Stomach Flashcards
foveolar cells
mucin secreting cells
How does the stomach protect itself against its acidity?
mucin
bicarbonate secreted by surface epithelium
vascular supply
Omphalocele
- persistent herniation of bowel into umbilical cord
- failure of abdominal wall to return to body cavity during development
- covered by peritoneum and amnion of cord
Gastroschisis
malformation of abdominal wall causing exposure of abdominal contents
Pyloric stenosis
congenital hypertrophy of smooth muscle of pylorus
- more common in males
- projectile vomiting in first 2-6 weeks of life
- visible peristalsis
- olive-like mass in abdomen
What are 6 general causes of abdominal pain?
- gastritis
- peptic ulcer disease
- gastroesophageal reflux disease (GERD)
- biliary colic
- irritable bowel syndrome
- pancreatitis
What are 4 symptoms of gastritis?
- nausea
- vomiting
- hematemesis-vomiting of blood
- epigastric pain
What leads to gastritis?
injury or impaired defenses
What is acute gastritis?
- transient process
- nausea, vomiting, epigastric pain
- superficial, erosive, ulcerative
- severe cases may hemorrhage
- Impairment of protective system: NSAIDs, ingestion, direct injury
-neutrophilic infiltrate
What is the treatment of acute gastritis?
removal of offending agent
pharmacologic acid blockade
tincture of time
What is chronic gastritis? What are the main causes?
more persistent
-most common cause is H pylori infection
other causes:
-autoimmune
What increases the risk for an H pylori infection? What are the 4 modes of virulence? What is the most common location of H pylori infection? What does H pylori increase the risk for?
Increased risk of infection
- poverty
- household crowding
- limited education
- AA or MA ethnicity
- Poor sanitation
- Birth outside US
Four modes of virulence:
- Flagella
- Secretion of ureases
- Adhesins
- Toxins
Antrum most common location
Increased risk of:
1. gastric adenocarcinoma due to intestinal metaplasia
- MALT
- lymphoid aggregates seen in MALT-subeptihelial plasma cells
How is the diagnosis of H pylori made?
- biopsy
- serologic testing for h pylori antibodies
- fecal detection
- urea breath test
What is the treatment of H pylori?
Triple
- PPI
- Amoxicillin
- Clarithromycin
Quadruple
- PPI
- Bismuth
- Tetracycline
- Metronidazole
Sequential therapy first
Chronic Gastritis: Autoimmune
SPARES THE ANTRUM
- antibodies to parietal cells and intrinsic factor
- vitamin b12 deficiency due to loss of IF–>pernicious anemia
- decreased pepsinogen 1 level due to loss of chief cells
- defective gastric acid secretion (achlorhydria)
- median age 60 years
- slight female>male
- increased risk of adenocarcinoma due to intestinal metaplasia
What does the decreased acid production seen in autoimmune gastritis lead to?
increase in gastrin release
and hyperplasia of antral G cells
What are symptoms of acute peptic ulcer disease? What are the causes of specific types of ulcers? What do the ulcers look like?
nausea, vomiting, coffee-ground hematemesis
stress ulcer: shock, sepsis, severe trauma
curling ulcers: severe burns, trauma
cushing ulcers: intracranial disease
ulcer are typically
What are they symptoms of chronic peptic ulcer disease?What are most often the causes?
Epigastric burning or aching pain occurring 1-3 hours after eating, worse at night, relieved by alkali or food
may also have nausea, bloating, belching
Most often due to
- H pylori
- NSAIDS
Location
- Most common in proximal duodenum and antrum (4:1)
- solitary in 80% of cases
Ulcer
-Sharply punched out defect, clean base
-perforation is complication
What is the treatment acute peptic ulcer disease?
stress ulcer prophylaxis with PPI or H2 blocker Target patients: Mechanical ventilation Severe burns Trauma Severe sepsis Intracranial injury Coagulopathy -acid blocking agents -treat underlying condition
How do you treat chronic peptic ulcer disease?
Eradication of H pylori if present
Remove offending agent
Surgery may be needed for bleeding or perforation
Zollinger Ellison Syndrome
-multiple ulcerations in GI tract due to hypersecretion of gastrin by tumor
What are risk factors for chronic peptic ulcer disease?
- NSAIDs
- Cigarette smoking
- high-dose corticosteroids
- alcoholic cirrhosis
- COPD
- Chronic renal failure
- Hyperparathyroidism
- Psychological stress
Fundic gland polyps
Sportic or associated with familial adenomatous polyposis
- -cystically dilated irregular glands lined by flattened parietal and chief cells
- well circumscribed and multiple
- located in the body and fundus
- not necessarily related to chronic gastritis
- not neoplastic
- males=females
- any age
Inflammatory and hyperplastic polyps?
50-60 years male=female -higher neoplastic risk when >1.5 cm -related to chronic gastritis -any location in stomach -multiple ovoid in shape,
Gastric adenoma polyp?
50-60 years
- male 3x more
- risk higher when >2 cm
- related to chronic gastritis
- ANTRUM
- intestinal type epithelium with variable degrees of dysplasia
- carcinoma can be present in up to 30% of adenomas
Extranodal lymphomas occur commonly in the GI tract especially the stomach what is a type of lymphoma that occurs?
Mucosa-associated lymphoid tissue (MALT)
-marginal zone b cell lymphomas
Carcinoid tumor arise from what? Where do they occur? What location is the most aggressive?
When is the peak incidence? What does carcinoid syndrome indicate?
- arise from neuroendocrine cells (G cells in the stomach)
- 40% occur in small intestine
- most agressive in midgut
- 60s
- carcinoid syndrome indicate metastasis
GIST: gastrointestinal stromal tumor
neoplasm of what?
Mesenchymal neoplasm of interstitial cells of Cajal: pacemaker cells for the cut
>50% in stomach
What do GIST look like?
solitary, well circumscribed fleshy, submucosal mass
Males>females
60s
75-80% gain of function mutation in gene encoding tyrosine kinase c-KIT
-symptoms related to mass effect or mucosal ulceration
What is the treatment of GIST?
Surgical resection if possible
Imatinib-inhibits tyrosine kinase activity of c-KIT and PDGRFA
Gastric Adenocarcinoma causes:
- H pylori infection
- chronic gastritis–>proinflammatory proteins - Epstein Barr virus
- 10% of cases; unclear mechanism
- proximal stomach, marked lymphocytic infiltrate - Mutations
- Germline mutation of CHD1 causing loss of E cadherin function (diffuse type)
- Familial adenomatous polyposis coli: mutations in APC genes (intestinal type)
Intestinal Gastric Adenocarcinoma
Bulky Glandular structures, exophytic mass or ulcerated tumor 55 yrs old Male X2 Incidence higher in high-risk areas
Diffuse Adenocarcinoma
-infiltrative growth, discohesive cells with large mucin vacuoles
-signet ring cells
-linitis plastica caused by desmoplastic reaction
-incidence same regardless of geography
males=females
What is the treatment for gastric adenocarcinoma?
surgical resection when possible; chemo minimally effective
-prognosis based on extent of nodal involvement whether metastasis is present at diagnosis
Metastatic gastric adenocarcinoma spread to the left supraclavicular node is called?
virchow node
Metastatic gastric adenocarcinoma often has distant metastases where?
liver
Metastatic gastric adenocarcinoma spread to periumbilical region it’s called?
sister mary joseph nodule (intestinal type)
Metastatic gastric adenocarcinoma spread to bilateral ovaries it’s called?
krukenberg tumor (diffuse type)
