Term
| Viral heptitis transmission and at risk population |
|
Definition
Hep A: Fecal-oral
Hep B: Parenteral, sexual, vertical
Hep C: Parenteral, sexual
Hep D: Parenteral, sexual
Hep E: Fecal-oral
Hep G: Parenteral
Hep A:Poor handling and food storage causes infections in restaurant patrons. Also areas of crowding and poor sanitation
Hep B:Vertical transmission from mother-child. Multiple sexual partners. People who received blood transfusions over a year ago
Hep C: Multiple sexual parners. IV drug users. Blood transfusions >10 years ago
Hep D: IV drug users
Hep E: Those traveling to endemic areas
Hep G: IV drug users. Dialysis pts. Blood transfusions. Hemopheliacs |
|
|
Term
|
Definition
Antibody to Hep A (anti HAV) appears only in the course of the illness. By the time of dx, Hep A would have been cleared from stool.
Bothe IgM and IgG anti-HAV are detectable in serum soon after onset
IgG: Takes months to develop and will make pt immune to HAV for their lifetime. If it is present, then the pt is pas infection. Titers of IgG anti-HAV peak after 1 mo and persist for years. IgG anti-HAV indicates previous exposure to HAV, noninfectivity and immunity. In US, about 30% of pop has serologic evidence of previous infection.
IgM Will be present from 4-10d- indicates acute infection. Peak titers of IgM anti-HAV occur during the first week of clinical dz and disappear w/in 3-6 mo. Detection of IgM anti-HAV is an excellent test for dx of acute HAV. |
|
|
Term
|
Definition
| Surface antigen measured in blood. If present, than pt has infection. This is the first evidence of infection, before clinical liver dz and implies infectivity |
|
|
Term
|
Definition
| An IgM or IgG antibody. IgM anti-HBc appears shortly after HBsAg is detected. Its presence in the setting of acute hep indicates a dx of acute Hep B. May also reappear during flares of previously inactive chronic hep. |
|
|
Term
|
Definition
| Specific antibody to HBsAg. Appears in most pts after clearance of HBsAg and afer successful vaccination against HepB. Disappearance of HBsAg and the appearance of anti-HBs signals recovery from HBV infection, noninfectivity and immunity. |
|
|
Term
| Other viral causes of hepatitis |
|
Definition
Other viral causes that should be included in ddx: HSV, spirochetal dz such as leptosirosis and syphilis, Brucellosis, Ricketsial diseases such as Q fever, drug induced liver disease, shock liver (ischemic hepatitis) and autoimmune hepatitis.
Mono: Requires exam of LUQ for splenomegaly (GENTLY! Don’t rupture it with palpation!). May be spread by saliva. Sx include fever, sore throat, lymphadenopathy, lympocytosis w/ abnormal lymphcytes similar to monocytes and heterophil antibody in serum.
CMV: Similar to mono found especially in immunocompromised pts. A group of herpesviruses infecting humans and other animals which has special affinity for salivary glands, causing development of characteristic inclusion in the cytoplasm or nucleus. Congenital infection may cause malformation or fetal death; infection in immunocompromised may be life threatening. |
|
|
Term
|
Definition
Fatty liver progressing to cirrhosis. Much more common than infective hep.
s/sx: Hx: EtOH x10 yr. Recent period of drinking w/ complaints of anorexia/nausea. Hepatomegaly, jaudice, abd tenderness, ascites, fever, encephalopathy.
Labs: no true lab test- dx is mad by hx of EtOH. Elevated AST, usually higher than ALT by 2x. Leukocytosisi w/ left shift; leukopenia occassionally seen but disappears w/ cessation of drinking; ALK slightly up; albumin dpressed; gamma globulin elevated; increased PTT. |
|
|
Term
| Complications of cirrhosis |
|
Definition
Esophageal varicies- dilated submucosal veins.
Hepatic encephalopathy- disorderd CNS fxn due to failure of liver to detoxify noxious agents of gut including ammonia. Diatary protein and GI bleeds make condition worse.
Ascities |
|
|
Term
|
Definition
| Prothrombin time- liver sythesizes prothrombin but needs vit K to do so. Interferene w/ Vit K metabolism can take place due to deficiency (dietary or defective intestinal absorption) or inadequate utilization secondary to destruction of liver parenchma. |
|
|
Term
|
Definition
Jaundice is caused by predominately unconjugated, and conjugated bilirubin in the serum and, biliary obstruction.
CONJUGATED: May result from impaired excretion of bilirubin from the liver due to –Hepatocellular disease, drugs, sepsis, extracellular biliary obstruction ans heredity d/o’s i.e. Dubin-Johnson syndrome.
UNCONJUGATED: May result from overproduction of bilirun due to hemolysis, impaired hepatic uptake of bilirubin due to certain drugs, impaired conjugation of bilirubin by glucuronide i.e. Gilbert’s syndrome.
BILIARY OBSTRUCTION: There may be RUQ pain, wt loss, dark urine & light stools. May result from a stone, carcinoma anywhere I the biliary system, or liver disease. |
|
|
Term
|
Definition
asymptomatic Stones are present but do not block the cystic duct. No prophylaxis cholecystectomy needed unless the gallbladder is calcified or the stones are larger than 3 cm in diameter. Or the patient is a candidate for cardiac transplantation.
symptomatic Stone becomes impacted in the cystic duct and inflammation develop behind the obstruction. Treatment of choice is laporoscopic cholecystectomy. |
|
|
Term
|
Definition
Assoc w/ gallstones (90%).
S/Sx: fever, sudden and stead RUQ pain. Attacks precipitated by fatty meal; vomiting, jaundice.
Tx: NPO, wait for acute attack to subside before s/p |
|
|
Term
|
Definition
| Inflammation of bile duct. Pain, fever and jaundice. |
|
|
Term
|
Definition
| Gallstones cause 30-75% of pancreatitis when lodged in ampulla of Vater. Epigastric pain radiating to back w/ n/v and anorexia. |
|
|
