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S2B1: Infectious Disease > GI Infections 2: Infections of the esophagus, stomach, duodenum, and liver > Flashcards

GI Infections 2: Infections of the esophagus, stomach, duodenum, and liver Flashcards

1
Q

What is esophagitis?

How does this present?

What are three etiologies that can lead to esophagitis?

What are 5 infectious causes?

A

Esophagitis: inflammation of the esophagus

Tends to occur in immunocompromised

Presentation:

dysphagia (difficulty swallowing) and odynophagia (pain with swallowing)

(above unique to infectious)

heartburn, retrosternal pain, n/v, fever, sepsis, abd pain, epigastric pain, and cough

Etiology:

GERD

Medications

Infections

5 common infectious causes

  1. Candida albicans (most common)
  2. CMV cytomegalovirus
  3. HSV herpes simplex virus
  4. HIV human immunodeficiency virus
  5. VZV varicella zoster virus
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2
Q

Which populations are more likely to get infectious esophagitis?

Which populations have more tendencies toward certain infectious etiologies?

A

Epidemiology

Most common in immunocompromised

AIDS, leukemia/lymphoma, diabetes, alcoholism, motility disorders, radiation/chemo

less than 5% in general population

Pathogenesis

Candida most common for all

HIV (low CD4) - fungal

AIDS - CMV>HSV

Transplant pts - HSV early, CMV 2-6 months after transplant

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3
Q

How is esophagitis diagnosed?

How is each infectious cause diagnosed?

A

Diagnosis of Esophagitis

odynophagia - unique to infectious esophagitis

EGD and biopsy

Diagnosis of Candida

Usually also have thrush

creamy white/pale yellow plaque in esophagus with raw base

sample and look for yeast

Diagnosis of HSV

abrupt onset

early lesions - small vesicle mid/distal esophagus

later lesions - ulcers with raised edges (volcano)

Biopsy edge of lesions looking for (tzanck test) multinucleated giant cells

Culture, histology

Diagnosis of CMV

gradual onset

ONLY in I/C hosts

EGD biopsy to culture

large, solitary, shallow ulcer or multiple discrete lesions at distal esophagus

Diagnosis of HIV

multiple small thrush-like lesions

during primary HIV infection

later on with deep giant ulcers

fistula formation, perforation, hemorrhage, or superinfections can occur

Diagnosis of VZV

usually has skin lesions consistent with chickenpox or shingles

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4
Q

How is esophagitis treated?

How is esophagitis prevented?

A

Treatment

Antifungal (Candida) or antiviral (HSV, HIV, VZV, CMV) depending on cause

Some use steroids to lower inflammation

Prevention

Avoid immunosuppression

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5
Q

What are 2 diseases of the stomach and duodenum caused by Helicobacter pylori?

A

Chronic active gastritis and Peptic Ulcer Disease

Peptic ulcer disease can be divided into Gastric Ulcer Disease and Duodenal Ulcer Disease based on location.

H.pylori is the most common cause of chronic active gastritis and of peptic ulcer disease.

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6
Q

How can you differentiate symptoms of chronic active gastritis versus someone with CAG that is critically ill?

A

Manifestations of Chronic Active Gastritis

  • often asymptomatic
  • pain or discomfort in pit of stomach or left upper abdomen
  • pain travels from belly to back
  • burning, gnawing, sore, vague discomfort
  • belching without relief, n/v

Manifestations of critically ill patient with chronic active gastritis

  • pale and sweaty
  • tachycardia
  • severe illness: bleeding from stomach, lightheaded/syncope
  • vomit blood
  • bloody or dark sticky, foul smelling stools
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7
Q

Describe the manifestations of peptic ulcer disease.

How can you tell the difference between gastric ulcers and duodenal ulcers in symptoms?

A

Manifestations of Peptic Ulcer Disease

gnawing or burning epigastric pain

bleeding with anemia, weakness, and/or fatigue

hematemesis, melena, or hematochezia

(bleeding mixed in stool, not hemorrhoid)

Gastric ulcers

Worse with eating

Duodenal ulcers

Relief with eating or antacids

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8
Q

How many people world wide are infected with H.pylori?

What population is this more common in?

How common is it to develop chronic active gastritis? Is this more prevelant in males or females?

What blood type is more likely to develop PUD?

What age groups are more common in duodenal ulcers versus gastric ulcers?

What is the ratio of male to female individuals with PUD?

A

Epidemiology

50% of world infected with H.pylori

More common in older adults

20% infected develop chronic active gastritis (1:1 male to female)

Peptic ulcers are very common and result in many hospitalizations

More likely in type O blood groups

duodenal ulcers - 25-75yrs more common

Gastric ulcers 55-65yrs more common

PUD with 2:1 male to female ratio

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9
Q

What are some long term consequences of H. pylori infection?

How is this transmitted?

A

Long-term infection can cause gastric adenocarcinoma or lymphoma

Transmitted person to person

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10
Q

What virulence factors contribute to the pathogenesis of H.pylori?

A

Virulence factors

Corkscrew motility - penetrate

pH sensing - directs to source of acid

urease - raises pH to survive

vac A toxin - vaculation and death of epithelium

cagA gene - affects host cell causing death and damage

Inflammation

Cytokines - reduce stomatostatin and increase gastrin levels causing more acid in the general area causing further damage

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11
Q

How is H.pylori infections diagnosed?

How is H.pylori infection established?

A

Diagnosis

Clinically - common signs and symptoms

Establish H.pylori infection

serological test - more false positives

C13 labeled urea test - broken down by urease resulting in radioactive CO2 release

endoscopy and biopsy

Stool EIA antigen test

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12
Q

What is fecal-borne viral hepatitis and the two etiologic agents that cause it?

A

Viral Hepatitis

Fecal-borne, a serious inflammatory disease of the liver associated with poor sanitation and is most common in developing countries

Etiologic Agents

Hepatitis A (HAV) and Hepatitis E (HEV) - single stranded RNA viruses

HEV is not endemic to US

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13
Q

What is the incubation period of fecal-borne viral hepatitis?

What percentage of adults and children are asymptomatic?

What are initial symptoms of viral hepatitis?

What are the classic symptoms of viral hepatitis?

A

Incubation: 14-45 days

84-94% of children are asymptomatic

5-25% of adults are asymptomatic, 66% have jaundice, common distaste for cigarettes

No chronic hepatitis with this

Initial symptoms

fever, malaise, fatigue, headache

Anorexia, n/v, RUQ pain, hepatosplenomegaly

Classic Symptoms

cholestasis - bile back up

icterus, jaundice, dark urine, clay-colored stools

Elevated AST, ALT, and bilirubin

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14
Q

Who are the natural hosts of fecal-borne viral hepatitis

What age group has the highest incidence of viral hepatitis? What living conditions increase incidence?

Which cause of viral hepatitis is not in the US?

When does viral shedding occur in the case of HAV?

What are the mortality rates of the two etiologies of viral hepatitis? What increases you mortality rate?

A

Natural hosts - humans and lower primates

highest incidence of infection in 25-39 year olds

HAV and HEV incidence higher in crowded living conditions

HEV not in US

No chronic carrier state

HAV shed virus 10 days before symptoms begin

HAV low mortality rate

HEV mortality rate (1-2%, 10x higher than HAV) even higher HEV fatality rate if pregnant (20%)

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15
Q

How is HAV and HEV transmitted?

What are common routes of transmission in the U.S.?

A

Person to person, fecal-oral route

HAV infection

  • raw/undercooked shellfish
  • daycare: diaper changes get rowdy, children are gross
  • poor sanitation
  • travel
  • MSM: fecal-oral transmission, any anal penetration
  • healthcare institutions
  • food service
  • illicit drug use
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16
Q

Describe the pathogenesis of fecal-borne viral hepatitis.

A

infects cells lining the oropharynx and intestines

viremia

infects liver from the blood

virus released into bile and shed in stools

usually self-limiting disease

17
Q

How is HAV and HEV diagnosed?

How is it treated?

How is it prevented?

A

Diagnosis

Classic symptoms:

EIA for IgM and IgG for HAV

+ for IgM = acute HAV

+ for IgG = previous HAV infection or vaccinated

Treatment

Supportive treatment and rest

Prevention

Vaccine for all children over 12 months - killed viral vaccine

Immunoglobulin given within 2 weeks of infections lessens severity

Passive immunization - human immune serum globulin (travelers)

18
Q

Which etiologies of viral hepatitis are blood borne?

A

Hepatitis B: partially dsDNA virus

Hepatitis C: ssRNA virus

Hepatitis D: ssRNA viroid

19
Q

What is the incubation period like with HBV versus HCV?

How likely is a patient to be asymptomatic?

What 2 things make an individual more likely to develop chronic infections?

A

Longer incubation period for HBV than HCV: 7-160 days

Many asymptomatic (children are more likely)

More likely to develop chronic infections if 1) asymptomatic on primary infection 2) infection with HCV vs B

20
Q

Who is more likely to be asymptomatic when infected with viral blood-borne hepatitis? What risk does this increase?

Describe the symptoms of acute blood-borne viral hepatitis infection.

Describe the later symptoms.

What is fulminant hepatitis? What infections increase the liklihood of this? What symptoms are associated?

What etiological agents are more common to cause chronic hepatitis? What other liver problems does this increas liklihood of?

A

Asymptomatic:

more likely in newborns and children, but also more likely to develop chronic hepatitis

Acute infection:

similar to fecal-borne
(fever, malaise, fatigue, HA, anorexia, n/v, RUQ abd pain, hepatosplenomegaly)

Later symptoms:

can be more severe than HAV infections (cholestasis)

Fulminant hepatitis (1% of patients)

more likely if HBV and HDV(wimpy) have infected the patient

severe liver damage; ascites and bleeding

liver shrinks rather than hepatomegaly

Chronic Hepatitis:

more common in HCV than HBV

10% of chronic hepatitis suffer liver cirrhosis and failure

If HDV superinfection of chronic HBV occurs fulminant or severe hepatitis is more likely

21
Q

Which etiological agent is associated with 80% of liver carcinoma cases?

What other hepatitis virus can cause liver carcinoma?

A

HBV is associated with primry hepatocellular carcinoma

HCV infections can also cause liver carcinoma

22
Q

How frequently do Hepatitis B infections become chronic?

What complications do chronic Hepatitis B typically come with?

How is this transmitted?

A

Hepatitis B

Cases have gone down

Few HBV infections become chronic (0.1-0.5%)

15-40% of chronic develop cirrhosis, liver failure of hepatocellular carcinoma (HCC)

20% of people with HCC have chronic HBV

Transmission

contact with HBV infected body fluids (blood, saliva, semen, vaginal secretions, breast milk)

Most commonly - sexual contact

Percutanous routes

Perinatal contact

Later contraction is better - less likely chronic

23
Q

How many cases of Hepatitis C are symptomatic?

How many HCV cases become chronic?

What complications does Hepatitis C frequently cause?

How is Hepatitis C transmitted?

A

Hepatitis C

Only 25-30% of cases are symptomatic

Many infected, mostly old because transfusions weren’t safe

>85% of HCV becomes chronic

Chronic liver disease in 70% of infected persons

Leading infectious indication for liver transplant

Transmission

most common - percutaneous
(IV drug use, transfusion, hemodialysis, renal transplant)

Perinatal

Sexual transmission - very low

24
Q

How is Hepatitis D transmitted?

A

Hepatitis D

Coinfection with HBV or superinfection of patients with chronic HBV

More likely to have severe liver disease

Transmission

percutaneous (IV drug users)

25
Q

How are blood-borne viral hepatitis infections diagnosed?

A

Diagnosis

Initial:
signs of cholestasis, altered liver enzymes, bilirubin, and alkphos, AST/ALT elevated

Acute Disease HCV:
RNA tests positive, serology negative. If RNA and serological tests are positive it is tough to know if acute or chronic

HDV:
Serology

HBV:

  • *HBsAg** detect HBV antigen
  • *Anti-HBs** and Anti-HBc detect antibodies to HBV antigens
26
Q

What three tests do you order when you suspect Hepatitis B?

What do they tell us?

A

Hepatitis B

Three tests to order

  1. HBsAg (Hepatitis B surface Antigen) - marker for virus circulating in blood stream
  2. Anti-HBs (Antibody to surface antigen) - typically not detectable at first because bound to virus, if detected means the individual will not develop chronic because they can get rid of it
  3. Anti-HBc (Antibody to core antigen) - does not bind to virus and get rid of it
27
Q

Again: what labs do you order when you expect Hepatitis B infection?

What lab findings would you expect for acute HBV Hepatitis during each phase of infection? What are these lab findings telling you?

How would lab values change based on vaccination?

A

Acute HBV Hepatitis

Assay for 2 things

HBsAg - HBV antigen assay

Anti-HBs and Anti-HBc - antibodies to HBV

Acute:
+ HBsAg (circulating virus) and Anti-HBc IgM

Window:
+ Anti-HBc IgM
There is no surface antigen or antibody to the surface antigen because they are binding each other and removing from serum

Early Convalescence:
+ Anti-HBs and Anti-HBc IgG
Antibodies to surface antigens are a good sign because there are more antibodies than antigens

Late convalescence:
+ Anti-HBc IgG
IgG antibodies to the core antigen indicates past infection and confirms not vaccination. BECAUSE a vaccination would use the surface antigen.

28
Q

Describe the serological results you would expect with chronic HBV infection.

Chronic persistent infection?

Chronic active infection?

A

Serological course of chronic Hepatitis B infection

You don’t see any antibody to surface antigen (Anti-HBs), but you do see surface antigen(HBsAg) stay because they aren’t being cleared

Chronic: HBsAg positive for 6 months

Chronic persistent:
+ HBsAg, Anti-HBc IgG, Anti-HBe(Antibody to hepatitis B envelope)
Less likely to be as severe as active

Chronic active:
+HBsAg, Anti-HBc IgG, HBeAg (envelope)
More severe than persistant

29
Q

How do you treat blood-borne hepatitis infections?

How can you prevent blood-borne hepatitis infections?

A

Treatment

Acute Hepatitis - supportive care

Chronic HBV - see pharm

Chronic HCV - see pharm (depends on pt and HCV genotype)

Prevention

Give hepatitis B vaccine to prevent both HBV and HDV

30
Q
A

S2B1: Infectious Disease (3 decks)

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