection of pituitary adenomaresection of pituitary adenoma
Adrenal neoplasmsAdrenal neoplasms: resection: resection Ectopic ACTHEctopic ACTH: resection if possible: resection if possible Bilateral adrenal hyperplasiaBilateral adrenal hyperplasia: may : may
need adrenalectomies (lifelong need adrenalectomies (lifelong glucocorticoid and mineralcorticoid glucocorticoid and mineralcorticoid replacement)replacement)
‘‘Medical’ AdrenalectomyMedical’ Adrenalectomy
Medications that inhibit steroidogenesisMedications that inhibit steroidogenesis Ketoconazole (600 to 1200 mg/day)Ketoconazole (600 to 1200 mg/day) metyrapone (exacerbates female metyrapone (exacerbates female
virilization) (2-3 g/day)virilization) (2-3 g/day) Mitotane(2-3 G/day)- slow onsetMitotane(2-3 G/day)- slow onset Aminoglutethinide (1g/day)Aminoglutethinide (1g/day) Ocreotide can work in 1/3 of patients.Ocreotide can work in 1/3 of patients.Major side affect is adrenal insufficiency, Major side affect is adrenal insufficiency,
therefore start at lowest dose and titratetherefore start at lowest dose and titrate
Drug Name:Drug Name:Metyrapone Metyrapone (Metopirone)(Metopirone)
Description:Description:Inhibitor of endogenous Inhibitor of endogenous adrenal corticosteroid synthesis. adrenal corticosteroid synthesis. Inhibits 11-B-hydroxylation reaction in Inhibits 11-B-hydroxylation reaction in the adrenal cortexthe adrenal cortex
..Adult Dose:Adult Dose:1 g/d PO divided qid; 1 g/d PO divided qid; increase gradually, not to exceed 4.5 increase gradually, not to exceed 4.5 g/dg/d
Drug Name:Drug Name:Ketoconazole (Nizoral)Ketoconazole (Nizoral) Description:Description:Imidazole broad-Imidazole broad-
spectrum antifungal agent that acts spectrum antifungal agent that acts on several of the P450 enzymes, on several of the P450 enzymes, including the first step in cortisol including the first step in cortisol synthesis, cholesterol side-chain synthesis, cholesterol side-chain cleavage, and conversion of 11-cleavage, and conversion of 11-deoxycortisol to cortisol.deoxycortisol to cortisol.
Adult DoseAdult Dose200-400 mg PO bid/tid200-400 mg PO bid/tid
Drug Name;Drug Name;Aminoglutethimide Aminoglutethimide (Cytadren)(Cytadren)
Description:Description:Inhibits conversion of Inhibits conversion of cholesterol to delta-5-pregnenolone, cholesterol to delta-5-pregnenolone, which, in turn, reduces the production of which, in turn, reduces the production of adrenal glucocorticoids, adrenal glucocorticoids, mineralocorticoids, aldosterone, mineralocorticoids, aldosterone, estrogens, and androgens.estrogens, and androgens.
Adult Dose:Adult Dose:250 mg PO bid initially; 250 mg PO bid initially; increase to 2 g qidincrease to 2 g qid
PrognosisPrognosis
Benign adrenal adenoma- 95% 5 year Benign adrenal adenoma- 95% 5 year survival, 90% 10 yearsurvival, 90% 10 year
Cushing’s disease (pituitary adenoma) Cushing’s disease (pituitary adenoma) same survival, but 10-20% transphenoidal same survival, but 10-20% transphenoidal resection failure rate over 10 years. resection failure rate over 10 years.
Ectopic ACTH survival depends on Ectopic ACTH survival depends on malignancymalignancy
Unknown cause of elevated ACTH- 65% 5 Unknown cause of elevated ACTH- 65% 5 year survival, 55% 10 year survivalyear survival, 55% 10 year survival
Adrenal carcinoma- median survival 7 Adrenal carcinoma- median survival 7 monthsmonths
Complications of Cushing's if Complications of Cushing's if UntreatedUntreated
DiabetesDiabetes HTNHTN Osteoporotic fractures and avascular Osteoporotic fractures and avascular
necrosisnecrosis InfectionsInfections NephrolithiasisNephrolithiasis PsychosisPsychosis
Hyperaldosteronism Hyperaldosteronism
Definition Definition
Aldosteronism is a condition Aldosteronism is a condition associated with hyper secretion of associated with hyper secretion of mineral corticoid aldosterone.mineral corticoid aldosterone.
Classification Classification
Primary aldosteronismPrimary aldosteronism Cause lie within the adrenal glandCause lie within the adrenal gland May be due to a adrenal leision May be due to a adrenal leision
which is benignwhich is benign It produce hypokalemia, It produce hypokalemia,
hypernatremia and secondary hypernatremia and secondary hypertension.hypertension.
Secondary Aldosteronism Secondary Aldosteronism Stimulus is extra adrenalStimulus is extra adrenal Condition include sodium wasting Condition include sodium wasting
renal disease, excessive laxative and renal disease, excessive laxative and diuretic use, dehydration , cirrhosis diuretic use, dehydration , cirrhosis with ascities, heart failure.with ascities, heart failure.
Primary aldosteronismPrimary aldosteronism
Definition Definition Primary aldosteronism indicate a Primary aldosteronism indicate a
primary autonomous overproduction primary autonomous overproduction of aldosterone with resultant of aldosterone with resultant suppression of renin angiotensin suppression of renin angiotensin system and decreased plasma renin system and decreased plasma renin activity activity
Incidence and prevalenceIncidence and prevalence
primary aldosteronism accounts for primary aldosteronism accounts for 0.05-2% of cases of 0.05-2% of cases of hypertensionhypertension in in the general populationthe general population
Twice common in women as in menTwice common in women as in men Usually occur in ages between 30 Usually occur in ages between 30
and 50. and 50.
Etiology Etiology
aldosterone producing adrenal aldosterone producing adrenal adenoma.adenoma.
Bilateral cortical nodular hyperplasiaBilateral cortical nodular hyperplasia Rarely adenocarcinomaRarely adenocarcinoma
Pathophysiology Pathophysiology
Due to hypersecretion of aldosteroneDue to hypersecretion of aldosterone
Increased renal tubular exchange of Increased renal tubular exchange of intratubular sodium for secreted intratubular sodium for secreted potassium and hydrogen ionspotassium and hydrogen ions
Hypernatremia hypokalemia Hypernatremia hypokalemia hypovolemiahypovolemia
Hypertension muscle weakness Hypertension muscle weakness hypertensionhypertension
Cerebral infarct, renal damageCerebral infarct, renal damage
Clinical manifestation Clinical manifestation
Usually asymptomaticUsually asymptomatic But findings include Hypernatremia But findings include Hypernatremia
hypokalemia and hypertension.hypokalemia and hypertension. Large urinary output leads to polydipsia Large urinary output leads to polydipsia Hypokalemia leads to metabolic Hypokalemia leads to metabolic
alkalosisalkalosis metabolic alkalosis causes adecrease in metabolic alkalosis causes adecrease in
ionized calcium levels which can result ionized calcium levels which can result in tetany and respiratory suppression.in tetany and respiratory suppression.
Diagnostic evaluationDiagnostic evaluation
Serum potassium decreasedSerum potassium decreased Urine PH- NEUTRAL TO ALKALINEUrine PH- NEUTRAL TO ALKALINE Serum sodium increasedSerum sodium increased Metabolic alkalosisMetabolic alkalosis Test for mineralocorticoid Test for mineralocorticoid
suppressibilitysuppressibility Radionuclide scanning technique to Radionuclide scanning technique to
visualize tumors.visualize tumors.
Management Management
Adrenalectomy Adrenalectomy Dietary sodium restrictionDietary sodium restriction Aldosterone antagonistAldosterone antagonist
Secondary Aldosteronism Secondary Aldosteronism
Definition Definition Secondary aldosteronism refers to an Secondary aldosteronism refers to an
appropriately increased production of appropriately increased production of aldosterone in response to aldosterone in response to activationof renin angiotensin activationof renin angiotensin system.system.
Etiology Etiology
Occurs in association with accelerated Occurs in association with accelerated phase of hypertension or on the basis phase of hypertension or on the basis of an underlying edema disorder like of an underlying edema disorder like cirrhosis or nephrotic syndrome.cirrhosis or nephrotic syndrome.
Narrowing of major renal arteries by Narrowing of major renal arteries by atherosclerosisatherosclerosis
Profound renal vasoconstriction.Profound renal vasoconstriction. Renin producing tumorsRenin producing tumors
Pathophysiology Pathophysiology
Due to etiological factorsDue to etiological factors
Narrowing of renal arteriesNarrowing of renal arteries
Decrease in renal blood flowDecrease in renal blood flow
Overproduction of reninOverproduction of renin
Hypokalemia, alkalosis, Hypokalemia, alkalosis, hypertension, increased aldosterone.hypertension, increased aldosterone.
Hypofunction of adrenal Hypofunction of adrenal cortexcortex
Primary adrenocortical Primary adrenocortical deficiency (addisons disease)deficiency (addisons disease)
Definition Definition Addison's disease is an uncommon Addison's disease is an uncommon
disorder resulting from progressive disorder resulting from progressive destruction of the adrenal cortex by destruction of the adrenal cortex by an autoimmune process or other an autoimmune process or other disease.disease.
Incidence Incidence
Usually rare , but may occur at any Usually rare , but may occur at any age and affect both sexes equally.age and affect both sexes equally.
Etiology and risk factorsEtiology and risk factors
Result from progressive destruction of Result from progressive destruction of adrenalsadrenals
Anatomic destruction of adrenal glandAnatomic destruction of adrenal gland Idiopathic atropy:autoimmune,adreno Idiopathic atropy:autoimmune,adreno
leukodystropyleukodystropy Surgical removal:bilateral adrenelectomySurgical removal:bilateral adrenelectomy infectioninfection
TuberculosisTuberculosis Fungal-histoplasma capsulatumFungal-histoplasma capsulatum ViralViral HaemorrhageHaemorrhage Invasion:metastasis from the Invasion:metastasis from the
lung,breast,Gi tractlung,breast,Gi tract Metabolic failure in hormone productionMetabolic failure in hormone production Congenital adrenal hyperplasiaCongenital adrenal hyperplasia Enzyme Enzyme
inhibitirs(metyrapone,ketoconazole)inhibitirs(metyrapone,ketoconazole) Cytotoxic agentCytotoxic agent ACTH blocking antibioticsACTH blocking antibiotics
Mutation in ACTH receptor geneMutation in ACTH receptor gene Adrenal hypoplasia congenitaAdrenal hypoplasia congenita RISK FACTORSRISK FACTORS a history of other endocrine a history of other endocrine
disordersdisorders Taking glucocorticoid for more than 3 Taking glucocorticoid for more than 3
weeks withsudden cessationweeks withsudden cessation Taking glucocorticoid more than once Taking glucocorticoid more than once
every other dayevery other day
PathophysiologyPathophysiology
Adrenal antibiotics(cytotoxic T Adrenal antibiotics(cytotoxic T lymphocytes)lymphocytes)
Autoimmune destruction of specific Autoimmune destruction of specific adrenal antigensadrenal antigens
Blocks the binding of ACTH to its Blocks the binding of ACTH to its receptorsreceptors
Inability of the adrenal cortex to Inability of the adrenal cortex to produce hormonesproduce hormones
Adrenal insufficiencyAdrenal insufficiency
Clinical featuresClinical features
Insidious onset of Insidious onset of fatigability,weakness,pigmentation of fatigability,weakness,pigmentation of skin,weight skin,weight loss,anorexia,nausea,vomiting,hypotloss,anorexia,nausea,vomiting,hypotension,pigmentation of mucus ension,pigmentation of mucus membrane,abdominal pain,salt membrane,abdominal pain,salt craving,diarrhea,constipation,syncopcraving,diarrhea,constipation,syncope and occassional hypoglycemiae and occassional hypoglycemia
AstheniaAsthenia is a cardinal symptom.early is a cardinal symptom.early it may be sporadicit may be sporadic
-More evident at the time of stress-More evident at the time of stress
-As adrenal function become more -As adrenal function become more impaiired the patient is continuously impaiired the patient is continuously fatiguedfatigued
HyperpigmentationHyperpigmentation appears as diffuse brown or bronze appears as diffuse brown or bronze
darkening of elbows,creases of the darkening of elbows,creases of the handhand
-Bluish black patches may appear on -Bluish black patches may appear on mucus membranemucus membrane
-Tanning following sun exposure-Tanning following sun exposure
-Arterial hypotension 80/50 or less-Arterial hypotension 80/50 or less Abnormalities of gi functionAbnormalities of gi function Mild anorexia with weight loss to Mild anorexia with weight loss to
fulminating nausea,vomitting,diarrhea fulminating nausea,vomitting,diarrhea and abdominal painand abdominal pain
Excessive irritability and restlessnessExcessive irritability and restlessness Axillary's and pubic hair decreased in Axillary's and pubic hair decreased in
women due to loss of adrenal women due to loss of adrenal adrogensadrogens
Diagnostic testsDiagnostic tests Serum sodium,chloride, and bicarbonate Serum sodium,chloride, and bicarbonate
decreaseddecreased Serum pottasium level elevatedSerum pottasium level elevated Low cortisol levelLow cortisol level Low aldosterone levelLow aldosterone level ACTH stimulation test :plasma ACTH will ACTH stimulation test :plasma ACTH will
be morebe more Blood count to assess anemiaBlood count to assess anemia Blood glucoseBlood glucose X ray,CT,MRIX ray,CT,MRI
ManagementManagement
Medical:Medical:
-all patients should receive specific -all patients should receive specific hormone replacementhormone replacement
--Glucocorticoid-Glucocorticoid-hydrocortisone(cortiso) hydrocortisone(cortiso) is the mainstay treatment is the mainstay treatment 20-30mg/day20-30mg/day
-To stimulate normal diurnal rhythm -To stimulate normal diurnal rhythm 2/32/3rdrd is taken in morning and 1/3 is taken in morning and 1/3rdrd eveningevening
Side effectsSide effects
-Insomnia,irritability,mental -Insomnia,irritability,mental excitementexcitement
Minerelocorticoid-Minerelocorticoid-fludeocortisone fludeocortisone 0.05-0.1mg/day orally0.05-0.1mg/day orally
-Maintain ample intake of Na-Maintain ample intake of Na
-Measure blood pressure or serum -Measure blood pressure or serum electrolyteelectrolyte
AndrogenAndrogen:DHEA 25-50mg/day orally:DHEA 25-50mg/day orally
Secondary adrenocortical Secondary adrenocortical insufficiencyinsufficiency
ACTH deficiency causes secondary ACTH deficiency causes secondary adrenocortical insufficiencyadrenocortical insufficiency
ETIOLOGYETIOLOGY
-prolonged administration of excess -prolonged administration of excess glucocorticoidsglucocorticoids
-deficiencies of multiple pituitary -deficiencies of multiple pituitary hormoneshormones
pathophysiologypathophysiology
Due to etiological factorsDue to etiological factors
Loss of adrenalresponsiveness to Loss of adrenalresponsiveness to ACTH and failure of pituitary ACTH ACTH and failure of pituitary ACTH releaserelease
Adrenal atropy and prolonged Adrenal atropy and prolonged pituitary adrenal insufficiencypituitary adrenal insufficiency
Adrenal insufficiency characterized Adrenal insufficiency characterized by low blood cortisol and ACTH levelsby low blood cortisol and ACTH levels
Clinical featuresClinical features
Weakness,fatigabilityWeakness,fatigability Severe dehydrationSevere dehydration HyponatremiaHyponatremia HyperkalemiaHyperkalemia GI disturbances include GI disturbances include
anorexia,nausea vomitting,weight anorexia,nausea vomitting,weight loss,diarrhealoss,diarrhea
Diagnostic testDiagnostic test
ACTH test:metyrapone and insulin ACTH test:metyrapone and insulin induced hypoglcemiainduced hypoglcemia
treatmenttreatment
Glucocorticoid therapyGlucocorticoid therapy
Acute adrenocortical Acute adrenocortical insufficiencyinsufficiency
Also called ADDISONIAN CRISIS OR Also called ADDISONIAN CRISIS OR ADRENAL CRISISADRENAL CRISIS
it may be a rapid and overwhelming it may be a rapid and overwhelming intensification of chronic adrenal intensification of chronic adrenal insufficiency of chronic adrenal insufficiency of chronic adrenal insufficiency usually precipiated by insufficiency usually precipiated by sepsis or surgical stresssepsis or surgical stress
causescauses
SepsisSepsis Surgical stressSurgical stress Acute haemorrhagic destruction of both Acute haemorrhagic destruction of both
glandsglands Septicemia with pseudomonas and Septicemia with pseudomonas and
meningococcemiameningococcemia Congenital adrenalhyperplasiaCongenital adrenalhyperplasia Drugs which inhibits steroids Drugs which inhibits steroids
synthesis(ketoconazole )synthesis(ketoconazole )
Clinical features Clinical features
Manifestations are related to degree Manifestations are related to degree of hormones deficiency and of hormones deficiency and electrolyte imbalance and include electrolyte imbalance and include
Suddenpenetrating pain at Suddenpenetrating pain at back ,abdomen and legsback ,abdomen and legs
Depressed or changed mentationDepressed or changed mentation Volume depletionVolume depletion
HypotensionHypotension Loss of consciousnessLoss of consciousness ShockShock Nausea and vomitingNausea and vomiting Fever Fever hypoglycemiahypoglycemia
managementmanagement
Replace steroidsReplace steroids
-hydrocortisone at 100mg iv bolus -hydrocortisone at 100mg iv bolus followed by 100mg every 8hrs for followed by 100mg every 8hrs for 24hrs24hrs
Replacement of Na and water Replacement of Na and water deficits-an isotonic solution usually deficits-an isotonic solution usually correct the volume depletion,salt correct the volume depletion,salt depletion and hypotensiondepletion and hypotension
Vasoconstrictive agent –dopamine Vasoconstrictive agent –dopamine as adjuant to volume depletionas adjuant to volume depletion
Sodium polysterene sulfonate orally Sodium polysterene sulfonate orally or as enema in combination with or as enema in combination with sorbital.it is a resin that releases Na sorbital.it is a resin that releases Na ions in exchange of K ionsions in exchange of K ions
Hypoglycemia corrected with 5% Hypoglycemia corrected with 5% dextrosedextrose
Adrenal steroidsAdrenal steroids
glucocorticoidsglucocorticoids
Evaluating patient prior to initiating Evaluating patient prior to initiating steroid therapysteroid therapy
1.1. Chronic infection-if TB is present Chronic infection-if TB is present steroid therapy should be given in steroid therapy should be given in conjunction in antitubercular drug conjunction in antitubercular drug
2.2. Diabetes mellitusDiabetes mellitus
3.3. Prolonged therapy may aggravate Prolonged therapy may aggravate DMDM
Osteoporosis with vertebral fracture Osteoporosis with vertebral fracture or comcompression is a high risk or comcompression is a high risk complicationcomplication
Peptic ulcer,gastric Peptic ulcer,gastric hypersecretion,esophagitishypersecretion,esophagitis
Hypertension or cardiovascular Hypertension or cardiovascular diseasesdiseases
Psychological difficulties-Psychological difficulties-sleeplessness is commonsleeplessness is common
hypoaldosteronismhypoaldosteronism
Isolated aldosterone deficiency Isolated aldosterone deficiency accompanied by normal cortisol accompanied by normal cortisol production occurs in association with production occurs in association with hyporeninism as an inherited hyporeninism as an inherited biosynthetic defect postoperatively biosynthetic defect postoperatively following removal of aldosterone following removal of aldosterone secreting adenoma,during protracted secreting adenoma,during protracted heparin or heparinoid administrationheparin or heparinoid administration
featuresfeatures
Unexplained hyperkalemiaUnexplained hyperkalemia Severe cases,urine sodium wastage Severe cases,urine sodium wastage
occurs at a normal salt intake.In occurs at a normal salt intake.In milder forms,excessive loss of urine milder forms,excessive loss of urine sodium occurs only with salt sodium occurs only with salt restrictionrestriction
pathophysiologypathophysiology
Due to renal disease,autonomic Due to renal disease,autonomic neuropathy extracellular fluid volume neuropathy extracellular fluid volume expansionexpansion
Plasma renin fail to rise following Na Plasma renin fail to rise following Na restriction and K changesrestriction and K changes
Failure of aldosterone level to riseFailure of aldosterone level to rise
Diagnostic testDiagnostic test
Serum K levelSerum K level ACTH stimulation testACTH stimulation test Renin and aldosterone levelsRenin and aldosterone levels
managementmanagement
Replace mineralocorticoidReplace mineralocorticoid 0.05-0.15mg fludrocortisones daily orally0.05-0.15mg fludrocortisones daily orally Patients with hyporeninic Patients with hyporeninic
hypoaldosteronism may require higher hypoaldosteronism may require higher dosesdoses
Potential risk in patient with Potential risk in patient with hypertension,mild renal insufficiency and hypertension,mild renal insufficiency and CCFCCF
Reduce salt intake and administer Reduce salt intake and administer frusemidefrusemide
pheochromocytomapheochromocytoma
DefinitionDefinition Pheochromocytoma is a Pheochromocytoma is a
catecholamine secreting tumor of the catecholamine secreting tumor of the chromaffin cells of the sympathetic chromaffin cells of the sympathetic nervous system that is usually found nervous system that is usually found in the adrenal medullain the adrenal medulla
Incidence and prevalenceIncidence and prevalence
Are rareAre rare In autopsy series the incidence is In autopsy series the incidence is
0.1^% in client with diastolic 0.1^% in client with diastolic hypertensionhypertension
Equal in men and womenEqual in men and women Rare after 60yrsRare after 60yrs
Etiology and risk factorsEtiology and risk factors
Unknown causeUnknown cause Familial bases-10% appear to have Familial bases-10% appear to have
familial syndromes-MEN 2A and 2B familial syndromes-MEN 2A and 2B syndromes,neurofibromatosissyndromes,neurofibromatosis
pathophysiologypathophysiology
The pathophysiology of the The pathophysiology of the pheochromocytoma is best pheochromocytoma is best appreciated with an understanding of appreciated with an understanding of catecholamine biochemistry. The catecholamine biochemistry. The following is an abbreviated version of following is an abbreviated version of the important steps in the the important steps in the biosynthesis and metabolism of biosynthesis and metabolism of catecholamines.catecholamines.
Tyrosine Tyrosine
Dihydroxyphenylalanine (DOPA)Dihydroxyphenylalanine (DOPA)
Dopamine (DA)Dopamine (DA)
Norepinephrine + Epinephrine Norepinephrine + Epinephrine
Homovanillic acid (HVA) + Homovanillic acid (HVA) + Vanillylmandelic acid (VMA)Vanillylmandelic acid (VMA)
an alteration in the regulation of the an alteration in the regulation of the catecholamine biosynthesis possibly catecholamine biosynthesis possibly suggests an alteration in the suggests an alteration in the feedback inhibition of tyrosine feedback inhibition of tyrosine hydroxylase, the key enzyme in the hydroxylase, the key enzyme in the production of catecholamines.production of catecholamines.
Location and morphologyLocation and morphology
In adult 80% are unilateral,10% are In adult 80% are unilateral,10% are bilateral.,10% are extra adrenalbilateral.,10% are extra adrenal
Size ranges from 100gm to 3 kgSize ranges from 100gm to 3 kg Tumors are highly vascular and Tumors are highly vascular and
made up of large made up of large polyhedral ,pleomorphic chromaffin polyhedral ,pleomorphic chromaffin cellscells
Less than 10% are malignantLess than 10% are malignant
Extraadrenal tumorsExtraadrenal tumors
Weigh 20-40gm and are less than Weigh 20-40gm and are less than 5cm diameter5cm diameter
Located in abdomen,urinary Located in abdomen,urinary bladder(10%) less than 3% seen in bladder(10%) less than 3% seen in neck within the sympathetic ganglianeck within the sympathetic ganglia
Clinical featuresClinical features
HypertensionHypertension - common manifestation- common manifestation -40% B>P elevation occur during -40% B>P elevation occur during
attackattack -often severe and not treated with -often severe and not treated with
antihypertensivesantihypertensivesParoxysmParoxysm/crisis:/crisis:-Occur in half of patients-Occur in half of patients-May be frequent or sporadic-May be frequent or sporadic
Sudden onsetSudden onset Last from a few mnts to several Last from a few mnts to several
hours or longerhours or longer Headache,profuse Headache,profuse
sweating,palpitationssweating,palpitations Apprehensions are commonApprehensions are common Pain in chest and abdomenPain in chest and abdomen Nausea and vomiting Nausea and vomiting pallorpallor
B.P elevated with tachycardiaB.P elevated with tachycardia Paroxyms may be precipitated by Paroxyms may be precipitated by
any activity that displaces abdominal any activity that displaces abdominal content.smoking,micturation may content.smoking,micturation may stimulate paroxysmsstimulate paroxysms
Activities that displaces abdominal Activities that displaces abdominal content include content include bending,exercising,straining,vigorous bending,exercising,straining,vigorous palpations of abdomen in pregnancypalpations of abdomen in pregnancy
Cardiac manifestations-sinus Cardiac manifestations-sinus bradycardia,arrythmias,angina,MI,cardbradycardia,arrythmias,angina,MI,cardiomyopathyiomyopathy
Carbohydrate intolerenceCarbohydrate intolerence HypercalcemiaHypercalcemia FeverFever PolyuriaPolyuria Urinary bladder pheochromocytomas-Urinary bladder pheochromocytomas-
produce typical paroxysms in relation produce typical paroxysms in relation to micturation,hematuria to micturation,hematuria
diagnosisdiagnosis
History and p/EHistory and p/E Lab testLab test
-elevated haematocrit due to -elevated haematocrit due to diminished plasma volumediminished plasma volume
-increased ESR due to production of -increased ESR due to production of interleukininterleukin
Assay of urinary catecholaminesAssay of urinary catecholamines
Assay of urinary VMA levelsAssay of urinary VMA levels
-performed on 24hr urine specimen-performed on 24hr urine specimen
-advice client to avoid -advice client to avoid tea,coffee,chocolate,vannilla for tea,coffee,chocolate,vannilla for atleast 2 days before the testatleast 2 days before the test
-normal less than 7mg in 24 hrs-normal less than 7mg in 24 hrs
Direct assay of catecholaminesDirect assay of catecholamines
-normal epinephrine-0.02-0.2mg/L-normal epinephrine-0.02-0.2mg/L
norepinephrine-0.1-0.5mg/Lnorepinephrine-0.1-0.5mg/L X-ray imaging,CT,MRIX-ray imaging,CT,MRI Pheochromocytomas of urinary Pheochromocytomas of urinary
bladder-cystoscopybladder-cystoscopy
complicationscomplications
CardiomyopathyCardiomyopathy Multisystem organ failureMultisystem organ failure Acute pancreatitisAcute pancreatitis Renal failureRenal failure
managementmanagement
Alpha-adrenergic blocking agentsAlpha-adrenergic blocking agents At low doses, alpha-adrenergic At low doses, alpha-adrenergic
receptor blockers may be used as receptor blockers may be used as monotherapy in the treatment of monotherapy in the treatment of hypertension. At higher doses, the hypertension. At higher doses, the agents may cause sodium and fluid to agents may cause sodium and fluid to accumulate. As a result, concurrent accumulate. As a result, concurrent diuretic therapy may be required to diuretic therapy may be required to maintain the hypotensive effects of maintain the hypotensive effects of the alpha-receptor blockers.the alpha-receptor blockers.
Drug Name :Drug Name :Phenoxybenzamine Phenoxybenzamine (Dibenzyline)(Dibenzyline)
Adult Dose:Adult Dose:10 mg PO bid initially; 10 mg PO bid initially; increase dose by 10-mg increments increase dose by 10-mg increments every other day until an optimal every other day until an optimal dosage is obtained; usual dosage dosage is obtained; usual dosage range is 20-40 mg PO bid/tidrange is 20-40 mg PO bid/tid
Drug Name: Drug Name: Phentolamine Phentolamine (Regitine)(Regitine)
Adult Dose:Adult Dose:Prevention or control of Prevention or control of hypertension in hypertension in pheochromocytomas: 5 mg IV/IM 1-2 pheochromocytomas: 5 mg IV/IM 1-2 h before surgery; repeat prn; h before surgery; repeat prn; administer 5 mg IV during surgery as administer 5 mg IV during surgery as indicated to control paroxysms of indicated to control paroxysms of hypertension, tachycardia, hypertension, tachycardia, respiratory depression, or seizuresrespiratory depression, or seizures
Drug Name:Drug Name:Prazosin Prazosin (Minipress)(Minipress)
Adult Dose: Adult Dose: 1 mg PO bid/tid 1 mg PO bid/tid initially; increase prn; not to exceed initially; increase prn; not to exceed 20 mg/d PO divided bid/tid20 mg/d PO divided bid/tid
Drug Category: Drug Category: Beta-adrenergic Beta-adrenergic blocking agentsblocking agents
These agents are used as adjunctive These agents are used as adjunctive therapy for cardiac effects. The therapy for cardiac effects. The agents inhibit chronotropic, inotropic, agents inhibit chronotropic, inotropic, and vasodilatory responses to beta-and vasodilatory responses to beta-adrenergic stimulation.adrenergic stimulation.
Drug Name:Drug Name:Propranolol Propranolol (Inderal)(Inderal)
Adult Dose: Adult Dose: Hypertension: 40 Hypertension: 40 mg/dose PO bid; may increase 10-20 mg/dose PO bid; may increase 10-20 mg/dose q3-5d; not to exceed 640 mg/dose q3-5d; not to exceed 640 mg/dmg/dPheochromocytoma preoperatively: Pheochromocytoma preoperatively: 60 mg/d PO for 3 d in divided doses; 60 mg/d PO for 3 d in divided doses; inoperable tumor, 30 mg/d PO in inoperable tumor, 30 mg/d PO in divided dosesdivided doses
Drug Name:Drug Name:Labetalol Labetalol (Normodyne, Trandate)(Normodyne, Trandate)
Adult Dose: Adult Dose: Incremental doses Incremental doses starting at 20-40 mg IV; a response starting at 20-40 mg IV; a response should be obtained within 5 min and should be obtained within 5 min and a maximum effect at 10 min; IV dose a maximum effect at 10 min; IV dose can be doubled q30-60min until can be doubled q30-60min until target BP is achieved; not to exceed target BP is achieved; not to exceed 300 mg total dose300 mg total dose
Drug Category: Drug Category: NitratesNitrates
These agents provide peripheral and These agents provide peripheral and coronary vasodilation.coronary vasodilation.
Drug Name: Drug Name: Sodium nitroprusside Sodium nitroprusside (Nipride, Nitropress)(Nipride, Nitropress)
Adult DoseAdult Dose0.3-0.5 mcg/kg/min IV 0.3-0.5 mcg/kg/min IV continuous IV infusion initially, titrate continuous IV infusion initially, titrate upward by 0.5 mcg/kg/min increments upward by 0.5 mcg/kg/min increments to effect; usual dose is 3-4 to effect; usual dose is 3-4 mcg/kg/min; infusion rates >10 mcg/kg/min; infusion rates >10 mcg/kg/min may lead to cyanide mcg/kg/min may lead to cyanide toxicitytoxicity
Drug Category: Drug Category: Antiarrhythmic Antiarrhythmic agentsagents
These agents alter the These agents alter the electrophysiologic mechanisms electrophysiologic mechanisms responsible for arrhythmia.responsible for arrhythmia.
Drug Name: Drug Name: Amiodarone Amiodarone (Cordarone)(Cordarone)
Adult DoseAdult DoseRapid loading: 5 mg/kg IV; Rapid loading: 5 mg/kg IV; not to exceed 450 mg; mixed in D5W not to exceed 450 mg; mixed in D5W infused over 10-30 min; not to infused over 10-30 min; not to exceed 50 mg/kgexceed 50 mg/kg
Drug Name:Drug Name:Lidocaine (Xylocaine)Lidocaine (Xylocaine) Adult DoseAdult Dose0.7-1.4 mg/kg IV push, 0.7-1.4 mg/kg IV push,
repeat in 5 min; not to exceed 300 repeat in 5 min; not to exceed 300 mg/h; follow with an infusion of 2-4 mg/h; follow with an infusion of 2-4 mg/kg/minmg/kg/min
Surgical managementSurgical management
Adrenalectomy Adrenalectomy
It is the surgical removal of one or both It is the surgical removal of one or both adrenal glands depending on tumors adrenal glands depending on tumors whether it is unilateral or bilateralwhether it is unilateral or bilateral
Techniques Techniques
Standard transabdominalStandard transabdominal
Thoraco abdominalThoraco abdominal
RetroperitonealRetroperitoneal
laproscopiclaproscopic
CARE OF THE PATIENT UNDERGOING CARE OF THE PATIENT UNDERGOING ADRENALECTOMYADRENALECTOMY
Adrenalectomy may be unilateral or Adrenalectomy may be unilateral or bilateral to treat adrenal tumors, bilateral to treat adrenal tumors, Cushing's syndrome, or Cushing's syndrome, or hyperaldosteronism. It is hyperaldosteronism. It is accomplished through abdominal or accomplished through abdominal or flank incision. Careful manipulation flank incision. Careful manipulation of the gland is necessary if surgery is of the gland is necessary if surgery is for pheochromocytoma to prevent for pheochromocytoma to prevent excessive release of epinephrine excessive release of epinephrine causing hypertensive crisis causing hypertensive crisis
Preoperative ManagementPreoperative Management BP and fluid volume are optimized.BP and fluid volume are optimized. Surgery and nursing care are explained to Surgery and nursing care are explained to
patient. Patient is shown where adrenal patient. Patient is shown where adrenal glands lie on top of kidneys and where glands lie on top of kidneys and where incision may be on abdomen or loin area.incision may be on abdomen or loin area.
BP will be checked frequently before and BP will be checked frequently before and after surgery and glucocorticoids will be after surgery and glucocorticoids will be given to cover period of stress (surgery) given to cover period of stress (surgery) because at least one adrenal gland will be because at least one adrenal gland will be removed.removed.
Patient is prepared as for major abdominal Patient is prepared as for major abdominal surgery surgery
Postoperative ManagementPostoperative Management Usual postoperative care for Usual postoperative care for
abdominal surgery includes frequent abdominal surgery includes frequent check of vital signs; assessment for check of vital signs; assessment for hemorrhage; turning, coughing, and hemorrhage; turning, coughing, and deep breathing; early ambulation; deep breathing; early ambulation; slow progression of diet when bowel slow progression of diet when bowel sounds return; and control of pain sounds return; and control of pain with scheduled opioid administration with scheduled opioid administration or patient-controlled analgesia I.V. or patient-controlled analgesia I.V. hydrocortisone (Solu-Cortef) is given hydrocortisone (Solu-Cortef) is given as directed to prevent adrenal crisis as directed to prevent adrenal crisis
Nonstressful environment is maintained, Nonstressful environment is maintained, rest is promoted, and meticulous care is rest is promoted, and meticulous care is given to protect the patient from infection given to protect the patient from infection and from other complications that could and from other complications that could cause adrenal crisis.cause adrenal crisis.
Serum sodium, potassium, and glucose are Serum sodium, potassium, and glucose are monitored for abnormality.monitored for abnormality.– Sodium and potassium may normalize, or Sodium and potassium may normalize, or
potassium may become elevated (because of potassium may become elevated (because of transient adrenal insufficiency after surgery).transient adrenal insufficiency after surgery).
– Electrolyte imbalances may persist for 4 to 18 Electrolyte imbalances may persist for 4 to 18 months after surgery.months after surgery.
Hypertension may persist for 3 to 6 months Hypertension may persist for 3 to 6 months after surgery after surgery
Hydrocortisone treatment causes Hydrocortisone treatment causes glucose to rise and worsens control glucose to rise and worsens control in patients with diabetes; may in patients with diabetes; may require additional treatment require additional treatment
ComplicationsComplications
Hemorrhage, adrenal crisisHemorrhage, adrenal crisis
Providing Patient EducationProviding Patient Education Teach patient with bilateral Teach patient with bilateral
adrenalectomy that glucocorticoid and adrenalectomy that glucocorticoid and mineralocorticoid replacement is mineralocorticoid replacement is necessary for rest of life.necessary for rest of life.
Administer additional doses I.M. in times Administer additional doses I.M. in times of stress.of stress.
Administer oral glucocorticoids after Administer oral glucocorticoids after unilateral adrenalectomy and teach unilateral adrenalectomy and teach patient that this treatment will be needed patient that this treatment will be needed for 6 months to 2 years after surgery until for 6 months to 2 years after surgery until remaining adrenal gland can remaining adrenal gland can compensate.compensate.
Encourage wearing or carrying this Encourage wearing or carrying this information at all times, so that information at all times, so that proper treatment can be instituted if proper treatment can be instituted if patient becomes unconscious.patient becomes unconscious.
Encourage follow-up to monitor for Encourage follow-up to monitor for signs of adrenal insufficiencysigns of adrenal insufficiency