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207 Cards in this Set
- Front
- Back
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Salivary gland secretions
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Parotid - serous
Submandibular - predominately serous Sublingual - predominately mucous |
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Major characteristics of saliva (5)
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HCO3
K+ Hypotonic Amylase Lingual lipase |
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Saliva and flow rate
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Low flow: lowest osmolarity (b/c ducts reabsorb Na and Cl)
High flow: highest osmolarity b/c no time for ducts to reabsorb ions In acinus, saliva osmolarity and composition is similar to plasma |
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Sialolithiasis (3)
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Submandib 90%
Recurrent pain and swelling w/ meals Middle-aged males |
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Sjogren Syndrome
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Immune-mediated destruction of salivary and lacrimal glands
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Head and Neck Squamous Cell Carcinoma (precursor, a/w)
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Precursor: leukoplakia
50% a/w HPV |
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Myenteric vs submucosal plexus
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Myenteric - b/w longitudinal and circular muscles, controls motility
Submucosal - sensory, controls secretions and blood flow |
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Neuronal control of lower esophageal sphincter
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Ach -> contraction
Nitric oxide and VIP -> relaxation |
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Normal esophageal histology
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Stratified squamous non-keratinizing epithelium
Changes to columnar at gastroesophageal juncture Upper 1/3 is striated muscle, middle is mixed, lower 1/3 is smooth muscle |
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Mallory-Weiss syndrome (path and 2 a/w)
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Mucosal lacerations at GE junction due to severe vomiting
-> Hematemesis A/w alcoholics and bulimics |
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Main mechanism of GERD and 4 others
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1. Transient LES relaxation
2. Increased intra abdominal pressure 3. Hypotensive LES 4. Crural diaphragmatic pinching 5. Hiatal hernias |
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GERD path
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Motility disorders -> acid exposure in esophagus
NOT too much acid production |
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Heartburn in pregnancy
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30-50%
Increased estrogen and increased abd pressure -> LES dysfunction |
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GERD rx (3)
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H2 antagonists
Antacids PPIs |
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3 causes of esophagitis
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Reflux
Infection (HSV-1, CMV, candida) Chemical ingestion |
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Barrett's esophagus path
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Distal squamous mucosa is replaced w/ metaplastic columnar epithelium as a response to chronic injury
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Barrett's esophagus (can lead to, caused by)
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Esophageal adenocarcinoma
Usually caused by GERD |
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2 types of esophageal carcinoma
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in US: adenocarcinoma
in World: squamous cell |
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Esophageal adenocarcinoma (sx, a/w. where?)
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Progressive dysphagia and wt loss
A/w Barrett's DISTAL |
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Esophageal squamous cell carcinoma (sx, 2 a/w, where)
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Dysphagia and wt loss
A/w alcohol and smoking Mid or distal |
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Achalasia (path, key symptom, key finding, 2 a/w)
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Loss of myenteric plexus NO neurons -> failure of LES relaxation -> uncoordinated peristalsis
Sx: progressive dysphagia to solids AND liquids Bird's beak on barium A/w scleroderma and 2/2 Chagas |
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Reflux esophagitis hist (3)
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Intraepithelial eosinophilia
Basal zone hyperplasia (increased thickness) Papillary elongation |
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Major sites of mucus and acid secretion in stomach
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Acid -> body (upper left)
Mucus -> antrum (bottom) |
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Gastrin (source, action, regulation)
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G cells in antrum of stomach
Increases gastric H+ secretion, gastric mucosa growth, and gastric motility Stimulated by eating (distension, peptides, vagal) |
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3 mechanisms for gastric acid secretion from parietal cells
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Histamine from ECL cells binds H2 receptor -> incr cAMP
Ach binds M3 receptor -> incr Ca Gastrin binds CKK2 receptor on parietal cells -> incr Ca and on ECL cells (incr histamine secretion) |
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3 phases of gastric acid secretion
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1. Cephalic via vagus Ach
2. Gastric phase: distension and peptides -> gastrin and Ach release 3. Intestinal phase: gastrin and absorbed amino acids stimulate parietal cells |
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3 things that slow gastric emptying
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Chyme
Fats Hypertonicity |
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Peptic ulcers and pain with meals
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Greater w/ meals = gastric ulcer
Decreases w/ meals = duodenal ulcer |
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Gastric ulcer (cause, h.pylori association, 1 key cause)
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Decreased mucosal protection against gastric acid
70% a/w h.pylori (urease test) NSAIDS commonly cause |
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Duodenal ulcer (cause, h.pylori association, histopath 2)
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Increased gastric acid secretion (zollinger-ellison) or decr mucosal proection
100% have h.pylori Clean, punched out margins w/ hypertrophy of Brunner's glands |
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Most common location for H.pylori in stomach
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Antrum
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How do NSAIDs cause gastric ulcers (2)?
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1. Topically injure mucosa by increasing permeability
2. Decrease prostaglandins which normally enhance gastric mucosal blood flow |
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Parietal cells (location, secretion, stimulus)
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Body (fundus)
HCl Gastrin, Ach, Histamine |
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Chief cells (location, secretion, stimulus)
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Body (fundus)
Pesinogen Ach |
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G cells (location, secretion, stimulus)
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Antrum
Gastrin Vagal, peptides (inhibited by somatostatin and H+) |
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Mucous cells (location, secretion, stimulus)
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Antrum
Mucus, pepsinogen Ach |
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Cholecystokinin (source, action, regulation)
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I cells in duodenum and jejunum
Increases pancreatic secretion and gallbladder contraction Decreases gastric emptying Increased by amino acids and fats |
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Secretin (source, action, regulation)
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S cells of duodenum
Increase HCO3 and bile acid secretion Inhibit gastric acid secretion Increased by acid and fats in duodenum |
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Somatostatin (source, action, regulation)
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D cells in pancreas and GI mucosa
Decreases gastric acid, pepsinogen, pancreatic, gallbladder, insulin and glucagon secretion Increased by acid and decreased by vagal stimulation |
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Vasoactive intestinal polypeptide (VIP) (source, action, regulation)
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Parasymp ganglia
Increases intestinal water, electrolyte secretion, relaxes smooth muscle and sphincters Increased by vagal distention and decreased by adrenergic input VIPoma -> copious diarrhea |
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2 inhibitors of parietal cell H+ secretion
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Prostaglandins and somatostatin
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Acute gastritis (path and several causes)
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Disruption of mucosal barrier -> inflammation
NSAIDs, alcohol, uremia, burns |
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Chronic gastritis (sx and 2 types)
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Usually few symptoms
Type A (fundus) - autoimmune AB to parietal cells -> pernicious anemia Type B (antrum) - most common, H.pylori -> incr risk of MALT lymphoma |
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Gastric carcinoma (type, 2 key findings)
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Almost always adenocarcinoma
Signet ring cells Acanthosis nigricans |
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Linitis plastica
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Diffusely infiltrative gastric adenocarcinoma
"Leather bottle" thickened, rigid appearance |
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Most common cause of acute vs chronic gastritis
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Acute - NSAIDs
Chronic - H.Pylori |
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Polyp: smooth, dome-shaped w/ hyperplasia of mucus secreting cells (path)
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Fundic gland polyp
Benign (path: PPIs -> incr serum gastrin ->glandular hyperplasia) |
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Polyp: increased cell density w/ picket-fence
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Adenomatous poly
Malignant potential A/w FAP APC gene mutation |
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H2 blockers (examples, moa, 3 uses)
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Cimetitidine, ranitidine
Block H2 receptors -> decr H+ secretion by parietal cells Peptic ulcer, gastritis, mild reflux |
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H2 blockers toxicity
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Cimetidine: P450 inhibitor
Gynecomastia in men, galactorrhea in women Diarrhea Headaches, confusion |
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Antacids tox (3)
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Affects absorption of other drugs
Overuse: AlOH -> constipation MgOH -> diarrhea CalciumCarbonate -> hypercalcemia, rebound acid All can cause hypokalemia |
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Sucralfate (moa, 1 tox)
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Bind ulcer base
Contains Al -> constipation |
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Misoprostol (moa, use, tox)
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PGE analog -> incr proudction and secretion of gastric mucous barrier and decr acid production
Prevention of NSAID-induced peptic ulcers Tox: Diarrhea, contraindicated in pregnancy (abortifacient) |
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PPIs (moa, use, tox)
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Irreversibly inhibit H/K ATPase in parietal cells
Uses: peptic ulcer, gastritis, reflux, zol-ellinger Tox: few but nausea, diarrhea, myopathy, skin rashes |
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Metoclopramide (moa, use, tox)
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D2 receptor antagonist -> incr resting tone, contractility, LES tone and motility
Use: diabetic and post surgery gastroparesis Tox: Parkinsonian, tardive dyskinesia |
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Bethanechol
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Prokinetic cholinergic agent
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H. pylori Rx (3)
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Metronidazole
Amoxicillin (or tetracycline) Bismuth |
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Ammonia metabolism
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Liver is only organ w/ complete urea cycle
In mito of hepatocytes: NH3 + CO2 -> Urea -> sinusoidal blood -> kidneys -> urine |
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Liver detoxification
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Phase I - CYP540 enzymes, unmasking or addition of polar groups
Phase II - conjugation |
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Bilirubin production and excretion
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RBC: hemoglobin -> biliverdin -> bilirubin
Circ: bilirubin+albumin Liver: bilirubin -> conj-bilirubin via UDPGT Bile: conj bilirubin -> small intestin urobilinogen via bacteria -> feces |
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Formation of bile
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Liver: Cholesterol -> bile salts ->
Gallbladder -> duodenum as bile salts via conjugation w taurine and glycine Bacteria produce secondary bile acids |
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Reabsorption of bile
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In terminal ileum
Via Na/Bile salt symporter |
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Secretory rate and composition of pancreatic juice
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High rates: lots of HCO3 little Cl
Low rates: little HCO3, lots of Cl B/c HCO3/Cl exchanger on luminal side of ductal cells |
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4 reasons pancreas doesnt digest itself?
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Enzymes secretes as zymogens
Enzymes are segregated into membrane bound compartments Pancreas has intracellular trypsin inhibitor Eneterokinase (activating enzyme) is distant from pancreas |
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3 phases of pancreatic secretions
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Cephalic- vagal -> lots of enzymes and little juice
Gastric- vagal, gastrin -> lots of enzymes, little juice Intestinal- secretin -> HCO3, CCK -> enzymes |
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Where is iron absorbed?
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Duodenum
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Pigment stones (2 types and composition)
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20%
Brown - bacteria or parasites Black - unconjugated bilirubin and calcium salts |
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Pigment stones risk factors
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Hemolytic anemias -> black stones
Chronic infection of biliary tree -> brown stones |
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Biliary colic
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Obstruction of common bile duct
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Cholesterol stones (4 a/w)
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80% of gallstones
A/w: female, fat, fertility, forty |
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Complications of gallstones (6)
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Cholecystitis, ascending cholangitis, acute pancreatitis, bile stasis
Biliary colic Gallbladder ileus |
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Gallstone disease clinical
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RUQ tenderness
Epigastric tenderness Pain radiating to back Jaundice |
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3 factors in gallstone formation
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Increased cholesterol
Decreased bile Phospholipids |
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Pancreas divisum
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10%
Ventral and dorsal ducts fail to fuse (ventral duct is main duct of Wirsung) Major drainage is by dorsal duct (the minor duct/papilla) predisposing to stenosis and chronic pancreatitis |
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Acute pancreatitis (definition and 3 clinical and main cause)
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Autodigestion of pancreas by pancreatic enzymes
Epigastric pain radiating to back Anorexia Nausea Cause: alcohol |
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Alcoholic acute pancreatitis path
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Alcohol stimulates enzyme secretion -> proteinaceous plugs in ducts -> blocked secretion -> buildup of digestive enzymes and leakage into interstitial space -> inflammation
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Acute pancreatitis labs and complications (5)
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Elevated serum amylase (sensitive) and lipase (specific)
DIC, ARDS, diffuse fat necrosis, hypocalcemia, hemorrhage |
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Chronic pancreatitis definition and 2 features
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Irreversible damage to pancreas
Fibrosis and destruction of endocrine cells |
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3 types of chronic pancreatitis
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Alcohol, hereditary, cystic fibrosis
All feature calcification |
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4 aspects to course of chronic pancreatitis
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Pain
Calcification Malabsorption Diabetes |
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Pancreatic pseudocysts
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Collection of pancreatic fluid with no epithelial lining
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Migratory thrombophlebitis
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Redness and tenderness on palpation of extremities (spontaneous venous clotting)
Pancreatic adenocarcinoma |
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Exocrine pancreas adenocarcinoma
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60% in head -> cause obstruction and jaundice
Distal tumors are clinically silent for a long time Highly fatal |
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Pancreatic endocrine tumor
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Single discrete tumor of islet cells
Eg: insulinoma, glucagonoma, gastrinoma |
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Acute vs chronic diarrhea
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4 wks
> 200 g of stool in 24 hr |
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5 types of diarrhea
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Osmotic
Malabsorption (fatty) Inflammatory Secretory Altered motility |
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Osmotic diarrhea (FOG limit, path)
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Fecal osmotic gap > 125
Large amts of osmotically active solutes in lumen cause water retention |
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Osmotic diarrhea (examples)
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Lactose intolerance
Osmotic laxative abuse |
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Hydrogen breath test (late vs early peak)
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Late peak = lactose intolerance (excess H2 produced by colonic bacterial fermentation)
Early peak = bacterial overgrowth into small intestine |
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Fecal osmotic gap
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290 - 2*([Na] + [K])
< 50 -> secretory diarrhea > 125 -> osmotic diarrhea |
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Malabsorptive diarrhea (5 examples)
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Small intestinal bacterial overgrowth
Increased bile salt losses (surgical resection of Ileum in Crohn's) Enzyme deficiency (pancreatic) Mucosal disease (celiac sprue, Crohn's) Celiac sprue |
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Small intestinal bacterial overgrowth syndrome (2 predisposing factors and pathophys, dx)
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Malabsorptive diarrhea
Due to: intestinal stasis or abnormal connections b/w distal and prox bowel -> reduced nutrient availability (bacteria consume) and bile salt inactivation due to unconjugation by bacteria Dx - early peak on H2 breath test |
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4 causes of malabsorptive diarrhea due to mucosal loss
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Extensive surgical resection
Extensive infarction Crohn's Celiac |
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Celiac disease path
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Wheat gliadin into lamina propria -> presented to T cells in conjunction w/ HLADQ2or8 -> tissue transglutaminase strengthens gliadin-Tcell binding -> incr T cell response -> TNFalpha, IFNg, IL4 -> inflammation
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Celiac disease histopath (4)
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Flattened villi
Intraepithelial lymphocytes Hyperplastic crypts Lamina propria inflammation |
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Celiac disease clinical (4)
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Crampy abd pain
Diarrhea, steatorrhea Iron deficiency Easy bruising |
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Celiac disease a/w
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Dermatitis herpetiformis - IgA deposits in skin w/ pruritic blistering
Small intestinal lymphoma and adenocarcinoma |
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Celiac disease dx
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Tissue transglutaminase Ab
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Secretory diarrhea (path, and FOG)
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Abnormal ion transport in intestinal epithelials
Decreased electrolyte absorption Fecal osmotic gradient < 50 |
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Secretory diarrhea 4 categories
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Congenital defects in ion absorption
Intestinal resection w/ decreased absorptive surfaces Diffuse mucosal disease w/ reduced enterocyte Abnormal mediators (changes in cAMP, bacterial toxins) |
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What type and how do Zollinger-Ellison and Carcinoid syndromes cause diarrhea
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Secretory
Z-E: gastrin -> acid inactivation of pancreatic enzymes and bile salts, damage to mucosa Carcinoid: serotonin, motilin, pg's -> incr motility, intestinal fluid and electrolyte secretion |
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Whipple disease (what type of diarrhea?)
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Distended macrophages containing lysosomes w/ organisms
-> malabsorptive diarrhea due to impaired lymphatic transport |
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Carcinoid tumors (epi, leads to, 4 symptoms, dx)
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50% of small intestine tumors
Produce 5-HT -> carcinoid syndrome: wheezing, right-sided murmurs, diarrhea, flushing Dx - 5-HIAA |
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Inflammatory bowel disease epi (2)
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Peak onset 15-25 y/o w/ bimodal at 50-65
m=f |
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Ulcerative colitis vs Crohn's (location, diarrhea, volume, distribution, inflammation, fibrosis, granulomas, fat malabsorption, rectal bleeding)
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UC: colon, small volume, diffuse, inflammation in mucosa, NO fibrosis, NO granulomas, NO malabsorption, rectal bleeding
Crohn's: ileum-colon, large volume, skip pattern, transmural inflammation, fibrosis + granulomas, fat malabsorption, 30% rectal bleeding |
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Ulcerative colitis path (5)
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Continuous
Erythema, punctate ulcerations Pseudopolyps Inflammation confined to mucosa Dysplastic crypts |
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Ulcerative colitis complications (2)
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Toxic megacolon
Colorectal cancer |
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Crohn's path (6)
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Segmental involvement
Thickened wall w/ narrowed lumen Transmural inflammation Cobblestone, patchy ulcers Mucosal granulomas String sign on bariumxray) |
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Antibodies in IBD
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UC: pANCA
Crohn's: ASCA |
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Surgery and smoking in IBD
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UC: curative, smoking improves
Crohn's: 90% recurrence, smoking worsens |
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Sulfasalazine (composition, activaton)
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Sulfapyridine-antibacterial
5-aminosalicyclic acid-anti inflammatory Activated by colonic bacteria UC and CD |
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NOD2/CARD15
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Crohn's disease
30% A/w with obstructive/stricturing phenotype |
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Crohn's complications (2)
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Osteoporosis
B12 deficiency |
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Micronodular vs macronodular cirrhosis
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Micro: uniform size, due to metabolic insult (alcohol, hemochromatosis, Wilson's)
Macro: varied size, due to significant injury leading to necrosis (post-infectious/drug-induced hepatitis) |
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Feathery/foamy hepatocyte degeneration
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Cholestasis
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Cirrhosis path
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Diffuse fibrosis with regenerative nodules
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7 major causes of cirrhosis
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Alcohol
Non-alcoholic fatty liver disease (NAFLD) Chronic viral hepatitis Chronic biliary disease Hereditary hemochromatosis Wilson's disease A1-AT |
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Hepatic fibrosis path
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Hepatic stellate cell normally stores vitA in space of Disse
Activation causes switch to myofibroblast like cells that makes collagen |
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Hepatic ballooning degeneration
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Acute viral hepatitis
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Acute viral hepatitis path (3)
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Mononuclear infiltrate
Ballooning degeneration Apoptosis |
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Councilman body and piecemeal necrosis
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Chronic hepatitis
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Alcoholic liver disease path
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Excess NADH from alcohol/acetaldehyde dehydrogenase -> lipid biosynth ->
Steatosis (fatty liver) Decr glutathione synth -> oxidative injury |
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3 morphologic forms of alcoholic liver disease
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Hepatic steatosis - short term change, macrovesicular fatty change
Alcoholic hepatitis - long-term, swollen necrotic hepatocytes, Mallory bodies Cirrhosis - regenerative micrnodules |
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Mallory bodies
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Alcoholic hepatitis
Intracytoplasmic eosinophilic inclusion |
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Alcoholic hepatitis LFTs
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AST > ALT (ration greater than 1.5)
BUT neither > 300 |
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Non-alcoholic fatty liver disease (morph/path, 2 causes)
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Steatosis + inflammation -> fibrosis
Caused by obesity/diabetes |
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Nutmeg liver
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Due to backup of blood into liver
Caused by R heart failure and Budd-Chiari Liver is mottled Can progress to necrosis -> cardiac cirrhosis |
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Hepcidin function
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Major regulator of iron, like insulin
Binds ferroportin in enterocytes to prevent iron going from cell into blood Also blocks iron release from macrophages and hepatocytes |
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Hereditary hemochromatosis classic triad
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Cirrhosis
Diabetes Skin pigmentation (bronze diabetes) HFE gene mutation |
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Hemochromatosis histopath
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Iron accumulation in hepatocytes and bile duct
NOT in Kuppfer cells- compare to secondary Fe overload |
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Wilson's disease pathogenesis and rx
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Inadequate hepatic copper excretion -> copper accumulation in brain, liver, kidneys, joints
Rx - penicillamine (chelator) |
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Wilson's disease 4 features
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ABCD
Asterixis Basal ganglia degeneration -> parkinsonian symptoms Ceruloplasmin down, cirrhosis, corneal deposits (Keyser-Fleischer rings) Dementia |
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Keyser-Fleischer rings
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Wilson's
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alpha-1 antitrypsin deficiency
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Misfolded gene products accumulate in hepatocellular ER
Decr elastic tissue in lungs -> panacinar emphysema |
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Primary biliary cirrhosis path (path sequence, 2 path features, dx)
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Autoimmune -> lymphocytic infiltrate -> GRANULOMAS
Incr serum mitochondrial Ab Florid duct lesions |
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Biliary cirrhosis clinical and labs (5 clinical, 3 labs)
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Pruritis
Jaundice Dark urine Light stools Hepatosplenomegaly Labs incr conj bilirubin, incr cholesterol, incr alk phos |
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Secondary biliary cirrhosis path
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Extrahepatic biliary obstruction (eg gallstone) -> incr pressure in intrahepatic ducts -> injury/fibrosis and bile stasis
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Primary sclerosing cholangitis path (path sequence, a/w)
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Unknown -> concentric onion-skinning of bile duct fibrosis -> "beading" of intra and extra hepatic ducts on ERCP
A/w IBD |
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Common benign liver neoplasms
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Hemangioma - small, incidental
Hepatic adenoma - a/w oral contraceptive use |
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Hepatic malignant neoplasms
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Metastases are most common
Multiple, nodular masses w/ central necrosis |
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Hepatocellular carcinoma
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A/w HBC, HCV, cirrhosis of any cause
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What malignancy is a/w oral contraceptive use?
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Hepatic adenoma
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Primary sclerosing cholangitis path a/w?
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Unknown -> concentric onion-skinning of bile duct fibrosis -> "beading" of intra and extra hepatic ducts on ERCP
A/w IBD |
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Common benign liver neoplasms
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Hemangioma - small, incidental
Hepatic adenoma - a/w oral contraceptive use |
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Hepatic malignant neoplasms
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Metastases are most common
Multiple, nodular masses w/ central necrosis |
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Hepatocellular carcinoma 3 a/w
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A/w HBC, HCV, cirrhosis of any cause
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What malignancy is a/w oral contraceptive use?
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Hepatic adenoma
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Gilbert's syndrome
|
Decr UDP-GT or decr bilirubin uptake
A-sx Normal direct, incr indirect |
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Crigler-Najjar syndrome
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Absent UDP-GT
Death w/in first few years |
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Dubin-Johnson syndrome
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Defective liver excretion ->
Incr conjugated bilirubin |
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Serum albumin: acute vs chronic liver disease
|
Normal in acute b/c has half-life of 20 days
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What clotting factors are made in liver?
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All but VIII
Have short-half life, so better test of acute liver disease than albumiin |
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Vitamin K dependent clotting factors
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2, 7, 9, 10, C, S
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Alkaline phosphatase elevation signals
|
Impaired bile flow
Distinguish incr from bone vs liver w/ g-glutamyl transpeptidase or 5' nucleotidase measurements |
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Increased anti mitochondrial antibody
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Primary biliary cirrhosis
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Increased AST and ALT > 500
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Heptaocellular disease (acute hepatitis, CHF, toxins)
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Hepatitis pathophys
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liver inflammation ->
hepatocyte membrane damage -> release of AST and ALT Failure to excrete bilirubin -> jaundice |
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Sx of acute hepatitis (4)
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Dark urine/Pale stool
Jaundice RUQ discomfort Fatigue and anorexia |
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Hepatitis and protective antibodies
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Protective Ab for HBV (anti-HBsAg) and HAV
NOT for HCV No vaccine for HEV |
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Presence of HBsAg indicates
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Acute or chronic infection
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Anti-HAV
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Detects both IgM and IgG
Positive in acute and someone w/ a past infection |
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Key features of HEV (3)
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Fulminant hepatitis in 20% pregnant women
Acute hepatitis in children No vaccine |
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What is the best way to test for early HBV infection?
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Anti-HBc IgM
Earliest host response |
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What is the serology difference in someone infected w/ HBV vs vaccinated
|
Infected has Anti-HBc and Anti-HBs
Vaccinated only has anti-HBs |
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When is Anti-HBcAg the only present marker?
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During the window period in which HBsAg is disappearing but anti-HBsAg is not yet detectable
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2 mechanisms for portal hypertension
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Increased resistance (smaller radius and less compliance due to collagen deposition)
Increase in portal inflow Increased resistance is the initial mechanism |
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Effect of portal htn on splanchnic vasculature
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Portal htn -> vasodilator release/decr clearance of vasodilators -> incr blood in splanchnic vasc -> incr portal inflow -> portal htn
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Hepatic venous pressure gradient
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Free hepatic venous pressure (IVC) - wedged hepatic venous pressure (Portal)
normal = 3-5 ONLY INCREASED IN INTRAHEPATIC SINUSOIDAL HTN |
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Pre-hepatic portal htn
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Portal thrombosis
Splenic vein thrombosis |
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Pre-sinusoidal portal htn
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Schistosomiasis (eggs are trapped in portal triad
Sarcoidosis Incr. resistance is at portal triad |
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Sinusoidal portan htn
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Increased HVPG
Cirrhosis |
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Post-sinusoidal portal htn
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Budd-Chiari
At level of central vein |
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Post-hepatic portal htn
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Hepatic venous thrombosis
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2 mechanisms of ascites
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Liver failure -> hypoalbuminemia -> decr oncotic pressure
Incr peripheral vasodilation -> perceived vol deficit -> decr cortical perfusion -> incr renin -> incr aldosterone -> incr Na and H2O retention |
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Serum ascites albumin gap
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Serum albumin - ascites fluid albumin
< 1.1 -> lots of protein in ascites fluid -> peritoneal leakage > 1.1 -> portal htn |
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Hepatic encephalopathy pathophys
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Incr ammonia (b/c failed liver metabolism to urea) -> upregulation of benzo receptors -> modulated GABA receptor activity -> hepatic encephalopathy
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Hepatic encephalopathy Rx
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Lactulose
Acidic pH decreases urease-producing bacteria Protonation of NH3->NH4 -> excretion |
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3 drugs associated with constipation
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Opiates
NSAIDs Iron supplements |
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2 metabolic causes of constipation
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Hypothyroidism
Hypercalcemia (depresses autonomic nerv system -> GI hypotonicity) |
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Colonic diverticulosis (a/w, pathogenesis, rx)
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A/w low fiber
Left side of colon Herniation of mucosa and submucoa through muscularis penetrating vasa rectae (weak points) -> incr intraluminal pressure Usually asymptomatic Rx - high fiber diet |
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Colonic diverticulosis complications
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Painless bleeding due to injury at vasa rectae
Diverticulitis |
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Diverticulitis (what is it, 3 clinical, 2 leads to)
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Inflammation and perforation of diverticula
LLQ pain, fever, leukocytosis Can lead to: abscesses, fistulas |
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Hemorrhoids: internal vs external
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Dilation of hemorrhoidal veins
Internal: painless External: pain |
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Anal fissures (a/w, sx (pain?))
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Trauma from stool, Crohn's, carcinoma
Extreme pain w/ defecation, bleeding |
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Most frequent location for ischemic bowel disease and 3 sx (one key)
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Colon, watershed area near splenic fixture for IMA and SMA
Sx: sudden onset abd pain -> diarrhea -> bleeding (most injury is due to reperfusion, not initial infarction) |
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2 idiopathic/functional constipations
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Slow colonic transit (accumulation of markers throughout colon on Sitz study)
Evacuatory failure/pelvic floor dysfunction (accumulation of markers in rectosigmoid in Sitz study) |
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Psyllium, methylcellulose, polycarbophil (class, moa, 3 tox)
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Bulk-forming agents for constipation or diarrhea
Sources of fiber -> enhance stool mass Tox: bloating, abd pain, drug interactions of absorption |
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Docusate, mineral oil (moa/use, tox)
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Stool softeners/surfactants for constipation
Lowers surface tension of stool Tox: fat malabsorption |
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Osmotic agents for constipation
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Water retention stimulates peristalsis
Tox: abd distention/flatulence For saline-based caution if renal/electrolyte disorders PEG, MgCitrate, Lactulose, Glycerin |
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Bisacodyl, senna, cascara
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Stimulant laxatives
Produce migrating colonic contractions |
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Loperamide, diphenoxylate+atropine
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Opioid derivates for anti-motility (anti diarrheals)
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Most common non-neoplastic polyp (where?)
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Hyperplastic
>50% found in rectosigmoid colon No malignant potential |
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Peutz-Jeghers (2 features, a/w?)
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Multiple non-malignant hamartomas throughout GI
Hyperpigmented mouth A/w incr risk of CRC and other malgiancies |
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Adenomatous polyp (risk increases w/ .. .3)
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Precancerous
Risk increase w/ size, villous histology, epithelial dysplasia |
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Familial adenomatous polyposis (what gene, where)
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Auto dominant APC mutation
100% progress to carcinoma Involves rectum |
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Hereditary non-polyposis colorectal cancer (Lynch Syndrome) (which gene? where?)
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Auto dom mutation of DNA mismatch repair genes
80% progress to carcinoma Proximal colon |
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2 pathways of colorectal carcinoma pathogenesis
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Adenoma-carcinoma sequence (85%): chromosomal instability, left-side colon, worse prognosis, APC/B-catenin -> KRAS
Microsatellite instability (15%) - rightside colon, better prognosis, includes HNPCC |
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Colorectal cancer staging (4)
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T1 - mucosa/submucosa invasion
T2 - muscularis invasion T3 - subserosal invasion T4 - direct invasion of other organs Early stage has 90% 5yr survival |
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Hypertrophic pyloric stenosis (2 clinical, 1 pathophys)
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Non-bilious projectile vomiting
1st born male 3-5wks Muscular layer hyperplasia |
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Intussusception (pathophys, clinical triad)
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Portion of small bowel telescopes into other bowel -> obstruction -> venous compression -> bowel edema
Intermitten abd pain, currant jelly stool, vomiting |
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Intermitten abd pain, currant jelly stool, vomiting
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Intussusception
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Hirschsprung's disease (pathophys, 1 clinical)
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Congenital megacolon
Angangliogenesis of distal bowel starting w/ anus and moving proximally -> incr contractions Infant w/ abd pain failing to pass meconium in 1st 48 hr |
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Omphalocele vs gastroschisi
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Omphalocele: covered by membrane, herniation of bowel through umbilicus, a/w trisomies
Gastroschisis: herniation lateral to umbilicus, not covered by membrane |
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Meckel's diverticulum (pathophys, complications)
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Incomplete obliteration of vitelline duct leading to true diverticulum near ileum
50% contain ectopic gastric musoca -> ulceration -> painless rectal bleeding |
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Meckel's diverticulum dx
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Technetium99 radio study
Only absorbed by gastric mucosa |
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Necrotizing enterocolitis
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Reduction in intestinal blood flow -> ischemia
Abd distension, high WBC, pneumotisis intestinalis is pathognomonic |
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Pneumotisis intestinalis
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Necrotizing enterocolitis
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