PTH 2403 Week 4 GI Tract Disorders 2025 PDF

PTH 2403 Unit 3: GI Tract Disorders 1. DYSPHAGIA Difficulty swallowing connection: esophagus is for food trachea is for air fistula creates and abnormality which connects them D: pouch called diverticulum (food is not supposed to be stuck and can cause necrosis) F: peristalsis is the contractio...

PTH 2403 Unit 3: GI Tract Disorders 1. DYSPHAGIA Difficulty swallowing connection: esophagus is for food trachea is for air fistula creates and abnormality which connects them D: pouch called diverticulum (food is not supposed to be stuck and can cause necrosis) F: peristalsis is the contractions of muscles to move through the system. No peristalsis is called achalasia C: if people have tumours in this location can be esophageal cancer or lung cancer if it is on the outside G: neurological aspects to dysphagia, runs through the cranial nerves (ie: stroke) (CNS damage) Cranial nerve 5: trigeminal, helps chew (10) Vagus nerve: helps swallow 2. HIATAL HERNIAS Hernia: protrusion/poking in an area that it does not belong in lower esophageal sphincter is effected if pushed above the diaphragm, type 1 (no longer in line with the diaphragm) (~90% of cases) Type 2: sphincter is in the right place, the upper part of the stomach is through the top opening (~5% of cases) M/f: heart burn/acid reflux, pyrosis, can cause risk for esophageal cancer Dx: endoscopy Tx : t1 : laparoscopic surgery to push it down T2: since stomach will become necrotic due to twisting it will be removed surgically e/t: crush injury, heimlick manuvar, being pregnant 3. GASTRIC DISORDERS gastritis :inflammation of the lining of the stomach e/t: spicy food, alcohol, medications pain : reported in LUQ 3. PYLORIC STENOSIS Narrow opening between stomach and duodenum Thickened pyloric sphincter, if food cant get through it will either decompose of will be vomited Peptic ulcer: stomach or duodenal ulcer caused by H. pylori, or overuse of NSAIDs (ibuprofen, naproxen) 4. PATHOGENESIS OF H. PYLORI Person to person (gastro oral transmission) (from the stomach to mouth) Ie; sharing food This bacteria creates urease which neutralizes the acid in the stomach, converts urea into NH3 (ammonia, alkaline) **link lymphoma and H pylori Dx: fast tests, non invasive UREA BREATH TEST: presence of carbon 13​ ​ STOOL SAMPLE: easier in children Both tests are very similar and is 50/50 Mx: clarithromycin, amoxicillin, pantoprazole ​ ​ ​ ​ ​ ​ Triple therapy Metronidazole is allergy to penicillin/amoxicillin Bismuth (found in peptobismol) is another option (quadruple therapy) 5. DUMPING SYNDROME​ Gastric Bypass Tx: of obesity to help lose weight Patho: accelerated gastric emptying M/f: extreme form of diarrhea (risk of dehydration; extreme volume of water and electrolytes) NO SUGAR ON AN EMPTY STOMACH; sugar is a water magnet 6. IBS Irritable Bowel Syndrome -​ Sporadic abnormal contractions -​ Vagus nerve controls m/f: 15% of people have this, change in bowel habits, pain or discomfort relieved w/BM P/f: stress (brain-gut axis), gut microbiome imbalances (e/t antibiotics, food sensitivity), 5-HT imbalance (serotonin) Splenic Flexure Syndrome: back pressure pressing on the spleen, where the large intestine kinks downwards 7. INTESTINAL OBSTRUCTIONS 1. INGUINAL HERNIA: small intestine poking through the abdominal wall, more common in males 2. VOLVULUS: part of intestine is twisted on itself, causes ischemia and has to be fixed to avoid necrosis (Sepsis will occcur w/necrotic tissue because it allows bacteria from the large intestine to escape into the body) 3. TELESCOPING (INTUSSUCEPTION): one component is sliding into another 4. INTERNAL TUMOR: intestinal cancer 5: DIVERTICULITIS 8. IBD Inflammatory Bowel Disease Patho (suspected): autoimmune; triggered by gut microbiome ​ ​ ​ ​ ​ 50/50 MALE AND FEMALE COMPLICATIONS CROHNS ULCERATIVE COLITIS Fistula because lesions can erode the wall of one which can go to the next thing that's touching it (distends the colon creating a toxic megacolon; must be treated surgically; risk for sepsis if it rips) Rectovaginal fistula is a possibility (feces will come out of vagina) Enterovesicle fistula is a possibility (males; fecal matter comes out of bladder) LEFT SIDE colonoscopy will reveal patchy inflamed tissue (skipped lesion), deep in the tissue (fissures) can affect small and large intestine RIGHT SIDE continuous inflammation (continuous lesions), surface level (occurs in mucosa) can affect large intestine 9. CELIAC DISEASE NO MORE GLUTEN Autoimmune Gluten binds to Gliadin that binds to tissue transglutaminase (people w/celiac will create antibodies). antibodies will attack tissue transglutaminase (TTG) and Gliadin intestinal lumen villi will begin to deteriorate through inflammatory response meaning there will be malabsorption causing weight issues (cant absorb nutrients) LABS: IgA: LOW TTG IgA: NEGATIVE (First line screen) Endomysial Antibody (EMA-IgA): NEGATIVE (confirmatory) TESTS IF PT IS IgA DEFICIENT: TTG IgG: POSITIVE (1st line) Deamidated Gliadin Peptide IgG (DGP-IgG): POSITIVE (confirmatory) IgA deficient people are prone to infections due to the antibodies 10. ACUTE APPENDICITIS e/t: little nugget of appendix gets an obstruction that cuts off circulation caused by a fecal stone (fecaliths, calculi, infections [gastro], neoplasm [new growth like tumour], ozempic use) Pain in RLQ and belly button; upon percussion will be firm and hard, distention may be present. 1-2: around 24 hours CASE STUDY: The Shade of It All (Exploring the GI-Renal Connection)​ A 67-year-old male client is self-medicating regularly with OTC naproxen for his long history of osteoarthritis of the knee. He is in the clinic today, visibly anxious, stating: "I’ve vomited a bit of blood in the last three days, and I’m passing very black stools, but I’m not urinating much." He sometimes feels a burning sensation in his stomach that is getting worse each week, but denies a history of GERD and does not drink alcohol. When the nurse asks the client to stand up, he reports dizziness. Additional Medical History: ​ The client has atrial fibrillation and is on warfarin. Stop prevention of clots ​ No known liver disease Hematology: ​ Hct = 0.28 LOW client is anemic from blood loss ​ Hb = 102 g/L LOW “ ​ MCV = Normal rbc size is normal ​ MCHC = Normal rbc hemoglobin % per cell is normal Coagulation: ​ INR = 2.9 NORMAL FOR A CLIENT ON WARFARIN Biochemistry: ​ Urea = 14 mmol/L HIGH (urinary retention, block??) ​ Creatinine = 141.4 µmol/L HIGH 1. Pathophysiology ​ Suggest the pathogenesis that has occurred in this client to explain the findings in his emesis and stools. Potentially a peptic ulcer due to regular use of NSAIDs (naproxen) and presence of blood in the stool Potentially ulcerative colitis due to bloody stool Upper GI bleed: client has developed peptic ulcers from NSAID use due to osteoarthritis Fresh blood from lesion of the stomach causes vomit to appear red; stool colour is tarry (melena) because bleed from the upper GI tract is digested and hemoglobin is transformed in structure so its colour changed to brown/black ​ Explain the origin of the client’s orthostasis. Orthostasis: dizziness from standing is due to anemia, orthostatic HOTN due to hypovolemic (loss of volume in blood) (low Hb, low Hct) Pt is bleeding A LOT because of warfarin (anticoag) 2. Evidence ​ Relate all lab results to the client’s pathogenesis (add comments next to each lab value, above) Refer to lab values ​ Explain why the client’s high urea level could indicate both GI bleeding and decreased kidney perfusion. Urea Kidney: decreased kidney perfusion causing the kidney to not excrete waste products such as urea Urea GI: blood is being digested in the stomach, urea is created through protein (byproduct) 3. Management of Disease Process Discontinue warfarin, stop naproxen, start a PPI, control bleeding (), IV fluid resuscitation (monitor Hb and Hct), transfusion (if Hb in less than 70g/L OR pt has symptomatic anemia), endoscopy (looking to see where the bleed is and cauterize) CASE STUDY 2 Kid who might be celiac Unit 4: Alterations to Liver, Gallbladder and Pancreatic Function 1. CHOLELITHIASIS Risk Factors and Pathogenesis (p.359) ​ Cholelithiasis is more common in fair-skinned females and Indigenous populations. List some other risk factors of gallstones. (see paragraph 1) ​ Biliary sludge often precedes cholelithiasis: what is biliary sludge a result of? (see paragraph 2) ​ Contrast the impact of small vs larger calculi. (see paragraph 3) ​ Define: cholecystitis. (see paragraph 3) Manifestations (p.360) ​ List the three types of cholelithiasis ○​ Which type is most common? ○​ Which type has a strong association with female hormones? ○​ Which type is associated with conditions that cause hemolysis? ​ Define: biliary colic ​ Locate the abdominal pain caused by cholelithiasis, and where it can radiate. Treatment strategies (p.360-361) ​ Describe the goal of using an NG tube with intermittent suctioning. ​ Describe: lithotripsy ​ Describe: cholecystectomy CHOLESTASIS Meaning: gallstones can be caused by oral contraceptives (estrogen and progesterone). estrogen slows movement of your gallbladder causing bile to collect and create stones Located in RUQ stones: yellow (cholesterol), caviar like, pale yellow stones can move and get stuck in the cystic duct (bile will be able to move) or can get stuck in the common bile duct (bile will not reach duodenum) M/F: common bile duct (clay coloured stool) since the bile is stuck there is no stercobolin being made, bilirubin backs up into GI tract and gets excreted stones can also get stuck in pancreatic duct 2. ACUTE PANCREATITIS #1 trigger is gallstones, alcohol, high trigs (fat)[too much in diet will overstimulate enzymes] other: mumps virus, medications (ie: Ozempic), post-ERCP (endoscopic retrograde cholagngiopancreatography) makes digestive enzymes Enzymes: hypovolemic shock: when enzymes leak into circulation causing vasodilation, neurogenic shock, DIC (disseminated intravascular coagulation), acute respiratory distress syndrome Septic shock, peritonitis (look for: tenderness of inner wall of abdomen TX: hemodynamics stabilization ENDOSCOPIC RETROGRADE CHOLANGIOPANCREATOGRAPHY camera gets snaked down esophagus to the duodenum, can irritate the pancreatic tissue 3. CHRONIC PANCREATITIS X in pancreas: longterm inflammation can turn into scar tissue (fibrosis) LABS [chronic pancreatitis] low fecal elastase in stool E/T Alcohol abuse, smoking, gallstones, recurring acute pancreatitis, AiP (autoimmune pancreatitis [labs: IgG4 antibodies]), Cystic fibrosis (thick mucus everywhere) M/F abdominal pain, N/V, weight loss (no appetite due to pain, can't digest enzymes/food), steatorrhea (fat in the stool; not breaking fat down), Secondary DM (pancreas stops making insulin) 4. CIRRHOSIS Primary Biliary Cholangitis (PBC): Autoimmune destruction of intrahepatic bile ducts Primary Sclerosing Cholangitis (PSC): Immune-mediated damage to intra- and extrahepatic bile ducts, often linked to UC. Hep C,B,D [chronic and most common to lead to cirrhosis] Autoimmune: Autoimmune Hepatitis (AiH) other: Fe overload (hereditary hemochromatosis), Cu overload (Wilson's disease), a1 antitrypsin deficiency Resistance to BF through fibrotic liver Hepatocytes can't do what they're supposed to PORTAL CIRCULATION AKA: liver circulation 1: scar tissue obstructs BF through liver (shrinks and tightens)[tried to take blood back to the heart but has a back up effect; high portal hypertension {lots of pressure in the portal vein}] 2: high pressure in anal area (causes hemorrhoids) 3: will not be able to absorb nutrients correctly 4: Back up of blood into the spleen (splenomegaly) 5: bulging esophageal varices (bulge in lumen in esophagus; risk for aspiration, perforation, bleeding from vomiting) Cirrhosis will shut down all organs unless eligible for transplant CASE STUDY: Gin & Toxic - A Case of Cirrhosis (Exploring the Multisystem Aspects of Liver Failure)​ ​ A 52-year-old male salesman was admitted to hospital after an episode of haematemesis. Endoscopy revealed the presence of esophageal varices. His varices were treated surgically, and no further bleeding occurred. The client was told to abstain from alcohol. He was readmitted 1 year later, drowsy and jaundiced with tremors and some edema. The client denied alcohol consumption over the last year. Results of biochemical investigations are shown below. Tremors due to extra ammonia in the plasma: Asterixis -​ Hepatic encephalopathy -​ Ammonia accumulation in the brain -​ TX: administer lactulose Additional Medical History: ​ Gynecomastia. Liver can’t handle estrogen anymore(impaired inactivation) ​ Frequent infections. Low WBC ​ Recurrent episodes of hypoglycemia Liver cannot store glycogen Biochemistry: ​ Ammonia = HIGH liver cells are compromised (ammonia to urea) ​ Bilirubin = HIGH impaired excretion of bilirubin leading to jaundice (over 50 is jaundice) ​ ALT = HIGH hepatocyte damage ​ ALP = HIGH bile duct impairment ​ GGT = HIGH marker of alcohol, impairment to bile duct and alcoholism ​ Urea = HIGH KIDNEY INJURY ​ Creatinine = HIGH KIDNEY INJURY ​ Ferritin = LOW liver cannot store iron ​ Vitamin B12 = LOW cannot store b12 in liver (scarred) ​ Albumin = LOW Impaired synthesis of albumin Hematology: ​ Hct = LOW r/t blood loss; anemia from low Fe and B12 ​ WBC = LOW backflow to spleen causing splenomegaly which destroys platelets and WBC  ​ PLT = LOW” splenomegaly Spleen tries to destroy odd looking cells like PLT and WBC Relates to Cirrhosis because 1. Evidence ​ Relate all lab results and manifestations to the pathogenesis of cirrhosis in this client.