Pathophysiologic relationship of alcoholism and anemia

Alcohol use disorder - Symptoms and causes - Mayo Clinic

pathophysiologic relationship of alcoholism and anemia

The most common etiologies are alcoholism, vitamin B12 and folate deficiencies, and When the peripheral smear indicates megaloblastic anemia Abstract; Pathophysiology; Diagnostic Strategy; Specific Causes of. Increased MCV is an indication of macrocytic anemia when any of the following with macrocytosis, found a significantly negative correlation between mean Although the macrocytosis of alcoholism may be secondary to poor nutrition with a. alcohol abuse. Learn more about anemia, how heavy drinking can cause, and how to pr. Alcohol's Relation to Blood Cells and Anemia.

The pancreas, likewise, may be the seat of acute disease, alcoholic pancreatitis, or long-continued injury that leads to chronic calcifying pancreatitis.

pathophysiologic relationship of alcoholism and anemia

Pseudocysts or abscesses may complicate acute disease. Both acute and chronic myocardial injury have been noted and aptly named alcoholic cardiomyopathy. Alcoholic myopathy rhabdomyolysisaffecting skeletal muscle, may occur alone or in conjunction with myocardial change.

In severe disease, myoglobinemia and myoglobinuria result. Alcoholics are particularly prone to have severe infections, probably because of acquired defects in host defenses.

Pneumonia is a common cause of death.

Anemia pathophysiology - Hematologic System Diseases - NCLEX-RN - Khan Academy

Other fatal infections, such as renal papillary necrosis, meningitis, and endocarditis, are additional hazards. Untreated pulmonary tuberculosis is occasionally observed at autopsy. Bone marrow dysfunction with megaloblastic anemia, thrombocytopenia, and granulocytopenia may be present singly or in some combination.

Hemolytic anemia also complicates alcoholism. Coagulation defects may occur in cirrhosis. Peripheral neuritis is a common complication. Premature testicular and ovarian atrophy appear in many patients. Alcoholic hepatitis steatohepatitis is a combination of fatty liver, diffuse liver inflammation, and liver necrosis often focal —all in various degrees of severity. The damaged hepatocytes are swollen with a granular cytoplasm balloon degeneration or contain fibrillar protein in the cytoplasm Mallory or alcoholic hyaline bodies.

Severely damaged hepatocytes become necrotic. Sinusoids and terminal hepatic venules are narrowed. Cirrhosis may also be present. Alcoholic cirrhosis is advanced liver disease characterized by extensive fibrosis that disrupts the normal liver architecture. The amount of fat present varies.

Pernicious anemia

Alcoholic hepatitis may coexist. The feeble compensatory attempt at hepatic regeneration produces relatively small nodules micronodular cirrhosis. As a result, the liver usually shrinks. In time, even with abstinence, fibrosis forms broad bands, separating liver tissue into large nodules macronodular cirrhosis—see Cirrhosis: Symptoms and Signs Symptoms usually become apparent in patients during their 30s or 40s; severe problems appear about a decade later.

pathophysiologic relationship of alcoholism and anemia

Fatty liver is often asymptomatic. In one third of patients, the liver is enlarged and smooth, but it is not usually tender.

Anemia Caused by Heavy Drinking

Alcoholic hepatitis ranges from mild and reversible to life threatening. Most patients with moderate disease are undernourished and present with fatigue, fever, jaundice, right upper quadrant pain, tender hepatomegaly, and sometimes a hepatic bruit.

Other manifestations of cirrhosis may be present. Cirrhosis, if compensated, may be asymptomatic. The liver is usually small; when the liver is enlarged, fatty liver or hepatoma should be considered. Symptoms range from those of alcoholic hepatitis to the complications of end-stage liver disease, such as portal hypertension often with esophageal varices and upper GI bleeding, splenomegaly, ascites, and portosystemic encephalopathy.

Portal hypertension may lead to intrapulmonary arteriovenous shunting with hypoxemia hepatopulmonary syndromewhich may cause cyanosis and nail clubbing.

pathophysiologic relationship of alcoholism and anemia

Acute renal failure secondary to progressively decreasing renal blood flow hepatorenal syndrome may develop. Chronic alcoholism, rather than liver disease, causes Dupuytren contracture of the palmar fascia see Figure: Dupuytren Contracturevascular spiders, myopathy, and peripheral neuropathy. In men, chronic alcoholism causes signs of hypogonadism and feminization eg, smooth skin, lack of male-pattern baldness, gynecomastia, testicular atrophy, changes in pubic hair. Undernutrition may lead to multiple vitamin deficiencies eg, of folate and thiaminenlarged parotid glands, and white nails.

In alcoholics, Wernicke encephalopathy and Korsakoff psychosis result mainly from thiamin deficiency. Rarely, patients with fatty liver or cirrhosis present with Zieve syndrome hyperlipidemia, hemolytic anemia, and jaundice. When the patient's alcohol consumption is in doubt, history should be confirmed by family members. Patients can be screened for alcoholism using the CAGE questionnaire need to Cut down, Annoyed by criticism, Guilty about drinking, and need for a morning Eye-opener.

There is no specific test for alcoholic liver disease, but if the diagnosis is suspected, liver function tests PT; serum bilirubin, aminotransferase, and albumin levels and CBC are done to detect signs of liver injury and anemia.

Its effect on AST is less pronounced. Serum gamma-glutamyl transpeptidase GGT increases, more because ethanol induces this enzyme than because patients have cholestasis or liver injury or use other drugs. Serum albumin may be low, usually reflecting undernutrition but occasionally reflecting otherwise obvious liver failure with deficient synthesis.

Indexes of the severity of liver disease are Serum bilirubin, which represents secretory function PT or INR, which reflects synthetic ability Thrombocytopenia can result from the direct toxic effects of alcohol on bone marrow or from splenomegaly, which accompanies portal hypertension.

pathophysiologic relationship of alcoholism and anemia

Neutrophilic leukocytosis may result from alcoholic hepatitis, although coexisting infection particularly pneumonia and spontaneous bacterial peritonitis should also be suspected. Imaging tests of the liver are not routinely needed for diagnosis.

If done for other reasons, abdominal ultrasonography or CT may suggest fatty liver or show splenomegaly, evidence of portal hypertensionor ascites. Ultrasound elastrography measures liver stiffness and thus detects advanced fibrosis.

Pathology of Alcoholism | American Journal of Clinical Pathology | Oxford Academic

This valuable adjunct can obviate the need for liver biopsy to check for cirrhosis and help assess prognosis. Its exact role is under study. If abnormalities suggest alcoholic liver disease, screening tests for other treatable forms of liver disease, especially viral hepatitis, should be done. Because features of fatty liver, alcoholic hepatitis, and cirrhosis overlap, describing the precise findings is more useful than assigning patients to a specific category, which can only be determined by liver biopsy.

Not all experts agree on the indications for liver biopsy. Proposed indications include the following: If iron accumulation is observed, measurement of the iron content and genetic testing can eliminate hereditary hemochromatosis as the cause.

For stable patients with cirrhosis, the American Association for the Study of Liver Diseases AASLD recommends that liver ultrasonography, with or without alpha-fetoprotein AFP measurement, should be done every 6 mo to screen for hepatocellular carcinoma 1. AASLD guidelines for the treatment of hepatocellular carcinoma. HepatologyJan 28 Epub ahead of print. Prognosis Prognosis is determined by the degree of hepatic fibrosis and inflammation.