deck_10249239 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 on EGD 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
Seen in 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
•Barrett’s esophagus
metaplasia associated w/ adenocarcinoma
•Reflux into pharynx, larynx, & tracheobronchial tree
•Apsiration → pulmonary fibrosis or chronic asthma•
GERD Treatment
Lifestyle modification:
•avoid foods that impair LES tone (fat, alcohol, peppermint, chocolate) or are 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
Malnourishment
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 ulcer
Most common cause = NSAID use
Stress Gastritis
Associated w/ shock, sepsis, respiratory failure, burns, hemorrhage, massive transfusions, or head injury
•Gastric bleeding occurs when coagulopathy, thrombocytopenia, INR >1.5, and aPTT >2x normal
Zollinger-Ellison Syndrome
•Gastroduodenal & intestinal ulceration d/t increased gastrin secretion
•Non-beta islet cell pancreatic tumor
•Primarily in men 30-50yo
Associated w/ MEN1```
Zollinger-Ellison syndrome (ZES)
S/S
Abdominal pain
Peptic ulceration
Diarrhea
GERD
ZES Treatment
Obtain fasting gastrin levels
Increasing 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
H receptor antagonists
Proton pump inhibitors 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, & Nizatidin
•inhibit basal & stimulated gastric acid secretion
•Cimetidine & Ranitidine bind to CYP450
PPIs
Proton pump inhibitors
Omaprazole, Pantoprazole, Esomeprazole, Lansoprazole, & Rabeprazole
•They inhibit hydrogen-potassium ATPase pump
The most potent drug available
•Inhibit ALL gastric acid secretion phases
•Interfere w/ Ketoconazole, Ampicillin, Iron, Digoxin, & Diazepam absorption
•Omaprazole & Iansoprazole inhibit CYP450
Prostaglandin Analogues
Misoprostol
•Is the onlyFDA approved •Contraindicated in pregnancy
•Enhances 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
Ulcerative Colitis 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
Ulcerative Colitis (UC) Complications
•Hemicolectomy when patient requires 6-8 units PRBCs w/in 24-48hrs
•Toxic megacolon - dilated transverse colon w/ loss •hallucinations triggered by electrolyte abnormalities & narcotics
•Perforations → peritonitis
•Obstruction d/t benign stricture formation
•Total proctocolectomy = curative
Crohn’s Disease
•IBD with acute or chronic bowel inflammation
•Can be Penetrating-fistulous or obstructing pattern
•Most common site = terminal ileum
Crohn’s S/S
Ileocolitis
•Recurrent episodes RLQ pain & diarrhea and fever indicates intraabdominal abscess formation
•Weight loss d/t anorexia & diarrhea
•Loss of digestive & absorptive surface → megaloblastic anemia & neurologic symptoms
•Hypoalbumenia,
•hypocalcemia, •hypomagnesemia, •coagulopathy,
•hyperoxaluria
•Vit. D deficiency
•hypocalcemia
glucocorticoid use
•B12 malabsorption → megaloblastic anemia & neurologic symptoms
•Diarrhea d/t bacterial overgrowth in obstruction areas, •fistulas,
•bile acid malabsorption,
•DecreasedH2O 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-inflammatoryGlucocorticoids moderate to severe Crohn’s only to induce remission & then taper (not maintenance)
•Antibiotics “pouchitis” (Ciprofloxacin & Metronidazole)Azathioprine, Methotrexate, Cyclosporine, & TacrolimusInfliximab & 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
manifestation
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 urine1° metabolite: 5-HIAA (5-hydroxyindoleacetic acid)
Carcinoid Crisis
•Intense flushing
•Diarrhea
•Abdominal pain
•Tachycardia
•Hypo or hypertension
Causes include stress, chemo, or biopsy
Avoid using Succinylcholine, Miva/Atracurium, Epi/NE, Dopamine, Isoproterenol, or Thiopental```
Carcinoid Tumor Treatment
Avoid flushingSerotonin receptor antagonists5HTZ or 5HT3 antagonistsH1/H2 antagonistsSomatostatin analoguesBronchoconstriction resistant to treatment β agonists worsen effects d/t mediator releaseTACE - 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)
•Post operative 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
•LISStent placement
•Opiods
•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 of exocrine & endocrine function
Chronic Pancreatitis| Causes
•Chronic ETOH abuse
w/ high protein diet
•Genetic defects (idiopathic chronic pancreatitis)
•Occurs with 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
•painless steatorrhea
•Diabetes when 90% exocrine fx is lost
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
•Melina stool 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 of effective colonic peristalsis & subsequent colon distention
Adynamic Ileus| Causes
Seriously ill hospitalized patients- Electrolyte disorders- Immobile- Narcotic/ anticholinergic medications- Surgical patientsExcessive 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
If untreated:→ R colon & cecum ischemia
