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FirstAid:GI > GI:Pathology > Flashcards

GI:Pathology Flashcards

1
Q

Salivary gland tumors are generally benign/malignant and occur in the _____ gland

A

Benign parotid

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2
Q

What is the most common salivary gland tumor?

A

Pleomorphic adenoma

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3
Q

What is the most common malignant tumor of the salivary glands?

A

Mucoepidermoid carcinoma

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4
Q

What a benign, cystic tumor of the salivary glands with germinal centers?

A

Warthin’s tumor

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5
Q

How do pleomorphic adenomas present? What are they composed of?

A

Painless, mobile mass

Cartilage and epithelium

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6
Q

Why do mucoepidermoid carcinomas often present as a painful mass?

A

Due to frequent involvement of the facial nerve

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7
Q

What is the problem in achalasia?

A

Failure of relaxation of the lower esophageal sphincter due to loss of the myenteric plexus–> high LES opening pressure and uncoordinated peristalsis

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8
Q

Does achalsia present with dysphagia to solids or liquids?

A

Progressive dysphagia to both

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9
Q

What does a barium swallow show with achalasia?

A

Dilated esophagus with an area of distal stenosis

**Bird’s beak appearance

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10
Q

Achalasia is associated with an increased risk for which malignancy?

A

Esophageal squamous cell carcinoma

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11
Q

What might secondary achalasia arise from?

A

Chaga’s disease

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12
Q

What is associated with esophageal dysmotility involving low pressure proximal to the LES

A

Scleroderma (CREST syndrome)

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13
Q

What does GERD commonly present as?

A

Heartburn and regurgitation upon lying down

Nocturnal cough, dyspnea, and adult-onset asthma

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14
Q

What causes GERD?

A

Decrease in LES tone

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15
Q

What is painless bleeding of dilated submucosal veins in the lower 1/3 of the esophagus?

A

Esophageal varices

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16
Q

What causes esophageal varicies?

A

Portal HTN

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17
Q

What are the three key things that esophagtits is caused by?

A
  1. Reflux
  2. Infection
  3. Chemical ingestion
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18
Q

What are three infections that commonly cause esophagitis>

A

Candida (white pseudomembrane)
HSV-1 (punched out ulcers)
CMV (linear ulcers)

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19
Q

What is Mallory-Weiss syndrome

A

Mucosal lacerations at the GE junction due to severe vomiting, leading to hematemesis

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20
Q

Who gets Mallory-Weiss syndrome?

A

Alcoholics

Bulimics

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21
Q

What is BoerHaave Syndrome?

A

Transmural esophageal rupture due to violent retching

**Been-Heaving Syndrome

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22
Q

What are esophageal strictures associated with?

A

Lye ingestion

Acid reflux

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23
Q

What is Plummer-Vinson syndrome a triad of?

A

Dysphagia (from esophageal webs)
Glossitis
Iron deficiency anemia

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24
Q

What happens in Barrett’s esophagus?

A

Glandular metaplasia–replacement of nonkeritonized stratified squamous epithelium with intestinal, non-ciliated columnar epithleium in the distal esophagus

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25
Q

What causes Barrett’s esophagus?

A

Chronic GERD

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26
Q

What are three complications that Barrett’s esophagus is associated with?

A

Esophagitis
Esophageal ulcers
Esophageal adenocarcinoma

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27
Q

What are the two types of esophageal cancer?

A

Adenocarcinoma

Squamous cell carcinoma

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28
Q

How does esophageal cancer usually present?

A

Progressive dysphagia from solids to liquids

Weight loss

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29
Q

What are the risk factors for esophageal adenocarcinoma?

A

Barrett’s/GERD
Obesity
Tobacco use

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30
Q

Which type of esophageal cancer is more common worldwide? In the US?

A

Worldwide: squamous
US: adeno

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31
Q

Where in the esophagus does squamous cell present? Adeno?

A

Squamous: upper 2/3
Adeno: lower 1/3

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32
Q

What are the 6 main malabsorption syndromes?

A 
Tropical sprue
Whipple's disease
Celiac sprue
Disaccharidase deficiency
Abetalipoproteinemia
Pancreatic insufficiency 
**these will cause devastating absorption problems
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33
Q

Cause of tropical sprue? Similar to:

A

Unknown cause, but responds to antibiotics

SImilar to celiac sprue–can affect whole SI

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34
Q

What organism causes Whipple’s disease?

Gram stain:

A

Tropheryma whipplei

Gram positive

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35
Q

What will Whipple’s disease present with histologically?

A

PAS positive, foamy PMNs in the intestinal lamina propria and mesenteric nodes

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36
Q

What are the three most common sx of Whipple’s disease

A

Cardiac sx
Arthralgias
Neurologic sx
**Foamy WHIPPed cream in a CAN

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37
Q

What causes celiac sprue?

A

Autoantibodies to gluten (gliadin) in wheat and other grains

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38
Q

What are the areas of the GI tract that are primarily affected by celiac sprue?

A

Distal duodenum

Proximal jejunum

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39
Q

What will be seen histologically with celiac sprue?

A

Loss of villi

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40
Q

What is the most common disaccharidase deficiency?

A

Lactase deficiency (leading to milk intolerance)

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41
Q

What kind of diarrhea will be seen with disaccharidase deficiency?

A

Osmotic diarrhea

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42
Q

What can cause self-limited lactase deficiency?

A

Injury to the villi, because lactase is located at the tips of the villi

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43
Q

With a lactose tolerance test, a patient is positive for lactase deficiency if: (2)

A
  1. Administration of lactose produces sx

2. Glucose rises <20 mg/dL

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44
Q

What is the chain of events that occurs in in abetalipoproteinemia?

A

Decreased synthesis of apolipoprotein B
Inability to generate chylomicrons
Decreased secretion of chol, VLDL into bloodstream
Fat accumulation in enterocytes

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45
Q

How does abetalipoproteinemia present?

A

Early in childhood with malabsorption and neurologic manifestations

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46
Q

What are three things that can cause pancreatic insufficiency?

A

Cystic fibrosis
Obstructing cancer
Chronic pancreatitis

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47
Q

Pancreatic insufficiency causes malabsorption of:

A

Fat

Fat soluble vitamins (A,D,E,K)

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48
Q

What will be increased in the stool of a patient with pancreatic insufficiency?

A

Neutral fat

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49
Q

What is autoimmune mediated intolerance of gliadin leading to steatorrhea?

A

Celiac sprue

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50
Q

What genetic factors is celiac sprue associated with?

A

HLA-DQ2
HLA-DQ8
People of northern european descent

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51
Q

What three antibodies will be found in celiac sprue?

A

Anti-endomysial
Anti-tissue transglutaminase
Anti-gliadin

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52
Q

Decreased mucosal absorption in celiac sprue primarily affects what area of the GI tract?

A

Jejunum

53
Q

What is used for screening for celiac sprue?

A

Serum levels of tissue transglutaminase antibodies

54
Q

What skin lesion will be found in association with celiac sprue?

A

Dermatitis herpetiformis

55
Q

What are the main RFs for squamous cell carcinoma of the esophagus?

A 
Alcohol use
Smoking
N-nitroso-containing foods
Betel nut chewing in Asia
Hot liquids 
Diverticula and esophageal webs
56
Q

What are Curlings and Cushings ulcers?

A

Two forms of acute gastritis:
Curling: burn→low volume→gastric sloughing
Cushing:brain injury→increased vagal stimulation→increase ACh→increased H+

57
Q

Causes of ACUTE (erosive) gastritis

A 
Stress
NSAIDs
Alcohol
Uremia
Burns
Brain injury
58
Q

What are the two types of chronic (non-erosive) gastritis?

A

Type A: fundus and body, autoantibodies to parietal cells

Type B: antrum, MC. H. pylori

59
Q

What type of gastritis leads to increased risk of malignancy?

A

Increased risk of MALT lymphoma with Type B (antral) chronic gastritis caused by H. pylori

60
Q

Precancerous condition where hypertrophies rugae of the stomach resemble brain gyri?

A

Menetrier’s disease: protein loss, pareietal cell atrophy, increase in mucus cells

61
Q

Skin manifestation of gastric adenocarcinoma?

A

Acanthosis nigracans

62
Q

What type of gastric cancer is associated with H pylori

A

Intestinal: lesser curvature, looks like a raised ulcer

**other RFs are dietary nitrosamines, chronic gastritis, type A blood

63
Q

What type of gastritis leads to pernicious anemia and achlorhydia?

A

Type A (body/fundus) chronic gastritis

64
Q

Presentation of diffuse gastric cancer

A

Signet ring cells

Thick and leathery wall (linitus plastica)

65
Q

Stomach met to left supraclavicular node

A

Virchow’s node

66
Q

Bilateral gastric cancer mets to the ovaries

A

Kruckenberg’s tumor: abundant mucus and signet rings

67
Q

Subcutaneous periumbilical metastasis from gastric cancer

A

Sister Mary Joseph nodule

68
Q

Gastic vs duodenal ulcers: pain with meals

A

More pain with gastric

Pain decreases with meals with duodenal

69
Q

Gastic vs duodenal ulcers: association with H. pylori

A

100% duodenal associated with H. pylori

Only 70% with gastric

70
Q

Gastic vs duodenal ulcers: cause

A

Gastric: decreased protection, NSAIDS
Duodenal: decreased protection and increased gastric acid (ZE)

71
Q

Gastic vs duodenal ulcers: risk of carcinoma

A

Gastric

72
Q

What is hypertrophied with duodenal ulcers/

A

Brunner’s glands

73
Q

Is hemorrhage from a duodenal ulcer more commonly posterior or anterior? Perforation?

A

Hemorrhage: posterior
Perforation: anterior

74
Q

Ulcer on the posterior wall of the duodenum, bleeding from what artery?

A

Gastroduodenal

75
Q

Ruptured gastric ulcer on the lesser curvature of the stomach, bleeding from what artery?

A

Left gastric

76
Q

What type of helper T cell mediates crohns vs UC?

A

Crohns: Th1
UC: Th2

77
Q

Is Crohns or UC associated with primary sclerosing cholangitis?

A

UC

78
Q

Cause of acute appendicitis in kids vs adults

A

kids: lymphoid hyperplasia
adults: fecalith obstruction

79
Q

Are most diverticula true or false?

A

False/acquired: attenuated muscularis externa, esp where the vasa recta perforate the muscularis externa

80
Q

MC location for diverticula

A

Sigmoid colon

81
Q

Causes of diverticulosis

A

Increased intraluminal pressure
Focal weakness
Low fiber diet
**common cause of hematochezia (fresh blood in stool)

82
Q

What will cause pneumaturia following diverticulitis

A

Colovesical fistula (between colon and bladder), passage of gas in the urine

83
Q

What causes Zenkers diverticulum

A

False div: hernitation of mucosa tissue at Killian’s triangle between the thyropharyngeal and cricopharyngeal parts of the inferior pharyngeal constrictor
Cricopharyngeal dysfunction

84
Q

MCC of small bowel obstruction?

A

Adhesions

85
Q

Pain after eating and weight loss in the elderly

A

Ischemic colitis, commonly at the splenic flexure and distal colon

86
Q

What is a tortuous dilation of vessels in the intestine leading to hematochezia, seen in older patients?

A

Angiodysplasia

87
Q

What type of colon polyp is precancerous?

A

Adenomatous (tubular, villous, tubulovillous)

88
Q

MC non-neoplastic colon polyp

A

Hyperplastic (>50% in the rectosigmoid colon)

89
Q

AD syndrome with multiple nonmalignant hamartomas through the GI and hyperpigmented mouth, lips, hands, genitalia

A

Peutz-Jeghers

90
Q

Mutation causing FAP

A

AD mutation in APC on chromosome 5q (2 hit hypothesis)

Thousands of polyps through the colon

91
Q

What is Garner’s syndrome

A

FAP
Osseous and soft tissue tumors
Congenital hypertrophy of the retinal pigment epithelium

92
Q

What is Turcot’s syndrome?

A

FAP

Malignant CNS tumors (medulloblastoma)

93
Q

What causes Lynch syndrome/HNPCC

A

AD mutation in DNA mismatch repair genes

94
Q

MC location for CRC?

A

Rectosigmoid

95
Q

What is the characteristic lesion seen on barium enema with CRC?

A

Apple core lesion

96
Q

How can be CEA be used in CRC?

A

Good for monitoring recurrence but not for screening

97
Q

What are the two molecular pathways leading to CRC?

A
  1. ABC/beta catenin 85%

2. Microsatellite instability 15%

98
Q

What is the progression of mutations seen in the APC pathway

A

APC → k-ras → p53/DCC

99
Q

What tumor type makes up 50% of small bowel tumors?

MC sites

A

Carcinoid

Appendix, ileum, rectum

100
Q

What are two things that will elevate amylase?

A

Acute pancreatitis

Mumps

101
Q

What is the mechanism of Reyes syndrome?

A

Aspirin metabolites decrease beta oxidation by reversible inhibition of mitochondrial enzymes

102
Q

What is the presentation of Reyes syndrome?

A

Kid treated with apirin after Inf B or VZV infection, other viral
Mitochondrial abnormalities, fatty liver, hypoglycemia, vomiting, hepatomegaly, coma

103
Q

What is the reversible change of the liver seen in alcoholics

A

Hepatic steatosis: macrovesicular fatty change

104
Q

What is seen microscopically with alcoholic hepatitis?

A 
Swollen and necrotic hepatocytes with PMN infiltration 
Mallory bodies (intracytoplasmic eosinophilic inclusions)
105
Q

Where is the majority of the sclerosis in alcoholic hepatitis

A

Around the central vein (zone III)

106
Q

What marker can be measured serialy for people with RFs for HCC?

A

AFP (increased in HCC)

107
Q

What are hepatic adenomas associated with?

A

Benign liver tumors associated with OCP and steroid use, regress spontaneously

108
Q

What tumors are associated with arsenic and polyvinyl chloride exposure?

A

Angiosarcoma; malignant tumor of endothelial origin

109
Q

How is Budd Chiari syndrome distinguished from liver congestion due to R heart failure?

A

No JVD in Budd Chiari

110
Q

Cirrhosis with PAS positive globules in the liver

A

alpha1 AT deficiency; gene product is aggregating in hecaptocellular ER
**codominant trait

111
Q

What is the difference between types I and II Crigler-Najjar?

A

Type II is less severe and responds to phenobarbital, which increases the activity of UDP glucuronyl transferase

112
Q

What is the inheritance of Wilson’s disease?

A 
AR recessive (chromosome 13)
Coppen normally excreted into bile by hepatocyte copper transporting ATPase (ATP7B gene)
113
Q

Where is a common location that Wilson’s disease causes cystic degeneration?

A

Putamen

114
Q

What kidney finding can result for wilson’s disease?

A

Fanconi syndrome (PT dysfunction)

115
Q

Micronodular cirrhosis, diabetes, and hyperpigmentation

A

Hemochromotosis: causes CHF and testicular atrophy

116
Q

What causes primary hemochromatosis?

A

C282Y or H63D (his to aspartate) mutation on HFE cene

117
Q

What presents with dementia, dyskinesia, dysarthria (difficulty speaking), and cirrhosis?

A

Wilson’s disease

118
Q

What HLA is associated with hemochromatosis?

A

HLA-A3

119
Q

Pruritus
Jaundice
Dark urine
Hepatosplenomegaly

A

Primary biliary cirrhosis
Secondary biliary cirrhosis
Primary sclerosing cholangitis

120
Q

Pathophys of PBC

A

Autoimmune rxn, lymphocytic infiltrate and granulomas (T cell attacking the bile ducts)

121
Q

Appearance of ducts in PSC

A

Concentrict onion skin bile duct fibrosis with alternating strictures and dilation with beading of the intra and extrahepatic bile ducts on ERCP

122
Q

Antibodies in PBC

A

+ anti mitochondrial

123
Q

Which biliary tract disease is UC associated with?

A

Primary Sclerosing Cholangitis

124
Q

Majority of pts with PSC are + for:

A

p-ANCA

125
Q

What causes secondary biliary cirrhosis?

A

Extrahepatic biliary obstruction (gallstone, biliary stricture, chronic pancreatitis, carcinoma of the pancreas head)
Increase in pressure in the intrahepatic ducts
Injury and fibrosis, bile stasis

126
Q

Tx for PBC

A

Ursodiol: bile acid that decreases cholesterol synthesis in the liver and changes the bile composition

127
Q

Trousseaus sign

A

Migratory thrombophlebitis–redness and tenderness on palpation of the extremities

128
Q

Courvoisier’s sign

A

Obstructive jaundice with a palpable, nontender gallbladder

129
Q

3 rfs for hepatic adenomas

A

OCPs
Anabolic steroids
Glycogen storage diseased

FirstAid:GI (5 decks)

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