Memorize - Microbiology

Front 1

Viral Hepatitis (What, Cause - RNA & DNA, Transmission route)

Back 1

1) An infection of the liver hepatocytes by viruses.
2) RNA: HAV, HCV, HDV, HEV, HGV
3) DNA: HBV
4) A & E = Fecal-oral route; BCD = BlooD, Blood to blood (Parenteral)

Front 2

Acute Viral Hepatitis (What, Cause, General dz course)

Back 2

1) Sudden illness w/ mild to severe course followed by complete resolution.
2) All of the hepatitis viruses.
3) General dz course (Variable incubation period):
....a. First: Systemic symptoms (fatigue, low-grade fever, muscle/joint aches, cough, runny nose, pharyngitis)
....b. ~2 Weeks: Often Jaundiced, Painful enlarged liver, Elevated liver-function enzymes

Front 3

Chronic Viral Hepatitis (What, Cause, General dz course)

Back 3

1) Prolonged course of active dz or silent asymptomatic infection.
2) HBV, HCV, and HDV.
3) Patient is often asymptomatic w/ only an enlarged tender liver & mildly elevated liver-function enzyme levels.

Front 4

Viral Hepatitis (Liver enzyme pattern, Dz progression)

Back 4

1) ALT & AST (Early change, High levels, ALT>AST); GGT, AP, & BR (Later change, Mildly elevated)
2) BR levels rise higher

Front 5

Cholelithiasis (Liver enzyme pattern, Dz progression)

Back 5

1) GGT, AP, & BR (High levels); ALT & AST (Mildly elevated)

Front 6

Hepatoctyes (Produce - enzymes)

Back 6

1) ALT & AST

Front 7

Bile canaliculi (Produce - enzymes, Carries)

Back 7

1) GGT & AP
2) Carries BR

Front 8

Hepatitis A Virus (Type, Family, Transmission, Incubation, Epidemiology)

Back 8

1) Naked icosahedral capsid w/ +ssRNA
2) Picornavirus
3) Fecal-to-oral route "HAVe you washed your hands???" (No Carriers)
4) Short incubation (3 Weeks)
5) 6000 cases reported a year and there are many more infections that are asymptomatic or unreported. 40% of people have serologic evidence of prior infection (Only 5% remember infection).

Front 9

Hepatitis A Virus (Vaccination, Etiology, Dx, Tx)

Back 9

1) Inactivated Hepatitis A vaccine; Routine pediatric vaccination since 2005, High risk adults (e.g. travelers)
2) Often mild course, often w/o jaundice or symptoms. A small percent, usually adults, will develop fulminant (severe) hepatitis. Death from HAV is very rare.
3) Acute Infection = Igm Anti-HAV; Old infection/Immune = IgG Anti-HAV; Incubation or no infection = No Anti-HAV Ig
4) If person is exposed, pooled immune serum globulin will prevent or decrease severity of infection if given during incubation period. Once infection is established, tx is only supportive.

Front 10

Hepatitis B Virus (Type, Family, Transmission, Incubation)

Back 10

1) Enveloped icosahedral capsid w/ ds circular DNA
2) Hepadnavirus
3) Parenteral, Sexual, & Maternal-fetal routes (Carriers)
....a. 90% transmission in mothers w/ HBeAg (10% w/o)
4) Long incubation (3 Months)

Front 11

Hepatitis B Virus (Mechanism of damage, Can cause, Complications)

Back 11

1. Cytotoxic T-cell damage --> Hepatocyte damage; Ab and HBsAg can for immune complexes and deposit in tissue -> Arthritis, Skin, and Kidney damage.
2) Can cause:
....a. Acute hepatitis
....b. Fulminant hepatitis - Severe acute hepatitis w/ rapid destruction of the liver.
....c. Chronic hepatitis
........1. Asymptomatic carrier - Never develops anti-HBsAg (Immunosuppresed states are more likely to fall into this group)
........2. Chronic-persistent hepatitis - Low-grade hepatitis
........3. Chronic active hepatitis - Acute hepatitis state that continue w/o normal recovery (> 6-12 months).
....d. Co-infection w/ HDV
3. Complications:
....a. Primary hepatocellular CA: HBV DNA becomes incorporated into hepatocyte DNA and trigger malignant growth.
....b. Cirrhosis: Permanent scarring and loss of hepatocytes.

Front 12

Hepatitis B Virus (Prevention/Vaccination, Etiology, Dx, Tx)

Back 12

1. Serologic test on donor blood
2. Active immunization: Recombinant vaccine. Gene for HBsAg is cloned in yeast and used to produce mas quantities of HBsAg used as the vaccine. Given to all infants (4 injections) and to adolescents and high-risk adults (3 injections)
3. Antiviral agents are used for tx of chronic active or persistent infection.
....a. Interferons (HBV DNA suppression and Seroconversion of HBeAg in 35%)
....b. Nucleoside analogs (Similar efffect, but need long-term or indefinite tx)
All therapies for HBV fail to eradicate HBV, so relapse of hepatitis is always a possibility.

Front 13

Hepatitis B Virus (Different forms/particles)

Back 13

1) Dane particle = Intact virus
2) HBsAg = Envelope + some disassociated capsid proteins; "Live virus and infection"
....a. anti-HBsAg = Protective; "Immune, Cure, No active Dz"
3) HBcAg = Viral core
....a. anti-HBcAg = Not protective; Tells us length of infection
........1. IgM = New Infection; IgG = Old Infection
4) HBeAg = Soluble cleavage product of the viral core; "Active Dz & Highly Infectious state"
....a. anti-HBeAg = Low infectivity

Front 14

Hepatitis D Virus (Type, Family, Transmission, Incubation, Epidemiology)

Back 14

1) Parenterally
2) Can only replicate w/ the help of HBV. "Hepatitis D is Defective and requires Hepatitis B as a Buddy"
....a. Uses HBV's envelope, HBSAg.
2) 2 Types of Infection:
....1. Co-infection w/ HBV -> Causes hepatitis similar to that of HBV alone. Anti-HBsAg will protect against both.
....2. Superinfection -> Results in acute hepatitis, which is more severe (higher rate of fulminant hepatitis, cirrhosis, and mortality). Patient's who are chronically infected w/ HBV cannot make anti-HBsAg, so remain chronically infected w/ both HBV & HDV.