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Pathology Q5 > GI diseases > Flashcards

GI diseases Flashcards

1
Q

Hepatitis A

A

1) HAV spreads by ingestion of contaminated
water or foods
– Fecal-oral contamination
2) small, nonenveloped, positive strand RNA virus
- can replicate in host cell
3) genus: hepatovirus
4) benign, self-limited disease
5) incubation of 2-6 weeks
- causes jaundice

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2
Q

what is common between all hepatitis viruses

A

1) cause disease in the liver
2) All of the hepatotropic viruses can cause acute
asymptomatic or symptomatic infection
- HAV and HEV do not cause chronic hepatitis in
the immune competent host!!!
- Only a small number of HBV-infected adult
patients develop chronic hepatitis
-* HCV is notorious for chronic infection (But can
be cured!)*

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3
Q

hepatitis A causes

A

1) DOESNT cause chronic hepatitis
2) fatality is 0.1-0.3%
3) clinical findings
- fatigue and loss of appetite
- jaundice
4) serological diagnosis
- recent infection: IgM antibody
- previous infection: IgG

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4
Q

hepatitis A contraction

A

1) consumption of raw oyster from seawater contaminated with human sewage
2) aka fecal oral

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5
Q

hepatitis B

A

1)Hepatitis B Virus (HBV)
– Member: Hepadnaviridae
- a family of DNA
viruses
2) One third of the world population has been
infected
- Spreads through minor breaks in the skin or
mucous membranes, unprotected sex,
intravenous drug abuse and from mother to child
3) Incubation period of 2 to 26 weeks

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6
Q

hepatitis B causes

A

1) acute hepatitis
2) non progressive chronic hepatitis
Progressive chronic disease ending in cirrhosis
3) Acute hepatic failure with massive liver necrosis
4) An asymptomatic healthy “carrier” state
HBV-induced chronic liver disease is a
precursor of hepatocellular carcinoma

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7
Q

hepatitis B symptoms

A

1) 65% of adults acquiring HBV have mild or no
symptoms
- Remaining 25% have nonspecific
constitutional symptoms of anorexia, fever,
jaundice and upper right quadrant pain
3) Chronic disease occurs in 5-10% of infected
patients
- Fulminant hepatitis is rare

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8
Q

hepatitis B transmission

A

1) Virus can be transmitted by both acutely or
chronically infected patients (including
asymptomatic carriers)
2) Vaccine is available
– Offered to individuals at risk of exposure
– Protection for up to ten years
– Three doses at 0, 1 and 6 months
– Seroconversion is confirmed by blood testing

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9
Q

hepatitis B diagnosis

A

1) Hepatitis B surface antigen (HBsAg)
- Indicates acute or chronic infection and carrier state
2) Hepatitis B surface antibody (Anti-HBs)
- Indicates past, resolved HBV infection
- It may persist for life, conferring protection
3) Hepatitis B e antigen (HBeAg)
- It signifies active viral replication
- Persistence is an important indicator of continued viral replication, infectivity, and
probable progression to chronic hepatitis
4) Hepatitis B core IgM antibody (IgM anti-HBc)
- Indicates recent infection
- It is concurrent with the onset of serum aminotransferase levels (indicative of
hepatocyte destruction)

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10
Q

acute disease

A

1) e antigen, surface antigen, and hepatitis B DNA will go down
2) virus is cleared
3) but the antibodies remain

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11
Q

chronic disease

A

1) the virus itself is still present

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12
Q

our patient had an acute infection with HBV
virus one year ago. If you would like to check if
the patient developed chronic hepatitis, which
of the following exams would you order now?

A

A. HBsAg
B. IgM anti-HBc
C. Anti-HBs
D. HBeAg
E. Anti-HBc

of course, test for antigen, but all could be appropriate in order to check if they are developing the ABs too

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13
Q

age of infection is best predictor of chronicity

A

1) younger is more likely to develop chronic
2) cure of HBV is diffucult
- inserts into host DNA
- limits active immune response
3) goals of treatment
- slow disease
- reduce liver damage
- prevent cirrhosis or liver cancer

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14
Q

hepatitis C

A

1) Major cause of liver disease worldwide
– 170 million people affected
– 3.6 million Americans
2) Small, single-stranded RNA virus, member of Flaviviridae
family
3) Transmission by blood transfusion, organ
transplantation, intravenous drug abuse and parenteral/
mucocutaneous exposure to blood or secretions
4) No vaccine is available
5) Incubation period of 4 to 26 weeks

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15
Q

hepatitis C progression

A

1) In 85% of the patients’ clinical course of the acute infection is
asymptomatic
- Chronic disease occurs in the majority of patients (80-90%)
– Cirrhosis eventually occurs in 20% of patients

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16
Q

hepatitis c serologic diagnosis

A

Serologic diagnosis:
– HCV RNA
- Detectable in blood for 1 to 3 weeks coincident with elevation in serum transaminases
In chronic disease, HCV RNA and serum aminotransferases levels persist
– Anti-HCV antibodies
- Detected in only 50 to 70% of patients with acute infection
- It may emerge only after 3 to 6 weeks
– Any individual with detectable HCV RNA in the serum needs close clinical
follow-up

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17
Q

Which of the following test results would be
diagnostic of chronic hepatitis C?

A

A. Elevated anti-HCV and low serum
transaminases
B. Elevated HCV RNA and serum transaminases
only for a period of 1-3 weeks
C. Non-detectable levels of both anti-HCV and
HCV RNA
D. Persistence of HCV RNA and serum
transaminases levels for months to years

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18
Q

hepatitis C cure

A
  • It is potentially curable
  • Direct acting antivirals (DAAs) are 90%
    effective in clearing HepC
  • Sofosbuvir/Ledipasvir (Harvoni)
  • Sofosbuvir/Velpatasvir (Epclusa)
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19
Q

hepatitis D

A
  • Single-stranded RNA virus
    ** Incomplete virus which requires HBV for its
    own capacity to infect and replicate
  • In western countries is restricted to
    intravenous drug abusers and patients who
    had multiple blood transfusions
  • It makes the clinical presentation of HBV more
    severe*
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20
Q

hepatitis D diagnosis

A

Serologic Diagnosis:
– HDV RNA
* Detectable in the blood and liver just before and in the
early days of acute symptomatic disease
– IgM anti-HDV
* Reliable indicator of recent HDV exposure
– Chronic delta hepatitis
* HBsAg and anti-HDV antibodies
* Vaccination for HBV also prevents HDV infection
Hepatitis D

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21
Q

hepatitis E

A

Positive-stranded RNA virus, Hepevirus genus
* Similar to HAV infection
* Common in the Third World
* Zoonotic disease (animal reservoirs)
* Water-borne infection (fecal-oral transmission)
* Young to middle aged adults
* High mortality rate among pregnant women
* Chronic disease in patients with AIDS or immunosuppressed transplant patients

22
Q

hepatitis E diagnosis

A

– HEV RNA and HEV virions
Detected by PCR in stool and serum before onset of
clinical illness
– IgM anti-HEV
Elevated during clinical illness and simultaneous with
serum aminotransferases
– IgG anti-HEV antibodies
Replace IgM antibodies after resolution of symptoms

23
Q

summary

A

1) The vowels (hepatitis A and E) never cause chronic hepatitis,
except HEV in immunocompromised and pregnant females
- Only the consonants (hepatitis B, C, D) have the potential to
cause “chronic” disease
- Hepatitis C is the single virus that is more often chronic than
not
- Hepatitis D, is a “defective” virus, requiring hepatitis B co-
infection for its own capacity to infect and replicate
- Hepatitis E is “endemic” in equatorial regions and frequently
epidemic

24
Q

clinico-pathologic syndromes of viral hepatitis

A
  1. Acute asymptomatic infection with recovery
  2. Acute symptomatic hepatitis with recovery
  3. Chronic hepatitis with or without progression to
    cirrhosis
  4. Acute liver failure with massive hepatic necrosis
    Acute symptomatic infection with recovery
  5. The disease can be divided into 4 phases
    – An incubation period
    – A symptomatic preicteric (pre-jaundice) phase
    – A symptomatic icteric (jaundice) phase
    – Convalescence
  6. Peak infectivity:
    – *Last asymptomatic days of the incubation period and the early
    days of acute symptoms
  7. It usually presents with jaundice
    *
25
Q

usually you do not get tested

A

unless serum aminotransferase is elevated and shown in bloodwork, OR syndromes or viral hepatitis

26
Q

chronic hepatitis syndromes

A
  1. Symptomatic, biochemical, or serologic evidence of
    continuing or relapsing hepatic disease for more than 6
    months
  2. Clinical findings:
    – Persistent elevation of serum transaminases
    – Prolongation of the prothrombin time, hyperglobulinemia,
    hyperbilirubinemia and mild elevations in alkaline phosphatase
    levels
    – Symptomatic patients: fatigue, malaise, loss of appetite, and
    occasional bouts of mild jaundice
    – Physical findings: mild hepatomegaly, hepatic tenderness and mild
    splenomegaly
27
Q

acute liver failure syndromes

A

– Liver transplantation may be the only option
– Viral hepatitis is responsible for about 10% of cases of
acute hepatic failure
– Globally Hepatitis A and E are the most common
causes
– Survival for more than a week may permit the
replication of residual hepatocytes
–* Recovery depends on surviving hepatocytes
undergoing cell division to restore missing parenchyma
– Liver transplantation may be the only option*

28
Q

histological features

A

1) hepatocyte injury can result in necrosis or apoptosis
- become eosinophilic
2) acute viral
- portal inflammation is minimal
- parenchymal injury is scattered
3) chronic viral
- scarring
- bands of dense scar extend between portal tracts
- cirrhosis
- mononuclear cell portal infiltration
- “ground glass” hepatocytes (hep B)
- lymphoid aggregates or follicles, superimposed FLD, bile duct injury (Hep C)

29
Q

Patients with long-standing HBV or HCV related
cirrhosis are at increased risk for

A

the development
of hepatocellular carcinoma

30
Q

liver failure

A

The most severe clinical consequence of liver disease
It may be the result of sudden and massive hepatic
destruction (acute liver failure)
Or, more often, chronic liver failure, which follows
upon years or decades of insidious progressive liver
injury
- 80-90% of hepatic functional activity must be lost
before hepatic failure ensues

31
Q

acute liver failure

A

1) Acute liver illness that occurs within 26 weeks of the
initial liver injury in the absence of a pre-existing liver
disease
2) It is caused by massive hepatic necrosis, most often
induced by* drugs or toxins*
3) Accidental or deliberate ingestion of acetaminophen
accounts for almost 50% of cases in the US
4) Other causes:
– Autoimmune hepatitis, other drugs/toxins, and acute
hepatitis A and B

32
Q

hepatocellular necrosis is due to

A
  • Direct toxic damage (as with acetaminophen)
    – Immune-mediated hepatocyte destruction (e.g.,
    hepatitis virus infection)
33
Q

acute liver failure findings

A
  • Nausea, vomiting, and jaundice
    – Life-threatening encephalopathy, and coagulation defects
    – Serum aminotransferases are markedly elevated
    – Liver is initially enlarged, but as parenchyma is destroyed,
    the liver shrinks dramatically
    – Decline of serum aminotransferases as the liver shrinks
    – Worsening jaundice, coagulopathy and encephalopathy
    – With progression, multi-organ system failure occurs and,
    if transplantation does not happen, death ensues
34
Q

cirrhosis

A

– A condition involving the whole liver
– Characterized by the formation of parenchymal
nodules separated by fibrous tissue
– It leads to progressive hepatocellular failure
and/or portal hypertension
– Predisposes the patient to hepatocellular
carcinoma

advanced disease: hepatic encephalopathy, bleeding
from esophageal varices (which develop from portal
hypertension) and bacterial infections

Impaired estrogen metabolism with
hyperestrogenemia in male patients:

35
Q

portal hypertension

A

1) It might occur in acute liver failure but is much more
common in chronic liver failure
- Increased resistance to portal blood flow
2) Prehepatic, intrahepatic and posthepatic circumstances
– Prehepatic conditions: obstructive thrombosis, narrowing of
portal vein before it ramifies within the liver, or massive
splenomegaly
– Posthepatic causes: severe right-sided heart failure,
constrictive pericarditis and hepatic vein flow obstruction
– Intrahepatic cause: cirrhosis

36
Q

portal hypertension consequences

A

1) Ascites (accumulation of excess fluid in the peritoneal
cavity)
2) Formation of portosystemic venous shunts
- Dilation of collateral vessels and development of new vessels
– Hemorrhoids in the rectum
– Esophageal varices may cause massive hematemesis and death
– Periumbilical region (caput medusae)
3) Congestive splenomegaly
4) Hepatic encephalopathy (confusion, changes in
consciousness, slurred speech…)

37
Q

alcoholic liver disease

A

1) Fatty change (steatosis)
- Completely reversible if there is abstention from
further alcohol intake

2) Alcoholic hepatitis
- Mallory bodies: these are usually present as clumped,
amorphous, eosinophilic cytoplasmic inclusions in degenerating
hepatocytes
-degree of fibrosis progresses, it leads to nodule formation,
distortion of liver architecture and micronodular cirrhosis

3) Hepatic fibrosis (steatofibrosis)

4) Cirrhosis (in late stages)

38
Q

End-stage alcoholic liver disease is
characterized by:

A

A. Steatosis
B. Micronodular cirrhosis
C. Inflammatory infiltrates involving portal
tracts
D. Ground-glass hepatocytes
E. Acidophil bodies

39
Q

chronic alcoholism

A

1) 50-60g/day of alcohol
2) pathologic effects
- Changes in lipid metabolism
– Decreased export of lipoproteins
– Cell injury caused by reactive oxygen species and
cytokines

40
Q

differences in ALD

A

1) gender
- women are more susceptible to hepatic injury
2) ethnic and genetic
- cirrhosis higher for AA than for white
- ALDH2 is in 50% of asians with low activity
3) comorbility
- iron overload and infections with HCV and HBV synergize with alcohol

41
Q

lab findings of alcoholic cirrhosis

A
  • Elevated serum aminotransferases
    – Hyperbilirubinemia
    – Variable elevation of serum alkaline phosphatase
    – Hypoproteinemia (globulins, albumin, and clotting factors)
    – Anemia
42
Q

inflammatory bowel diseases

A

Chronic condition resulting from inappropriate
mucosal immune activation
1) Two main disorders:
– Ulcerative Colitis and Crohn’s disease
- Ulcerative colitis: colon and rectum and extends only
into the mucosa and submucosa
- Crohn disease: may involve any area of the GI tract and
is typically transmural

43
Q

crohns disease

A

1) Chronic inflammatory condition which may affect any
part of the whole gastrointestinal tract
- Presence of multiple, separate, sharply delineated areas of disease,
resulting in skip lesions
2) young adults
3) transmural perforation
4) Chronically: thickening and rigidity with fibrosis causing luminal
narrowing and obstruction- strictures
5) Ulcers may be deep and fissuring and may penetrate into the wall causing
adhesions or fistulas between the bowel and adjacent structures

44
Q

crohns disease complications

A

Malabsorption of vitamin B12 and bile salts leading to megaloblastic anemia and
fat malabsorption
– Serum protein loss
– Chronic iron deficiency anemia
– Extracolonic manifestations: migratory polyarthritis, ankylosing spondylitis,
erythema nodosum and uveitis
– Small increased risk of colonic adenocarcinoma

45
Q

clinical manifestations of crohns

A
  • Intermittent attacks of relatively mild diarrhea, fever
    and abdominal pain
    – Acute presentation:* right lower quadrant pain, fever,
    and bloody diarrhea*
    – Periods of active disease are interrupted by
    asymptomatic periods
    – Disease reactivation associated with: physical or
    emotional stress, specific dietary items and cigarette
    smoking
46
Q

ulcerative colitis

A

1) similar to crohns but no skip lesions
2) pancolitis
- typically involves the rectum
3) broad based ulcers
- usually does not perforate mucosa
4) pseudopolyps
5) toxic mega colon may occur in severe acute disease

47
Q

ulcerative colitis microscopic features

A

– Inflammatory process is diffuse and limited to the
mucosa and superficial submucosa
– Granulomas are not present

48
Q

ulcerative colitis clinical features

A

– Relapsing disorder
– Attacks of bloody diarrhea with stringy, mucoid material
– Lower abdominal pain, and cramps that are temporarily
relieved by defecation
– The initial attack may be severe enough to constitute a
medical or surgical emergency
– 30% of patients require colectomy within the first 3 years
of presentation because of uncontrollable symptoms

49
Q

ulcerative colitis causes

A

– Infectious enteritis precedes disease onset in
some cases
– In other cases, the first attack is preceded by
psychological stress
– Initial onset of symptoms have been reported
shortly after smoking cessation

50
Q

inflammatory bowel disease

A

The risk of colonic epithelial dysplasia and
adenocarcinoma is increased in patients who
have had IBD for more than 8 to 10 years

Pathology Q5 (6 decks)

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