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UF COM GI > GI Exam 2 > Flashcards

GI Exam 2 Flashcards

1
Q

The histological hallmark of ulcerative colitis is…

(hint: acute on chronic)

A

crypt abcesses. note the neutrophils within the crypts.

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2
Q

Risk for progression from adenoma to carcinoma in the colon is related to… (3 things)

A
  1. polyp >2cm
  2. sessile growth (as opposed to pedunculated)
  3. villous histology
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3
Q

Name the disease:

Malabsorption due to chronic immune mediated reaction to
dietary gluten (most pathogenic component is gliadin; protein
fraction of wheat, rye and barley).

A

What is celiac disease?

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4
Q

In what populations is celiac disease most common?

A

1% in Caucasians of European ancestry. There is a genetic predisposition,

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5
Q

Which human leukocyte antigens are particularly prevalent in patients with celiac disease?

A

Virtually all patients are + for HLA DQ2 or HLA DQ8. These are actually the MHCs that macrophages use to present deaminated gliadin to NKCs and Tcells

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6
Q

Prevalence of celiac disease is higher in pts with __________.

A

Down’s syndrome

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7
Q

What is the treatment for celiac disease?

A

Treatment: lifelong gluten free diet.

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8
Q

Steps of injury in celiac disease:

Once absorbed, (protein) is deamidated by (enzyme).
Deamidated (protein) is presented by antigen presenting cells via MHC class II.
Helper T cells mediate tissue damage including (3 things)

A

Steps of injury in celiac disease:

Once absorbed, gliadin is deamidated by tissue transglutaminase (TTG).
Deamidated gliadin is presented by antigen presenting cells via MHC class II.
Helper T cells mediate tissue damage including cytokine release, killer T cell activation, and Bcells releasing anti-TTG

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9
Q

On microscopic examination, the damage done by celiac disease is most prominent in the (portion of GI).

A

duodenum (jejunum and ileum
are less involved).

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10
Q

The lab test for celiac disease is (2 items).

A

IgA anti TTG & anti endomysial antibodies.
•
IgG antibodies useful in individuals with IgA deficiency
(increased incidence of IgA deficiency in celiac disease).

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11
Q

Which disease do these various degrees of villous blunting demonstrate?

A

celiac disease

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12
Q

Which disease does this image demonstrate?

A

celiac disease

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13
Q

Histological hallmarks of celiac disease are (3 items).

A

increase intraepithelial lymphocytes, increased plasma cells in the lamina propria, and villous blunting.

Mucus cells are still present unlike in autoimmune enteropathy.

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14
Q

Children with celiac disease present with (3 items), whereas adults present with (2 items).

A

Children : abdominal distention, diarrhea and failure to thrive.
•
Adults : chronic diarrhea and bloating.

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15
Q

Patients with (GI disease) can also present with (associated medical condition pictured).

A

Patients with celiac disease can also present with dermatitis herpetiformis (itchy blistering skin lesions due to IgA deposition at the tips of dermal papillae).

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16
Q

Celiac disease is associated with which 2 malignancies?

A

Enteropathy associated T cell lymphoma (EATCL)
•
Small intestinal adenocarcinoma.

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17
Q

Celiac disease and autoimmune enteropathy both present with watery diarrhea, villous diarrhea, intraepithelial lymphocytic infiltrate, and in some cases, anti-TTG Ab. How do you distinguish autoimmune enteropathy from celiac disease? (2 items)

A
  1. Villous atrophy not responding to
    dietary restrictions.
    -
  2. Circulating gut autoantibodies against goblet cells and and enterocytes are present (unique).
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18
Q

What is the CVID triad?

A

absence of plasma cells, lymphoid hyperplasia, presence of giardia lamblia

UpToDate: Patients may suffer from chronic lung disease, gastrointestinal and liver disorders, granulomatous infiltrations of several organs, lymphoid hyperplasia, splenomegaly, or malignancy …the most common reported disorders were pneumonia, autoimmunity, splenomegaly, and bronchiectasis

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19
Q

Common variable immunedeficiency (CVID) presents with

Diarrhea at 2nd 3rd decades.
-
Nodular lymphoid hyperplasia and
absence of plasma cells.

A

Common variable immunedeficiency (CVID) presents with

failure of B cell maturation, defective
antibody production, and decreased serum
immunoglobulins.
-
Diarrhea at 2nd 3rd decades.
-
Nodular lymphoid hyperplasia and
absence of plasma cells.

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20
Q

Common variable immunedeficiency (CVID) presents with

failure of B cell maturation, defective
antibody production, and decreased serum
immunoglobulins.
-
(?)
-
Nodular lymphoid hyperplasia and
absence of plasma cells.

A

Common variable immunedeficiency (CVID) presents with

failure of B cell maturation, defective
antibody production, and decreased serum
immunoglobulins.
-
Diarrhea at 2nd 3rd decades.
-
Nodular lymphoid hyperplasia and
absence of plasma cells.

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21
Q

Common variable immunedeficiency (CVID) presents with

failure of B cell maturation, defective
antibody production, and decreased serum
immunoglobulins.
-
Diarrhea at 2nd 3rd decades.
-
(?)

A

Common variable immunedeficiency (CVID) presents with

failure of B cell maturation, defective
antibody production, and decreased serum
immunoglobulins.
-
Diarrhea at 2nd 3rd decades.
-
Nodular lymphoid hyperplasia and
absence of plasma cells.

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22
Q

Which two mimickers of celiac disease
can have villous blunting and increased epithelial lymphocytes?

A

CVID and autoimmune enteropathy.

CVID you won’t see plasma cells in the lamina propria

Autoimmune enteropathy you won’t see goblet cells

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23
Q

Patients who have (disease) might present with malabsorption secondary to villous blunting and a travel hx to tropical regions ( e.g.,Caribbean

A

tropical sprue. don’t confuse with celiac disease.

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24
Q

Tropical sprue occurs secondary to (?).

A

aerobic bacterial contamination. Per Osmosis, Klebsiella, E. coli, Enterobacter

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25
Q

Tropical sprue presents with (histology) similar to celiac disease.

A

Variable villus blunting with increased intraepithelial
lymphocytes.

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26
Q

Unlike in celiac disease, tropical sprue predominantly affects the (GI tract segment) .

A

Duodenums less commonly involved. Typically
jejunum and ileum .

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27
Q

Tropical sprue is treated with (2 items).

A 
Folate (to counteract malabsorption) and broad
spectrum antibiotics (to fight bacterial etiological agent).
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28
Q

Patients who have Mycobacterium avium infection present with (presentation) and are (illness script).

A

Diarrhea, weight loss, fever.
•
HIV/AIDs with CD4 + cell counts 100/µl.

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29
Q

On histology, infection with Mycobacterium avium looks like (appearance).

A

Villi distended by diffuse
histiocytic infiltrate and foamy macrophages. PAS+ and acid fast

+

Histiocytes are stationary phagocytic cells in connective tissue.

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30
Q

Whipple disease presents with (presentation) predominantly in (population)

A

Whipple disease presents with diarrhea, abdominal pain especially after meals, weightloss 2/2 malabsorption, encephalopathy, lymphadenopathy, arthralgias predominantly in middle aged white males. Cardiac involvement might also be seen.

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31
Q

On histology, (disease) shows foamy macrophages full of Tropheryma whippleii and dilated lacteals in the small intestine resuling in fat malabsorption and steatorrhea.

A

whipple disease. don’t confuse with MAI. both are PAS D positive. Only MAI is acid fast blue positive (unlike Tropheryma whippleii ).

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32
Q

Giardia

Source: ?

Presentation: ?

Tx: ?

A

Giardia

Source: contaminated water such as pools, lakes, streams…

Presentation: watery diarrhea

Tx: metronidazole

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33
Q

Name that bug

A

Giardia. See the falling leaves?

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34
Q

A man living with AIDs presents to his PCP with 3 weeks of persistent, watery diarrhea and a CD4 count <100. A biopsy from his GI is seen below. Name that bug.

A

Cryptosporidium. The little blue dots are classic presentation on histo

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35
Q

A patient presents with profuse, watery diarrhea after a 2 week course of apicillin. This is what her colon looks like. Name that bug.

A

C. diff. Pseudo membranous colitis.

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36
Q

A patient presents with profuse, watery diarrhea after a 2 week course of apicillin. This is what her colon looks like. What’s this lump, and what caused it?

A

Volcano-like muco-purulent exudate comprisd of of mucin, fibrin, and neutrophils. C. diff.

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37
Q

How do you diagnose C. diff, and how do you treat it?

A

Diagnosis by detection of C. difficile toxin and treat with oral vanco or metronidazole (Flagyl)

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38
Q

Ischmic Colitis

Ischemic damage to colon is most likely to occur at (area). It presents with (sx) and (sx); patients might also have (sx). Patients with (predisposing factor) are most at risk.

A

Ischmic Colitis

Ischemic damage to colon is most likely to occur at splenic flexure (watershed area of superior mesenteric artery) or sigmoid colon. It presents with postprandial pain and weight loss; patients might also have bloody diarrhea. Patients with atherosclerosis of SMA are most at risk.

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39
Q

What are the top three microscopic findings in ischemic bowel injury?

A
  1. surface injury resulting in loss of mucus from crypts
  2. whithered appearing crypts
  3. hyalinization of lamina propria
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40
Q

Necrotizing Enterocolitis

Is a (cause) enterocolitis that predominantly affects (population). (portion of GI) most commonly involved. It presents with (3 things). Imaging will show (3 things). Grossly, (1 thing) is seen.

A

Necrotizing Enterocolitis

Is a multifactorial enterocolitis that predominantly affects premature neonates within a few weeks of birth. Terminal ileum, cecum and right colon most commonly involved. It presents with abdominal distention, feeding intolerance, and bloody stools. Imaging will show dilated bowel loops, pneumatosis and pneumoperitoneum, portal venous gas in liver. Grossly, coagulative necrosis of intestinal wall is seen.

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41
Q

The two main pathologic correlates of microscopic colitis are (1) and (2). Both are characterized by (sx) and (exam finding).

A

The two main pathologic correlates of microscopic colitis are collagenous colitis and lymphocytic colitis. Both are characterized by watery diarrhea and normal endoscopy.

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42
Q

Name the disease

This disease is usually seen in (population) with (sx). It affects (populations) equally and is associated with (disease). Microscopy seen below.

A

Lymphocytic Colitis

This disease is usually seen in middle aged to elderly individuals with chronic nonbloody diarrhea. It affects males and females equally and is associated with autoimmune disease (20%-60% of these patients). Microscopy seen below. Increased lymphocytic infiltration of epithelium (>20 IELs/100 epithelial
cells) and surface epithelial injury.

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43
Q

Collagenous Colitis

Population: ?

Presentation: ? and ?

Microscopic appearance: Thickening of (?) layer. Demonstrable by (?) stain, but generally not required. Measures (?) microns (vs 1 2 microns in normal subjects. Increased (?)

A

Collagenous Colitis

Population: middle-aged woman

Presentation: watery diarrhea and normal endoscopy.

Microscopic appearance: Thickening of subepithelial collagen layer. Demonstrable by trichrome stain, but generally not required. Measures 10-30 microns (vs 1-2 microns in normal subjects. Increased intraepithelial lymphocytes (>20 IELs/100 cells).

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44
Q

On microscopy, (dz) shows surface epithelium injury and sloughing, increased lamina propria cellularity, and capillaries and inflammatory cells included in collagen layer. Patient, most likely a middle-aged woman, will present with watery diarrhea.

A

On microscopy, collagenous colitis shows surface epithelium injury and sloughing, increased lamina propria cellularity, and capillaries and inflammatory cells included in collagen layer. Patient, most likely a middle-aged woman, will present with watery diarrhea.

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45
Q

Diversion colitis

Pathology: (initial insult) –> changes in luminal flora –> (effect on microbiome) –> nutritional deprivation –> (result).

Treatment: mucosal recovery often seen with restoration of fecal flow.

A

Diversion colitis

Pathology: Diverted fecal stream –> changes in luminal flora –> decreased short chain fatty acids –> nutritional deprivation –> cellular injury.

Treatment: mucosal recovery often seen with restoration of fecal flow.

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46
Q

Diversion colitis

Pathology: Diverted fecal stream –> (changes) –> decreased short chain fatty acids –> (result) –> cellular injury.

Treatment: (tx)

A

Diversion colitis

Pathology: Diverted fecal stream –> changes in luminal flora –> decreased short chain fatty acids –> nutritional deprivation –> cellular injury.

Treatment: mucosal recovery often seen with restoration of fecal flow.

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47
Q

Pseudopolyp is a buzz word for…

A

ulcerative colitis. These are areas of healing ulcerations

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48
Q

cobble stoning seen on endoscopy is a buzzword for…

A

crohn’s dz.

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49
Q

air in the peritoneal cavity (aka sub-diaphragmatic free air) on XR points to…

A

perforated bowel. Eg. s/p cancer –> obstruction.

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50
Q

Symptoms and histologic confirmation of enteropathy associated T cell lymphoma demonstrates (??).

A

Symptoms and histologic confirmation of enteropathy associated T cell lymphoma demonstrates clonal expansion of intraepithelial lymphocytes with aberrant phenotype.

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51
Q

Hepatitis E is also known as…

A

“enteric non-A, non-B”

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52
Q

Typical signs and symptoms of hepatitis include…

  1. (general)
  2. (MSK)
  3. (liver)
  4. (liver)
A

Typical signs and symptoms of hepatitis include…

  1. an initial phase of mild fever, anorexia, nausea and vomiting, lasting for a few days
  2. some persons may also have abdominal pain, itching w/o skin lesions, rash, or arthralgia.
  3. jaundice (yellow colour of the skin and whiteness of the eyes), with dark urine and pale stools; and
  4. hepatomegaly
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53
Q

Definitive diagnosis of hepatitis E infection is usually based on (?). Additional testing includes (?).

A

Definitive diagnosis of hepatitis E infection is usually based on serology (IgM Ab in blood). Additional testing includes RT-PCR to detect the hepatitis E virus RNA in blood and/or stool

Must first eliminate HBV, HCV & HAV, so this is a diagnosis of exclusion

54
Q

Hep E is spread via (?) transmission. It is seen in (geographic area).

A

Hep E is spread via fecal-oral transmission (mainly water-borne). It is seen in under-developed countries.

55
Q

Hep E is endemic in (3 areas). Most cases in the U.S. are related to some travel history.

A

Hep E is endemic in latin America, northern Africa, Asia. Most cases in the U.S. are related to some travel history.

56
Q

Pathogenesis of Hep E

(?) –> multiplies in intestinal epithelium –> (?) –> travels to liver

A

Pathogenesis of Hep E

ingested –> multiplies in intestinal epithelium –> enters blood stream –> travels to liver

57
Q

Pathogenesis of Hep E

ingested –> (?) –> enters blood stream –> travels to (?)

A

Pathogenesis of Hep E

ingested –> multiplies in intestinal epithelium –> enters blood stream –> travels to liver

58
Q

Hep E has an incubation period of (time) incubation. Presentation is mostly (?) in children

A

Hep E has an incubation period of 2-8 weeks incubation. Presentation is mostly sub-clinical in children

59
Q

Acute hepatitis E is clinically similar to HAV except (?) levels are higher and (?) is deeper and more prolonged

A

Acute hepatitis E is clinically similar to HAV except bilirubin levels are higher and jaundice is deeper and more prolonged

60
Q

Patients with Hep (?) are symptomatic for a few weeks after virus is no longer shed in stool.

A

Patients with Hep E are symptomatic for a few weeks after virus is no longer shed in stool.

61
Q

The normal case-fatality rate of Hep E is (?), but (?) in pregnant women.

A

The normal case-fatality rate of Hep E is 1-2%, but 10- 20% in pregnant women.

62
Q

There is no chronic carrier state for Hep (?) or Hep (?). The disease is self-limited.

A

There is no chronic carrier state for Hep A or Hep E. The disease is self-limited.

63
Q

Treatment for Hep E is (?) since the dz is self-limiting and there is no chronic or carrier state

A

Treatment for Hep E is supportive care since the dz is self-limiting and there is no chronic or carrier state

64
Q

To prevent Hep E transmission, (?) and avoid (?) when traveling to endemic regions

A

To prevent Hep E transmission, cook foods and avoid contaminated water when traveling to endemic regions

65
Q

A (?) vaccine against Hep E is in clinical trials, but as yet, no vaccine is available in the U.S.

A

A viral protein (subunit) vaccine against Hep E is in clinical trials, but as yet, no vaccine is available in the U.S.

66
Q

Most outbreaks of Hep E are associated with (source). There is minimal (?) transmission.

A

Most outbreaks of Hep E are associated with fecally contaminated drinking water. There is minimal person-to-person transmission.

67
Q

The reservoir for (?) and (?) is the Aedes mosquito.

A

The reservoir for Dengue Fever and Yellow Fever is the Aedes mosquito.

68
Q

The reservoir for Dengue Fever and Yellow Fever is the (?).

A

The reservoir for Dengue Fever and Yellow Fever is the Aedes mosquito.

69
Q

Dengue is also known as (??) fever.

A

Dengue is also known as “break bone fever”.

70
Q

Severe Dengue fever can present with (?) and (?).

A

Severe Dengue fever can present with thrombocytopenia and spontaneous bleeding, esp. petechiae and melena.

71
Q

Yellow fever is a hemorrhagic fever meaning it can present with spontaneous bleeding in the (?) and (?).

A

Yellow fever is a hemorrhagic fever meaning it can present with spontaneous bleeding in the GI tract (hematemesis, hematochezia) and mucous membranes (eyes, nose, mouth).

72
Q

(?) are viruses that are transmitted by arthropod vectors (usually mosquitoes and ticks). It isn’t technically a taxonomic family of viruses.

A

Arboviruses are viruses that are transmitted by arthropod vectors (usually mosquitoes and ticks). It isn’t technically a taxonomic family of viruses.

73
Q

Flaviviridae is an (?) virion. It has an (?) capsid, 40 – 50 nm and is (?)

A

Flaviviridae is an enveloped, spherical virion. It has an icosahedral capsid, 40 – 50 nm and is heat labile and easily inactivated by detergents

74
Q

Flaviviruses like yellow fever, dengue fever, and Hep C are (linear/segmented/coiled), (+/-) sense (ssRNA/ssDNA)

A

Flaviviruses like yellow fever, dengue fever, and Hep C are linear, plus sense ssRNA

75
Q

Flaviviruses

5’ end of genome is (?); 3’ end (?)

A

Flaviviruses

5’ end of genome is capped; 3’ end not polyadenylated – a looped structure

76
Q

In order to be replicated, Flavivirus requires the (?)!

A

In order to be replicated, Flavivirus requires the virally encoded RNAdependent RNA polymerase!

77
Q

Flavivirus repliactes in (?)

A

Flavivirus repliactes in host cell cytoplasm.

78
Q

Togavirus (?) whereas Flavivirus exits the host cell through (?0

A

Togavirus buds through the plasma membrane whereas Flavivirus exits the host cell through the ER or Golgi.

79
Q

Structural proteins are required in (?) amounts. Flaviviruses have the structural proteins (?) on the RNA to ensure they will be the most efficiently translated to protein

A

Structural proteins are required in stoichiometric amounts. Flaviviruses have the structural proteins ordered first on the RNA to ensure they will be the most efficiently translated to protein

80
Q

The non-structural proteins of Flavivirus and Togavirus are mainly (?) needed for replication.

A

The non-structural proteins of Flavivirus and Togavirus are mainly enzymes needed for replication.

Enzymes are catalytic (a little goes a long way). Not stochiometric

81
Q

The structural proteins of Togavirus are encoded on a (?) that is transcribed off the viral genome.

A

The structural proteins of Togavirus are encoded on a subgenomic RNA polycistronic transcript that is transcribed off the viral genome.

82
Q

Humans are usually a (?) host for alphavirus

A

Humans are usually a dead-end host for alphavirus

83
Q

The sylvan or “jungle” cycle of flavi/alpha/toga viruses involves transmission between (?) and (?). The virus can then be transmitted to a human working in the jungle.

A

The sylvan or “jungle” cycle of flavi/alpha/toga viruses involves transmission between non-human primates and arthropods (usually mosquito spp). The virus can then be transmitted to a human working in the jungle.

84
Q

The urban cycle of alpha/flavi/toga viruses involves transmission of the virus between (?) and (?). The virus is usually introduced by a viremic human who encountered the virus in the jungle.

A

The urban cycle of alpha/flavi/toga viruses involves transmission of the virus between humans and mosquitos. The virus is usually introduced by a viremic human who encountered the virus in the jungle.

85
Q

Dengue and Yellow fever (both flaviviridae) can cause (?) symptoms

A

Dengue and Yellow fever (both flaviviridae) can cause hepatitis-like symptoms

86
Q

Flavi and Toga viruses induce a strong interferon response early in the infection: (?)-like symptoms BEFORE (?)-like symptoms appear

A

Flavi and Toga viruses induce a strong interferon response early in the infection: fever and flu-like symptoms BEFORE hepatitis-like symptoms appear

87
Q

Note the same flavivirus can cause primarily (sx) in some patients, or present with (sx) in others!

A

Note the same flavivirus can cause primarily encephalitis in some patients, or present with liver symptoms in others!

88
Q

Infection Cycle of Flavivirus

1) Virus replicates in (?) following infection and then gain access to the bloodstream via (?) causing the first wave of viremia.
2) Then replicates in (cells) of (organs).
3) Second wave of viremia (much higher level) occurs as virus is released from these structures
4) The seeding of target organs at this stage determines type of clinical symptoms and severity. The target organs effected depends on (?) and differences in (?).

A

Infection Cycle of Flavivirus

1) Virus replicates in dentritic cells/monocytes following infection and then gain access to the bloodstream via lymphatics causing the first wave of viremia.
2) Then replicates in macrophages, endothelial cells or liver and spleen.
3) Second wave of viremia (much higher level) occurs as virus is released from these structures
4) The seeding of target organs at this stage determines type of clinical symptoms and severity. The target organs effected depends on degree of viremia and differences in tissue tropism and host immune status.

89
Q

Yellow fever is characterized by (?) with degeneration of (3 organs). The mortality rate is (?)% during epidemics

A

Yellow fever is characterized by severe systemic disease with degeneration of liver, kidney and heart. The mortality rate is 50% during epidemics

90
Q

Dengue induces classic “breakbone” fever presenting with (5 sx) lasting (?) days. (severe presentation) can occur in 0.25% of these dengue fever cases

A

Dengue induces classic “breakbone” fever presenting with high fever, headache, rash, back muscle, and bone pain lasting 6-7 days. Hemorrhagic fever and shock can occur in 0.25% of these dengue fever cases

91
Q

(?) to one Dengue serotype causes more severe disease with infection of another serotype via (?)

A

Non-neutralizing Ab to one Dengue serotype causes more severe disease with infection of another serotype via Fc receptors on macrophages.

Wiki: Ab-dependent enhancement occurs when non-neutralizing Ab facilitate entry into host cells, leading to increased infectivity. Dengue is a rare example.

92
Q

Liver damage in hepatitis infection is due to (?)

A

Liver damage in hepatitis infection is due to cell mediated immune response

93
Q

Infection with a hepatitis virus is diagnosed with (?) or (?)

A

Infection with a hepatitis virus is diagnosed with viral antigen detection or PCR

94
Q

Generally, there are no vaccines for arboviruses. There is a (?) vaccine for (?). Otherwise, prevention is via (?)

A

Generally, there are no vaccines for arboviruses. There is a live attenuated vaccine for Yellow Fever. Otherwise, prevention is via control of insect population

95
Q

What are “Dane particles”?

A

The 42 nm virions, which are capable of infecting hepatocytes.

96
Q

What test should be ordered that would be diagnostic (if positive) for acute hepatitis A infection?

A] Hepatitis A virus (HAV) total antibody (HAVAb)

B] Hepatitis D virus antibody (HDVAb).

C] Human immunodeficiency (HIV) viral load.

D] Electron microscopy for the Dane particle.

E] Hepatitis A virus IgM antibody (HAV IgM antibody).

A

What test should be ordered that would be diagnostic (if positive) for acute hepatitis A infection?

A] Hepatitis A virus (HAV) total antibody (HAVAb)

B] Hepatitis D virus antibody (HDVAb).

C] Human immunodeficiency (HIV) viral load.

D] Electron microscopy for the Dane particle.

E] Hepatitis A virus IgM antibody (HAV IgM antibody).

Answer A does not distinguish acute HAV hepatitis from recovery from immunization. HDV (answer B) does not relate to HAV. HIV worsens viral hepatitis but HIV infection does not equal HAV infection. The Dane particle is the HBV particle (virion). HAV IgM antibody is positive transiently with acute infection and following HAV immunization.

97
Q

How is the diagnosis of ACUTE HCV infection made?

A

Clinically. There is no laboratory test to identify acute HCV infection

98
Q

HCVAb can be present in ___________, __________ or in persons who have ________________.

A

HCVAb can be present in acute infection, chronic infection or in persons who have recovered from HCV infection.

In the U.S., testing for HCV IgM antibody is presently not available as the test appears not to be sufficiently reliable to gain FDA approval.

99
Q

PCR detection of HCV RNA does not ____________________________________.

A

PCR detection of HCV RNA does not distinguish acute from chronic HCV infection.

100
Q

A positive Hepatitis B virus core IgM antibody (HBc IgM antibody) is diagnostic for (acute/chronic?) hepatitis B infection.

A

A positive Hepatitis B virus core IgM antibody (HBc IgM antibody) is diagnostic for acute hepatitis B infection.

101
Q

A positive ________ is diagnostic for acute hepatitis B infection.

A

A positive Hepatitis B virus core IgM antibody (HBc IgM antibody) is diagnostic for acute hepatitis B infection.

102
Q

Positivity for HBsAg indicates _____ infection (either acute or chronic) or the hepatitis B carrier state.

A

Positivity for HBsAg indicates active infection or the hepatitis B carrier state.

  • active can be acute or chronic*
  • HBsAg is the HB surface antigen*
103
Q

Positivity for (serology??) indicates active infection or the hepatitis B carrier state.

A

Positivity for HBsAg indicates active infection or the hepatitis B carrier state.

104
Q

It is extremely rare for HBsAb and HBsAg to be ____ _____. Therefore if a person is HBsAb _____, they are almost certainly HBsAg ______. Some reports have documented the coexistence of HBsAg and HBsAb in patients with ______ HBV.

A

It is extremely rare for HBsAb and HBsAg to be positive simultaneously. Therefore if a person is HBsAb positive, they are almost certainly HBsAg negative. Some reports have documented the coexistence of HBsAg and HBsAb in patients with chronic HBV.

105
Q

Positivity for HBsAg indicates _____ infection (either ____ or ______) or the hepatitis B _____state

A

Positivity for HBsAg indicates active infection (either acute or chronic) or the hepatitis B carrier state

106
Q

During recovery from acute HBV infection, _____ can be negative and _______ antibody can still be positive for a period of time.

A

During recovery from acute HBV infection, HBsAg can be negative and HBc IgM antibody can still be positive for a period of time.

107
Q

If present, HB_?Ag_ indicates infection and is always present along with HB_?_Ag.

A

If present, HBeAg indicates infection and is always present along with HBsAg.

108
Q

Detection of ___ DNA by PCR would indicate infection, or if there is a relatively low copy number (<105 copies/mL ), this could be consistent with the ___ _______ state.

A

Detection of HBV DNA by PCR would indicate infection, or if there is a relatively low copy number (<105 copies/mL ), this could be consistent with the HBV carrier state.

109
Q

Because the

_______ of HBV polymerase overlaps the HB?Ag ___, it is possible that some mutations in the HB?Ag region correspond to mutations in the ______, conferring resistance to current antiviral therapies.

A

Because the reverse transcriptase region (rt) of HBV polymerase overlaps the HBsAg ORF, it is possible that some mutations in the HBsAg region correspond to mutations in the rt ORF, conferring resistance to current antiviral therapies.

110
Q

HB?Ag is a protein from the hepatitis B virus that circulates in infected blood when the virus is _____ ______. The presence of HB?Ag suggests that the person is _____ and is __________________________.

A

HBeAg is a protein from the hepatitis B virus that circulates in infected blood when the virus is actively replicating. The presence of HBeAg suggests that the person is infectious and is able to spread the virus to other people.

111
Q

The HBV carrier state is defined by…

  • HBsAg ______.
  • HBeAg _______.
  • HBV serum DNA ________.
  • AST & ALT ________.
  • Liver biopsy shows __________.

I.e. there is evidence of HBV infection (e.g., ?????) but there is no evidence of active disease and HBV DNA copy number is ___.

A

The HBV carrier state is defined by…

  • HBsAg positive longer than 6 months.
  • HBeAg negative
  • HBV serum DNA <105 copies/mL (e.g., negative or lower copy number)
  • AST & ALT persistently normal
  • Liver biopsy shows no significant inflammation or necrosis

I.e. there is evidence of HBV infection (e.g., HBsAg +) but there is no evidence of active disease and HBV DNA copy number is low.

112
Q

Positive serum HBeAg indicates a __________. Though carriers are negative for HBeAg, they are still able to _________.

A

Positive serum HBeAg indicates a HIGH level of infectivity. Though carriers are negative for HBeAg, they are still able to spread the virus.

113
Q

The presence of HBV DNA in HBsAg-negative individuals is defined __________________. ___ is caused by (1/2), or (2/2). These patients may also be negative for HB?Ag

A

The presence of HBV DNA in HBsAg-negative individuals is defined as occult HBV infection (OBI). OBI is caused by variant viruses (S-escape mutants) undetectable by HBsAg commercial kits, or infection with wild-type viruses that are strongly suppressed in their replication activity. These patients may also be negative for HBeAg

***infection with suppressed wild type is most likely***

114
Q

OBI may be involved in different clinical contexts including …

  • transmission of HBV by ___ or ___
  • ___ when an immunosuppressive status occurs.
  • the development of ____
  • may have an important role in ___.
A

OBI may be involved in different clinical contexts including …

  • transmission of HBV by blood transfusion or liver transplantation
  • acute reactivation when an immunosuppressive status occurs.
  • the development of cirrhosis
  • may have an important role in hepatocarcinogenesis.
115
Q

The success of the vaccination programs has now been challenged by the discovery of mutant viruses showing ___ ___ ___ in HB?Ag, which may lead to evasion of ____-____ _____

A

The success of the vaccination programs has now been challenged by the discovery of mutant viruses showing amino acid substitutions in HBsAg, which may lead to evasion of vaccine-induced immunity

116
Q

Positivity for HB?Ab and negativity for HB?Ab indicates previous immunization: the immunogen is HB?Ag and therefore HB?Ab does NOT develop after immunization.

A

Positivity for HBsAb and negativity for HBcAb indicates previous immunization: the immunogen is HBsAg and therefore HBcAb does NOT develop after immunization.

117
Q

Positivity for HBsAb and HBcAb with a negative HBsAg indicates _____ _____ HBV infection.

A

Positivity for HBsAb and HBcAb with a negative HBsAg indicates recovery from HBV infection.

118
Q

Suppose that this person had the following test results, what is the correct interpretation?

HBsAg = Positive.

HBc IgM Ab = Positive.

HBsAb = Negative.

A

Suppose that this person had the following test results, what is the correct interpretation?

HBsAg = Positive.

HBc IgM Ab = Positive.

HBsAb = Negative.

acute infection

119
Q

Suppose that this person has the following test results:

HBsAg = Negative.

HBcAb = Negative.

HBsAb = Positive.

Can he serve as a liver donor to a person who is not infected with HBV?

A

Yes

He has been immunized against HBV as indicated by the fact that he is positive for HBsAb and lacks HBcAb. HBcAb is only acquired after natural infection. The lack of HBcAb indicates that this is not a state of recovery from HBV infection.

120
Q

HB?Ab is only acquired after natural infection.

A

HBcAb is only acquired after natural infection.

Appears at the onset of symptoms in acute HBV and persists for life.

121
Q

HBcAb is only acquired after _____ ______.

A

HBcAb is only acquired after natural infection.

122
Q

Acute liver failure can occur in 1 in 1000 cases of H?V hepatitis. Because chronic liver disease does not occur, neither ____ nor ______ ____ should be increased in frequency in persons recovering from H?V hepatitis.

A

Acute liver failure can occur in 1 in 1000 cases of HAV hepatitis. Because chronic liver disease does not occur, neither cirrhosis nor hepatocellular carcinoma should be increased in frequency in persons recovering from HAV hepatitis.

123
Q

Positive HAV ___ _______ indicates infection.

A

Positive HAV IgM antibody indicates infection.

Have to see IgM specifically. Otherwise you won’t know if the +Ab are from current or resolved infection, or from immunization.

124
Q

HB?Ab develops in a person who has recovered from infection with HBV or who has been successfully vaccinated against HBV.

A

HBsAb develops in a person who has recovered from infection with HBV or who has been successfully vaccinated against HBV.

125
Q

The presence of HB?Ab indicates previous or ongoing infection with HBV in an undefined time frame.

A

The presence of HBcAb indicates previous or ongoing infection with HBV in an undefined time frame.

126
Q

The presence of HBcAb indicates ____ or ____ infection with HBV in an undefined time frame.

A

The presence of HBcAb indicates previous or ongoing infection with HBV in an undefined time frame.

127
Q

AST stands for ______ ___________

A

AST stands for Aspartate Aminotransferase

128
Q

AST has two main functions:

  1. ???
  2. ???
A

AST has two main functions:

  1. Deaminate Aspartate to Oxaloacetate
  2. Transamination of alph-ketoglutarate to glutamate
129
Q

Was is the function of Alanine Aminotransferase (ALT)?

A

To deaminate alanine to pyruvate

and

transamination of alph-ketoglutarate to glutamate

130
Q

What are the essential amino acids?

Pvt. Tim Hall

A

Phenylalanine, Valine, Tryptophan, Threonine, Isoleucine, Methionine, Histidine, Arginine, Lysine, Leucine

The must be included in the diets of humans

131
Q

In addition to total bilirubin, is direct or indirect bilirubin measured?

A

Direct

UF COM GI (4 decks)

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