Metabolic derangements that accompany liver failure

1. Coagulopathy: prolonged prothrombin time; in severe cases, partial thromboplastin time may be prolonged. Because the damaged liver cannot use vitamin K, patients must be treated with fresh frozen plasma.

2. Jaundice/hyperbilirubinemia: elevated conjugated and unconjugated bilirubin with hepatic damage (vs. biliary tract disease).

3. Hypoalhuminemia: liver synthesizes albumin.

4. Ascites: due to portal hypertension and/or hypoalhuminemia. Ascites can be detected on physical exam by shifting dullness or a positive fluid wave. Possible complication is spontaneous bacterial peritonitis -infected ascitic fluid that leads to sepsis. Look for fever and/or change in mental status in a patient with known ascites. Do a paracentesis, and examine the ascitic fluid for white blood cells (especially neutrophils), Gram stain, culture and sensitivity, glucose (low with infection), and protein (high with infection). Usually caused by 1!. coli, S. prieiimonme, or other enteric bugs. Treat with broad.-spectrum antibiotics.

8. Portal hypertension: seen with cirrhosis (chronic liver disease); causes hemorrhoids, varices, caput medusae.

6. Hyperammonemia: liver clears ammonia. Treat with decreased protein intake (source of NH3) and lactulose (prevents absorption of ammonia). Last choice is neomycin (stops bowel flora from making NH3).

1. Hepatic encephalopathy: mostly due to hyperammonemia; often precipitated by protein, GI bleed, or infection.

8. Hepatorenal syndrome: liver failure causes kidney failure (idiopathic).

9. Hypoglycemia: liver stores glycogen.

10. Disseminated intravascular coagulation: activated clotting factors usually cleared by liver.

Biliary tract disease: jaundice may be caused by bile duct obstruction. Look for markedly elevated alkaline phosphatase, conjugated bilirubin that is more elevated than unconjugated bilirubin, pruritus, clay colored stools, and dark urine that is strongly bilirubin-positive. Unconjugated bilirubin is not excreted in the urine because it is tightly bound to albumin.

1. Common bile duct: obstruction with gallstone: look for history of gallstones or the four Fs (female, forty, fertile, fat). Ultrasound can often image the stone; if not, use endoscopic retrograde cholangiopancreatography.

2. Common bile duct obstruction from cancer: usually pancreatic cancer, sometimes cholangiocarcinoma or bowel cancers.

3. Cholestasis: often from medications (oral contraceptives, phenothiazines, androgens) or pregnancy.

4. Primary biliary cirrhosis: middle-aged woman with no risk factors for liver or biliary disease, marked, pruritus, jaundice, and positive antimitochondrial antibodies; rest of work-up is negative. Cholestyramine helps with symptoms, but no treatment (other than liver transplantation) is available.

5. Primary sclerosing cholangitis: young adults with inflammatory bowel disease (usually ulcerative colitis); presents like cholangitis.

6. Cholangitis; Charcot's triad = fever, right upper quadrant, pain, and jaundice. Treat with antibiotics, and remove stones surgically or endoscopically.

Esophageal disorders: dysphagia is usually an esophageal complaint. Patients may present with atypical chest pain.

1. Achalasia; hypertensive lower esophageal sphincter (LES), ingbr'nplete relaxation of LES, and loss or derangement of peristalsis. Achalasia is usually idi opathic but may be secondary to Chagas' disease (South America). Patients have intermittent dysphagia for solids and liquids with no heartburn. Barium swallow reveals dilated esophagus with distal "bird-beak" narrowing. Diagnosis can be made with esophageal manometry. Treat with calcium channel blockers, pneumatic balloon dilatation, and, as a last resort, surgery (myotomy).

2. Diffuse esophageal spasm/nutcracker esophagus: both have irregular, forceful, painful esophageal contractions that cause intermittent chest pain. Diagnose with esophageal manometry. Treat: with calcium channel blockers and, if needed, surgery (myotomy). (See figure, top of next page.)

3. Scleroderma: may cause aperistalsis due to fibrosis and atrophy of smooth .muscle. Lower LES becomes incompetent, and patients may develop GERD. Look for positive antinuclear antibody and mask-like fades, other autoimmune symptoms (CREST ~ calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, telangiectasias).

4. Barrett's esophagus: columnar metaplasia due to acid reflux; must be followed with periodic endoscopy and biopsies to rule out progression to adenocarcinoma.

Pancreatitis: more than 80% of cases are due to alcohol arid, gallstones. Other causes include hypertriglyceridemia, viral infections (mumps, coxsac.kie virus), trauma, and medications

tWfuse fisopbageal spasm. IFrom James EC, Corry RJ, Perry JF; Principles of Basic Surgical Practice, Philadelphia, Hanley & Belfus, 1987, with permission,)

(steroids, azathioprine). Patients have abdominal- pain radiating to tlic back, nausea and vomiting that does not relieve the pain, leukocytosis, and elevated amylase/lipase, Perforated peptic ulcer disease also may have elevated amylase and presents similarly, but patients have free air on abdominal x-ray and history of peptic ulcer disease,

Herbal Remedies For Acid Reflux

Herbal Remedies For Acid Reflux

Gastroesophageal reflux disease is the medical term for what we know as acid reflux. Acid reflux occurs when the stomach releases its liquid back into the esophagus, causing inflammation and damage to the esophageal lining. The regurgitated acid most often consists of a few compoundsbr acid, bile, and pepsin.

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