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From Flashcardlet > Pathology - Exam 2 - GI Liver > Flashcards

Pathology - Exam 2 - GI Liver Flashcards

1
Q

Hiatal Hernia: what happens to the tissues (anatomically/pathologically)

A

Dilated portion of stomach protrudes above diaphragm

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2
Q

Hiatal Hernia: Is it rare OR common / what are the symptoms when it does occur?

A

Common but usually asymptomatic

Heartburn, reflux esophagitis

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3
Q

Hiatal Hernia: what are the dangers of this disease

A

Danger: ulceration, bleeding

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4
Q

Hiatal Hernia: what are the 2 diff types?

A
  • sliding:

* rolling:

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5
Q

Mallory-Weiss Syndrome: what happens at the tissue level

A

Gastro-Esoph junction tears

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6
Q

Mallory-Weiss Syndrome: cause?

A

Severe vomiting (chronic alcoholics)

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7
Q

Mallory-Weiss Syndrome: symptoms?

A

Symptoms: bleeding, pain, infection

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8
Q

Mallory-Weiss Syndrome: treatment? prognosis?

A

Treatment: cauterization whats bleeding
Prognosis: usually heals; sometimes fatal

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9
Q

Barrett Esophagus: what happens histologically at the cell level

A

Replacement of squamous epithelium by columnar epithelium with goblet cells

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10
Q

Barrett Esophagus: this disease is complication of what medical issue?

A

Complication of long-standing reflux esophagitis

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11
Q

Barrett Esophagus: what is the potential danger of this?

A

Danger: 30-100x risk of adenocarcinoma

bc metaplasia can lead to dysplasia

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12
Q

Barrett Esophagus: treatment?

A

Treatment: screen for high-grade dysplasia

and can laser the messed up epithelium

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13
Q

Esophageal Carcinoma: 2 types

A

adenocarcinoma
AND
squamous cell carcinoma

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14
Q

esophageal carcinoma:

Adenocarcinoma vs squamous cell carcinoma: where is each type most common

A 
A = most common in US
SCC = most common in world
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15
Q

esophageal carcinoma:
Adenocarcinoma vs squamous cell carcinoma:
RISK FACTORS?

A 
A = barrett esophagus
SCC = esophagitis, smoking, alcohol, genetics
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16
Q

esophageal carcinoma:
Adenocarcinoma vs squamous cell carcinoma:
where are they seen

A 
A = Distal 1/3 of esophagus
SCC = Middle 1/3 of esophagus
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17
Q

esophageal carcinoma:
Adenocarcinoma vs squamous cell carcinoma:
SYMPTOMS??

A

same Symptoms for both:

  • gradual harm not easily noticed (insidious);
  • late obstruction
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18
Q

what would the difference between esophagus bleed puke vs. stomach bleed puke look like

A 
E = bright red blood
S = coffee grind puke
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19
Q

gastritis: definition

A

Chronic mucosal inflammation

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20
Q

gastritis: symptoms

A

Symptoms: asymptomatic, or discomfort

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21
Q

gastritis: causes?

A

Causes:
*Helicobacter pylori,
OR
*autoimmune gastritis = attack of parietal cells
- no intrinsic factor (required for making B12)
- no acid

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22
Q

gastritis: danger of developing what?

A

intestinal metaplasia (columnar to squamous)

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23
Q

who “discovered”/ H. Pylori

A

Barry Marshall and Robin Warren
(via mistake in the lab)
no one believed them
so Barry Marshall drank it –> nobel prize

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24
Q

how does H.pylori change the environment of the stomach?

A

has urease that creates ammonia to raise the pH so they can survive in such an acidic environment.

  • makes the host cell:
  • release cytokines
  • neutrophils spit off free radicals
  • creates holes/vacuoles in the cells
  • immobilize helper T-cells
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25
Q

H. pylori can cause 2 things

A 
acute gastritis
AND 
chronic gastris
or 
ULCERS
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26
Q

H. pylori infection
can lead to asymptomatic gastritis
which can lead to what

A

symptomatic gastritis
ulcer
carcinoma
lymphoma

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27
Q

Acute gastritis

A

Acute mucosal inflammation (usually transitory)

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28
Q

Acute gastritis: causes

A

H. pylori, NSAIDS, alcohol, smoking

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29
Q

Acute gastritis: 2 types or “presentations”

A

Superficial or full-thickness

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30
Q

Acute gastritis: can lead to what dangerous occurrence?

A

Can lead to erosions

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31
Q

Acute gastritis: sympotoms?

A 
Asymptomatic 
or 
pain, 
vomiting, 
hematemesis
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32
Q

Ulcers: what happens at the tissue level

A

Erosion of mucosa into submucosa

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33
Q

Ulcers: causes?

A

Causes: H. pylori, NSAIDs

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34
Q

Ulcers: symptoms?

A

Symptoms: epigastric pain

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35
Q

Ulcers: dangers?

A

Danger: bleeding, perforation

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36
Q

How does Helicobacter cause ulcers?

A
  • Bugs hide in mucous and attract inflammatory cells
  • Inflammatory cells release toxins but can’t kill bugs easily
  • Host causes damage by continual, ineffective immune response!
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37
Q

Gastric Carcinoma: 2 types?

A

intestinal type
AND
diffuse types

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38
Q 
Gastric Carcinoma: intestinal type
where does it arise from?
risk factors?
morphology?
any symptoms??
A

Intestinal type

  • Arises in intestinal metaplasia
  • Risk factors: chronic gastritis, bad diet
  • Glandular morphology
  • Generally asymptomatic
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39
Q 
Gastric Carcinoma: diffuse 
where does it arise from?
risk factors?
morphology?
any symptoms??
A

Diffuse type

  • Arises from gastric glands
  • Risk factors undefined
  • Signet ring morphology (hard to find for pathologist - scary!)
  • Generally asymptomatic
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40
Q

what is one of the first symptoms of stomach cancer?

A

usually left (or sometimes right) superclavicular node is super swollen = VIRCHOW’s NODE

(b/c left drains abdomen / right drains thorax)

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41
Q

Gastric Carcinoma’s can also present as _________?

A

“LINITIS PLASTICA”
rigid “leathery” “wall” - usually from diffuse stomach cancer
(but can be from metastasis of something else)

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42
Q

Intestines: Diverticulosis: what happens at tissue level?

A

Mucosa/submucosa herniates through muscle wall

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43
Q

Intestines: Diverticulosis: risk factors?

A

Older patients, low fiber diet

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44
Q

Intestines: Diverticulosis:what part of intestines does it usually happen?

A

sigmoid colon

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45
Q

Intestines: Diverticulosis: any symptoms??

A

Asymptomatic

*unless infected = “diverticulitis”

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46
Q

Inflammatory Bowel Disease: 2 types? (2 diff diseases)

A

Crohns Disease

Ulcerative Colitis

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47
Q

Inflammatory Bowel Disease: Crohn Disease (FEATURES)

A 
*Crohn Disease
Anywhere
Patchy
Transmural
Poor response to surgery
Increased risk of cancer
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48
Q

Inflammatory Bowel Disease: ulcerative colitis (FEATURES)

A 
*Ulcerative Colitis
Colon only
Continuous
Superficial
Good response to surgery
Increased risk of cancer
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49
Q

location of disease: crohn disease vs. ulcerative colitis

A 
C = anywhere (systemic inflammatory disease)
U = colon only
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50
Q

pathological presentation/place : crohn disease vs. ulcerative colitis

A 
C = patchy
U = continuous (end of sigmoid colon and "up")
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51
Q

layers of tissue involvement: crohn disease vs. ulcerative colitis

A 
C = transmural (thru all the layers)
U = superficial (inflammation only affects mucosa)
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52
Q

response to surgery: crohn disease vs. ulcerative colitis

A 
C = poor (b/c patchy - can pop up anywhere)
U = good (b/c you know where the lesion is - take it out and be done)
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53
Q

risk of cancer?: crohn disease vs. ulcerative colitis

A

BOTH have increased risk of colon carcinoma

C = slightly less risk

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54
Q

signs/symptoms: crohn disease vs. ulcerative colitis

A 
C = crampy intermittent pain and discomfort, fever
U = bloody diarrhea
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55
Q

Adenoma: general features.

A
  • Common! 50% of people >60.

* Benign glands that may become dysplastic

56
Q

Adenoma: when is it more dangerous?

A

More dangerous when:
Large (>1 cm)
Villous architecture
Severely dysplastic

57
Q

Adenoma: what is the biggest risk factor of those for it becoming malignant?

A

SIZE = bigger, >1 cm = bad news bear

58
Q

Adenoma: 2 types

A

tubular (looks like a mushroom)

villous (looks like a sea sponge)

59
Q

Colon Carcinoma: usually arises from what tissue finding?

A

Almost always arises in adenomatous polyp

(colon adenoma) –> colon adenocarcinoma

60
Q

Colon Carcinoma: risk factors/lifestyle risks

A

Diet: low fiber, high fat, lots of refined carbs

61
Q

Colon Carcinoma: symptoms?

A 
Symptoms: 
silent for years
fatigue, 
weakness, 
iron-deficiency anemia (bc bleeding)
occult bleeding (initially see anemia) 
"BRB" = bright red blood
crampy pain
62
Q

Colon Carcinoma: prognosis

A

based on stage
5 year prognosis: 4% (stage 4) - 90% (stage 1)
(don’t memorize #’s just understand)

63
Q

Liver: diseases we discussed

A 
Hepatitis
Alcoholic liver disease
Hemochromatosis
Wilson disease
Carcinoma
64
Q

Viral Hepatitis:

A

some asymptomatic

65
Q

Viral Hepatitis: most common sign of acute HEP

A

acute = jaundice

66
Q

Viral Hepatitis: most common sign of CHRONIC HEP?

A

Chronic = cirrhosis (fibrous tissue when liver trying to mend itself)
* this can lead to liver failure

67
Q

Viral Hepatitis: fulminant?

A

very dangerous

leads to liver failure

68
Q

Viral Hepatitis: which is highest chance of chronic?

A

HEP C

69
Q

Viral Hepatitis: which have chance of carcinoma

A

HEP B & HEP C

HEP C more bc greater chance of chronic

70
Q

cells prominent in ACUTE HEP

A

lymphocytes all over the place

71
Q

cells prominent in CHRONIC HEP

A

lymphocytes around portral tract which can lead to fibrosis around these areas of inflammation

72
Q

what happens (histologically) to hepatocytes infected with HEP

A

can see changes in the hepatocytes too = ground-glass hepatocytes (viruses sitting in the cytoplasm of the cells)

73
Q

JAUNDICE: what happens to the bilirubin during HEP infection jaundice

A

build up of conjugated
-or-
unconjugated bilirubin

74
Q

Conjugated hyperbilirubinemia

A
  • DEC liver excretion (bc of hepatitis)

* DEC bile flow (tumor blocking bile duct)

75
Q

Unconjugated hyperbilirubinemia

A
  • INC production (bc of hemolytic anemia)

* DEC uptake (bc of hepatitis)

76
Q

Hepatocyte integrity: lab tests?

A

Serum aspartate aminotransferase (AST)

Serum alanine aminotransferase (ALT)

77
Q

Biliary function

A

*Serum bilirubin (total and direct)
(total = making more or blacking into blood - can’t excrete)
*Serum alkaline phosphatase (from biliary epi cells)

78
Q

Hepatocyte function

A 
Serum albumin (down? not making? or peeing out?)
Prothrombin time (coagulation factors made in liver)
79
Q

Cirrhosis: pathological presentation @ tissue level

A

Fibrotic bands in liver,
-and-
nodular liver

80
Q

Cirrhosis: causes?

A

Causes: alcoholism, hepatitis

81
Q

Cirrhosis: what diseases does this lead to

A

Leads to:

  • portal hypertension
  • and-
  • liver failure
82
Q

Cirrhosis: risks associated?

A

Increased risk of liver carcinoma

83
Q

Portal Hypertension: why/how does it occur?

A

Decreased blood flow through liver

84
Q

Portal Hypertension: biggest cause?

A

Biggest cause: cirrhosis

85
Q

Portal Hypertension: symptoms?

A

Symptoms
*ascites (fluid in peritoneal cavity)

  • venous shunts: (where portal and systemic share capillary beds) –> can rupture –> (esophageal varices, hemorrhoids)
  • congestive splenomegaly (big spleen)
  • hepatic encephalopathy
86
Q

Portal Hypertension: what are Esophageal varices

A

dilated vessels in esoph where shared with hepatic portal system

87
Q

Portal Hypertension: what is Caput medusae

A

dialated surface veins on abdomen

88
Q

Liver Failure: definition?

A

End point of severe liver disease

89
Q

Liver Failure: causes

A

Causes:
fulminant hepatitis,
cirrhosis,
drug overdose

90
Q

Liver Failure: symptoms?

A 
Symptoms: 
jaundice, 
edema, 
bleeding, 
hyperammonemia
91
Q

Liver Failure: can lead to diseases/syndromes in other organs - what are they

A

Multiple organ-system failure:
*Hepatic encephalopathy - stupor coma and death prob due to ammonia

*Hepatorenal syndrome - kidneys failing bc of crap blood flow to liver

92
Q

Oral Manifestations of Liver Injury

A 
Hematomas, 
gingival bleeding
Jaundiced mucosa
Glossitis (in alcoholic hepatitis)
Reduced healing after surgery
93
Q

Alcoholic Liver Disease: effects on liver

A

Effects on liver:
steatosis (accumulation of fat),
hepatitis,
cirrhosis

94
Q 
Alcoholic Liver Disease: 
how much do you need to drink to cause damage?
short term vs. long term?
which is reversible?  
which is more severe?
A

Short-term ingestion of 8 beers/day
- reversible steatosis

Long-term ingestion of 5 beers/day
- severe injury

note: Beer and binge drinking are risky

95
Q

Alcoholic Liver Disease: hepatitis (see slide 77)

A

liver cell necrosis
inflammation
mallory bodies - (associated w/ alcoholic HEP only)
fatty change

96
Q

Alcoholic Liver Disease: steatosis (see slide 77)

A

fatty change
perivenular fibrosis

(possibly reversible but not if continued exposure)

97
Q

Alcoholic Liver Disease: cirrhosis (see slide 77)

A

fibrosis

hyperplastic nodules

98
Q

what pathological/histological “feature” is seen only in Alcoholic Hepititis but not Viral?

A

Mallory Bodies

99
Q

Alcoholic Liver Disease: what is the prognosis if pt decides to abstain

A

Abstinence: 5ys is 90%

100
Q

Alcoholic Liver Disease: prognosis if pt continues to drink?

A

Continued drinking: 5ys drops to 50-60%

101
Q

Alcoholic Liver Disease: causes of death?

A 
*Causes of death in end-stage alcoholism:
Liver failure
Massive GI bleed
Infection
Hepatorenal syndrome
Hepatocellular carcinoma
102
Q

Hereditary hemochromatosis:
what mode of heredity?
what do you see serologically in the body?

A

Autosomal recessive disease:

- see INCREASED body iron

103
Q

Hereditary hemochromatosis:
what mutation causes?
what is this gene’s purpose?

A

Cause: mutations in hemochromatosis gene

gene purpose = regulates iron absorption

104
Q

Hereditary hemochromatosis: symptoms?

A

Cirrhosis,
skin pigmentation,
liver carcinoma

105
Q

Hereditary hemochromatosis:
how diagnosed?
treatment?

A

Early detection = phlebotomy,
treatment = iron chelators
can lead to –> normal life expectancy

106
Q

Wilson Disease:
what type of heredity?
what element is at wrong level in body
(too much? too little?)

A

Autosomal recessive disease:

see: INCREASES body copper

107
Q

Wilson Disease: cause?

A

Cause: mutation in gene regulating copper excretion

108
Q

Wilson Disease: symptoms?

A

Symptoms:
acute and chronic liver disease,
neuropsychiatric manifestations,
Kayser-Fleisher rings in cornea (slide 85)

109
Q

Wilson Disease: trx?

A

Treatment: copper chelation therapy

110
Q

Hepatocellular Carcinoma: associated with what diseases?

A 
Strongly associated with :
hepatitis B 
Hepatitis C, 
chronic liver disease, and 
aflatoxins
111
Q

Hepatocellular Carcinoma: symptoms

A

Rapid increase in liver size,
worsening ascites,
fever and pain

112
Q

Hepatocellular Carcinoma: what is seen serologically?

A

VERY HIGH alpha fetoprotein level

113
Q

Hepatocellular Carcinoma:
prognosis?
what usually causes death?

A 
Median survival 7 months 
*death from: 
bleeding, 
liver failure, 
cachexia
114
Q

what is the Most common malignancy in the liver

A

Metastatic Carcinoma: Usually multiple lesions

115
Q

Metastatic Carcinoma: most common cancer places/types that it came from (“primary”)

A 
Most common primaries: (know first three)
colon, 
lung, 
breast, 
pancreas, 
stomach.
116
Q

Cholelithiasis: what are the 2 different types of gall stones you can get?

A

Cholesterol stones

pigment stones

117
Q

Cholelithiasis: compare the 2 types of stones.

A
  • Cholesterol stones: Female, Fat, Fertile, Forty

* Pigment (bilirubin) stones: more in Asian countries, seen in hemolytic anemia and biliary infections

118
Q

Cholelithiasis: symptoms?

A

Symptoms: None, or excruciating pain

119
Q

Cholelithiasis: complications

A 
Complications: 
cholecystitis, 
empyema, 
perforation, 
fistula, 
obstruction, 
pancreatitis
120
Q

Normal Pancreas: what are it’s 2 functions?

A

exocrine
AND
endocrine

121
Q

Normal Pancreas: exocrine pancreas

  • what does it make?
  • what diseases are seen when there is a problem with the exocrine part?
A 
Exocrine pancreas
-Makes enzymes for digestion
-Diseases:
   Pancreatitis, 
   cystic fibrosis, 
   tumors
122
Q

Normal Pancreas: endocrine pancreas

  • what does it make?
  • what diseases are seen when there is a problem with the endocrine part?
A 
Endocrine pancreas
- Makes:
    insulin, 
    glucagon, 
    other hormones
- Diseases: 
     Diabetes, 
     tumors
123
Q

Acute Pancreatitis: “definition?”

A

Acute inflammation
-and-
reversible destruction of pancreas

124
Q

Acute Pancreatitis: symptoms

A

Symptoms: abdominal pain radiating to back

125
Q

Acute Pancreatitis: main causes?

A

Main causes: alcoholism, gallstones

126
Q

Acute Pancreatitis: labs used for Dx?

A 
Labs for DX:
elevated serum:
* amylase 
-and-
* lipase
127
Q

Acute Pancreatitis: prognosis?

A

Prognosis: Most recover,

but 5% die in first week

128
Q

Chronic Pancreatitis: technical definition?

A

Longstanding, irreversible pancreatic destruction

129
Q

Chronic Pancreatitis: most related to what?

A

Most are alcohol related,

however, some idiopathic

130
Q

Chronic Pancreatitis: Symptoms?

A

Symptoms: silent, or bouts of jaundice and pain

131
Q

Chronic Pancreatitis: prognosis?

A

Prognosis: poor (50% mortality over 20 years)

132
Q

Pancreatic Carcinoma: epidemiology?

A

4th leading cause of cancer death in US

HIGHLY invasive

133
Q

Pancreatic Carcinoma: biggest risk factor?

A

Biggest risk factor: smoking

134
Q

Pancreatic Carcinoma: symptoms?

A

Silent until late; then pain, jaundice

135
Q

Pancreatic Carcinoma: prognosis?

A

Very high mortality: 5ys <5%

136
Q

Pancreatic Carcinoma: which is more deadly? exocrine or endocrine?

A

exocrine

From Flashcardlet (51 decks)

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