GI pouch- Exam 3- Ross Flashcards
By what physiologic mechanisms is the gastric mucosa protected?
bicarbonate and mucus production
What 3 regulatory systems stimulate the stomach’s production of acid
neurocrine: acetylcholine released by **vagal nerve for production of acid
paracrine: local release of hormone: histamine released from stomach wall cells stimulates acid production
endocrine components: gastrin produced by G cells of stomach
increase gastric acid by parietal cells
Digestive enzymes: proteases
-list 3 tyoes
- Pepsinogen/Pepsin
- Trypsinogen
- chymotrypsinogen
Pepsinogen/pepsin=
- produced by chief cells in stomach wall
- cleaved from pepsinogen to pepsin by hcl
- primary cause of mucosal damage in esophageal reflux
Trypsinogen=
a serum protease secreted by pancreas cleaved by enteropeptidase to trypsin
Chymotrypsinogin=
serum protease secreted by pancreas converted into active form by trypsin
Mucosal defense: 3 layer
list 3 layers
- mucus
- surface epithelial cells
- microvascular system
Describe the mucous layer of the mucosal defense
-bicorbonate-phospholipid : physiochemical barrier especially to Hydrogen ions
Describe the surface epthelial cells of the mucosal defense layer
=mucus production, intracellular tight junctions
–>prostaglandins: inhibit acid production, regulate release of bicarb rate limiting production step is controlled by cyclooxygenase (COX-1,COX-2 inflammatory)
Describe the microvascular system of the mucosal defense
-provides subepithelial defense / repair also supplying micronutrients.
B is mucosal defense
3 level barrier= Pre epithelial, epithelial, and subepithelial
-HCO3 (bicarb) coming up from vascular system turning into h20 and co2
Describe the “constant attack” on the GI system
- acid, pepsin, bile acids, pancreatic enzymes, bacteria and drugs
- when this defense breaks down inflammation ensues and ulcer forms
-Gastric acids (Hydrochloric acid )and pepsin destroy gastric and duodenal mucosa. Mucus and bicarbonate ion secretions protect mucosa. Prostaglandins protect mucosa by enhancing mucus and bicarbonate production and by enhancing mucosal blood flow
Gastritis=
- chronic or acute inflammation of gastric mucosa: multiple etiologies
- -dx made by endoscopy and is histological
PUD=
- both gastric and duodenal is a more chronic illness characterized by the formation of recurrent ulcers (>5mm in size) in the stomach an proximal duodenum
- -definitive dx made by upper GI or endoscopy
Dyspepsia=
continuous or recurrent upper abdominal pain it’s a symptom not a pathophysiologic condition
Gastritis- is NOT to be interchanged with _____
dyspepsia
Sx of Gastritis
-acute vs chronic epigastric pain (dyspepsia)
-Generally non-erosive
inflammatory cell infiltrate
-Infectious: usually acute: H.Pylori, CMV
- Granulomatous: as in Chron’s dz
- If involving astral cells can cause **pernicious anemia
-**endoscopic sub epithelial hemorrhages: no major bleeding as no art/vein in mucosa
Infectious Gastritis
-Bacterial- rapidly progressive, rare, life-threatening
-Viral- CMV(cytomegalovirus) in the immunocompromised/
immunosuppressed patient
- Fungal- Candida in immunocompromised patients
- Parasitic- among others -Anisakis marina from raw fish or sushi can become embedded in gastric mucosa
Erosive and Hemorrhagic Gastritis: “stress gastritis:”
- MC caused by?
- endoscopic findings?
Most commonly caused by: Stress Meds Alcohol Portal hypertension
Endoscopic findings:
- Subepithelial hemorrhages
- Petechiae
- Erosions
Stress gastritis:
erosions may occur rapidly following?
- Mechanical ventilation*
- Coagulopathy*
- Major physical or thermal trauma
- Shock
- Sepsis
- Head injury
- Hepatic, renal or multiorgan failure
**very ill Pts in the ICU
Peptic ulcer disease (PUD)=
-etiology?
- etiology 12% males usually due to alcoholism
- 10% fem usually due to NSAIDs
- 15,000 deaths
PUD= disruption of mucosal integrity of stomach or duo leading through to the muscularis mucosa into deeper layers to a local defect due to active inflammation
Ulcer is defined as ____
is a breakdown in the mucosal surface, through the muscularis mucosa into deeper layers to a local defect due to active inflammation.
alcohol
->5 mm in size
H. Pylori=
-produces?
-Helix shaped curved gram neg rod with flagella that penetrate through mucosa of stomach to a less acidic environment
-produces ammonia which is cytotoxic to lining cells of stomach
and also a focus of inflammatory response
-thereby decreasing the protective layer and harming the epithelial cells (added by pepsin)
____% of those infected with H pylori are asymptomatic
80%, (most ppl dont develop ulcers)
H. Pylori testing (list methods)
- serum antibody: IgG levels : variable accuracy depending on lab vs home commercial test
- urea breath test: Best established test ** KNOW
- stool antigen : simple and accurate less expensive
- -With noninvasive Testing
- -Discontinue PPIs 7-14 days prior to testing by breath or feces
-Endoscopy- not indicated specifically but if being performed for another reason, biopsy can be obtained
H. pylori: testing is indicated for? (3 things)
- Active or past history of PUD
- Gastric MALToma (mucosa-associated lymphoid tissue lymphoma)
- Family history of gastric carcinoma (especially if Asian descent)
Peptic Ulcer Presentation:
-Duodenal? (sx)
- Burning pain 1-3 hours after meals, relieved by food
- Epigastric pain (vague discomfort, cramping, hunger pangs)
- Nocturnal pain with early morning awakening
- usually within 3cm of pylorus
Peptic Ulcer Presentation:
Gastric? (Sx)
- Not common to see post-prandial epigastric pain
- Weight loss
- later in life peak 6th decade
- **associated with malignancy
Peptic Ulcer Treatment
Antacids H2 blockers: (cimetidine/or ranitdine) PPIs (omeprazole, iansoprazole) -Sucralfate -Bismuth -H. Pylori
Another H. Pylori–indications for testing
- test if you only plan to treat
- test and treat for under 50 with no worrisome flags
- obtain your pre-test probability before hand
- -ELISA: IgG antibodies: sensitivity not good
- -Stool antigen: good sensitive and specificity
High pretest: if negative retest
Low pretest: if negative then unlikely to be H pylori
-if positive, consider retest with another modality
SLide 21
GO OVER
H Pylori education?
-Usually 2 Abxand a PPI for 2 weeks
- Triple therapy: (if Pt failed 1st therapy)
- -Tetracycline, metronidazole, bismuth
- -Clarithromycin, tetracycline, bismuth
- -PPI + 2 of these-> Amoxicillin, metronidazole, clarithromycin
-Quadruple therapy:
Metronidazole, TCN, bismuth, PPI
When should you scope ppl?
- family hx of gastric cancer
- GI bleed
- Weight loss
42 yo male with epigastric discomfort for past month. It is intermittent and is described as a burning sensation. It occasionally makes him short of breath. It is is relieved with food. It was so intense that it required an ED visit. He is here for follow up.
PMH: HCO
Meds: atorvastatin
ROS: no weight loss/gain, chronic knee pain
Social: occasionally drinks etoh, non-smoker, lives with girlfriend
PE: BMI 28, 150/70, 86, 18 97.8 95%
- you could tx him for h pylori without testing him, OR you could get an h pylori test on him
- also think about pancreatitis, and gallstones
- get a GOOD alcohol hx
Work up of Dyspepsia: scope or not?
-definitive diagnosis made by endoscopy, although not all pt require endoscopy
age >50 with new symptoms weight loss persistent vomiting dysphagia Gi bleed Iron def anemia abdominal mass family hx of GI malignancy
-complicated cases need a scope
Work-up of dyspepsia:
- consider alternative diagnosis labs :lft’s, lipase, ekg
- H.pylori
-If complicated then will need a scope
PUD: Reasons for Treatment Failure
Non-compliance NSAIDs or ASA Zollinger-Ellison Cigarette smoking Malignancy -If all of the above excluded, can continue PPI for 8 weeks and still refractory, surgical consult
Cigarette smoking retards _____ _______.
get them to stop!!
ulcer healing (PUD tx failure reason_
GERD:
- changes in ______ epithelium
- those who have chronic reflux disease will change their esophageal epithelium
- the squamous epithelium is replaced by metaplastic columnar epithelium, this is called Barrett esophagus and carries higher risks of cancer.
Upper GI Bleed:
is defined as:
- bleeding originating above ligament of Treitz* KNOW
- Hematemisis, clarify: is it BRB or coffee-ground emesis = UGI
- Melena: could be upper or lower
Hematemisis=
the vomiting of blood.
Melena=
dark sticky feces containing partly digested blood.
the production of melena, following internal bleeding or the swallowing of blood.
GI Hemorrhage from PUD
- not always a brisk vomiting of blood
- can be hematemesis
- can be melanotic stool
- Decreased hematocrit/Elevated BUN
Treatment:
- -Appropriate resuscitative procedures if needed
- -Endoscopy- preferred diagnostic procedure
- -High dose oral or IV PPI in high risk of re-bleed x 3 days
- -Long term prevention- r/o H. pylori ->PPI or H2 blocker
- -Surgery
ross says: if Pt is vomiting blood–> start the Pt on 2 IV lines, get a CBC (check Hct levels)
-high dose PPI
Vomiting Blood: Mallory-Weiss syndrome
=non penetrating mucosal tear at gastroesophageal junction
- occurs after forceful vomiting
- blood tinge/fleck
- no specific treatment–> will heal on its own
44 year old female sent over from clinica compazina due to low H/H. Been following for several weeks now 6/24. Pt asymptomatic . Hx of PUD dx by scope 4 years ago. Takes medications.
ROS: tired all the time
- 130/80, 88, 20,90% at rest
- PE pale conjunctiva
- Guiac pos no frank blood
6/24= very anemic
-this is peptic ulcer disease case with failed tx
Autoimmune (Pernicious Anemia)=
=antibodies to parietal cell leading to decreased acid production as well as decreased Intrinsic factor production
- Achlorhydria leads to significant hypergastrinemia
- and decreased levels of intrinsic factor (IF)
- (IF) needed to absorb B12 in the duodenum
- Endoscopy with biopsy is recommended at the time of diagnosis with pernicious anemia and any suspicious findings periodically reexamined
51y/o male vomiting awoke him from sleep. He states it was purple vomit, he did not know if with blood He no longer drinks ETOH, quit 4 years ago. Had a hx of vomiting blood 4 years prior had esophageal varicies that were banded. No hx of bleeding since then.
Vomiting is accompanied with some pain but not much 2/10.
VS 115/60, HR 110, 33, 94% sat, 97.2, DS 120 pain 0/10
PE: Pale face, almost icteric, pale mucosa, **perioral cyanosis
Oral pharynx: moist, dark material on back of tongue
AB: soft non-tender, no distention, normal BS.
rest of exam non contributory
What important PE component is missing?
What important PE component is missing? rectal exam!!! (it was positive)
-note: his hematocrit was VERY low. He had exophageal varices
Gastric Cancer=___ MC death related cancer in the world
2nd MC
Gastric cancer dx=
-few complaints
PE: usually normal
-Labs may not be helpful until it reaches an advanced stage
–*EGD- procedure of choice for diagnosis of gastric cancer, with deep biopsy
(thought to be related to smoked or salted foods that bacteria degrade to carcinogenic nitrites)
Risk factors for Gastric Cancer
- chronic H. Pylori infections increases risk 5-20%
- achlorhydria : increase in serum gastrin an inducer of gastric epithelial cell proliferation - Pernicious anemia
- gastrojejunostomy : removal of portions of stomach
Gastric cancer: Pts can have which kind of carcinoma?
-adenocarcinoma**
–>Intestinal
Early, then late adenoma, then carcinoma
- Environmental causes
- H.pylori
- Dietary factors
- Smoking
-Diffuse
Gastric cancer: MC metastasis?
Metastases to multiple organs- most commonly the liver
Gastric Cancer: AGA recommends an ____ be performed in Pts
EGD!!**
-Older than 45 years with new-onset dyspepsia
-Younger than 45 years with “alarm symptoms” (wt. loss, recurrent vomiting, dysphagia, evidence of bleeding, anemia)
Gastric Cancer: tx
- Surgical resection is the only curative procedure
- Fairly resistant to conventional chemotherapy and radiation therapy
Gastric cancer: prognosis of adenocarcinoma?
- 18.6% 5-year survival rate in men and 25.2% in women
- 4-6 month life expectancy in untreated, advanced disease with liver metastases
- 4-6 weeks in patients with peritoneal carcinomatosis
Gastric cancer: gastric lymphoma–> most are?
- Most are non-Hodgkin’s lymphomas
- Submucosal involvement
Gastric cancer: gastric carcinoid tumors–> arise from? Risk factors?
- Arise from GI neuroendocrine cells (MEN-1)
- Risk factors: Pernicious anemia and chronic atrophic gastritis
Gastric Cancer:
-Gastrointestinal Stromal Tumors (GIST)?
- Intra-abdominal mesenchymal tumors
- Usually asymptomatic until quite large
- Can be benign to highly aggressive
- Endoscopy with biopsy and histologic examination
- Endoscopic ultrasound to determine depth of invasion
-*Most useful clinical predictor of outcome is **mitotic index
Zollinger-Ellison Syndrome (Gastrinoma) (ZES)
=Excessive secretion of gastric acid by a gastrinoma
-Can be located in the: Pancreas Duodenal wall Lymph nodes Other or unknown
-Most in the “gastrinoma triangle”
ZES:
-demographic?
-Slightly more common in males
Average age 40s
ZES:
- ___ of gastrinomas are malignant
- ____ have already metastasized to liver at presentation
- 2/3
- 1/3
ZES: almost ____% of gastrinomas are associated with MEN1
-25%
ZES: what lab would you order?
**get fasting gastrin level
if elevated, think ZES
Another sx of ZES?
Ulcers with no H. Pylori or NSAID use
MEN type 1=wermer’s syndrome pay attention to..
-peptic ulceration,
ZES:
-Pts present with..
- symptoms of gastric acid hypersecretion
- 70-80% of patients have or have had a peptic ulcer
- 60% of patients present with GERD or GERD/esophageal symptoms
Screening for ZES
- Refractory ulcers or frequent recurrences
- Giant ulcers >2cm
- Ulcers distal to the duodenal bulb
- Multiple duodenal ulcers
- Ulcer complications
- Fasting gastrin level
- *MEN-1
Imaging in ZES
- Somatostatin receptor scintigraphy(SRS) with single photon emission computed tomography (SPECT)
- CT and MRI have low sensitivity for small tumors
Treatment of ZES
-Immediate and long-term control of gastric hypersecretion
- Specific treatment for the gastrinoma
- -Metastatic
- -Localized disease
-95% 15-year survival rate in patients who do not have liver metastases
Gastroparesis =
=delayed or impaired gastric emptying Sx: -early satiety, nausea and postprandial vomiting of undigested food -can be debilitating -causes: Diabetes -neuromuscular dysfunction: diabetics
Gastroparesis: tx
treat by small meals, increase nutrition via liquids, low fat diets
–acute management with anti-emetics, IVF (Ross say’s give Ativan, or benzos)
Cyclic Vomiting Syndrome=
- usually children, uncommon in older adults although making a resurgence with the use of marijuana
- can be triggered by food allergies
- can last days to weeks
- need GI referral and electrogastrografic studies: usually a sympathetic nerve issue
- cannabinoid hyperemesis syndrome= daily smokers feel nausea and vomit for hours. hot showers assist in feeling better
tx: hot showers and STOp smoking
