Talk a tiny bit about H. pylori and what it is.

- it's a flagellated bacteria that does not stain on a normal H and E stain and is really hard to culture.

- Uniquely produces urease, and so makes a bunch of ammonia to surround it to protect from the gastric acid. We use this in the breath test.

- causes gastritis (antral predominant, nonatrophic pangastritis, or corpus predominant atrophic gastritis) - that last one can lead to intestinal metaplasia, dysplasia and then gastric cancer. The last one is also the most likely to creat a gastric ulcer.

- antral predominant are the ones more likely to cause duodenal ulcers.

What clinical testing can we do in someone that we suspect may have an H pylori infection? (Or we want to rule it out)

- in most cases do serology, but histology is the best

- Can also do breath testing for non-tissue

- Other tissue tests include CLO-rapid urease test (that bubble pack thing) and culture, but that is done very rarely.

How do you treat H pylori infection?

- PPI / clarithromycin /  either amxocillin or metronidazole

- cure rate about 80%

- check afterwards to make sure they're treated.

Explain the COX and NSAID thing in relation to what causes gastric ulcers

- Both COX 1 and 2 break down arachidonic acid into prostaglandins (and thromboxane for COX-1 for platelet aggregation)

- COX-1 is in the stomach, platelets, kidney and endothelium, and is good for GI mucosal integrity, platelet aggregation and renal function.

- COX-2 is on macrophages, leukocytes, fibroblasts and endothelium and is good for inflammation, mitogenesis, bone formation and maybe others.

*activity of COX-2 is induced by injury wheras COX-1 is active all the time.

*downside of COX-2 specific inhibitors is cost, if you use ASA it doesn't matter, and increased risk of CV complications.

Name some H2 receptor agonists and describe what they do

- ranitidine, famotidine, mizatidine, cimetidine.

- inhibits histamine stimulated acid secretion (reduces it by like 50%)

- good for duodenal ulcers but not as much gastric ones

- not as effective in NSAID users.

* Ohhhhh 2 DINE again!

Name some PPIs and describe what they do

- Omeprazole, lansoprasole, pantoprazole

- cuts acid by about 95%

- more effective than H2 R antagonists.

- good for those using ASA

* Those good "OLEd" PPIs with help ya!

It case it comes up which it totally won't, describe Zollinger-Ellison syndrome

- CP: multiple ulcers (and w/o NSAID/HP), complicated ulcers, duodenal distal to the ampulla of Vater, water diarrhea and/or nephrolithiasis due to hypercalcemia.

- Dx: serum gastric level (> 1000 ng/ml) and secretin stimulation test (positive when rise in gastrin by 200 ng/L)

- Tx: find gastroma and take it out (that's what caused the increase in gastrin and all the ulcer stuff by the way). Can do MRI, Angiogram, Octreotide scan (binds to somatostatin R found on these tumors), endoscopic U/S or intraoperative U/S. Those little guys can be easy to miss.

As far as I can remember from jsut hearing it, how do you work up a person who come to you with stomach pain?

- ask about red flags for cancer. If they are over 50 (I think) and have never had this type of pain before, loosing weight, anemia, trouble swallowing, do an endoscopy.

- ask if they are on NSAIDs or ASA, see if it helps to stop if you can

- ask if they are on PPIs, if they are then it's suuuuper probably not an ulcer

- test them for serum H pylori test. If it comes back + then treat it with abios plus PPI and see if it goes away, if it's - then treat with PPI to see if it goes away

- if PPIs don't help and you haven't seen an NSAID or ASA cause, then just endoscopy them although they'll probably be normal.

What are the 4 layers of the stomach? Describe esprically what happens at the mucosa.

Mucosa: columnar epithelium secretes mucus, surface epithelium invaginated with gastric pits, each pit contains ~ 5 glands.

- gastric glands in different areas of the stomach have different types of specialzed epithelial cells.

- Fundus and Body: oxyntic (or parietal) glands have parietal, cheif and endocrine cells

- Antrum and Pyloris: their glands are mostly made up of mucous producing cells but G cells and parietal cells play a role as well.

Submucosa, Muscularis propria and Serosa

Define and discuss the role of the following in promoting gastric motility:(a.) receptive relaxation, (b.) antral contraction, (c.) vagal innervation, and (d.) food.

RR: relaxation of the sphinters and muscles of the stomach. PSNS innervation controls relaxation of the pylorus.

AC: the antrum is the first part of the pyloris. so here it will mix food and propel it to the duodenum

VI: PSNS control! vagal fibres form Auerbach's plexus and Meissner's plexus and thus can sense when the stomach is distended (so then it causes contractions!

Food: when food gets in the mouth there is relaxation of both upper and lower sphinters i think. Food in the stomach causes mechanical distension of the stomach and esophagus, causing intrinsic nerves and the vagal nerve to cause peristalsis.

How does acid get released into the stomach?

Gastric glands: ~80% of glands, in oxyntic mucosa within the corpus of the stomach secretes gastric juice in response to food and peristalsis.

Gastric juice: HCl, Pepsin, IF, mucus, bicarbonate, water, minerals.

Pyloric glands: ~ 15% of glands, secretes mucus and gastrin

- H+ ions are formed in parietal cell from dissociation of water, then the hydroxyl ions combine with CO2 to become bicarb ion (this is mediated by carbonic anhydrase), bicarb ion is then exchanged for Cl-, then H+ and Cl- are secreted separately from parietal cells and get together in the lumen. H+ by a H+/K+ ATPase antiporter and Cl- by a K+/Cl- symporter (both out).

- Note how K+ is recycled here. The Na+/K+ can help drive this by making the K+ gradient that the Cl- will use to get out of the cell.

How is acid neutralized once it's in the duodenum?

- gastric acid (HCl) is neutralized by sodium bicarbonate which is secreted by the pancreas in response to secretin. 

- comes from "S cells"

- HCl + NaHCO3 to NaCl + H2CO3

- the H2CO3 gets turned into CO2 and H20 by carbonic anhydrase.

In what ways does our body stimulate the stomach to secrete acid?

Neural: post-gang vagus neurons terminate in the myenteric and submucosal plexus near the parietal cells and release Ach which directly diffuses toward parietal cells and binds to M3 receptors causing influx of Ca2+ causing the end result, acid secretion.

Paracrine: via release of histamine from Enterochromaffin-like (ECL) cells and also via release of somatostatin from D-cells. The 2 pathways are antagonistic! Histamine (via ECL) is pro-acid, and somatostatin (via D-cells) downregulates acid.

Hormonal: Cholecystokinin (CKK), peptide YY, enterogastrone, secretin and GASTRIN (the major one). Histamine from ECL cells is the #1 stimulator of gastrin stimulation. Gastrin is regulated by negative fbk (gastric acidity)

Pepsinogen

- precursor to pepsin

- made by cheif cells in gastric glands located in the stomach and duodenum

- 2 major forms, Pepsinogen A and B

- conversion to pepsin at a pH below 5

- secretion stimulated by Ach, CCK and neuropeptide substance P

- secretion inhibited by PGE2 and somatostatin

Intinsic Factor

- glycoprotein produced by parietal cells in the stomach

- PEPSINOGEN = CHEIF CELLS

- IF = PARIETAL CELLS

- needed for absorption of vit B12 in terminal ileum.

- pernicious anemia is an autoimmune disease which acts against intrinsic factor.

Describe the "cephalic phase" of gastric secretion.

- stimuli are sight, smeel, taste or thought of food

- activeate enteric neurons via PSNS preganglionics in the vagus

- release of Ach from vagus which binds to G cells and makes them secrete Gastrin

- Gastrin, Ach and histamine stimulate parietal cells to secrete acid and gastric motility is induced.

Describe the "gastric phase" of gastric secretion.

- food in stomach stimulates acid secretion in 3 ways

1- distension of the somach wall is sensed by stretch R, activating a neural reflex to stimulate Ach secretion

2- peptides and aas in fod stimulate G cells to release gastrin

3- food acts as a buffer, faising the pH and removing the stimulus for somatostatin secretion.

Net results:

- secretory and motor funcitons of the stomach activated

- acid and pepsinogen secreted (pepsinogen from cheif cells!)

- pepsinogen is converted into pepsin

- vigourous grinding and mixing contractions take place.

What is a cheif cell?

- also called peptic cell or gastric zymogenic cell, it releases:

- pepsinogen

- gastric lipase (together with the lingual lipase make up the acidic lipases)

- chymosin (made by infants to curdle the milk they ingest)

- stimulated by the vagus nerve and the acidic environment of the stomach. Gastrin and Secretin can also act as secretagogues.

- it works in conjuction with the parietal cell which releases gastric acid which will convert the cheif cells pepsinogen to pepsin.

Describe the intestinal phase of gastric secretion.

- small intestines first need to neutralize the acid and absorb nutrients

- the small intestine sends inhibitory signals to the stomach to slow down it's secretion and motility.

- main purpose is to activate -ve fbk to reduce acid secretion

2 mechanisms

1- neural: distension of small intestine and chemical and osmotic irritation of mucose is transmitted as gastric-inhibitory impulses, call "enterogastric reflex"

2- hormonal: enterogastrones = hormones that inhibit stomach acid secretion.

- CCK and secretin are released from intestinges during this phase, and they also act as enterogastrones.

*However CCK stimulates digestion of fat and protein! Secretin also does more than one thing, but mostly inhibits gastric acid secretion by parietal cells.

Describe the mucosal layer of the stomach (later you will describe how the mucus protects the stomach)

3 parts: epithelium, lamina propria and muscularis mucosa.

- surface mucus cells are simple columnar epithelium that secrete alkaline mucus in response to friction due to roughage in the diet or due to chemical stimuli like ethanol.

Describe the water layer, mucus, cell adherance and cell restitution, blood flow and prostaglandins, all playing a role in gastric mucosal protection.

Water layer: gel layer formed on epithelium, doesn't let H+ in, can protect against bile salt injury. *Mucus blocks pepsin but not H+! It's this unstirred water layer just under the mucus layer that neutralizes the H= with HCO3-.

Cell adherence and resitution: adherent mucus gell layer which is percolated by HCO3- secretion from underlying epithelial cells. It acts as a physical barrier against luminal pepsin. Restitiution is an epithelial layer process which involves rapid migration of healthy cells from gastric pits or duodenal crypts.

Blood flow: removes acid that gets through the barrier. Specially adapted vascular network which also provides a supply of HCO3- for transcellular transport and/or diffusion into the mucus layer.

Prostaglandins: decrease acid secretion by inhibiting pepsinogen. Simulates mucus/bicarb secretion and increases mucosal blood flow.

How do carbohydrates get digested in the stomach?

-       ptyalin (an alpha amylase) from salivary glands hydrolyzes starch into maltose

-       starch digestion continues in the stomach for up to 1 hour

-       food mixes with stomach secretions

-       salivary enzyme activity is finally blocked by acidic gastric secretions

however, 30-40% of starches will have been hydrolyzed to maltose before ptyalin is inactivated by acidic conditions

How do carbohydrates get digested in the small intestines?

-       digestion by pancreatic alpha amylase

-       within 15-30 minutes after chyme empties from stomach into duodenum, almost all starches will have been digested

-       almost all starches will be converted to maltose and other small glucose polymers before passing beyond the duodenum

-       cells lining villi of small intestine contain four enzymes: 1.) lactase, 2.) sucrase, 3.) maltase, and 4.) alpha-dextrinase

final product of all carbohydrate digestion are monosaccharides

How do proteins get digested in the stomach?

-       pepsin will break down proteins only in acidic environments (pH 2-3)

-       pepsin able to digest protein collagen

- pepsin is only able to break down 10-20% of total protein digested

How do proteins get digested in the small intestine?

-       enterocytes which line villi of small intestines have a brush border which consists of many microvilli

-  the enzyme peptidase is in the membrane of the microvilli and there aretwo types: aminopolypeptidase and dipeptidase. They split the remaining polypeptides into amino acids

How do lipids get diested in teh stomach? In the intestine?

Stomach

- only small amount of TGs are digested in the stomach by lingual lipase.

- < 10% of fat digestion.

Intestine

-       bile helps in emulsification of fat

-       pancreatic lipase and to a lesser extent, enteric lipase, help convert Tgs into monoglycerides and free fatty acids

>90% of fat digestion

What are some of the potential effects of truncal vagotomy on gastric physiology?

-       side effects may include:

-       * chronic diarrhea *

-       * abnormal gastric emptying or delayed gastric emptying *

-       impairs receptive relaxation and gastric accommodation

-       as a result, gastric emptying of fluids is increased

-       duodenogastric reflux

-       weight loss

-       cramps

-       sudden gross gastric distension

-       acute dilation of the stomach

-       increased risk of gallstones

What is a "gastric emptying study"?

- it's a dx procedure and measures the speed with which food emties from stomach to the small intestine.

- pt eats a radioactive meal

- to test pts who may have to slow or too fast (rare) emtypin. Symptoms of slow would be nausea, vomitng and fullness after eating. Fast would be diarrhea, weakness or light-headedness after eating.

Used also to:

- detect GE reflux

- detect aspiration

- evaluate N/V

- evaluate why a child is not gaining weight or having abdominal pain.

What are the basal and maximal acid secretion tests?

Series of tests involving 2 parts:

1- Basal secretion test: collecting residual gastric acid from a fasting pt and basal secretion every 15 minutes for 4 hours

2- Maximal acid test/gastric acid stimulation test: IM admin of a drug stimulating gastric acid, then they collect stmach secretions every 15 minutes for 90 minutes.

They look at: appearance, blood, bile, pH, volume, H+/L, /volume and /hour.

For pts with: obscure gastric pain, loss of app, weight loss, suspected PUD, severe gastritis, and ZE syndrome.

*you would do the second one if the first one showed an abnormalitty.

*both require gastric intubation

*don't do to pts who have esophageal problems, aortic aneurysm, severe gastric bleeding of CHF.

Describe the mucosa and how it's got different types of specialized epithelial cells depending on the site?

Mucosa:

-       contains most secretory cells, columnar epithelium secretes mucous

-       surface epithelium invaginated with gastric pits. Each pit contains ~ 5 glands

-       gastric glands in different areas of stomach have different types of specialized epithelial cells

Fundus and Body:

      Oxyntic (or parietal) glands – parietal, chief, endocrine cells

Antrum and Pyloris:

Glands mostly made up of mucous producing cells but others play important role (e.g. G cells, parietal cells)

What's the normal pH of the stomach?

Describe what they release and what they have receptors for:

ECL cells

G cells

D cells

Enterochromaffin Like (ECL) Cells:

            Release histamine

            Receptors for gastrin, acetylcholine, somatostatin, cholecystokinin (CCK) and secretin.

G Cells:

Release gastrin

Receptors for CCK_B , gastrin releasing peptide, acetylcholine 

D Cells:

            Release somatostatin (inhibit ECL cells)

Receptors for CCK_A

What does acetylcholine do? Histamine (H2)?

Acetylcholine – cholinergic innervation via vagus

                        Stimulate parietal cells directly

                        Stimulate gastrin release (G cells)

                        Increases parietal cell sensitivity to gastrin and ECL cell to histamine

                        Inhibit somatostatin (D cells)

                        In Parietal Cells: Increase calcium entry into cells

                                                Increased calcium in cytoplasm

                                                Inositol triphosphate involved (G protein linked)

Histamine –   most important source of gastric acid

(H2)                Primarily derived from ECL cells (gastrin and vagus inputs)

                        Major stimulant for both parietal and chief cells

In Parietal Cells: Receptor stimulation stimulates G protein coupled receptor, Leads to increased cAMP

                                                cAMP stimulates protein kinases

What does gastrin do? Somatostatin?

Gastrin –        Released from G cells

                        Stimulate ECL cell to release histamine* and stimulate partial cell directly

                        Excess stimulation leads to hypertrophy of both ECL and parietal cells

Somatostatin -           Released from D Cells

                        Inhibit ECL cells from releasing histamine and G Cells from releasing gastrin

                        In Parietal Cells: Opposite effect of histamine (inhibit G protein generation) 

What do gastric prostaglandins do? CCK?

Prostagladins –Secreted by almost all cells in the stomach

Main ones in stomach are PG E₂, I₂ and F_2a

                        In Parietal Cells: Opposite effect of histamine (inhibit G protein generation)

Cholecystokinin -     Secreted by endocrine cells

Different forms act on ECL, G (CCK_B ) and D (CCK_A) cells

How do antacids work?

Antacids :

(salts of Aluminum, Calcium, Magnesium, Sodium Bicarbonate)

Mechanism of Action:

Neutralize acid in stomach. Usually increases pH into 2 – 3 range

Liquid formulations (suspensions) largest particle surface area

Pharmacokinetics:

Bioavailability varies amongst agents with bicarbonate being the highest

            Duration of acid neutralization variable but only a few hours at most

given before meals and at bedtime

Efficacy:

            Based on acid neutralizing capacity of the salt and formulation used

            Calcium carbonate the most potent on a molar basis (Al the least)

Equivalence Amongst Agents: All the same at appropriate dosage

Mostly for symptom relief of mild dyspepsia or breakthrough symptoms on other agents

Side Effects:

Constipation (aluminum and calcium salt) , diarrhea (magnesium salts)

Drug interactions – can bind drugs in GI tract e.g. iron, quinolones, antifungals

Excess use can lead to hypophosphatemia

Calcium based agents can (rarely) cause milk alkali syndrome

Magnesium and sometimes aluminum salts contraindicated in renal failure

Sodium bicarbonate can provide significant sodium load (e.g. CHF, ascites) and gas

How do H2 (Histamine) receptor blockers work?

Histame 2 (H2) Receptor Blockers:

(Cimetidine, Famotidine, Nizatidine, Ranitidine)

Mechanism of Action:

Reversible competitive H₂ receptor blockers on parietal cells

Pharmacokinetices:

            Bioavailability of most agents 50 %

            Half life: 1 – 3 hours. All can given od or bid

            Extensively cleared by the kidneys – adjust dose in renal dysfunction

Efficacy:

            Decrease acid production by 50-75%. PUD healing rate 80- 90%

            Equivalence Amongst Agents: All the same at appropriate dosage

Side Effects:

Many drug interactions with cimetidine alone, other agents rare

Occasional S.E. include increased LFTs, diarrhea, headache

Tolerance a concern (esp IV formulations)

How do PPIs work?

Proton Pump Inhibitors

(esomeprazole, lansoprazole, omeprazole, pantoprazole, rabeprazole)

Mechanism of Action:

Block H+ release from parietal cell

Prodrugs that concentrate 1000 X in the secretory canaliculi of the parietal cell (pH 1)

Once in canaliculi are protonated to their active form which binds irreversibly (?) to proton pump (H⁺/K⁺ ATPase)

Evidence to suggest that covalent binding of most PPIs to the ATPase may be overcome by intracellular reducing agents such as glutathione

Pharmacokinetics:

All broken down by stomach acid so formulated in enteric coated preparations

Bioavailability:  60 - 90 %

            Half life: 1 hour but effects last up to 3 days (50 % at 24 hrs). Given od or bid

            Extensively cleared by the liver (genetic polymorphism CYP2C19)

Efficacy:

The gold standard for acid supression. Heals ulcers quicker than H2 blockers.

Best suited for refractory PUD, Zollinger Ellison syndrome and mod – severe GERD

Equivalence Amongst Agents: likely all the same at appropriate dosage

Side Effects:

Low frequency of SE but expensive.

Drug interactions: rarely of any clinical significance

See a compensatory increase in gastrin. Leads to hyperplasia of ECL and parietal cells.

Increased gastrin levels associated with cancers in rats but not humans.

May see rebound acid hypersecretion a few (e.g. 3) weeks after stopping therapy abruptly but there is large interpatient variability

How does Misoprostil work?

Mechanism of Action:

PG E1 analog. Decrease cAMP generation arising from histamine stimulus

Antisecretion < H2 blockers + mucosal protection via increase mucous and bicarbonate

May increase blood flow.

Inhibition of acid secretion more important than improving defense

Prodrug – free acid is the active form

Pharmacokinetics:

            Bioavailablilty: 90 %

            Half Life: active metabolite 30 min. Inhibits acid production for at least 3 hrs

            Renally cleared

Efficacy:

Only role is in prevention of NSAID induced ulcers

Better than H2 blockers at preventing gastric ulcers from NSAIDs (equal to PPIs)

Arthrotec has only 400 mcg/day. Require 600 mcg/day for adequate gut protection.

Side Effects:

Diarrhea frequent - 20-40 % pts on 800 mcg/day. Dose related.

Abdominal pain (10 %), nausea, bloating

Contraindicated for use in pregnancy (abortifacient)

Describe prokinetic agents

Prokinetic Agents (Domperidone, Metoclopramide)

Dopamine antagonists and serotonin agonists generally increase motility via cholinergic mechanisms

Mechanism of Action:

dopamine receptor antagonists but appears main effect on upper GI tract with metoclopramide alone is via 5HT4 stimulation

Domperidone peripheral D2 blocker – poor CNS penetration

Both decrease gastric emptying time, increase lower esophageal sphincter pressure

Pharmacokinetics:

            Bioavailablilty:  80 %

            Half Life: ~ 6  hours, both given before meals and at bedtime

            Mostly metabolized in liver

Efficacy:

Similar to H2 blockers in GERD and non ulcer dyspepsia. No role in PUD

Metoclopramide: more side effects than H2 blockers

Domperidone: use to be more expensive than H2 blockers – generic brand now cheaper

Side Effects:

Diarrhea, headache

Dose related CNS effects with metoclopramide: drowsiness, anxiety, dystonic reactions, Parkinsonian effects.

Galactorrhea can occasionally occur with both

Cisapride works thru 5HT4 stimulation (better than metoclopramide) but was removed from the market due to fatal arrhythmias 

Erythromycin, a motilin agonist, is occasionally used for diabetic gastroparesis

In what layer are the glands in the GI tract?

- some are in mucosa and some in submucosa.

- mucosa is where you will also find the MALT

If you were cutting a GI tube right through, what layers would you hit in order?

- mesentery

- Serosa epithelium

- serosa connective tissue

- Muscularis externa longitudinal muscle

(myenteric nerve plexus)

- Muscularis externa circular layer

(submucosal nerve plexus)

- Submucosa

- Mucosa muscularis layer

- Mucosa lamina propria (where the glands would be, looks like CT area)

- Mucosa epithelium

- lumen!

What are the basic mucosal forms in the GI tract?

Protective form: in the oral cavity, pharynx, esophagus and anal canal

- stratified non-keratinized squamous epithelium

Secretory form: only in stomach!

- columnar epithelium. Mucosa consists of closely packed tubular glands (simple or branched)

Absorptive form: entire small intestine

- columnar epithelium, mucosa arranged into villi

Absorptive/Protective form: entire large intesting

- columnar epithelium. mucosa arranged into closely packed straight tubular glands.

What does the Lamina Propria offer to the mucosa? What about the muscularis mucosa?

Lamina Propria

- structural support (CT!)

- contains blood vessels ad glands

- lymphatic

- immune/defense cells

- nerve fibres

Muscularis mucosa

- thin muscle layer

- provides local movement (gland secretion) and folding of the mucosa.

What do you have to say about the submucosa of the GIT?

What do you have to say about the muscular proper layer of the GIT?

- inner layer is circular, outer longitudinal

- contains nerve plexus-myenteric (AURBACH)- ANS

- synchronized contractions of peristalsis!

*Hischsprung/aganglionic megacolon is a congenital absence of innervation causin abnormal dilation of the colon and paralysis of peristalsis.

Describe the serosal layer of the GIT

- it's an outer layer of CT, contains major nerves and cessels

- if the gut is in the peritoneal cavity, it's called serosa, and is covered by mesothelium

- elsewhere is called adventitia and merges with retroperioteneal tissues.

Describe the 4 layers of esophageal tissue

Mucosa: stratified squamous

Submucosa: esophageal glands (mucus) in upper third

Muscular proper: upper esophagous is striated, middle is a mix, and lower is smooth muscle

Adventitia: cause remember it's outside of the peritoneum.

Describe GERD (this is from the histology lecture, so very basic info)

- it's from decreased sphincter tone or hiatal hernia

- repeated GERD leads to esophagitis, inflammation, pain and eventually a change from squamous to glandular epithelium (Barret's syndrome)

- ulceration

- 5-10% proceed to carcinoma

- esophageal stricture.

What are the very broad strokes causes of dysphagia?

- Obstruction

- Motility disorders: Achalasia, Diffuse esophageal spasm, scleroderma

Describe the 4 layers of the stomach wall (I may have said stomach before but that was actually the description of the typical GIT, not specifically the stomach)

- Mucosa: simple columnar epithelium with Rugae (longitudinal folds) when empty

- Submucosa: dense CT

- Muscular proper (3 layers!): oblique, circular, longitudinal

- Serosa: simple squamous

What is the basic structure of a gastric gland?

- starts with the gastric pit, then as it gets deeper these are the types of cells more often found:

- G-cells

- mucous neck cells

- parietal cells

- chief cells (they look like they stain darker than parietal cells and are maybe a bit bigger)

*That can vary depending on where in the stomach you are though, in the pyloric place there's no cheif cells, in the cardia there's mostly jsut mucus cells. Fundic mucosa's got it all.