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48 Cards in this Set
- Front
- Back
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GERD:
develops from? dammage leads to? sx? Alarm sx? |
-gastric reflux
-pharyngitis, laryngitis, esophagitis, eareache, asthma, aspiration pneumonia -1. dysphagia: food stuck in esophagus via benign stricture 2. Bleeding: hemategemsis + sig. erosion, comromise of lining of esophagus 3. other: regurgitiation w/ hoarseness, cough, wheezing(laying down at ngiht), dental erosion, ginigival erythema |
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GERD Pathogensis
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1. Inappropriate relaxation of LES sphincter
2. Hiatal Hernia: age related protrusion of esophagogastric jxn and stomach into chest, intefers with disphragm swallowing fxn 3. Defective clearance fxn: defective neutralization of reflux material 4. -smoking, -low pH foots, carminatives(garlic, onions, peppermint) fatty food- decrease lower esophageal pressure -NSAIDs |
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GERD Complications
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(BASE)
Barret's Espophagus(squamous-->columnar metaplasia) Aspiration Esophageal Ulcers Stricture |
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GERD Diagnosis
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-Heart burn
-Alarm symptoms: dysphagia, weight loss, GI bleeding, chest pain, upper airway symptoms -Barium swallow: dysphagia - Ambulatory 24 hr pH monitoring -endoscopy-esophagitis/barrets -Maometry-surgery |
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GERD Treatment:
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-lifestyle
-antacids, H2 blockers, proton pump inhibitors -surgery: spincter competence, remove barret's lesions |
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Other Esophageal Conditions
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-infectious esophagitis(c. albicans, HSV, cMV in immunocompromised)
-esophageal motor disorders-dysphagia due to neuromuscular disorders(stroke, parkinsons, myasthenia gravis) -Achalasia: failure to releax of lower sphincter -Structural: Zenkers diverticulum: outpouching of pharyngeal mucosa |
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Gastritis
defn? caused by? |
-inflammation fo stomach mucosa
-h. pylori -autoimmune -chemical gastritis via NSAIDs(prostaglandins)/alcohol -reactive: phyiscal stress -special:radiation/infection |
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Gastritis Pathogenesis
types? |
1. Acute H. Pylori: Mild dyspepia(epigastric pain and discomfort, nausea & vomiting) post acue infection, 4-5 days
2. Chronic Infection -progressive H. Pylori damage -asymptomatic or recurrent epigastric pain, nausea, vomiting -acid production w/o negative feedback system -atrophy & ulceration not common |
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Gastritis Management
Diagnosis: Treatment: |
-Serology(IgG, IgA antibodies for pylori)
-Urease testing of antral biopsy by endoscopy -C14 urea breath test -avoid causaitive agents -pH > 3.5 prevents ulcerations and bleeding -erradicate pylori |
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Peptic Ulcer Disease
defn? classificaiton? assoicated with? areas involved? |
-sharp circumscribed loss of tissue lining in digestive tract(place exposed to gastric acid/pepsin)
-acute: multiple superifical chronic: single deep with thickened margins -Gastritis -Gastric Ulcers -Duodenal Ulcers |
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PUD Predisposing Factors
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-H Pylori
-Asprin/NSAIDs -Genetic -Stress -Zollinger-Ellison syndrome(gastrin producing tuor) -Idiopathic |
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PUD Sx
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-Epigastric Pain
-Tarry stools:blood in GI tract-->Feces -Nausea -Excessive Salivation |
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PUD complications
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-Perforations
-Hemorrhage(more serious in gastric vs. duodenal) -Gastric Outlet obstruction(narrowing via fibrosis) -Intracitiblity: failure ulcer to heal despite H. Pylori treatment |
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PUD Diagnosis
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-Radiography of upper GI
-Endoscopty-fiberoptics -Test of Pylori: biposy, rapid urease, seorlogy, breath -Test of blood in stool.micropscopic vkeeding |
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PUD Treatment
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-Block secretion of acid
-Stop NSAID use -Nuetralize stomach via coating agents -Eradicate H. pylori -surgery |
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Inflammatory Bowl Diseases
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-UC or/and Crohns
-Chronic inflam of GI tract -Need clinical, endoscopic and hiological characertisics -Family |
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UC
etilology? -defn? -smoking makes it worst? -cancer risk? |
-unknown
-mucosal inflam in rectum and colon(termianl end of bowl), only in submucoas/mucosa -no -increase risk of colon cancer |
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UC Clinical Features
Sx? Complications? |
-diarrhea with blood in stool, abdoominal plane, rectal bleeding/hypersensitivity, weight los, fever
-local: massic hemorrhage, colonic stricture, polyp, adenocarcinoma, toxic colon dilation, perforation -oral lesions in UC = Pyostomatitis Vegetans |
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UC Management
diagnosis? treatment? |
-Barium enema, endoscopy(colonoscopy), biopsy
-medical: anti-inflammatory and immunosuppressive drugs -surgical: removal of colon and rectum is curative(illeal puch-to-anal anastomosis rectal fxn |
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Crohn's Disease-Granulomatous Enteritis
etiology? defn? -sx? -complcations? |
-none
-granulomatous inflammation involving in part of the GI tract(mostly proximal), can penetrate lining -abdominal pain, diarrhea, weight loss, no bleeding -intestinal obstruciton, -malaabosprtion -fistula, -abscess formation -mucosal ulcers break through interstinal wall-->leakage -Rectal: perforation and penetration |
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Crohn's Disease:
Diagnosis: Treatment: |
-radiogrpahy, endoscopy, biopsy
-Medical: immunosppression, anti-TNF antibody Surgical: only with complication hyperalimentation if significant absoprtion problems |
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Diarrhea-acute:
duration? due to? Sx? |
2-3 weeks
infection via bacterial toxins, viruses, parasites which cause immesne secretion of water-do not slow down with fasting ex. C.Diff-->pseuomembranous colitis abdominal pain, watery or bloody diarrhea & fever(dysentery) |
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Diarrhea-Chronic
-duration -due to? |
4 weeks or greater
-Malaabsoprtion: inaibility to absorb fat -Osmotic: watery diarrhea that SLOWS with FASTING: via poorly absorbed solutes(Mg laxatives, lactose, sorbitol) -inflammatory: IBDs, food alergies, radiation -Motility disorder-irritbal bowel syndrome |
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Diarrhea Diagnosis
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-RBC, WBC, parasites, bacteria, toxins in stool
-sigmoidoscopy(terminal end of bowle) and biopsy -fecal fat(malabsoprtion) -24 hr stool volume measurement -hormones: Zolinger Ellison: gastrin Pancreatic adenomas: Vasoactive intestinal peptide |
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Diaarhea Treatment
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Antibacterial and antiprotozoal therapy
Opiates: slow down peristalsis Bismut subalicylate(Peptobismol) coating agent, inhibit colonization of enterotxoin producing bacteria, reduce inflammation -Replace loss fluid |
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Irritable Bowel Syndrome
Sx? results from? diagnosis? Treatment? |
-chronic/recurrent abdominal pain, defecation disturbance, heaches, fatigue, menstural pain, psychological distress
-exclusion of other gi disorders and dyfxn -dietary modifecation, antispamotics, anti-diarrhea meidcation, psychological counseling, atni-depressants, anxiolytics |
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Diverticular disease
inovles? related to? complications? |
-herniations/ouptuching in the mucosa/susbmocusa through bowel muscle at sites where arteries penetrate
-low fiber diet: small stool volume-->smaller colonic diameter -diverticulitis: diverticula become impacted with mass-->inflammation, erosion, perforation and bleeding |
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Diverticulosis clinical features
Sx? Diagnosis? treatment? |
-Diverticulitis: lower left pain, bleeding, masses
-barium enema, UT scan, Ultrasound, Colonscopy(rule out colon cancer) -medical: antibiotics, IV fluid -Surgical |
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Appendicitis
defn? results from? pathogensis? Sx? Diagnosis? Treatment? |
-impaction of fecal matter in appendix leading to bleeding thromobsis and possibly explosion
-ulceration of lumen and/or obstruction -LR abodominal pain, rebound pain, loss of apetite, nausea, vomiting, fever -Elevated WBC count -Spiral Ct scan and ultraound -surgical |
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Dental Implication of GI Disorders
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-peptic ulcer disease: avoid NSAIDs, corticosteroids, increase acid of sotomach
-IBD: avoid corticosteroids, watch for hematologica effects of immunosuppresive drugs, broad/long term antibiotics |
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Jaundice
characterized by? classificaitons? caused? |
-Yellow pigment of skin, sclera, mouth from elevate bilirubin levels in blood steam
-conjugated: direct bilirubin, unconjugated: indirect bilirubin -excessive breakdown of erythrocytes -failure of liver of metabolize -obstruction of drainage of biliary system |
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bilirubin excretion process
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-bilirubin(water insoluble)-->Bilirubin diglucornide(water soluble) [excereted]
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types of Jaundice
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1. Hemolysis--> unconjugated bilirubin
2. Failure of liver: any cause including various froms of Hep. conjugated/unconjugated 3. Failure of drainage-may involve intrhepatic process(cirrhosis) or extrahepatic obstruction(cholelithiasis) mostly conjugated |
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Hepatitis A
-transmited? -duration and limiations? -IgM =? -IgG =? -vaccine? |
-RNA virus, sexually, oral fecal
-15-145 days, genreally short and self -limiting -acute -immunity to hep A -yes |
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Hepatitis B
-transmited? -duration? -acute = -limitations? |
-sexually, perinatal, parenteral
-1-6 months -fatigue, nausea, poor appetite, jaundice, anorexia, helatic tenderness/enlargement -self limited or lead to chronic liver disease and hepatomas |
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Hepatitis B Serology
Viral components? Chronic carriers show? Silent Carriers Can lead to? |
S: surface
C: core E: fragments of core(very sick wehn expressed) Sustained S levels, up and down E, E levels follow liver inflammation Constant level of S w/p E change manifestions everywhere including glmoerulonephritis |
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Pattern of Acute Hepatitis B
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-HBsAG rises and falls quickly as antibodies rise
-IgM = acute hep B -IgG = prvious exposure -HBeAg-detected nect, but replaced by anti-HBe -HBeAg = max viral activity and infectivity -IgG anti-HB = immunity -HBsAg 6+ months = chronic Hb |
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Clinical Aspects of Hep B
other complications? vaccine? passive immunity? |
-Ag/Ab-->extrahpeatic problems (rash, urticaria, arthritis, vasculitis, glomerulonephritis
-available -HBIG |
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Hep C
transmitted? complications? manifestations? |
-blood transfusion, sexually
-chronic hepatitis, cirrhosis -rashes, rhematoid arthritis, glomerulonephritis |
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Hep C clinical aspects
Diagnosis: Treatment? |
-anti-HCV antibodies, Rt-PCR, Serum transaminas enzymes(ALT,AST)
- alhpa interferon, Ribavirin |
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Other Types of Hepaitits
D E G |
D: Requires hep B, causes further infection seen in high risk HBV infeected people(IDUs)
E: Fecal Oral, waterborne, self-limited, particularly effect pregnant women G: GBV-C: in chronically infected hep C patients, transmitted sexually, blood borne, non pathogeneic |
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Hepatitis Diagnosis
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Elevated transaminases ALT, AST
Elevated bilirubin Lower levels of albumin(vs. globulin) Psoitive serologies |
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complications of Hepatitis
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-Chronic Liver disease(cirrhosis)
-Protal HTN-->varices -Ascites: fluid in peritoneal space -Hepatic encephalopathy-increase fluid to brain via bilirubin increases |
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Obstructive Diseases
caused by? |
-intrahepatic(cirrhosis)/extrahepatic(gall stones)
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Choleithiasis
defn? risks? leads to? stones made from? bilirubin stones result from? |
-stone formation in gall bladder
-rapid weight lost/fasting -chronic/acute obstruction and inflammation(cholecystitis) -cholosterol or birle -chronic hemolysis ex: sick cell disease |
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Cholelithiasis Clincal Features
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UR pain, anusea, vomiting
cholecystitis -->fever and chills |
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Cholelithiasis
Diagnosis? Treatment? |
-ultrasound
-CT -endoscopic exam(2 holes scope) -MR cholangiography -Blood tests, elevated bilirubin, transaminases -Urine has bilirubin--> turns dark dissolve stones via bile acid lithotripsy endoscopic removal of stones laproscopic surgery |
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Dental implications of liver diseseases
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-know hep type and status as hepatic viruses are present in saliva during active infeciton
-check liver fxn and determine patients abilit yot metolize drugs -perform coagulation tests -hematologic abnormalties -referral for lacohol counseling? |
