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GI Test > Stomach, Small intestine/colon, Salivary gland, Pancreas, and Oral Cavity Pathology > Flashcards

Stomach, Small intestine/colon, Salivary gland, Pancreas, and Oral Cavity Pathology Flashcards

1
Q

What are the normal damaging factors to the gastric muscosa?

A
  • Gastric acidity

- Peptic enzymes

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2
Q

What are the normal protective factors to the gastric muscosa?

A
  • Surface mucus secretion
  • Bicarbonate secretion into mucus
  • Mucosal blood flow
  • Epithelial barrier function
  • Epithelial regenerative capacity
  • Elaboration of prostaglandins
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3
Q

What are some external factors that damage the gastric mucosa?

A
  • H. pylori infection
  • NSAIDs
  • Tobacco
  • Alcohol
  • Gastric hyperacidity
  • Duodenal-gastric reflux
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4
Q

What are some internal factors that damage the gastric mucosa?

A
  • Ischemia
  • Shock
  • NSAIDs
  • Radiation
  • Chemotherapy
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5
Q

What do exogenous prostaglandins do?

A
  • Inhibit acid secretion
  • Stimulate mucus and bicarbonate secretion
  • Alter mucosal blood flow
  • Provide dramatic protection against wide variety of agents which cause acute mucosal damage
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6
Q

What is the molecular defect of FAP?

A
  • APC/WNT pathway
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7
Q

What are the target genes in FAP?

A
  • APC
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8
Q

What is the transmission of FAP?

A
  • AD
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9
Q

What is the histology of FAP?

A
  • Tubular, villous, typical adenocarcinoma
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10
Q

What is the molecular defect of MYH-associated polypsis?

A
  • DNA mismatch
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11
Q

What are the target genes of MYH-associated polypsis?

A
  • MYH
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12
Q

What is the transmission of MYH-associated polypsis?

A
  • AR
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13
Q

What is the histology of MYH-associated polypsis?

A
  • Sessile serrated adenoma; mucinous adenocarcinoma
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14
Q

What is the molecular defect of hereditary nonpolyposis colorectal cancer?

A

DNA mismatch repair

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15
Q

What are the target genes of hereditary nonpolyposis colorectal cancer?

A
  • MSH2

- MLH1

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16
Q

What is the transmission of hereditary nonpolyposis colorectal cancer?

A
  • AD
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17
Q

What is the histology of hereditary nonpolyposis colorectal cancer?

A
  • Sessile serrated adenoma; mucinous adenocarcinoma
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18
Q

What is the molecular defect of sporadic colon cancer?

A
  • APC/WNT pathway
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19
Q

What are the target genes of sporadic colon cancer?

A
  • APC
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20
Q

What is the histology of sporadic colon cancer?

A
  • Tubular, villous; typical adenocarcinoma
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21
Q

What is the peak age for colonic adenocarcinoma?

A
  • 60-70s
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22
Q

What is the clinical presentation of FAP?

A
  • AD disorder in which patients develop numerous colorectal adenomas as teenagers
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23
Q

What do carcinomas in the distal colon look like?

A
  • Tend to be annular lesions that produce “napkin-ring” contractions and luminal narrowing
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24
Q

What is Peutz-Jeghers syndrome?

A
  • AD syndrome that presents at a median age of 11 years with multiple GI hamartomatous polyps and mucocutaneous hyperpigmentation
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25
Q

What regions of the body are hyperpigmented in Peutz-Jeghers?

A
  • Lips
  • Nostrils
  • Buccal mucosa
  • Palmar surfaces of hands
  • Genitalia
  • Perianal region
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26
Q

What is the LOF mutation in Peutz-Jeghers?

A
  • STK11
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27
Q

What is fatal in Peutz-Jeghers?

A
  • Intussusception
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28
Q

What do people with Peutz-Jeghers most at risk for?

A
  • Risk of colon, breast, lung, pancreatic, and thyroid cancer
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29
Q

In whom is IBD more likely?

A
  • Teens/early 20s
  • Caucasians
  • 3-5x more likely in Ashkenazi Jews
  • Most common in North America, Europe, and Australia
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30
Q

What area of the GI tract does Crohn’s disease affect?

A
  • Any area of the GI tract but most commonly involves the terminal ileum, ileocecal valve, and cecum
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31
Q

What area of the GI tract does ulcerative colitis affect?

A
  • Colon only
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32
Q

What is the distribution of crohn disease?

A
  • Skip lesions

- Have creeping fat

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33
Q

What is the distribution of ulcerative colitis?

A
  • Diffuse
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34
Q

What is the earliest sign of crohn disease?

A
  • Aphthous ulcer

- Multiple lesion often coalesce into elongated, serpentine ulcers oriented along the axis of the bowel

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35
Q

Is there a stricture in crohn disease?

A
  • Yes
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36
Q

Is there a stricture in ulcerative colitis?

A
  • Rarely
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37
Q

What does the colonic wall look like in crohn disease?

A
  • Thick
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38
Q

What does the colonic wall look like in ulcerative colitis?

A
  • Thin
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39
Q

What does the inflammation look like in crohn disease?

A
  • Transmural
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40
Q

What does the inflammation look like in ulcerative colitis?

A
  • Limited to mucosa
41
Q

What do the ulcers look like in crohn disease?

A
  • Deep, knife like
42
Q

What do the ulcers look like in ulcerative colitis?

A
  • Superficial, broad-based
43
Q

What is the clinical presentation of crohn disease?

A
  • Perianal fistula (in colonic disease)
  • Fat/vitamin malabsorption
  • Malignant potential with colonic involvement
  • Common recurrence after surgery
  • No toxic megacolon
44
Q

What is the clinical presentation of ulcerative colitis?

A
  • No perianal fistula
  • No fat/vitamin malabsorption
  • Malignant potential
  • Surgery is curative
  • Toxic megacolon is present
45
Q

What are the presenting symptoms of crohn disease?

A
  • Abdominal pain
  • Diarrhea
  • Nausea
  • Vomiting
  • Weight loss
46
Q

What are the presenting symptoms of ulcerative colitis?

A
  • Abdominal pain
  • Rectal bleeding
  • Bloody diarrhea
47
Q

What else is pseudomembranous colitis called?

A
  • Antibiotic associated colitis or antibiotic associated diarrhea
48
Q

What causes pseudomembranous colitis?

A
  • Disruption of the normal colonic microbiota by antibiotics allows overgrowth of C. difficile
49
Q

What are the pseudomembranes made up of?

A
  • An adherent layer of inflammatory cells and debris are not specific and may also be present in ischemia or necrotizing infections
50
Q

What is the presentation of pseudomembranous colitis?

A
  • Fever
  • Leukocytosis
  • Abdominal pain
  • Cramps
  • Watery diarrhea
  • Dehydration
51
Q

What is potentially fatal complication of pseudomembranous colitis?

A
  • Toxic megacolon
52
Q

How is diagnosis made of pseudomembranous colitis?

A
  • Presence of C. difficile toxin
53
Q

What are effective therapies for antibiotic resistant or hypervirulent C. difficile?

A
  • Metronidazole and vancomycin
54
Q

What is xerostomia?

A
  • Lack of saliva
55
Q

What is the etiology of xerostomia?

A
  • Most frequently due to medications
  • Major feature in Sjogren syndrome
  • Radiation therapy
56
Q

Which salivary gland is most affected by mucoepidermoid carcinoma?

A
  • Parotid gland but could show up in others
57
Q

What is the chromosomal translocation of mucoepidermoid carcinoma?

A
  • (11:19)(q21;p13)
58
Q

What is the prognosis of mucoepidermoid carcinoma based on?

A
  • Grade
59
Q

What is the clinical manifestation of acute pancreatitis?

A
  • Abdominal pain
  • Pain is constant, intense, and referred to the upper back and, occasionally the left shoulder
  • Anorexia, nausea and vomiting are common
60
Q

What are the laboratory findings in acute pancreatitis?

A
  • Elevation of serum amylase and lipase during the first 4-12 hours following the onset of pain
  • Serum lipase is the most specific and sensitive marker of acute pancreatitis (remains elevated for 8-14 days
  • Glycosuria and hypocalcemia could result from saponification of necrotic fat
61
Q

What signs are associated with acute pancreatitis?

A
  • Periumbilical ecchymosis (Cullen’s sign)

- Ecchymosis of the flank (Grey Turner’s sign)

62
Q

What causes the ecchymosis of the abdomen in acute pancreatitis?

A
  • Liberated pancreatic enzymes causing the diffusion of fat necrosis and inflammation in the retroperitoneal or intra abdominal bleeding
63
Q

What does the ecchymosis of the abdomen in acute pancreatitis mean?

A
  • Not specific but associated with severe acute pancreatitis and mortality
64
Q

What is the ratio of men to women in acute pancreatitis? What are the causes?

A
  • 6:1 male to female in alcoholism

- 1:3 male to female in biliary tract disease

65
Q

What is present in around half of acute pancreatitis patients?

A
  • Gallstones
66
Q

What is the pathogenesis of acute pancreatitis?

A
  • Tissue damage commences and trypsin can activate factors found in the blood including components of coagulations, complement, kallikrein, and fibrinolytic pathways
  • The resulting inflammation and small vessel thrombosis causes further damage to acinar cells, amplifying intrapancreatic enzyme activiation
67
Q

What does the CFTR gene do?

A
  • Epithelial anion channel. LOF mutations alter fluid pressure and limit bicarbonate secretion, leading to inspissation of secreted fluids and duct obstruction
68
Q

What does the PRSS1 gene do?

A
  • Cationic trypsin. GOF mutations prevent self-inactivation of trypsin
69
Q

What does the SPINK1 gene do?

A
  • Inhibitor of trypsin. Mutations cause LOF, increasing trypsin activity
70
Q

What does CASR gene do?

A
  • Membrane-bound receptor that senses extracellular calcium levels and controls luminal calcium levels . Mutations may alter calcium concentrations and activate trypsin
71
Q

What does the CTRC gene do?

A
  • Degrades trypsin, protects the pancreas from trypsin related injury
72
Q

What does the CPA1 gene do?

A
  • Exopeptidase involved in regulating zymogen activation
73
Q

What are some basic alterations in the morphology of acute pancreatitis?

A
  1. Microvascular leak and edema
  2. Fat necrosis
  3. Acute inflammation
  4. Damage, including autodigestion, of pancreatic parenchyma, and
  5. Blood vessel destruction with interstitial hemorrhage
74
Q

What is chronic pancreatitis defined as?

A
  • Prolonged inflammation of the pancreas associated with irreversible destruction of exocrine parenchyma, fibrosis, and, in the late stages, loss of endocrine parenchyma
75
Q

What is the most common cause of chronic pancreatitis?

A
  • Long-term alcohol use
76
Q

How many forms are there of autoimmune pancreatitis?

A
  • Two
77
Q

What is autoimmune pancreatitis type 1?

A
  • Associated with the presence of immunoglobulin G4 (IgG4) –> secreting plasma cells in the pancreas and is one manifestation of a systemic IgG-related disease
78
Q

What is autoimmune pancreatitis type 2?

A
  • Restricted to the pancreas with the exception of a subset of patients with ulcerative colitis.
79
Q

What do both variants of the autoimmune pancreatitis mimic?

A
  • Pancreatic carcinoma, including presentation as a mass lesion in the pancreatic head on imaging
80
Q

How is the diagnosis of chronic pancreatitis made?

A
  • High degree of suspicion
  • Repeated bouts of abdominal pain
  • Persistent back pain
  • Calcifications
  • Pseudocyst
  • Pancreatic exocrine insufficiency
  • Diabetes mellitus
81
Q

What can all lead to significant morbidity and contribute to mortality?

A
  • Chronic malabsorption
  • Pancreatic exocrine insufficiency
  • Diabetes mellitus
82
Q

What is a dominant problem in chronic pancreatitis?

A
  • Severe, chronic pain
83
Q

What happens in patients with hereditary pancreatitis associated with PRSS1?

A
  • Mutations have a 40% lifetime risk of developing pancreatic cancer
  • RIsk of pancreatic cancer is only modestly elevated with other forms of chronic pancreatitis
84
Q

What is leukoplakia?

A
  • A white patch or plaque that cannot be scraped off and cannot be characterized clinically or pathologically with any other disease
85
Q

What is a special quality of leukoplakia?

A
  • Up to 25% are precancerous
86
Q

What is erythroplakia?

A
  • A red, velvety, possibly eroded area within the oral cavity that usually remains level or may be slightly depressed in relation to the surrounding mucosa
87
Q

Which is less common: leukoplakia or erythroplakia?

A
  • Erythroplakia
88
Q

What is a special quality of erythroplakia?

A
  • Is more ominous because it is almost always associated with severe dysplasia/CIS
89
Q

What causes most orofacial herpetic infections?

A
  • HSV-1 is most common

- Oral HSV-2 (genital herpes) can occur

90
Q

What is the primary age of oral HSV?

A
  • Typically occur in children between 2 and 4, are often asymptomatic
91
Q

What do the vesicles of HSV look like?

A
  • Range from lesions of a few millimeters to large bullae

- First filled with a clear, serous fluid, but rapidly to yield painful, red-rimmed, shallow ulcerations

92
Q

When do the HSV vesicles usually clear?

A
  • Spontaneously clear within 3-4 weeks
93
Q

What test can be used for HSV?

A
  • Tzanck test
94
Q

What is the most common fungal infection of the oral cavity?

A
  • Candidiasis
95
Q

What factors influence clinical infection of candidiasis?

A
  • Strain of C. albicans
  • Composition of individual oral flora
  • Immune status of the patient
96
Q

What is important for the protection against Candida infection?

A
  • Neutrophils, macrophages, and Th17 cells
97
Q

What does histology look like for Candida?

A
  • Pseudohyphae, budding yeast, and human epithelial cells
98
Q

What is an important diagnostic clue for Candida?

A
  • Pseudohyphae

GI Test (10 decks)

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