Abdominal Surgery: Stomach

Question 1

___________is the presence of one or more ulcerative lesions in the stomach or duodenum. Etiologies include Helicobacter pylori infection (most common), prolonged NSAID use (NSAID-induced ulcer), conditions associated with an overproduction of stomach acid (hypersecretory states), and stress.

Answer 1

Peptic ulcer disease (PUD)

Question 2

How does the approach for Peptic ulcer disease eval differ in pts older and younger than 60?

Answer 2

Usually, patients younger than 60 years of age can be managed with testing for H. pylori infection or with empirical acid suppression therapy. Older patients and those with high-risk clinical features benefit from an esophagogastroduodenoscopy (EGD) and biopsies to confirm the diagnosis or rule out differential diagnoses (especially gastric cancer).

Question 3

Erosions are more superficial than ulcers. Ulcers involve damage to the gastric mucosa extending beyond the _______________ layer into the submucosa.

Answer 3

muscularis mucosa

Question 4

The two major contributing factors to the development of PUD are …

Answer 4

The two major contributing factors to the development of PUD are…
H. pylori infection
and
nonsteroidal anti-inflammatory drug (NSAID) use.

Helicobacter pylori infection
Associated with 40–70% of duodenal ulcers and 25–50% of gastric ulcers
Chronic NSAID use

Question 5

Inhibit COX-1 and COX-2 → decrease in prostaglandin; production → erosion of the gastric mucosa

Answer 5

NSAID pathophys behind peptic ulcer disease

Question 6

Parietal cells, what do i do

Answer 6

Secrete hydrochloric acid (HCl) and intrinsic factor
Stimulated by acetylcholine, histamine, and gastrin
Inhibited by prostaglandins and somatostatin

Question 7

Mucosal cells

Answer 7

Secrete protective mucus
Stimulated by acetylcholine, prostaglandins (which inhibit HCl secretion), and secretin

Question 8

Chief cells

Answer 8

Secrete pepsinogen
Stimulated by acetylcholine, gastrin, secretin, and vasoactive intestinal polypeptide (VIP)

Question 9

How does eating impact pain in someone with peptic ulcer disease?

Answer 9

Gastric ulcer–> pain increases
Duodenal–> pain releif

Question 10

What peptic ulcer patients get eval w/ EGD

Answer 10

Patients > 60 years of age, or > 45 years of age in areas with high gastric cancer prevalence
Patients with red flags for dyspepsia: on a case-by-case basis [23]
Patients unresponsive to empiric medical therapy (e.g., H. pylori eradication therapy, PPI trial therapy)

Question 11

A peptide hormone that stimulates gastric acid secretion and increases stomach motility. It is secreted by G cells in the antrum of the stomach and the duodenum.

Answer 11

Gastrin

Question 12

A hormone produced by duodenal S cells. Increases pancreatic bicarbonate secretion and bile secretion into the duodenum. Decreases gastric acid secretion.

Answer 12

Secretin

Question 13

How does h pylori lead to ulcers?

Answer 13

H. pylori secretes urease → alkalinization of acidic environment → survival of bacteria in gastric lumen
Release of cytotoxins (e.g., cagA toxin) → disruption of the mucosal barrier and damage to underlying cells

Question 14

What duodenal ulcers are more likely to perforate?

Answer 14

Duodenal ulcers of the anterior wall are more likely to perforate than ulcers of the posterior wall.

Posterior ulcers are more likely to bleed and anterior ulcers are more likely to perforate: Postal workers wear Blue collars and should not have an Antisocial Personality.

Question 15

What is the malignant potential of gastric ulcers?

Answer 15

High malignant potential (progression to cancer in 5–10% of cases)

Question 16

Ulcer associated with burns

Answer 16

Curling ulcer: severe burns → decreased plasma volume → decreased gastric blood flow → hypoxic tissue injury of stomach surface epithelium → weakening of the normal mucosal barrier

“hot curling iron”

Question 17

Ulcers Associated with brain injury

Answer 17

Cushing ulcer: brain injury → increased vagal stimulation → increased production of stomach acid via acetylcholine release

Question 18

The main risk factor for developing gastric cancer is _______________________

Answer 18

The main risk factor for developing gastric cancer is infection with Helicobacter pylori.

Question 19

A type of gastritis characterized by enlargement of the mucosal folds (rugae) due to hyperplasia of the gastric mucosa. Causes excess mucus production, protein loss, and parietal cell atrophy with decreased acid production. Manifestations include epigastric pain, anorexia, weight loss, vomiting, and edema secondary to protein loss.

Answer 19

Ménétrier disease/ Giant hypertrophic gastritis

Question 20

How does gastric cancer tend to present?

Answer 20

Early stages of gastric cancer:
Often asymptomatic

Late stages of gastric cancer:
General signs
Weight loss
Signs of chronic iron deficiency anemia
Signs of gastric outlet obstruction
Dysphagia
Abdominal pain
Early satiety
Vomiting

Signs of upper gastrointestinal bleeding:
Hematemesis
Melena

Signs of metastatic disease:
Hepatomegaly
Ascites
Left supraclavicular adenopathy (Virchow node)
Palpable umbilical nodule (Sister Mary Joseph node)
Palpable mass on digital rectal examination (Blumer shelf)
Ovarian mass (Krukenberg tumor)
Paraneoplastic syndromes
Leser-Trélat sign
Malignant acanthosis nigricans

Question 21

Answer 21

Leser–Trélat sign

Back of a patient with colon cancer

Numerous light brown, raised lesions of different shapes and sizes are visible. A few spots show a scaly surface with a stuck-on appearance while others are smooth.

The sudden development of multiple seborrheic keratoses in association with paraneoplastic syndrome, as is the case here, is referred to as “Leser-Trélat sign.” Seborrheic keratosis can also occur naturally in the process of aging.

Question 22

A metastatic tumor of the ovary, most commonly caused by diffuse gastric cancer (signet ring cell carcinoma). Other primary sites include other types of gastric cancer as well as breast cancer, endometrial cancer, and colon cancer.

Answer 22

Krukenburg tumor

Question 23

An enlarged periumbilical lymph node. Classically associated with metastatic gastric cancer but can develop in other abdominopelvic malignancies (e.g., gallbladder, pancreas, kidneys, testicles, prostate, ovaries).

Answer 23

sister mary joseph nodule

Question 24

What chemotherapies do we have for gastric cancers that you should know?

Answer 24

Trastuzumab is added to the chemotherapy regimen for HER2-positive metastatic disease.

For the forms of cancer associated with HER2 gene overexpression and the medication used for treatment, think: TRUST HER, GaBriel (TRUSTuzumab; HER2; Gastric cancer; Breast cancer).

Because there are no early signs, gastric cancer is often diagnosed very late. Around 50% of cancers have already reached an advanced stage that does not allow for curative treatment due to tissue invasion and metastases.

Question 25

Gastric cancer spreads hematogenously to…

Answer 25

Skeleton
Liver
Lung
Brain

The Skeleton (bones), Liver, Lung, and Brain are the structures most commonly affected by hematogenous spread of gastric cancer: Zombie SKELETONs don’t LIVE LONG (lung) without eating BRAINs.

Question 26

What paraneoplastic signs should you look for in patients with gastric cancer?

Answer 26

malignant acanthosis nigrans and leser trelat sign

Question 27

a pathologically increased growth of bacteria in the small intestine

Answer 27

Small intestinal bacterial overgrowth (SIBO)

Question 28

dysfunctional pyloric sphincter → rapid emptying of glucose-containing chyme into the small intestine → quick reabsorption of glucose → hyperglycemia → excessive release of insulin → hypoglycemia and release of catecholamines

Answer 28

Late dumping syndrome

Question 29

A complication of procedures compromising the pyloric sphincter (e.g., distal gastrectomy) that presents with gastrointestinal discomfort (nausea, vomiting, cramps, diarrhea), shakiness, hypoglycemia, hunger, and decreased level of consciousness late after eating (after hours). Symptoms result from absorption of carbohydrate-rich chyme in the small intestine and subsequent hyperglycemia and excessive release of insulin, leading to compensatory hypoglycemia and a surge in catecholamines.

Answer 29

Late dumping syndrome

Question 30

dysfunctional or bypassed pyloric sphincter → rapid emptying of undiluted hyperosmolar chyme into the small intestine → fluid shift to the intestinal lumen → small bowel distention → vagal stimulation → increased intestinal motility

Occur within 15–30 minutes after meal ingestion
Include nausea, vomiting, diarrhea, and cramps
Vasomotor symptoms such as sweating, flushing, and palpitations

Answer 30

early dumping syndrome

Question 31

Suspect _______________________ in a patient with previous gastric surgery and hypoglycemia. Occur hours after meal ingestion, Include signs of hypoglycemia (e.g., hunger, tremor, lightheadedness)
GI discomfort

Answer 31

late dumping syndrome

Question 32

Gastric MALTomas: association with _________________infection

Answer 32

H. pylori

Question 33

Non-gastric MALTomas are frequently associated with ________________

Answer 33

Non-gastric MALTomas are associated with autoimmune conditions

Salivary MALToma: parotid enlargement

Question 34

A subtype of metaplastic (chronic) atrophic gastritis that is characterized by chronic inflammation of the gastric mucosa with atrophy, gland loss, and metaplastic changes. Chronic infection with Helicobacter pylori is the most common cause of this subtype.

Answer 34

Environmental metaplastic atrophic gastritis

EMAG or “type b” gastritis

Question 35

What is the treatment for MALT lymphoma?

Answer 35

First-line: H. pylori eradication therapy
If H. pylori eradication therapy fails: radiotherapy or chemotherapy

Question 36

What is a MALT lymphoma?

Answer 36

Mucosa-Associated Lymphoid Tissue (MALT) lymphoma (also called MALToma or extranodal marginal zone lymphoma) is a B-cell non-Hodgkin lymphoma (NHL)

Question 37

A penetrating duodenal ulcer can form an abscess where?

Answer 37

liver

Question 38

An upper endoscopy shows a large nodular mass on the anterior wall of the lesser curvature of the gastric stump. Biopsy samples are obtained, showing polypoid, glandular formation of irregular-shaped and fused gastric cells with intraluminal mucus, demonstrating an infiltrative growth.
What is the most likely mass?

Answer 38

gastric adenocarcinoma.

Question 39

Bacterial overgrowth of the small intestine caused by stasis in a surgically created blind loop, e.g., following partial gastrectomy with Billroth-II or Roux-en-Y reconstruction. The overproliferation of bacterial flora may result in dysfunctional intestinal digestion and malabsorption. Symptoms typically include nausea, diarrhea, abdominal bloating, and flatulence.

Answer 39

Blind loop syndrome

Question 40

Pt w/hx of gastrectomy. The patient now presents with symptoms of malabsorption, including diarrhea, vitamin B12 deficiency (anemia, paresthesias, loss of vibratory sensation and proprioception), hypoalbuminemia (peripheral edema), and weight loss, all of which suggest

Answer 40

Blind loop syndrome leading to SIBO

Question 41

What are the symptoms of SIBO/presentation of SIBO?

Answer 41

The patient presents with symptoms of malabsorption, including diarrhea, vitamin B12 deficiency (anemia, paresthesias, loss of vibratory sensation and proprioception), hypoalbuminemia (peripheral edema), and weight loss

Question 42

What is the inital tx for early dumping syndrome?

Answer 42

The diagnosis of early dumping syndrome is primarily clinical, and dietary modifications are the initial treatment of choice. In early dumping syndrome, large amounts of carbohydrate-rich food are emptied rapidly into the small intestine, causing fluid shifts and sympathetic activation. To prevent this, initial treatment involves frequent, small, low-carbohydrate meals to reduce the osmotic load on the small intestine. Other behavioral modifications (e.g., 30–60 min of supine rest) may also be helpful. Symptoms of early dumping syndrome are usually self-limiting and resolve after a few months.

Dumping syndrome that is not adequately controlled with dietary modification can be treated with octreotide.

Question 43

What physical exam finding indicates gastric dialation?

Answer 43

tympanitic epigastric mass and a succussion splash on abdominal auscultation

Question 44

tympanitic epigastric mass and a succussion splash on abdominal auscultation should raise concern for

Answer 44

gastric dialation concerning for Gastric Outlet Obstruction (GOO)

Question 45

What is the difference in the cause of GOO in patients w/peptic ulcer disease?

Answer 45

acute PUD, which can cause obstruction via inflammation-induced edema and tissue deformation

chronic PUD, which is most commonly seen in individuals with long-term NSAID use or those with Helicobacter pylori infection, GOO can result from scarring and tissue fibrosis.

Question 46

In patients with GOO, persistent vomiting can lead to _______________________ alkalosis and prerenal AKI

Answer 46

hypokalemic hypochloremic metabolic

Question 47

________________________is the first-line treatment for gastric MALT lymphomas.

Answer 47

H. pylori eradication therapy (e.g., amoxicillin, clarithromycin, and omeprazole) for 10–14 days

Question 48

Upper gastrointestinal endoscopy reveals an ulcerating mass in the gastric antrum. Biopsies of the mass show diffuse infiltrates of small lymphoid cells that are positive for CD20 antigen. This is highly suspicious for…

Answer 48

Helicobacter pylori-associated gastric MALT lymphoma

Question 49

Uncontrolled gastrin secretion–> parietal cell hyperplasia–> ulcers and such and inactivation of pancreatic enzymes

Answer 49

zollinger-ellison (gastrinoma)