GI Conditions: Part 1 Flashcards
GI bleeds
Erosion of the mucosal lining of the GI tract
Caused by: Tears, erosions from ulcers, CA (ruptured vascular neoplasms, or malignant neoplasms causing leaking/invasion into vascular spaces)
Assessing GI bleeds
COLOR:
- Bright blood = Close to mouth or rectum
- Darker blood = Digested; farther from mouth/rectum
AMOUNT:
- Large bleeds (>1 L) require immediate correction; usually not malignant
- Smaller bleeds may be malignant (in older adults)
ASSESSMENT:
- Fast, large bleeds (losses of whole blood) = Hgb and Hct are normal at first; assess volume, BP, oxygenation, and physical exam
- Slow, small bleeds (anemia) = Fluid status gets restored, but Hgb and Hct are low
Location of GI bleed
Upper and lower GI bleeds are differentiated by the ligament of Treitz (anatomical landmark between the duodenum and jejunum)
Blood characteristics:
1. HEMATEMESIS (blood in vomit): Upper GI bleed; can be either (1) Frank (active, bright red) or (2) Coffee-grounds (digested, mixed with gastrin)
- MELENA (dark, sticky feces containing partly digested blood): Upper and lower GI
- HEMATOCHEZIA (BRBPR): Lower GI or massive upper GI
- OCCULT: Blood in the feces that is not visibly apparent and is typically asymptomatic (normal stools/gastric secretions); often found in older adults who are anemic, and can be associated with colon CA
Upper GI bleeds
Sources:
1. Peptic ulcer disease (most common, >50%)
- Gastritis/Duodenitis from NSAID use (15-30%)
- Varicose veins from portal HTN (10-20%)
- Mallory-Weis tears at GE junction (5%)
Other: Esophagitis (3-5%), malignancy (3%), nasopharyngeal bleed (swallowed to stomach), aortoenteric fistula, angiodysplasia, and hemophilia
Mallory-Weiss tear
Linear lacerations at GE junction caused by prolonged/severe vomiting (80-90% resolve spontaneously)
At risk: Alcoholism, acute alcohol ingestion trauma, inflammation (gastritis, esophagitis), and chemotherapy
S/S: Hematemesis (frank or coffee-grounds), abdominal pain, retching, melena
Portal HTN and varices
Portal vein: large vein that carries blood from the GI tract, spleen, and pancreas to the liver
Portal HTN and subsequent destruction of sinusoidal capillaries caused by obstruction or increased resistance to blood flow (d/t cirrhosis) results in the formation of varices across the esophagus and stomach
ASYMPTOMATIC unless a vessel ruptures; S/S: Hematemesis, melena, shock, death
Lower GI bleeds
Sources:
1. DIVERTICULOSIS: Small pouches formed of weakened lower intestinal wall (diverticula) d/t bleeding, inflammation, or infection; Risk factors: >40 y/o, smoking, obesity, sedentary lifestyle, and diet; S/S: LLQ pain, N/V/D, fever, tenderness, constipation
- HEMORRHOIDS: External/internal varices of the veins in the anus and rectum (internal varices can be asymptomatic until passing stool); Risk factors: Pregnancy, obesity, and low-fat diets; S/S: Hematochezia (BRBPR), itching, pain, and swelling
Esophageal obstruction
Caused by:
- Intrinsic blockage: Tumors, stricture from scar tissue or GERD, eosinophilic esophagitis, radiation therapy
- Extrinsic blockage: FB obstruction
Location:
- Upper esophageal obstruction: discomfort 2-4 sec. after swallowing
- Lower esophageal obstruction: discomfort 10-15 sec. after swallowing
Complications: Aspiration pneumonia, malnutrition, dehydration, choking
S/S: Retrosternal pain, regurgitation of undigested food, unpleasant taste, V/, weight loss; and dysphagia (most prominent symptom)
ACHALASIA: Defect of the lower esophageal sphincter characterized by failure to relax; food sits in the lower esophagus, and irritates the mucosa (increasing the risk for esophageal CA)
Esophageal CA
Diagnosed by endoscopy with biopsy
Tx: Surgery (poor prognosis)
Esophageal CA: Squamous cell carcinoma
Typically affects the epithelial cells that line the upper two-thirds of the esophagus (more common in the DEVELOPING world)
Risk factors: Male, >50 y/o, smoking, alcohol consumption, betel nut/hot drink/caustic substance consumption, idiopathic achalasia
S/S: Asymptomatic until advanced; Dysphagia (first symptom), followed by weight loss, hoarseness, coughing, and chest pain
Poor prognosis: 40% cure rate if found early; 5% 5-year survival rate if found in stage IV
Esophageal CA: Adenocarcinoma
Typically affects the lower third of the esophagus; glandular cells transform into intestinal cells d/t chronic exposure to gastric acid (more common in the DEVELOPED world)
Risks: Male, obesity, GERD, Barrett’s esophagus (esophageal cells transform into intestinal duodenal cells), CA
S/S: Indigestion, heart burn, dysphagia, V/, chest pain, hoarseness, coughing
Similar prognosis to esophageal SCC
Obstruction: Stomach and intestines
Gastric outlet obstructions are caused by: Tumors, inflammation d/t duodenal ulcer, FB; and babies may have congenital pyloric stenosis
Causes of intestinal obstruction:
- Postoperative ileus d/t drugs and neural paralysis during manipulation
- FB
- Mechanical obstructions
Mechanical obstructions of the intestines
Mechanical obstructions:
1. HERNIATION: A protrusion of the abdominal contents through an acquired or congenital area of weakened or defective abdominal wall
- VOLVULUS: Twisted loop of bowel; can occur by accident
- ADHESIONS: Bands of scar-like tissue between segments of the bowel; may result from postoperative abdominal surgeries
- INTUSSUSCEPTION: Part of the intestine slides into an adjacent part of the intestine, resulting in strangulation and loss of blood supply; most common cause of mechanical intestinal obstruction in children
Vomitus
Location of obstruction:
1. PLYORUS: Early, profuse vomiting of clear gastric fluid
- PROXIMAL SI: Mild distention and vomiting of bile-stained fluid
- DISTAL SI: Pronounced distention; vomiting can contain fecal material
Peptic ulcer disease (PUD)
Chronic mucosal ulceration of (1) the stomach or (2) duodenum d/t mucosal imbalances and damaging forces of gastric acid and pepsin
Caused by: NSAIDs and H. pyloric infection (most common); Stomach CA, Zollinger-Ellison syndrome (pancreatic gastrinoma), Crohn’s disease, stress, burns, trauma, sepsis, and mucosal ischemia
Gastric and duodenal ulcers
Types of peptic ulcers:
1. GASTRIC (more common in women): Epigastric pain 1-2 hours after eating (worsens after eating); S/S: Hematemesis or melena, heart burn, chest discomfort and early satiety (common), indicative of gastric CA (in the elderly), and weight LOSS
- DUODENAL (more common in men): Epigastric pain 2-5 hours after eating (relieved with eating); S/S: Melena or hematemesis, heart burn and chest discomfort (less common), pain that awakens at night, and weight GAIN
Complications from peptic ulcers
Complications:
1. HEMORRHAGE (20% of patients): Blood vessels damaged as ulcer erodes into the muscle of the stomach or duodenal wall; S/S: Hematemesis (coffee grounds), melena, dizziness, pallor, sweating, chills, restlessness, anxiety
- PERFORATION: Ulcer erodes completely through the wall; S/S: Epigastric pain with referred shoulder pain, guarding, rigidity, absent bowel sounds, distention; Peritonitis: inflammatory infection of the abdominal cavity
- PYLORIC STENOSIS: Fibrotic scar tissue at the pyloric sphincter; S/S: Severe N/V/ after eating, persistent hunger but early satiety, and epigastric pain
Acute gastritis
Acute mucosal inflammatory process of the entire mucosal lining of the stomach
Epithelial damage is exacerbated by:
- Neutrophilic infiltration
- Increased acid secretion (H. pylori increase gastrin secretion by inhibiting somatostatin release)
- Decreased bicarb. secretion
- Hypoperfusion
- Disruption of the mucosal layer
Risk factors: NSAIDs and corticosteroid use (most common causes); H. pylori, excessive alcohol consumption, smoking, drugs, chemicals, infections, parasites, fungal infections, age, obesity, and stress
S/S: Recurring N/V/, abdominal pain and discomfort, feeling of burning in the stomach, and early satiety
Chronic gastritis
Chronic mucosal inflammatory changes leading eventually to mucosal atrophy and intestinal metaplasia
Types:
- Type A: Fundic (autoimmune)
- Type B: Antral
Caused by: H. pylori infection, toxins (alcohol and cigarette-smoking), motor and mechanical, radiation, granulomatous conditions (Crohn’s disease)
Chronic gastritis: Fundic (type A)
Autoimmune atrophic gastritis that involves the body and fundus of the stomach; antibodies are directed against parietal cells, resulting in low acid secretion and pernicious anemia (no intrinsic factor)
S/S: Symptoms of anemia (vitamin B12 def.), asymptomatic bleeding, erosive epigastric pain
Chronic gastritis: Antral (type B)
Most common form of chronic gastritis in the U.S.; predisposed to gastric CA
S/S: N/V/, abdominal pain, hematemesis (uncommon)
Inflammatory bowel disease
Chronic AUTOIMMUNE conditions resulting from inappropriate mucosa immune activation
Umbrella term for:
- Crohn’s disease
- Ulcerative colitis
Risk factors: FHX, smoking, NSAID use, environmental factors, and diet
Complications: Increased risk for colon CA, inflammation elsewhere (skin, eye, joint), bile duct scarring, liver damage, blood clots in intestinal tract vasculature
Crohn’s disease and ulcerative colitis
CROHN’S DISEASE: Intermittent areas of inflammation creating fistulas/abscesses spanning full thickness of the bowel (risk for B12 def.); S/S: Crampy abdominal pain; Complications: Fistulas, abscess, obstruction
ULCERATIVE COLITIS: Progressive inflammation of the mucosa and submucosa, typically starting at the rectum; S/S: Hematochezia and bloody D/; Complications: Hemorrhage, toxic megacolon, pseudo-polyps (do not tend to have ulcers, erosions, or abscesses)
GERD
Stomach contents reflux into the esophagus causing inflammation
Caused by: Reduced resting tone of cardiac sphincter, increased pressure on stomach (pregnancy, coughing, lifting, obesity, large meals), and spicy/acidic foods
S/S: Heartburn, chronic cough, laryngitis, epigastric pain within 1 hour of eating
Long-term complications:
- Esophagitis
- Barret’s esophagus: pre-cancerous metaplasia of esophagus
- Esophageal CA (adenocarcinoma)
Diarrhea
Types of diarrhea:
1. OSMOTIC: Non-absorbable substances (i.e. sugars, laxatives) in the intestines draw water into the lumen by osmosis, causing large-volume D/ (lactose intolerance)
- SECRETORY: Ion imbalance d/t excessive mucosal secretions, Cl- or bicarb-rich fluid, or inhibition of net sodium absorption, causing large-volume D/ (cholera, E. coli infection)
- MOTILITY (functional): Excessive intestinal motility decreases transit time, mucosal surface contact, and opportunity for fluid absorption (irritable bowel disease)
Complications: Dehydration, electrolyte imbalance (hyponatremia, hypokalemia), metabolic acidosis (loss of bicarb.), and weight loss
Constipation
Infrequent or difficulty defecation; Normal: ~2-3 times/day to few times/week
Caused by:
1. Normal-transit constipation (functional): Normal rate of passage, but difficulty with stool evacuation from low fiber or -fluid diet
- Slow-transit constipation: Impaired colonic motor activity with infrequent bowel movements and straining
- Pelvic floor dysfunction: Failure of pelvic floor muscles or anal sphincters to relax with defecation
- Secondary: Actual disease process or condition (i.e. stroke)
