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GI

QuestionAnswer
RUQ pain -cholecystitis, hepatitis, pancreatitis, perforated ulcer,right renal pain
RLQ pain apendicitcitis,abd aortic disection or rupture,ruptured ectopic prego,PID, irinary +calculus, hernia,ovarian or testicular torsion,rt ovarian cyst
LUQ pain -pancreatits, gastritis, left renal pain
LLQ pain diverticulitis, aortic dissection or rupture, ruptured extopic pregnancey,left ovarian cyst,PID,urinary calculus,hernia,ovarioan or testicular tosion
Epigastric pain -gastritis,esophagitis,pancreatitis,cholecystis, aortic aneurysm,myocardial ischemia
Diffuse pain -intestinal obstruction,preforation,peritonitis
Visceral pain -walls of hollow organs due to inflammation,distention, ischemia.*not localized-DULL,CRAMPY,DIFFUSE
Somatic pain Localized-sharp or stabbing/guarding-caused by bacteria, chemicals,
Referred pain originates in a region other than where it is felt
Sudden onset= perforation of organ
Gradual onset blockage of organ
Diaphram high pitch sounds
Cullens sign discoloration over the umbilicus-late sign
Turners sign discoloration over flanks-late sign
Ascites sign of CHF
Upper GI bleeding within the GI tract proximal to the ligament of Treitz-where duodenum and jejunum meet
Orthostatic hypotension 10-20 mmHg drop in systolic and 10-20 increase in pulse
Mallory-Weiss syndrome mucosal tear in the distal esophagus-bleeding is arterial-occurs afterviolent vomiting,forced coughing, trauma
Esophageal Varies Swollen veins of esophagus-35% mortality rate if vessel ruptures,DUE to portal hypertention(primary cause)-Cirrosis,, high pressure causes esophageal veins to dilate
Esophageal S/S painless bleeding,shock,dysphagia(swallowing)burning or tearing,clotting time increases sue to back up in spleen, plts are destroyed,liver is not producing proteins
Esophageal TX IV fluid 20cc/kg,Sengstaken-blkemore tube, sclerotherapy(thrombus forming frug into vein itself
Acute Gastroenteritis Inflammation of the stomach/intesine-causes hemorrhage and erosion of mucosal/sub mucosal layer-sdestruction of villi=H2o and nutrients not absorbed=diarrhea
Acute gastroenteritis causes alcohol,ASA,NSAID, ingestion of chemicals, infections
" S/S N/V,bloody/MUCUS diarrhea, melena,abd cramps,dehydration,Hypokalemia,acidosis or alkalosis
Chronic Gastritis Inflammation of gastric lining-due to infections, passed on by fecal -oral route, infected food or water-S/S same as acute G
Peptic Ulcers breakdown of gastric or duodenal mucosal defence-caused by imbalance between production of acid->males -Caused by Helieobacter pylori,NSAIDs,cigs,alcohol,
Duodenal Ulcer -prox duodenum(small intestines)2-3xs more common that gastric ulcers,25-50yr,genetic-PAIN AT NIGHT/EMPTY STOMACH-blocked pancreatic duct can cause this-relieved by food for 2-3hrs
Gastric Ulcer only in the stomach,>50,PAIN AFTER MEAL/FULL STOMACH,no pain at night,because of acid production
Zollinger ellison syndrom gastrin secreting tumors(signals stomach to produce acids
HCL converts pepsinogen to its active form to breakdown protein
Peptic ulcers S/S rigid boardlike abd,sudden intense steady epigastric pain,RUQ, radiates to back, dimished bowel sounds,hemorrhage :TX:H2blockers-Zantac/pepcid,Antacids, antibiotics
Drugs that block or decrease gastric acid secretion H2 receptor antagonists, Tagamet,Zantac,Pepcid, Axid
Antacids Aluminim, magnesium, calcium,sodium bicarbonate
Lower GI consist of Jejunum,Ileum,large intestine, rectum,anus
most common cause of lower GI bleeding is Diverticulosis
Lower GI bleeding S/S Cramp,N/V,stool changes,bright red blood , distention or ecchymosis
Ulcerative COlitis Idiopathic inflammatory bowel disprder (IBD)-unknown origion, ulcers along mucosal layer of colon.75% involve rectum or rectosimoid portion,inflammation starts at rectum extends proximally-20-40yrs,immune system overreacts to intestinal bacteria
Pancolitis when the entire large intestine is involved
Proctitis when only the rectum is involved
Ulcerative S/S bloody diarrhea,contains mucus,N/V,fever, weightloss,abd cramping,limited to lower quadrants,lyte abn,perforation,ecchymosis,distention
Crohn's Disease (IBD),runs in families,white males,can occur from mouth to rectum,affects Ileum,colon-hypertrophy and fibrosis of muscles undersubmucosal layer-diameter decreases causing fissures.
Increased levels of suppressor T-cells means inflammatory process
Diverticulitis -complication of diverticulosis-small outpuching of tissue that push thru outermost layer of intestine(muscle)-inflammation of diverticula secondary to infection due to obstructed fecal matter
Diverticulitis S/S LLQ pain, most in sigmoid colon, fever, WBC high,melena,comstipation,diarrhea
Divertiluitis pathology 1.stool passes sluggish,colon responds withmuscle spasms,by raising pressure causes herniation through openings in muscles forming diverticula,poop gets trapped,bacteria develops,infection and inflammation
Hemorrhods small masses of swollen veins-occur in anus and rectum
Internal hemorrhoids involve inferior hemorrhoidal plexus, bleeds during defication
Bowel obstruction partial or complete-due to hernias,intussusception (overlaps) and volvulus (twisting on itself) Adhesions-most common area is the small intestines
Adhesions union or normally seperated tissue by fibrous band of new tissue-develops due to abd surgery and inflammation-develop die to abd sx and inflammation
Bowel obstr S/S fever,DIFFUSE VISCERAL pain,peritonitis, shock, ecchymosis, decreased bowel sounds
Appendicitis inflammation of vermiform appendix,kids n young adults-caused by obstruction of lumen by fecal material,inflames lymphoid tissue
Appendicitis S/S low grade fever,pain begins periumbilical,then localizes to RLQ (MCBURNEYS point),once ruptured diffuse pain-peritonitis
Gallbladder stores 30-50cc of bile produced by liver-excreted into the duodenum
Cholecystitus inflammation of the gallbladder
Cholelithiasis formation of gallstones-causes 90%of cases-2 types:
Cholesterol Based gallstones most common,associated w/obese,middle aged,women,whom are fertile 4F's
Bilirubin based gall stones formed by breakdown of hemoglobin in RBC's
Sphincter of Oddi allows entrance of bile from the liver to the intestines
Formation of stones patho bile from liver travels thru the common bile duct thru Sphincter of Oddie, it closes when intestines had enough bile, excess bile goes to gall bladder,if bile becomes supersaturated with bilirubin or cholesterol the bile salts erode the membrane and cause
back up and inflammation occurs-prostoglandins release,leads to reduced blood flow
Chronic Cholecystiitus bacterial infection
Acalculus Cholecsistis (no stones) burns,sepsis,DMI,multiple organ failure
Cholecystitus S/S RUQ pain, MURPHEYS SIGN(reffered pain to RT shoulder,colicky,pain after meal high in fat (increases bile release),N/V,warm skin,DARK URINE/light stools TX:DEMORAOL or STADOL-NOT MORPHINE!!
Pancreatitis inflammation of pancreas-most common cause is alcoholism,mechanical and vascular causes,ifectious dx-30-40% mortality due to sepsis and shock >3 s/s =severe pancreatitis
mild pancreatitis epigastric pain,N/V,elevated amylase and lipase
Severe pancreatitis refractory hypotensive shock and bloos loss,jaundice,respiratory failure
pancreas acini cells produce enzymes involved in digestion,produces bicarbonate juice to buffer acidic juice from stomach
Islets of Langerhans Beta cells (75%)insulin,Alpha (20%) glucagon,Delta (5%)somastatin
Hepatitis injury to liver cells either by inflammation or infection
Viral Hepatitis (A,B,C,D,E) 60-70% of all cases
Alcoholic hepatitis 20-30%
Kuffer cells (in liver) breakdown RBC's, bacteria
Liver Fx digestive,storage,Detox,production of bile 60-1000ml per day, carbohydrate metabolism, amino acid metabo-proteinmetabo,synthesis of plasma proteins
Bile Salts made of cholesterol n other stuff,used in small intestines for emulsification and absorbption, reabsorbed in ileum and carried back to liver
Hepatitis A spread by fecal0oral,rarely causes hepatic inj,TX.immune globulin
Hepatitis B serum hepatitis,blood borne
Hepatitis C most common blood borne infection,blood borne,needle sticks,less severe than HBV,TX:imunoglobs,ribavirin(antiviralmed)
Endogenous Interferon critical against ciral infections,produced by invaded cells,doesnt kill, prevents virus from moving and reproducing
Hepatitis D occurs in pts with HBV,sexually transmitted and needle sharing,TX:prevention of HBV
Hepatitis E waterborne infection,chronic hep does not develop,mortlity high for pregos
Hepatitis S/S Sudden onset of Malaise,muscle aches,weak,anorexia,N/V,weightloss, diarrhea,constipation,clay colored stool,jaundice,dark urine,photophobia,cough
Cirrhosis Chronic,irreversable degenerative Dx of the liver,most common cause alcohol, viral hep B or C-slow developing-bld backs up in portal system causing portal HTN due to obstructed liver
Created by: rebeccabelleth