Lecture 8 Gastrointestinal diseases Flashcards
ESOPHAGEAL
Normal Function
Transport food from mouth to stomach, peristalsis, prevent backflow
Interfered by obstruction, dysfunction, punching, reflux/regurg
ESOPHAGEAL
Obstruction
Foreign objects, nodes, cancers, etc.
S/Sx:
Dysphagia (w/ solids, liquids as it progresses)
Chest pain/angina like
Regurgitation of undigested food
Has not reached the stomach yet!
Muscle/Innervation Dysfunction PNS -> rest/digest
PNS input compromise -> disruption of sensory or motor pathway
Muscle/Innervation Dysfunction Failure to contract
Dilation d/t collagen structure damage (scleroderma, connective tissue dx., Chagas dx)
Muscle/Innervation Dysfunction Failure to Relax
Diffuse spasms
Can present as chest pain/angina
Achalasia (Contract & Relaxation Issue)
Triad of S/Sx
Incomplete LES (lower esoph sphincter) relaxation
Increased LES tone
Aperistalsis of lower ⅔ of esophagus
Barium swallow test -> bird beak; dilated, tortuous esophagus
Diverticula
Outpouching of esophagus
Obstruction increases contractions (where its closest to the obstruction)
Leads to wall weakness
Congenital or lymph node related
Pulsion Diverticulum
Proximal to obstruction
Zenker Diverticulum
Behind upper esophageal sphincter
Reflux general
Backwash of acid through LES
Burning of esophageal mucosa -> esophagitis
Reflux etiology
Incompetent sphincter
Hernial distortion
Excess pressure from impaired stomach emptying
reflux s/s
Worse when bending over or lying down after eating
Heartburn
Epigastric pain
Chest pain
Sour, bitter taste in mouth d/t stomach contents
Complications
Barrett’s Esophagus -> metaplasia of epithelium d/t damage -> esophageal adenocarcinoma
Esophagitis
Etiology
Medications (chemo)
Radiation
Crohn/s Dx
Infection
Esophageal Varices
Varix: abnormal dilation of artery, vein, lymphatic vessel
Increased risk for rupture causing esophageal bleeding
Esophageal Varices etiology
Liver disease, portal HTN
Esophageal Varices s/s
Asymptomatic until there is rupture
Hematemesis
HypoTN Sx
Tachy
Abdominal bloating
Severe -> hypovolemic shock
Esophageal Cancer histology/etiology
Adenocarcinoma
GERD-induced Barrett’s esophagus is precursor
Squamous Cell Carcinoma
Smoking and alcohol is precursor
Esophageal Cancer s/s
Dysphagia
Indigestion
Reduced appetite, regurgitation
Chronic cough, hoarseness
Respiratory sx if trach becomes compressed
STOMACH General
Normal -> produce acid to break down food, produce intrinsic factor for Vitamin B12 absorption, digested food through pyloric sphincter to duodenum
Stomach parietal cells
Pump H+ into stomach in exchange for K+
Stimulated by gastrin, histamine, acetylcholine
Inhibited by somatostatin, prostaglandin, secretin, VIP
Makes sure not too acidic when entering the small intestine
stomach mucus cells
protective layer, regulated by prostaglandin
Acute Gastritis etiology
NSAIDS, alcohol, bile
Uremia, decreased O2 delivery, ingestion of harsh chemicals
Acute Gastritis s/s
Epigastric pain
N/V
Severe -> mucosal erosion, ulceration, hemorrhage
Peptic Ulcer Disease (PUD) etiology
Decreased Mucosal Protection
Prolonged NSAID use (decreases prostaglandin fxn)
Cox-2 inhibitors
Tobacco/alcohol
Stress Related Mucosal Disease -> physiological (ischemia, shock from sepsis, burns and hemorrhage)
Many inpatients get anti-ulcer prophylaxis
Decrease in perfusion
Increased Acid Secretion
Zollinger Ellison Syndrome
Increased gastrin (increases acid pdxn and ulceration multi-site)
Peptic Ulcer Disease (PUD) Dx
secretin injection -> if pancreas is normal, no change to gastrin secretion (if not normal, see a paradoxical increase in gastric acid)
Peptic Ulcer Disease (PUD) sx
Pain IMMEDIATELY after eating -> gastric ulcer
Relief with vomiting + antacids (acidity going down)
Pain HOURS after meal -> duodenal ulcer
Relief with eating
Epigastric pain
N/V
Melena (black stool)
Appetite changes
Severe/perforation of duodenal or gastric wall
Acute abd pain, air under diaphragm, visible on radiograph
Peptic Ulcer Disease (PUD) Tx
Neutralize acids
PPI (omeprazole) to inhibit parietal cells
Decrease parietal cell stimulation by H2 blockers (histamine stimulates acid release)
Vagotomy to sever vagus nerve PNS input to acid secretion
Increase mucosal defense
Sucralfate viscous gel barrier
Prostaglandins decrease stomach acid
Antibiotics for H.Pylori
Peptic Ulcer Disease (PUD)
Bleeding -> may be first indication of ulcer
Perforation -> rarely first indication of ulcer
Obstruction
Secondary to edema or scarring, mostly in chronic ulcers
Duodenal ulcers more likely to obstruct food vs gastric
D/t less area for food to move!
Chronic Gastritis etiology
Autoimmune
Radiation
Mechanical injury (NG tube)
Crohns
Reflux of bile or pancreatic secretion
Chronic Gastritis complications
Mucosal atrophy
Intestinal metaplasia
Dysplasia
Gastritis cystica
Loss of Intrinsic Factor general
Normally If is produced from parietal cells
Type II Hypersensitivity
Pernicious anemia
Autoimmune gastritis -> antibodies form against parietal cells
Loss of Intrinsic Factor s/s
Megaloblastic anemia
Atrophic glossitis (smooth beefy red tongue)
Malabsorptive diarrhea
CNS changes
Marrow deficiency
Obstruction etiology
Foreign body
Gastric polyp
Gastric cancer
External -> pancreatic tumor
obstructions s/s
Vomiting
Early satiety
Abdominal distention
Congenital Pyloric Stenosis
Projectile vomiting after feeding, frequent refeeding demand
Palpable olive like mass
Visible waves of peristalsis (stomach tries to overpower stenosis but fails)
Gastroparesis general
Paralysis of the stomach
Gastroparesis etiology
Nerve damage (ex. Diabetic neuropathy)
Acetylcholine blockers
Since PNS nerves release Ach at the synapse
Drugs that decrease gastric motility (opioids)
Gastroparesis s/s
Indigestion
Bloating
Early satiety; prolonged; loss appetite
Upper abdominal pain
N/V
Regurgitation of partially undigested food
Acid reflux and heartburn
Blood glucose fluctuations d/t malabsorption
Constipation
Gastric Cancer etiology
Etiologies of gastritis predispose someone to gastric cancer development
Gastric Cancer s/s
N/V
Early satiety
GI bleed
Usually occur in late stage of dx/ prognosis is poorer
SMALL INTESTINE (normal fx & interference)
Normal function -> absorption
Interferences -> obstruction, tumor, bleeding, malabsorption
Malabsorption
Digestion Problem
Gastroparesis
Failure of enzyme secretion into gut lumen
Pancreatic insufficiency or failure
Decreased digestive enzymes
Liver disease or gallbladder obstruction
Resulting decreased bile acids
absorption problems etiology
Reduced surface area
Damage to absorbing mucosa
Biochemical/metabolic
Obstruction of lymphatics and lacteals by tumors
absorption problems s/s
Abdominal pain + distention
Bloating
N/V
Diarrhea
Steatorrhea
Small Bowel Tumor (benign)
Adenoma, lipoma, leiomyoma
Small Bowel Tumor (malignant)
Adenocarcinoma (gland lining organ), lymphoma, carcinoids, GIST, sarcoma
Small Bowel Tumor s/s
Bleeding
Obstruction
N/V
Abdominal pain
Weight Loss
Fatigue
bowel obstruction etiology
Hernia, adhesion, intussusception
Tumors
Nearby tumors from other organs
Gallstones
Inflammatory (Crohn’s)
bowel obstruction s/s
Abdominal pain
N/V
Lacking appetite
Malaise
Diarrhea
Dehydration (tachy + low urine output)
Severe constipation
Complete small bowel obstruction -> medical emergency!
All others can be medically or interventionally managed
LARGE INTESTINE
(normal fx & interference)
Normal Fxn -> Water and Na+ reabsorption, delivery of stool to outside
Interference -> Diarrhea, constipation, (muscle fxn, obstruction), tumors, inflammation, bleeding
Hirschsprung’s Disease (Aganglionic Megacolon)
Functional obstruction of the colon
Problem of chronic constipation in children
Massive nerve malformation -> dilation
Colonic Diverticula (general)
Low fiber -> excess work on large intestines to squeeze stool -> weakened -> diverticulum forms (irregular pouch usually in descending colon)
Colonic Diverticula s/s
Intermittent cramping
Lower abdominal discomfort
Abdominal distention
Diverticulosis -> GI bleeding, LLQ pain Severe -> rupture, adherence to bladder, or air/feces in urine
Enterocolitis (definition)
Inflammation of colon secondary to infection, ischemia, drugs, injury, IBD
Enterocolitis
Changes in bowel pattern
Diarrhea
Abdominal pain
Urgency
Incontinence, Lower GI bleed
Colon Cancer (etiology)
Common -> colon adenocarcinoma
Genetic, regular screening after age 50 with fecal occult blood testing
Colon Cancer s/s
Abdominal pain
Lower GI bleed
Intestinal obstruction
IBS Dx
Abdominal pain at least 3 days per month over 3 months
Following defecation and change in stool frequency/form
IBS S/s
Chronic relapsing abdominal pain
Bloating
Changes in bowel habits
Diarrhea. Constipation, mixed subtypes predominance
IBD (general)
Chronic condition from inappropriate mucosal immune activation
In combination with host-microbe interactions and epithelial barrier issues
Comprised of
Ulcerative Colitis
Crohn Disease
H pylori - Mechanism of gastric injury and protection
Increases gastric secretion, initiating inflammation and susceptibility to acid damage
NSAIDs - Mechanism of gastric injury and protection
Inhibit COX 1 & 2, reducing prostaglandin production and mucosal protection
Tobacco - Mechanism of gastric injury and protection
Inhibits prostaglandin synthesis
Promotes oxidative stress and reduces bicarb -> inhibits neutralization of gastric acid
Result -> weakened mucosal barrier
alcohol - Mechanism of gastric injury and protection
Increases membrane permeability leading to cell death
Impairs mucosal blood flow and suppresses prostaglandin synthesis
Gastric Hyperacidity - Mechanism of gastric injury and protection
Overwhelms and degrades mucosal defenses
Ex. Zollinger-Ellison syndrome and continuous acid secretion
Duodenal-Gastric Reflux - Mechanism of gastric injury and protection
Reflux of bile acids, pancreatic enzymes, etc disrupt mucosal barrier
Toxic to gastric epithelial cells
What factors increase risk for peptic ulcer formation/disease?
H. Pylori infection
Long term NSAID use
Smoking
Excessive alcohol consumption
Corticosteroid use
Family/Past Medical history
Stress related -> shocks (burns, sepsis, hemorrhage)
gastric ulcer vs duodenal ulcer
GU- Worse with eating
Occur shortly after meals
DU-Relieved by eating but…
Worsens 1-3 hours after meal or at night
Associated with increased acid secretion
What are the results of a secretin test to determine if there is normal pancreatic function vs. a pancreatic tumor (gastrinoma)?
Normal
Secretin stimulates bicarbonate production -> increased pancreatic juice pH
Gastrinoma (pancreatic tumor)
Secretin paradoxically increases gastrin levels (more acidic)
Key differentiator is a higher vs lower pH
What are complications from chronic gastritis?
Mucosal atrophy (significant loss of parietal cell mass)
Intestinal metaplasia
Normal stomach cells adapt to become more like intestinal cells after prolonged irritation
Precancerous!
Dysplasia (abnormal growth and development)
Gastritis Cystica
Cyst formation in the stomach
What are the types of intestinal obstructions? (mechanical)
Adhesions, hernias, tumor formation
What are the types of intestinal obstructions? (functional)
Paralytic ileus
Muscle dysfunction or nerve dysfunction
What are the types of intestinal obstructions? (complete vs partial)
Partial can be managed by NPO, NG tube, decompression, IV fluid
Complete is surgical emergency
Irritable Bowel Syndrome (IBS)
vs
Irritable Bowel Disease (IBD)
IBS: Functional disorder, no structural abnormalities
Dx: abdominal pain 3 days per month for 3+ months with improvement after defecating
With change in stool frequency or form
Diarrhea/Constipation predominant or both
IBD: Chronic condition
Involves inflammation with potential structural changes
Comprised of Crohn’s and Ulcerative Colitis
Liver failure s/s - metabolic
Hypoglycemia
Hypoalbuminemia (edema)
Hepatic encephalopathy
Liver Fx
Stores glycogen
Glucose access
Hormone metabolism (from vitamin)
Substance detoxification (by making things water soluble for excretion)
Produces bile
Conjugates bilirubin for excretion
Liver failure s/s - impaired detoxification
Jaundice
Bleeding and bruising (d/t low synthesis of clotting factors)
Liver failure s/s - portal HTN
Esophageal varices
Ascites
Splenomegaly
Liver failure s/s - overall
Reduced immune fxn
Decreased bile production
Signs/Symptoms by System
Skin: Jaundice, spider angiomas, palmar erythema, bruising.
Abdomen: Ascites, hepatomegaly (if not shrunken in cirrhosis), caput medusae (dilated abdominal veins).
Neurological: Confusion, lethargy, asterixis, coma (hepatic encephalopathy).
Gastrointestinal: Nausea, vomiting, esophageal varices (hematemesis), anorexia.
Cardiovascular: Hypotension (reduced albumin and vascular tone).
Explain how ascites occurs in liver cirrhosis
Portal HTN and hypoalbuminemia increase capillary oncotic pressure
Fluid now pushed out and leaks into the peritoneal cavity
Know location and causes of portal hypertension
pic on doc
Etiology: Pre-hepatic
Portal vein thrombosis/ increased pressure in portal venous system
External compression by tumors or cysts
Structural abnormalities
etiology: Intrahepatic
Cirrhosis, hepatitis, fibrosis, liver tumors
Anything disrupting normal liver blood flow inside the liver
NASH (nonalcoholic steatohepatitis)
etiology: post hepatic
Right HF
IVC thrombosis/obstruction
Pericarditis
Thickened pericardium impeding venous return from liver
etiology: general
Alcohol abuse with high risk cirrhosis
Chronic viral hepatitis
Autoimmune liver disease
Obesity and infection
Understand bile metabolism and general causes for jaundice
Bilirubin is a byproduct/component of bile, helps digest fats
Stored in gallbladder
Secreted into duodenum
Impaired liver function, bile duct obstruction, or excessive RBC breakdown -> bilirubin accumulation
Accumulation in bloodstream (unconjugated) -> yellow discolorations
AST/ALT
Elevated indicate hepatocyte injury
Alk Phos
Elevated indicates cholestasis (slowing/stalling of bile flow)
Bilirubin
High levels indicate impaired excretion/metabolism
Albumin
Low levels suggest chronic disease
Albumin synthesized in liver to maintain capillary oncotic pressure
Prothrombin Time (PT)
Prolonged PT indicates poor synthesis of clotting factors
How are amylase and lipase levels affected in acute pancreatitis?
Amylase/Lipase levels increased d/t damage and inflammation in pancreatic tissue -> released into bloodstream
hepatities
transmission, vaccines, tx, prevention
