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239 Cards in this Set
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can be a primary or secondary manisfestation of several infections (Yellow fever, EBV, HSV, CMV, Lassa Fever) and/or noninfectious conditions (alcoholic cirrhosis)
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viral hepatitis
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inflammation of the liver
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viral hepatitis
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RQ: detectable signs of viral hepatitis
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RQ: elevated liver enzyme levels, jaundice (icterus), malaise, fever
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primary viral hepatitis agents
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Hepatitis A-G
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Hepatitis A Virus (HAV)
aka ... taxonomic group? |
enterovirus 72 of the picornaviradae
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Hepatitis B Virus (HBV)
TQ: *RNA or DNA?* which taxonomic group? |
TQ: *DNA* virus of the Hepadnaviradae
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Hepatitis C Virus (HCV)
aka... taxonomic group? |
nee NonAnonB (NANB) an enteriovirus
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TQ: Hepatitis D Virus (HDV)
*aka..*. RNA or DNA? taxonomic group? |
TQ: *aka Delta agent*
defective RNA virus currently only member of Deltaviridae |
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Hepatitis E Virus (HEV)
taxonomic group? |
provisionally in caliciviridae
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TQ: Hepatitis F (HFV)
variant of what virus? |
TQ: variant of HBV
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TQ: Hepatitis G Virus (HGV)
homologous to ... |
TQ: 25% homologous to HCV genome but doesn't cause symptoms
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HAV
how many serotypes? enveloped or not? thermotolerant or not |
single serotype,
unenveloped- since's there's no envelope it's thermotolerant and cold tolerant acid stable |
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TQ: how is HAV spread?
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TQ: it's in stool 2-3 weeks before and 1 week after jaundice
*fecal-oral* or contaminated food (*shellfish*) or *water*, oro-anal sex |
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why is parenteral transmission of HAV rare?
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parenteral "around the gut"
rare b/c of short viremic phase |
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where does HAV grow then spread and multiply
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assumed to grow in intestinal epithelium then spread to liver and multiply in parenchymal cells
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which antibody responds first to HAV?
TQ: is there life-long immunity to HAV? |
TQ: IgM - largest, most efficient. then switches to IgG -giving *life long immunity*
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is HAV a zoonoses
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no, shellfish are intermediate hosts, use chimps as experiemental hosts
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does severity of HAV increase or decrease with age?
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increases: 75% of adult cases have jaundice
childhood infection tend to be anicteric (milder)- less jaundics cases |
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is mortality of HAV high or low
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low. 90% of pts recover fully w/in 3 months
5% have recurrence of milder dx, then recover |
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TQ: do people chronically carry HAV
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TQ: no, *no chronic carrier state* known. endemicity requires sporadic subclinical infection
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responsible for 25% of clinically apparent hepatitis worldwide
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HAV
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highest incidence of HAV found in which populations
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Amer. Indians, Alaskan natives, institutionalized children and in daycare
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in undeveloped countries when do people have anti HAV antibodies?
how by are seropositive by 50 yrs in developed countries? |
undevl. most have antibody by 10 yrs
devel. 50% seropostive by 50 yrs old |
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what's given in the passive immunization of HAV? is it long term or temporary
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Immune Serum Globulin, it's expensive and temporary but you won't become ill and doesn't interfere with natural immunization
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who's given the HAV vaccine?
is it active or inactive? |
inactivated formalin, universally recommended b/c it's less expensive.
Before it was given at 2 yrs, recommended for those at risk and living in states with high annual incidence (CA) |
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TQ: *HBV is also known as or causes what?*
how is it spread? |
TQ: *serum hepatitis*
spread from sexual contact (50%) or from blood transfusion |
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is HBV a zoonoses?
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no but it can infect chimps and gibbons - can't be cultured b/c cells don't retain wild type markers used for viral attachment
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RQ: Dane particle is associated with what virus?
how many layers does it have DNA or RNA |
RQ: HBV
two layers dsDNA |
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what is strange about the DNA of HBV?
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one of the strands is incomplete so that 15-50% is single stranded
has 4 genes DNA polymerase with reverse transcriptase activity |
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what antigens are associated with HBV?
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HBsAg = surface antigen (AKA Australia antigen)
HBcAG, HBeAg = core antigens |
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chronic carriers of HBV have a large excess of what antigen? - it's a source of HBV vaccine antigen
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HBsAg, a positive or prolonged presence indicative of carrier status and a way to diagnose
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how do you tell when a person + for HBV has a low risk of transmission?
when does it "arise" |
when anti-HBeAb is found in high amounts, "arises" during incubation
HBcAg and HBeAg are dimers |
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how long is the incubation of HBV?
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long: 6 weeks to 6 months (average is 10 weeks)
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what's going on in the proliferative phase of HBV?
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viral DNA in hepatocyte - actis as an episomal template (part of the chromosome) for complete virions but replication is inefficient, makes more empty capsids than comple virions
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what happens in hepatocytes infected by HBV that are not destroyed by the host's immune system?
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viral DNA may be integrated with host DNA, stops viral replication and liver damage
still have risk of hepatocellular carcinoma (Primary Liver Cancer) |
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which phase of HBV includes jaundice?
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icteric (preicteric, icteric, convalescent)
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symptoms of preicteric (prodromal) HBV
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malaise, lethargy, anorexia, nausea, vomiting, abdominal and upper right quandrant pain
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what might you find in an HBV patient in the icteric phase?
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bilirubinemia and bilirubinuria (dark urine) followed by jaundice
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HAV and HBV are dramatically differnt in that the convalescent stage may be protracted with malaise lasting for weeks, months, or in older folks-a year
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HBV - malaise lasting for weeks, months or longer
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the severity of HBV is affected by 3 things:
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1. portal of entry-needle most serious
2. infective dose (0.0001mL sufficient for disease) 3. intensity of host's CMI response (massive response produces more severe disease but assoc w/ lower carrier rate) |
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what are the 6 outcomes of HBV
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1. transient subclinical infection
2. acute hepatitis 3. fulminant hepatitis 4. healthy carrier 5. persistent infection 6. chronic active hepatitis |
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which HBV 'outcome' is fatal
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fulminant hepatitis
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are transient subclinical HBV infected people healthy carriers or non-infective
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they are not healthy carriers and are non-infective
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what antigen is found in HBV healthy carriers?
how often are they fully resolved? |
HBsAg
50% are resolved, others remain as asymptomatic carriers for life |
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do most persistant HBV infections resolve?
what can they develop into? |
extrahepatic disease (polyarteritis nodosum, glomerulonephritis)
Chronic active hepatitis (10-30%) |
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TQ: chronic active hepatitis from HBV can progress into..
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TQ: *cirrhosis* or *primary hepatocellular carcinoma (PHC)*
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TQ: when are most HBV infections acquired
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TQ: early in life: *perinatally* (not transplacentally)
{HBV- B for Birth} |
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TQ: how is HBV virus shed from healthy carriers
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TQ: semen, saliva, tears, breast milk (*not stool*)
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TQ: are many of those infected with HBV at birth become chronic carriers
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TQ: 95% - develop either chronic active hepatits, cirrhosis, or PHC
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what reduced the infection of HBV
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RIA blood screening
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TQ: how is HBV 'historically transmitted'?
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TQ: tatooing, piercing, venereally, *IV drug use*, *blood transfusions*
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TQ: how is HBV prevented?
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TQ: *Recombivax*~recombinant subtype vaccine - given to baby, can be given 12 hours after birth
~HBIG (hep B immunoglobulin) - given to mom or others that may have been exposed |
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is HCV RNA or DNA, ss or ds?
enveloped or not |
ssRNA
enveloped |
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what was HCV's former name
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NonA NonB
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TQ: which Hepatitis strain is most known for *post-transfusion hepatits (PTH) and IV drug use*
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TQ: Hepatitis C
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TQ: most frequent reason for liver transplant
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TQ: HCV (leading cause of liver disease in the Western world) {lame mneumonic: C as in Cut you open for a new liver, tell me you won't remember that!}
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TQ: what's a characteristic feature of HCV?
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TQ: *episodic elevation of liver enzymes/they're sometimes normal
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TQ: is jaundice with HCV more or less severe than HBV?
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TQ: less severe jaundice but more frequently leads to chronic active hepatitis--> *cirrhosis in 5-10 years*
~*HCV is also most frequent reason for liver transplant in the US* |
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TQ: what is done for the prevention or to cure HCV?
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TQ: no cure or prevention b/c the *virus is unstable* --many variants
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TQ: *high titers of what do not protect against subsequent infection or recurrent illness from endogenous strain?
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TQ: anti-HCV IgG
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TQ: HDV aka...
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TQ: Delta agent
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the capsid of HDV has which antigen
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HBsAg
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TQ: HDV is entirely dependent on what for its survival
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TQ: *HBV for reverse transcriptase
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TQ: when a person has a superinfection with HDV, what other disease is often included?
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TQ: HBV
TQ: HDV can only be transmitted from *host to host* that's what Johnny said was a test question |
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TQ: what could be the outcomes of HDV/HBV superinfection
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TQ: *self-limiting*, *high rate of chronic active hepatitis*, or severe hepatitis (high mortality)
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TQ: where is HDV commonly found?
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TQ: *{think D for desert} *africa, middle east, southern italy (also russia, romainia, parts of S. america)
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where is HBV commonly found?
TQ: is HDV found there also |
China and South east Asia
TQ: No, ironically HDV is not common there |
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who has HDV in the US?
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IV drug users (in NE) and hemophiliacs (from blood transfusions)
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is HEV DNA or RNA?
enveloped or not TQ: member of what taxonomic group? |
ss RNA
nonenveloped TQ: *Caliciviridae* {remember CALI: cal-E} |
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TQ: how is HEV spread?
TQ: who is most commonly affected? |
TQ: ~*fecal-oral, like *HAV {mneumonic:E, E, E for feeeecal. HAV: A: anus (assoc w/ fecal matter), TV channel A&E}
TQ: ~ *young adults most commonly affected* |
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TQ: what are some similiarities and a difference b/t HEV and HAV?
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similarities: fecal-oral, acute and often severe dx *w/out chronic sequelae*), uncommon in children
TQ: differences: *HEV high mortality rate among pregnant women*, *HEV uncommon in elderly* {don't worry.. about HEV.. if you're elderly. but oh no.. if you're prego} you're all going to ace this test with my rhyming skillz |
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why are STDs now called STIs?
can any come from animals/zoonoses? |
~b/c many are acute or asymptomatic
all are infectious ~no zoonoses |
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Herpes Simplex Virus-I (HSV-I)
4 conditions: |
herpes labialis
gingivostomatitis keratoconjunctivitis encephalitis and meningits |
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HSV-2
2 conditions: |
genital herpes
herpes neonatorum |
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do any STIs evoke permanent portective immunity?
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NO
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Herpes Virus:
DNA or RNA? enveloped or not? |
dsDNA
enveloped |
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TQ: is Herpes Virus prevalent?
does Herpes Virus persist in the host indefinitely? |
TQ: ~yes, very prevalent -almost everybody has become infected *familial transmission* but majority not symptomatic
~yes, you have the host indefinitely but it's typically latent. *recurrent symptoms associated with immunosuppressive therapy* |
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where does the HSV multiply?
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slowly in the nucleus of the host cell so it doesn't kill it
buds from nuclear membrane |
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TQ: how can you tell the area where HSV is replicating?
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TQ: *a histopathological lesion* - intranuclear inclusions idential (*Cowdry type A*) [i don't know what that means]
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what virus is most responsive to chemotherapy?
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herpes viruses- only for symptomatic relief
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TQ: how do primary infections of HSV present?
what are recurrences called? |
TQ: ~*often inapparent*- you can have it awhile before having symptoms
~*it's considered reactivation, not reinfection* (b/c you have it for life) |
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what is the portal of entry for HSV?
TQ: *where are virions shed from? |
~skin and mucus membranes-direct contact
TQ: ~virions shed in *saliva* |
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TQ: what the most common disease manisfestation caused by HSV-1?
when is it acquired? |
TQ: ~*herpes labialis - 70% of pop seropositive by 45 y/o
~acquired early in life |
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TQ: what manisfestation of HSV-1 is moslty seen in young children?
what are the symptoms? TQ: how does it present in young adults? |
~gingivostomatitis
TQ: ~children: fever, drooling, sore mouth (b/c of *pharyngeal erythema* and edema), mouth and gums covered with vesicles that rupture (*resemble chicken pox*) TQ: ~young adults: *pharyngitis* or tonsillitis (also occurs with genital herpes with orogenital contact) |
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TQ: what are complications AIDS patients might have if also infected with HSV-1?
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TQ: *esophagitis*-acute onset, painful, difficult swallowing, substernal pain
can get secondary candidiasis |
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TQ: where is HSV-1 retained for life?
how does it reappear? |
TQ: in sensory nerve root ganglia of the *trigeminal nerve* - stressors may reactivate disease --> cluster of vesicles around the mucocutaneious junction of the lips
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TQ: what manisfestation of HSV-1 can cause blindness?
how might you get it? |
TQ: keratoconjunctivitis- from autoinoculation (from yourself)
dendritic ulcer of cornea and conjunctiva -->scarring -->blindness (*most common cause of corneal damage and blindness in the industrialized world*) |
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what is the rare but fatal manisfestation of HSV-1?
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encephalitis and meningitis - currently the major cause of fatal sporadic encephalitis in US, survivors suffer permanent neurological damage
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TQ: what are some local symptoms of HSV-2?
TQ: what are some systemic symptoms? |
TQ: ~local: painful vesiculopustular lesions -burst and form *genital ulcers*; in females-discharge, itching, *inguinal lymphadenopathy*
TQ: ~systemic: fever, malaise, myalgias, *photophobia*, small amt may develop menigitis |
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TQ: *where is HSV-2 retained in your body?
*are recurrences more common with HSV-1 or 2 |
TQ: *lumbar and sacral sensory ganglia* {remember Dr. Dain's drawing of roman numeral two, II -->between the legs}
~*more common recurrences with HSV-2 but episodes are shorter and milder* *self-limiting* |
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primary infection may be subclinical but severe disease often occurs, esp in females
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HSV-2
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does HSV-2 cause cervical carcinoma?
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no, but there is a high association. may be a cofactor for development of cancers but is not likely to be a sole cause of it
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TQ: is herpes neonatorum passed transplacentally?
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TQ: no, herpes 2 *doesn't cross the placenta*
*greatest risk is when there's a primary maternal infection during labor* |
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TQ: what is the most common infection worldwide?
~what number Herpes virus is it? HHV_ |
TQ: Epstein-Barr Virus (aka Human Herpes Virus 4: *HHV4)* 90-95% of adults are seropositive
[chicken pox is HHV3] |
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TQ: ~*what do half of those infected with Epstein-Barr virus develop?
~*heterophile + or -? |
TQ: ~*infectious mononucleosis* (*aka glandular fever*)
~*heterophile + {mneumonic: going to the bar is a positive experience: Barr, hetero +} |
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how is Epstein-Barr virus spread?
is it contagious with "household contacts"? |
~oral contact, virus is in saliva and B cells (not in feces, urine or genital secretions)
~not very contagious with household contacts- the secret to its success is that only some people have symptoms and they shed the virus months after recovery |
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most common manifestation of Epstein-Barr virus infection?
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infectious mononucleosis (gladular fever)-initial development in lymphoid tissue of oropharynx (esp tonsils) hard to distinguish from other infections
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what is the target cell for Epstein-Barr virus resulting in infectious mononucleosis?
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B lymphocyte - the envelope glycoprotein attaches to CD 21 receptor on the B cell (polyclonal activation)
causes them to proliferate and make plasma cells and antibodies but not neccessarily the right ones- takes lots of energy (why pt is tired) |
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TQ: symptoms of infectious mononucleosis (EPV)
willl they have life long immunity to recurrence? |
TQ: -fever (104F or 40 C)
-convalescence, depression, don't want to overexert self -sore throat -enlarged lymph glands -*hepatosplenomegaly* (elevated enzyme levels (AST, ALT) *mimics viral hepatitis* ~most have life long immunity to recurrence |
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what is seen in immunosuppressed (impaired Tc cell activity) in someone with Epstein-Barr Virus?
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progressive lymphoproliferative disease
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who develops progressive lymphoproliferative disease from Epstein-Barr virus?
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-kids with primary immunodeficiency (SCID-severe combined immunodeficiency)
-transplant pts on cyclosporin A (drug that suppresses T cells) -AIDS pts |
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TQ: *E. Africa'*s most common childhood cancers -affects node in jaw
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TQ: *Burkitt's lymphoma* -associated with *Epstein-Barr virus*
the kids are immunosuppressed b/c of malaria |
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two cancers associated with Epstein-Barr virus
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~Burkitt's lymphoma-E. Africa, affecting nodes in jaw
~Nasopharyngeal Carcinoma (NPC)-most common cancer in certain parts of China, SE Asia, Africa and eskimos |
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aka Human Herpes Virus 5 (HHV5)
is it better to 'get this' as a child |
~cytomegalovirus- about 40% in US are seropositive, up to 100% in undeveloped countries
~usually subclinical if acquired during early childhood |
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what does cytomegalic inclusion disease (CID) resemble? {Boss will try to confuse you with SCIDS: associated with Epstein-Barr Virus/progressive lymphoproliferative dx}
TQ: symtoms of CID? |
~resembles *erythroblastosis foetalis*:Rh incompatible dx b/t mom and baby, but CID can't be "cured" with transfusions. *infant can shed virus for years
TQ:~*hepatosplenomegaly*, CNS abnormalities (hearing, IQ), *jaundice*, thromobcytopenia, petechiae, pneumonities (but only 10-20% infect manifest with some signs of disease) |
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TQ: what the major viral cause of congenital abnormalities?
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TQ: cytomegalovirus : causing cytomegalic inclusion disease (CID), infant can shed virus for years
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how can cytomegalovirus be spread?
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during delivery or from breast milk
mostly asymptomatic, possibly b/c infant acquired mom's antibodies |
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TQ: how are EBV mononucleosis and CMV mononucleosis different?
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TQ: EBV : *pharyngitis and lymphadenopathy. CMV-neither of those
CMV- *heterophile - (heterophile antibody is absent) {lame mneumonic CMV sounds like DMV, which is well known as being a negative experience DMV-->CMV heterophile -} EBV heterophile +{a Bar is a + positive experience} |
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how is cytomegalovirus shed?
is it spread for life? |
~in saliva: urine, semen, cervical secretions, breast milk, transplanted organs
~shed intermittently for life |
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TQ: how does risk of infecting unborn baby with cytomegalovirus increase?
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TQ: if mom has CMV before preganancy-baby has little chance of getting it
-big risk if mom gets mono whle pregnant, but most asymptomatic b/c *mom passes on antibodies* |
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TQ: how can CMV be passed on?
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TQ: *intrauterine* (transplacentally?), *perinatal* (during delivery, breast feeding), oral contact with fomites (esp in day cares), venereal, blood transfusion
{CMV- M- Mom's uterus & V- vagina} |
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most frequent cause of transfusion-acquired mononucleosis
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CMV cytomegalovirus
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is Human Papillomavirus (HPV)
DNA or RNA? enveloped or not? which taxonomic group? |
dsDNA, nonenveloped, Papovaviridae
certain types infect certain types of tissues-(papillomas or warts: common, flat, plantar anogenital and laryngeal papillomatosis) |
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TQ: second leading cause of cancer related death in women (after lung cancer)
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TQ: *Human Papillomavirus -->cervical cancer*
implicated in development of squamous cell dysplasias and carcinomas of the genital tract |
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TQ: how does cancer develop from HPV?
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TQ: ~infection of basal cells in strat. squamous epithelium - causes proliferation
~*Koilocytosis -a cytopathic effect: enlarged vacuolated cytoplasm with shrunken nuclei* |
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TQ: *condyloma acuminatum aka...
how does it grow? how does it metastasize? |
~* aka anogenital warts* from HPV {the only semi helpful way to remember it is to think of condyleeza rice, it's more helpful if you don't like the Bush administration} {keep this straight from condylomata lata- which if from syphilis}
~exophytic growth (grows outward) but also grows into myometrium ~can metastisize through lymph |
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TQ: which types of HPV are most common?
~*which accounts for most of the cancer cases?* |
TQ: HPV 16 and 18
*HPV 16 accounts for half of cancer cases* |
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TQ: typical form of anogenital warts:
*atypical form: treatment: |
~typical: soft, raised, fleshy, lesions (HPV 6, 10, 11, 40-45)
~atypical:flat (*HPV 16*, 18, 31) TQ: *associated with increased risk of cervical, penile and anal carcinoma* ~treatment:caustics, cauterization or surgical excision |
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TQ: most prevalent STI in the US
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TQ: HPV- but it's not tracked by the CDC
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TQ: prevention of HPV
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TQ: *vaccine against HPV 16*, inoculation of virus like particles, done prior to puberty
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leading cause of death in Africa and 4th leading cause of death worldwide
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AIDS/HIV
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is HIV
DNA or RNA? enveloped or not? taxonomic group? + or - sense |
~2 copies of ssRNA
~enveloped ~group D Lenitvirus- related to a group of nontransforming cytopathic retroviruses {vs transforming retroviruses that are cancer causing} ~ +sense |
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TQ: how is HIV transmitted?
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TQ: ~venereally
~IV drug use ~*blood transfusions* *Like HBV but HIV requires greater exposure b/c free infectioius virus is present in small quantities* ~*in utero* (transplacental?) and *perinatal* (*some in breast milk*) |
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TQ: highest risk group for HIV in US and worldwide...
*fastest growing risk group...* |
TQ: ~in US: homosexual/bisexual males with multiple partners
~worldwide:70-75% of infections acquired heterosexually *fastest growing risk group is female sex parteners of male IV drug users* |
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this transmission account for almost all childhood cases
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in utero and perinatal
-all infants of HIV+ moms have antibodies at birth but only 25-40% are infected with the virus |
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TQ: can HIV be passed on by casual contact, air-borne transmission and arthropod vectors (ie mosquitos)
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TQ: no ( HBV is also not tranmissable this way)
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what's the 'secret to HIVs success'?
is the incubation time variable? |
~antigenic diversity
~very variable 2-15 years (avg 5-8 years) depends on how well you can regenerate T Helper cells |
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TQ: what is the target cell for HIV?
what happens? |
TQ: ~targets cells with *CD4 receptors* (*T4 or helper lymphocytes*, certain *macrophages*, *monocytes* and *Langerhans cells*)
~viral envelope glycoprotein120-CD4 contact results in conformational change of glycoprotein so it can attach to CCR coreceptor which allows viral entry |
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how does HIV enter cell? (short answer)
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via receptor-mediated endocytosis or fusion - often involving syncytia or giant cell formation
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TQ: HIV replication kills what directly and indirectly?
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TQ: *T4 cells - indirectly via apoptosis
*doesn't kill macorphages and monocytes* but infects them early on-they're used as *vehicles for transport of HIV to lymph nodes and CNS*, they are resistant to cytolytic infection (esp isolated in CNS from immune effector cells) |
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why is there a higher incidence of Pneumocystis pneumonia in AIDS than in other immunosuppressed conditions?
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poor antigen presentation and defective chemotaxis in infected aleolar macrophage
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the secretion of what in AIDS patients explains chronic fevers?
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enhanced secretion of Interleukin-1, an endogenous pyrogen
Tumor Necrosis Factor Alpha-could explain the 'wasting' slimness see in Africa |
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TQ: where is the primary resevoir of infectious HIV?
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TQ: *in the lymph nodes* - where it's predominately found in the middle (chronic or latent phase) and they're mostly asymptomatic
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why is there such a considerable genomic diversity seen with HIV
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b/c of hypervariable regions of envelope glycoprotein- gradually changes HIV from M tropic to more T tropic agent
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TQ: in what stages is HIV most contagious?
~*in the chronic or latent phase, where does viral replication take place?* |
~in the early (acute) and final (crisis) stages. has highest viremia (detectable virus in the blood)
~*replication of virus is predominately in the lymphoid tissue* |
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when is a person said to have AIDS
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when CD4+ counts are below 200
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what is Kaposi's sarcoma associated with?
what is it? |
~HIV - a rare skin cancer, might be cause by a separate infectious agent (HHV8 or Kaposi sarcoma HV)
~proliferation of endothelial cells lining lymph channels |
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what is B cell lymphoma (non-Hodgkins) accociated with?
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~HIV- thought to be a comlication of Epstein-Barr infection
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TQ (matching):what is a common cause of death in early cases of HIV? (in about 60% of the cases)
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TQ: *Pneumocystis jiroveci (nee carinii) pneumonia (PCP)*
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TQ(matching): name of the systemic infection involving several organ systems in people with HIV?
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TQ: *toxoplasmosis*- causes encephalitis, responsible for half of mass lesions found in CNS
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TQ (matching):*most common fungal agent infecting AIDS patients
~(matching) *what causes chronic diarrhea in AIDS pts <1month |
TQ: *C. albicans or Candidiasis*
candidiasis- esophageal, tracheal or pulmonary *cryptosporidiosis* |
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TQ: can HSV-2 cause aseptic meningitis?
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TQ: yes, it's usually mild and self-limiting
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TQ: can HSV-2 cause aseptic meningitis?
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TQ: yes, it's usually mild and self-limiting
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TQ: what drugs can be used for Herpes viruses?
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TQ: chemotherapy drugs *Acyclovir* or Zovirax-for symptomatic relief only
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TQ: what is used to transcribe vRNA (of HIV) to cDNA?
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TQ: *enzymes: *reverse transcriptase
then the DNA is incorporated into the host's genome |
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TQ: heterophile + and - both lead to what infectious disease?
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TQ: infectious mononucleosis
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TQ: ~*interstitial cell pneumonia* and *chorioretinitis* is associated with what virus
~chorioretinitis is it also known as? |
TQ: ~assoc with CMV mononucleosis
~AKA *pizza pie retinitis* ~the person may also have hepatitis, arthritis and carditis |
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TQ: if a mother was infected with HSV-2 prior to her pregnancy, will the baby become infected?
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TQ: the greatest risk of infection at birth (intrapartum) is associated with active primary maternal infection {tricky Boss question, no clear answer, I think the baby won't be infected b/c at birth the mom would not still be in the active primary state}
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TQ: where is HEV commonly found?
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TQ: blood borne in *Asia, India, sub-Saharan Africa and Mexico*
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TQ: 80% of liver cancer among Asian Americans is due to...
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TQ: HBV
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TQ (matching): what three bacteria(?) are associated with AIDS and skin lesions?
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TQ: *Cryptococcosis, Histoplasmosis or Coccidioiodomycosis* - extrapulmonary and/or disseminated with skin lesions
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TQ (matching): in patients with AIDS, what age do you see disseminated *CMV*?
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TQ: >1 month old, commonly affects eyes (25% have chorioretinitis-pizza pie retinitis, 10% have GI lesions)
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TQ (matching):in patients with AIDS, what other virus might they have if they have persistent mucocutaneious ulcers or pulmonary infections?
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TQ: in patients >1month old with *HSV* and AIDS
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TQ (matching): leading cause of death worldwide among HIV + people
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TQ: ~TB
disseminated *mycobacteriosis*, cause by typical TB or atypical species (eg. MAI complex) |
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TQ: many AIDS pts have neurological symptoms caused by what?
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TQ: ~*AIDS encephalopathy or dementia complex*
~gliosis of cerebral cortex, necrosis or gray and white matter, demyelination of white matter ~may involve inflammation b/c of infected monocytes and macrophages |
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what's the treatment for people with HIV/AIDS?
what are the side effects |
~chemotherapy, a "cocktail" of AZT, ddi and protease inhibitors
reduces viral activity enough to be undetectable, increases T cell count ~neg. effects: diabetes, heart disease, vascular necrosis-->hip replacement |
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do we have drugs to cure viral diseases?
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NO, we only have vaccines to prevent infection. drugs don't cure you once you have the virus
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signs of hepatitis (A-G)
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malaise, jaundice, fever, increased liver enzymes
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compare the Australia antigen and the Dane antigen
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Australia: on the surface of the virus
Dane: the complete virus, consists of 2 concentric layers |
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which virus has oncogenic potential and is associated with cervical cancer?
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HSV-2, but doesn't neccessarily cause cervical cancer
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True or False: Epstein-Barr virus is largely asymptomatic in childhood.
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True
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what virus is associated with inguinal lymphodenopathy?
what virus is assoc w/ cervical lymphodenopathy? |
HSV-2 - inguinal
EBV - cervical |
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True or False: Epstein-Barr virus targets Tcells.
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False: targets B cells
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what are the target sites of infective mononucleosis?
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B lymphocytes
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cytomegalovirus is shed for life in...
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breast milk, saliva, urine, semen
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most prevalent STI in the US
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HPV - Human Papilloma Virus
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what harbors HIV?
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lymphocytes (monocytes) and macrophages
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which virus is associated with herpes labialis
|
HSV-1
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TQ: which virus is assoc. with pharyngeal erythema and edema
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TQ: HSV-1
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TQ:which virus is assoc with photophobia?
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TQ: HSV-2
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TQ: which virus is assoc with Burkitt's lymphoma?
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TQ: EBV
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which viruses are dsDNA?
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All herpes viruses: HSV-1 and 2, EBV, CMV, Varicella Zoster
HBV HPV |
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which virus is assoc with nasopharyngeal carcinoma
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EBV
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which herpes virus is spread sexually?
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HSV-2. the rest can be spread by kissing/saliva or mucus membranes
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which virus reporduces in the host cell nucleus?
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HSV-1
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which virus is assoc with gingivomastitis?
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HSV-1
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which virus is assoc with interstitial cell pneumonia?
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CMV
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which virus is assoc with keratoconjunctivitis?
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HSV-1
|
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which virus is assoc. with hepatosplenomegaly and jaundice?
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CMV
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95% of adults are seropositive for what virus?
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EBV
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which virus is associated with herpes neonatorum?
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HSV-2
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most common manisfestation of tertiary syphillis
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aortic aneurysm
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associated with condylomata lata
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syphilis (don't get confused with the condy--anogenital warts)
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TQ: world's leading cause of treatable blindness:
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TQ: *chlamydia-a chronic suppurative follicular keratoconjunctivitis*, lesions heal with scarring
{HSV-1 most common cause of corneal damage and blindness in industrialized world} |
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causes genital elephantiasis, rectal strictures, acute epididymus, PID
|
chlamydia- i didn't couldn't find acute epididymus but an old final review had this question twice
-gonorrhea also causes PID |
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True or False: infective mononucleosis can be caused by the same virus as Burkitt's carcinoma
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true: EBV
|
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True or False: with infective mononucleosis the circulating cell that's infected is the T lymphocyte.
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False: B lymphocyte
|
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True or False: the microscopic changes in the liver in infective mononucleosis resemble viral hepatitis
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True
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True or False when regarding infective mononucleosis: exposure during childhood often results in asymptomatic infection
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True
|
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True or False: the microscopic changes in the lymph nodes in a pt with infective mononucleosis resemble Hodgekin's Disease
|
False
|
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primary resevoir of this virus is in lymph nodes
|
HIV/AIDS
~may also be found in monocytes and macrophages |
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what is the hypothesis of why some people are not infected by HIV
|
they lack CCR5 receptor
or if they are heterozygous- slows the onset of AIDS |
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causative agents of Pelvic Inflammatory disease (PID)
|
Neisseria gonorheoeae
Chlamydia trachomatis |
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TQ: bacterial STI that's 'famous for having a short incubation time'
~*can it be spread by fomites?* |
TQ: gonorrhea: 2-7 days
*can be spread by fomites but it's rare* |
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TQ: True or False: gonorrhea is* tissue type specific*
|
True: hangs around mucosal surfaces lined by*transitional* or *columnar epithelium* (urethra, cervix, anal canal, throat, conjunctiva ) doesn't go into gonads
|
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what does this pertain to "attachment to microvilli by pili and multiplication evokes a chronic purulent inflammatory response"
|
gonorrhea- neutrophils predominate
diagnosis: finding lots of phagocytosed diplococci in gram-stained smears of the exudate |
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TQ: there's no protective immunity induced by gonorrhea and healing of gonorrhea involves scar, what's the importance?
|
TQ: repeated infection may lead to extensive scarring/fibrosis
*ORCHITIS* (shouldn't it be no orchitis b/c it doesn't involve the testis) |
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can scar tissue from gonorrhea impair fertility?
|
yes; but it's functional sterility, doesn't involve testis
|
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what does salpingitis mean?
what's causes it? what organs are not involved in women? |
~inflammed fallopian tubes- can progress and burst
~caused by gonorrhea ~doesn't involve uterus or ovaries |
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TQ: ectopic pregnancy, bacteremia, endocarditis, arthritis, infertility and sterility can all be cause by...
|
TQ: gonorrhea-->*PID pelvic inflammatory disease* *by Neisseria gonorrhea* and *Chlamydia trachomatis*
|
|
how do you diagnose gonorrhea?
|
men: smear
women (or if rectal or pharyngial infection): do a culture or lacroscopy |
|
TQ: what does chemoprophylactic eyedrops in newborns prevent?
|
TQ: *conjunctival infection* *opthalmia neonatorum*- gonorrhea infection
|
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TQ: second most commonly reported STD
|
TQ: *gonorrhea* (behind chlamydia)...herpes would be first but that's not reportable
|
|
factors contributing to spread of gonorrhea:
|
-human resevoirs can be asymptomatic
-penicillin resistant strains (absolute refractoriness PPNG strains (Penicillinase Producing N. gonorrhea) -birth control pills-create salutary environment, b/c of horomone shift? |
|
how is trachoma transmitted?
|
direct contact, fomites, and filth flies (mechanical vectors)
{chlamydia} |
|
TQ: most frequent form of chlamydial infection in US, *may be most common bacterial STI in the world*
|
TQ: chlamydial urethritis or cervicitis
-also causes 50% of *non-gonococcal urethritis (NGU)* -*chlamydia may be most common STI in world* |
|
compare the incubation time and duration of symptoms of gonorrhea and chlamydia
|
chlamydia: incubation time is longer, symptoms more prolonged (and hidden)
|
|
which STI is Teiter's syndrome the most severe complication in men
|
chlamydia: genital infection, polyarthritis, conjunctivitis
|
|
TQ: how can one acquire inclusion conjunctivitis?
|
TQ: newborns from *mom with chlamydial cervicitis*. baby can also get neonatal pneumonia {inClusion ConjunCtivitis: Chlamydia Cervicitis}
adults: contaminations with genital secretions or unchlorinated pools |
|
TQ: what is primarily found in tropics:
*begins as genital ulcer*, granulomatous and suppurative (pus) -->inflammation of inguinal lymph nodes-->*bubos* that drain. *genital elephantiasis* but most resolve w/out treatment |
TQ: *lymphogranuloma venereum* : from chlamydia trachomatis
|
|
TQ:~what STI is an intracellular parasite of columnar epithelial cells
~*does it resolve on it's own?* |
TQ: ~chlamydia
~*yes, self-limiting* |
|
TQ: which morphological form of chlamydia is the* infectious form*?
which is the *dividing form*? |
TQ: infectious: elementary body
dividing: reticulate body |
|
why is chlamydia rigid?
what does this mean it's resistant to? |
rigidity maintained by disulfide bonds so it's resistant to penicillin
|
|
TQ: why is syphilis known as *'the great imposter'*
*what's the causative agent?* |
it's often misdiagnosed as something else, b/c it occurs in so many areas- in blood vessels
*causative agent: treponema pallidum* |
|
how is syphilis transmitted?
|
most often by sexual intercourse, rarely transplacentally
it's never casually transmitted |
|
TQ: primarily an infectious of blood vessel walls
|
TQ: syphilis: *inflammation of blood vessel endothelium, blocks lumen causing obliterative endarteritis which underlies all damage seen*
repair involves scarring and *fibrosis* |
|
TQ: chancres (primary lesion)
cause: *when does it appear* *how does it heal?* |
TQ:syphilis
only 30% of males and 50% of females have them, otherwise they'll move onto secondary phase *appears b/t 10-90 days (avg 3 weeks) *heals spontaneously, self-limiting* |
|
TQ: -*condylomata lata*-around moist areas
-macular skin rashes commonly involving palms and soles -oral lesions that appear as white patches |
TQ: syphilis- *most infectious when chancres and condylomata latas are present* (*secondary phase*)
oral lesions look like candida |
|
in latent phase of syphilis, what might cause a chronic slowly developing damage
|
an endotoxin and DH (i don't know what that is)
|
|
TQ: *aortic aneurysm* and mesaortitis are associated with what stage of what STI
|
TQ: *tertiary stage of syphilis
mesaortitis is the dialation of the media of the vessel -->weakening |
|
TQ: *neurosyphilis may present as...
affects which part of CNS |
chronic meningitis, tabes dorsalis or general paralysis
~affects posterior roots and columns of spinal cord, atrophy of brain |
|
TQ: *gumma is associated with what STI?
what does it resemble? |
TQ: ~*syphilitic gumma*- lesions of liver, bones, testis or skin with rubbery necrotic center
~resembles granulomas of TB |
|
can syphilis be transmitted transplacentally?
|
yes- during second trimester
|
|
characteristic triad of congenital syphilis
|
1. interstitial keratits and choroiditis (saddle nose)
2. Hutchinson teeth (barrel incisors) 3. 8th cranial nerve deafness |
|
spirochete who's growth can be slowed by PPNG (penicillin producing N. gonorrhea).
associated with cocaine trafficking |
syphilis
|
|
this STI is dropping to new lows in most places, except San Fran. LA and Seattle
|
syphilis
|
|
can non-syphlitic treponematoses be transmitted transplacentally?
|
no
|
|
TQ: *Yawa (frambesia): agent
~*what resembles Yaws and what does it look like? |
TQ: ~t. (pallidium) pertenue: Non-syphlitic treponematoses: *strawberry lesion* (initial lesion called *mother yaw* (framboise)*
~bejel (endemic syphilis) -*primary and secondary lesions in oral cavity* |
|
TQ: causative agent of *chancroid* (soft chancre)
what does it look like? *where is it found in the world?* |
TQ: *haemophilus ducreyi* a bacteria
-red lesion, becomes pustular, ulcerates and has soft ragged edges, *found in tropics and subtropics* |
|
treatment for chancroid
|
antibiotics-clears all bacteria and lesions heal in 1-2 weeks
|
|
TQ: STI that is a *protozoan, has *flagellates*
|
TQ: *trichomoniasis : trichomonas vaginalis **it's eukaryotic**
irritates but doesn't penetrate mucosal surfaces |
|
TQ: *strawberry mucosa*
*seen in what stage only?* |
TQ: *trichomoniasis: small blisters on surfaces of urogenital tracts
*seen only in the trophozoites stage* |
|
TQ: heavy, greenish, thick, foul-smelling, foamy dishcarge in females
*typically asymptomatic in males* |
*trichomoniasis
*males are vectors* in this situation {men are tricky: trich-omoniasis} |
|
what predisposes one to a symptomatic infection of trichomoniasis?
|
loss of normal vaginal acidity (an increase of pH)
|
|
TQ: *often coexists with gonorrhea
|
TQ: *trichomoniasis
|
|
Are these Gram + or -
staph aureus clostridium listeria |
gram +
|
|
Are these gram + or -
E. coli salmonella shigella |
gram -
|
|
TQ: incubation time for HCV
|
TQ: 2-26 weeks (avg 6-12 weeks)
|
|
TQ: most common enterics in US
|
TQ: rotavirus, Norwalk virus and *E. coli*
|