MOD 7 Flashcards
liver inflammation
Hepatitis
viral hepatitis lasting < 6 months
ACUTE VIRAL HEPATITIS
Viral Hepatitis A and E
Acute
Viral Hepatitis B and D
Acute &
Chronic
Viral Hepatitis C
Chronic
Most Common Viral
Hepatitis Worldwide
Hepatitis A Virus
does HEPATITIS A VIRUS have Acute Symptoms ONLY, true or false?
true
HEPATITS E VIRUS
Very Similar to Hep A; But HIGH
MORTALITY in PREGNANCY
pathogenesis of hepatitis E virus
Virus is Directly Cytopathic to the Liver
transmission via parenteral route or
equivalent
Hepatitis B Virus
occurs during 3rd trimester or early
post-partum
vertical transmission
HBsAg +ve, HBeAg +ve mothers
90% of infants affected
HBsAg +ve, anti-HBe +ve mothers
10-15% affected
Surface Antigen
HBsAg
E antigen (a component of HBV
core); marker of viral replication
HBeAg
Core Antigen( cannot be meassured in serum )
HBcAg
Both HBsAg and HBeAg
are present during acute hepatitis B
Anti-HBs follows HBsAg clearance
and confers long term immunity
Anti-HBe and anti-HBc appear during the
acute and chronic phases of the illness
but do not provide immunity
Transmission is chiefly parenteral
Hepatitis C Virus
most
common cause of post-transfusion
hepatitis
HCV
infectious only in the presence of HBV
because HBV surface antigens are required
for replication
Hepatitis D Virus
2 patterns of transmission
of HDV
o nonparenteral transmission by close
personal contact in endemic areas
(Mediterranean)
o transmission by blood products in
non-endemic areas (IV drugs, blood
transfusions)
Types of infection of HDV
o coinfection: simultaneous HBV and
HDV infection
o superinfection: appears as clinical
exacerbation in a chronic HBV
patient
- fecal-oral transmission occurring in
epidemics in Asia, Africa, Central America - most have mild disease, but in 3rd trimester
of pregnancy 10-20% have fulminant liver
failure
Hepatitis E Virus
metabolized by hepatic cytochrome P450
system
Acetaminophen
Cholestasis in 1% after 4 weeks; often with
fever, rash, jaundice, pruritus and
eosinophilia
Chlorpromazine
20% develop elevated transaminases but <
1% develop clinically significant disease
- susceptibility to injury increases with age
INH
May rarely cause cirrhosis, especially in the
presence of obesity, diabetes, alcoholism
- Scarring develops without symptoms or
changes in liver enzymes, therefore biopsy
may be needed in long-term treatment
Methotrexate
can cause same histology and clinical
outcome as alcoholic hepatitis
Amiodarone
Imbalance of cholesterol and its solubilizing
agents, bile salts and lecithin concentrations
Cholelithiasis
(80%) = mixed (> 70%
cholesterol by weight), radiolucent
o risk factors
▪ female, fat, fertile, forties
▪ North American First Nations
peoples have highest
incidence
▪ diabetes mellitus (DM),
pancreatitis
▪ malabsorption, terminal ileal
resection or disease (e.g.
inflammatory bowel diseases
Cholesterol
(20%), may be radioopaque
pigment stones
composed of unconjugated
bilirubin, calcium, bile acids
smooth green/black to brown pigment stones
associated with cirrhosis,
chronic hemolytic states
black pigment stones
associated with bile
stasis, (biliary
strictures, dilatation
and biliary infection
(Clonorchis sinensis)
calcium bilirubinate stones
- Inflammation of gallbladder resulting from
sustained obstruction of cystic duct by
gallstone (80%) - No cholelithiasis in 20% (acalculous)
acute cholecystitis
sudden cessation of
inspiration with deep RUQ
palpation
Murphy’s Sign
Inflammation of the Stomach Lining
Gastritis
Most common bacteria in chronic gastritis
Helicobacter Pylori
(Most Common)
- inc. Attack (Hyperacidity, Zollinger Ellison
Syndrome) Or - dec Defense (**H.Pylori, Stress, Drugs
[NSAIDs & Corticosteroids], Smoking)
peptic ulcer disease
Autodigestion of Pancreas > Reversible
Inflammation > +/- Necrosis
- Can lead to Systemic Inflammatory
Response Syndrome
o > Shock
o > Acute Renal Failure
o > Acute Respiratory Distress
Syndrome
acute pancreatis
Etiology of pancreatis
50% - Gallstones (Cholelithiasis) >
Ampulla/Common Bile Duct Obstruction
- 40% - Alcohol Abuse
- 10% Infections/Metabolic
o Produces Toxins:
o Travelers Diarrhea
Enterotoxigenic E. coli
o Active Intestinal
Invasion/Destruction
o Traveller͛s Dysentery
Enteroinvasive E. coli
Sporadic disease in babies and
children
Enteropathogenic E. coli
The Serious One:
o Produce Verotoxin > Destroys
Platelets & RBCs > HEMOLYTICUREMIC SYNDROME > Kidney Failure
+ Bleeding + Dysentery
Entero-Hemorrhagic E. coli
-food poisoning
Onset Within 4hrs
o *Vomiting, *Stomach Cramps,
Diarrhea
TOXIGENIC DIARRHEA
Pathogenesis:
- > Dysentery
- Can cause Septicemia
- Also, Fever - rose spots - delirium -
perforation of bowel
SALMONELLA; TYPHOID͟
bacteria in poor food handling
staph aureus
bacteria in cereal
Bacillus Cereus
Risk to Pregnant Women & Immunocompromised
Listeriosis
Profuse Rice-Water Stools
CHOLERA
Adult Diarrhea
Norovirus (80%)
Diarrhea in children <3 years old
rotavirus
transmission of cholera
oral-fecal transmission
The passage of infrequent or hard stools
with straining
Constipation
Fecal-Oral - (Ingestion of Dormant Cysts in
Contaminated Food/Water)
PARASITIC GUT INFECTIONS
(Protozoa & Helminths)
Not Toxigenic; Rather, it covers the brush
border > Malabsorption
Giardia
Ingestion of oocysts (Contaminated
Drinking Water/Public Pools)
- Can survive Chlorination
CRYPTOSPORIDIUM
Ingestion of oocysts (Fecal Oral)
ENTAMOEBA HISTOLYTICA
(The Amoebic Dysentery)
clinically significant helminths are “soil
transmitted”
HELMINTHIC INFECTIONS
Infection via swallowing infected eggs
a. Ascaris lumbricoides (roundworm)
b. Trichuris trichiura (whipworm)
Infection via Active skin penetration
a. Strongyloides stercoralis (threadworm)
b. Ancylostoma duodenale (hookworm)
