Incidence of GI/GU Disorders

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Presentation transcript:

Gastroenterology “A Cute Abdomen” Dr Baxter Larmon Professor UCLA School of Medicine

Incidence of GI/GU Disorders Every year about 62 million people are diagnosed with a gastrointestinal disorder. The incidence and prevalence of most digestive diseases increase with age, although there are exceptions.

Morbidity & Mortality of GI/GU Disorders In 1992, GI disorders cost nearly $107 billion in direct health care expenditures. Currently, GI disorders result in nearly 200 million sick days, 50 million visits to a physician, 16.9 million days lost from school, 10 million hospitalizations, And nearly 200,000 deaths per year.

General Pathophysiology General Risk Factors Excessive Alcohol Consumption Excessive Smoking Increased Stress Ingestion of Caustic Substances Poor Bowel Habits Emergencies Acute emergencies usually arise from chronic underlying problems.

Etiology of Pain Inflammation Foreign chemical Bacterial contamination Stimulation of nerve endings. Irritation Stretching, distention, bleeding

Visceral vs. Somatic Visceral pain Somatic pain Caused by stimulation of autonomic nerve fibers that surround a hollow viscus Cramping or gas type Generally diffuse drill Somatic pain Produced by Bacterial or chemical irritation of autonomic nerve Guarding Don’t want to move Superficial

Solid Organs Dull and steady in nature. More localized. Bleeding Within capsule, Rupture;

Hollow Organs Colicky, crampy, dull, or gassy, Typically intermittent. Diffuse and poorly localized. Path of a tube. The place where the patient is feeling the most pain may not be the most tender on palpation.

Hollow Organs Usually associated with Bleeding nausea, vomiting, tachycardia, diaphoresis; Bleeding within the organ itself;

Referred Pain Definition Cause Pain in area removed from tissue that caused the pain Caused by visceral fibers that synapse in the spinal cord Cause same spinal segment, skin has more receptors, unable to distinguish,

Referred Pain NOT ALL ABDOMINAL PAIN IS OF ABDOMINAL ETIOLOGY.

General Assessment Scene Size-up & Initial Assessment Scene clues. Identify and treat life-threatening conditions. Focused History & Physical Exam Focused History Obtain SAMPLE History. Obtain OPQRST History. Associated symptoms Pertinent negatives

General Assessment Physical Exam General assessment and vital signs Abdominal assessment Inspection, Auscultation, and Palpation, Percussion Cullen’s Sign: Discoloration around the umbical area Grey-Turner’s Sign: Discoloration in the flank area

Let’s Review a Physical Exam of the Abdomen

General Treatment Maintain the airway. Support breathing. High-flow oxygen or assisted ventilations. Maintain circulation. Monitor vital signs and cardiac rhythm. Establish IV access. Transport in position of comfort.

Specific Illnesses The Gastrointestinal System Upper Gastrointestinal Tract Lower Gastrointestinal Tract Liver Gallbladder Pancreas Appendix

Upper Gastrointestinal Bleeding Causes Peptic Ulcer Disease Gastritis Esophagitis Duodenitis

Upper Gastrointestinal Bleeding Etiology PERCENT Peptic Ulcer 45 Gastric erosions 23 Varices 10 Mallory-Weiss Tear 7 Esophagitis 6 Duodenitis Other 2

Upper Gastrointestinal Bleeding Signs & Symptoms General abdominal discomfort Hematemesis and melena Classic signs and symptoms of shock Changes in orthostatic vital signs Treatment Follow general treatment guidelines. Begin volume replacement using 2 large-bore IVs. Differentiate life-threatening from chronic problem.

Esophageal Varices Cause Portal Hypertension Chronic alcohol abuse and liver cirrhosis Ingestion of caustic substances

Esophageal Varices Signs & Symptoms Treatment Hematemesis, Dysphagia Painless Bleeding Hemodynamic Instability Classic Signs of Shock Treatment Follow General Treatment Guidelines. Aggressive Airway Management Aggressive Fluid Resuscitation

Acute Gastroenteritis Cause Damage to Mucosal GI Surfaces Pathologic inflammation causes hemorrhage and erosion of the mucosal and submucosal layers of the GI tract. Risk Factors Alcohol and tobacco use Chemical ingestion Systemic infections

Acute Gastroenteritis Signs & Symptoms Rapid Onset of Severe Vomiting and Diarrhea Hematemesis, Hematochezia, Melena Diffuse Abdominal Pain Classic Signs of Shock Treatment Follow General Treatment Guidelines. Fluid Volume Replacement. Consider Administration of Antiemetics.

Peptic Ulcers Pathophysiology Erosions caused by gastric acid. Terminology based on the portion of tract affected. Causes: Alcohol/Tobacco Use H. pylori

Peptic Ulcers Signs & Symptoms Treatment Abdominal Pain Observe for signs of hemorrhagic rupture. Acute pain, hematemesis, melena Treatment Follow general treatment guidelines. Consider administration of histamine blockers and antacids.

Lower Gastrointestinal Bleeding Pathophysiology Bleeding distal to the ligament of Treitz Causes Diverticulosis Colon lesions Rectal lesions Inflammatory bowel disorder

Lower Gastrointestinal Bleeding Signs & Symptoms Determine acute vs. chronic. Quantity/color of blood in stool. Abdominal pain Signs of shock. Treatment Follow general treatment guidelines. Establish IV access with large-bore catheter(s).

Crohn’s Disease Pathophysiology Inflammatory bowel disease, ? Autoimmune etiology Can affect the entire GI tract. Pathologic inflammation: Damages mucosa. Hypertrophy and fibrosis of underlying muscle. Fissures and fistulas.

Crohn’s Disease Signs and Symptoms Treatment Difficult to differentiate. Clinical presentations vary drastically. GI bleeding, nausea, vomiting, diarrhea. Abdominal pain/cramping, fever, weight loss. Treatment Follow general treatment guidelines.

Diverticulitis Pathophysiology Signs & Symptoms Treatment Inflammation of small outpockets in the mucosal lining of the intestinal tract. Common in the elderly. Diverticulosis. Signs & Symptoms Abdominal pain/tenderness. Fever, nausea, vomiting. Signs of lower GI bleeding. Treatment General treatment guidelines.

Hemorrhoids Pathophysiology Signs & Symptoms Treatment Mass of swollen veins in anus or rectum. Idiopathic. Signs & Symptoms Limited bright red bleeding and painful stools. Consider lower GI bleeding. Treatment General treatment guidelines.

Bowel Obstruction Pathophysiology Blockage of the hollow space of the small or large intestines Hernias

Bowel Obstruction OR Pathophysiology Occlusion of the intestinal lumen that results in blockage of the normal flow of intestinal fluids OR

Bowel Obstruction Pathophysiology Twisting of the bowel

Bowel Obstruction Pathophysiology Adhesions

Bowel Obstruction Signs & Symptoms Treatment Decreased Appetite, Fever, Malaise Nausea and Vomiting Diffuse Visceral Pain, Abdominal Distention Signs & Symptoms of Shock Treatment Follow general treatment guidelines.

Accessory Organ Diseases GI Accessory Organs Liver Gallbladder Pancreas Appendix

Appendicitis Pathophysiology Inflammation of the vermiform appendix. Frequently affects older children and young adults. Lack of treatment can cause rupture and subsequent peritonitis.

Cholecystitis Pathophysiology Inflammation of the Gallbladder Cholelithiasis Chronic Cholecystitis Bacterial infection Acalculus Cholecystitis Burns, sepsis, diabetes Multiple organ failure

Pancreatitis Pathophysiology Inflammation of the Pancreas Classified as metabolic, mechanical, vascular, or infectious based on cause. Common causes include alcohol abuse, gallstones, elevated serum lipids, or drugs.Viral Hepatitis A viral inflammatory disease: 1. Hepatitis A Virus (HAV), 2. Hepatitis B Virus (HBV), 3. Hepatitis C Virus (HCV) aka non-A, non-B hepatitis, 4. Hepatitis D Virus (HDV) only occurs in individuals with HBV, 5. Hepatitis E Virus (HEV).

Cirrhosis Infection Toxins Altered immune response; Viral hepatitis Toxins ETOH Altered immune response; Vascular disturbance;

Urology & Nephrology

Anatomy & Physiology Ureters Urinary Bladder Urethra Testes Epididymus and Vas Deferens Prostate Gland Penis

General Mechanisms of Nontraumatic Tissue Problems Inflammatory or Immune-Mediated Disease Infectious Disease Physical Obstruction Hemorrhage

General Pathophysiology, Assessment and Management Differentiating GI and Urologic Complaints Pathophysiologic Basis of Pain Causes of Pain Types of Pain Visceral pain Referred pain

Renal and Urologic Emergencies Risk Factors Older Patients History of Diabetes History of Hypertension Multiple Risk Factors Renal and Urologic Emergencies Acute Renal Failure Chronic Renal Failure Renal Calculi Urinary Tract Infection

Acute Renal Failure Pathophysiology Prerenal Acute Renal Failure Dysfunction before the level of kidneys Most common and most easily reversible Renal Acute Renal Failure Dysfunction within the kidneys themselves Postrenal Acute Renal Failure Dysfunction distal to the kidneys

Acute Renal Failure Assessment Focused History Change in urine output Swelling in face, hands, feet, or torso Presence of heart palpitations or irregularity Changes in mental function

Acute Renal Failure Physical Assessment Altered mental status Hypertension Tachycardia ECG indicative of hyperkalemia Pale, cool, moist skin

Acute Renal Failure Physical Assessment Edema of face, hands, or feet Abdominal findings dependent on the cause of ARF

Renal Calculi Pathophysiology Results when “too much insoluble stuff” accumulates in the kidneys. Stone types Calcium salts Struvite stones Uric acid Cystine

Renal Calculi Assessment Focused History Physical Exam Severe pain in one flank that increases in intensity and migrates from the flank to the groin Painful, frequent urination with visible hematuria Prior history of calculi Physical Exam Difficult due to patient discomfort Tachycardia with pale, cool, and moist skin

Urinary Tract Infection Pathophysiology Risk Factors Increased risk in female or catheterized patients Sexual activity Lower and Upper UTIs Urethritis Cystitis Prostatitis Pyelonephritis Community-acquired vs. nosocomial infections

Urinary Tract Infection Assessment Focused History Abdominal pain Frequent, painful urination A “burning sensation” associated with urination Difficulty beginning and continuing to void Strong or foul-smelling urine Similar past episodes

Thanks for listening Blarmon@mednet.UCLA.edu