Pathophysiology (Prunuske) Flashcards
Zollinger-Ellison Syndrome (gastrinoma)
- -Caused by gastrin-secreting tumor (usually)
- -Excess H+ secretion and hyperplasia and hypertrophy of parietal cells
- -95% of patients get gastric ulcers
Gastric and duodenal ulcers
- -H. pylori infection
- -Poor secretion of mucus, bicarb by surface epithelium
- -Stress can contribute (not cause)
- -Irritation w/EtOH, acid, digestive enzymes, bile
- -Treat w/antibiotics and PPI, stop NSAIDS
GI peptic ulcer pathophysiology
- -Gastrin levels increased (somatostatin inhibition during fasting state not activated)
- -Increased gastrin can cause acid hypersecretion, pepsin secretion, hyperplasia of ECL and parietal cells and stomach contractions
- -NSAIDs further exacerbate due to inhibition of protective factors from PG
Achlorhydria
- -Reduced acid secretion
- -Possible causes: aging , gastric resection, genetics, auto-immune attack of H+/K+ ATPase, PPIs, infection
- -Bacterial overgrowth, diarrhea, pneumonia
- -Hip fractures, iron deficient anemia (decreased Ca++ and iron absorption)
- -Decrease in pepsin activation doesn’t cause problems
Pyloric stenosis
Congenital condition where pylorus fails to relax after meal–> malnutrition and dehydration
–Treat with surgical myotomy
Gastroparesis
- -Reduced gastric emptying often because of diabetic neuropathy
- -Vagus and enteric nerves fail to generate enough force to empty stomach contents
- -Treat with prokinetic drugs
Dumping syndrome
- -Rapid, gastric emptying (often from gastric bypass, vagotomy, high-sugar meals)
- -Rapid entry of contents into duodenum represents osmotic challenge and water moves to lumen causing hypovolemia and reduced BP
- -Nausea, weakness, dizziness, sweating, shakiness, diarrhea, heart palpitations
Peptic ulcer disease
- -Scarring and ulcers near pylorus can delay emptying
- -Duodenal ulcers can lead to rapid gastric emptying from loss of duodenal negative feedback mechanism
Vomiting (emesis)
- -Expulsion of contents of stomach contents through reverse peristalsis of the intestine
- -Often preceded by nausea (sensation vomiting will happen)
- -Can cause Mallory-Weiss tear if forceful enough
What coordinates emesis mechanisms?
- -Vomiting center in medulla
- -Increased salivation (bicarb) protects teeth enamel
- -Retro-peristalsis (starting from middle of small intestine) into stomach through relaxed pyloric sphincter
- -Can be preceded by retching
- -Glottis closes to prevent aspiration of vomit
Does the stomach contract during process of vomiting?
No, except at the annular notch. Control is mediated by extrinsic nerves
What inhibitors are used to suppress vomiting?
Inhibitors of DA, Histamine and 5-HT
What are some emetic stimulants?
- -Stimulation of pharynx
- -Sensory input from higher centers
- -Vestibular info
- -Irritants or blockage in GI tract
- -Blood-borne emetics
Hereditary pancreatitis
- -Mutation in trypsinogen PRSS1 gene–> activates digestive enzymes in pancreas
- -Autosomal dominant
Pancreatitis causes
- -Cystic fibrosis
- -Occlusion of pancreatic duct
- -EtoH
Pancreatitis effects
- -Upper abdominal pain from autodigestion of pancreatic tissue
- -Vomiting and sympathetic activation
- -Elevated serum amylase and lipase levels
- -Malabsorption of fat and fat-soluble vitamins
- -Steatorrhea
- -Malignancy, diabetes, infections
Cirrhosis
Hardening of liver from irreversible deposition of excess collagen
Cirrhosis effects
Jaundice, abdominal ascites, esophageal varices, hepatic encephalopathy, GI bleeding
Cirrhosis pathology
–Oxidative stress (alcohol, infection) –> Kupffer cells release cytokines–> collagen production by stellate cells–> collagen accumulates–> increases resistance to blood flow and reduces hepatocyte function
Cholestasis
Impaired bile secretion
Primary biliary cirrhosis
Destruction of cholangiocytes
Primary sclerosing cholangitis
Inflammation of bile ducts
Pregnancy and relation to cholestasis
Progesterone reduces gallbladder smooth muscle tone
Cholestasis effects
- -Bile accumulates in liver–> metabolic dysfunction
- -Itch (bile regurgitates into plasma)
- -Hypercholesterolemia
- -Deficiency of fat soluble proteins
Cholelithaisis size, symptoms, prevalence
- -Grain of sand to golf ball size
- -RUQ pain, fever, many lack symptoms
- -20% of people have
Cholesterol stones
Caused by increased cholesterol or decreased bile acids treat with bile acid
Pigment stones
Calcium salts of unconjugated bilirubin, can be caused by hemolytic anemia, infection of biliary tract that leads to deconjugation
Treatment for cholelithiasis
Laparoscopic cholecystectomy
Diverticulum
Single pouch protruding from alimentary tract. Usually false, not true.
Diverticulosis
Multiple diverticula
Diverticulitis
Impacted with feces, inflamed, painful, hemorrhage (if blood vessel erodes)
Causes of mesenteric ischemia
- -Occlusive mechanisms
- -Non-occlusive mechanisms (include prolonged reflex vasoconstriction or vasodilator toxins from gut)
Effects of mesenteric ischemia
- -Postprandial pain
- -Sitophobia
- -Necrosis of tops of villi
- -Loss of barrier function of wall of gut an uptake of vasodilator toxins (endotoxin) from gut causing septic shock
Consequences of removal of ileum
Can’t transport bile salts back to liver–> steatorrhea
Osmotic diarrhea
Small bowel overgrowth of bacteria leading to increased production of organic acids that pull water from blood stream by osmosis
Secretory diarrhea
Infection leads to excess secretion of Cl-, drawing water into lumen
What is fluid flux in diarrhea dependent on?
Surface area available for ion transport and residence time in lumen
- -East-West vector: increased by surface area
- -North-South vector: influenced by motility–>transit time.
What antidiarrheal works to slow transit time to increase fluid absorption?
Loperamide
Borborygmi
Rumbling noise created by movement of gas in bowels
Causes of small intestine bacterial overgrowth syndrome
Delayed small intestine transit time and diverticulum
Small intestine bacterial overgrowth syndrome presentation
- -Gas and bloating (due to fermentation)
- -Anemia (competition for B12 uptake)
- -Steatorrhea (deconjugate bile acids)
- -Toxins alter epithelium
How do you diagnose small intestine bacterial overgrowth?
Hydrogen breath test
Xerostomia definition
Subjective sensation of dryness in oral mucosa
Xerostomia causes
- -Sjogren syndrome
- -Lots of meds (esp. muscarinic antagonists)
- -Secondary to head and neck radiation
- -Dehydration
- -Sialolithiasis
- -Nerve damage related to injury or diabetes
- -Postmenopausal hyposalivation
Xerostomia consequences
- -Increased likelihood of opportunistic infections
- -Halitosis
- -Tooth decay (decreased oral pH)
- -Decreased taste
- -Speech problems
- -Dysphagia > malnutrition
Treatment of xerostomia
Gum, artificial saliva, switch meds, parasympathomimetics
What leads to halitosis in xerostomia?
Production of hydrogen sulfide by bacteria and accumulation of dead cells
Dysguesia
Abnormal taste changes. Can occur from infection, aging, nutritional deficiencies
Dysphagia/Odynophagia (causes and consequences)
Causes: structural abnormalities (cancer, diverticula) or functional abnormalities (stroke etc.)
Consequences: can lead to aspiration and malnutrition
Primary diagnostic technique of dysphagia/odynophagia?
Videofluroscopic swallowing study. Barium swallowed with food and observed with x-ray
GERD definition
Reflux of gastric acid contents into esophagus due to relaxation of lower esophageal sphincter
Causes of GERD
Obesity, pregnancy, eructation, hiatal hernia
Achalasia definition
Failure of LES to relax and in some cases lack of proximal peristalsis
Manometry
Measures how tightly muscles contract when swallowing
Portal hypertension
Gastric blood flow diverts and leads to formation of varices
