Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
57 Cards in this Set
- Front
- Back
|
What are the common features of acute viral hepatitis (clinical manifestations, physical signs, lab findings)?
|
Upper right quad abdominal pain, nausea, anorexia, fatigue, fever, malaise
Jaundice and hepatomegaly LABS: elevated liver enzymes (ALT/AST), bilirubin in the blood and urine, Alkaline phosphatase, LDH |
|
|
When do the symptoms usually arise from Hepatitis infections?
|
most are after incubation period and start at the icteric portion of the disease
The only ones that start preicteric are malaise, anorexia, and fever/rash/arthritis |
|
|
What are the incubation periods for the hepatitis infections? How is damage caused to the liver by hepatitis infection?
|
LONG INCUBATION: weeks to months
Damage is uaully caused by immune system killing most hepatocytes |
|
|
What are acute vs chronic infections; how do they resolve?
|
Acute: resolves within a short period of time/immune system will either win or the host will lose
chronic: last for an indefinite period of time and the virus reaches a balance with the immune system here |
|
|
Which Hepatitis viruses causes chronic viral hepatitis and what can chronic hepatitis lead to?
|
B, C, D are chronic
immune sys fails to clear inf can lead to cirrhosis and or hepatocellular carcinoma 70% HCC are attributable to HEP B or HEP C |
|
|
Which Hepatitis viruses have a vaccine?
|
Hep A and Hep B?
These viruses are low in number because of vaccine |
|
|
Which Hepatitis are rarely seen in the USA?
|
D and E are rarely seen in the USA
|
|
|
Which virus can survive better, enveloped or nonenveloped?
|
NONENVELOPED
naked one has a tough protein coat while the enveloped one only has a lipid coat and will die once it is broken by stomach acid |
|
|
what types of viruses are enteric?
|
Hep A and E
ingested and invade out of the gi tract Other viruses are enterovirus, rotavirus, norwalk virus, adenovirus, astrovirus |
|
|
Describe General properties of Hep A virus: what is the family, the composition, stability, and host?
|
Picornaviridae family, (+)ssRNA virus
ONLY ONE HEP A SEROTYPE EXISTS Very stable in environment low pH and is NONENVELOPED Humans are the only known host |
|
|
What is the Hep A transmission?
|
Fecal Oral
crowding, poor hygiene, community outbreaks such as contam water, food, shellfish Household transmission is common Asymptomatic individuals are HUGE source of new infection 1996 vaccine |
|
|
What is the hep A pathogenesis?
|
Ingest it, replicate it in the oropharnyx/gi tract, transport to the lvier, shed in bile and transit to intestine, shed in feces, brief viremia, cellular immune response of clinical disease and control
No chronic infection and protective antibodies develop which give lifelong immunity |
|
|
Which antibodies are made in response to acute and chronic infections and when are they made for Hep A?
|
We make IgM and IgG to this
The acute response is from IgM and the lifelong protection is IgG IgM made in serum by ELISA detected within 5-10 days before symptoms lasting six months IgG made 4-6 weeks after onset of symptom and last a lifetime |
|
|
What does definitive diagnosis of an infection of Hep A require?
|
antibody total detecting both IgM and IgG at some point
|
|
|
What are clinical features of Hep A virus?
|
Average 28 day incubation, older you are the greater your jaundice chance because your immune system is much better developed and jaundice occurs because of the body fighting the virus
Fulminant hepatitis: fulminant hepatitis (liver failiure) or cholestatic hepatitis (bile obstruction) Typically an acute disease with a low mortality rate with severity of symptoms increasing in time |
|
|
How do you control Hep A virus?
|
Vaccine: formalinh inactivated killed virus with two doses. Intra muscular delivery, routine vaccination in children at 1 year of age, travelers or those at high risk of infection
THIS VACCINE GIVES LIFE LONG IMMUNITY CONTROL: prevent with sanitation and hand washing |
|
|
what are properties of killed/inactivated vaccines?
|
no infection causing ability, no reversion to pathogenic form, medium to low immunogenicity, no special storage, strong induction of antibody, poor cd8+ response variable mucosal delivery possibiliies
|
|
|
Where did HEP E first start?
|
kashmir valley, india
only one patient had hepA antibody |
|
|
What is Hep E virus family and it's general descriptions (relations, transmissions, how/when/where does it occur, which virus is it related to,
|
Hepeviridae related to norwalk virus or calicivirus group,
non enveloped +ssRNA genome Fecal oral drinking water route little p2p evidence or blood or sexual transmission with a lot secondary attack rate occurs where virus is, seasonly in tropics after rainy/floody, no evidence of chronic infections |
|
|
What are clinical features of Hep E virus?
|
average 40 day incubation
low fatality cept with preg PREG HAVE HUGE FATALITY Illness severity increases with age4 FULMINANT HEPATITIS IS RATE indistinguishable symptoms from other hepatitis Greater risk of serious HepE disease occurs in people with preexisting chronic liver disease |
|
|
How do you diagnose Hep E and control it?
|
No commercial test available: do serology for IgG and IgM and you can also look for virus detection
No Vaccine in USA but two recombinant ones with capsid protein developed and trialed in asia Prevention with clean drinking water |
|
|
What types of viruses are HEP A and E?
|
Enteric and Acute
|
|
|
What are the two types of hepatitis?
|
infectious: hep A
Serum associated: hep B serum associated are much longer incubation period |
|
|
What are general properties of Hep B virus?
|
HEPADNAVIRIDAE family
ENVELOPED partially dsDNA virus which replicates with RNA intermediate HUMAN ONLY HOST 2 bill infected and 350 mill chronically infected 100K die each year assoc with cirrhosis and HCC |
|
|
How do you transmit Hep B virus?
|
sexual, parenteral, perinatal
THREE B bedroom baby and perinatal HIGH in blood, serum, wound exudates; moderate in semen vaginal fluid and saliva; low in urine feces sweat tears breast milk |
|
|
What are the outcomes of infection with Hep B?
|
Average 120 day incubation
90% of acute infection adults recover Chronic persistent: asymptomatic Chronic active: symptomatic Fulminant is rare hepatoma: HCC |
|
|
How does Hep B do pathogenesis?
|
viral replication in liver, liver damage due to immune response
CTL responders resolve infections in msot cause with inefficient CTL response you get a chronic infectgion |
|
|
What is rate of infection associated with?
|
High rates of Chronicity
|
|
|
What are the clinical features of Hep B Virus?
|
120 day incubation, jaundice risk increased with age, chronic infection increased with lower ages
premature mortality from liver disease will be about 25 percernt |
|
|
How does vaccine work?
|
It allows you to make AB against Ag
When body see Ag, if it has Ab it will go bind to the protein and neutralize virus. MUST HAVE AB against surface Ag |
|
|
Which antigens does the Hep B virus have? and what components does Hep B virus have
|
HBsAg: surface
HBcAg: core HBeAg: extra core four open reading frames Viral DNA, Reverse transcriptase |
|
|
How do you diagnose Hep B Virus?
|
HBsAg is general marker
HBs antibody for recovery and immunity to infection HBc IgM marker for acute HBc IgG past or chronic infection HBV DNA tests show active virus replication and used to monitor response to therapy antibody for HBe shows virus is not replicating |
|
|
What is the single most important Antigen to search for during HEP B Vaccine?
|
HBsAG made in mass quantities
If it is present you have current acute or chronic infection If it is a no: you have resolved infection or you never had it |
|
|
Why is the antibody for HBsAg not detected till later? What is the problem associated with this?
|
because it is being used up by binding to the HbsAg
HBsAg mops up the antibody because there are SO MANY MADE! causing a six month delay to the detection Complexes can deposit into joints and skin causing pain or rash You will not see Hbs antibodies in chronic infection |
|
|
Where do we see HBcAg?
|
ONLY FOUND IN INTACT viral particles, not like HBsAg
WE MAKE anitbody against HBc We see IgM early and IgG late |
|
|
What does HBeAg and HBeAg antibody HBe tell us about Hep B infections?
|
If it is present the virus is replicating, if the antibody is present the virus is not really replicating
monitor the progress of the infection |
|
|
How do you prevent Hep B?
|
Recombinant peptide faccine with pure HBsAg made in yeast
Passive Vaccine: Hep B immunoglobins IgGs for post exposure In patients with HBV or infatns with HBV +ve mothers: give either |
|
|
How does HBV replicate?
|
Viral DNA injects into host DNA
when transcribed, the longest piece transcribed mRNA will be viral DNA including. This will make stuff when expressed Also, RT will come thru and make it into DNA in cytoplasm |
|
|
How do you treat HBV?
|
Give them RT inhibitors or nuceloside analog reverse transcriptase inhibitors can can cause DNA chain termination
Give them interferons which are human proteins that induce antiviral state lamivudine, tenofovir, telbivudine, entecarcir, adefovir |
|
|
What type IFN are used for antiviral state and how do they work?
|
Interferons are human proteins that induce antiviral state by blocking protein synthesis and degrading RNA molecules by inducing interferon stimulated genes
They induce cell mediated immunity which increased potential for liver damage during infection |
|
|
What are general props of Hep D?
|
Delta agent, can't replicate on own, DEFECTIVE. needs HBV to code surface protein
infection is qith coinfection with HBV ssRNA enveloped with HDV Ag and HBsAg which is derived from HBV |
|
|
How do you transmit hep D?
|
Percutaneous exposures via drug injection, permucosal exposure via sex contact
IVDA and their partner are at risk for Hep D infection |
|
|
What are clinical features of Hep D infection?
|
Coinfection: HepB and HepD at the same time with 90% full recovery; lo risk for chronic infection
Super infection: HepB infected then later infected with HepD leaving to a chronic HDV infection, HBV chronic infection and HDV super and then HDV chronic occurs VERY HI RISK OF SEVERE CHRONIC LUNG DDISEASE FROM FULMINANT HEPATITIS |
|
|
What happens with coinfection?
|
Most patient clear both infection with the more severe acute disease often seen
Enhanced clearance of HBV Every HepB patient should be tested for HDV IgG antibody |
|
|
How do you diagnose and prevent HDV?
|
Serologic diagnosis: antibody for HDV IgM is acute and hi amounts in chronic reactivation
HDV Ag for acute and chronic infection a IgG for late acute or chronic Active infection via Pcr Prevention by prophylaxis and education |
|
|
What are general properties of Hep C virus?
|
Flavivirus: same family as yellow fever, dengue, and west nile
(+)ssRNA enveloped virus 90% of NonA, NonB infections Major cause of post transfusion hep 200 million carrier world wide |
|
|
How does Hep C replicate?
|
Typical positive sense ssRNA
Genome acts as mRNA and then gets translated and also replicated PROTEASE DRUG TARGET for treatment |
|
|
What is the leading cause of liver transplant?
|
Hep C causign 40% of chronic liver disease
70% are unware of their infection |
|
|
How do you transmit HCV?
|
Percutaneous injection with needle sticking
perinatal via permucosal sexual in hi risk sexual practice negligible with monogamous and significant with multiple partners neonatal: less than five percent with increased if mom has HIV Household tranmission is rare Healthcare transmission happens with a 2 percent risk following needle sstick injury |
|
|
what are clinical features of HEP C infection?
|
45 day avg incubation, acute illness is 25%
acute case ftality is low chronic is 70-85% chronic hep is 70% cirrhosis is 5% inoculum size, genotype, age, strrength of immune response, route of infection are all factors that affect outcome |
|
|
What factors affect HCV infection?
|
Increased alcohol intake esp for women, age greater than 40 at time of infection, HIV co infection, male gender, chronic hbv coinfection
|
|
|
What's so special about genetic variability?
|
evolution, undergo antigenic variation in infected individuals
viral polymerase has a low error rate with a high amount of virons produced |
|
|
How do you diagnose Hep C?
|
antibodies to hep c virus via EIA
HCV recombinant immunoblot assay nucleis acid test for hcv rna AND NEGATIBVE FOR IGM AGAINST HAV AND HBV |
|
|
What are diagnostic tests for HCV?
|
Serology: antiHCV antibody
RIBA: recombination immunoblot assay NAT: nucleic acid testing detecting viral RNA in serum Qualitative: confirms infection; quantitative: determines viral load genotyping: predicting treatment response Gold standard: nearly 100% sensitive and specific |
|
|
Which tests shows active infection for Hep C infection?
|
NAT test
|
|
|
How do you treat Hep C?
|
PEG interferon alpha, ribavirin
Protease inhibitor: boceprevir, telaprevir |
|
|
What are the time periods with the three major viral hepatitis?
|
Hep A is acute
Hep B is acute perinatal or chronic Hep C is acute or chronic |
