Exam 3: GI Pathophysiology Flashcards
After a meal, blood pH shifts:
More alkaline d/t shift of H+ into lumen of stomach, HCO3- into blood
Once food enters duodenum, blood pH shifts:
Back to normal; HCO3- is dumped into lumen to increased pH
Hiatal hernia is caused by:
Stomach moving through opening in diaphragm by esophagus
Sequalae of hiatal hernia:
Trapping of food in esophagus and heartburn/regurg
Achalasia is:
Loss of inhibitory innervation of LES, leading to food sitting in esophagus instead of moving into stomach
Causes of achalasia:
Aperistalsis
Incomplete relaxation of LES
↑ tone of LES
Sequlae of achalasia:
Dysphagia
Mucosal inflammation/ulceration
Squamous cell carcinoma (5%)
Cause of esophageal varices:
Impaired hepatic portal blood flow –> portal HTN –> blood backup to esophagus
% of cirrhosis pts with esophageal varices:
2/3rds
Sequelae of esophageal varices:
Rupture & hemorrhage
Hematemesis
Mortality rate of ruptured esophageal varices:
20-30% per episode with a 70% recurrence rate
Barrett’s esophagus is:
Metaplastic change from esophageal cells to stomach cells
Contributing causes to GERD:
Obesity
Hiatal hernia
Vagal nerve abnormalities
Cause of Barrett’s esophagus:
Long standing GERD
Sequelae of Barrett’s esophagus:
Adenocarcinoma
Two types of esophageal cancers:
Squamous cell carcinoma
Adenocarcinoma
Conditions predisposing to SCC:
Tobacco use
Alcohol use
Achalasia
Drinking very hot tea??
Conditions predisposing to adenocarcinoma:
Barrett’s esophagus/GERD
S/s of esophageal CA:
Dysphagia
Obstruction
(Typically late in progression)
Chronic gastritis can lead to:
Peptic ulcers
Acute gastritis can lead to:
Acute gastric ulceration
Normal stomach pH:
1.5
Gastric pits are:
Depressions in epithelial lining containing gastric glands
Chief cells produce:
Gastric juice enzymes
Parietal cells produce:
Stomach acid
Chronic gastritis/PUD usually caused by:
H. pylori
H. pylori survives in stomach by:
Secreting ammonia as buffer against gastric acid
S/s of H. pylori:
Upper abdo discomfort
N/V
Ulcers
Peptic ulcers are:
Chronic lesions anywhere in the GI tract exposed to acid, although 98% are in proximal duodenum/stomach (4:1)
Causes of peptic ulcers:
H. pylori NSAIDs Smoking Alcohol Corticosteroids Stress
S/s of peptic ulcers:
Epigastric pain
N/V
Hemorrhage
Perforation
NOT cancer
Acute gastritis is:
Acute, usually transient, mucosal inflammation
Causes of acute gastritis:
Just about anything NSAIDs ETOH Smoking Chemo Uremia Sepsis Ischemia, shock, stress Ingestion Trauma to stomach
S/s of acute gastritis:
Epigastric pain
N/V
Hematemesis
Melena
Most common type of stomach cancer:
Gastric carcinoma (> 90%)
Causes of intestinal-type adenocarcinoma:
Nitrites/nitrates Smoked, pickled, salty food ↓ in fruit/veg consumption Chronic gastritis H. pylori
Causes of diffuse carcinoma:
Not well understood
Four layers of intestine from outermost to innermost:
Serosa
Muscularis
Submucosa
Mucosa
If starches are not absorbed or broken down:
Bacteria will eat them, leading to cramps and bloating
Non-digested proteins in the bloodstream cause:
Inflammation and the creation of antibodies/immune response
Monosaccharide uptake is aggressive due to:
Glucose and galactose being taken in via Na+ cotransporters
Most at-risk blood supply in the GI system:
Splenic flexure
Developmental problem behind Hirchsprung’s:
Aganglionic segment of distal colon lacks Meissner & Auerback plexuses and thus has no peristalsis
Sequelae of Hirchsprung’s:
Obstruction
Enterocolitis
Perforation
After removal of large segment: chronic diarrhea d/t minimal H2O absorption
Tx of Hirchsprung’s:
Removal of aganglionic segment
Worst case scenario for ischemic bowel disease:
Transmural infarction - 90% mortality rate
Five causes of ischemic bowel disease:
Arterial thrombosis Arterial embolism Venous thrombosis Non-occlusive ischemia Mechanical obstruction
Cause of hemorrhoids:
Straining during defecation
Pregnancy (caval obstruction backs up to portal-caval anastamoses)
Hepatic portal hypertension
Secretory diarrhea:
Caused by bacterial infections
Ex. cholera
Can lose 1L/hr!
Cholera causes diarrhea by:
Causing epithelium to lose Cl- into the lumen, which inhibits Na+ uptake and H2O uptake
Osmotic diarrhea:
Due to non-digestible agents in the lumen that act as osmotic agents
Ex. GoLytely
Exudative diarrhea:
Due to destruction of epithelial layer - not enough viable tissue, poor absorption
Ex. shigella, salmonella, campylobacter, etc
Malabsorption diarrhea:
Ex. lactose intolerance, giardia, lympatic obstruction d/t fat buildup
Bacterial feeding on ingested food causes bloating, gas, diarrhea
Deranged motility diarrhea:
D/t surgery or hyperthyroidism
Usually ↓ motility but can sometimes be ↑
Dx’ing CD vs UC:
Colonoscopy - UC will be in the colon with pseudopolyps
X-ray - can show wall thickening
Distribution of ulcerative colitis:
In the colon in one continuous section, starting at anus and going backwards
Distribution of Crohn’s disease:
Anywhere from mouth to anus, usually in intestines
Skip lesions
Deep fissures, not ulcers
Diverticula are:
Pouches protruding out of the bowel
Diverticulitis is:
When diverticula get inflamed
Sequelae of diverticulitis:
Perforation
Fistula formation
S/s of diverticulitis:
LLQ pain
Bleeding
Tx of diverticulitis:
Fiber
Types of mechanical bowel obstruction:
Herniation
Adhesions
Intussception
Volvulus
Types of pseudo-obstructions:
Paralytic ileus
Bowel infarction
Myopathies/neuropathies
Colonic tumor becomes invasive when:
Penetrates the muscularis mucosae and enters submucosal layer
S/s of colorectal carcinoma:
Pain
Obstruction
Changes in bowel habits
S/s of left-sided colorectal CA:
Visible blood in stool, LLQ pain
S/s of right-sided colorectal CA:
Fatigue
Weakness
Iron deficiency anemia
