Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI II Exam 1 > Pathoma: Gastric Disorders > Flashcards

Pathoma: Gastric Disorders Flashcards

1
Q

_____ is a congenital malformation in the anterior wall that leads to the exposure of the abdominal contents to air

A

gastroschisis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is an omaphacele?

A

Persistant herniation of the bowel into the umbilical cord. Bowel doesnt return into the body cavity as we develop => abdominal contents covered in peritoneum and amnoin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

When does pyloric stenosis present?

A

NOT at birth: 3-6 weeks because it takes time to develop.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Who is pyloric stenosis more common in?

A

M

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Sx of pyloric stenosis?

A

3-6 weeks after birth

  1. Projectile nonbilous vomiting
  2. Olive like mass in abdomen and visible peristalsis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is gastritis?

A

inflammation of the gastric mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the 2 types of gastritis?

A

Acute gastritis => acid damage to the stomach due to imbalance between mucosal defenses and acid production => causes

  • Superficial inflammation
  • Erosion (loss of epithelium => extend to mucosa)
  • Ulcer (loss of mucosa)

Chronic gastritis=> chronic inflammation of the stomach mucosa due to either H.pylori and AI gastritis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the mucosal defenses?

A
  • Mucosa defenses protect against acid
      1. Mucosa lined by epithelium (epithelial cells = foveolar cells = make mucus and layer)
      1. HCO3-
      1. Blood flow => provides nutrients and carry acid away
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Risk factors for acute gastritis?

A
  1. Severe burn (Curling ulcer)
  2. Increased intracranial pressure (Cushing ulcer)
  3. Shock (multuple “stress” ulcers seen in ICU pt)
  4. NSAIDS (decreased PGE2 => NL; decrease acid production and increase mucus and bicarb and increase BF)
  5. Heavy alcohol consumption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Acid damage in acute gastritis causes what?

A
  1. Superficial inflammation
  2. Erosion
  3. Ulcers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Chronic AI gastritis causes chronic gastritis how?

A
  • T-cell mediated AI reaction (type 4) that destroys gastric parietal cells, located in the fundus and body.
    • Produces Ab against parital cells or IF, which do not cause damage but are a side effect.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Chronic gastritis due to chronic AI gastritis

A
  1. Atrophy of mucosa with intestinal metaplasia
    1. => increase risk for gastric adenocarcinoma (intestinal type)
  2. Achlorhydria => Increase in gastrin => G-cell hyperplasia in antrum
  3. Megaloblastic (pernicious anemia) d/t decreased IF (made by parietal cell) => decreased vit B12.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What do we see with intestinal metplasia of the gastric mucosa?

A

Goblet cells!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Chronic H.pyloris gastritis is due to..

A

H.pylori induced acute AND chrponic inflammation (most common form 90%) in the antrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Sx of Chronic H.pyloris gastritis

A
  1. Epigastric abdominal pain
  2. Increase risk for ulceration (PUD)
  3. Gastric adenocarcinoma (intestinal type)
  4. MALToma (B-cell)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Triple therapy for Chronic H.pylori induced gastritis causes

A
  • Resolves gastritis/ulcer
  • Reverses intestinal metaplasia (metaplasia is reversible)
17
Q

What confirms that H.pylori is gone

A
  1. Negative urea breath test
  2. Lack of stool antigen
18
Q

PUD produces

A

solitary mucosal ulcer in the proximal duodunum (90%) or distal stomach (10%

19
Q

Duodenal ulcers are due to ______

A
  1. H. pylori (90%)
  2. ZE syndrome: gastrinoma => increase gastrin => + parietal cell => increase acid production => duodenal ulcer
20
Q

Duodenal ulcers presents with epigastric pain that ________ with meals

A

IMPROVES

duodenum makes HCO3- when stomach senses food

21
Q

Diagnostic endoscopic biopsy shows what for duodenal ulcers

A

Ulcer with hypertophy of brunners glands (which makes mucus to protect)

22
Q

Duodenal ulcers usually arise in the ______ duodenum; but when they arise in _________ duodenum, we can see…

A
  • anterior duodenum
  • posterior duodenum
    • Bleeding from the gastroduodenal A.
    • Acute pancreatitis
23
Q

Gastric ulcers are due to ______

A

H.pylori (75%) and others; NSAIDS/bile reflux

24
Q

Gastric ulcers presents with epigastric pain that ________ with meals

25
Q

Gastric ulcers usually arise in the ______ and can cause what

A
  • Lesser curvature of antrum
  • Rupture => bleed due to L. gastric A.
26
Q

DDx of ulcers include _____

27
Q

_______ ulcers are almost NEVER malignant and rarely biopsied

28
Q

Gastric ulcers can be caused by ________

A

Gastric carcinoma (intestinal type)

29
Q

On endoscopy, how can we tell the difference between a benign ulcer and malignant ulcer

A
  • Benign ulcer: small (<3cm), punched out and surrounded by NL/flat margins
  • Malignant ulcer: large, irregular with heaped up margins
30
Q

What is required for definitive diagnossis of ulcer malignancy

GI II Exam 1 (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions