on 18-Nov-2021 (Thu)

Abraham Lincoln ( / ˈ l ɪ ŋ k ən / ; February 12, 1809 – April 15, 1865) was an American lawyer and statesman who served as the 16th president of the United States from 1861 until his assassination in 1865.

The life cycle of this organism outside of a human can be summed up in six stages:

The adult Echinococcus granulosus, which is about 3-6 mm in length, resides in the bowel of its definite host.

Gravid proglottids release eggs that are passed in the feces.

These eggs are then ingested by a suitable intermediate host, including sheep, goat, swine, cattle, horses and camels. The eggs then hatch in the bowels and release oncospheres that penetrate the intestinal wall. These oncospheres then migrate through the circulatory system to various organs of the host.

At the organ site, the oncosphere develops into a hydatid cyst. This cyst enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior.

These cyst-containing organs are then ingested by the definite host, causing infection. After ingestion, the protoscolices evaginate, producing protoscolexes.

The scolexes of the organisms attach to the intestine of the definite host and develop into adults in 32-80 days.

The life cycle then continues in humans:

Humans can become infected if they ingest substances infected with Echinococcus eggs.

The eggs then release oncospheres in the small intestine.

...

The life cycle of Echinococcus is illustrated below (courtesy of DPDx)⁵:

from a functional point of view, the liver is organized into acini, with both hepatic arterial and portal venous blood entering the acinus from the portal areas (zone 1) and then flowing through the sinusoids to the terminal hepatic veins (zone 3); the intervening hepatocytes constitute zone 2. The advantage of viewing the acinus as the physiologic unit of the liver is that this perspective helps to explain the morphologic pat- terns and zonality of many vascular and biliary diseases not explained by the lobular arrangement

Hepatocytes have distinct polarity. The basolateral side of the hepa- tocyte lines the space of Disse and is richly lined with microvilli; it exhibits endocytotic and pinocytotic activity, with passive and active uptake of nutrients, proteins, and other molecules. The apical pole of the hepatocyte forms the canalicular membranes through which bile components are secreted. The canaliculi of hepatocytes form a fine network, which fuses into the bile ductular elements near the portal areas.

In hepatocellular diseases (such as viral hepatitis and alcoholic liver disease), features of liver injury, inflammation, and necrosis predomi- nate. In cholestatic diseases, such as gallstone or malignant obstruction, primary biliary cholangitis (previously referred to as primary biliary cirrhosis), and some drug-induced liver diseases, features of inhibition of bile flow predominate. In a mixed pattern, features of both hepato- cellular and cholestatic injury are present (such as in cholestatic forms of viral hepatitis and many drug-induced liver diseases).

Typical presenting symptoms of liver disease include jaundice, fatigue, itching, right-upper-quadrant pain, nausea, poor appetite, abdominal distention, and intestinal bleeding.

The manifestations of liver disease include constitutional symptoms such as fatigue, weakness, nausea, poor appe- tite, and malaise and the more liver-specific symptoms of jaundice, dark urine, light stools, itching, abdominal pain, and bloating. Symp- toms can also suggest the presence of cirrhosis, end-stage liver disease, or complications of cirrhosis such as portal hypertension. Generally, the constellation of symptoms and their patterns of onset rather than a specific symptom points to an etiology

Diarrhea is uncommon in liver disease except with severe jaundice, in which a lack of bile acids reaching the intestine can lead to steatorrhea.

The pain arises from stretching or irritation of Glisson’s capsule, which surrounds the liver and is rich in nerve endings. Severe pain is most typical of gallbladder disease, liver abscess, and severe sinusoidal obstruction syndrome (previously known as veno-occlusive disease) but is also an occasional accompaniment of acute hepatitis

Jaundice is the hallmark symptom of liver disease and perhaps the most reliable marker of severity. Patients usually report darkening of the urine before they notice scleral icterus. Jaundice is rarely detectable with a bilirubin level <s.

Major risk factors for liver disease that should be sought in the clin- ical history include details of alcohol use, medication use (including herbal compounds, birth control pills, and over-the-counter medica- tions), personal habits, sexual activity, travel, exposure to jaundiced or other high-risk persons, injection drug use, recent surgery, remote or recent transfusion of blood or blood products, occupation, accidental exposure to blood or needlestick, and familial history of liver disease.

Vertical spread of hepatitis B can now be prevented by passive and active immunization of the infant at birth, although addition of antiviral therapy during the third trimester of pregnancy is now recommended for mothers with levels of HBV DNA >200,000 IU/mL. Vertical spread of hepatitis C is uncommon, but there are no reliable means of prevention. Transmission is more common among HIV-co-infected mothers and is also linked to prolonged and difficult labor and delivery, early rupture of membranes, internal fetal monitoring, and a high viral load

Hepatitis E infection can become chronic in immunosuppressed individuals (such as trans- plant recipients, patients receiving chemotherapy, or patients with HIV infection), in whom it presents with abnormal serum enzymes in the absence of markers of hepatitis B or C.

Alco- hol consumption associated with an increased rate of alcoholic liver disease is probably more than two drinks (22–30 g) per day in women and three drinks (33–45 g) in men. Most patients with alcoholic cirrho- sis have a much higher daily intake and have drunk excessively for ≥10 years before onset of liver disease

Alcoholism is usually defined by the behavioral patterns and consequences of alcohol intake, not by the amount. Abuse is defined by a repetitive pattern of drinking alcohol that has adverse effects on social, family, occupational, or health status. Dependence is defined by alcohol-seeking behavior, despite its adverse effects. Many alcoholics demonstrate both dependence and abuse, and dependence is consid- ered the more serious and advanced form of alcoholism

family history can be helpful in assessing liver disease. Familial causes of liver disease include Wilson disease; hemochromatosis and α 1 antitrypsin deficiency; and the more uncommon inherited pedi- atric liver diseases—that is, familial intrahepatic cholestasis, benign recurrent intrahepatic cholestasis, and Alagille syndrome. Onset of severe liver disease in childhood or adolescence in conjunction with a family history of liver disease or neuropsychiatric disturbance should lead to investigation for Wilson’s disease. A family history of cirrhosis, diabetes, or endocrine failure and the appearance of liver disease in adulthood suggests hemochromatosis and should prompt investiga- tion of iron status. Abnormal iron studies in adult patients warrant genotyping of the HFE gene for the C282Y and H63D mutations typical of genetic hemochromatosis. In children and adolescents with iron overload, other non-HFE causes of hemochromatosis should be sought. A family history of emphysema should lead to investigation of α 1 antit- rypsin levels and, if levels are low, for protease inhibitor (Pi) genotype