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Adrenal crisis

medicines

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Adrenal crisis

Adrenal crisis with hypotension must be treated immediately. Patients should be evaluated for an underlying illness that precipitated the crisis.

1. If the diagnosis of adrenal failure is known, hydrocortisone, 100 mg IV q8h, should be given, and 0.9% saline with 5% dextrose should be infused rapidly until hypotension is corrected. The dose of hydrocortisone is decreased gradually over several days as symptoms and any precipitating illness resolve, then is changed to oral maintenance therapy. Mineralocorticoid replacement is not needed until the dose of hydrocortisone is less than 100 mg/day.

2. If the diagnosis of adrenal failure has not been established, a single dose of dexamethasone , 10 mg IV, should be given, and a rapid infusion of 0.9% saline with 5% dextrose should be started. A Cortrosyn stimulation test should be performed . Dexamethasone is used because it does not interfere with subsequent measurements of cortisol. After the 30-minute plasma cortisol measurement, hydrocortisone, 50 mg IV q8h, should be given until the test result is known.



Incidental Adrenal Nodules

Adrenal nodules are a common incidental finding on abdominal imaging studies. Most incidentally discovered nodules are benign adrenocortical tumors that do not secrete excess hormone, but the differential diagnosis includes adrenal adenomas causing Cushing's syndrome or primary hyperaldosteronism, pheochromocytoma, adrenocortical carcinoma, and metastatic cancer.


I. Evaluation. The imaging characteristics of the nodule may suggest a diagnosis but are not specific enough to obviate further evaluation.


A. Patients who have potentially resectable cancer elsewhere and in whom an adrenal metastasis must be excluded may require needle biopsy of the nodule. Pheochromocytoma should be excluded with measurement of 24-hour urine catecholamines before biopsy.

B. In patients without known malignancy, the diagnostic issues are whether a syndrome of hormone excess or an adrenocortical carcinoma is present. Patients should be evaluated for symptoms suggestive of pheochromocytoma (episodic headache, palpitations, and sweating) and signs of Cushing's syndrome. Plasma potassium and dehydroepiandrosterone sulfate and 24-hour urine catecholamines should be measured, and an overnight dexamethasone suppression test or 24-hour urine cortisol should be performed.


II. Management. Patients with hypertension and hypokalemia should be evaluated for primary hyperaldosteronism in consultation with an endocrinologist. Abnormalities of cortisol secretion should be evaluated further. If clinical or biochemical evidence of a pheochromocytoma is found, the nodule should be resected after appropriate a-adrenergic blockade with phenoxybenzamine. Elevation of plasma dehydroepiandrosterone sulfate or a large nodule suggests adrenocortical carcinoma. A policy of resecting all nodules greater than 4 cm in diameter appropriately treats the great majority of adrenal carcinomas while minimizing the number of benign nodules that are removed unnecessarily. Most incidental nodules are less than 4 cm in diameter, do not produce excess hormone, and do not require therapy. At least one repeat imaging procedure 3–6 months later is recommended to ensure that the nodule is not enlarging rapidly (which would suggest an adrenal carcinoma).

A 62-year-old man with lung carcinoma has rapid progression of bilateral lower-extremity weakness to paralysis over several hours and bilateral lower-extremity hypesthesia. He loses bowel and bladder continence. His arm strength is not affected. Which of the following statements concerning this patient is true?

a. Differential diagnosis includes compressive myelopathy, Guillain–Barré syndrome, Eaton–Lambert syndrome, or paraneoplastic neuropathy.
b. MRI of the spine or myelography could be postponed.
c. Hyperreflexia and increased muscle tone are always found early in this disorder.
d. The only treatment option is with intravenous steroids.
e. The only treatment option is surgical decompression.

The correct answer is a
a. The patient has spinal cord compression due to vertebral metastasis. Spinal cord compression in the thoracic spinal cord region will produce sensory and motor changes below the level of the lesion. Cervical involvement will involve both arms and legs. Pain is not universal and should not dissuade the clinician from making this diagnosis. Because of the possibility of recovery of function, rapid diagnosis and intervention with radiation therapy or surgery is indicated. Sometimes patients will exhibit 'spinal shock' soon after development of compression and have flaccidity and hyporeflexia. Definitive diagnosis with either MRI or myelography should be made in the patient as soon as possible. Although compressive myelopathy from vertebral metastasis is the most likely diagnosis, differential diagnoses should include Guillain–Barré syndrome, Eaton–Lambert syndrome, or paraneoplastic neuropathy.



it looks like oncologic emergency
abnormal neurologic exam with back pain, lung cancer hx. even loss of sphincter control- emergent MRI, steroid, but plain radiographs of spine when normal exam(erosion /loss of pedicle, collapse of vertebral body, paraspinous mass)
emergency tx. - high-dose steroid and RTx
when it comes to surgery(laminectomy) - refractory to RTx. progressive neurologic sign even Rtx., recurrent on the previous Rtx. site,..

Which one of the following statements about hepatitis B e antigen (HBeAg) is LEAST accurate?

A HBeAg can be detected transiently in the sera of patients ill with acute hepatitis B infection
B The presence of HBeAg in the serum is correlated with infectiousness
C The absence of HBeAg in the serum rules out chronic infection caused by the hepatitis B virus
D HBeAg is immunologically distinct from HBsAg but is genetically related to HBcAg
E The disappearance of HBeAg from the serum may be a harbinger of resolution of acute hepatitis B infection

The answer is C
Hepatitis B e antigen (HBeAg) is a protein that is associated with the HBV core particle. HBeAg is a soluble protein found only in HBsAg-positive serum and is immunologically distinct from HBsAg as well as from intact HBcAg, an antigen expressed on the hepatitis B virus nucleocapsid core. Interestingly, both HBcAg and HBeAg are encoded on the so-called C-gene of the hepatitis B genome. Owing to the close association of HBeAg and HBsAg, the presence of HBeAg in the serum is linked with infectiousness, and the antigen is present during the viremic period of acute hepatitis B. HBeAg correlates well with viral replication, and detection of HBeAg persistence predicts for the subsequent development of chronic hepatitis B infection; however, the absence of HBeAg in serum does not preclude the development of chronic hepatitis B infection. In acute hepatitis B, the disappearance of HBeAg from serum often presages resolution of the acute infection; however, HBeAg-negative persons should be considered infectious until antibody to HBsAg is no longer detected in the serum.

All the following factors portend a poor survival rate during an attack of acute pancreatitis EXCEPT

A hyperbilirubinemia
B hypoalbuminemia
C hypocalcemia
D hypoxemia
E discolored peritoneal fluid

The answer is A
Serum bilirubin elevations >68 mol/L (.4.0 mg/dL) occur in about 10 percent of patients with acute pancreatitis, are usually transient, and do not portend a poor prognosis unless they are accompanied by very high levels of serum lactic dehydrogenase



ranson criteria(poor px.)
at admission:
age>55years
leukocytosis>16,000/mm3
hyperglycemia>200mg/dl
serum LDH>400IU/L
serum AST>250IU/L
during intial 48hr
hematocrit fall>10%
fluid sequestration>4000ml
hypocalcemia<8mg/dl
hypoxemia(pO2<60mmHg)
BUN rise >5mg/dl after IV fluids
hypoalbuminemia<3.2g/dl
i think discolored peritoneal fluis is sequestration or pancreatic necrosis
 

Near-Drowning

Predisposing factors include youth, inability to swim, alcohol and drug use, barotrauma (in scuba diving), head and neck trauma, and loss of consciousness associated with epilepsy, diabetes, syncope, or dysrhythmias. Near-drowning is defined as survival for at least 24 hours after submersion in a liquid medium.


I. Pathophysiology. Much has been made of the differences in pathophysiology between fresh- and salt-water drownings. However, the major insults (i.e., hypoxemia and tissue hypoxia related to / mismatch, acidosis, and hypoxic brain injury with cerebral edema) are common to both. Hypothermia, pneumonia, and, rarely, DIC, acute renal failure, and hemolysis also may occur.


II. Treatment. Begin with resuscitation, focusing on airway management and ventilation with 100% oxygen. Establish an IV line with 0.9% saline or lactated Ringer's solution. The Heimlich maneuver is not indicated unless upper airway obstruction is present.

A. Immobilize the cervical spine, as trauma may be present.

B. Treat hypothermia vigorously

C. Manage pulmonary complications. Administer 100% oxygen initially, titrating thereafter by ABGs. Intubate the patient endotracheally and begin mechanical ventilation with positive end-expiratory pressure (PEEP) if the patient is apneic, is in severe respiratory distress, or has oxygen-resistant hypoxemia. Administer bronchodilators if bronchospasm is present.

D. Reserve antibiotics for documented infection. Prophylactic glucocorticoids have no role.

E. Manage metabolic acidosis with mechanical ventilation, sodium bicarbonate (if the pH is persistently <7.2), and BP support.

F. Cerebral edema may occur suddenly within the first 24 hours and is a major cause of death. Treatment of cerebral edema does not appear to increase survival ,and intracranial pressure monitoring does not appear to be effective. Nevertheless, if cerebral edema occurs, hyperventilate the patient to a PCO2 of no less than 25 mm Hg, and administer mannitol (1–2 g/kg q3–4h) or furosemide (1 mg/kg IV q4–6h). Treat seizures aggressively with phenytoin. The routine administration of glucocorticoids is not recommended. Hypothermia or barbiturate 'coma' is not indicated. It may be necessary to sedate and paralyze the patient to reduce oxygen consumption and facilitate intracranial pressure management.


III. Observation. Admit patients who have survived severe episodes of near-drowning to an ICU. Noncardiogenic pulmonary edema may still develop in those individuals with less severe immersions. Admit any patient with pulmonary signs or symptoms, including cough, bronchospasm, abnormal ABGs or oxygen saturation as measured by pulse oximetry (SpO2), or abnormal chest radiograph. Observe the asymptomatic patient with a questionable or brief water immersion for 4–6 hours and discharge the patient if the chest radiograph and ABGs are normal. However, if a documented long submersion, unconsciousness, initial cyanosis or apnea, or even a brief requirement for resuscitation has occurred, the patient must be admitted for at least 24 hours.






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