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ADV PATH > 1P-GIT > Flashcards

1P-GIT Flashcards

1
Q

Failure of organ dev’t

A

AGENESIS

*d/t absence of primordial cells

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2
Q

Arrest in development or maldevelopment

Sx: regurgitation during feeding

A

ATRESIA

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3
Q

Partial/ complete obstruction d/t fibrous thickening or scarring

A

STENOSIS

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4
Q

Most common type of esophageal atresia

A

Proximal end: blunted

Distal end: fistula with trachea

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5
Q

Defect in diaphragm: abd. viscera herniate to thoracic cavity

*CXR: gas bubbles

A

DIAPHRAGMATIC HERNIA

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6
Q

Abdominal musculature defect; organs protrude thru umbilical cord opening

A

OMPHALOCELE

*membranous sac present

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7
Q

Defect in all layers of abd. wall; organs are outside the peritoneal cavity, usually to the right of UC.

A

GASTROSCHISIS

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8
Q

Heterotopic gastric mucosa: facts

A
  • circular, flat, orange to red area
  • MC site: Postcricoid region or upper 3rd of esoph. –> - aka: inlet patch
  • usually asymp; may produce dysphagia
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9
Q

Heterotopic pancreatic tissue (pancreatic

acinar metaplasia) factors:

A
  • congenital
others:
- advancing age
- Helicobacter
pylori infection
- female gender
- GERD
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10
Q

MECKEL DIVERTICULUM’s rule of 2s

A 
○ 2x more common in males
○ 2% of the population
○ 2 feet of the ileocecal valve
○ 2 inches in length
○ 2 types of mucosa
○ Presentation before the age of 2
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11
Q

MECKEL DIVERTICULUM’s results from the failed involution of the ___?

A

Vitelline duct or Omphalomesenteric duct

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12
Q

Assoc. risk factor of PYLORIC STENOSIS

A

Erythromycin,

Azithromycin in utero exposure

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13
Q

Genetic assoc. factor of PYLORIC STENOSIS

A

Turner syndrome (45X), Trisomy 18 (Edwards syndr)

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14
Q

Male, newborn (3rd to 12th wk)

Sx: New onset regurgitation, projectile non-bilious
vomiting aft. feeding

PE: Firm, ovoid, 1-2cm abd. mass @ left/medial side + hyperperistalsis

What is the dx & tx?

A

PYLORIC STENOSIS

Tx: Myotomy (pyoloromyotomy)

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15
Q

Failure of neural crest cells migration to wall of colon d/t premature arrest of NCC migration or premature death of ganglion cells

A

HIRSCHSPRUNG DISEASE

→ aka : Congenital Aganglionic Megacolon

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16
Q

Biopsy is done for dx of HIRSCHSPRUNG DISEASE. What immunohistochemical stain is being used?

A

Acetylcholinesterase

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17
Q

Genetic involvement of HIRSCHSPRUNG DISEASE

A
  • RET gene (& EDNRB gene)

- 10% occur in children with Trisomy 21 (Down syndr)

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18
Q

Male, newborn (upto 1st yr of life) presents w/ abdominal
gaseous distention, delayed meconium passage, and tight anus

PE: No peristalsis

A

HIRSCHSPRUNG DISEASE

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19
Q

MC site of HIRSCHSPRUNG DISEASE

A

Distal colon

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20
Q

MC site of MECKEL DIVERTICULUM

A

Antimesenteric border of ileum

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21
Q

Trisomy 21 (Down syndr)

A

HIRSCHSPRUNG DISEASE

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22
Q

Turner syndrome (45X), Trisomy 18 (Edwards syndr)

A

PYLORIC STENOSIS

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23
Q

High amplitude contractions of the distal
esophagus (d/t loss of
the normal coordination of ICOL smooth muscles)

A

Nutcracker Esophagus

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24
Q

Repetitive, simultaneous contractions of

the distal esophageal smooth muscle (= Uncoordinated propulsion of food)

A

Diffuse Esophageal Spasm

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25
Q

High pressure on LES

A

Hypertensive Lower Esophageal Sphincter

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26
Q

CC: feeling of food stuck @ back of throat; Halitosis

A

ZENKER DIVERTICULUM

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27
Q

Mucosal outfoldings that are non-circumferential

A

MUCOSAL WEBS

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28
Q

Mucosal outfoldings that are circumferential

A

SCHATZKI RINGS

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29
Q

SCHATZKI RINGS: A rings

A

squamous (above

GEJ)

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30
Q

SCHATZKI RINGS: B rings

A 
squamo-columnar,
gastric glands (below GEJ)
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31
Q

Dilated veins in the distal esophagus; seen in patients with portal HTN, cirrhosis d/t alcohol or schistosomiasis

A

VARICES

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32
Q

Complication of chronic GERD; Precursor lesion to Esophageal

Adenocarcinoma

A

BARRET’S ESOPHAGUS

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33
Q

Mgt for BE indefinite for dysplasia (IND) or low-grade

dysplasia (LGD)

A

Anti-reflux medical therapy and repeat

endoscopy with biopsy in shorter period of time.

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34
Q

Mgt for BE of high-grade dysplasia (HGD)

A

Endoscopic ablative therapy (radiofrequency

ablation and cryoablation)

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35
Q

T or F: Most patients with BE never

develop dysplasia or adenocarcinoma.

A

TRUE

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36
Q

Carcinoma that has penetrated through
the basement membrane of the glands of esophagus
into the lamina propria or muscularis
mucosae, but not below.

A

Intramucosal adenocarcinoma of BE

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37
Q

HPI:
Swallowing difficulties
Progressive weight loss
Hematemesis

PMH: Chr. GERD

A

ADENOCARCINOMA of esoph.

*from BE

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38
Q

Genetic factor of Esoph. AdenoCA

A

Mutation of TP53, CDKN2A(p16/INK4a)

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39
Q

Main features used to suggest an origin for an

esophageal adenocarcinoma from Barrett mucosa

A

Identification of goblet cells adjacent to the
neoplasm and the epicenter of the tumor being
located on the esophageal side of the GEJ.

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40
Q

MC site of Esoph. SQUAMOUS CELL CARCINOMA

A

Middle & lower thirds

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41
Q

Mutagenesis of Esoph. SQUAMOUS CELL CARCINOMA

A
  • Alcohol & Tobacco use
  • Polycyclic Hydrocarbons, Nitrosamines
  • Amplification of transcription factor SOX2
    gene
  • HPV infection
42
Q

Px presents w/ esoph. tumor w/c is circumferential,
ulcerated, & has sharply demarcated margins.

PSHx: Alcohol & tobacco use

A

SQUAMOUS CELL CARCINOMA

43
Q

Common sites of metastasis of Esoph. SQUAMOUS CELL CARCINOMA

A

LIVER, LUNG, ADRENAL

GLANDS

44
Q

Causes of STRESS-RELATED MUCOSAL DISEASEs

A

Trauma; extensive burns;

intracranial disease; major surgery; serious medical disease

45
Q

PEPTIC ULCER DISEASE: causes & complications

A

CAUSES: H. pylori infection, NSAID use, Smoking

COMPLICATIONS: Bleeding, Perforation, obstruction

46
Q

Sx assoc. w/ excess TGF-alpha

A
  • Hypochlorhydria or achlorhydria
  • Hypoproteinemia

(MENETRIER DISEASE/ HYPERTROPHIC GASTROPATHY)

47
Q

Diffuse hyperplasia of foveolar epithelium w/c has an increased risk for adenocarcinoma

A

MENETRIER DISEASE/ HYPERTROPHIC GASTROPATHY

48
Q

Parts affected in MENETRIER DISEASE/ HYPERTROPHIC GASTROPATHY

A

Greater curvature
Body
Fundus

*Antrum is spared

49
Q

Hyperplasia
primarily affecting the secretory portion of
the fundic gland

A

ZOLLINGER-ELLISON SYNDROME

50
Q

ZOLLINGER-ELLISON SYNDROME is assoc. with what syndrome?

A

MEN (Multiple Endocrine Neoplasia) type 1

51
Q

ZOLLINGER-ELLISON SYNDROME mainly involves what kind of cells?

A

Parietal cells
ECL cells

*both resulting from gastrin stimulation

52
Q

Generally small, sessile, and multiple, with a smooth or slightly lobulated contour; randomly distributed in the stomach

A

HYPERPLASTIC POLYPS

53
Q

Tend to arise
in a background of hypochlorhydria, low levels of pepsinogen I,
hypergastrinemia, chronic gastritis, and gastric atrophy

A

HYPERPLASTIC POLYPS

54
Q

Multiple small polypoid projections in the

gastric fundus or body

A

FUNDIC GLAND POLYP

55
Q

FUNDIC GLAND POLYP occur in?

A
  • Sporadically
  • Pxs w/ ZES
  • Long term PPI tx
  • Pxs w/ FAP
56
Q

Molecular alteration in FUNDIC GLAND POLYP

A
  • Sporadic fundic gland polyps: mutation of
    β-catenin gene
  • With FAP: second hit alterations in APC gene
57
Q

Cystically dilated irregular
glands lined by parietal, chief, and foveolar mucosal
cells

A

FUNDIC GLAND POLYP

58
Q

Associated with familial adenomatous polyposis

(FAP) and background of chronic gastritis

A

GASTRIC ADENOMA

59
Q

Type of GASTRIC ADENOMA w/ higher tendency for malignant transformation

A

Intestinal-type adenomas

60
Q

Known as linitis plastica/ signet ring adenoCA

A

Diffuse type gastric adenoCA

61
Q

Molec. pathogenesis involved in diffuse type gastric adenoCA

A

CDH1 gene

62
Q

Molec. pathogenesis involved in both diffuse & intestinal type gastric adenoCA

A

TP53

63
Q

Molec. pathogenesis involved in sporadic intestinal type gastric adenoCA

A
  • WNT pathway
  • Beta catenin
  • APC gene
64
Q

Identified precursor lesion for both diffuse & intestinal type gastric adenoCA

A
  • Diffuse type: No identified precursor lesion

- Intestinal type: Barrett’s Esophagus; Flat dysplasia and Adenoma

65
Q

GASTRIC ADENOCARCINOMA advanced stages sx

A

weight loss, anorexia, early satiety

66
Q

Female patient – signet ring on bilateral ovaries,

diffused type gastric carcinoma

A

Krukenberg tumor.

67
Q

H. pylori infection provides the necessary background in which this tumor develops

A

MALT Lymphoma

68
Q

MALT Lymphoma molec pathogenesis

A

Translocation AP12-MLT fusion gene

69
Q

Small, sharply outlined, and covered by a flattened mucosa; linked to PPI tx

A

CARCINOID TUMORS/ Well differentiated-Neuroendocrine tumors

70
Q

Most important prognostication factor for WDNETs

A

Location

o Foregut: rarely metastasize; cured by resection.
o Midgut: Aggressive
o Hindgut: Incidental; more benign

71
Q

Mesenchymal neoplasm of the abdomen

A

GASTROINTESTINAL STROMAL TUMOR

72
Q

GIST location

A 
● 60% occur in the stomach.
● 60% submucosal growing towards lumen
creating a smooth projection.
● 30% are subserosal
● 10% are intramural
73
Q

Carney Triad

A
  • Nonhereditary syndrome of GIST
  • Paraganglioma
  • Pulmonary chondroma
74
Q

Most common site of Metastasis of GIST

A

LIVER
LUNGS
PERITONEUM

75
Q

Mutagenesis of GIST

A

Gain of function of c-KIT gene

76
Q

Becomes emergency when there is bowel obstr’n → need to do reduction

A

INTESTINAL HERNIA

77
Q

Obstructive sx bec peristalsis is affected;

Caused by surg. procedures/ infxn/ peritoneal inflam’n.

A

INTESTINAL ADHESION

78
Q

MC site of VOLVOLUS

A
  • MC: Sigmoid colon

- Other sites: cecum, small bowel, stomach, transverse colon.

79
Q

Lymphoid hyperplasia precedes this, and are particularly seen during the first 5 years of life

A

Intussusception

80
Q

Watershed zones

A

Splenic Flexure, Sigmoid Colon and Rectum

81
Q

An immune-mediated disease due to an abnormal
response certain proteins in
genetically susceptible people.

A

CELIAC DISEASE

82
Q

Characterized by scalloping and denting of the duodenal folds with markedly atrophic or absent villi.

A

CELIAC DISEASE

83
Q

Endoscopically, small bowel shows white lipid-filled

plaques in the mucosa which represents macrophages in the lamina propria

A

WHIPPLE DISEASE

84
Q

Flask-like outpouchings alongside the taenia coli caused by Elevated intraluminal pressure

A

SIGMOID DIVERTICULAR DISEASE

85
Q

Thin wall composed of flattened or atrophic
mucosa, compressed submucosa, often absent
muscular layer

A

SIGMOID DIVERTICULAR DISEASE

86
Q

Main complications of diverticulosis

A

Hemorrhage, perforation, and diverticulitis.

87
Q

TX: Acute uncomplicated diverticulitis vs patients with

complications of diverticulitis

A

Acute uncomplicated : Abx
With complications of diverticulitis: Surgical
resection

88
Q

HYPERPLASTIC POLYP size & location

A

Left colon; <5 mm

89
Q

Genetic defect in juvenile polyposis

A

inherited inactivating mutations of the SMAD4 or BMPR1A genes,

90
Q

The standard treatment for adenomatous polyps

A

polypectomy, followed by repeated

colonoscopy.

91
Q

TUBULAR ADENOMA size

A

Measure less than 1 cm

92
Q

Sometimes clusters of dysplastic glands in an
adenomatous polyp are seen beneath the
muscularis mucosae and may lead to a
mistaken diagnosis of malignant transformation

A

“Pseudoinvasion”

93
Q

Represent the earliest identifiable

“adenomatous” change; numerous in colons harboring carcinoma

A

“Aberrant crypts”

94
Q

Large polyps located at the right side of the colon

A

SESSILE SERRATED ADENOMAS

95
Q

100% of untreated cases progress into Colorectal

Adenocarcinoma

A

FAMILIAL ADENOMATOUS POLYPOSIS

96
Q

Genetic involvement in FAP

A

● Autosomal Dominant Disorder
● APC gene
● Other genes: MYH gene

97
Q

Genetic defect in LYNCH SYNDROME/ HNPCC

A
  • MLH1
  • MSH2

-Also, MSH6, PMS2

98
Q

Genetic defect in INT. ADENOCARCINOMA

A

APC
KRAS
TP53

99
Q

T or F: Smooth muscle tumors situated higher up in the colon have a higher incidence of malignancy.

A

TRUE

100
Q

T or F: Colorectal malignant lymphomas are nearly

always of non- Hodgkin type.

A

TRUE

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