33 GIT Flashcards

1
Q

SIALADENITIS

A

Inflammation of the salivary gland

Most commonly due to an obstructing stone (sialolithiasis) leading to Staphylococcus
aureus infection; usually unilateral

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2
Q

mucocele

A

results from blockage of salivary duct

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3
Q

renula

A

like mucocele but when sublingual duct affected

connect 2 bellies of myloid muscle

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4
Q

non specific bacterial sialadanitis in location?

A

submandibular

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5
Q

viral location

A

parotid

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6
Q

tumors of salivary gland list
benign and malignant

A

bening
pleopmorphic adenoma
warthin tumor

malignant
mucoepidermoid carcinoma
adenoid cystic carcinoma
acinic cell tumor

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7
Q

most benign and malignat tumors arise from

A

benign from bigger gland
malignat from smaller

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8
Q

PLEOMORPHIC ADENOMA
define
where
capsule?

A

A. Benign tumor composed of stromal (e.g., cartilage) and epithelial tissue; most
common tumor of the salivary gland
B; Usually arises in parotid; presents as a mobile, painless, circumscribed mass at the
angle of the jaw
C, High rate of recurrence; extension of small islands of tumor through tumor capsule
often leads to incomplete resection (Fig. 10.5).
D. Rarely may transform into carcinoma, which presents with signs of facial nerve
damage (facial nerve runs through parotid gland)

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9
Q

WARTHIN TUMOR
define
where
risk factor
laterality

A

A. Benign cystic tumor with abundant lymphocytes and germinal centers (lymph
node-like stroma); 2nd most common tumor of the salivary gland
B, Almost always arises in the parotid

male smokers

bilateral

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10
Q

MUCOEPIDERMOID CARCINOMA

A

Malignant tumor composed of mucinous and squamous cells; most common
malignant tumor of the salivary gland

Usually arises in the parotid; commonly involves the facial nerve

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11
Q

congenital anomalies of esophagus

A

ectopic gastric tissue
congenital cysts
impaired diaphram so hernia
esophageal web
achalasia

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12
Q

achalasia
define
causes plus type
clinical
may develop

A

A. Disordered esophageal motility with inability to relax the lower esophageal
sphincter (LES)
B. Due to damaged ganglion cells in the myenteric plexus
1. Ganglion cells of myenteric plexus are located between the inner circular
and outer longitudinal layers of the muscularis propria and are important for
regulating bowel motility and relaxing the l.ES.
2. Damage to ganglion cells can be idiopathic (primary ) or secondary to a known insult {e.g.,
Trypanosoma cruzi infection in Chagas disease),
C. Clinical features
1. Dysphagia for solids and liquids
2. Putrid breath
3. High LES pressure on esophageal manometry
4. ‘Bird-beak’ sign on barium swallow study
5. Increased risk for esophageal squamous cell carcinoma
may develop squamous cell carcinoma

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13
Q

hiatal hernia
types
complications

A

axial/sliding

paraesophageal / non axial

complications
ulceration
obstruction
reflux esophagitis

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14
Q

diverticula
define
types

A

outpouching of esophageal mucosa

zenker
traction
epiphrenic

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15
Q

ZENKER DIVERTICULUM
where
cause of zenker
aka

A

A, Outpouching of pharyngeal mucosa through an acquired defect in the muscular
wall (false diverticulum)
B, Arises above the upper esophageal sphincter at the junction of the esophagus and
pharynx
C, Presents with dysphagia, obstruction, and halitosis (bad breath)

cause
ues stenosis

pulsation diverticula

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16
Q

traction diverticula
where
cause
symproms

A

midpoint

caused by tb infection mediastinal lymadenopathy

asymptomatic

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17
Q

MALLORY-WEISS SYNDROME
define
caused by
present as
risk or may develop what syndrome

A

A, Longitudinal laceration of mucosa at the gastroesophageal (GE) junction

B Caused by severe vomiting, usually due to alcoholism or bulimia

C. Presents with painful hematemesis

D. Risk of Boerhaave syndrome—rupture of esophagus leading to air in the
mediastinum and subcutaneous emphysema

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18
Q

ESOPHAGEAL VARICES

A

A. Dilated submucosal veins in the lower esophagus
B. Arise secondary to portal hypertension
1. Distal esophageal vein normally drains into the portal vein via the left gastric
vei 11.
2, In portal hypertension, the left gastric vein backs up into the esophageal vein,
resulting in dilation (varices).
C. Asymptomatic, but risk of rupture exists
1. Presents with painless hematemesis
2. Most common cause of death in cirrhosis

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19
Q

esophagitis types

A

reflux esophagitis or gerd

infectious and chemical esophagitis

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20
Q

GASTROESOPHAGEAL REFLUX DISEASE (GERD )

A

A. Reflux of acid from the stomach due to reduced LES tone
B. Risk factors include alcohol, tobacco, obesity, fat-rich diet, caffeine, and hiatal
hernia.
C. Clinical features
1. Heartburn (mimics cardiac chest pain)
2. Asthma (adult-onset) and cough
3. Damage to enamel of teeth
melena
4. Ulceration with stricture and Barrett esophagus are late complications.

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21
Q

BARRETT ESOPHAGUS
define
types
criteria to diagnose

A

A. Metaplasia of the lower esophageal mucosa from stratified squamous epithelium to
nonciliated columnar epithelium with goblet cells
seen in 10% of patients with GERD
1. Response of lower esophageal stem cells to acidic stress
B. May progress to dysplasia and adenocarcinoma

long segment and short segment
>< 3cm

criteria
endoscopy
histology

22
Q

tumors of esophagus
most where
benign or mal common
3 morphologic patterns
metastasise locations
types

A

middle most tumors
benign most

3 morphologic
flat
protruded most
excavated or ulcerated

metastasis
upper cervical
middle mediastinal
lower celiac

23
Q

adenocarcinoma
define
where

A

is a malignant proliferation of glands; most common type of esophageal carcinoma in the West

Arises from preexisting Barrett esophagus; usually involves the lower one-third
of the esophagus

24
Q

Squamous cell carcinoma
define
where

A

is a malignant proliferation of squamous cells; most common esophageal cancer worldwide

Usually arises in upper or middle third of the esophagus;

major risk, factors Include
i. Alcohol and tobacco (most common causes)
ii. Very hot tea
III. Achalasia
iv. Esophageal web (e.g., Plummer-Vinson syndrome)
v. Esophageal injury (e.g., lye ingestion)

25
Q
  1. Symptoms include progressive dysphagia (solids to liquids), weight loss, pain,
    and hematemesis.
  2. Squamous cell carcinoma may additionally present with hoarse voice (recurrent
    laryngeal nerve involvement) and cough (tracheal involvement).
A
26
Q

CONGENITAL gastric pathologies

A

heterotopic rests
diaghramatic hernia
pyloric stenosis

27
Q

pyloric stenosis
define
presentation
types

A

A. hypertrophy of pyloric smooth muscle;

B. Classically presention
1. Projectile nonbilious vomiting
2. Visible peristalsis
3. Olive-like mass in the abdomen

C. Treatment is myotomy.

congenital and acquired

28
Q

congenital pyloric stenosis
sex
clinical presentation
physical exam results

A

male
clinical
regurgutation
vomiting

physical examination
palpable mass
visible perstalisis

29
Q

acquired pyloric stenosis from what

A

PUD
antral gastritis

30
Q

gastritis
define then type

A

acute and chronic and special type

31
Q

ACUTE GASTRITIS
define
due to
risk factors

A

A. Acidic damage to the stomach mucosa

B. Due to imbalance between mucosal defenses and acidic environment
1. Defenses include mucin layer produced by foveolar cells, bicarbonate secretion
by surface epithelium, and normal blood supply (provides nutrients and picks up
leaked acid).

C. Risk factors
1. Severe burn (Curling ulcer) — Hypovolemia leads to decreased blood supply.
2. NSAIDs (decreased PGE.)
3. Heavy alcohol consumption
4. Chemotherapy
5. Increased intracranial pressure (Cushing ulcer)—Increased stimulation of vagus
nerve leads to increased acid production.
6. Shock—Multiple (stress) ulcers may be seen in ICU patients.

D. Acid damage results in superficial inflammation, erosion (loss of superficial
epithelium), or ulcer (loss of mucosal layer).

32
Q

acute gastritis presentation or manifestation or diagnosis

A

neutrophil infiltration in the epithelium

33
Q

concurrent erosion and hemorhage with acute gastritis termed as

A

acute erosive hemorhagic gastritis

34
Q

chronic gastritis
results in
errosion?
associated with / risk factors
2 important

A

results in mucosal atrophy and intestinal metaplasia

absent erosion

associated with
H. pylori
automimmune

35
Q

Chronic autoimmune gastritis
define
where
causes

A

is due to autoimmune destruction of gastric parietal cells, which are located in the stomach body and fundus.

Associated with antibodies against parietal cells and/or intrinsic factor; useful for diagnosis, but pathogenesis is mediated by T cells (type IV hypersensitivity)

Clinical features
i. Atrophy of mucosa with intestinal metaplasia
ii. Achlorhydria with increased gastrin levels and antral G-cell hyperplasia
iii. Megaloblastic (pernicious) anemia due to lack of intrinsic factor
iv. Increased risk tor gastric adenocarcinoma (intestinal type)

36
Q

Chronic H pylori gastritis
define
where
virulence factors 4
pathogenesis
types / patterns 2

A

is due to H pylori-induced acute and chronic
inflammation; most common form of gastritis (90%)

  1. H pylori ureases and proteases along with inflammation weaken mucosal defenses; antrum is the most common site
    motility, adhesins (BabA bind blood group O), toxins (CagA and VacA)
  2. Presents with epigastric abdominal pain; increased risk for ulceration (peptic
    ulcer disease), gastric adenocarcinoma (intestinal type), and MALT lymphoma
  3. Treatment involves triple therapy.
    i. Resolves gastritis/ulcer and reverses intestinal metaplasia
    ii. Negative urea breath test and lack of stool antigen confirm eradication of H pylori.

pathogenesis
h.pylori produces pro inflammatory cytokines

types
antral type
pangastritis

37
Q

Antral type h pylori
acid
and develop what

A

increased acid
increased doudenal ulcer

38
Q

pangastritis type h pylori

A

causes atrophy then adenocarcinoma
reduce acid
increased IL 1B

39
Q

special type gastritis

A

eosinophilic gastritis
lymphocytic gastritis
granulomatous gastritis

40
Q

PUD
define
lesion characterize
location/type

A

Breach in the mucosa that extends from muscularis to submucosa

chronic solitary lesions <4cm

lactions
duodenal and antral/gastric

41
Q

Duodenal ulcer
cause 2
where
ulcer looks like

A

is almost always due to H pylori (> 95%); rarely, may be due to ZE
syndrome
1, Presents with epigastric pain that improves with meals
2. Diagnostic endoscopic biopsy shows ulcer with hypertrophy of Brunne r glands.
3. May rupture leading to bleeding from the gastroduodenal artery (anterior ulcer)
or acute pancreatitis (posterior ulcer)

anterior duodenum

punched out

pain 2 hours after meal

42
Q

Gastric ulcer

A

is usually due to H pylori (75%); other causes include NSAlDs and bile reflux.
1. Presents with epigastric pain that worsens with meals
2. Ulcer is usually located on the lesser curvature of the antrum.
3. Rupture carries risk of bleeding from left gastric artery.

43
Q

i. Benign peptic ulcers are usually small (< 3 cm), sharply demarcated
(“punched-out”), and surrounded by radiating folds of mucosa

ii. Malignant ulcers are large and irregular with heaped up margins

A
44
Q

ulcers askanazi layers 4

A

necrotic debris
inflammation
granulation formation
scar

45
Q

gastric carcinoma
define
classification
metastasize to

A

Malignant proliferation of surface epithelial cells (adenocarcinoma)

classification
intestinal and diffuse

virchow and paraumblical nodes

supraclavicular and suster mary joseph

46
Q

Intestinal type
where
lesion crcter
risk factors
name why

A

(more common) presents as a large, irregular ulcer with heaped up margins; most commonly involves the lesser curvature of the antrum (similar to gastric ulcer)

Risk factors include intestinal metaplasia (e.g., due to H pylori and autoimmune gastritis), nitrosamines in smoked foods (Japan), and blood type A.

gland resemble colonic glands so name

47
Q

Diffuse type
characteristics 2
cell and tissue

A

is characterized by signet ring cells that diffusely inliltrate the gastric
wall ; desmoplasia results in thickening of stomach wall (linitis plasties)

Not associated with H pylori, intestinal metaplasia, or nitrosamines

48
Q

less common tumors gastric

A

gastric lymphoma
GIST
carcinoid tumor

49
Q

GIST
from what cells

A

cells of cajal which control peristalisis

increased autoantibody agaists tumor supression genes

50
Q

most common source of metastatic gastric cancer

A

systemic lymphoma

51
Q
A