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LOL REDO GI II BC NO WAY > Dobson #1 > Flashcards

Dobson #1 Flashcards

1
Q

Who is more likely to get periodontitis and why?

A

down syndrome patients because they are more likely to get leukemia

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2
Q

What makes up the normal flora in healthy gingiva?

A

facultative gram positive

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3
Q

what is the composition of plaque?

A

anaerobic and microaerophilic gram negative bacteria

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4
Q

what is important for protection against candida infection?

A

neutrophils, macrophages, and Th17 cells

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5
Q

histologic features of candida?

A

pseudohyphae and bidding yeast

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6
Q

name an example of a deep fungal infection

A

zygomycetes can cause Mucor–> rhinocerebral mucromycosis

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7
Q

who does mucormycetes primarily affect?

A

diabetics, and the fungus may spread from nasal sinuses to the orbit and brain

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8
Q

what is scarlet fever due to?

A

pyrogenic toxin from group A beta hemolytic bacteria

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9
Q

most at risk for HPV related cancers of head and neck?

A

white, non-smoking 35-55 men

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10
Q

what cancer is associated with premalignant lesions?

A

classic opscc

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11
Q

What is over expressed in HPV oral SCC?

A

p16

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12
Q

what is over expressed in oral cancer caused by alcohol/tobacco?

A

Cyclin D1

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13
Q

what is the most frequent cause of xerostomia?

A

medications: anticholinergic, antidepressant/antipsychotic, diuretic, antihypertensive, sedative, muscle relaxant, analgesic, and antihistamine drugs

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14
Q

bacterial cause of sialadenitis?

A

staph aureus/ strep viridans (secondary to stone)

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15
Q

What is the most common lesion of the salivary glands?

A

mucocele

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16
Q

how do mucocele’s appear?

A

blue translucent hue

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17
Q

how can nonspecific sialadenitis be characterized?

A

unilateral involvement of a single gland

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18
Q

what are the genetic aberrations associated with pleomorphism adenoma?

A

PLAG1 overexpression

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19
Q

histologic feature of pleomorphism adenoma?

A

epithelial elements and mesenchymal elements

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20
Q

what’s important to remember about mucoepidermoid carcinomas?

A

prognosis is dependent on grade

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21
Q

what is an omphalacele?

A

when the abdominal musculature is incomplete and viscera herniate into the ventral membranous sac

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22
Q

what is gastroschisis?

A

when all the layers of the abdominal wall fail to develop- from the peritoneum to the skin

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23
Q

what are the complications associated to meckel diverticulum?

A

complications related to ectopic gastric or pancreatic tissue

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24
Q

What is pyloric stenosis associated with?

A

turner syndrome and trisomy 18; or erythromycin or azithromycin within first 2 weeks of life

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25
Q

what is Hirschspring disease?

A

aganglionic megacolon due to arrested migration of NCCs into the gut

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26
Q

How does Hirschspring disease present?

A

functional obstruction and the rectum is always involved

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27
Q

what are 3 functional causes of esophageal obstruction?

A

nutcracker esophagus, DES, and systemic sclerosis

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28
Q

what is a complication due to increased esophageal pressure?

A

Zenker diverticulum

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29
Q

what are esophageal webs associated with?

A

GERD, C-GVHD, and celiac disease

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30
Q

achalasia is characterized by a triad of what?

A

incomplete LES relaxation, increased LES tone, and aperistalsis of the esophagus

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31
Q

what is the cause of primary achalasia?

A

ganglion cell degeneration

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32
Q

where does the tear occur in mallory-weiss syndrome?

A

gastric side of the gastroesophageal junction

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33
Q

where does the tear occur in Boerhaave’s syndrome?

A

complete rupture at the distal esophagus

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34
Q

what is the most frequent cause of esophagitis?

A

reflux of gastric contents into the lower esophagus

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35
Q

how can you determine the cause of viral esophagitis?

A

the endoscopic appearance

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36
Q

how does HSV viral esophagitis look?

A

it typically causes punched-out ulcers

37
Q

how does CMV viral esophagitis look?

A

CMV causes shallower ulcerations and is marked by characteristic nuclear and cytoplasmic inclusions

38
Q

where are most of the benign neoplasms of the esophagus located?

A

most are submucosal

39
Q

what is are the characteristics of benign neoplasms of the esophagus?

A

most are mesenchymal, with smooth muscle tumors being the most common

40
Q

there are 2 malignant neoplasms of the esophagus- what are they?

A

squamous cell carcinoma and adenocarcinoma

41
Q

what geographic distribution is at more risk for squamous cell carcinoma of the esophagus?

A

iran, central china, Hong kong

42
Q

what is the highest risk group for squamous cell carcinoma of the esophagus?

A

> 45, males, african americans 8x more likely

43
Q

where do most squamous cell carcinomas of the esophagus occur?

A

in the middle third of the esophagus

44
Q

what are 3 specific risk factors for esophageal scc?

A

if you have tylosis, HPV (+/-), HIV

45
Q

what is typically the first symptom of an esophageal scc?

A

aspiration of food due to an acquired TE fistula

46
Q

where are the highest rates for esophageal adenocarcinoma?

A

US, UK, Canada, australia

47
Q

who is the highest risk group for esophageal adenocarcinoma?

A

caucasians, 7x more common in men

48
Q

What are the risk factors for esophageal adenocarcinoma?

A

barrett esophagus, tobacco, radiation

49
Q

where are esophageal adenocarcinomas commonly found?

A

distal 1/3 esophagus

50
Q

what do esophageal adenocarcinomas look like microscopically?

A

the tumors typically produced mucin and form glands

51
Q

how do esophageal adenocarcinomas commonly present?

A

pain or difficulty swallowing, progressive weight loss, hematemesis, chest pain, and vomiting

52
Q

what is the most common cause of diffuse atrophic gastritis?

A

autoimmune gastritis

53
Q

what happens to long-standing chronic gastritis that involves the body/fundus?

A

it could lead to mucosal atrophy and/or intestinal metaplasia–> both are risk factors for adenocarcinoma

54
Q

when looking for H. pylori, what stain should you use?

A

warthrin-starry stain

55
Q

5 features of autoimmune gastritis?

A
  1. antibodies to parietal cells and IF 2. reduced serum pepsinogen I (chief cells are collateral damage) 3. Endocrine cell hyperplasia 4. Vitamin B12 deficiency 5. defective gastric acid secretion
56
Q

what is gastrin secretion like in autoimmune gastritis?

A

it is markedly increased BECAUSE THE ANTRUM IS SPARED DUH SO G CELLS ARE THERE AND CAN STILL STIMULATE GASTRIN

57
Q

what could come from Type B chronic gastritis?

A

peptic ulcer, adenocarcinoma, MALToma

58
Q

what could come from type A chronic gastritis?

A

atrophy, pernicious anemia, adenocarcinoma, carcinoid tumor

59
Q

how is lymphocytic (an uncommon form of gastritis) characterized?

A

by thickened folds covered by small nodules with central aphthous ulceration

60
Q

how do peptic ulcers appear?

A

are solitary; round-oval, sharply punched out defect; HEAPED UP MARGINS= MALIGNANCY NOT PUD

61
Q

where are peptic ulcers most common?

A

proximal duodenum

62
Q

How is intestinal metaplasia recognized?

A

by the presence of goblet cells

63
Q

what are two diseases that causes hypertrophic gastropathy?

A

Menetrier disease and zollinger-ellison syndrome

64
Q

what are the risk factors associated with zollinger-ellison syndrome?

A

multiple endocrine neoplasia

65
Q

what etiology of hypertrophic gastropathy is associated with adenocarcinoma?

A

menetrier disease

66
Q

what is the causes of menetrier disease?

A

over expression of TGF-alpha

67
Q

what are the symptoms associated with menetrier disease?

A

hyponatremia, weight loss, diarrhea

68
Q

what are the symptoms associated with Zollinger-ellison syndrome?

A

peptic ulcers

69
Q

how is zollinger ellison syndrome characterized?

A

doubling of the oxyntic mucosal thickness

70
Q

what is the most common benign tumor of the stomach? (polyp)

A

inflammatory and hyperplastic polyps

71
Q

what are inflammatory and hyperplastic polyps associated with?

A

H. pylori

72
Q

what is the most common malignancy of the stomach?

A

adenocarcinoma

73
Q

what geographical region has a higher risk of adenocarcinoma of the stomach?

A

japan, chile, costa rica, and eastern europe

74
Q

early symptoms of both types of adenocarcinoma of the stomach include what?

A

dyspepsia, dysphagia, and nausea

75
Q

incidence of cancer of the gastric cardia is on the rise. Why so?

A

barrett esophagus and may reflect the incidence of chronic GERD and obesity

76
Q

what are the two types of gastric adenocarcinomas?

A

diffuse gastric cancer and intestinal type gastric cancer

77
Q

what is a key step in the development of diffuse gastric cancer?

A

loss of E-cadherin

78
Q

what is the histology of diffuse gastric cancer?

A

signet ring cells that are discohesive and do not form glands; large intracellular mucin vacuoles that push nucleus to the periphery= signet ring cells

79
Q

what is a morphological feature of diffuse gastric cancer?

A

linitis plastica: appearance when there are large areas of infiltration, diffuse rugal flattening, and a thick rigid wall

80
Q

What is intestinal type gastric cancers-bulky cancer strongly associated with?

A

APC mutations; mutations that result in increased signaling via the Wnt pathway; and gain of function mutation in gene encoding B-catenin

81
Q

most gastric adenocarcinomas involve what?

A

the antrum- the lesser curvature is involved more often than the greater

82
Q

which translocation is most common in MALToma?

A

t(11;18)(q21;q21)

83
Q

what are the most common symptoms of MALToma?

A

dyspepsia and epigastric pain

84
Q

histologically, how does MALToma look?

A

takes the form of a dense lymphocytic infiltrate in the lamina propria- the lymphocytes infiltrate the gastric glands focally to create diagnostic lymphoepithelial lesions

85
Q

What are the clues that you are dealing with a neuroendocrine tumor (carcinoid tumor)?

A

cutaneous flushing, sweating, bronchospasm, colicky abdominal pain, circumscribed yellow mass, salt and pepper chromatin, neurosecretory granules

86
Q

what is the most common mesenchymal tumor of the abdomen?

A

GIST

87
Q

what do GISTs arise from?

A

interstitial cells of cajal

88
Q

when children present with GIST tumors what should you consider?

A

Carney syndrome triad and Carney-stratakis dyad–> increased risk in neurofibromatosis type 1

89
Q

approximately 75% of all GISTS hace oncogenic, gain of function mutations in what?

A

the receptor tyrosin kinase KIT (cKIT)

LOL REDO GI II BC NO WAY (2 decks)

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