gastro school part 2

most commonly put in an esophageal stent so that the path remains a little open so that its not uncomfortable for the patient and they can still eat and drink

to determine prognosis and treatment-- they have an adventitia and not a serous layer so its very easy for them to metastasize--- tumors limited to the mucosa can be endoscopically resected

Tylosis- a condition that is associated with hyperkeratosis of the palms and soles of the feet and also increased chances of developing esophageal SCC

• rhomboid protease usually regulates how much EGF is released--but when mutation it is hyperactive and releases a lot of EGF 

SCC: used to be predominant but adenocarcinoma has come more prevalent

Adenocarcinoma: is more associated with: GERD, barretts, and obesity  (more in the distal areas of the esophagus) 

SCC is more associated alcohol (more in the proximal areas of the esophagus)

both are associated with tobacco

SCC is of the epithelial cells and adenocarcinoma is of the glands

squamous cell type

developing squamous cell cancers in other areas-- so those with oral cancers are more likely to develop esophageal cancers and vice versa (secondary location can be elsewhere too like the lungs)

oral cancer

• retromolar areas
• tongue floor (underneath the tongue)

k-ras gain of function---increased proliferation and differentiation

• tobacco 
• age
• alcohol 
• HPV-oral cancers induced by HPV have a better response to tx 

diet--vegetables and fruits

H pylori and tobacco

higher education, obesity, and tobacco

as volume goes up emptying increases and as nutrient density goes up emptying goes down

there are slow waves--NOT AP SO THE FREQUENCY OF SLOW WAVES IS NOT CHANGED BY NEURAL/HORMONAL INPUT-- at which the GI tract is resting at-- from this point you can have hyperpolarization which is stimulated by NE and other sympathetics (prevents contraction) OR you can have depolarization by stretch, ach which cause motility

• -parasympathetic preganglia synapses at the plexuses  
• -sympathetic preganglia synapses at the pre-vertebral region and postganglia synapse at the plexus

the muscle layer below the mucosal cell layer is involved in absorption and secretion--submucosal plexus 

the muscles of the inner (C) and outer layer (longitudinal) are involved in moving the food along the tract--myenteric plexus

gas

I am not giving you this because you are depressed but there is something going on in your brain that is affecting the pain you are experiencing"

• anticholinergics to slow down motility; antagonize the Ach 
• dicyclomine 
• hyoscyamine 

works the same way as tegaserod--tegaserod was pulled from the market because of it causing heart issues

constipation type has fewer EC cells (less Ach: decreased bowel movements) 

diarrhea: increased number of EC cells

induces motility and secretions

• -frequent stronger contractions 
• -perception of pain happens at lower balloon volumes (heightened perception) 
• -functional mri--give a trigger to someone with IBS--different parts of the brain light up

For all three types Creactive protein and calprotectin 

IBS-diarrhea: stool studies, IgA Ttg antibody (celiac disease)..colonoscopy 

• IBS mixed: stool, XR
• IBS constipation: XR, psychologic testing 

• 
• persistent diarrhea-- in IBS its usually intermittent

• constipation is more common in females 
• diarrhea type equal prevalence 
• and alternating more common in females too

used to characterize bowel movements--lower categories are more associated with constipation and higher categories are more associated with diarrhea

• reccurent abdominal pain atleast once a week for the past 3 months associated with atleast 2 of the following: 
• stool frequency change
• stool form change 
• related to defecation 

no obvious cause

heart burn symptoms that do not improve with proton pump inhibitor, no evidence on testing-- and they are associated with certain psychological states

• -recurrent abd pain 
• -functional dyspepsia (upper abdomen-- early satiety, nausea, bloating) 
• -IBS

gastroparesis

inhibits D2 receptors but also can activate 5HT4 receptors (seratonin effect is to move along the contents of the GI)

avoid things that slow down gastric emptying--avoid bulky foods like fibers-- drinks fluid based diets and eat less but more frequent meals 

there are motility drugs

obtain a CT scan and endoscopy, if negative then order a Gastric emptying test--gold standard for diagnosing this condition, other tests are just to rule out other causes like GOO

surgical procedures can affect the vagus nerve which can affect motility

Diffuse esophageal spasms---can ultimately lead to achalasia

• -NO supplement (nitrates)
• -calcium channel blockers--calcium produces      contraction 
• -Botulin toxin-- prevents Ach release

-neurons that release NO (relaxes the lower esophageal sphincter are damaged)--can be due to chagas disease (T. cruzi), measles etc 

IF YOU SEE SOMEONE PRESENTING WITH ACHALASIA--ALWAYS CONSIDER MALIGNANT CAUSE OF SXS

things tend to get caught above the sternal notch-(symptoms can differ but good rule of thumb) skeletal muscle affected

• stroke
• MS--
• parkinsons 
• Dermatomyositis 
• Polymyositis

Scleroderma can do both-- smooth and skeletal

are both released from the duodenum in response to food and stimulate the release of insulin from pancreas-- gastric inhibitory also goes and inhibits the release of gastrin.

both will stop releasing insulin when blood glucose range is in normal limits

• Gastrin
• CCK
• Secretin
• GIP
• Motilin

similar-- except the sulfate group on the CCK is actually imperative to the function-- the sulfur group on the gastrin is not

hypokalemia 

Mg is known to cause renal and cardiac issues because of the fluid loss 

calcium carbonate: avoid giving with milk because it can cause milk alkali syndrome

• are used to coat the ulcers so that they dont get agitated 
• they also allow HCO3 release so that it can neutralize the acid 

sucralfate requires an acidic environment so avoid use with PPIS

are most effective at preventing nocturnal acid reflux--gastrin and Ach are more involved in meal acidity--but can still use before you dine

5HT4 agonist

NK1 antagonist--use prophylactically together with 5HT3 antagonist and steroids for treating nausea and vomiting.

hyoscine

• – Stimulates motility of small intestine at low doses
• – Inhibits motility and intestinal secretions at high doses
• – Particularly useful to treat chemotherapy-induced diarrhea

This is therapeutic in some patients who have IBD and diarrhea

• 5HT4 agonist 
• 5HT3 antagonist

Activates chloride channel (CLC-2) on apical membrane of intestinal epithelia

Activates CFTR which stimulates chloride secretion into the lumen

• Sorbitol
• and polyethylene glycol 

all within the same category that Mg Al and everything belongs to

Stimulant laxatives work by stimulating enteric nerve endings and blocking fluid re-absorption. These actions promote peristalsis.

Bisacodyl

doesn't cross the BBB and increases Ach--which increases gastric emptying but can also be used to increase esophageal tone and increase the amplitude of the peristaltic wave

used to treat GI symptoms associated with delayed stomach emptying

• – Feeling full, bloating, belching, nausea, heartburn and stomach ache
• – Gastrokinesis- Often associated with diabetes

• antibiotics-- phenytoin, trimethoprim, methotrexate
• because your gut bacteria can make folate as well as vitamin K

Give vitamin B9 9 months of pregnancy and 1 month after to prevent neural tube defects and folate deficiency-- anytime you have any condition that is producing a lot of cells-cancer, pregnancy-- you need folate supplementation

B1-- and this impairs glucose breakdown-- in these patients however THIAMINE should be given before dextrose to prevent worsening symptoms

• make NADH which is important to make 3 ATP 
• -it also inhibits lipolysis in fat tissues so less fatty acids are packaged into VLDL and LDL

• podagra: 
• -facial flushing (caused by prostaglandins--so you can take aspirin beforehand)
• -hyperglycemia 
• -hyperuricemia--can lead to gout 

Hepatic artery flow is faster than the portal vein and so will appear more orange 

the common bile duct has flow but it is too slow for the doppler to pick up

supplies the left lobe and the intermediate lobe

fluid air level in the stomach

the ileum is very linear while the large intestines have bubble curves

the jejuneum is a feathery substance

the ligament of trietz should be seen after the midline (vertebral body will mark the midline--normal anatomy)

XR is good for gas patterns, air, foreign bodies 

CT is good to use anytime you are going in blind and do not really know what to expect

Ultrasound: best for structures that are closer to the skin (biliary and liver)

proliferation that elongates the tube but also closes the entire tube and have to undergo recanalization to open it up 

also have to form a septum (splanchnic mesoderm) to seperate the trachea and the esophagus

• 
• outer layer of the GI organs is derived from the splanchic mesoderm (visceral)

inner layer of the GI wall is derived from the somatic mesoderm(parietal)

everything else when in doubt is splanchic

remove waste products and retrieving nutrients

gut tube (foregut, midgut, and hindgut) is attached to the yolk sac via the vitelline duct--from the midgut region 

hindgut gives the allantois (urachus post-development) which is connected to the umbilical stalk)--

both the vitelline duct and the allantois are endodermal structures 

Not all lesions found in the mouth are cancerous-- lichen planus is an autoimmune disorder associated with precancerous lesions: plaque, ulcerations, erosions, nodules, erythema--but these same findings can also be present in cancer--two different causes for similar set of symptoms