GI Tract Signs & Symptoms Pathophysiology PDF

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European University Cyprus

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Konstantinos Ekmektzoglou

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GI tract pathophysiology nausea vomiting

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This document discusses the pathophysiology of common gastrointestinal (GI) tract signs and symptoms, including nausea, vomiting, abdominal pain, diarrhea, malabsorption, incontinence, and constipation. It covers definitions, the vomiting process, triggers, and various causes of acute and chronic GI problems.

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Pathophysiology of the most common signs and symptoms from the GI tract (Nausea and Vomiting, Abdominal Pain, Diarrhea, Malabsorption, Incontinence, Constipation) Konstantinos Ekmektzoglou MD, PhD, FESBGH Assistant Professor School of Medicine European University Cyprus November 2023 Nausea and V...

Pathophysiology of the most common signs and symptoms from the GI tract (Nausea and Vomiting, Abdominal Pain, Diarrhea, Malabsorption, Incontinence, Constipation) Konstantinos Ekmektzoglou MD, PhD, FESBGH Assistant Professor School of Medicine European University Cyprus November 2023 Nausea and Vomiting Definitions Vomiting: forceful expulsion of stomach contents from the mouth due to involuntary contractions of the abdominal, thoracic and GI (smooth) muscles • spontaneous • provocative Nausea: feeling of wanting to vomit, often associated with autonomic effects like salivation, pallor, sweating • frequently precedes actual vomiting • vomiting does not follow necessarily Retching: a strong, involuntary, unproductive effort to vomit • associated with abdominal muscle contraction but without expulsion of gastric contents through the mouth 3 Vomiting process • Complex process • CNS • ANS • Vomiting center and chemoreceptors • Neurotransmitters • • • • • Acetylcholine Histamine Dopamine Noradrenaline Serotonin • Visceral efferent fibers 4 5 Triggers causing nausea and vomiting Chemotherapeutics Digoxin - L-Dopa Uremia Toxins - Drugs Visceral pain Visceral obstruction Pregnancy Stress Travelers' nausea 4th ventricle chemoreceptors Mucosal chemoreceptors Vagus nerve Vomiting center Vagus nerve Vomiting center Unknown 4 The process of vomiting CTZ stimulation Motor nervous system Parasympathetic nervous system Sympathetic nervous system Heaving or retching before actual vomiting increased salivation Deep breathing preceding the actual vomiting to protect lungs from aspiration Relaxation of the pyloric sphincter that guards the lower end of the stomach to bring up content from the gut Abdominal pressure rises and thoracic pressure lowers The abdominal muscles contract to expel the contents of the stomach Activation of the sympathetic nervous system: sweating, palpitation and rapid heart rate 5 Causes of acute nausea and vomiting in adults Infections Acute hepatitis Acute gastroenteritis Ovarian Torsion Peritonitis Acute Appendicitis Renal colic Acute abdominal pain Biliary colic Acute Pancreatitis Acute Cholecystitis 8 Causes of acute nausea and vomiting in adults Intestinal ileus Ileus Paralytic ileus Volvulus Acute glaucoma Sigmoid torsion Meningitis CNS Diseases CNS tumors Medications Drugs 9 Causes of chronic nausea and vomiting in adults GI Diseases Metabolic Diseases Peptic Ulcer Disease Uremia Pyloric Stenosis Hypercalcemia Gastric/Pancreas Cancer Diabetic gastroparesis Chronic Pancreatitis Diabetic ketoacidosis Superior Mesenteric Artery Syndrome Hyperthyroidism Gastrectomy -> Bile Reflux Gastritis Addison Disease 10 Causes of chronic nausea and vomiting in adults Neuropsychological Diseases Other Migraine Malignant hypertension Labyrinth Diseases Labyrinth Diseases Psychogenic Vomiting Pregnancy Anorexia nervosa Radiotherapy Bulimia nervosa Idiopathic cycling vomiting 11 Vomiting as a Side Effect Medications where vomiting has been reported as a SE in >5% of the cases Cytostatic and chemotherapeutic agents Opioids Hormones Corticosteroids, estrogen Antiasthmatic Antibiotics Theophylline Macrolides, Vancomycin, Sulfonamides, Tetracycline, Isoniazid, Rifabicin Meds used in neurology Amphetamines, L-Dopa Meds used in cardiology B-blockers, digoxin, spironolactone, Ca channel blockers Meds used in gastroenterology (!!!) Sulfasalazine Meds used very often (!!!) ASS, NSAIDs 12 Hyperemesis (excessive vomiting) clinical consequences • Syndrome Mallory-Weiss • Syndrome Boerhaave • Electrolyte and metabolic disorders • Hypovolemia • Hypochloremic metabolic alkalosis • Significant weight loss 13 Work-up History Physical examination Signs and Symptoms Lab tests Imaging 14 History • How long? • Relationship to meals? • Contents of vomitus? • Diabetes? • Other chronic diseases? • Psychiatric disease? • Medications? • When was last menstrual period? • Any previous surgeries? • Alcohol / drugs? Relationship to meals Early morning vomiting Pregnancy Alcoholism Before or during meals Psychogenic vomiting After the meals GI disease (e.g. stomach) 16 Associated symptoms • Vertigo, dizziness, headache, focal neurological symptoms • Chest or abdominal pain • Fever, myalgias • Diarrhea • Jaundice • Weight loss, anorexia 17 Physical Examination • Abdominal exam • Rectal exam • Cardiopulmonary exam • Neurological exam including funduscopic exam (papilledema) • Vital signs • BP and pulse tilt test • Emesis content and odor • Food, blood, bile, feces 18 Laboratory studies • Electrolytes, glucose, BUN/creatinine • Calcium, albumin, total serum proteins • CBC • LFTs • Pregnancy test • Urinalysis • Serum lipase  amylase 19 Additional studies •Tumor markers •Hormones • Ophthalmology exam • ECG 20 Imaging • Plain abdominal films Imaging • Plain abdominal films Imaging • Abdominal ultrasonography or CT if pain is key feature Imaging • EGD • Gastric outlet obstruction / duodenal obstruction • Peptic ulcer disease • Gastroparesis Imaging • Radiopaque marker emptying studies or radionuclide scintigraphy • Diabetic gastroparesis Abdominal Pain Lecture Outline • Causes of abdominal pain • Location of abdominal pain • Types of abdominal pain • Acute abdominal pain • Chronic abdominal pain Abdominal Pain • One of the most common reasons for outpatient and ER visits • A plethora of diseases may present with abdominal pain as the main symptom • An organized approach is needed Abdominal causes of abdominal pain • Esophagitis / GERD • Esophageal spasm • PUD • Gastric outlet obstruction • Bowel obstruction • Intussusception • Bowel perforation • Cancer • CD / UC • Gastroenteritis • Appendicitis • Cholecystitis • Choledocholithiasis • Pancreatitis • Cholangitis • Mesenteric ischemia • AAA rupture • Diverticulitis • Ectopic pregnancy • Pelvic inflammatory disease • Incarcerated Hernia • Hepatitis • Splenic infarct/abscess • IBS Other causes of abdominal pain • Systemic • Infectious –DKA • Thoracic –Strep pharyngitis –Alcoholic ketoacidosis – Myocardial (more often in infarction/ Unstable –Uremia children) angina –Sickle cell disease –Rocky Mountain –Pneumonia –Porphyria Spotted Fever –Pulmonary embolism –SLE –Mononucleosis –Herniated thoracic –Vasculitis • Abdominal wall disc (neuralgia) –Glaucoma –Muscle spasm • Genitourinary –Hyperthyroidism –Muscle hematoma –Nephrolithiasis / UTI • Toxic –Herpes zoster –Testicular torsion –Methanol poisoning –Renal colic –Heavy metal toxicity –Scorpion bite –Black widow spider bite Abdominal Pain Location Types of Abdominal Pain •Visceral –Crampy, achy, diffuse –Poorly localized •Somatic –Sharp, cutting, stabbing –Well localized •Referred –Distant from site of generation –Symptoms, but no signs Visceral Pain • Stretching of nerve fibers of walls or capsules of organs • Crampy – Dull - Achy • Often unable to lie still • Bilateral innervation • Foregut organs (stomach, duodenum, biliary tract) produce pain in the epigastric region • Midgut organs (most small bowel, appendix, cecum) cause periumbilical pain • Hindgut organs (most of colon, including sigmoid) as well as the intraperitoneal portions of the genitourinary tract cause pain initially in the suprapubic or hypogastric area. Parietal Pain • Irritation of fibers that innervate the parietal peritoneum • Usually anterior abdominal wall • Localised to the dermatome superficial to the site of painful stimulus Pain evolution Visceral Parietal • Non specific • • • • Localised tenderness Guarding Rigidity Rebound Referred Pain • Pain or discomfort perceived at a site distant from the affected organ because of overlapping transmission pathways • Reflects embryologic origin Referred Pain • subdiaphragmatic irritation • ipsilateral supraclavicular or shoulder pain • gynecologic pathology • back or proximal lower extremity pain • biliary tract disease • right infra-scapular pain • myocardial ischemia • mid-epigastric, neck, jaw, or upper extremity pain • ureteral obstruction • ipsilateral testicular pain Acute abdominal pain • Less than a couple weeks • Usually present since days to hours • Don’t forget about the chronic pain that has acutely worsened • Usually immediate attention is required • Surgical vs. nonsurgical Chronic abdominal pain • Present for months to years • Usually not life threatening • Outpatient work-up • Constipation, IBS, dyspepsia the most common causes… • Diagnosis easily in younger patients, but pay attention in patients >55 years old Approach to the patient • History: of PARAMOUNT importance • Location, quality, severity, radiation, exacerbating or alleviating factors, associated symptoms • Medical history • including sexual and menstrual • Social history • including alcohol, drugs, domestic abuse, stressors, travel etc. • Family history • IBD, cancers, etc • Medication • Chronic and recent History: what to ask for O: P: Q: R: S: T: onset provocation /palliation quality/quantity region/radiation severity/scale timing/time of onset History: associated symptoms • Gastro – intestinal • • • • Nausea Vomiting Dyspepsia Change in bowels • Genitourinary • Gynaecologic • Weight loss • Bleeding History: complementary elements • Medical History • • • • • DM HT Liver Disease Renal Disease Sexually Transmitted Infections • Surgical History • Abdominal Surgery • Pregnancies • Deliveries/ Abortions/ Ectopic • Trauma • Consultations/ Presentations • Meds • NSAIDs • Steroids • OCP/ Fertility Drugs • Narcotics • Immunosuppressant • Chemotherapy agent • Allergies • Contrast • Analgesic Physical examination • Vitals (incl postural) -> always document!!! • General appearance • Systematic physical examination • Jaundice, signs of chronic liver disease • Costovertebral angle tenderness • Abdominal exam • FIRST Look, THEN listen, THEN feel • Digital Recta Examination • Pelvic exam, Genito-Urinary examination • Musculoskeletal examination Physical examination • Lots of bedside information • Distressed vs. non distressed • Lying still -> peritonitis • Writhing -> renal Colic Laboratory tests •Labs • CBC, electrolytes, BUN, Cr, coagulation • Amylase and lipase, LFTs • Urine analysis • B-Human chorionic gonadotropin • Lactate • Toxin-drug screen • H. pylori serology • FOBT • ECG • anyone with upper abdominal pain or elderly Imaging • Imaging • Plain films • Computer tomography • Ultrasound • MRI • Angiography • Endoscopy • EGD • Colonoscopy • ERCP/EUS Radiology • Plain film • Exclude perforation • Exclude small bowel obstruction Radiology • Plain film • Useful for renal stones, but CT is the primary investigation modality Abdominal Ultrasound • Biliary Disease • Gynecologic complaints • Rule out ectopic pregnancy • Appendicitis in children • No radiation Computer tomography • CT is accurate for: • Renal colic • Appendicitis • Diverticulitis • AAA • Intra-abdominal abscesses • Mesenteric Ischaemia • Bowel Obstruction • Avoid repeated CT scans • Limit use in younger patients • Avoid where possible in pregnant females Acute (surgical) abdomen • The first thing to be considered in acute abdominal pain • Early identification is very important • prognosis worsens rapidly with delay • Important to get surgeons involved early if this is even mildly suspected • This is a clinical diagnosis • Presentation is usually bad • Fevers, tachycardia, hypotension • Tender abdomen, possibly rigid • Presentation can vary with other demographic and medical factors • Advanced age • Immunosuppression Acute abdomen Most common causes • • • • • Acute appendicitis Acute cholecystitis Acute pancreatitis Diverticulitis Acute peritonitis • rupture of a hollow viscus or as a complication of inflammatory bowel disease or malignancy • • • • • • Mesenteric ischemia Ruptured abdominal aortic aneurysm Ruptured ectopic pregnancy Ovarian torsion Ureteral colic -pyelonephritis Small bowel obstruction Acute abdomen • Work-up • Start with stat labs • Surgical abdominal series (plain films) • Consider stat CT if readily available • Sometimes patients go straight to surgery • Surgeons should get involved early • guidance and early intervention Special populations Elderly • May lack physical findings despite serious pathology • Reduced diagnostic accuracy • Risk of Vascular Catastrophes • Assume surgical cause until proven otherwise • 30-40% of elderly with acute abdominal pain need surgery • Biliary Disease is the commonest cause Special Populations Women of Childbearing Age • PREGNANCY should be always included in DD • B-Human chorionic gonadotropin in all women of childbearing age and acute abdominal pain • Lactate • Atypical clinical presentations due to gravid uterus that displaces intra-abdominal organs • Pregnant women still get common surgical abdominal conditions • Cholecystitis • Choledocholithiasis - cholangitis Diarrhea Definition •Diarrhea is defined as painless loose or watery stools during ≥75% of defecations for the prior 3 months, with symptom onset at least 6 months prior todiagnosis •Stool volume may increase to >200 g in 24 hours. However… • Collecting and weighing stools is neither practical nor required except in a clinical researchsetting • A good working definition is three or more loose or watery stools perday • A definite decrease in consistency and increase in frequency based upon anindividual baseline • Acute(<14 days)or chronic(>30 days) Key questions duringhistory • Duration? • Acute diarrhea up to 2 weeks /Chronic diarrhea lasting 4 weeks or more • Characteristics? • volume, frequency, consistency • Presence of mucus, pus, orblood? • Associated tenesmus? • a constant urgency to defecate, accompanied by pain, cramping, andinvoluntary straining • • • • • • • Does diarrhea occur at night? Are the stools greasy or oily? Frothy? Foul-smelling? Floating on the surface? Medications? Recent travel? Diet patterns? Baseline bowel habits? Risk factors for immunocompromise? Small bowel vs.colon Small bowel • watery diarrhea • large volume • abdominal cramping • bloating, gas, weight loss • Rarely fever • No blood orinflammatory cells Colon • frequent and regular • small volume • often painful bowel • fever may be present • bloody or mucoidstools Acute diarrhea • Diarrhea = increased water content of the stool • impaired water absorption • active water secretion by thebowel • In severe infectious diarrhea, > 20 /day • defecation occurring every 20 or 30 minutes • Total daily volume of stool may > 2 liters • volume depletion and hypokalemia • Most patients with acute diarrhea • 3 - 7movements per day • stool volume < 1 liter/day Etiology • Mostcases of acute infectious gastroenteritis are probably viral • stool culture has been positive in only 1.5 to 5.6% • In contrast, bacterial causes are responsible for most cases of severediarrhea • Protozoa are less commonly identified as the etiologic agents of acute gastrointestinalillness Etiology Infectious origin Bacteria Salmonella Campylobacter Shigella Escherichia coli 0157:H7 Clostridium difficile Non- infectious origin Virus Norovirus Adenovirus Rotavirus Protozoa Cryptosporidium Giardia Cyclospora Entamoeba histolytica Drugs Food allergies IBD Thyrotoxicosis Carcinoid syndrome Acute Diarrhea – General Approach •Careful history to determine symptoms’duration •Frequency and stoolcharacteristics •Signs of extracellular volumedepletion • decreased skin turgor, orthostatic hypotension •Fever and peritonealsigns • invasive enteric pathogen Acute Diarrhea - FurtherEvaluation? • Profuse watery diarrhea with signs of hypovolemia • Small volume stools with blood and mucus • Bloody diarrhea • Fever • Six unformed stools per day; illness duration >48h • Severe abdominal pain • Recent use of antibiotics or hospitalized patients • Elderly (70 years of age) or immunocompromised Responsible pathogens persite Small Bowel Colon Bacteria Salmonella Escherichia coli Clostridium perfringens Staphylococcus aureus Aeromonas hydrophila Bacillus cereus Vibrio cholera Campylobacter Shigella Clostridium difficile Yersinia Vibrio parahaemolyticus Enteroinvasive E. coli Plesiomonas shigelloides Viruses Rotovirus Norovirus Cytomegalovirus* Adenovirus Herpes simplex virus Protozoa Cryptosporidium* Entamoeba histolytica Microsporidium* Isospora Cyclospora Giardia lamblia Foodborne acute diarrhea -Timing • Symptoms that begin within six hours suggest ingestion of a preformed toxin of Staphylococcus aureus or Bacillus cereus • Symptoms that begin at 8 to 16 hours suggest infection with Clostridium perfringens • Symptoms that begin at more than 16 hours can result from viral or bacterialinfection • Food contamination with enterotoxigenic orenterohemorrhagic E. coli • Recent antibiotic use • Search for Clostridium difficile Diagnostic Approach •Blood and white cells instool • Low sensitivity, suggestive of invasivebacteria (?) •Stool cultures • Immunocompromised patients, severe,inflammatory diarrhea underlying IBD •Ova and Parasite studies • Persistent diarrhea +/- travel to specialregion • Persistent diarrhea with exposure to infants in daycare centers • MSM, patients withAIDS • Community waterborne outbreak • Bloody diarrhea with few or no fecal leukocytes • intestinal amebiasis Diagnostic Approach • Endoscopy is usually NOTneeded • IBD vs. infectious diarrhea ->biopsies • Diagnosing C. difficile infection (pseudomembranes) in patientswho are toxic and tissue culture assays results pend • Decreased need for endoscopy due to ELISA for C. difficile toxins A and B • In immunocompromised patients (egCMV) • Suspicion of ischemic colitis with unclear diagnosis after clinical and radiologic assessment Treatment Oral rehydration solutions Empiric antibiotic therapy Symptomatic Treatment Antibiotic TreatmentIndications • moderate to severe travelers' diarrhea (>4 stools /d, fever, blood, pus, or mucus in the stool) • > 8 stools /day, volume depletion, symptoms > 1 week • Immunocompromised • bacterial diarrhea with fever, bloody diarrhea • NO for suspectedEHEC • empiric therapy: oral fluoroquinolone • E.g. ciprofloxacin 500 mg twice daily, 3-5days Symptomatic Treatment • Loperamide (Imodium): symptomatic treatment of patients with acute diarrhea when NO fever and NO bloody stools • 4 mg) initially, then 2 mg after each unformed stool • Maximum 16 mg/day for 2 days. Dietary Recommendations • Adequate nutrition is important • enterocyte renewal • Short period of consumingonly liquids • Boiled starches and cereals (eg, potatoes, noodles, rice, wheat, and oat) • Gradual reinsertion of allfoods Approach ToThe Patientwith ChronicDiarrhea Sub-types ofDiarrhea • Osmotic • Secretory • Motility Induced Chronicdiarrhea • Osmotic Diarrhea: solutes • Carbohydrates, laxatives • Secretory Diarrhea: • Defects in ion absorption • Cl-/HCO3- or NA+/H+ exchange • Abnormal mediators: cAMP, cGMP,etc • Motility induced Diarrhea • Rapid transit leads to decreasedabsorption • Inflammatory Diarrhea • Inflammation and ulceration compromise the mucosalbarrier • Mucous, protein, bloodreleased into the lumen • absorption diminished Osmotic Diarrhea • Lactose-Dairy products • Sorbitol-Sugar free gum, fruits • Fructose-Soft drinks, fruit • Magnesium-Antacids • Laxatives-Citrate, NaSulfate Osmotic Diarrhea History • Ask about ingestionpf: • Laxatives, unabsorbed carbohydrates, magnesium containing products • Can be watery or loose • No blood, minimal cramping, nofever! • Diarrhea stops when patientfasts! • Stool analysis • Osmotic gap > 125 Osmotic Diarrhea Work-up • Stool electrolytes (Na+ andK+) • Stool osmolality • pH • NOT FEASIBLE in everyday clinicalpractice • HISTORY is the key! • Remove potential etiology factor SecretoryDiarrhea History • Diarrhea is usually watery • Non-bloody • Persistent during fast • Non-cramping SecretoryDiarrhea Causes Causes of Dysmotility Diarrhea Irritable bowel syndrome Carcinoid syndrome Resection of the ileo-cecalvalve Hyperthyroidism Post gastrectomy syndromes Constipation Constipation as causeof Dysmotility Diarrhea • “Overflow” diarrhea • Extremely common! • Often in elderly with fecalincontinence • Fiber enriched diet, fleet • Colon cancer • Partial obstruction due tomass • Recent alteration in bowel habits, lower abd pain • >55 years Inflammatory Diarrhea • Inflammatory bowel disease • Celiac Disease • Chronic infections • Amoeba • C. Difficile, aeromonas • Other parasites • HIV, CMV, TB, InflammatoryDiarrhea History • Bloody diarrhea • Tenesmus, cramping • Fever, malaise, weight loss • Family History of IBD? • Recent Travel abroad? Modern Sub-types ofDiarrhea • Inflammatory • IBD, parasitic infections, fungal, TB, viral, Sprue(?),rare bacteria • Watery • Secretory, osmotic and some motilitytypes • Fatty • Pancreatic insufficiency, sprue, bacterial overgrowth, large small bowel resections FattyDiarrhea • Malabsorption • pancreatic disease • bacterial overgrowths • Sprue • Greasy, floating stools • Measure 24 hourfecal fat • > 5g per day = fat malabsorption Chronic Diarrhea GeneralApproach • History • Inflammatory, watery orfatty? • Are there any obviousassociations? • Foods (lactose!), candies, medications, travel,stress, medications Is the patientconstipated? Is there any weight loss or abdominal pain? Are there any night timesymptoms? Familyhistory? • IBD, IBS • Are there any other medicalconditions? • Thyroid, DM, Collagenvascular • • • • Chronic Diarrhea PhysicalExamination •Vital Signs, general appearance •Abdomen – tenderness, masses, organomegaly •Rectal exam – Sphincter tone and squeeze •Skin – rashes, flushing, •Thyroid mass?? •Edema? ChronicDiarrhea Work-up (Initial) • Address any obvious causes!!! • Labs • CBC, Chemistry, • Stool analysis • Wt., Na+, K+, osm, pH, Fat assessment(sudan) • O&P, C Diff. stool? WBC? Chronic Diarrhea Work-up(Further) •If subtype not clear… •Stool elastase, TTG,Anti-EMA •Colonoscopy/FS and EGD with SB biopsy •CT Scan, SBFT etc When to Refer aPatient? Inflammatory Watery Fatty Refer to GI Wait labs Refer to GI Secretory Treat infection Treat IBS Osmotic Stop offending agent However… Consider fecal incontinence Consider constipation Consider IBS Minimal work-up. Malabsorption Normal nutrient absorption requires 3 steps: • Luminal and brush border processing • Absorption into the intestinal mucosa • Transport into the circulation. An impairment in intestinal absorption and functioning is known as intestinal insufficiency or deficiency intestinal insufficiency or deficiency is a decrease in gut absorptive function not requiring iv supplementation for health and/or growth maintenance • Malabsorption is impaired absorption of nutrients caused by any disruption in the process of normal absorption • Impaired digestion of nutrients within the intestinal lumen or at the brush border membrane can also interfere with nutrient absorption. • This is known as maldigestion. Malabsorption and maldigestion differ pathophysiologically but the processes of digestion and absorption are interdependent. Therefore, in clinical practice, malabsorption refers to deficiencies in the process of both absorption and digestion. malabsorption disorders can originate from the • Liver • Pancreas • Stomach • Intestines Absorption into the Intestinal Mucosa Acquired cases of malabsorption in the mucosal absorptive phase may include • A brush border enzyme deficiency • a brush border transport deficiency, • or an enterocyte defect. Lactase is an enzyme present in the brush border membrane of the small intestine. Lactose, hydrolyzed by lactase, is found in mammalian milk. Most humans’ lactase activity declines after age 2 to 3 years. Only about 35%can digest lactose beyond the age of 7 to 8 years. Lactose malabsorption refers to low lactase activity without symptoms. Lactose intolerance is defined when the malabsorption causes symptoms. Transport into the Circulation • Transport of absorbed nutrients into the general circulation is the final stage of absorption. • Lipid transport depends on the lymphatic system. Obstruction in the lymphatic system can impair absorption of lipoproteins and lead to • fat malabsorption • steatorrhea, • chylous ascites and/or • protein-losing enteropathies Primary intestinal lymphangiectasis, secondary obstructions from lymphoma, and infectious causes such as Whipple disease are all possible causes of lymphatic obstruction. Incontinence Definition • recurrent frequent uncontrolled leakage of stool and/or stool staining for more than 1 month Incidence • 1,4-18% • higher in middle-aged women, elderly and nursing patients • Gas – soft or liquid stool – solid stool • Passive or with awareness • Mild - moderate - severe Pathophysiology • Abnormal Anorectal or Pelvic Floor Structures • • • • • Anal sphincter muscles Puborectalis muscle Pudendal nerve NS, ANS, spina cord Rectum • Abnormal Anorectal or Pelvic Floor Function • Impaired anorectal sensation • Fecal impaction • Altered Stool Characteristics • Increase volume, loose consistency, hard stools, retention • Miscellaneous • Physical mobility, cognitive function • Drugs, psychosis • Food intolerance Constipation Definition Constipation • infrequent, difficult passage of stool with the sensation of incomplete bowel emptying Prevalence • 14% in the general population • 30% more common in non-white population • more common in women (3:1) The definition of chronic constipation has evolved to encompass more than a decreased number of stools per week. It includes a constellation of symptoms such as: • excessive straining • a sense of incomplete evacuation • failed or lengthy attempts to defecate • use of digital manoeuvres for evacuation of stool • abdominal bloating • hard consistency of stools Classification By course • Acute By etiology • • Bowel obstruction • Primary (functional) • Poor diet and insufficient exercise • Slow transit time Chronic • Secondary • • • • • Mechanical Drugs Endocrine Neurological Connective tissue disorders Secondary constipation Mechanical Drugs Endocrine/Metabolic Neurological CRC, diverticulosis, strictures, volvulus hemorrhoids, opiates , iron supplements, antacids, anticholinergics, antidepressants, CCB hypothyroidism, DM hypokalemia, hyperparathyroidism Multiple sclerosis, diabetic neuropathy, stroke, Hirschsprung, Parkinson, Chagas (megacolon), botulism Connective Tissue Disorders scleroderma, amyloidosis IBS colonic Constipation Assessment • History • dietary habits • medication use • Mobility • stool character and frequency • problems with defecation • anorectal pain In children delayed passage of meconium?? (e.g., Hirschsprung disease) voluntary withholding of stool (e.g., squatting, crying, crossing ankles, hiding) fecal (overflow) incontinence Functional Constipation (Rome IV criteria) • At least two of the following must have occurred in ≥ 1/4 of defecations during the past 12 weeks with onset of symptoms ≥ 6 months ago: • Passage of stool < 3 times/week • Passage of hard or lumpy stool • Sensation of anorectal obstruction/blockage • Manual aid to evacuate stool • Straining during attempts to defecate • Sensation of incomplete evacuation Constipation Physical Examination •Inspect the anorectal area • Fissures • Hemorrhoids •Anal wink reflex • Anal contraction when a cotton pad runs along all 4 quadrants around anus • Absence suggestive of pathology (sacral nerve injury) •Digital rectal examination • Mass (CRC?, fecal impaction?) • Sphincter tone (pelvic floor dysfunction) Constipation Further Investigation • Laboratory • Electrolytes (exclude hypokalemia) • Hormones (TSH, hypothyroidism) • Glucose (diabetes) • Imaging • X-ray, radiopaque markers for slow transit constipation • Colonoscopy • Especially if alarm symptoms, age >50, acute onset Constipation Alarm Features • Family history (e.g. CRC, IBD) • Iron deficiency anemia • Blood in stool • Palpable abdominal mass • Reduced stool caliber • Rectal prolapse • Significant unexplained weight loss • Sudden onset of new change in bowel habit • Persistent constipation, despite treatment • > 50 years of age and no previous screening for colorectal cancer Constipation Treatment • Diagnose and treat any underlying conditions. • Adults (step-up approach) • Lifestyle changes • high-fiber diet (psyllium seed husk, wheat bran) • increased fluid intake • exercise • Administer osmotic laxatives • Stimulant laxatives • Biofeedback training • helpful in treating disturbances in defecation

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