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66 Cards in this Set
- Front
- Back
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other than ABC what are some other viral causes of hepatitis |
CMV |
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what is the clinical difference btwn ACUTE hep ABC
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nothing
remmeber A wont go chronic and neither will E |
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what are the 4 ways a Hep ABCDE infection can go
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1. no sx
2. acute, get some jauncise, resolution 3. FULMINANT hepatitis 4. chronic hep (hep C often asx until it gets chronic) |
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what are the fecal oral Heps, what are the others
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A/E
BCD- blood |
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tell me about the VIRUS that causes HepA
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picornaviridae
+ sence ssRNA highly restitant, naked. capsid proteins bind to liver |
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tell me about Hep A transmission and disease onset
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fecal oral- shed 3-week before and 1 week after onset
Acute disease only common in restaurants, daycare, shellfish, food, irrigated water |
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what does Hep A do once in body
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1. you eat poo
2. hep A goes to intestine 3. enters blood 4. has protein that lets it stay in liver 5. some get in bile 6. some get in stool- shed virus 3 weeks before and 1 week after onset of ACUTE sx (never a chronic disease, +ssRNA) |
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where is Hep A endemic
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WORLDWIDE- fecal oral, due to bad hygeine and sanitation
*infections in kids are milld/asx more common in west. about 50 a year in AZ |
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does Hep A have an abript or insidious onset
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ABRUPT, its an acute illness that resolves
virus is shed before onset of sx |
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what are the clinical features of a Hep A infection
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acute, abrupt onset, shed virus before and a little after illnedd
jaundice/icterus fever, fatigue, N, anorexia, abd pain Later- dark urine, pale stool. sx for like a month |
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this disease is classified by...
A child eats contaminated food and then starts to shed virus for several weeks, the kid then gets sick- fever, fatigue, anorexia, nausea. They then become yellow, their urine is dark and their poo is clay color. whats the deal. why is the poo pale |
hep A- acute disease (all of the Heps will ahve a simliar acute phase) A will recover and no chronic disease. fecal oral spread
Pale stool bc hepatocytes arent able to break down bilirubin- its NOT bc there is an excess of bili being secreted into the lumen of the GI |
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how does Hep A cause disease
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1. ingested- fecal oral
2. HAV gets into hepatocytes and replicates 3. virus gets into bile and then GI 4. poo out virus for weeks (3 weeks before, 4 weeks during disease, 1 week after) 5. HUMORAL and CMI- non perm liver damage occurs via ADCC, and CTL elimination of infected hepatocytes 6. jaundice occurs bc of liver damage |
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what mediates the liver damaged caused by HAV
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Humoral- ADCC
CMI- CTL *both kill hepatocytes, non perm damage *get better in like 4 weeks w/o complications **life long immunity |
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do you get life long immunity with Hep A
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yep
its a mild disease |
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A 23-year old man presented to the ER with a 5 day history of fever, jaundice, dark yellow urine, and pale colored stools. He also complained of malaise, fatigue, abdominal pain, intermittent nausea, vomiting, and loss of appetite. He denied a history of IV drug use and had no sexual contacts for the past six months.
VS: T 38.4oC, P 94/min, R 14/min, BP 124/80 mmHg PE: Icteric patient with hepatomegaly; no splenomegaly What is your next course of action? If this patient has HAV what will AST/ALT look like 1. 10-60 Normal 2. 100-200 3. 250-400 4. >500 |
blood work adn serology
>500, HUGE increase in HepA Serology will be + for IgM antiHAV |
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how is HepA tx
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post exposure prophylaxis with Ig
PREVENT with vaccine- start at 1 yo dont eat poo |
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tell me about the VIRUS hepE
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hepeviridae
+ssRNA, cytoplasmic replication naked- resitant **presents like hepA, also spread like A (fecal oral) |
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whats teh clinical of HepE
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JUST like hep A- fever, anorexia, nausea. progress to jaundice, dark pee adn light poo
**E is more fatal than A, less common bc limited to mexico, europe, africa |
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where is Hep E endemic
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mexico, europe, arfica
Not common here. it presents just like A but its a little more serious A was worldwide E gets 15-40yo |
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what are the sx of acute hep E
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Not a chronic disease
abrupt onset of fever, maliase, anorexia, jaundce etc **simliar to HepA sx but can be more severe 2-8 week incubation |
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does humoral and CMI cause liver damage in hepE
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yep, just like in HepA
CMI- CLT humoral- ADCC **its a HepA mimic, same clinical, same serology (except its anti HEV) **AST/ALT >500 like in HepA **serology and recept travel are the only way to distinguish E and A |
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HepA and HepE are SOO simliar, what about vaccine
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vaccine for A not for E
E tx is symptomatic, prevent spread- dont eat poo **serology and recept travel are the only way to distinguish E and A |
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tell me about the Hep B virus
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1. hep-a-DNA-viridea
2. small ENVELOPE (A/E no envelope) 3. dsDNA- dane particle |
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whats the dane particle
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a clever name for hep B virus
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what are the Ag that are associated with HepB? what do they mean when they show up in serum, what about AB to them
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HBsAG- surface AG
HBcAG- core AG HBeAG- highly transmissible part of HBV core, indicates LOTS of replication If we see these AG we have been infected if we see ANTI... AntiHBsAG- immunized AntiHBcAG- infected AntiHBeAG- AB to e AG, low transmission |
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tell me about HBV replication
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1. dsDNA completion in cytoplasm by viral DNA polymerase
2. transcription in nucleus, use host RNA polymerase. Full length cRNA used to make -DNA. shorter mRNA used to make viral protein 3. - DNA for partial + DNA synthesis 4. budding, release of virions + HBsAG |
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why do kids get chronic hep B more than adults
1. tranaminase is not via IV drugs as is common in adults 2. ther immune system is less mature 3. the infection does is lower |
** less mature immune system why do kids get chronic hep B more than adults
** immune response is responsible for clearing disease |
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what creates an excess of HBsAG in the blood
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dane particles (mature virions) and HbSAG are released into blood stream
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whats the transmission of HepB
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Blood- sex, IVDU
Perinatal |
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whats the dist of HepB
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worldwide (same as A)
8 genotypes **pretty common, 150 cases in AZ/year |
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what is the onset of HepB like, what are the 3 outcomes of infection
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insidious (constrast to A and E which were abrupt)
1. Acute hep w/resolution: hep inflammation, fever, nausea, RUQ pain. jaundice, dark urine, resolves 3-6 months 2. Acute Hep --> fuliminant hep. rapid progression to liver necrosis. acute severe sx and fatal 3. Chronic hep either persistent or active. --> cirrhosis, liver failure, primary hepatocellular carcinoma |
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what outcome of Hep B is this
1. hepatic inflammation, fever, nausea,RUQ pain, jaundice, dark urine, pale stool. resolves 3-6 months 2, acute hepatitis--> liver necrosis 3. persistnat infection --> cirrhosis, liver failure, primary hepatocellular carcinoma |
1, acute hep B w/resolution
2. acure HepB ---> fulminant hep 3. chronic hepatitis |
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whats the pathogensis of hep B
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enters blood, infected hepatocytes (no perm damage at this stage)
viral DNA enters hepatocytes --> latent an effective CMI-->acute hepA and resolution INEFFECTIVE CMI- chronic hepB, Immune complex deposition, cirrhosis, PHC (primary hepatocellular carcimona) |
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what is the first indicator of acute HepB infection
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HBsAG
HbeAG **occures before onset of sx ALT/AST dont get higher until sx occur |
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what does the serology look like for a chronic hEP B infection
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1. liver enzymes elevated for longer
2. HbsAG, HbeAG, HBV DNA persist NO antiHBs Late appearance of anti HBe |
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A 27-year old woman presents to the clinic with fever, chills, HA, malaise, anorexia and abdominal pain for several days. She came in because she noticed her eyes had turned yellow and she developed a very bothersome generalized itching. She admitted to using IV drugs for years, frequently sharing needles with friends. She had had one sexual partner in the past year.
VS: T 38.8oC, P 104/min, R 16/min, BP 112/70 mmHg PE: Mild distress due to pruritis. Icterus and jaundice present; hepatomegaly with tenderness. Blood: Hematocrit: 31% WBC: 9,400/uL Differential: 32% PMNs, 52% lymphs, 5% atypical lymphs Chem: ALT 2730 IU/L, AST 2390 IU/L, bilirubin 6.8 mol/L |
AST adn ALT are high
maybe HepB- get a hep panel |
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whats the disease state
-HBsAG -anti HBc -anti HBs |
susceptible, never immunized
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whats the disease state
-HBsAG +anti HBc +anti HBs |
infected, immune
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whats the disease state
-HBsAG -anti HBc +anti HBs |
immunized,
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whats the disease state
+HBsAG +anti HBc +IgM anti HBc -anti HBs |
acute infection,
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whats the disease state
+HBsAG +anti HBc -IgM anti HBc -anti HBs |
chronic infection
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whats the tx for hep B
acute fulminant chronic |
acute- sx
fulminant- transplant chronic- IF, transplants |
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how is HepB prevented
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Vaccine
HB Ig |
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serology: AB to HAV and HCV were absent. IGsAG and IgM anti ABc were present. whats the dx
1. acute HBV 2. chronic HBV 2. acute HEV since anti IgG HBV are absent 4. non viral hepatitis, pt is immune doe to presence of |
acute HBV
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tell me about the HepD virus
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viriod! its not a virus at all, -ssRNA
envelope has HBsAG- MUST have HBV infection inorder for HVD |
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tell me about replication of HVD
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Replication is unusual:
Host RNA pol II makes an RNA copy, replicates the genome, and makes mRNA. The delta antigen is produced. The delta antigen, genome, and HBsAg are packaged and released from the cell. this is the one that is a viroid and needs HBV inorder for HDV to occur |
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does everyone who is HBV have HDV
does everyone with HDV have HBV |
no
yes, MUST have B in order to get D |
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what is the disease like in HepD
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like B but more severe
coinfection with B and D --> SEVERE disease. can bechronic but more often you revocer with immunity |
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what is the course of a B+D hep coinfection
what about superinfection |
coinfection- more severe in acute stage. usually recover with immunity
superinfection. increased chronic hep, increased fulminant hep and cirhossis, can include hepatic encephalopathy and massive hepatic necrosis |
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at what age do hyou initiate hep B vaccine
1 birth 2. 2 months 3. six months 4. one year 5. 1 years |
birth
do hep A at 1 year |
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whats the pathogenesi sof hep D
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enters liver cells, hep B required for replication
HDV causes CPE- which damages the liver the immune response is also responsible for the sx. HBsAg offers some protection |
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what does serology look like for B D coinfection
what about superinfection |
IgM againse HepDAG and HBcAG
HBsAG clears and you get apprearance of anti HBs In a super infection you detect: HDV HBsAG is present IgM anti HDV is there for MONTHS IgG anti HDV presnt Both: HDVAG or RNA Increased ALT/AST |
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whats teh tx for HepD
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get vaccinated against HepB!!
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tell me aboiut the hep C VIRUS
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flaviviridae
+ssRNA, envelope E1, E2 bing CD81 on hepatocytes |
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what virus has E1 and E2 in its envelope, what do they bind to in the liver cells
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Hep C
binds to CD81 in liver HepC also binds to LDL and LDLreceptor |
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what is the replication of Hec C like
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like normal, its +ssRNA, virus released by exocytosis so they can steal their envelope from host
recall envelope has E1 and E2 which bind to CD81 in liver cells |
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where is HepC endemic
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worldwide!
genotype 1a 1b are most common here |
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how is HCV transmitted
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contact with blood- transfusion, IVDA, cocaine
Adults more infected than kids pretty common |
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what is the liklihood an acute hep C will progress to chronic
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super common, ofthen there is no acute phase but goes to chronic
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whats acute hepC like
what about chronic |
acute- insidious, often not clinicaly apparent
chronic- simlar to HBV, MUCH more fatal! and MUCH more common |
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whats the pathogenesi of HepC
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gets in liver cells and replicates
CMI determines outcome of disease HCV- INHIBITS NK cells--> decreased IFNg (defining cytokine for CMI) and inhibits the CMI, low DC, delay of Th1 cells |
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what hep interferes with CMI
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hep C
CMI needed to clear infection BUT hep C will inhibit it! blocks NK cell and inhibits IFNg (recall IFNg is the defining cytokine for CMI) |
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what do AB to HepC do
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nothing, not protective and immunity may not be life long
** can get tissue damage in liver bc of chronic inflammation |
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A 48-year-old man presented to the clinic for a physical exam, his first in many years. He was asymptomatic, but a routine chemistry panel showed elevated transaminases. He denied IV drug use, but on further questioning, recalled having received a blood transfusion 25 years ago after an appendectomy.
VS: T 37oC, P 72/min, R 12/min, BP 124/76 mmHg PE: Unremarkable What can you rule out at this point? What do you suspect? Blood/Urine: Hematocrit: 45% WBC: 6,200/uL Differential: Normal Chem: ALT 145 IU/L, AST 124 IU/L, urine bilirubin normal Do you still suspect HCV after these results? |
ASL adn ALT are no where near as high as was seen in HepA and E
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tell me about seroconversion in hepC
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happens 7-31 weeks adter infection but not all pts seroconvert
**liver biopsy to determine amt of damage |
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tx for Heo C
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dont drink
dont take hepatotoxic drugs dont spread the virus with sex and drugs |
