• Mucus cells will secret mucus to protect from stress and acid
• Parietal cells secrete an intrinsic factor which is important for absorbing B vitamins
• Chief cells will secrete pepsinogen which is important for the formation of pepsin in the presence of acids (this is important in ulcers)
• G cells will produce gastrin and will stimulate production of HCl (excess gastrin will have gastric syndrome and will have many ulcers)

3 functions of gastric acid

1. —to kill micro-organisms
2. —to activate pepsinogen (converts it to pepsin)
3. breaks down connective tissue in food

1. heartburn
2. burping
3. belching
4. bitter taste
5. regurgitation
6. water brash
7. chronic cough

1. Gastric function abnormalaties
2. Transient LES relaxation
3. Dysfunction of antireflux barrier
4. abnormal esophageal transit clearance
5. pressure gradient across LES
6. increase in intra abdominal pressure

1. defects in defense mechanism
2. loss of LES pressure (inappropriate relax or increase in gastric pressure)
3. aggresive factors, acid/pepsin

Risk factors for GERD

1. factors that lower LES pressure-Diet, Alcohol, Smoking, Drugs.
2. factors that increase inta abdominal pressure- obesity, Prego, Bending over

1. H. Pylori
2. NSAIDs
3. Gastric Acid and pepsin
4. smoking

1. Bicarbonate
2. Mucus
3. Prostaglandin
4. Growth Factor
5. Mucosal regeneration

Increases acid and pepsin secretion

decreases Bicarbonate secretion

1. H pylor
2. increase in parietal cells
3. high gastrin secretion after meals
4. failure in feedback mechs (acid doesn't inhibit gastrin release)
5. rapid gastrin emptying overwhelms buffering capacity of bicarbonate rich pancreatic secretions
6. NSAID use
7. Smoking leading to more acid production
8. decreased bicarbonate secretion 

1. inhibits COX-1 (responsible for good prostaglandins in gut)
2. disrupts mucosal integrety
3. decreases mucosal blood flow (cell death)
4. decreases cell regeneration
5. direct GI irritation
6. antiplatelet effect
7. ion trapping
8. increased acid secretion

• epigastric pain that is

1. not well localized
2. annoying burning gnawing aching
3. pain when they eat

• patients pain

1. on an empty stomach
2. during the night
3. between meals
4. relieved by food and antacids
5. episodic followed with symptomatic periods then no occurance

Hematemesis

perforation 

diarrhea

obstruction

nausea

vomiting

weight loss

weakness

Melena

decreased Hct, Hgb

increased BUN/ Cr ratio

erosive esophagitis

esophageal strictures

barrett's esophagus

esophageal cancer

laryngeal cancer

past medical history

rule out other causes

trial of acid suppressing therapy

endoscopy

24 hr esophageal pH monitoring

• lifestyle modifications
• Antireflux surgery (typically if drugs dont work and after 5 yrs it may come back)
• endoscopic therapies

1. weight loss
2. avoid tight fitting clothes
3. avoid spicy, acidic, high fat food, chocolate, caffeine, peppermint, and large meals
4. smoking cessation
5. reduce alcohol intake
6. don't lie down after you eat for 3 hrs
7. avoid drug induced causes
8. elevate head of bed 6-8 inches

1. Antacids PRN (Al/Mg, Calcium, Na bicarb)
2. LOW dose H2 receptor antagonist prn (ranitidine, famotidine)
3. alginic acid (gaviscon)

1. full dose H2 antagonist
2. Proton pump inhibitor (severe GERD)
3. metoclopramide, bethanechol, sucralfate

Ca>Mg>Al

with the liquids being better then solids

1. How long does it take for an antacid to work
2. how long will it work for on an empty stomach/full stomach
3. when should you not give an antacid for GERD

1. 5 min
2. 20-30min/60-90 min
3. when its nocturnal GERD

1. dont heal mucosal
2. Al, and Mg accumulate in renal dysfunction
3. Mg causes diarrhea and Al, Ca cause constipation

1. cimetadine (most drug interactions)
2. ranitidine
3. Nizatidine
4. Famotidine

1. effective in healing erosive disease in mold GERD
2. more effective then antacids in reasing intragastric pH
3. lasts 6-12 hrs

1. effective only in mild GERD
2. tolerance (50% loss of efficacy, not overcome by increased dose)
3. side effects
4. elderly can develop confusion if they have renal impairment

• most effective acid suppression therapy
• prevents Nsaid induced ulcers
• well tolerated
• helps the healing

half life 1 hr

action 24h

they increase LES pressure and gastric emptying 

last line of therapy due to side effects

drug interaction of antacids

drug interaction of PPI

• antacids block absorption of antibiotics
• PPI blocks ketoconazole or anything that requires an acidic environment for absorption

• invasive are- rapid urease test, biopsy with histology, (culture and polymerase chain reaction used in reasearch)
• noninvasive- elisa, urea breath test, fecal antigen test

Gastric ulcer treat with PPI for 6-8 weeks

duodenal treat with PPI for 4 weeks

1. Triple therapy- PPI twice a day, clarithromycin 500mg bid, amoxicillin 1000mg bid (or metronidazole 500mg bid) up to 14 days
2. quadruple therapy- PPI bid, bismuth subsalicylate 575mg qid, metronidazole 250mg qid, tetracycline 375mf qid up to 14 days

1. Salvage therapy is PPI bid, levofloxacin 500mg qd, amoxicillin 1000mg bid, for up to 12 days
2. sequential therapy- PPI bid, amoxicillin 1000mg bid for 5 days then PPI bid, clarithromycin 500mg bid, tindazole 500mg bid

1. PPI 30 min before a meal
2. bismuth can blacken the tongue and stool
3. metronidazole elevates INR
4. report recurrent bleeding
5. avoid NSAIDs

1. stress ulcer occurs at pH< 3.5
2. prevent complications
3. be cost effective
4. continuous infusions better for intermittant dose
5. avoid antacids in neonates

sucralfate

PPI

H2 blocker

1. PPI works how to reduce acid secretion
2. how much does it inhibit acid secretion by
3. why give PPi 30 min before a meal

1. PPi's block the final common pathway (proton pump)
2. PPi's inhibit 90% of acid secretion
3. They are entericly coated so that they only dissolve in alkaline ph of intestine then are abosrbed and will rapidly diffuse to parietal cell canaliculus where it will have it’s action

they all bind to cysteine 813

pantoprazole in addition will bind to cysteine 822

1. at pH <4 will split off into anions and bind to cations in ulcers
2. stimulate prostaglandins
3. complexes with mucous thus decreasing mucus degradation by pepsin
4. This can't be used with antacids

1. 15 cc of stool enter rectum and activate strecth receptors
2. involuntary decrease of smooth muscle in the internal sphincter passing it to the outer sphincter
3. child relaxes outer sphincter squats and increases pressure from the abdomin
4. MAGIC

If they continually refuse to poop then the water will come out and it will stretch the rectum and lead to impactation

what is encopresis

what causes this

1. fecal soiling as a result of leaking stool from distended rectum
2. fecal retention, damage to corticospinal tract, from anxiety or passive aggresive behavior (attention)

1. drugs- barium, bismuth, Fe, opiates, Ca/Al
2. excessive milk/lack of fiber
3. lead ingestion
4. hirschsprung disease
5. hypothyroid
6. infant botulism
7. intestinal obstruction or strictures

produce 1-2 soft stools a day

find the cause and treat

1. change in diet increase fiber, and water
2. rectal stimulation in small children
3. try to avoid using laxatives and use them sparingly

glycerin suppository

miralax

1. unhurried potty time 5-10 min after meal
2. keep a log and use reward system
3. diet and water reccomendations
4. med info if needed

1. <3 years old
2. dehydration/weight loss
3. fever
4. sever tummy pain
5. blood in stools
6. >48 hrs in duration
7. lethargic
8. no urine output for 6-9 hrs infant, 12 hrs child

1. oral rehydration therapy 4-8 oz per watery stool
2. keep eating a regular diet avoiding high fat and sugar food
3. loperamide if over 6 and has no GI bug
4. bismuth if over 6 and has no bug esp virus due to reyes

1. keep eating
2. don't use OTC anti diarrhea meds unless cleared
3. wash hands, toys, and clothes
4. when to call dr

what are the two major disorders in IBD

Ulcerative Colitis

Crohns disease

what are the two classifications of ulcerative colits

1. Distal- proctitis (inflammation of the rectum), proctosigmoiditis (inflammation of the rectum and colon
2. extensive-left sided colitis extends to the sphlenic flexor, extensive goes to the hepatic flexor, pancolitis is the entire colon

how does uc manifest

1. relapsing episodes of bloody mucoid diarrhea
2. fever tachycardia
3. toxic megacolon, perirectal abscess

describe crohns disease

can occur anywhere in the GI tract

coblestone in appearance

transmural (inflammation goes through all the layers of the GI tract and in the submucosa

fistulas

1. IBS-C this is hard lumpy stools >25% of time with mushy watery stool <25%
2. IBS-D this is loose mushy stools >25% of the time with hard lumpy stools<25%
3. IBS-M this is when you have both types >25% of the time
4. IBS-U is when you can't figure it out

1. women with IBS have a much lower quality of life then men
2. women are 2 times more likely to be diagnosed
3. men describe difficulties with finance and work

1. GI motility issues
2. visceral hyperglesia (sensation of food hurts, feel pain instead of full)
3. psychopathology (linked to abuse

1. anemia
2. fever
3. weight loss >10lbs
4. extreme diarrhea or constipation
5. recent antibiotic use
6. rectal bleeds
7. symptoms onset after 50
8. nocturnal symptoms

antispasmodics

bulking agents

antidarrheals

stool softener

antidepressants

Cl channel activator

probiotics

seratonin agonist

antispasmodics- dicyclomine, hyoscyamine, peppermint oil

antidepressant- tricyclic, SSRI

1. mild- < 5 (usually 2-4) semi-formed stools/day with little blood/mucus
2. moderate- More severe diarrhea (4-6 BM’s/day with more bleeding than mild disease
3. severe-Frequent liquid stool (>6-10) with blood and pus

1. mild to moderate- able to tolerate po foods/med
2. moderate to sever- failed to respond to treatment
3. sever/ fulminant- persistant symptoms in spite of steroids
4. remission- asymptomatic or without inflammatory sequelae
5. steroid dependent or chronic active chrohns- needs chronic steroids to stay symptom free

1. sulfasalazine for flairs(active ingredient mesalamine)
2. aminosalicylates (mesalamine, balsalazide, olsalazine) these are good to induce remission and maintain it (higher doses to induce remission)
3. Lialda is used to induce remission for UC
4. corticosteroids used for exacerbations (for moderate or above)
5. immunomodulators like 6-MP (used for maintanece and to help reduce corticosteroids)
6. methotrexate to induce remission only in crohns
7. cyclosporine to induce remission
8. we use biologicals as a last line with lots of fistules

what allergies prevent patients from taking the sulfazalazines and mesalamine

sulfa allergies for sulfazalazine

and aspirin for both

1. mild-moderate- if distal topical or oral aminosalicylates, if extensive oral sulfasalazine or aminosalicylate
2. moderate-sever-oral aminosalicylate, oral prednisone or infliximab
3. severe-fulminant- hydrocortisone, then cycosporine for non responders to iv corticosteroids
4. maintanence oral aminosalicylates

NA restriction (under 2G)

avoid EtOH

Tips

paracentesis

Diuretis

• loop- furosemide, torsemide, bumetanide
• aldosterone antagonist/ K-sparing diuretics- spironolactone amiloide

if they have >250PMN/mm3

find this by multuplying polys and WBC together

give antibiotics ceftriaxone, or fluroquinolones

give albumin to avoid hepatorenal toxicity

non-selective beta blockers (propanolol, nadolol, carvedilol)

endoscopic variceal ligation

1. lactulose titrated to 2-3 bms daily
2. rifaximin 550 bid
3. metronidazole
4. neomycin

liver transplant, TIPS, MARS, dialysis

drugs- albumin, octreotide, midodrine

1. AST levels can be altered by cardiac damge or muscle damage
2. ALTlevels altered by only the liver

albumin

prealbumin

INR

PT

alkaline phosphatase

5'nucleotide

gamma glutamyl transpeptidase 

prego

infiltrative diseaseinflammatory disease of bile ducts

drugs

biliary stricture

gallstones

tumors

aids

primary sclerosing cholangitis

EtOH consumption

chronic viral hepatitis

metabolc liver disease

cholesatasis

drugs and herbals

strains A and R

strains B and C

do we always need to treat HEP

in the us it is transmitted sexually or via IV drug use

in asia typically transmitted from mother to child

interferon alpha

pegylated interferon alpha 2 (main therapy)

below are all nucleoside analogs

lamivudine

adefovir

entecavir (main therapy)

telbivudine

tenofovir (main therapy)

ALT (3 months)

CBC

TSH

HBV DNA (3-6 months)

treating naive patient .5 mg qd

experienced patient 1 mg qd

what should be monitored in tenofovir aside from viral and liver function

MALE

older age

ethnicity

immunosuppression

uncontrolled depression

organ transplant

autoimmune hepatitis

untreated thyroid disease

prego

under 2

peginterfeuron alpha

ribavirin

(for 48 weeks, stop if no response after 24 weeks)

liver with centrilobular necrosis

less commonly nephrotoxic

SAFE- •sulfate and glucuronide pathways (glutathione will take the toxic metabolite and convert it to APAP glutothiene)

TOXIC- CYP450 pathway

acute to overdose

developed within a few hours

lasts 24 hrs

nonspecefic signs (N/V, anorexia, pallor, sweets, malaise)

1. occurs at 24-48 hrs after ingestion
2. may have improvement in phase one symptoms
3. elevation in AST, ALT and INR
4. right upper quadrent tenderness
5. decrease in piss

occurs 3-5 days after ingestion

hepatic failure

renal failure

this is when you die

elevated liver enzymes

coagulation effects

encephalopathy

this will occur within 2 weeks of ingestion

this will happen if you survive phase 3

this is when you start to go back to normal liver function

when do you send a child <6 to the ER

takes>10g or 200mg/kg

intentional OD

unknown dose

>10g/ >200mg/kg in 24h

>6 g or >150mg/kg over per 24 hr for two days

>4g or 100mg/kg per day or if susceptable to toxicity

liver disease

EtOH (induces cyp enzymes)

malnutrition (glutothione depletion)

induced cyp 2e1

starvation

1. activated charcoal if brought with in 2 hrs
2. wait 4 hrs to assess patient using rumack mathew line if above the give antidote (N-acetylcysteine

what is the mechinism for N-acetylcysteine

1. EARLY- glutothione precursar and replacement, increases sulfate conjugation
2. LATE- scavanges oxygen free radical, improves microcirculatory blood flow

loading dose 140mg/kg

maintanence dose 70mg/kg q4h for 17 doses (72 h)

loading dose 150mg/kg over 1 hr

1st maintanence 50mg/kg over 4 hrs

second maintence 100mg/kg over 16 hrs

flushing 

urticaria

angioedema

bronchospasms

NA products

CaCO3

short duration

systemic absorption

acid rebound

belching

15% systemically absorbed can lead to hypercalcemia

milk-alkali syndrome (decreased parthyroid lvls)

acid rebound

constipating max 8g a day

acts as an osmotic laxative

5-10% absorbed systemically and can lead to kidney toxicity

slow acting

constipating

phosphat depleting

tastes bad

acetylcholine was only option and only decreased H production 40-50%

many side effects

1- block H binding to parietal cell H2 R after

  release from ECL cells by gastrin

  or vagal stim.

  2- decreases the response of parietal cells

  to direct stim. by gastrin or ACh in

  presence of H2 blk