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GI II Exam I AP > GI pathology > Flashcards

GI pathology Flashcards

1
Q

Increased ALT and AST but AST is < ALT

A

Do viral serology

+ = hepatitis

-  = autoimmune hepatitis (ASM, ANA) 
WIlson disease (ceruloplasmin)
Hemochromatosis (Fe saturation)
alpha-antitrypsin (serum level) 
drugs and toxins
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2
Q

ceruloplasmin

A

wilson disease

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3
Q

AST > ALT <500 IU/L

A

Hepatitic cause

Alcoholic liver disease

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4
Q

increased ALK phos and GGT

A

cholestatic –>get imaging diameter of common bile duct

1 cm = extrahepatic

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5
Q

cholestatic Intrahepatic cause of jaundice

AMA +

A

primary biliary cirrhosis

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6
Q

AMA - cholestatic intrahepatic cause of jaundice

A

Primary sclerosing cholangitis

pregnancy

cholangiocarcinoma

hereditary syndromes

GVH and HVG

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7
Q

extrahepatic cholestatic causes of jaundice

A

pancreatic CA

gallstones

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8
Q

what does the liver catabolize

A

estrogen
drugs
toxins
NH3

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9
Q

Zone 1

A

highest O2

affected first by viral hepatitis and toxins

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10
Q

Zone 3

A

lowest O2
closest to central vein

at risk for hypotension and congestion

increased drug metabolism

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11
Q

Dendritic cells in the liver

A

DCs in the liver are uniquely positioned to monitor the portal circulation. they are in the space of Disse and are part of innate immune response

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12
Q

stellate cells

A

inside space of disse

fat soluble vitamin storage

fibrosis production

can contract and push fluid along in the space of disse

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13
Q

kupffer cells

A

inside sinusoids

part of innate immune system

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14
Q

where does Detox/
Delivery of synthesized/
metabolized products
( like bilirubin) to hepatocytes//system go

A

bile canaliculi to canal of hering to bile duct

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15
Q

space of Disse

A

lymph fluid is in this space

The hepatic lymph primarily
comes from the hepatic sinusoids. Fluid filtered out
of the sinusoids into the space of Disse flows through
the channels traversing the limiting plate either independently
of blood vessels or along blood vessels and
enters the interstitial space of either the portal tract,
sublobular veins, or the hepatic capsule.

if there is blockage in space of disse or mall then ascites occurs

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16
Q

what special types of cells are in the canal of hering

A

Canal of hering- bile is delivered to canal of hering which is a very small bile duct  delivered to bile ducts of portal tracts
-stem cells of liver may be located in the canal of hering – source of regeneration of the hepatocytes

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17
Q

what is the space of Mall

A

lymphatic fluid flows from space of Disse into the portal area filling the space of Mall and then flowing into the larger portal lymphatics to the thoracic duct

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18
Q

what is sythesized in the liver

A

albumin

clotting factors (VIII, XI)–> liver transplant cures hemophilia A

acute phase reactants

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19
Q

in terms of mechanisms of cell injury what is generally the stage of irreversibility

A

membrane damage

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20
Q

what is fetor hepatis

A

distinctive smell of breath “musty” “sweet and sour” from shunting and dimethyl sulfide made by gut bacteria

seen in chronic liver failure

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21
Q

macronodular cirrhosis

A

> 3mm viral causes

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22
Q

micronodular

A

<3mm ethanol

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23
Q

in cirrhosis, what activates stellate cells into myofibroblasts

A

PDGFR-Beta

TNF

Kupffer cells release cytokines and chemokines that stimulate fibrogenesis in stellate cells

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24
Q

what is the most common cause of isolated increase in AST and ALT in typical Americans

A

NASH

Nonalcoholic Steatohepatitis

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25
Q

in what types of liver disease will you find the highest levels of aminotransferases

A

acute viral or ischemic liver injury , or toxic liver injury

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26
Q

cirrhotic pt’s and chronic hepatitis pt’s may have aminotransferases at what level?

A

within reference range

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27
Q

what is the significance of the t 1/2 life of albumin of 20 days

A

Albumin binds conjugated bilirubin- if the conjugated bili is elevated for extended periods of time, the conjugated bili can strongly bind to albumin- delta bilirubin is this complex – the half life of albumin is about 20 days so this delta bilirubin is going to be present in the blood for long periods of time – important to understand this delta bili . If you allow bile to run through the duct again the pt’ stays yellow for a while b/c you have to wait for the albumin to clear before the deposition of conjugated bili can actually go away

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28
Q

Increase in IgA

A

alcoholic liver disease

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29
Q

Increase in IgM

A

primary biliary cirrhosis

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30
Q

increase in IgG

A

autoimmune hepatitis

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31
Q

mean incubation period of hep A

A

1 month

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32
Q

mean incubation period of Hep B

A

3 months

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33
Q

mean incubation period of Hep C

A

2 months

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34
Q

mean incubation period of Hep e

A

1 month

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35
Q

why is it hard to develop a vaccine for Hep C

A
  • This genomic instability and antigenic variability have hampered development of a vaccine…no vaccine
  • Elevated titers of anti-HCV antibody do not confer effective immunity
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36
Q

Hairy leukoplakia is caused by what

A

EBV

may be first sign of HIV

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37
Q

99mTc nuclear scan

A

meckel diverticulum–> will show gastric mucosa and symptomatic meckel’s diverticula have ectopic gastric or pancreatic cells within them

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38
Q

if you have a positive Tzanck test what will you see?

A

multinucleated giant cells within inclusions

inclusions represent the herpes virus particles inside the nucleus

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39
Q

when do you lose ameloblasts

A

loss of ameloblasts? You lose these before the tooth ruptures through the gum

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40
Q

failed involution of vitelline duct

A

meckel’s diverticulum

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41
Q

what causes double bubble sign

A

annular pancreas

duodenal atresia

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42
Q

where are the regional lymph nodes located for the colon ?

A

periocolonic adipose tissue attached to the bowel

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43
Q

where do colon cancer cells travel to if they migrate into a vascular space

A

travel via lymphatics

get to liver by tumor cells invading into veins–> goes to portal vein–> right to liver

brain? travels through liver sinusoids, central vein–> hepatic vein–> IVC–> through lungs–> left side heart–> brain

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44
Q

when malignant colonic cells mets to the liver, where will they most likely stop and begin to multiply and grow–> becoming metastatic nodule

A

sinusoidal lumen

space of disse

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45
Q

what paraneoplastic syndrome is most common with colonic adenocarcinoma

A

nephrotic syndrome- membranous glomerulopathy, immune complexes, autoAb’s against antiphospholipase A2 receptor

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46
Q

how do malignant colonic tumor cells get to the regional lymph nodes?

A 
float
invade into them
diffuse
pushed mechanically 
and probably sucked into
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47
Q

what are the genes involved with HPV associated squamous cell carcinoma

A

E6/E7 oncogenic proteins

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48
Q

what is the central dot sign

A

ciliopathy- congenital defect

these represent the portal veins and the empty space around the veins are the dilated cysts

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49
Q

what is a ground glass appearance of the liver indicative of

A

Hep B

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50
Q

Type I autoimmune hepatitis

A

female predominance
young to perimenopausal

elevated IgG

ANA, ASMA

negative AMA

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51
Q

Type 2 autoimmune hepatitis

A

Children and teenagers

AMA

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52
Q

rare but potentially fatal syndrome of mitochondrial dysfunction with massive microvesicular steatosis

occurs in children that receive aspirin for fevers

A

reye syndrome

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53
Q

cause of hepatocellular necrosis in zone 3

A

acetaminophen

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54
Q

what is vinyl chloride associated with?

A

Angiosarcoma

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55
Q

what is budd-chiari syndrome associated with

A

oral contraceptives

Budd-Chiari syndrome is an uncommon condition induced by thrombotic or nonthrombotic obstruction of hepatic venous outflow and characterized by hepatomegaly, ascites, and abdominal pain.

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56
Q

what are some substances or conditions that are associated with Zone 1

A

Fe overload

allyl alcohol

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57
Q

what are some substances that are associated with zone 3 hepatotoxicity

A

CCL4

Acetaminophen

Ethanol

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58
Q

what pattern of injury does oral contraceptives cause

A

cholestasis

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59
Q

Acetaminophen

A

Zone 3 necrosis
Toxicity is from a metabolic by-product –> NAPQI

Toxicity is greatly enhanced by concurrent ETOH consumption (upregulation of cytochrome P-450 system…CYP2E1)

Commonly used for suicide – commonest cause of acute liver failure
- In the US, 50% overdoses are unintentional

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60
Q

Antidote for Acetaminophen

A

N-acetyl cysteine

restores GSH

must be given within 8-12 hours

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61
Q

Isoniazid

A

First line anti-TB drug with toxic metabolite (Fibrosis and cirrhosis)

1% get hepatitic damage; 10-20% show increase in ALT

62
Q

methotrexate and the liver

A

Used to treat immune diseases (psoriasis, rheumatoid arthritis..)

Hepatotoxic with fatty change and fibrosis –cirrhosis

macrovascular fatty change

63
Q

tetracycline and the liver

A

microvesicular fatty change

64
Q

where do the patterns of disease of alcohol toxicity occur and what are the 3 patterns

A

begin in zone 3

hepatic steatosis (fatty change)

alcoholic hepatitis

cirrhosis

65
Q

mallory bodies and AST>ALT are seen in what

increased ALK phos and GGT

leukocytosis (mainly neutrophilic)

Malaise, fever, jaundice, RUQ pain

A

alcoholic hepatitis

Mallory bodies–> represent tangles of intermediate keratin filaments complexed with proteins like ubiquitin

66
Q

copper overload

A

wilson disease

67
Q

what are the 5 cancers associated with smoking

A

pancreas
lung
HNSCC (squamous cell carcinoma of head and neck)

bladder
esophagus

68
Q

what happens to flow in the hepatic artery as portal vein undergoes occlusion

A

increases

this holds true in cirrhosis as well

if there is acute occlusion , then the hepatic artery can’t catch up, but if the occlusion is slow/chronic, the hepatic artery will adapt and deliver adequate blood flow

under conditions of reduced portal venous flow with induction of the hepatic arterial buffer response, preferential shunt perfusion leads to a disproportionally increased contribution of perfusion of sinusoids with hepatic artery-derived blood. This guarantees maintenance of oxygen supply despite an overall reduction of nutritive blood flow.

space of Mall. Chemicals in this space/ environment…we think adenosine and NO…control the flow in this shunt…making sure enough O2 is getting to the hepatocytes

69
Q

in hypovolemic shock, which area of the liver is injured first (necrotic changes)

A

zone 3 (around central vein) necrosis (also seen in acetominophen poisoning)

70
Q

what happens to the liver with CHF

A

Increased sinusoidal pressure in zone 3 leads to hepatocyte and sinusoidal endothelial cell damage in Zone 3–> this activates stellate cells and leads to fibrosis (beginning in zone 3) “cardiac cirrhosis”

nutmeg liver

can lead to cardiac cirrhosis

71
Q

benign hepatocyte neoplasm in young women taking oral contraceptives

A

hepatic adenoma

72
Q

what virus is associated with hepatocellular carcinoma

A

HBV

73
Q

presents in the background of cirrhosis

elevated AFP

A

HCC

AFP is a major plasma protein produced by the yolk sac and the liver during fetal development. It is thought to be the fetal form of serum albumin.

74
Q

occurs in young patients with normal livers

looks like focal nodular hyperplasia but is malignant

has no association with HBV, HCV or cirrhosis

single large hard mass

micro–> shows malignant hepatocytes with characteristic stromal fibrosis

A

Fibrolamellar carcinoma (5% of HCC’s)

75
Q

Arises from bile duct epithelium and resembles other adenocarcinomas
60% are perihilar (Klatskin tumor)
Risk factors: primary sclerosing cholangitis, congenital biliary cystic diseases, thorotrast exposure, parasites (liver fluke)
Hematogenous route of metastasis in ~ 50%
Frequently difficult to differentiate from metastatic carcinoma from breast or pancreas
Lethal tumor (median survival 6 months)

A

cholangiosarcoma

76
Q

Constitutional: fatigue, weakness, weight loss
Estrogenic: spider angiomata, palmer erythema, gynecomastia, testicular atrophy

seen in what?

A

chronic liver disease cirrhosis

77
Q

HFE gene

cysteine-to-tyrosine substitution at amino acid 282 (called C282Y)

A

hereditary hemochromatosis

autosomal recessive

78
Q

HFE

histadine-to-aspartate substitution at amino acid 63 (called H63D)…worldwide distribution…mild disease.

A

hereditary hemochromatosis

79
Q

HAMP

HJV

A

mutations in juvenile hemochromatosis

80
Q

chronic inflammation and IL-6 lead to increased activation of hepcidin transcription

what is the effect on Fe

A

Fe is not absorbed into the blood in sufficient amounts and the person becomes iron deficient…so called “iron deficiency of chronic disease” =
“anemia of chronic disease”

hepcidin is an acute phase reactant

So, if there is no hepcidin …Fe is constantly being absorbed into blood stream…and abnormally deposited in tissues like the liver, heart, pancreas

81
Q

what is the presentation of hemochromatosis

A

most common symptoms now include fatigue, malaise, arthralgia, and loss of libido (endocrine

unexplained cirrhosis, bronze-colored skin, diabetes (and other endocrine diseases), joint inflammation, and heart disease in middle-aged white men

iron stains blue with prussian blue stain

transferrin saturation increased, normal TIBC , increased serum ferritin

HFE mutation (C282Y)

82
Q

what is the classic triad of complications in hemochromatosis

A

skin pigmentation

cirrhosis- iron activates stellate cells to induce fibrosis

diabetes

83
Q

auto recessive disorder

WD gene

impaired biliary excretion of copper
failure to incorporate copper into ceruloplasmin

kayser-fleischer rings

mutation in Cu-ATPase ATP7B

A

Wilson disease

copper accumulates in liver, brain and eye

Liver disease: acute fulminant hepatitis, chronic active or cirrhosis

CNS: behavioral and/or Parkinson-like, strange smile (dystonia of muscles of the face- risus sardonicus)- basal ganglia lesions

Eye: Kayser -Fleischer rings*** - by the time these are visible, there should already be neurological symptoms

84
Q

what are the lab findings in wilson disease

A

low serum ceruloplasmin (screening)
increased urine copper (specific)
Increase liver copper content by biopsy (most sensitive, highest PPV+)
Serum copper is highly variable as it depends on ceruloplasmin level

lymphocytes are the main infiltrate in the liver without inflammation

rhodanine stain for copper is positive

85
Q

autosomal recessive

very low serum levels of protease inhibitor –> deficiency leads to emphysema and hepatic disease

A

Alpha 1 antitrypsin deficiency

most common abnormal variants is PiZZ

Protease normally inhibits 1) neutrophil elastase 2) cathepsin G, 3) proteinase 3…all made by neutrophils at site of inflammation

Defect blocks release of α1-antitrypsin from hepatocytes
Mutant alpa1-antitrypsin is abnormally folded which leads to the “unfolded protein response”…accumulates in hepatocyte…activates caspases and induces apoptosis…cirrhosis

Lack of inhibitor to neutrophil proteases in lung allows alveolar damage →emphysema

86
Q

how do you make the diagnosis of alpha 1 antitrypsin deficiency

A

Decreased serum α1- antitrypsin level

Phenotyping for PiZZ

Liver biopsy shows accumulated α1-antitrypsin (abnormal protein folding)…

round to oval PAS positive cytoplasmic inclusions in hepatocytes - begin around the periportal area first and then spread to central vein region

87
Q

progressive destruction of the small to medium bile ducts

antimitochondrial antibodies (AMA) * directed against the E2 component of pyruvate dehydrogenase complex (PCD-E2) in small bile duct epithelial cells in Hering’s canal closest to the portal tract (periportal)

more common in women middle aged

pruitis

non- caseating granulomas , florid duct lesions (involves ductular epithelium)

A

Primary biliary cirrhosis (PBC)

You see massive leukocytic infiltration in the portal tracts (lymphocytes and plasma cells)

88
Q

how is the AMA test in primary biliary cirrhosis done

A

This is an immunofluorescence study/picture. A drop of the patient’s serum (which pathologically contains AMAs) is placed on normal test tissue. The serum and tissue are incubated and the abnormally present AMAs in the patient’s serum bind to the PDC-E2 in the normal mitochondria of the tissue specimen. The test specimen (patient’s serum-normal tissue) is then washed and a drop of fluorescently tagged anti-anti-mitochondrial antibody is incubated on the tissue. This anti-anti- mitochondrial antibody binds to the AMAs binding to the tissue. This positive reaction can be seen with fluorescent light activation and is seen as bright green staining in the cytoplasm of the test cells. If there were no AMAs in the patient’s serum, no bright green reaction would be seen.

89
Q

A progressive disease of liver characterized by cholestasis with obliterative fibrosis of intra and extrahepatic bile ducts (with dilation of preserved segments)

most present in Chronic inflammatory bowel disease

male, age 40

cholelithiasis

65% have pANCA, 50% have ANA (Antinuclear Ab)
and 50% have increased serum IgM

onion skinning appearance of bile duct!

A

primary sclerosing cholangitis

what confirms the diagnosis?
-beading of bile ducts (ERCP or MRI)

90
Q

Causes in Adults
Obstruction by gallstones
Malignant neoplasms of biliary tree/head of pancreas
Strictures from previous surgery in the bile duct tree
PBC,PSC

Causes in Children
Biliary atresia
Choledochal cysts
Cystic fibrosis

see nodular formation with regeneration ductular proliferation, bile lakes

A

secondary biliary cirrhosis
-results from prolonged obstruction of the biliary tree

cholestasis, then escape of bile, then inflammatory reaction to bile, then fibrosis (biliary cirrhosis)….may be complicated by ascending cholangitis

91
Q

bile duct hamartomas

small clusters of dilated ducts or cysts within fibrous stroma

the portal area gets a disorganized bile duct proliferation but those ducts do NOT drain or connect to normal biliary system

A

von meyenburg complex

92
Q

hundreds of biliary epithelium lined lesions

PKD1 associated

common fatal association with this disease is subarachnoid hemorrhage from rupture of berry aneurysm in circle of willis

A

polycystic liver disease

autosomal dominant polycystic kidney disease clinical extrarenal manifestations

93
Q

bile duct cysts only

cyst + hepatic fibrosis

A

caroli disease

94
Q

PC1 and PC2 abnormalites

A

altered mechanosensation by tubular cilia
altered calcium flux

associated with cysts- abnormal bile ducts

don’t know what the fuck he’d ask about this

95
Q

what is the most common congenital dilatation of the bile duct

A

choledochal cysts

96
Q 
fat
female
fertile 
forty
flatulent
A

cholelithiasis

cholesterol stones

97
Q

radiolucent
at 20% CaCO3 become radiopaque

due to increased hepatic cholesterol and/or decrease bile salts/lecithin

abnormal bile flow

↓GB motility: fasting; weight loss, progesterone
heredity (25%): Pima Indians (have ↑cholesterol secretion & ↓bile salts )
Crohn disease: ?disrupted enterohepatic bile salt circulation

A

cholesterol stones

98
Q

what are the 4 steps of stone formation

A
  1. Increased production/saturation
    2. Crystallization (nidus)
  2. Flow (volume, turbulence)
  3. Accretion (matrix/sludge)
99
Q

what is the cause of strawberry gallbladder?

A

cholesterolosis

supersaturated bile and ↑mucosal uptake…can present clinically like acute/chronic cholecystitis …usually with stones (mechanism unknown if stone absent)

100
Q
  • formed from polymers of unconjugated bilirubin (bilirubin calcium salts)
  • small (
A

BLACK PIGMENT STONES

101
Q
  • formed from unconjugated bilirubin + cholesterol
  • soft, “soapy” to feel, laminated, may not be picked up on X-ray
  • commoner in bile ducts than gallbladder; radiolucent
  • associated with E. coli infection (bacterial cholangitis)
  • common in Asia because of liver flukes (C. sinensis)
A

BROWN PIGMENT STONES

102
Q

what is the evolution of the disease of acute cholecystitis

A
  1. Acute obstruction: stone blocks cystic duct→ CCK causes GB contraction → mid-epigastric, colicky pain, N & V
    1. Stone impaction: ↑mucous behind obstruction → chemical irritation and bacterial overgrowth (E. coli, gut flora) → acute inflammation → pain shifts to RUQ, continuous aching pain, ± radiation
    2. Bacterial infection: invasion of GB wall → peritonitis → + rebound, Murphy’s sign, neutrophilia, 90% resolve < 1 month
    3. Gangrenous necrosis: compression of wall vessels → full thickness necrosis → perforation → peritonitis

most common cause of acute cholecystitis is gallstones

103
Q

what is the HIDA scan

A

radioactive dye (given IV) is excreted by the liver (GB not seen in acute cholecystitis …even up to 3 hrs…stone blocks duct)

dye normally fills the gallbladder and will later be seen in the small bowel

Helpful b/c if the gallbladder doesn’t appear then it is obstructed! – surgical reason/cause to remove the gallbladder

104
Q

Caused by stasis/obstruction in biliary tract…stone…tumor

 - There is secondary bacterial infection…organism is typically from duodenum
 - E. coli, Klebsiella, enterobacter ….

Infection moves up the biliary tree into the liver bile duct system…sometimes resulting in multiple small liver abscesses

A

acute/ascending cholangitis

105
Q

what is the presentation of a pt with acute ascending cholangitis

A

Charcot’s triad:

  • fever
  • jaundice
  • abd pain

bile duct is filled with neutrophils/pus

106
Q

Rokitanski-Aschoff sinuses

porcelain gallbladder

A

chronic cholecystitis

these are inflammation with occasional mucosal outpouchings -areas where the gallbladder is constricting due to long-standing inflammation

surface mucosa is pulled down into the wall of the mucosa

porcelain- due to dystrophic calcification of gallbladder– high risk for adenocarcinoma ***

107
Q

most common gallbladder carcinoma

A

adenocarcinoma

2x more common in women

native americans and hispanics

no symptoms til advanced stge

ERBB2 (Her2-neu) overexpressed in 2/3

poor survival

108
Q

what are the main causes of cholangiocarcinomas

A

primary sclerosing cholangitis

choledochal cysts

flukes

painless jaundice

109
Q

Villous blunting and flattening

increase in intraepithelial lymphocytes

A

celiac disease

chronic diarrhea with steathorrhea

10% have dermatitis herpetiformis = subepidermal blistering skin lesions

110
Q

most common cause of chronic gastritis

A

H. pylori

111
Q

what do parietal cells secrete

A

Gastric acid (HCl)

intrinsic factor (Vitamin B12 absorption)

112
Q

polyhydraminos

child unable to feed

A

atresia of esophagus

113
Q

hamartomatous polyps
autosomal dominant
entire GI tract

splayed smooth muscle in the polyp

age 10-15
mutated STK11, AMP kinase-related pathways
mucocutaneous hyperpigmentation (think lips)

increased risk of thyroid, breast, lung, pancreatic and bladder cancers

A

Peutz-Jeghers syndrome

114
Q

MLH1, MSH2 microsatellite instability (DNA mismatch repair defect)

A

10-15 % of sporadic cases of colon carcinoma (adenocarcinoma)
right sided

sessile/serrated

115
Q

APC/beta catenin multiple hits

A

classic adenoma (colon adenocarcinoma)

left sided

typical tubular/villous

also seen in familial adenomatous polyposis syndrome

116
Q

syndrome with esophageal tears from severe vomiting. Most cases occur in the
context of alcohol abuse.

A

mallory weiss

117
Q

M>F

FAP related (APC/WNT pathway) , HNPCC related

P53
occurs in gastric antrum and pylorus

forms bulky tumors and masses that ulcerate

heaped up borders and central ulceration

demonstrates malignant gland formation invading the muscular wall of stomach

associated with h, pylori

A

Intestinal (non-signet ring) or usual type of gastric adenocarcinoma

118
Q

M=F
no association with h. pylori

CDH1/E - cadherin mutations

p53

Germline loss-of-function mutation in tumor suppressor gene CDH1 (encodes E-cadherin)

very poor survival rates

do not tend to ulcerate but infiltrate diffusefly in to the wall of the stomach- thick , hard like a wine flask

linitis plastica –> gastric walls is markedly thik and rugal folds are lost

A

diffuse-type signet ring gastric adenocarcinoma

see signet rings

119
Q

t11;18
t1;14
t14;18

h. pylroi related

constitutive activation of NF-kB- promotes b cell growth and survival

arises at sites of previous inflammation

50% disappear with Ab Tx

CD19+ and CD20 +

diagnosis:
lymphoepithelial lesions in the gastric epithelium with neoplastic lymphocytes surrounding and infiltrating gastric glands

A

MALTOMA

120
Q

arises from interstitial cells of Cajal (pacemaker cells)

M>F, age 60

80% have tyrosine kinase c-KIT (CD117)

15% have PDGFA mutations

arises from mesenchyme NOT epithelial

Responds to Imatinib

A

Mesenchymal (gastro-intestinal stromal tumor) GIST

121
Q

punched out lesions in the esophagus in immunocompromised

A

herpes simplex

122
Q

well differentiated neuroendocrine carcinoma

salt and pepper in the nuclei of tumors

serotonin release:

  • skin flushing
  • diarrhea, abd pain,
  • asthma, bronchoconstriciton
  • strongly associated with mets
A

carcinoid tumors

123
Q

pANCA found in what

A

75 % of UC

124
Q

occurrence of a liver abscess after an episode of

diarrhea most likely results from infection with

A

Entamoeba histolytica

125
Q

Infection with Tropheryma whippelii

A

causes Whipple disease,

which may involve any organ, but most often affects intestines, central nervous system, and joints

126
Q

A 35-year-old woman has had increasing lower back pain for 5 years. At various times during the past year, she also
has had arthritic pain involving the knees, hips, and wrists. A stool sample is positive for occult blood. A pelvic radiograph
shows changes consistent with sacroiliitis. A colonoscopy is performed, and she undergoes a total colectomy. The figure
shows the gross appearance of the colectomy specimen. What is the most likely diagnosis?
□ (A) Dysregulated CD4+ T-cell responses
□ (B) Cross-reaction of antibodies against gut bacteria
□ (C) Auto-antibodies directed against tropomyosin
□ (D) Mutations in the NOD2 gene
□ (E) Germline inheritance of the APC gene mutation

A

The segment of the colon shows the diffuse and severe ulceration characteristic of ulcerative colitis. The
inflammation shown is so severe that areas of mucosal ulceration have produced pseudopolyps or islands of residual
mucosa. Ulcerative colitis is a systemic disease; in some patients, it is associated with migratory polyarthritis, ankylosing
spondylitis, and primary sclerosing cholangitis. The pathogenesis of ulcerative colitis is unclear, but is most likely mediated
by a T-cell response to an unknown antigen (but not a gut infection), leading to an imbalance between T-cell activation
and regulation. The CD4+ T cells present in the lesions secrete damaging substances.

127
Q

NOD2

A

crohn’s

128
Q

protein losing enteropathy

excessive secretion of TGF-alpha

A

Metetrier disease - type of hypertrophic gastropathy

enlarged rugal folds

this is diffuse hyperplasia of foveolar epithelium of body and fundus

129
Q

pt’ presents with multiple peptic ulcers b/c of this gastrin secreting tumor

A

zollinger-ellison

130
Q

F>M

sporadic and in pt’s with FAP

proton pump inhibitor related

Upper GI endoscopy reveals 3 circumscribed, round, smooth lesions in
the gastric body from 1 to 2 cm in diameter. Biopsies are taken and microscopically show the lesions to consist of irregular
glands that are cystically dilated and lined by flattened parietal and chief cells

A

fundic gland polyp

131
Q

most common in the antrum, have intestinal metaplasia with dysplasia, and are
precursors to adenocarcinoma; they may occur with FAP

M>F

arise in chronic gastritis

epithelial dysplasia

A

gastric adenoma

132
Q

most common bacteria in biofilm in mouth

A

streptococcus mutans

133
Q

LL37

A

produced by neutrophils and made in the salivary glands.

produces Kostmann Disease- with horbbile peridontitis

134
Q

mutlinucleated giant cell inclusions

establishes latency in trigeminal ganglion and recurs on lip or lower face

A

Tzanck test for Herpes Simplex Virus

135
Q

what are the 2 types of initial HSV-1 infections

A

90% age 2 to 4 yr; asymptomatic or mild, transient orofacial blisters

10% Acute Herpetic Gingivostomatitis numerous variable-size mucosal ulcers

136
Q

Pseudo-hyphae…budding blastoconidia

white - easy to scrape off

A

oral candidiasis

candida albicans

137
Q

associated with immune suppression and EBV

lateral tongue

doesn’t scrape off

balloon cells

A

hairy leukoplakia

138
Q

hypertrophy of filiform papillae on the dorsal surface of the tongue, usually due to a lack of mechanical stimulation and debridement. This condition often occurs in individuals with poor oral hygiene (eg, lack of tooth brushing, eating a soft diet with no roughage that would otherwise mechanically debride the dorsal surface of the tongue).

A

black hairy tongue

139
Q

white patch/plaque that cannot be scraped off and is due to increased keratin

A

Leukoplakia

hyperplasia/hyperkeratosis

Hyperkeratosis alone is NOT a premalignant change
But, 5 - 25% leukoplakia do contain premalignant findings
Biopsy is needed to evaluate if premalignant changes present

140
Q

what is the prognosis of erythroplakia

A

less common than leukoplakia, but more ominous … represents highly vascular eroded mucosa …” ~ 90% have dysplasia or CIS, some have invasive SCC

141
Q

oral pharynx squamous cell carcinoma is most likely caused by what

A

HPV type 16 (tonsils, base of tongue, oral pharynx) and have p16, E6 and E7 mutations

these have better prognosis usually

whereas SCC of the oral cavity are usually due to chronic alcohol/tobacco use, mutaitons in p53, NOTCH1

142
Q

parotid gland acinar epithelial cell type

A

serous

143
Q

Acute onset of bilateral (~90% cases) tender, self-limited swelling of parotid or other salivary glands lasting 2+ days

Major complication: Testicular inflammation (orchitis) occurs ~40% of postpubertal males. Sequela may be sterility.

A

mumps!

144
Q

SS-A (Ro) and SS-B(La) antibodies

angular chelitis -corners of mouth

dry eyes and mouth

commonly associated with RA

women

A

Sjogren’s

immunologically mediated destruction of the lacrimal and salivary glands

Biopsy of the lip (to examine minor salivary glands) is essential for the diagnosis of Sjögren syndrome.

145
Q

50% all salivary gland tumors and 70% of benign neoplasms

Location: 60% - parotid, 40% - submandibular/sublingual; rare - in minor salivary glands.

Termed “Mixed Tumor” because both epithelial and mesenchymal (myxoid - cartilage) elements - neoplasm arises from multipotential basal myoepithelial cells

Carcinoma in this disease develops In 5-yrs , 2% develop carcinoma. In 15-yrs period, 10% of those unresected will develop cancer.

white glistening tumors

A 
pleomorphic adenoma (mixed tumor) 
benign
146
Q

arises almost exclusively in the parotid gland (the only tumor virtually restricted to the parotid) and occurs more commonly in males than in females, usually in the fifth to seventh decades of life

more common in smokers

On microscopic examination these spaces are lined by a double layer of neoplastic epithelial cells resting on a dense lymphoid stroma (lymphocyte follicles) sometimes bearing germinal centers

Double layer of tall eosinophilic epithelial cells over a lymphoid stroma

A

Warthin Tumor (Papillary Cystadenoma Lymphomatosum)

147
Q

Parotid is the predominant site
[Parotid contains ~75% salivary tissue mass]

Slow-growing, but relentless:
difficult to excise and treat

Grade most important prognostically

Low-grade: locally aggressive, rarely metastasizes
>95% 5-yr and 10 year survival

High-grade: Invasive, frequent metastasis

A

mucoepidermoid carcinoma

148
Q

Difficult to Treat
“Perineural invasion”
Tumor spreads via peripheral nerves with numerous “skip” or non-contiguous tumor extensions

“swiss cheese” appearance

A

adenoid cystic carcinoma

149
Q

receptor tyrosine kinase RET

associated w/ down syndrome

A

hirschsprung disease

150
Q

, presents as a triad of postcricoid dysphagia, esophageal webs, and iron deficiency anemia.[1] It most usually occurs in postmenopausal women.

often complain of a burning sensation with the tongue and oral mucosa, and atrophy of lingual papillae produces a smooth, shiny, red dorsum of the tongue.

Symptoms include:
Dysphagia (difficulty in swallowing)
Pain
Weakness
Odynophagia (Painful swallowing, also called Algiaphagia)
Atrophic glossitis
Angular stomatitis
increased risk of carcinoma
A

Plummer–Vinson syndrome (PVS

151
Q

CREST

A

calcinosis - calcium deposits in skin

Raynaud’s phenomenon

Esophageal dysfunction- acid reflux and decrease in motiliyt of esophagus- rubber hose like tube

Sclerodactyly - thickening and tightening of the skin on the fingers and hands

Telangiectasis - dilation of capillaries causing red marks on surface of skin

10% of pt’s with primary biliary cirrhosis have CREST

anti-DNA topoisomerase (anti-Scl 70)

152
Q

bacterial enterocolitis infection associated with guillan barre sydnrome

A

campylobacter

GI II Exam I AP (8 decks)

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