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1P-GIT Flashcards

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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
High pressure on LES
Hypertensive Lower Esophageal Sphincter
26
CC: feeling of food stuck @ back of throat; Halitosis
ZENKER DIVERTICULUM
27
Mucosal outfoldings that are non-circumferential
MUCOSAL WEBS
28
Mucosal outfoldings that are circumferential
SCHATZKI RINGS
29
SCHATZKI RINGS: A rings
squamous (above | GEJ)
30
SCHATZKI RINGS: B rings
``` squamo-columnar, gastric glands (below GEJ) ```
31
Dilated veins in the distal esophagus; seen in patients with portal HTN, cirrhosis d/t alcohol or schistosomiasis
VARICES
32
Complication of chronic GERD; Precursor lesion to Esophageal | Adenocarcinoma
BARRET'S ESOPHAGUS
33
Mgt for BE indefinite for dysplasia (IND) or low-grade | dysplasia (LGD)
Anti-reflux medical therapy and repeat | endoscopy with biopsy in shorter period of time.
34
Mgt for BE of high-grade dysplasia (HGD)
Endoscopic ablative therapy (radiofrequency | ablation and cryoablation)
35
T or F: Most patients with BE never | develop dysplasia or adenocarcinoma.
TRUE
36
Carcinoma that has penetrated through the basement membrane of the glands of esophagus into the lamina propria or muscularis mucosae, but not below.
Intramucosal adenocarcinoma of BE
37
HPI: Swallowing difficulties Progressive weight loss Hematemesis PMH: Chr. GERD
ADENOCARCINOMA of esoph. *from BE
38
Genetic factor of Esoph. AdenoCA
Mutation of TP53, CDKN2A(p16/INK4a)
39
Main features used to suggest an origin for an | esophageal adenocarcinoma from Barrett mucosa
Identification of goblet cells adjacent to the neoplasm and the epicenter of the tumor being located on the esophageal side of the GEJ.
40
MC site of Esoph. SQUAMOUS CELL CARCINOMA
Middle & lower thirds
41
Mutagenesis of Esoph. SQUAMOUS CELL CARCINOMA
- Alcohol & Tobacco use - Polycyclic Hydrocarbons, Nitrosamines - Amplification of transcription factor SOX2 gene - HPV infection
42
Px presents w/ esoph. tumor w/c is circumferential, ulcerated, & has sharply demarcated margins. PSHx: Alcohol & tobacco use
SQUAMOUS CELL CARCINOMA
43
Common sites of metastasis of Esoph. SQUAMOUS CELL CARCINOMA
LIVER, LUNG, ADRENAL | GLANDS
44
Causes of STRESS-RELATED MUCOSAL DISEASEs
Trauma; extensive burns; | intracranial disease; major surgery; serious medical disease
45
PEPTIC ULCER DISEASE: causes & complications
CAUSES: H. pylori infection, NSAID use, Smoking COMPLICATIONS: Bleeding, Perforation, obstruction
46
Sx assoc. w/ excess TGF-alpha
- Hypochlorhydria or achlorhydria - Hypoproteinemia (MENETRIER DISEASE/ HYPERTROPHIC GASTROPATHY)
47
Diffuse hyperplasia of foveolar epithelium w/c has an increased risk for adenocarcinoma
MENETRIER DISEASE/ HYPERTROPHIC GASTROPATHY
48
Parts affected in MENETRIER DISEASE/ HYPERTROPHIC GASTROPATHY
Greater curvature Body Fundus *Antrum is spared
49
Hyperplasia primarily affecting the secretory portion of the fundic gland
ZOLLINGER-ELLISON SYNDROME
50
ZOLLINGER-ELLISON SYNDROME is assoc. with what syndrome?
MEN (Multiple Endocrine Neoplasia) type 1
51
ZOLLINGER-ELLISON SYNDROME mainly involves what kind of cells?
Parietal cells ECL cells *both resulting from gastrin stimulation
52
Generally small, sessile, and multiple, with a smooth or slightly lobulated contour; randomly distributed in the stomach
HYPERPLASTIC POLYPS
53
Tend to arise in a background of hypochlorhydria, low levels of pepsinogen I, hypergastrinemia, chronic gastritis, and gastric atrophy
HYPERPLASTIC POLYPS
54
Multiple small polypoid projections in the | gastric fundus or body
FUNDIC GLAND POLYP
55
FUNDIC GLAND POLYP occur in?
- Sporadically - Pxs w/ ZES - Long term PPI tx - Pxs w/ FAP
56
Molecular alteration in FUNDIC GLAND POLYP
- Sporadic fundic gland polyps: mutation of β-catenin gene - With FAP: second hit alterations in APC gene
57
Cystically dilated irregular glands lined by parietal, chief, and foveolar mucosal cells
FUNDIC GLAND POLYP
58
Associated with familial adenomatous polyposis | (FAP) and background of chronic gastritis
GASTRIC ADENOMA
59
Type of GASTRIC ADENOMA w/ higher tendency for malignant transformation
Intestinal-type adenomas
60
Known as linitis plastica/ signet ring adenoCA
Diffuse type gastric adenoCA
61
Molec. pathogenesis involved in diffuse type gastric adenoCA
CDH1 gene
62
Molec. pathogenesis involved in both diffuse & intestinal type gastric adenoCA
TP53
63
Molec. pathogenesis involved in sporadic intestinal type gastric adenoCA
- WNT pathway - Beta catenin - APC gene
64
Identified precursor lesion for both diffuse & intestinal type gastric adenoCA
- Diffuse type: No identified precursor lesion | - Intestinal type: Barrett’s Esophagus; Flat dysplasia and Adenoma
65
GASTRIC ADENOCARCINOMA advanced stages sx
weight loss, anorexia, early satiety
66
Female patient – signet ring on bilateral ovaries, | diffused type gastric carcinoma
Krukenberg tumor.
67
H. pylori infection provides the necessary background in which this tumor develops
MALT Lymphoma
68
MALT Lymphoma molec pathogenesis
Translocation AP12-MLT fusion gene
69
Small, sharply outlined, and covered by a flattened mucosa; linked to PPI tx
CARCINOID TUMORS/ Well differentiated-Neuroendocrine tumors
70
Most important prognostication factor for WDNETs
Location o Foregut: rarely metastasize; cured by resection. o Midgut: Aggressive o Hindgut: Incidental; more benign
71
Mesenchymal neoplasm of the abdomen
GASTROINTESTINAL STROMAL TUMOR
72
GIST location
``` ● 60% occur in the stomach. ● 60% submucosal growing towards lumen creating a smooth projection. ● 30% are subserosal ● 10% are intramural ```
73
Carney Triad
- Nonhereditary syndrome of GIST - Paraganglioma - Pulmonary chondroma
74
Most common site of Metastasis of GIST
LIVER LUNGS PERITONEUM
75
Mutagenesis of GIST
Gain of function of c-KIT gene
76
Becomes emergency when there is bowel obstr'n → need to do reduction
INTESTINAL HERNIA
77
Obstructive sx bec peristalsis is affected; | Caused by surg. procedures/ infxn/ peritoneal inflam'n.
INTESTINAL ADHESION
78
MC site of VOLVOLUS
- MC: Sigmoid colon | - Other sites: cecum, small bowel, stomach, transverse colon.
79
Lymphoid hyperplasia precedes this, and are particularly seen during the first 5 years of life
Intussusception
80
Watershed zones
Splenic Flexure, Sigmoid Colon and Rectum
81
An immune-mediated disease due to an abnormal response certain proteins in genetically susceptible people.
CELIAC DISEASE
82
Characterized by scalloping and denting of the duodenal folds with markedly atrophic or absent villi.
CELIAC DISEASE
83
Endoscopically, small bowel shows white lipid-filled | plaques in the mucosa which represents macrophages in the lamina propria
WHIPPLE DISEASE
84
Flask-like outpouchings alongside the taenia coli caused by Elevated intraluminal pressure
SIGMOID DIVERTICULAR DISEASE
85
Thin wall composed of flattened or atrophic mucosa, compressed submucosa, often absent muscular layer
SIGMOID DIVERTICULAR DISEASE
86
Main complications of diverticulosis
Hemorrhage, perforation, and diverticulitis.
87
TX: Acute uncomplicated diverticulitis vs patients with | complications of diverticulitis
Acute uncomplicated : Abx With complications of diverticulitis: Surgical resection
88
HYPERPLASTIC POLYP size & location
Left colon; <5 mm
89
Genetic defect in juvenile polyposis
inherited inactivating mutations of the SMAD4 or BMPR1A genes,
90
The standard treatment for adenomatous polyps
polypectomy, followed by repeated | colonoscopy.
91
TUBULAR ADENOMA size
Measure less than 1 cm
92
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
“Pseudoinvasion”
93
Represent the earliest identifiable | “adenomatous” change; numerous in colons harboring carcinoma
“Aberrant crypts”
94
Large polyps located at the right side of the colon
SESSILE SERRATED ADENOMAS
95
100% of untreated cases progress into Colorectal | Adenocarcinoma
FAMILIAL ADENOMATOUS POLYPOSIS
96
Genetic involvement in FAP
● Autosomal Dominant Disorder ● APC gene ● Other genes: MYH gene
97
Genetic defect in LYNCH SYNDROME/ HNPCC
- MLH1 - MSH2 -Also, MSH6, PMS2
98
Genetic defect in INT. ADENOCARCINOMA
APC KRAS TP53
99
T or F: Smooth muscle tumors situated higher up in the colon have a higher incidence of malignancy.
TRUE
100
T or F: Colorectal malignant lymphomas are nearly | always of non- Hodgkin type.
TRUE

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