Gastrointestinal Flashcards
Achalasia
Esophageal motility disorder (neuromuscular)
Outflow obstruction d/t inadequate LES relaxation
Achalasia S/S
Dysphagia
Heartburn
Chest pain
Achalasia Diagnosis
Esophagram reveals “bird’s beak” appearance
EGD
Esophageal manometry
Achalasia Type 1
Classic minimal esophageal pressure
Treatment = myotomy
Achalasia Type 2
Entire esophagus pressurization
Best outcome
Achalasia Type 3
Esophageal spasm w/ premature contractions
Worst outcome
Achalasia Treatment
Palliative Relieve obstruction (does not correct lacking peristalsis)
Distal Esophageal Spasm
Diffuse esophageal spasm
Elderly patients
ANS dysfunction
Distal Esophageal Spasm Diagnosis
Esophagram reveals “corkscrew” or “rosary bead” esophagus
Distal Esophageal Spasm Treatment
Pain mimics angina
Responds to Nitroglycerin
GERD
Gastroesophageal reflux disease
LES incompetence
GERD S/S
Heartburn
Regurgitation
Less common include dysphagia & chest pain
GERD Complications
Chronic peptic esophagitis
Strictures
Ulcers
Barrett’s metaplasia associated w/ adenocarcinoma
Reflux into pharynx, larynx, & tracheobronchial tree
Aspiration → pulmonary fibrosis or chronic asthma
GERD Treatment
Lifestyle modification Avoid foods that impair LES tone (fat, alcohol, peppermint, chocolate) & acidic Pharmacological - PPI ↑pH & allows esophagus to heal - H2 antagonists Surgical = Nissen fundoplication
↑aspiration risk associated w/ ___ mL & ___ pH
25mL or 0.4mL/kg
pH <2.5
Esophageal Diverticula
Esophageal structural disorder w/ outpouchings
Most common locations:
- Pharyngoesophageal (Zenker’s diverticulum)
- Mid-esophageal
- Epi-phrenic (supradiaphragmatic)
Hiatal Hernia
Stomach herniates into thoracic cavity via diaphragm esophageal hiatus
Asymptomatic
Esophageal Tumors
Progressive dysphagia to solid food & weight loss
Poor survival rate (lymph node metastasis)
Adenocarcinoma
Mortality rate about 50%
Esophageal Tumor Treatment
Esophagectomy (curative or palliative)
Thoracic epidural
Esophageal Tumors Complications
ARDS
Malnourished
Dehydration
RLN injury risk
Peptic Ulcer Disease
Epigastric pain exacerbated by fasting & improved by eating
H. Pylori
Associated w/ PUD
Induces acid secretion via pro-inflammatory cytokines
Gastric Ulcer
1/3 duodenal
Benign ulcers
Most common cause = NSAID use
Stress Gastritis
Associated w/ shock, sepsis, respiratory failure, burns, hemorrhage, massive transfusions, or head injury
Gastric bleeding when coagulopathy, thrombocytopenia, INR >1.5, and aPTT >2x normal
Zollinger-Ellison Syndrome
Gastroduodenal & intestinal ulceration ↑gastrin secretion Non-beta islet cell pancreatic tumor Primarily men 30-50yo Associated w/ MEN1
ZES S/S
Abdominal pain
Peptic ulceration
Diarrhea
GERD
ZES Treatment
Obtain fasting gastrin level
↑PPIs dosages
Surgical tumor resection
PUD Complications
Bleeding
- Hemorrhage = leading cause of death
Perforation (risk 10%)
- Severe epigastric pain caused by highly acidic gastric contents in peritoneum
Obstruction
- Gastric outlet obstruction
- Cause = edema & inflammation in the pyloric channel & duodenum 1st portion
PUD Treatment
Antacids H2 receptor antagonists PPIs Prostaglandin analogues Cytoprotective agents Anticholinergics
Antacids
Aluminum hydroxide
Magnesium hydroxide
Avoid in chronic renal failure patients → hypermagnesemia & neurotoxicity
TUMS = calcium carbonate (milk-alkali syndrome hypercalcemia, hyperphosphatemia, & renal calculi)
HCO3 → metabolic alkalosis
H2 Receptor Antagonists
Cimetidine, Ranitidine, Famotidine, & Nizatidine
Inhibit basal & stimulated gastric acid secretion
Cimetidine & Ranitidine bind to CYP450
PPIs
Proton pump inhibitors
Omeprazole, Pantoprazole, Esomeprazole, Lansoprazole, & Rabeprazole
Covalent, irreversible bond
Inhibit hydrogen-potassium ATPase pump
Most potent drug available
Inhibit ALL gastric acid secretion phases
Interfere w/ Ketoconazole, Ampicillin, Iron, Digoxin, & Diazepam absorption
Omeprazole & Iansoprazole inhibit CYP450
Prostaglandin Analogues
Misoprostol only FDA approved
Contraindicated in pregnancy
Enhance mucosal HCO3 secretion, stimulate mucosal blood flow, & ↓mucosal cell turnover
Most common side effect = diarrhea
Cytoprotective Agents
Sucralfate provides physiochemical barrier, enhances defense & repair
Most common side effect = diarrhea
Colloidal bismuth (Pepto) MOA unknown & neurotoxicity risk
Anticholinergics
Inhibit muscarinic receptors activation in parietal cells
Negative side effects
Not routinely used
Post-Gastrectomy
Dumping Syndrome
Hyperosmolar gastric contents enter into proximal small bowel
Fluid shifts into small bowel lumen
Results in plasma volume contraction & acute intestinal distention
Early Dumping Syndrome
Symptoms 15-30min after meal (nausea, epigastric discomfort, diaphoresis, cramps, diarrhea, tachycardia, palpitations, dizziness, syncope)
Late Dumping Syndrome
Symptoms 1-3hrs after meal
Vasomotor symptoms 2° to hypoglycemia d/t excessive insulin release
Dumping Syndrome Treatment
Dietary modifications (fewer simple sugars) & less fluid consumption during meals Octreotide therapy - admin SQ before meal or depot injection monthly - Inhibit release vasoactive peptides from gut, ↓peak plasma levels, & slow intestinal transit
Post-Gastrectomy
Alkaline Reflux Gastritis
Clinical triad:
- Post-prandial epigastric pain associated w/ N/V
- Evidence bile reflux into stomach
- Histologic evidence gastritis
Treatment = divert intestinal contents from contact w/ gastric mucosa (diversion)
Inflammatory Bowel Disease
Ulcerative colitis
Crohn’s disease
Ulcerative Colitis
IBD
Involves rectum & extends proximally to involve part or all colon
Mucosal disease
UC S/S
Diarrhea, rectal bleeding, tenesmus (feeling incomplete BM), passage mucus, & cramps
Anorexia, N/V, fever, weight loss
Low serum albumin & leukocytosis when severely ill
UC Complications
Hemicolectomy when patient requires 6-8 units PRBCs w/in 24-48hrs
Toxic megacolon - dilated transverse colon w/ loss haustrations triggered by electrolyte abnormalities & narcotics
Perforation → peritonitis
Obstruction d/t benign stricture formation
Total proctocolectomy = curative
Crohn’s Disease
IBD
Acute or chronic bowel inflammation
Penetrating-fistulous or obstructing pattern
Most common site = terminal ileum
Crohn’s S/S
Ileocolitis
Recurrent episodes RLQ pain & diarrhea
Fever indicates intraabdominal abscess formation
Weight loss d/t anorexia & diarrhea
Loss digestive & absorptive surface → megaloblastic anemia & neurologic symptoms
Hypoalbuminemia, hypocalcemia, hypomagnesemia, coagulopathy, hyperoxaluria, & nephrolithiasis
Vitamin D deficiency, hypocalcemia, & glucocorticoid use
B12 malabsorption → megaloblastic anemia & neurologic symptoms
Diarrhea d/t bacterial overgrowth in obstruction areas, fistulas, bile acid malabsorption, ↓H2O reabsorption
1/3 patients at least 1 symptoms outside intestines (arthritis or renal calculi)
IBD Surgical Treatment
NOT curative
Severe IBD → total proctolectomy & end ileostomy
Most common surgery = small intestine resection
Removal > 2/3 small intestine → short bowel syndrome & need parenteral nutrition
IBD Crohn’s Surgical Complications
Hemorrhage
Sepsis
Neural injury
IBD Medical Treatment
5-ASA (Mesalamine) to treat mild to moderate IBD
- Antibacterial & anti-inflammatory
Glucocorticoids moderate to severe Crohn’s only to induce remission & then taper (not maintenance)
Antibiotics “pouchitis” (Ciprofloxacin & Metronidazole)
Azathioprine, Methotrexate, Cyclosporine, & Tacrolimus
Infliximab & Natalizumab
Carcinoid Tumors
Tumors originate in GI tract
< 1/4 first found in the lung
Secrete GI peptides/vasoactive substances
Often found incidentally (suspected appendicitis)
Sometimes contain GI peptides
Midgut more likely to release substances than foregut carcinoids
Carcinoid Syndrome
Approximately 10%
Serotonin & vasoactive substances released into systemic circulation
Carcinoid Syndrome S/S
Sudden onset flushing & diarrhea Flushing d/t histamine (admin H1 & H2 blockers) Hypo or hypertension Bronchoconstriction Cardiac manifestations
Carcinoid Syndrome
Precipitating Factors
Stress, alcohol, exercise, certain foods, & drugs such as catecholamines, pentagastrin, & SSRIs/SNRIs
Carcinoid Syndrome Diagnosis
Measure urinary or plasma serotonin
Serotonin metabolites present in urine
1° metabolite: 5-HIAA (5-hydroxyindoleacetic acid)
Carcinoid Crisis
Intense flushing Diarrhea Abdominal pain Tachycardia Hypo or hypertension Causes include stress, chemo, or biopsy AVOID Succinylcholine, Miva/Atracurium, Epi/NE, Dopamine, Isoproterenol, or Thiopental
Carcinoid Tumor Treatment
Avoid flushing
Serotonin receptor antagonists
5HTZ or 5HT3 antagonists
H1/H2 antagonists
Somatostatin analogues
Bronchoconstriction resistant to treatment β agonists worsen effects d/t mediator release
TACE - trans-arterial chemoembolization w/ or w/o chemotherapy
Acute Pancreatitis
Pancreas inflammatory disease caused by digestive enzyme
Autodigestion prevented by enzymes being packaged in precursor form, protease inhibitors synthesis, & low calcium concentrations ↓trypsin activity
Acute Pancreatitis
Causes
Gallstones & ETOH abuse
Hypercalcemia (hyperparathyroidism & AIDs)
Postop pancreatitis after CABG & ERCP
Acute Pancreatitis
S/S
Excruciating mid-epigastric pain that radiate to the back
Sitting/leaning forward ↓pain
Abdominal distension w/ ileus
Dyspnea indicates pleural effusion or ascites
Low grade fever
Hypotension & tachycardia
Shock d/t hypovolemia (blood & plasma exudation into retroperitoneal space, kinins release, & systemic pancreatic enzymes effects)
↑serum amylase & lipase
Diagnosis CT w/ contrast
Acute Pancreatitis
Treatment
ERCP (when caused by gallstones) Aggressive IVF admin Colloid replacement NPO to rest pancreas - NJ tube feeding NG tube LIS Stent placement Opioids Stone extraction Sphincterotomy
Acute Pancreatitis
Differential Diagnoses
Perforated duodenal ulcer Acute cholecystitis Mesenteric ischemia Bowel obstruction Acute MI Pneumonia
Acute Pancreatitis
Complications
Shock, hypoxemia, ARDS, GI hemorrhage & coagulation defects, DIC, infection or abscess formation
Chronic Pancreatitis
Chronic inflammation leads to irreversible damage to pancreas
Loss exocrine & endocrine function
Chronic Pancreatitis
Causes
Chronic ETOH abuse
Especially w/ high protein diet
Genetic defects (idiopathic chronic pancreatitis)
Occurs w/ CF & hyperparathyroidism
Chronic Pancreatitis
Diagnosis
History chronic ETOH abuse + pancreatic calcifications
Thin or emaciated - maldigestion proteins & fats
Normal serum amylase
U/S reveals enlarged pancreas or pseudocyst
ERCP most sensitive imaging test
Chronic Pancreatitis
S/S
Epigastric pain that radiates to back
Frequent after eating
1/3 painless
Steatorrhea when 90% exocrine function lost
Diabetes d/t impaired or lost endocrine function
Chronic Pancreatitis
Treatment
Manage pain, malabsorption, & diabetes
Opioids
Celiac plexus blockade
Pancreatic jejunostomy - internal surgical drainage procedure
Endoscopic stent placement & remove stones
Enzyme supplements to help fat & protein absorption
Insulin replacement/therapy
Upper GI Bleed
Most common
Due to peptic ulcer disease
Mortality >30% elderly, esophageal varices, cancer, & hospitalized patients
1° cause of death MODS rather than hemorrhage
Upper GI Bleed
Diagnosis
Upper endoscopy after hemodynamic stabilization Cardiopulmonary concerns d/t blood & gastric content aspiration risk Prefer ETT (secured airway)
Upper GI Bleed
S/S
Hypotension & tachycardia
Orthostatic hypotension
Melena indicated bleeding ABOVE the cecum
↑BUN
Upper GI Bleed
Treatment
Endoscopic coagulation - perforation risk
Epi injection
Endoscopic ligation (bleeding varices)
Trans-jugular intrahepatic portosystemic shunt (TIPS) esophageal varices resistance to treatment → worsen encephalopathy
Mechanical balloon tamponade via Blakemore-Sengstaken tube
Refractory GI bleeding → oversew ulcer or perform gastrectomy
Lower GI Bleed
Usually from diverticulosis or tumor
Common in older patients
Lower GI Bleed
Diagnosis
Sigmoidoscopy to exclude anorectal lesions
Colonoscopy
Lower GI Bleed
S/S
Bright red blood & clots via the rectum
Lower GI Bleed
Treatment
Angiography embolic therapy
Surgical intervention required about 15%
Lower GI Bleed
Usually from diverticulosis or tumor
Common in older patients
Lower GI Bleed
Diagnosis
Sigmoidoscopy to exclude anorectal lesions
Colonoscopy
Lower GI Bleed
S/S
Bright red blood & clots via the rectum
Lower GI Bleed
Treatment
Angiography embolic therapy
Surgical intervention required about 15%
Adynamic Ileus
Formerly known as acute colonic pseudo-obstruction
Massive dilation w/o mechanical obstruction
Loss effective colonic peristalsis & subsequent colon distention
Adynamic Ileus
Causes
Seriously ill hospitalized patients - Electrolyte disorders - Immobile - Narcotic/ anticholinergic medications - Surgical patients Excessive SNS & lack PSNS input
Adynamic Ileus
Diagnosis
CXR proximal colon dilation & decompressed distal colon w/ air in rectosigmoid region
Adynamic Ileus
Treatment
Correct electrolyte abnormalities Avoid narcotics & anticholinergics Mobilization Tap water enemas NG suction Conservative treatment usually takes 2 days
Neostigmine IV (monitor bradycardia), repetitive colonoscopy, and/or cecostomy placement
Untreated → R colon & cecum ischemia
