Presentation is loading. Please wait.

Presentation is loading. Please wait.

Gastrointestinal Disorders. Disorders of Nutrition Alterations in: Ingesting Digesting Absorbing Eliminating.

Similar presentations

Presentation on theme: "Gastrointestinal Disorders. Disorders of Nutrition Alterations in: Ingesting Digesting Absorbing Eliminating."— Presentation transcript:

1 Gastrointestinal Disorders

2 Disorders of Nutrition Alterations in: Ingesting Digesting Absorbing Eliminating

3 Ingestion Anorexia Pica Nausea & Nausea Esophageal Atresia Tracheoesopheal fistula Cleft lip/palate Anorexia Nervosa Pyloric Stenosis Projectile Vomiting

4 Maldigestion Lactic Deficiency Pancreatitis Cystic Fibrosis

5 Malabsorption Intestinal Parasites Gastrectomy Loss of Stomach as Reservoir for Food Dumping Syndrome Loss of Intrinsic Factor Celiac Disease (Sprue) Cholecystitis/Cholelithiasis Regional Enteritis (Crohn’s Disease)

6 Elimination Diarrhea Osmotic Changes Secretory Changes Mucosal Damage Altered Motility Crohn’s Disease Ulcerative Colitis

7 Submucosa Lumen Circular muscle longitudinal muscle Myenteric plexus Submucosal plexus PSNSSNS Basic Structure of the GI tract

8 ENTERIC NERVOUS SYSTEM Myenteric Submucosal PSNS Pelvic nerves SNS Ach NE Smooth muscle Secretory Cells Endocrine Cells Blood Vessels Enteric Nervous System Influenced by ANS

9 Gastric Motility LES fundus Antrum pylorus approx 3 contractions per minute receptive relaxation

10 Control of Gastric Emptying GASTRIC EMPTYING PSNS + SNS - Duodenal acid secretin- Duodenal fats CCK - Duodenal hypertonicity -

11 Small and Large Bowel Motility Small Intestine 2-4 hours to traverse Segmental contractions to mix Peristaltic waves to move forward Large Intestine Slow progression at 5-10 cm per hour Segmental contractions produce haustra 1-3 mass movements per day

12 Secretion in the Stomach Parietal Cells HCL Intrinsic Factor Chief Cells Pepsinogen Surface epithelia and mucous cells HCO3- and mucus

13 Gastric Parietal Cell Acid Secretion muscarinic receptor H 2 receptorgastrin receptor AchHistamine Gastrin Vagus Mast Cells G cells Control of Acid Secretion

14 Secretion in the Small Intestine Secretions from Pancreas HCO3-, Proteases, Lipases, Amylases Secretion from Gallbladder Bile acids, pigment, phospholipid Secretions from intestinal epithelia Brush border enzymes

15 Brush Border Enzymes Lactase:lactoseglucose, galactose Sucrase:sucrosefructose, glucose Dextrinase:cleaves amylose branch points Glucoamylase: maltoseglucoses Only Monosaccharides are Absorbed

16 Digestion and Absorption of Proteins Pepsin: 15% of peptide bonds broken Pancreatic proteases Trypsin Chymotrypsin Carboxypeptidases Brush Border Peptidases cleave into 1 to 4 aa chains

17 Digestion and Absorption of Fat Bile salts are amphipathic molecules that break up large fat globs into droplet Lipase are water soluble - only work at surface of droplet Triglycerides --------> FFA and glycerol Bile forms micelles with FFA to keep soluble. FFA are lipid soluble so absorb directly

18 Reabsorption of Bile Bile is reabsorbed at terminal ileum Passive diffusion and active transport Transported to liver via portal blood ALL reabsorbed bile is taken up on first pass by liver Entire bile pool circulates 2 to 5 times per meal. 5-10% lost per day in stool

19 GI Disorders

20 Dysphagia Neuromuscular: pharynx Stricture or tumor: Progressive solid food dysphagia Achalasia: esophageal motility disorder, loss of peristalsis in lower 2/3 plus impaired LES relaxation Mallory-Weiss syndrome: mucosal tears at distal esophagus, bleeding, pain

21 Oropharyngeal vs Esophageal Nasal regurgitation Airway obstruction with eating Coughing when swallowing Immediate regurgitation Hoarse voice No airway distress Late regurgitation Chest pain @ meals Frequent heartburn Presence of collagen disease Presence of Left supraclavicular node

22 Dyspepsia Present with heartburn, indigestion, epigastric distress Up to 2/3 will have no identifiable cause One-half will have relief from placebo Symptom profile does not differentiate between GERD, PUD, and non-ulcer dyspepsia (functional) Physical exam is rarely helpful

23 Diagnosis NSAID: suspect PUD and treat Helicobacter pylori: urea breath test or biopsy during endoscopy GERD: Trial of H2 therapy Functional: may improve with agents that increase motility Zollinger-Ellison syndrome: gastrin level

24 PUD with H. pylori H. pylori is nearly always a factor in non- NSAID peptic ulcer disease Conventional therapy with H2 blockers or H+ pump inhibitors has a 75-80% one-year recurrence rate Treatment for H. pylori reduced recurrence rate to less than 5%

25 High fever? Bloody diarrhea? YESNO Noninflammatory watery large volume periumbilical pain small volume LLQ pain + fecal leukocytes Viral: rotavirus, Norwalk S. aureus food poisoning Giardia Shigella, Salmonella, C. difficile, E. coli (bad) Campylobacter, HIV- associated Rehydrate, symptomatic Culture and treat Acute Infectious Diarrhea Inflammatory

26 Chronic Diarrhea: Stool Studies Stool Osmolality: normal gap < 50 Laxative screen: Mg, PO4, SO4 Fecal leukocytes: Inflammatory disease Ova and parasites: Giardia, cryptosporidium Fecal Fat analysis: > 10 g/24 hrs indicates malabsorption Fecal weight: > 1000 g is secretory

27 Osmotic Diarrhea: Lactase Def. Incidence 90% of Asian Americans 95% of Native Americans 50% of Mexican Americans 60% of Jewish Americans 25% of other Caucasians DX: empiric trial of lactose-free diet for two weeks

28 Inflammatory Bowel Disease Ulcerative Colitis Involves only the colon and rectum Mucosal layer is affected Hallmark is bloody diarrhea and lower abdominal cramps Associated with increased cancer risk after 8- 10 years of disease

29 Assess UC Disease Severity Number of stools per day Hematocrit Sed rate Albumin level

30 Crohn Disease Intermittent bouts of fever, diarrhea, and RLQ pain May have RLQ mass, tenderness Can affect any portion of GI tract 30% are small bowel only 50% are small and large bowel 15-20% are large bowel only

31 Crohn Disease Transmural process in the intestinal wall predisposes to fistula formation If suspected, obtain upper GI series with small bowel follow through plus either colonoscopy or barium enema Suggestive findings are ulcerations, strictures, and fistulas RX: stop smoking, drugs similar to UC

32 Compare and Contrast – CD & UC Crohn’s Disease “Skip” Lesions (granulomatous) Terminal ileum Diarrhea/Constipation Alternates – Less Bloody Malignant Potential (not totally determined) Proned to Develop Abcesses & Fistula formation Ulcerative Colitis Continuous ulceration of mucosa of colon Colon, rectum – distal Watery diarrhea – has mucus/pus – may be bloody – common Proned to develop colon carcinoma rare abcess/fistula formation

33 Motility Diarrhea: IBS Irritable bowel syndrome is a chronic (>3months) functional disorder with no identifiable pathology Fluctuations in stool frequency and consistency (no nocturnal diarrhea) Perceived abd distention, bloating, pain Often associated with anxiety or depression

34 IBS It is not IBS if fever, bloody stools, nocturnal diarrhea, or weight loss are present Consider checking CBC, sed rate, albumin, and stool for occult blood to rule out inflammatory disease, consider lactose-free trial. RX: restrict caffeine, gas producing food, high fiber. Rx depression

35 Occult GI Bleeding Detected by FOBT: worry colorectal CA Indicated for iron deficiency anemia in males or postmenopausal females Unless S&S suggest Upper GI etiology (heartburn, dyspepsia PUD) start with colonoscopy (or barium enema) If no source, follow with endoscopy

36 Acute Abdominal Pain Tension: spasm, associated with intense peristalsis (irritant, infection, obstruction) Ischemia: intense constant pain (bowel strangulation, volvulus adhesion) Inflammation: first localized to serosa covering inflamed part then extends to abdominal wall causing reflex muscle spasms (rigidity, involuntary guarding)

37 Assessment of the Pain Is it nongastric? consider aortic aneurysm, ectopic pregnancy, PID, kidney Is it an acute surgical abdomen? Involuntary guarding, rigidity Absent bowel sounds Is there shock

38 Localization of Abdominal Pain Stomach, duodenum: mid epigastric Small bowel: periumbilical Colon: low abdomen, midline Rectum: sacrum and perineum Gallbladder: mid epigastric radiates to RUQ or right scapula Pancreas: mid epigastric radiate to back Appendix: RLQ, but variable

39 Bowel Obstruction Presentation Pain, distention, vomiting, obstipation Evaluation Flat and upright abdominal film Small bowel: less urgent intestinal tube, decompression Large bowel: urgent, danger of cecal perf immediate surgical consult

40 Types of Bowel Obstruction Mechanical Obstruction * Adhesions * Tumors * Impaction * Strangulated Hernia * Volvulus “Twisting” * Intussusception (telescoping) Functional Obstruction * Bowel Manipulation (surgery) * Narcotic Anesthesia * Peritonitis

41 “itis”EtiologyClinical Findings esophagitisreflux (GERD)- pain after meals - “heartburn” gastritis -PUDASA, ETOH- epigastric pain H. pylori regional enteritis? Etiology- diarrhea with (Crohn) blood and mucus ulcerative colitis? Etiology- bloody diarrhea “Itis” from TOP to BOTTOM

42 “itis”EtiologyClinical Findings diverticulitislow fiber dietlow abdominal pain, fever appendicitisobstruction- RLQ pain, fever “fecalith”- rebound pain peritonitisperforation- severe pain, ileus bowel ischemia- guarding, rigid pancreatitisbiliary disease- pain to back, shock ETOH- high lipase, amylase

43 “Itis” from TOP to BOTTOM “itis”EtiologyClinical Findings cholecystitischolelithiasis- RUQ pain - steatorrhea hepatitisviral, acute ETOH- jaundice, big liver - high AST, ALT - flu-like symptoms

44 Appendicitis Etiology: Obstruction by fecalith, inflammation Presentation: RLQ pain (classic, but may be anywhere), N&V, fever, diarrhea, RLQ tenderness Evaluation: CBC, abdominal ultrasound RX: immediate surgical consult

45 Diverticulitis Etiology: Microperforation with peridiverticular inflammation Presentation: Elderly with LLQ pain, severe constipation, nausea, fever Evaluation: CBC, abd film, CT if peritoneal signs Rx: NPO, antibiotics, IV fluids

46 Liver, biliary, and pancreatic anatomy

47 Acute Pancreatitis Etiology: unknown Associated with ETOH, biliary disease Presentation: Severe epigastric and back pain Evaluation: CBC, glucose, calcium, electrolytes, amylase, lipase (renal studies) Severity index

48 During first 48 hours HCT drop of >10% BUN rise >5 mg/dl PaO2 < 60 Calcium < 8 mg/dl Fluid sequestration of > 6 liters Severity Scale: Pancreatitis Initially Age over 55 WBC > 16,000 Blood glucose > 200 Base deficit > 4 Serum LDH >350 AST > 250

49 Pancreatitis Severity Mortality RateNumber of criteria 1% 16% 40% 100% 0-2 3-4 5-6 7-8

50 Cholecystitis Etiology: 95% associated with stone in cystic duct Presentation: Often obese female, fever, RUQ pain with scapular or epigastric pain, colicky, N&V Evaluation: CBC, RUQ ultrasound, HIDA scan RX: Prompt cholecystectomy

51 Steatorrhea Pancreatic steatorrhea: > 90% of exocrine function lost Bile salt deficiency: decreased ileal reabsorption (Crohn) blocked secretion (cholestasis) Bacterial overgrowth syndromes: stasis of small bowel contents Mucosal defects: Celiac disease (sprue)

52 Jaundice Jaundice occurs with bilirubin level > 3 mg/dl (normal 0.2-1.2) Increased RBC breakdown Impaired liver uptake of bilirubin Impaired excretion of bilirubin

53 Functions of the Liver Nutrient metabolism (glucose, protein, fat, fat soluble vitamins) Production of serum proteins and enzymes (albumin, clotting factors etc.) Detoxification of hormones, drugs Bile synthesis (conjugation of bilirubin) Urea synthesis

54 Structure of liver lobule

55 Manifestations of Liver Dysfunction Impaired protein synthesis bleeding (clotting factor deficiency) edema (hypoproteinemia) immune deficiency (substrate for antibody) Accumulation of toxins and hormones feminization (excess estrogens) poor metabolism of drugs spider nevi (estrogen)

56 Manifestations of Liver Dysfunction Inadequate bile synthesis increased bilirubin level jaundice Inadequate urea synthesis increased blood ammonia level (NH 3 ) hepatic encephalopathy Release of marker enzymes into blood AST (SGOT) ALT (SGPT)

57 High Direct Bilirubin Hepatocellular injury: hepatitis drugs hemochromatosis Alpha-1 antitrypsin deficiency Cholestasis: stones, tumors, strictures cholangitis

58 Acute Hepatitis Etiology: acute liver inflammation and cellular injury: viral, toxic Presentation: jaundice, anorexia, fatigue, diffuse abd discomfort, dark urine Evaluation: History of viral or toxin exposure, AST, ALT, Alk phos, bilirubin, serology for viral hepatitis

59 TypeAB+(D)CE Transmissionoral-fecalblood andblood andoral-fecal body fluids Riskcontaminatedsexual, IVsexual, IVwaterborne food Prognosisgoodmore severe85% chronic? 5% carrier B+D more severe Viral Hepatitis

60 Acute Toxic Hepatitis Etiology: exposure to hepatotoxin or its metabolite Evaluation: No definitive tests: history of exposure is important negative viral serology screen improvement after discontinuing drug if alcohol is the toxin, AST > ALT, 2:1

61 Chronic Alcoholic Liver Disease Etiology: chronic, heavy ETOH exposure Only 15-20% of alcoholics develop liver disease Men > 4-6 drinks/day, Women > 3-4/day Pathogenesis: unknown Presentation: fatty liver hepatitis cirrhosis

62 Cirrhosis of the Liver Fibrotic liver loss of hepatocellular functions obstruction to bloodflow from the gut Etiology Chronic alcohol use (most common) Biliary (obstruction in bile drainage) Postnecrotic (viral, toxic hepatitis) Cardiac (right heart failure, liver congestion)

63 To vena cava From GI tract Hepatic vein Portal vein jaundice bleeding low albumin -edema immune deficient estrogen excess encephalopathy cell failure portal hypertension ascites esophageal varices hemorrhoids anorexia Liver Cirrhosis

64 Treatment & Monitoring Abstinence from alcohol Restore nutrition: (high protein diet unless hepatic encephalopathy) Monitor PT, AST, ALT, albumin, bilirubin Vitamin K Abnormal PT despite vitamin K indicates a severely compromised liver

65 Treatment & Monitoring Ascites: caput medusae: flow outward from navel sodium restriction spironolactone monitor for spontaneous bacterial peritonitis If ascites is present, high likelihood of esophageal varices

66 Treatment & Monitoring Hepatic Encephalopathy Altered mental status due to accumulation of toxins, including ammonia (NH 3 ) Precipitated by GI bleed, drugs, increased shunting of blood around liver Monitor NH 3 level lactulose withhold protein

67 Liver Cancer May and usually does have similar clinical manifestations to cirrhosis. Liver cancer is almost always metastatic. The survival rate s less than 5%.

68 Balloon tamponade of esophageal varices

69 Study Well & Do GREAT Next Week The End…..

Download ppt "Gastrointestinal Disorders. Disorders of Nutrition Alterations in: Ingesting Digesting Absorbing Eliminating."

Similar presentations

Ads by Google