made in liver

emulsifies fats (cuts through grease)

glycogen and protien is made

destroys RBC's

detoxifies body

clotting factors are made there

amylase (starches)

lipase (fats)

tripsinogen-->tripsin (protien digestion)

insulin and glucagon

somatostatin(?)

alter closure strength of LES or inc. intraabdominal pressure, inc. gastric acidity, obesity, pregnancy, cigarettes, fatty foods, ETOH, caffiene, chocolate, sitting, supine or side lying, NGT, hiatal hernia,

Meds may dec. LES Fx: theophylline, morphine, birth control pills

lose weight

eat small freq. meals

avoid eating before bed

avoid tobacco

avoid irritating food/drink

elevate HOB

antacid medications

surgery: nissen fundoplication

barret esophagus: Histological changes (squamous to columnar)

vomiting blood

esophageal cancer

disorder of the GI tract caused by action of acid and pepsin

usually in stomach or duodenum (gastric or duodenal)

gastric problems tends to cause duodenal ulcers and vise versa (?)

gastric ulcers-->breakdown of gastric mucosal and epithelial barrier

duodenal ulcers-->excess secretion of acid

helicobacter pylori infection

Also: stress(glucocorticoids inc. acidity in stomach), smoking, heredity, ETOH, NSAIDS, bile acids

may be asymptomatic

epigastric pain (eating makes it feel better, acid has something to work on)

hematemesis(bright red), coffee ground emesis(digested blood, often gastric ulcers)

melena (bleeding digests down into SI, stool black and tarry, often duodenal)

hematochezia (bright red blood through rectum (hemorrhoids))

hemoptysis

endoscopy, barium swallow, biopsy

H/H dec.

reduce gastric acidity

eradicate H. Pylori and prevent reccurence

meds to block acid secretion

antibiotics to Tx H. Pylori

avoid smoking, ASA, NSAIDS, stress, ETOH, Caffeine

no specific diet, avoid foods that inc. acidity (dairy may not be good, avoid high protien diet)

Surgery: vagotomy (vagus nerve) and pyloroplasty

hemorrhagic shock

acid spill into peritoneal cavity(peritonitis)-->can cause septic shock

acid spill into back of stomach-->pancreatitis

probably autoimmune, possibly genetic and environmental

(smoking dec. risk)

bloody diarrhea (most common)

abd. pain before defication

hematopenia(?)

inflammatory disease that extends through all layers of intestinal wall

proximal colon, terminal ileum

probably genetic

smoking inc. risk

bloody diarrhea(most common)

sharp colic pain(sharp, deep, intestinal pain)

malabsorption problems

steatorrhea

exacerbation and remission

slowly progressive

perforation

peritonitis

obstruction

hemorrhage

GI cancer risk lower that colitis

1. dec. diarrhea: (no antidiarrhea meds, need to get rid of blood), rest bowel, TPN

2. inc. nutrition: high protien, high calorie (if tolerated), low residue liquid supplement that can be absorbed in small intestine, vitamin/mineral supplements

3. reduce inflammation: pharmacologic, esp corticosteroids (for crohn, metronidazole)

intralumen pressure inc.-->dec. venous drainage-->thrombosis-->edema-->bacterial invasion-->necrosis-->gangrene-->perforates

rarely self resolves or stutters, inflammation usually become steadily worse

necrosis

abscess

burst appendix

peritonitis

waves of periumbilical pain (may start out as feeling need to pass BM but becomes acute

nausea

pain migrates to mcBurney's point

pain becomes steady

rebound tenderness (pain on release), guarding

physical examination by surgeon

sometimes CT

sometimes ultrasound for child or pregnant woman

appendectomy (laparoscopic or classic)

pain meds will be withheld until diagnosis (pain is main symptom)

no laxative (inc. motility)

herniation in of mucosa and submucosa into the colon wall (pouch)

low fiber diet (fiber is shock absorber for bowel)

diverticula show up where BV's are in wall

very common in westernized countries

dull left quadrant or mid abd. pain

anorexia

flatus

constipation and/or diarrhea

fever

lower abdominal pain

mucus or trace blood in stool

physical examination

exploratory laparotomy

no colonoscopy (could perforate)

rest bowel

 NPO

NGT to sxn(dec. peristalsis)

IV fluids and antibiotics

surgery: ligation of diverticula or bowel resection

loss of propulsive ability

surgery(abd. shutdown by SNS)

mech: impaction, diverticula, adhesions, twisted intesting, tumor, inflammation, edema, intusseption(rolling socks together)

Funct: abd surgery, peritonitis, hypokalemia, spinal fracture, narcotics

small bowel secretes fluid and electrolyes; or obstruction-->fluid and gas accumulate-->impeded venous return-->bowel wall edema-->inc. bowel wall pressure-->from there

1. bacterial escape into blood;strangulation necrosis(causes bacteria to escape into blood)-->sepsis-->shock

2. fluid escape into peritoneum; perforation (causes fluid to escape into peritoneum also)-->peritonitis-->sepsis-->shock

depends upon site

reverse peristalsis(first undigested food, 2nd bile, 3rd vomit feces)

dehydration

pain

constipation

gas distention(raises diaphragm, inhibits respiration)

F&E imbalance: Na, Cl, K and HCO3 dec., extracellular loss (even further dehydration)

Abd X-ray, barium studies, CBC

H/H inc. (dehydration?)

BUN inc.

decompress bowel

mech: insertion of intestinal tube

surgery: excision, resection, ostomy

funct: rest bowel, prevent distention with gastric suction

meds may or may not be effective in stimulating bowel

cholelithiasis

age

female

native american

obese

rapid wt loss from obesity

pregnancy

(fat, female, and 40)

not well understood

cystic duct clogs-->bile stasis occurs in gall bladder-->inflammation escalates-->empyema may develop in gall bladder-->gangrene or necrosis may occur-->gall bladder may rupture

H&P

abd. ultrasound

sometimes CT or ERCP(endoscopic retrograde cholangialpancreatography?)

WBC

laparoscopic cholecystectomy (puncture and suck gall bladder out)

open cholecystectomy

chemodissolution (oral bile salts, not common)

lithotripsy

antibiotics

ETOH abuse (causes pancrease to secrete thick protein rich juice that dries up and blocks duct)

gallstone obstruction

infections, toxins

heredity

structure abnormality

ischemia

pregnancy and others

secreted by pancreatic acinar cells

inactive form of tripsin

1. pancreatic duct obstruction-->digestive enzymes seep into parenchyma of pancreas-->pancreas autodigests-->edema-->necrosis-->hemorrhage

2. acinar cells injured-->intracellular trypsinogen activated early-->pancreas autodigests-->edema-->necrosis-->hemorrhage

steady, boring pain that gradually intensifies

pain reaches max level several hours from start

pain starts in epigastric or LUQ and often penetrates to the back

N/V

Exquisite(unbearable) tenderness

fever

ascites(goes to mediastinum and pleura)

severe anxiety

secondary bacterial infection

possible hyperglycemia

hemorrhage

sepsis

respiratory distress

renal failure

shock

inc. serum lipase

inc. serum amylase

inc. WBC

inc. ALT, AST, ALP

inc. BUN

dec. Hct (pulling fluid into blood to compensate for shock)

dec. Ca (saponification)

albumin (inc. or dec.)

Xray(left base atelectasis, elevated diphragm, pseudocyst, enlarged pancreas, bowel changes)

CT, US

conservative management: NPO(dec. pancreatic enzymes), NGT to sxn, opioids(demerol hits hard, morphine causes sphincter of Oddi to spasm), TPN, Calcium

Antibiotics, suportive care for above problems

Non conservative: ERCP

jaundice

lethargy

malaise

myalgia

arthralgia

anorexia

N/V

abd pain

diarrhea

constipation

fever

itching from bile salt accumulation

rest

nutrition

route: feces

symptoms: often asymptomatic, malaise, anorexia, nausea, low grade fever, RUQ pain

jaundice: sometimes absent in children, most adult develop, lasts about two weeks

Diagnosis: anti HAV igG (previous infection), anti HAV IgM

route: blood, sex, per enteral(?), perinatal(developing countries)

symptoms: early signs insidious, r/t immune system (rashes, uticaria, joint pain), malaise, anorexia, nausea, low grade fever, RUQ pain

Jaundice: degree and duration same as HAV

route: sex(not very common), IV drug use

symptoms: usually asymptomatic, if symptoms occur, mild

jaundice: usually none

alcoholic (long term ETOH abuse)

post necrotic (HBV and HCV toxins)

biliary cirrhosis (obstruction)

cardiac cirrhosis (right sided heart failure, hepatomegaly) (rare)

portal vein

hepatic artery

bile duct

1. destruction of hepatocytes, scarring, and fibrosis-->dec. liver Fx

2. Hardened liver tissue-->inc. pressure on portal vein(portal HTN)-->retrograde pressure-->enlargement of esophageal, umbilical, and superior rectus veins-->esophageal varices, hemorrhoids, caput medusae -->bleeding,

3. dec. vit K absorption(from large intestine)--> more likely to bleed

4. portal HTN-->splenomegaly--dec. platelets, WBC(infection), RBC(weak)

5. portal HTN and dec. protien synthesis-->ascites in abdomen

6. dec. ammonia metabolism-->inc. ammonia levels-->hepatic encephalopathy

ascites

hematemesis(often fatal)

bleeding tendency overall

prominent abd wall veins (caput medusae)

internal hemorrhoids

confusion

irritability

infection

asterixis (liver flap, holding hands up)

inc. AST, ALT, LDH

dec. albumin

inc. PT

liver biopsy

nutritious diet with adequate calories and protein(protein is limited for hepatic encephalopathy, will break down to ammonia)

vitamin supplement

adquate rest

eliminate exposure to hepatotoxins

remove biliary obstructions

prevent infections

liver transplant

paracentesis (limited over time because of F&E imbalance)

albumin

low sodium/mod. protein/fluid restricted diet

O2 and HOB raised to reduce respiratory compromise (laid flat they can drown)

gentle skin hygiene

ligation

sclerotherapy

cautery

balloon tamponade

IV vasopressin(more often octreotide)

senstaken-blakemore(?)

restrict protein

antibiotics/amoxycillin to reduce intestinal bacteria (they produce ammonia?)

Lactulose (promotes freq. bowel mov'ts, ammonia is formed in bowels)