Microbiology and Pathophysiology Flashcards
What causes hyperestrinism in cirrhosis? What are the signs?
Liver normally metabolizes circulating estrogens – damaged hepatocytes cannot break androstenedione down leading to increased estradiol levels
Signs:
- gynecomastia
- spider angiomata (telangiectasia with central red spot and outward extensions like a spider’s web)
- testicular atrophy
What is hepatic encephalopathy? Why does it occur? Treatment?
Cirrhosis/hepatic dysfunction and consequent shunting of blood through collateral circulation around the liver leads to build-up of ammonia (neuropsychiatric dysfunction)
- Ammonia created in GI tract by enterocytic catabolism (glutamine) and bacterial catabolism of protein in the colon
- Ammonia enters circulation and enters liver via portal vein to be detoxified to urea
- Impaired liver detoxification (cirrhosis, collateral circulation) leads to accumulation of ammonia in blood
Can be triggered by stressors (GI bleed, infection, renal failure) that either increase NH3 production or decrease NH3 removal.
Treatment:
- lactulose (breakdown by gut flora acidifies and creates NH4+ which is not absorbable – an ammonia trap!)
- rifaximin (kills GI bacteria, so less production)
Infant presents in first month with persistent jaundice, muscle rigidity, lethargy, seizures? Lab values?
Crigler-Najjar syndrome
absence of uridine glucuronyl transferase (UGT)
increased unconjugated bilirubin
(fat soluble and cannot be excreted, so deposits in brain – kernicterus)
What is the enzyme in hepatocytes that conjugates bilirubin? What is the result of mildly decreased activity? Severe deficiency?
Uridine glucuronyl transferase (UGT)
Gilbert syndrome = mildly decreased activity
asymptomatic or mild jaundice with increased UCB
Crigler-Najjar syndrome = absent UGT
very early presentation with jaundice, kernicterus, elevated UCB
20yo with jaundice and unconjugated bilirubinemia during periods of stress (fasting, exercise)?
Gilbert syndrome - mild unconjugated hyperbilirubinemia due to mild UGT deficiency
If alkaline phosphatase (ALP) is elevated, what enzyme should be tested next?
elevated ALP of unclear etiology should be followed up with gamma-glutamyl transpeptidase
ALP elevated in liver disease and in bone disease.
To clarify the importance of a moderately elevated ALP, the hepatic gamma-glutamyl transpeptidase (GGTP) should be evaluated.
GGTP is predominantly present in hepatocytes and biliary epithelia (also some in other tissues), but NOT in bone. Used to determine whether elevated ALP is of hepatic or bony origin.
Fulminant hepatitis with high mortality rate?
Hepatitis E
non-enveloped (fecal-oral transmission), RNA virus
What hepatitis B marker indicates high transmissibility/infectivity? Vertical transmission possible? Prevention?
HBeAg - envelope antigen (also lack of anti-HBeAg antibody)
soluble protein that is a marker of viral replication and increased infectivity
Vertical transmission from mother to child possible (high probability with HBeAg-positive mother)
all newborns of mothers with hepatitis B immune globulin (HBIG) followed by active HBV vaccine
What is chronic hepatitis risk for a newborn with HBV through vertical transmission? What are the histological findings?
HIGH risk of progression to chronic hepatitis in an infected infant
Histological findings show MILD liver injury because HBV is not inherently cytotoxic and the neonatal immune system is still immature.
What is the delta agent? What does it require in order to infect?
Hepatitis D virus
only capable of causing infection when encapsulated with HBsAg!!
What does HBsAg suggest? HBeAg? Anti-HBsAg? Anti-HBcAg IgM and IgG?
HBsAg: present during symptomatic acute Hepatitis and around in chronic
HBeAg: indicates active viral replication and infectivity
Anti-HBsAg: indicator of noninfectivity and immunity against HBV
Anti-HBcAg IgM: acute phase of disease!! most specific for acute HBV
AntiHBcAg IgG: recovery portion of HBV (resolved and chronic states(
At risk of what hepatitis with unprotected sex? Other means of transmission?
Hepatitis B (also Hepatitis D, which is dependent on HBV infection) FAR less commonly - Hepatitis C (spread by blood)
Parenteral (piercing of skin or mucus membranes – childbirth, semen, saliva, sweat, tears), sexual, maternal-fetal
Transmission of Hepatitis A? Presentation?
fecal-oral
also contaminated water or food (raw or steamed shellfish common)
- MOST OFTEN silent or subclinical (anicteric/no jaundice observed) in children
- but can also have acute onset with malaise, fatigue, anorexia, nausea, vomiting, mild abdominal pain, hepatomegaly
What does primaquine do in the treatment of malaria?
added to chloroquine in the treatment of Plasmodium vivax and Plasmodium ovale in order to eradicate hypnozoites, the intrahepatic stages of these species, which cause relapse.
Traveler returned from Africa with recurrent fevers, chills, sweating that occurs every 48hrs. Blood smear shows RBC inclusions.
Malaria from Plasmodium vivax or ovale
48 hour cycle / tertian malaria
fever on first and third days
