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Hypernatremia: Addison’s disease involves aldosterone deficiency, leading to renal sodium wasting and hyponatremia rather than sodium retention. Reduced sodium reabsorption contributes to decreased intravascular volume. Elevated sodium levels are not consistent with primary adrenal insufficiency.

Hypokalemia: Aldosterone deficiency reduces potassium excretion in the distal nephron, resulting in potassium retention. This mechanism leads to hyperkalemia instead of low potassium levels. Hypokalemia is more characteristic of excess mineralocorticoid activity.

Weight gain: Clients with Addison’s disease commonly experience weight loss due to decreased appetite, chronic fatigue, and impaired metabolism. Cortisol deficiency reduces gluconeogenesis and energy availability. Weight gain is more typical of hypercortisol states such as Cushing’s syndrome.

Pulmonary embolism: A pulmonary embolism results from a thrombus, typically originating in the deep veins of the lower extremities, that travels to the pulmonary circulation. It is not an immediate complication of penetrating chest trauma. The acute mechanism does not align with embolic obstruction.

Pulmonary hypertension: Pulmonary hypertension develops gradually due to chronic vascular or cardiac conditions affecting pulmonary circulation. It does not present acutely following trauma. The timeline and mechanism are inconsistent with this diagnosis.

Cardiac tamponade: Cardiac tamponade results from rapid accumulation of fluid in the pericardial sac, usually following penetrating injury to the heart itself. Although possible with anterior chest trauma, symptoms would include hypotension, jugular venous distention, and muffled heart sounds rather than isolated respiratory distress.

Unexplained weight gain: Type I diabetes is characterized by absolute insulin deficiency, which prevents glucose uptake into cells. This leads to a catabolic state rather than anabolic storage. Weight gain is not expected at initial diagnosis.

Polyuria: Hyperglycemia causes osmotic diuresis as excess glucose is excreted in the urine, pulling water with it. Increased urine output is a classic manifestation of diabetes mellitus. However, it is a symptom rather than the most defining metabolic consequence.

Hypertension: Elevated blood pressure is not a typical early finding in type I diabetes. Hypertension may develop later due to chronic complications such as nephropathy. It is not an expected manifestation at initial diagnosis.

Hypertension and low heart rate: Hypovolemic shock results in decreased circulating blood volume and reduced cardiac output. The compensatory response involves sympathetic activation rather than bradycardia or elevated blood pressure.

Increased urine output and fever: Hypovolemia leads to decreased renal perfusion, causing oliguria rather than increased urine output. Fever is not a defining feature of hypovolemic shock and suggests an infectious or inflammatory process instead.

Metabolic alkalosis and slow respiratory rate: Hypovolemic shock commonly leads to metabolic acidosis due to tissue hypoxia and lactic acid accumulation. Respiratory compensation typically involves tachypnea, not bradypnea.

Though painful, pancreatitis does not lead to malabsorption syndromes: Inflammatory injury to the pancreas impairs exocrine enzyme secretion needed for fat, protein, and carbohydrate digestion. Reduced pancreatic enzyme availability can lead to steatorrhea and nutrient malabsorption, particularly with recurrent or severe episodes.

Acute pancreatitis is not reversible: Acute pancreatitis is often reversible with supportive care once the inflammatory trigger is removed. Pancreatic tissue can recover if necrosis and complications are limited. Irreversibility is more characteristic of chronic pancreatitis.

Acute pancreatitis is often caused by Hepatitis B: Viral hepatitis primarily affects hepatic tissue rather than pancreatic parenchyma. While rare viral causes of pancreatitis exist, Hepatitis B is not a common or typical etiologic factor.

Biliary colic and fever: Biliary colic is typically associated with gallstone obstruction of the cystic duct, and fever suggests an acute infectious or inflammatory process such as cholecystitis. This presentation is episodic and colicky rather than chronic and progressive. It does not explain weight loss and abdominal distension related to chronic liver disease.

Bloody stools and diarrhea: These findings are more suggestive of lower gastrointestinal pathology such as inflammatory bowel disease, ischemic colitis, or gastrointestinal bleeding. Chronic liver disease may cause coagulopathy, but overt bloody stools and diarrhea are not primary features. The symptom pattern does not align with RUQ pain and ascites.

Epigastric pain and brash: Epigastric pain with acid regurgitation is characteristic of gastroesophageal reflux disease or peptic ulcer disease. These conditions do not account for jaundice, abdominal distension, or systemic effects such as weight loss and weakness. The pain location and associated findings point away from hepatic pathology.

Hyperlipidemia: Elevated lipid levels contribute to systemic atherosclerosis affecting coronary and peripheral arteries. It does not directly increase pulmonary vascular resistance or cause chronic pulmonary hypertension. The right ventricle is not primarily affected.

Renal disease: Chronic kidney disease affects fluid balance, blood pressure regulation, and metabolic function. While it may contribute to systemic hypertension or volume overload, it does not cause primary pulmonary vascular changes that lead to cor pulmonale.

Aortic stenosis: Aortic valve narrowing increases left ventricular afterload and can result in left-sided heart failure. The resulting hemodynamic burden is on the left ventricle rather than the pulmonary circulation. Right-sided failure in this condition occurs through different mechanisms.

Check for lower extremity pitting edema: Left-sided heart failure primarily causes blood to back up into the pulmonary circulation rather than systemic veins. This leads to pulmonary congestion rather than peripheral edema. While edema may eventually develop if right-sided involvement occurs, it is not the first or most urgent assessment.

Measure current urine output: Reduced cardiac output in left-sided HF can decrease renal perfusion, potentially leading to oliguria. Assessing urine output is important for overall fluid balance and kidney function. However, it does not provide immediate information about pulmonary status or oxygenation, which are more acutely threatened in left-sided HF.

Monitor for jugular vein distension: Jugular vein distension reflects elevated systemic venous pressure associated with right-sided heart failure. In isolated left-sided HF, JVD is typically absent, making it a lower priority assessment. Focusing on JVD does not detect pulmonary complications caused by left ventricular dysfunction.

Hyperplasia: Hyperplasia is an increase in the number of cells in a tissue or organ in response to a stimulus. It does not involve a change in cell type, so it does not explain the replacement of normal esophageal epithelium with a different cell type in Barrett’s esophagus.

Hypertrophy: Hypertrophy is an increase in the size of existing cells, usually in response to increased workload or stress. It does not involve a change from one cell type to another, making it unrelated to the cellular changes seen in Barrett’s esophagus.

Anaplasia: Anaplasia is the loss of differentiation and structural organization of cells, typically seen in malignant tumors. It involves abnormal, poorly functional cells rather than the adaptive, protective cell type change observed in metaplasia.