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Surgery Clerkship- Amboss Study Plan > Abdominal Surgery- Stomach > Flashcards

Abdominal Surgery- Stomach Flashcards

1
Q

Peptic Ulcer Disease (PUD)

A

the presence of one or more ulcerative lesions in the stomach or lining of the duodenum.

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2
Q

PUD risk factors

A
  • Chronic gastritis caused by H. pylori, a curved, flagellated gram-negative rod
    • Duodenal ulcers: up to 90% are due to H. pylori infection
    • Gastric ulcers: up to 80% are due to H. pylori infection
  • Long-term use of NSAIDs
  • Long-term use of NSAIDs plus glucocorticoids
  • Smoking
  • Chronic alcohol consumption
  • Rare risk factors:
    • Zollinger-Ellison syndrome (can result in duodenal ulcer)
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3
Q

Zollinger-Ellison syndrome

A
  • gastrin-secreting neuroendocrine tumor that is most often localized to the duodenum and pancreas.
  • part of multiple endocrine neoplasia (MEN) syndrome]
  • elevated serum gastrin and low gastric pH
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4
Q

PUD Pathophysiology

A
  • Helicobacter pylori gastritis: increased acid secretion, decreased protective factors/mucus production
  • NSAIDs inhibit COX-1 and COX-2 → decrease in PGE2 (normally decreases gastric acid secretion and increases HCO3- and mucus secretion) → gastric mucosa erosions
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5
Q

PUD clinical features for both gastric and duodenal

A

∼ 70% of patients with PUD are asymptomatic

  • Dyspepsia: postprandial heaviness, early satiety, and gnawing, aching or burning epigastric pain
  • Pain relief with antacids
  • Potential signs of internal bleeding (anemia, hematemesis, melena)
  • Stool sample positive for occult blood
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6
Q

PUD Clinical signs for gastric ulcers

A

Pain increases shortly after eating →weight loss

nocturnal pain in 30-40% patients

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7
Q

PUD clinical features for duodenal ulcers

A
  • pain increases 2–5 hours after eating
  • Pain on an empty stomach (hunger pain) that is relieved with food intake → weight gain
  • nocturnal pain 50-80% patients
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8
Q

Stress Ulcer

A

Acute damage to the gastric mucosa, resulting from increased levels of endogenousglucocorticoids and decreased blood flow to the stomach.

  • Causes: polytrauma, major surgery, SIRS, kidney failure, etc.
  • Types
    • Curling ulcer:
    • Cushing ulcer:
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9
Q

Curling Ulcer

A

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

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10
Q

Cushing Ulcer

A

In patients with brain injury, increased vagal stimulation leads to increased production of stomach acid via acetylcholine release.

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11
Q

Nonulcer dyspepsia:

A

Symptoms including bloating, nausea, and belching persisting ≥ 3 months without organic cause

(synonym: functional dyspepsia)

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12
Q

PUD Diagnostic Approach

A
  • ≤ 60 years of age without alarm features: Urea breath test for H. pylori
  • > 60 years of age or presence of ≥ 1 alarm features: EGD with biopsies and rapid urease testing for H. pylori
  • Negative for H. pylori infection and NSAID intake; trial therapy unsuccessful
    • Measure serum gastrin level at baseline and after secretin stimulation test: high levels in gastrinoma (Zollinger-Ellison syndrome)
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13
Q

PUD Alarm Features

A
  • Certain symptoms: progressive dysphagia, painful swallowing (odynophagia), and/or persistent vomiting
  • Signs of active GI bleeding (e.g., melena, unexplained iron-deficiency anemia)
  • Signs of malignancy (e.g., unintended weight loss, lymphadenopathy, palpable mass)
  • Family history of upper GI malignancy in a first-degree relative
  • Jaundice
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14
Q

PUD EGD

A
  • MOst Accurate Test
  • Biopsy samples from:
    • Edge and base of the ulcer (essential to rule out malignancy)
    • Helicobacter pylori testing
  • If active bleeding, EGD can be performed for diagnosis and subsequent hemostasis treatment (electrocautery)
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15
Q

PUD Tx

H. Pylori Positive

A

eradication therapy (with antibiotics and a PPI) and supportive treatment → continue PPIs for 4–8 weeks → follow-up

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16
Q

PUD tx

h. pylori negative

A

medical acid suppression (with a PPI) and supportive treatment for 4–8 weeks → follow-up

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17
Q

PUD Supportive treatment

A

Discontinue NSAIDs

Restrict alcohol use/smoking/emotional stress

Avoid eating before bedtime

18
Q

PUD Surgical Treatment

A

surgical intervention is rarely needed.

  • Indications
    • Refractory syndromes despite appropriate medical treatment
    • If cancer is suspected
    • Complications that cannot be treated endoscopically
  • Partial gastrectomy (Billroth I/II)
19
Q

PUD Complications

A
  1. Bleeding (posterior ulcers)
  2. Perforation (anterior ulcers)
  3. Subhepatic abcess
  4. Gastric Outlet Obstruction
  5. Fistula Formation
  6. Malignant Transformation
  7. Postgastrectomy Syndromes
20
Q

Subhepatic Abscess

A
  • Etiology: may result from a perforated duodenal or gastric ulcer
  • Clinical presentation: fever and vomiting
  • Diagnosis: subhepatic gas on abdominal x-ray
21
Q

Gastric Outlet Obstruction

A

condition of obstruction of the pyloric channel or duodenum

  • Etiology
    • Malignancy (most common)
    • Acute PUD → inflammation and edema
    • Chronic PUD → scarring and fibrosis
22
Q

Gastric outlet obstruction clinical findings

A
  • Postprandial, nonbilious vomiting
  • Succussion splash
  • Early satiety
  • Weight loss
23
Q

Gastric outlet obstruction diagnosis

A
  • Upper endoscopy (confirmatory test): identification of the gastric pathology
  • Laboratory tests: hypokalemic hypochloremic metabolic alkalosis
24
Q

Malignant Transformation of PUD

A
  • Gastric ulcers: high malignant potential (progression to cancer in 5–10% of cases) → malignancy should be ruled out with biopsy
  • Duodenal ulcers: usually benign
25
Q

Gastric Cancer Risk Factors

A

Exogenous

  • Diet rich in nitrates and/or salts
  • Nicotine use
  • Low socioeconomic status

Endogenous

  • Atrophic gastritis
  • H. pylori infection
  • Gastric ulcers
  • Partial gastrectomy
26
Q

Gastric Cancer Clinical findings

A

Gastric cancer is often asymptomatic.

  • General signs
    • Weight loss
    • Chronic iron deficiency anemia; fatigue
  • Gastrointestinal signs
    • Abdominal pain
    • Early satiety
    • Nausea or vomiting
    • Acute gastric bleeding (hematemesis or melena)
  • Late stage gastric cancer
    • Gastric outlet obstruction
    • Hepatomegaly, ascites
    • Virchow’s node
    • Sister Mary Joseph’s node
    • Malignant acanthosis nigricans
27
Q

Malignant acanthosis nigricans

A

Presents as verrucous or papulous, hyperpigmented, pruritic skin lesions with rapid growth. Mainly affects the neck, genital area, and axillae.

28
Q

Virchow’s node

A

left supraclavicular adenopathy, located where the thoracic duct joins the subclavian vein at the venous angle.

29
Q

Sister Mary Joseph’s node

A

umbilical node indicating metastasis from a gastrointestinal or abdominopelvic malignancy

30
Q

Krukenberg tumor

A

an ovarian malignancy comprised of signet ring cells that has metastasized from a primary site, most commonly the stomach

31
Q

Gastric Cancer Pathology

A
  • Adenocarcinoma (90% of cases)
  • Signet ring cell carcinoma
    • Multiple signet ring cells = round cells filled with mucin, with a flat nucleus in the cell periphery
32
Q

Gastric Cancer Tx

A
  • Endoscopic resection
  • Trastuzumab is indicated for HER2+ gastric adenocarcinomas
  • Surgery
    • Radical gastrectomy and lymphadenectomy (operative standard)
    • Roux-en-Y gastric bypass
33
Q
A
34
Q

Postgastrectomy Maldigestion

A
  • Iron deficiency → supplement iron
  • Pernicious anemia due to lack of intrinsic factor, usually produced by gastric parietal cells → supplement vitamin B12
35
Q

Postgastrectomy:

Small intestinal Bacterial Overgrowth

Clinical Features/ Diagnosis

A
  • diarrhea,
  • steatorrhea,
  • weight loss,
  • malabsorption (e.g., deficiency of vitamin B12, A, E, D, zinc, and iron)

Diagnostics

  • Positive lactulose breath test
36
Q

Postgastrectomy:

Small intestinal Bacterial Overgrowth

A

Definition: bacterial overgrowth within the small intestine

Causes

  • Anatomic abnormalities: blind loop syndrome

Pathophysiology:

  • bacterial overgrowth → bacteria deconjugate bile acids, increase vitamin B12 turnover, and produce increased amounts of vitamin K and folic acid

Treatment: antibiotics and parenteral supplementation

37
Q

Dumping Syndrome

A
  • rapid gastric emptying due to either defective gastric reservoir function or pyloric emptying mechanism, or anomalous postsurgery gastric motor function.
  • Early dumping
    • rapid emptying of undiluted chyme into the small intestine caused by a dysfunctional or bypassed pyloric sphincter
38
Q

Dumping Syndrome

Clincal Features

A
  • Appears within 15–30 minutes after ingestion of a meal
  • Nausea,
  • vomiting,
  • diarrhea, and
  • cramps,
  • vasomotor symptoms such as sweating, flushing, and palpitations
39
Q

Dumping Syndrome Managment

A
  • Dietary modifications: Small meals that include a combination of complex carbohydrates and foods rich in protein and fat to cover protein and energy requirements are preferable.
  • 30–60 min of rest in the supine position after meals
40
Q

Mucosa-Associated Lymphoid Tissue (MALT) lymphoma

A
  • is a B-cell non-Hodgkin lymphoma (NHL) that typically affects elderly patients in the 7th and 8th decades.
  • Gastric MALTomas are frequently associated with Helicobacter pylori (H. pylori) infection
  • nongastric MALTomas are rather associated with autoimmune conditions
41
Q

MALT Lymphoma Clinical Features

A
  • Gastric MALTomas
    • Abdominal pain
    • Melena, hematemesis, potentially anemia
    • weight loss
  • Non-gastric MALTomas:
    • Salivary MALToma: parotid enlargement
42
Q

Gastric MALToma

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

Surgery Clerkship- Amboss Study Plan (6 decks)

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