gastritis, peptic ulcer disease, and gastric cancers

generic term used to describe inflammation, infection, or damage to the stomachs mucosal lining

gastritis

categories of gastritis

nonerosive, erosive/hemorrhagic, infectious

gastric irritation and atrophy caused by cellular changes or weakened host mechanisms

nonerosive gastritis

areas of the stomach

fundus, body, pyloric region

common causes of nonerosive gastritis

pernicious anemia, h. pylori infxn

an autoimmune disease resulting in vit B12 malabsorbtion due to dec intrinsic factor

pernicious anemia

what will you see on lab results specifically for pernicious anemia

see anti-intrinsic factor antibodies in 70% of pts

how do we treat pernicious anemia related gastritis

parenteral B12 and Proton Pump Inhibitors

how is nonerosive gastritis caused by H. pylori transmitted

oral-oral or fecal-oral transmission

how common in nonerosive gastritis caused by H.pylori

80% of adults in developing countries and 30-40% of adults in US

what cell secretes intrinsic factor

parietal cells

tell me about the H.pylori bacteria

gram neg bacillus w spiral shape flagella, can move within the mucus environment of the gastric mucosa, and secretes ammonia as a buffer defense against gastric acid

what can cause macrocytic anemia

vit b12 deficiency (perniciouos anemia if autoimmune) and folate deficiency

stomach body predominant infections of H.pylori result in ____

gastric atrophy and irritation

stomach antrum predominant infections of H.pylori result in ____

erosions and ulcers (erosive and hemorrhagic or peptic ulcer disease)

nonerosive gastritis caused by H. pylori risk factors

family members or close relations with a hx of “ulcers”, similar sx, or known H. pylori infxn

nonerosive gastritis caused by H. pylori sx

loss of appetite, midepigastric pain/tenderness, nausea, maybe vomiting

noninvasive physical is low yield for a pos dx but can rule out other ddx

nonerosive gastritis caused by H. pylori dx

fecal antigen immunoassay, urea breath test, serological ELISA (enzyme lined immunosorbent assay, not often used bc bad accuracy)

biopsy (not used primarily for H.pylori dx but can be work up for other ddx)

upper endoscopy w biopsy for active infection based on urease production

what do we have to do first before doing a fecal antigen immunoassay or urea breath test

fecal and breath tests both require cdiscontinuing of Proton pump inhibitors for 7-14d and abx for 28d

h.pylori gastritis tx (erosive or nonerosive)

mostly 14d regimine, must be at least 7 days min

standard triple combo of Proton Pump Inhib + clarithromycin + amoxicillin (or metronidazole if PCN allergy)

tet for eradication 4wks after completing tx, sx improve after 7-14d

what mechanisms can cause erosive/hemorrhagic gastritis

gastric mucosal erosion either from inhibition of the normal mucosal defenses allowing gastric acid to damage tissues OR local damage from ingested items

common causes of erosive/hemorrhagic gastritis

meds (NSAIDS), H.pylori antral infxn, alc, stress, portal hypertension, consumed irritants

erosive/hemorrhagic gastritis risk factors

chronic NSAID use, severe medical illness or injury (stress induced), chronic or binge alc use, liver disease, family member w hx of ulcers or H.pylori, preferring spicy or acidic foods

erosive/hemorrhagic gastritis sx

loss of appetite, midepigastric pain/tenderness, nausea, black stools, vomiting (coffee grounds puke or bright red blood), nasogastric suction with the coffee ground or bright red blood, maybe melena on digital rectal exam

erosive/hemorrhagic gastritis dx

upper endoscopy, H.pylori labs, labs may show anemia due to chronic bleeding, positive fecal occult blood

diagnostic of choice for erosive/hemorrhagic gastritis

upper endoscopy

erosive/hemorrhagic gastritis tx for stress induced cause

PROPHYLAXIS (Proton pump inhibitors PO or IV for all severely ill or injured pts

tx damage and hemorrhage (continuous PPI infusion and PO sucralfate suspension, possible endoscopic repair)

erosive/hemorrhagic gastritis tx for NSAID induced

stop NSAIDS or reduce to minimal dose or switch to selective COX-2 inhibitors (COX-1 is mainly involved w somach and duedenal cytoprotectie prostaglandins and since normal NSAIDS inhibit COX 1 and 2 normal enzymes will dec gastric mucosal protection)

take NSAIDS w food from now on, begin PPI meds for 2-4wks, if sx dont improve do an endoscopy

erosive/hemorrhagic gastritis caused by alc or irritating foods

stop drinking or eating the food, begin PPI, H2 blocker, or sucralfate for 2-4wks

erosive/hemorrhagic gastritis tx for portal htn caused

propanolol to dec portal HTN

tx underlying liver disease

PPI or sucralfate to help sx but wont reverse the pathology

the destruction of the gastric or duedenal mucosa by digestive factors like acid and pepsin, due to impaired or overwhelmed mucosal defense mechanisms

peptic ulcer disease

how deep do peptic ulcers extend

usually over 5mm through the muscularis mucosae (second layer of stomach cells, deep to gastric glands)

where is peptic ulcer disease most often found

5x more commonly found in duedenum bc bc right outside of stomach and less protection from the acid there

peptic ulcer disease causes

NSAIDS and H. pylori infxn for 90%

what is the MOST common cause of peptic ulcer disease

H. pylori infxn

why is H. pylori the most common cause of peptic ulcer disease

bc H. pylori presence physically reduces teh natural protective barrier increasing the tissue damage from gastric contents AND

H. pylori presence creates local tissue inflammation worsening tissue damage created by gastric contents

why do NSAIDS cause peptic ulcer disease

because NSAIDS inhibit COX-1 which leads to impaired mucosal defenses

peptic ulcer disease risk factors

family members or close living arrangements w ppl affected by ulcers and/or have known H. pylori infxn

long term NSAID use

peptic ulcer disease sx

anorexia, nausea

midepigastric pain (hunger like gnawing pain, pain wakes pts from sleep and becomes severe as it perforates, “classic pain”, pain worse 2-5hrs after a meal when acid is secreted in the absence of a food buffer and worse at night between 11-2 when acid secretion is maximal, improved w food buffers)

midepigastric tenderness

if the ulcer perforates see rigid abdomen w guarding and peritoneal signs

possible melena based on time of bleeding

labs to run for peptic ulcer disease

H. pylori serum test, breath urea test, fecal testing, CBC to identify possible anemia, digital rectal exam for pos fecal occult blood (remember to discontinue PPI for 7-14d for fecal and breath tests and abx for 28d)

may see free air on upright Xray (indicates perforation)

biopsy can be taken immediately to confirm non-malignancy

what is the most definitive dx for peptic ulcer disease

upper endoscopy (not always needed)

red flags (for malignancy) with “ulcer” or “gastritis” type sx require _____

EGD

red flags that would indicate malignancy

weight loss, over 50yo, melena, dysphagia, family hx of cancer, pos fecal occult blood test, anemia, bleeding, sx continue despite medical tx, blood in puke, odynophagia, recurrent vomiting, severe abdominal pain

peptic ulcer disease tx if caused by NSAIDS

stop using NSAIDS or switch to selective COX-2 NSAID and start a proton pump inhibitor for 4-6wks

an acquired condition caused by hypertrophy and spasms of the pyloric sphincter resulting in gastric outlet obstruction

pyloric stenosis (aka gastric outlet obstruction)

when dose pyloric stenosis mostly happen

most commonly occurs in the first weeks of life but can be delayed

mostly in men, familial relationship, infants who are exposed to macrolides (esp at first 2wks olf) inc risk

what causes primary adult acquired pyloric stenosis

mostly idiopathic

what causes secondary adult acquired pyloric stenosis

secondary to local. inflammation, caused by

chronic gastritis, chronin peptic ulcer disease, gastric cancer, chronic gallbladder disease

bouverets syndrome is a rare complication of a biliodigestive fistula (big stone occludes the pyloric duoedenal region

pyloric stenosis sx

increasingly frequent and forceful puking (forceful and projectile, NOT spitting up)

emesis contains NO BILE (means obstruction proximal to duodenum

pts are starving despite vomiting

report that after feeding the stomach becomes enlarged with visible peristaltic waves. as stenosis progresses pt will experience malnutrition, weight loss and fatigue

pyloric stenosis physical exam findings

hypertrophied pylorus may be palpated in the epigastric region (“olive” like)

in late disease see: weight loss, dehydration, lethargy, failure to thrive

pyloric stenosis labs

hypochloremia, metabolic alkalosis, and high BUN all from repetitive vomiting

pyloric stenosis xray results

dilated stomach w little to no gas in intestines

pyloric stenosis ultrasound results

elongated and thickened pylorus

pyloric stenosis imaging of choice

ultrasound

pyloric stenosis barium swallow study results

“string sign”

pyloric stenosis tx

stabilize severely ill pts, correct dehydration and metabolic abnormalities

surgical pyloromyotomy (a longitudinal incision and blunt dissection of the hypertrophic pylorus) can be done by laparoscopic, right upper quadrant transverse incision, infra umbilical rim or circumumbilical techniques

post op do ad lib feeding aka start feeding directly after surgery (shortens time to full feeding and helps recover faster)

pyloric stenosis prognosis

feeding can be resumed in most infants within a few hrs post surgery

3 main types of gastric neoplasms

gastric adenocarcinoma, gastric lymphoma, gastric carcinoid tumor

2 cellular variants of gastric adenocarcinoma

intestinal type (resembnled intestinal cellular cancers w glandular structures)

diffuse type (poorly differentiated, without glandular formations)

gastric adenocarcinoma risk factors

chronic H. pylori infxn, pernicious anemia, smoking, diets high in nitrates and salt and low in vit C, family hx of gastric cancer (may consider prophylactic gastrectomy in pts w genetic mutation and higher than 60% chance of getting gastric cancer)

gastric adenocarcinoma sx

dyspepsia, vague midepigastric pain, loss of appetite, early satiety (late in disease)

pts usually asymptomatic until disease is super advanced

gastric adenocarcinoma physical exam findings

(occur late in disease)

midepigastric tenderness, weight loss, maybe melena, maybe pallor depending on amount of blood lost

gastric adenocarcinoma dx

upper endoscopy (good in early and late disease)

endoscopy w biopsy highly sensitive for cancer

labs (good in late disease)
pos fecal occult, anemia due to chronic disease or iron deficient, high liver enzymes due to metastases

CT scan on chest and abdomen/pelvis to delineate extension of cancer

endoscopic ultrasound better than CT to determine depth of tumor invasion into stomach tissues

gold standard dx for gastric adenocarcinoma

upper endoscopy

the T in the TNM staging system stands for

size and extend of the primary tumor

the N in the TNM staging system stands for

the number of nearby lymph nodes that have cancer (for gastric adenomas will check the lymph node on the ciliac trunk)

the M in the TNM staging system stands for

whether the cancer has metastasized

gastric adenocarcinoma tx

surgical resection (ONLY curative option) (laproscopic or open)

perioperatice chemo improves survival rates of localized or locoregional disease

palliative surgery or chemo for no curative disease

tumor that can be the primary site or site of metastasis from primary lymph node lymphoma

gastric lymphoma

what is the 2nd most common type of gastric cancer

primary gastric lymphoma

what is the largest risk factor for primary gastric lymphoma

H. Pylori

what kind of gastric lymphoma has reed-sternberg cells and is more treatable w inc survival rates

hidgkins

gastric lymphoma sx

vague midepigastric pain, weight loss, early satiety late in disease, melena, systemic sx of fatigue and pain if cancer is diffuse

maybe pallor

gastric lymphoma dx

upper endoscopy w biopsy (deliniates type of cancer and identifies possible H.pylor infxn)

pos fecal occult

anemia due to chronic disease or iron def

elevated liver enxymes

lymph node biopsy pos for lymphoma

H. pylor breath, fecal, or serological testing

CT scan of chest, abdomen, pelvis to deleniate extension of cancer

bone marrow biopsy

gastric lymphoma tx

stage w TNM, tx H. pylori infxn (causes complete regression of lymphoma in 75% of pts w minimally invasive disease)

chemo/radiation

rare gastric tumors that only makeup 1% of gatric cancers and most occur in conjunction w pernicious anemia

gastric carcinoid tumors

carcinoid syndrome seen in gastric carcinoid tumors

skin fushing that can be accompanied by hypotension, venous telangiecsasia, diarrhea, bronchospasm

gold standard to dx all gastric cancers

upper endoscopy w biopsy

gastric carcinoid tumors tx

if 1 small local tumor: resection

if many carcinoids localized: radical gastrectomy w regional lymphadenectomy

if pts have any of these sx they immediately need an upper endoscopy: (red flags for cancer)

new onset GERD over 50to

GERD not relieved by proton pump inhibitrs

progressive dysphagia

recurrent vomiitng

pos fecal occult stool

melena

hematemesis or anemia

severe, unexplained abdominal pain

weight loss/anorexia

family hx of stomach cancer