Term
| Signs and Symptoms of acute or chronic liver disease |
|
Definition
Fatigue
Anorexia
Dark colored urine
Light colored stools (Acholic)
Bone fractures
Hyperpigmentation
Pruritis
RUQ discomfort
Insomnia
Jaundice
Bleeding diathesis
Sexual dysfunction |
|
|
Term
|
Definition
alanine aminotransferase, SGPT, serum glutamic pyruvic transaminase
Enzyme mainly found in liver, sometimes kidneys, heart, muscle, pancreas
More specific for liver damage
Released when there is liver damage into the bloodstream; therefore can detect elevated levels in liver disease, normal <40 IU/l |
|
|
Term
|
Definition
aspartate aminotransferase, SGOT, Serum glutamic-oxaloacetic transaminase
Enzyme found in liver, heart, and muscle cells, less specific for liver disease, normal <40 IU/l |
|
|
Term
|
Definition
Found particularly in liver, bones, and GI tract
Used to identify biliary disorders, normal ~20-140 IU/L
Hydrolase enzyme, removes phosphate groups |
|
|
Term
| LDH: lactate dehydrogenase |
|
Definition
Checks for tissue damage, found in heart, liver, kidney, skeletal muscle, brain, lungs, blood cells
Not very specific for liver damage |
|
|
Term
| GGT: Gamma-glutamyl transpeptidase |
|
Definition
Found mostly in the liver
Normal Adult Female Range: 0 - 45 U/L
Normal Adult Male Range: 0 - 65 U/L
Can also be elevated in alcoholics
Very Sensitive, but nonspecific indicator of hepatic injury |
|
|
Term
|
Definition
3.5-5.5 gm/dL
Mainly synthesized in the liver
Protein that carries nutrients
Assesses changes in liver ability to produce albumin |
|
|
Term
| PT/INR: Prothrombin time and International Normalized Ratio |
|
Definition
extrinsic pathway of coagulation
PT: 11-16 seconds
INR: 0.8-1.2, on anticoagulants: 2.5-3.5
Assesses changes in the liver ability to produce clotting factors
Reflects acute or chronic changes in liver function |
|
|
Term
|
Definition
Product of heme metabolism
80% derived from hemoglobin, 20% from other hemoproteins and free heme
Hemoglobin travels to spleen is catabolized with the help of 2 enzymes: heme oxygenase and biliverdin reductase-->biliverdin-->unconjugated (indirect, not water soluble) bilirubin then travels by binding to albumin to the liver diffused into the hepatocytes to be conjugated into a water soluble bilirubin (direct, conjugated)-->released in urine and feces |
|
|
Term
| Unconjugated (Indirect), not water soluble |
|
Definition
Can cross BBB, can’t be excreted, toxic levels can build up, 96% of bilirubin is unconjugated
Hemolysis (autoimmune, anemia, sickle cell)
Drug toxicity (Rifampin)
Thalassemia minor (ineffective erythropoises-leading to destruction of red cell precursors)
Gilbert’s Syndrome (benign, mutation in gene leading to underactivity of bilirubin–uridine diphosphate glucuronyl transferase bilirubin-UGT)
Crigler-Najjar (kernicterus can occur, neonatal disorder, omplete loss or very low levels of hepatic bilirubin-UGT)
Gallstones |
|
|
Term
| Direct Hyperbilirubinemia, Conjugated |
|
Definition
Conjugated, water soluble, excreted
Biliary obstruction
Hepatitis, Cirrhosis
Dubin-Johnson syndrome (benign, no tx necessary)
Excretion of organic anions is impaired
Rotor Syndrome
Disorder of hepatic storage |
|
|
Term
|
Definition
Total bilirubin
between 0.2 and 1.2 mg/dL
Direct bilirubin
0-0.3 mg/dL (30% of total bilirubin)
Indirect bilirubin
Indirect bilirubin=Total bilirubin-Direct bilirubin
0.2-0.9 mg/dL
Total bilirubin=Direct + indirect |
|
|
Term
| Etiology of ALT/AST/Alk phos elevations |
|
Definition
ALT-predominant
AST-predominant
Alkaline Phosphatase-predominant
Nonhepatic |
|
|
Term
|
Definition
| Hep B, C, acute viral hepatitis, steatosis, medications, hemochromatosis, autoimmune, Wilson’s |
|
|
Term
|
Definition
Alcohol related AST/ALT ratio, >2
Cirrhosis |
|
|
Term
| Alkaline Phosphatase-predominant |
|
Definition
| Cholestatic-PBC, PSC, obstruction |
|
|
Term
|
Definition
Extensive scarring of the liver leading to complications/decompensation
Complications include
Encephalopathy
Portal Hypertension
Ascites
Varices
Cancer |
|
|
Term
|
Definition
Caput medusae
JVD
Neuro sx
Ascites
Anasarca
Spider veins
Palmar erythema
Jaundice/Icterus |
|
|
Term
| Fulminant Hepatic Failure/ Acute Liver Failure FHF/ALF |
|
Definition
“A potentially reversible condition, the consequence of severe liver injury, in which encephalopathy developed within 8 weeks of the appearance of the first symptoms, in the absence of preexisting liver disease”
The latter characteristic was later modified, and it is generally accepted that FHF can occur in patients with some degree of liver impairment
Coagulopathy is also noted, INR >1.5 |
|
|
Term
| FHF/ALF Most common causes |
|
Definition
| Drug induced, in particular Acetaminophen, viral hepatitis, shock, ischemia, infiltrating malignancy, autoimmune |
|
|
Term
|
Definition
If FHF is suspected, hospitalization is required
Cerebral edema, primary cause of death
PSE
Coagulopathy
ARF (Acute renal failure)
Cardiopulmonary instability due to vasodilation |
|
|
Term
|
Definition
Results from an increase in resistance to portal flow and increase in portal venous inflow
Increase in vascular resistance
Increase in portal blood flow |
|
|
Term
| Splenomegaly in Portal HTN |
|
Definition
| occurs due to backflow from liver, and blood is shunted from portal system to systemic circulation |
|
|
Term
|
Definition
| Cirrhosis--> portal (sinusoidal) HTN--> splanchnic (circulation of GI tract) and systemic vasodilatation--> decreased effective arterial blood volume-->activation of neurohumoral systems (RAAS, SNS, ADH)--> |
|
|
Term
|
Definition
Ultrasound can pick up 100mL of fluid, paracentesis can identify etiology of ascites
SAAG: Serum albumin-ascitic fluid albumin
DDX: Cardiac, carcinoma, TB
SAAG >1.1gm/dL
If ascites protein <2.5gm/dL: cirrhosis
Ascites protein >2.5gm/dL: cardiac, HF
SAAG <1.1 gm/dL
Investigate peritoneal process, cancer, TB |
|
|
Term
|
Definition
JVD, anasarca, hepatorenal syndrome
Can develop spontaneous bacterial peritonitis, SBP, fluid becomes infected, can lead to sepsis
Infection from GI tract, bacterial translocation in absence of perforation, then travels to mesenteric lymph nodes
~70% of advanced liver disease patients
Impaired local and systemic immune defenses allow bacteria to grow
Gram negative bacteria-most common
DX made by paracentesis and ascitic fluid positive and elevated PMN >250 cells/mm3 |
|
|
Term
|
Definition
Paracentesis: removal of fluid using ultrasound and needle
Temporary
Low salt diet
Diuretics
Spironolactone, Lasix
Soy milk ~3 glasses daily
IV albumin
Low albumin levels |
|
|
Term
|
Definition
Renal failure due to cirrhosis, altering blood flow and blood vessel tone in the kidneys
Renal vasoconstriction
Kidneys appear normal, and function normally when removed from a pt who has HRS and transplanted into another individual
~40% of patients with ascites will develop HRS
Oliguria (low urine output) in cirrhotics in absence of proteinuria |
|
|
Term
|
Definition
Rapidly (~2weeks) decline in kidney function, creatinine >2.5, CrCl <20 ml/min, high mortality rate, SBP, Large volume paracentesis without volume expansion
Mortality rate ~50% after one month |
|
|
Term
|
Definition
Slower onset/progression
Development of ascites, and not responding to diuretics leading to HRS |
|
|
Term
|
Definition
10% of hospitalized patients, 18% of patients within the 1st year of cirrhosis diagnosis
Precipitating factors: diuretics, GI bleed
Renal failure is usually irreversible unless liver transplant is performed, long-term need a transplant |
|
|
Term
|
Definition
Avoid nephrotoxic agents: diuretics, iv contrast, etc
TIPS procedure-shunt placed to reduce blood pressure in PV
Hemodialysis with IV albumin (~20-40grams/daily)
Octreotide/midodrine |
|
|
Term
|
Definition
| The intrahepatic shunt (transjugular intrahepatic portosystemic shunt [TIPS]) provides a conduit for portal venous blood flow directly into the hepatic vein while bypassing the hepatic parenchyma. |
|
|
Term
|
Definition
| Form when increased venous pressure leads to development of collateral circulation diverting the obstructed blood flow to the systemic veins |
|
|
Term
| Variceal Complications/Diagnosis/ Treatment |
|
Definition
Can grow and rupture, 8% chance of growing/forming per year in cirrhotics
Diagnosis: MRI, Upper endoscopy
Treatment: Variceal banding, beta blockers-Carvedilol, Nadolol, TIPS |
|
|
Term
|
Definition
Develops when the liver is unable to remove certain toxins and travel to the brain
Neuropsychiatric signs: initial: insomnia, confusion, personality changes, forgetfullness, coma, also have fetor hepaticus (almond breath)
Grade I-IV
Most common toxin: ammonia
Elevated in patients with PSE |
|
|
Term
|
Definition
Ammonia absorbed by GI tract, travels to liver to be converted to urea then excreted by the GI tract and kidneys
In cirrhotics, ammonia builds up due to liver not being able to convert ammonia to urea and ammonia travels to brain and crosses BBB
Can develop in patients who had a TIPS procedure due to shunting |
|
|
Term
|
Definition
Diets low in ammonia and protein
Food containing high ammonia levels: cheese, onion, gelatin, potatoes, ham, etc
Avoid psychoactive drugs: benzodiazepines, ethanol,
Neomycin, Flagyl, Xifaxan, Lactulose |
|
|
Term
|
Definition
All patients with elevated LFT’s should be tested for autoimmune, genetic, viral markers
Imaging should be done on all patients
Cholestatic and alkaline phosphatase pertains to bile ducts
Symptoms: Fatigue, anorexia, jaundice, malaise, pruritis, changes in color of stool/urine, RUQ discomfort
Cryptogenic: unable to identify cause of cirrhosis due to extensive damage to hepatocytes, most likely cause is NASH |
|
|
Term
|
Definition
| Inflammation of the liver, which in turn causes damage to the liver over time, not necessarily causing elevation in liver enzymes |
|
|
Term
| most common Causes of hepatitis |
|
Definition
NASH, fatty liver disease
Alcohol
Viral
Drug-induced
Genetics
Autoimmune |
|
|
Term
|
Definition
Autoimmune hepatitis
Primary Sclerosing Cholangitis
Primary Biliary Cirrhosis |
|
|
Term
|
Definition
Alpha1-antitrypsin deficiency
Hemochromatosis
Wilson’s disease |
|
|
Term
| most common toxin found in encephalopathy |
|
Definition
|
|
Term
| Alpha1-Antitrypsin Deficiency A1AT |
|
Definition
Autosomal codominant, inherited disease
Most common in Europe
Common phenotype MM-normal, mutated phenotypes MS, MZ, SS, ZZ, etc
One gene from each parent
Mutated gene cannot leave liver, builds up and eventually damages hepatocytes. Lungs also suffer since protein not available to protect lungs from antiproteases
COPD, Emphysema, cirrhosis
Testing is via labs, A1AT serum and phenotype
Important not drink and smoke. No tx available for for liver, can prescribe breathing treatments, inhalers for lungs |
|
|
Term
|
Definition
Need to screen with imaging every 6 months due to increased risk for hepatocellular cancer
Women typically harder to diagnose due to menstrual cycle and loss of iron
Heterzygotes or Homozygotes
Heterozygote: (one gene mutation) 10% Caucasian in U.S. and western Europe
Homozygote: (2 gene mutation) 0.5%
Testing: Iron serum, iron saturation >45%, ferritin >300, HFE genotype, MRI and liver bx showing increase in iron
Iron Serum and saturation, ferritin will all be elevated
Treatment: phlebotomy, diet low in iron |
|
|
Term
|
Definition
Autosomal recessive, 1/30,000 people
Accumulation of copper in liver, eyes, brain
Mutation in Wilson disease protein (ATP7B)
Signs/Symptoms: Kayser and Fleischer ring-eye, neurological and psyc disorders
Testing: Ceruloplasmin, if low, test 24hr urine copper studies, if elevated-diagnosis can be made, liver bx |
|
|
Term
| Accumulation of copper in liver, eyes, brain |
|
Definition
| Copper->duodenum->help of albumin->liver->removed from portal circulation->liver uses some copper, synthesizes and secretes the copper-containing protein ceruloplasmin, and excess copper is excreted in bile |
|
|
Term
|
Definition
Unknown etiology, immune system attacks liver
Some think medication, infections, can trigger it
Females>Men, affects all ethnicity and ages
Accounts for 5.9% transplantation in U.S., 2.6% in Europea
Can overlap with PBC and PSC |
|
|
Term
| Autoimmune hepatitis Diagnosis |
|
Definition
Lab work: LFT’s,ANA, AMA, SMA, anti-LKM1, quantitative immunoglobulins (IgM, particularly IgG, IgA), liver bx
Typically elevated AST/ALT, >10 fold |
|
|
Term
| Autoimmune hepatitis treatment |
|
Definition
Treatment includes suppressing immune system
Steroids: Reduces inflammation in the liver
Immunosuppressants: Imuran, Cellcept, rarely Prograf
Ursodiol
Acts as an anti-inflammatory effect, unknown pathway Usually want to taper off of steroids once liver enzymes normalize and AIH is in remission, then keep a constant dose of immunosuppresants and ursodiol-less toxic if kept on for a long period of time |
|
|
Term
|
Definition
| Acts as an anti-inflammatory effect, unknown pathway Usually want to taper off of steroids once liver enzymes normalize and AIH is in remission, then keep a constant dose of immunosuppresants and ursodiol-less toxic if kept on for a long period of time |
|
|
Term
| Primary Biliary Cirrhosis PBC |
|
Definition
Chronic cholestatic disease
Affects bile ducts
Thought to be triggered by genetic/environmental substances
Females > Males, 50-60 year olds
Usually found in the elderly since patients remain asymptomatic for decades
May present earlier on if something triggers an autoimmune response |
|
|
Term
| PBC associated symptoms/diseases |
|
Definition
Sicca Syndrome=dry mouth/eyes also common with this
Pruritis
Osteoporosis also assoc with this disease
Bone formation is inhibited and bone resorption is low/normal
Therefore bone density/DEXA scan is recommended
Hyperlipidemia: HDL(good cholesterol) is elevated compared to LDL (bad cholesterol)
This is due to lipid malabsorption due to decreased bile acid secretion
Therefore you see Xanthelasma-cholesterol built up around eyes, Xanthoma-cholesterol deposits in skin |
|
|
Term
| Primary Biliary Cirrhosis |
|
Definition
AMA positive (in 95% of patients), bile ducts affected, more common to the small intrahepatic bile ducts
Therefore alkaline phosphatase will be elevated
Immunoglobulins, in particular IgM usually elevated
Mild elevations in AST/ALT
MRI/MRCP-helps with diagnosis, irregular appearing bile ducts
Liver bx-helpful, but not necessary if AMA positive, elevated alk phos, and abnormal MRI/MRCP indicating PBC, irregular bile ducts |
|
|
Term
|
Definition
Treatment includes Ursodiol
Some antacids/bile acid binding sequestrants may interfere with urso, so need to be given at separate times
Cholestyramine is usually given to help alleviate pruritis, but needs to be given 2-4hrs separately from Urso
Usually take with food, when bile is released
If overlap with AIH, may need steroids or immunosuppressants with ursodiol |
|
|
Term
| Primary Sclerosing Cholangitis PSC |
|
Definition
Chronic, cholestatic liver disease
Fibrosing inflammatory process that leads to strictures in the biliary system
Includes both intra- and extrahepatic bile ducts, mid and large bile ducts
60-80% have IBD, in particular UC
Males 75% > Females
Primary vs Secondary
Secondary includes bile duct damage by recurrent pancreatitis, intra-arterial chemo, surgical trauma, choledocholithiasis |
|
|
Term
|
Definition
Cholangitis episodes can occur: fever chills
Abx treatment necessary
Labs: LFT’S, primarily alk phos elevation, anti-neutrophil cytoplasmic antibody 50-80% (p-ANCA in particular)
IgG levels are elevated in 60% of pts
Imaging: MRCP/ERCP
ERCP complications include pancreatitis, bacterial cholangitis, used to be gold standard
MRCP- >80% sensitivity and >87% specificity-now more commonly used
Cholangiographic assessment-dx of large duct PSC
Can do ultrasound and CT scan, but non-specific
Can show thickening, indicating inflammation |
|
|
Term
|
Definition
| cholangiocarcinoma 10-15%, cirrhosis |
|
|
Term
|
Definition
Liver Bx
“Onionskin” appearance
Tx:
Ursodiol
Percutaneous tx: IR uses same techniques as ERCP, but done through skin
ERCP to help with strictures and flow of bile
Balloon dilation |
|
|
Term
|
Definition
|
|
Term
| Nonalcoholic Fatty Liver Disease NAFLD |
|
Definition
Fatty infiltration of the liver, eventually damaging hepatocytes and leading to scarring then cirrhosis
1/3 of patients with fatty liver disease, and elevated LFT’s will progress to cirrhosis
Diagnosis of NASH (nonalcoholic steatohepatitis) can be made by liver bx |
|
|
Term
|
Definition
|
|
Term
|
Definition
Typically seen in overweight patients, metabolic syndrome, ? genetics
NASH implies fatty liver with elevated liver enzymes, inflammation (Mallory body accumulation on liver bx)
Fatty liver disease is a condition, where there is fat on the liver, and is playing a role in damage |
|
|
Term
| NAFLD Diagnosis and Treatment |
|
Definition
Bx can be similar to patients with alcohol related liver disease, but dx is made if alcohol is excluded
Fatty infiltration can be seen on ultrasound
MRI with fat quantification can measure how much steatosis is on liver
Treatment: Tx underlying cause, HTN, DM, hyperlipidemia, weight loss, diet, exercise |
|
|
Term
| Drug Induced/Chemical/Toxin related Hepatitis |
|
Definition
Medications (OTC, prescribed) and chemicals (bleach, paint) causing liver enzyme elevation, particularly AST and ALT, can sometimes be 10x’s ULN
Most commonly seen medications: Statins, Diclofenac, Macrobid, Acetaminophen, Amiodarone, Augmentin, medications for TB (Isoniazid), Methotrexate, Minocycline |
|
|
Term
| Drug/Chemical/Toxins Induced Hepatitis |
|
Definition
Illicit drugs: Cocaine
Herbal
Shark cartilage, glucosamine chondrotin, Ephedra, Kava Kava
Mushroom: Amanita phalloides, tx with activated charcoal and gastric lavage via NG tube, can use PCN-G, milk thistle-no trials to prove efficacy
Toxin
Chloroform, Toluene (paint thinner), Trichloroethylene (industrial solvent) |
|
|
Term
| Drug/Chemical/Toxin induced Hepatitis Treatment |
|
Definition
Remove offending agent
May take up to 6 months to a year for liver enzymes to normalize
Pts that are older, have other co-morbidities, on immunosuppresion, pre-existing liver disease take longer to recover
Can rarely activate autoimmune response, if so, treat with steroids, then taper, and add ursodiol
Unsure if autoimmune response was underlying and drug triggered it, or if drug triggered an autoimmune response that was not previously present |
|
|
Term
|
Definition
Leading cause of Acute liver failure (ALF)
ALF can occur in pts exceeding 10gm/qd
Severe liver damage can occur in pts ingesting doses as low as 3-4gm/qd
Aminotransferases can be seen as high as 3,500 IU/L |
|
|
Term
| Acetaminophen Toxicity Treatment |
|
Definition
If ingested within 4 hours, can use activated charcoal, prior to starting N-acetylcysteine, NAC
N-acetylcysteine, NAC-antidote |
|
|
Term
| Alcohol related liver injury |
|
Definition
According to the 2008 National Survey on Drug Use and Health, slightly more than half of Americans aged 12 or older (51.6 percent) reported being current drinkers of alcohol.
One half of all cases of cirrhosis in the US are due to alcohol abuse
>20-30 gm/day |
|
|
Term
| Alcohol related Liver Injury tx |
|
Definition
Patients develop a fatty liver that eventually leads to fibrosis and cirrhosis
TX: stop drinking, attend AA, support groups, rehab
Not a transplant candidate if alcohol consumption is < 6 months and no signs of rehab is shown |
|
|
Term
|
Definition
Hepatocellular carcinoma (HCC) results in between 250,000 and one million deaths globally per year
2nd leading cancer death worldwide
In U.S., 9th leading cause of cancer death
Men (5th most common) > Women (7th most common)
Most common causes are from Hepatitis B and C ~80% |
|
|
Term
|
Definition
Top priority for transplant, need for surgeon, interventional radiologist, and oncologist to see patient for tx options
Hepatic resection
transarterial chemoembolization (TACE)
Majority of blood supply is from artery-inject with chemo agents then occlusion of artery with embolization
Typically used in non-resectable tumors
Radiofrequency ablation
heating the tissue to temperatures above 50°C
Nexavar (sorafenib)-oral therapy
Some studies have shown coffee consumption >2 cups, may prevent HCC |
|
|
Term
|
Definition
< 6 months
Self-resolution
No development to cirrhosis |
|
|
Term
|
Definition
Fecal-Oral route
27nm in size
Family PicoRNAviridae
Incubation period: 15-45 days
Acute hepatitis, usually self-limiting, no chronicity
Vaccination available |
|
|
Term
|
Definition
Replicates in liver, excreted in bile, and shed in stool
Found commonly in poor sanitary areas, men who have sex with men, uncooked food, IVDU, healthcare settings
Symptoms usually occur 2 weeks after peak infectivity and include:
Malaise, fever, jaundice, abdominal discomfort, fatigue, anorexia, dark urine, etc.
After jaundice and elevated liver enzymes appear, person’s infectivity decreases
Children can shed virus longer than adults |
|
|
Term
|
Definition
Once exposed either by vaccination or infection, hepatitis A IgM Ab persists for 4-12 months.
Hepatitis A IgM Ab or IgM anti-HAV=Test for acute hepatitis A and indicating recent exposure
After antibodies form, hepatitis A Ab total is positive
Hepatitis A Ab total or anti-HAV=IgM and IgG are positive, therefore ensuring protection against hepatitis A either by exposure or vaccination |
|
|
Term
|
Definition
Vaccine available
Inactivated or killed virus
0, 6 month doses
Majority of the patients will develop an immunity
Cannot receive vaccination if you are allergic to Erythromycin, ? during pregnancy
Children born after 1997 in the U.S. have all been offered the vaccination by their Pediatrician (Recommended for children aged 2+, minimum 12 months) |
|
|
Term
| Hepatitis A Post-exposure |
|
Definition
Rest, fluids, if severe, may need hospitalization
If exposure is within 2 weeks, can receive single dose of IG (immunoglobulin), more than 85% effective in preventing virus
IG lasts approximately 3 months
Helps prevent spread of virus, will still need vaccination |
|
|
Term
|
Definition
Parenteral route, blood, fluids, etc
Size 45nm
Family HepaDNAviridae
Acute and Chronic infection
Highly contagious
Can lead to cirrhosis and hepatocellular cancer
Vaccine available
Never really cured of disease since it is a DNA virus |
|
|
Term
|
Definition
Symptoms usually appear 60 days after exposure-similar symptoms to Hepatitis A
Symptoms can last up to 6 months after exposure
Approximately 95% of patients resolve infection on their own
If resolution does not occur after 6 months of infection, considered chronic infection
Chronic infection can lead to cirrhosis and cancer |
|
|
Term
|
Definition
1. HBsAg
2. anti-HBs=Hep Bs Ab
3. anti-HBc=Hep B core Ab
4. IgM anti-HBc=Heb B core Ab IgM
5. HBeAg
6. anti-Hbe=Hep Be Ab
7. Hep B DNA |
|
|
Term
|
Definition
Vaccine
0, 1, 6 month dose
Can receive first dose at birth
Made from protein found in yeast, cannot receive vaccination if allergic to yeast
Immunoglobulin available for post-exposure prophylaxis, should be given within 14 days |
|
|
Term
|
Definition
Various treatment available
Interferon
Antiviral thereapy
Viread
Baraclude
Tyzeka
Epivir |
|
|
Term
|
Definition
Parenteral route, blood, fluids, etc
~50nm-60nm
Family Flaviviridae (RNA virus)
IVDU, tattoos, blood transfusions, needle-stick, 3-5% sexual spread and birth
Acute and chronic
Can lead to cirrhosis and cancer
Can cure disease since it is an RNA virus |
|
|
Term
|
Definition
Approximately 20% of patients exposed to the virus clear it on their own, 80% develop chronicity
75% of people with HCV in the U.S. don’t know they have it
Can remain asymptomatic for decades
Approx 3.2 million people in the U.S.
Incubation period approx 15-150 days
Various genotypes, most common are 1-6
Most common in the United States is 1, which is the hardest to treat, easiest is 2, then 3 and 4 |
|
|
Term
|
Definition
| and hinder blood flow (can’t use |
|
|
Term
| Extrahepatic manifestations of HCV |
|
Definition
Cryoglobulins are antibodies
Skin biopsy can identify
90% caused by HCV
Can affect kidney function (glomerulonephritis)
Rheumatoid factor can be positive
Various types, similar to vasculitis
Treatment is to treat underlying |
|
|
Term
|
Definition
Best initial screen
Indicates active or past infection
Not very sensitive |
|
|
Term
|
Definition
Positive during active infection, viral load
Very Sensitive
Quantitative and qualitative |
|
|
Term
|
Definition
Confirms if patient was ever exposed to hepatitis c
Indeterminate value, meaning not sure if patient was exposed to infection or not |
|
|
Term
|
Definition
Treatment length depends on genotype
Interferon
Weekly injection
Ribavirin
Daily PO
New medication
Incivek and Victrelis
New antiviral medications, directly attacks virus |
|
|
Term
|
Definition
Hepatitis Delta Virus
RNA virus
Coinfection with Hepatitis B
Highest mortality rate due to both Hepatitis B and D
Transmission similar to hepatitis B
Testing: Hepatitis D Ag and anti-HDV, viral load
Treatment: Tx hepatitis B |
|
|
Term
|
Definition
Transmission: Fecal-oral, similar route as HAV
RNA virus
No tx, self limiting
Can cause fulminant hepatic failure, especially in pregnant females
Africa, Asia, Middle east, Central America
More prevalent during heavy rainfall |
|
|
Term
|
Definition
|
|
Term
Hepatitis A Ab IgM
POSITIVE, everything else NEGATIVE |
|
Definition
|
|
Term
Hepatitis A Ab total
POSITIVE, everything else neg |
|
Definition
|
|
Term
Hepatitis BsAg
Hepatitis BcAb IgM
Hep B DNA
ALL POSITIVE |
|
Definition
|
|
Term
Hepatitis BsAb
POSITIVE, everything else negative |
|
Definition
|
|
Term
Hepatitis BsAg
Hepatitis BcAb
HepBeAb
Hep B DNA
ALL POSITIVE |
|
Definition
|
|
Term
Hepatitis BsAg
Hepatitis BcAb
HepBeAg
Hep B DNA
POSITIVE |
|
Definition
|
|
Term
Hepatitis BsAg
Hepatitis BcAb
HepBeAb
Hep B DNA |
|
Definition
|
|
