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895 Cards in this Set
- Front
- Back
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What is another name for the myenteric plexus? Where is it? Main function? auerbach's plexus
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external muscle layer
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What are the 2 muscle layers of the GI system inner circular
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outer longitudinal
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What is a cell of Cajal pacemaker cell in the GI that has a lower threshold
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can set the # of depolarizations and contractions in an area of GI
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describe the physiology of peristalisis Lumen is stretched
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triggers muscle behind bolus to contract and muscle in front to relax
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Describe the chewing reflex periodontal loading causes jaw muscles to relax and mandible to drop w gravity
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stretch receptors then signal for muscle contraction
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What are the important components of the oral prep phase Lip closure
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cheek tonicity
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What are the 3 key components to dental caries fermentable sugar
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plaque (for anaerobic conditions)
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Child is getting cavities before age 3: Nursing bottle syndrome
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given fruit juice in bottle in crib
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how does mono appear in the mouth palate irritation
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tonsillitis
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Pathogens associated with shellfish cholera
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norovirus
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what is included in the swallowing center of the brain nonvagal nuclei
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nucleus ambiguus
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Describe secretins release and role when duodenal contents have a pH <3.5
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secretin stops gastric emptying
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What is somatostain released in response to low pH
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slows HCl production
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1. medulla inhibits emptying
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pepsin and HCl. Somatostatin also released
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3. Secretin
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GIP and CCK released"
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brush border acts on maltose
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sucrose
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Bile secreted makes soluable
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into cell
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Upper esophagus
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dysphagia and foul smelling vomit Zenker
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What causes esophageal stenosis fibrous thickening of the submucosa. congenital or from reflux
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caustic agents
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Dysphagia
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problems vomitting
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Esophagus with acute neutro infiltrates that can progess to necrosis
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ulceration or granulation esophagitis
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genetics of adenocarcinoma of the esoph p53
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rb
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How does alpha amylase digest starches hydrolyzes the alpha 1
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4 linkages
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what 3 digestive components are found in saliva Alpha amylase
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lingual lipase
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What enzymes does the pancreas release amylase
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lipase
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then at the lumenal brush border endopeptidase
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aminopeptidase and dipeptidase finnish the job."
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Hartnup disease tryptophan deficiency
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pellagra like
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What gases are found in flatus "N2
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CO2
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What is the sequence of events in vommitting UES open
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thrust out jaw
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What is the main pharmacologic goal in treating PUD Controlling acid secretion
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eliminate H. pylori
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Use for PPI PUD
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GERD
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What GI drugs cause P450 inhibition Cimetidine
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Omeprazole
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MOA sucralfate interacts with HCl and forms a paste that creates a barrier for mucosa
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increases Prostaglandin synth
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What drugs interact with sucralfate "Slows absorption of dioxin
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anticoags
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dont mix with antacids
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H2 blocks
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MOA of misoprostol increase Mucous
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NO
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ADR misoprostol Diarrhea
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gas
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MOA bismuth subsalicylate "binds to mucous glycoproteins
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protects against acid and bile
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What are key Abx for H. pylori metranoidazole
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tetracycline
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3 prokinetics "Metaclopramide- Blocks D2
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inc Ach
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aka sineropedic dysphagia" Webs
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etrophic tongue
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Most common causes of dysphagia Achalasia
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scleroderma
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What is a zenker's diverticulum "false diverticulum
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only the mucosa is involved
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Symptomatic Diffuse Esophageal Spasm Crushing substernal pain
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dysphagia
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Cushing (CNS trauma
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loss of vagal tone)"
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What diseases are linked to PUD chronic gastritis
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smoking
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Where are lesions found in D-PUD close to the pylorus
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often paired lesions.
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PUD microscopically "fibropurulent exudate
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necrosis
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What is the pathogenesis of H pylori inflammatory reaction inc cytokines
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inc gastrin
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where is gastritis due to H pylori antral
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high acid production
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what is the appearence of H pylori infected tissue erythematous
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course/nodular
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Causes of reactive gastropathy chemical injury
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NSAID
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Increased IgE leveles
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parasites
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idopathic
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celiac"
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crohns
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sarcoid
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Common gastric polyp
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single/multi
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Large dilated glands
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elongated branch crypts hyperplastic polyp
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Polyploid type of GC solid mass projecting into lumen
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may have ulceration
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Ulcerating type GC grows down
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mimic peptic ulcer
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Diffuse adenocarcinoma no true mass
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walls of stomach thickened (linitis plastica)
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Dysphagia
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weight loss
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button like protrusions
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yellow tan and firm
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prognosis hindgut carcinoid incidental
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almost never met
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GIST demographics "males
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60 yo
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or carneys triad- women
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paraganglioma
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Carney's triad women with GIST
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paraganglioma
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where do you find gastric xanthomas lesser curve
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antrum
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Non inflammatory diarrhea is water
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osmotic
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Dysenteric diarrhea is mucous
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blood
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What causes non inflammatory diarrhea viruses
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parasites
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what risk factors enhance spread of diarrhea crowing
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hygeine
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Pathogenesis of viral mediated GE cytopathic
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blunting of villi
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Important parts of hx when dealing with GE What
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how well was it cooked
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What pathogens are associated with vomitting norovirus
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S. aureus
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What are the causes of inflammatory diarrhea Shigella
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campylobacter
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Heat Labile (meat
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vegs)"
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C. perfringes toxin "heat labile
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spores are heat resistant
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What species of vibrio are more common in the US parahemolyticus
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vulnificus
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5-72 hr incubation and is cleared in 1-3 days
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watery diarrhea parahaemolyticus
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Mechanism of cholera toxin A and B subunits
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activates cAMP
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MOA of ETEC Heat Labile toxiin same as cholera
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cAMP activated pumps
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HUS causes renal failure
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morality low but kidney function reduced
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Enteroinvasive E coli "inflammatory
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resembles shigella (ecoli ferments lactose)
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non motile non lactose fermenting
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varied symtoms shigella
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which shigella causes dysentary dysenteria
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flexerni
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Pathogenesis of shigella "invasive by phagocytosis
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escapes lysosome
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What does campy infection look like "dysenteric
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fever
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how do you test for gastroporesis pt eats an egg with radioactive tracer
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if 50% of tracer remains in stomach after 90 min
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What needs to be ruled out when considering gastroporesis pyloric channel block
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ulcer
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Tx for gastroporesis metacopamid
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erythromycin
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Consquences of H pylori infection gastritis
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peptic ulcers
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DOC for H pylori Clarithromycin
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amoxicillin
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what are the explainations if a pt has a nonhealing ulcer after PPI
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H pylori tx
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Courvoisier's law "large gallbladder
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no jaundice
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small gallbladder
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jaundice and pain= stone in common bile duct
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large gallbladder
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no pain
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Boas Sign run fingers down back
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hypersensitivity of skin T11-L1 positive sign for cholecystitis
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Ca
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K
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The trouble with celiac's gliadin (alcohol soluable part of gluten) induces proliferation of lymphocytes
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esp CD8
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what HLA genes are involved in celiac HLA-DQ2
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DQ8
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Histological staging of celiac "Marsh 1- some lymphocyte infiltration
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minor villi blunting
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Marsh 2- more lymphocytes
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crypts longer and branching
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Marsh 3- villous atrophy
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lots of lymphocytes
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Autoimmune Enteropathy "X linked
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seen in children
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Genes related to autoimmune enteropathy "IPEX
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FOXP12 (3)
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Presentation and sequelae of abetalipoproteinemia infant failure to thrive foul smelling greasy stool
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lipid membrane defects (acantholytic RBCs)
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Presentation of whipples malabsorption
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CNS symptoms
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TH1
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17
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get lots of cellular dmg from bacteria and cytokines
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get inappropriate inflammation"
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most common sites for crohns terminal ileum
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ileocecal valve
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what are the early lesions in crohns aphtous ulcers
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can progress into serpentine linear ulvers
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clinical presentation of Crohn "diarrhea
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fever
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what is CT enterography good for "finding mural thickening
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differential for pt with celiac AMI
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whipple
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Gluten containing grains wheat
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oats
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sulfasalzine compound that breaks down to ASA in colon
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reduces inflam
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Hamartomatous polyps are associated with peutz jegeher
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cowden
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What do the polyps in Juvenile polypolyposis look like less than 3 cm
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pedunculated
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mucocutaneous hyperpigment around moth
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palms
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What malignancies are associated with Peutz jegers breast
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colon
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Conkite Canada "nonhereditary
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older peeps
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diarrehea
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weight loss
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what do hyperplastic polyps look like 5 mm
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smooth nodular
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colon
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thyroid
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Tubular adenoma small on pedestel
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cylindrical
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Villus adenoma large more sessile
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slender villi
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Tubulovillus adenoma mixed
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villus component more at risk for malignancy
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hyperemic
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friable
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traits of distal colon tumors "annular
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circumferential portions of bowel
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cramping
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constipation
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Histological features or adenocarcinoma tall columnar
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desmoplastic
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sites of metastasis for adenocarcinoma local lymph nodes
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bones
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basaloid pattern
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squamous or mucinous differentiation Tumors of the anal canal
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diagnosis of UC sigmoidoscopy
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complete circumferential inflammation with ulceration. biopsy shows non specific inflammation
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what bile issues do people with crohns disease have bacteria deconjugate bile and is excreted as diarrhea
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as a result more cholesterol is diverted to bilary tree to make more
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highest chance of malignant polyp many
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large and dysplastic
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the compromising of what vasculature can result in ischemic bowel celiac
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SMA
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Patchy and segmental involvement
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hemorrhagic
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mesenteric venous thrombosis atrophy of surface epithelium
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acute inflam
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angiodysplasia abnormal formation of blood vessels
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presents in older pop
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meckels diverticulum persistence of vitelline duct
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solitary
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What can cause a diverticulosis to become diverticulitis diet including seeds
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can progress into abscess
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How does giardiasis present abdominal distention
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malabsorb
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cryptosporidium acid fast
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intracellular
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what are the 3 AIDS defining parasites cryptosporidium
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isospora
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What is the unique virulence factor for microsporidiosis polar tubule
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penetrates cell membrane
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Entameba histolytica "very virulent
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disseminates to liver and lungs
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diloxanie
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paromomycin
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if there is an issue with the spleen or stomach what part of the liver should you place your attn to the left side
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most of the blood flow from those organs enters the left lobe of the liver
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Myogenic response have local control by releasing NO
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CO2
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Hepatic arterial buffer response can release adenosine and when blood flow is slow the hepatic arterioles will dilate
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when it is fast they stay constricted as the adenosine is washed away
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how do the centroacinar cells of the intercalated ducts produce bicarb H2O and CO2 and carbonic anhydrase. secrete H+ into the blood
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get small acid tide but is buffered so no large pH shift
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LFTs showing active HAV infection "if ALT is still rising
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pt is infected
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when ALT declines
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pt is most likely clear of virus"
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difference between PTC and ERCP "PTC evaulates the liver
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bile ducts
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children
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itchy butts enterobius vermicularis
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tx for tapeworms (Taenia spp
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E. granulosis
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Lifecycle of malaria mosquito bites
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injects sporozoites
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MOA of chloroquine CQ blocks the conversion of heme to hemazoin
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heme kills plasmodium
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caution in using abx against diarrhea "promote resistance
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can cause HUS in 0157:H7 infected pts.
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pathogenesis of c diff toxin a causes diffuse lymphocytic infiltrate in lamina propria leading to edema and bulging
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epithelium seperates and creates malabsorption. pancolitis
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CT
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then endoscopy"
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complications in c diff toxic megacolon
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transverse volvulus
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tx of c diff "Metronidazole
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vanco if really bad (never IV)
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what parasite is treated with abx
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and what abx cyclospora tx with bactrim
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RNA
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naked icosahedral"
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Long Filamentous- most numerous
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non infectious
|
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HBV coinfection with HDV not too bad
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pt can recover
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HBV and HDV superinfections pt was HBV infected previously and is infected with HDV
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very bad prognosis
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how is HBV transmitted Sexual contact
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IVDA
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HCV transmission "IVDA
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Blood
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Symptoms of acute hepatitis fever
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fatigue
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when is someone considered immune tolerant for HBV exposed infants
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HBeAg positive
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what does an acute HBV infection appear serologically first thing that appears is HBsAg
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shortly after get anti-HBc
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anti HBs -" susceptible
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not exposed
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how does the liver interact with fats in the fasted state HSL is activated by glucagon
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TG is carried to liver by albumin
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what tests measure liver integrity AST
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ALT
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BR
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AP
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what is feathery degeneration seen in cholestasis
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bile accumulation within hepatocytes
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in a proliferation liver you will see mitoses
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string like chords
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HLA with viral ag
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CD8 targets and kills.
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virus initiates an inflammatory rxn
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resulting in cell death"
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jaundice
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ascites
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associations with hep C MPGN
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lymphoma
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pathogenesis of cirrhosis "collagen I and III deposit in the lobules
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liver may be enlarged at first but becomes contracted and shrunken
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how does alcohol enhance oxidative stress "impairs methionine
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decreases glutathione levels making liver more prone to oxidation
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body cannot refuse iron
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absorbs too much in intestine
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what triad of symptoms will lead u to hemochromotosis as a dx "liver abnormalities
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hemoglobin problems
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primary sclerosing cholangitis "inflammation
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fibrosis
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What do FNH lesions look like "clearly demarcated
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central fibrosing scar (stellate)
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you have a liver sample in pathology and it tests positive for alpha 1 antitrypsin
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what kind of lesion was removed from the pt FNH
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Distinguish LCA from FNH LCA does not have a central scar
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can look relatively normal. LCA can result in massive hemorrhage. LCA will also be encapsulated
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abd pain
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ascites
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Gross appearance of HCC multiple
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size varies
|
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Microscopic view of HCC trabecular growth pattern (solid or tubular)
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varied differentiation
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spindle cells
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multinuclear cells"
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Fibrolamellar carcinoma "young pts
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no cirrhosis
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Collagen I
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III
|
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lungs
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diaphragm
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extrahepatic sequelae of HCC can invade portal vein
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and create vena cava syndrome
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gross appearance of hepatoblastoma solid
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well circumscribed
|
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microscopic hepatoblastoma immature hepatocytes
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extramedullary hematopoeisis
|
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Mets to liver Bowel
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breast
|
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central necrosis
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umbilication
|
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may retain some characteristics of source tissue (smooth muscle
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pigmentation)"
|
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impaired estrogen metab- palmar erythema
|
spider angiomas"
|
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hepatorenal syndrome normal appearing kidneys
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sodium retention
|
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what do you look for in acscitic fluid color
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clarity
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surgery
|
illness
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what is ranson imrie criteria how you make a decision on pt care for someone with acute pancreatitis
|
taken at admission and 48 hrs
|
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admission criterea "age
|
cbc
|
|
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complications of pancreatitis PE
|
ARDS
|
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uncomplicated diverticulosis bloated
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flatulence
|
|
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complicated diverticulosis "diverticulitis ->abscess
|
peritonitis
|
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dont do DCBE
|
use CT"
|
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abd pain- better after poop
|
change in freq and consistancy"
|
|
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hemorrhage
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necrosis
|
|
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chronic pancreatitis begin to get fibrosis and destruction of exocrine
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can eventually take out endocrine
|
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lots of fibrosis
|
depressed ducts"
|
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lymphoplasmacytic sclerosing pancreatitis autoimmune pancreatitis
|
lots of plasma cells
|
|
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bulk laxatives sound like plants cuz they are basically
|
absorb water and distend lumen to encourage peristalisis
|
|
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pancreatic pseudocyst accumulations of necrotic hemorrhagic material
|
no epithelial lining
|
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serous cystadenomas benign glandular tissue
|
clear straw colored fuild
|
|
|
intraductal papillary mucinous neoplasm men
|
head of pancreas
|
|
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solid pseudopapillary neoplasm "well circumscribed masses
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locally aggressive
|
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irregular outpatchings
|
benign"
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hard stellate gray poorly defined
|
hard lesions
|
|
|
Sx of pancreatic cancer pain
|
obstructive jaundice
|
|
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acinar cell carcinoma zymogen granules
|
trypsin and lipase production (stains copper color)
|
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pancreatoblastoma "rare
|
children
|
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risks for cholelithiasis "female
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>40
|
|
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4 Fs
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fat fertile females forty
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|
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e coli
|
ascaris infection
|
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Charcot Triad "RUQ
|
fever
|
|
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morphology of chronic cholecystitis "gb wall may be thickened
|
gray
|
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xanthogranulomatous cholecystitis shrunken
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nodular
|
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fever
|
chills
|
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reynolds pentad RUQ pain
|
Fever
|
|
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Cancer of extrahepatic bile ducts "primary sclerosing cholangitis
|
UC
|
|
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acanthosis nigricans "hyperplastic
|
hyperpigmented
|
|
|
Define prehension
|
The obtaining of food to be consumed by hand or mouth
|
|
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Describe the difference between control and regulation of the digestive system
|
"control is on/off
|
|
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What is the major regulator of the Dig System
|
extrinsic autonomic system
|
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What is another name for the myenteric plexus? Where is it? Main function?
|
"auerbach's plexus, external muscle layer, motor control"
|
|
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What is the location and function of the submucosal plexus
|
"submucosa
|
|
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What are the 2 muscle layers of the GI system
|
"inner circular, outer longitudinal"
|
|
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What are the 2 exceptions to the 2 layer rule
|
"stomach- has 3 (oblique layer)
|
|
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Describe the shape of section of GI when the inner circular layer contracts
|
occludes lumen but lengthens tube
|
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Describe the shape of a section of GI when the outer longitudinal contracts
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shortens segment but opens lumen
|
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What area of the brain is controlling GI movement
|
Dorsal motor cortex
|
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What is a cell of Cajal
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"pacemaker cell in the GI that has a lower threshold, can set the # of depolarizations and contractions in an area of GI"
|
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if you see this chart what are the x and y axis
|
"Y- mV
|
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Tonic vs Phasic
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"Tonic- prolonged contractions like in sphincters
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(cycles/min)"
|
"3- stomach
|
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what is the only area in the GI that does not need an AP to contract
|
stomach
|
|
|
What is the sympathetic effect on BER
|
raises the depol threshold
|
|
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What is rhythmic segmentation
|
mixing type of movement that ensures enzyme activity throughout the chyme (ensures digestion)
|
|
|
What kind of contration does the colon use
|
"Haustration for mixing
|
|
|
describe the physiology of peristalisis
|
"Lumen is stretched, triggers muscle behind bolus to contract and muscle in front to relax"
|
|
|
What muscles are used for crushing food
|
masseter and medial pterygoid
|
|
|
Describe the chewing reflex
|
"periodontal loading causes jaw muscles to relax and mandible to drop w gravity, stretch receptors then signal for muscle contraction"
|
|
|
What are the important components of the oral prep phase
|
"Lip closure, cheek tonicity, nasal breathing"
|
|
|
Parotid secretes ______ saliva
|
watery
|
|
|
Submandibular secretes ______ saliva
|
mixed (amylase and Ca++)
|
|
|
Sublingual secretes _______ saliva
|
Mucous
|
|
|
Contents of saliva early in production
|
"isotonic to plasma
|
|
|
in saliva production what ions are taken out and added
|
"Na and Cl reabsorbed into plasma
|
|
|
What are the 4 phases of the normal swallow
|
"Oral prep
|
|
|
Describe the pharyngeal phase
|
"begins when bolus reaches the anterior tonsilar arch
|
|
|
Why is swallowing a problem in people with respiratory issues
|
can attempt to take a breath while swallowing and will aspirate
|
|
|
How many deciduous teeth are there
|
"20
|
|
|
What teeth are missing in a child
|
no premolars or third molars
|
|
|
How many permanent teeth
|
"32
|
|
|
When does the eruption of permanent teeth happen
|
"6-7
|
|
|
Hypodontia
|
some missing teeth (less than 6)
|
|
|
Oligodontia
|
missing more than 6 teeth
|
|
|
Anodontia
|
missing all primary or permanent teeth
|
|
|
Mesiodens
|
midline supernumerary tooth between middle incisors
|
|
|
What 2 syndromes are associated with supernumerary teeth
|
"Cleidocranial dysostosis
|
|
|
Parulus
|
Gum boil abscess on labial or lingual side of mouth
|
|
|
What are the 3 key components to dental caries
|
"fermentable sugar, plaque (for anaerobic conditions), S. mutans"
|
|
|
Child is getting cavities before age 3:
|
"Nursing bottle syndrome, given fruit juice in bottle in crib"
|
|
|
Plaque
|
thick mucous film that can harden
|
|
|
Periodontitis
|
tartar on teeth causes gums to recede
|
|
|
Other name for meth mouth
|
"ANUG
|
|
|
Hairy Tongue
|
some disease processes prevent filliform papillae from shedding giving tongue hairy appearence
|
|
|
Apthous
|
"most common oral ulcer
|
|
|
Where does one get apthous sores
|
"non keratinized surfaces
|
|
|
what causes apthous sores
|
unknown (autoimmune? hormones?)
|
|
|
Pyogenic granuloma
|
"overgrowth of granuloma tissue
|
|
|
how does mono appear in the mouth
|
"palate irritation, tonsillitis"
|
|
|
Primary syphilis
|
chancre inside or around mouth
|
|
|
2ndary syphilis
|
on palate
|
|
|
tertiary syphilis
|
"oral nasal fistula
|
|
|
2 signs of congenital syphilis
|
"Hutchinsons (screwdriver) incisors
|
|
|
What pathogen is commonly found in flooded areas
|
cholera
|
|
|
Pathogens associated with shellfish
|
"cholera, norovirus"
|
|
|
Key symptom to distinguish viral gastroenteritis vs bacterial
|
viral can have associated vommitting
|
|
|
Where do 2ndary and tertiary peristalic waves begin
|
above the bolus
|
|
|
in relation to atmospheric pressure the pressure in the esophagus is _____-
|
lower
|
|
|
what is included in the swallowing center of the brain
|
"nonvagal nuclei, nucleus ambiguus, and the dorsal motor nucleus"
|
|
|
What nucleus controls the striated portions of the esophagus
|
nucleus ambiguus
|
|
|
What is the unsung role of the stomach
|
stores food for release over time
|
|
|
What does CCK do
|
increases gastric distensibility and slows emptying
|
|
|
Where is CCK released from
|
intestine
|
|
|
what is retropulsion
|
larger chunks of chyme are deflected back into the fundus of the stomach as smaller pieces are allowed into the duodenum
|
|
|
Describe secretins release and role
|
"when duodenal contents have a pH <3.5, secretin stops gastric emptying"
|
|
|
What causes the release of CCK
|
high fat content in duodenum
|
|
|
What is the real name of housekeeping waves
|
Migrating motor complex
|
|
|
What are the only 2 real sphincters
|
UES and external anal
|
|
|
What is somatostain
|
"released in response to low pH, slows HCl production"
|
|
|
What does gastrin stimulate
|
HCl and histamine
|
|
|
What does histamine do
|
stimulates HCl
|
|
|
How is HCl produced
|
CO2 and H2O combine by carbonic anhydrase to from H2CO3 which dissociates. HCO3 is absorbed into blood and H is pumped into the stomach along with Cl (and K)
|
|
|
what are the 3 phases of gastric secretion
|
"cephalic
|
|
|
What occurs during the cephalic phase
|
secretion of gastrin -> HCl and pepsin release (pepsinogen until low pH)
|
|
|
What occurs during gastric phase
|
stretch receptors release more gastrin. most HCl released now
|
|
|
What happens during intestinal phase
|
"low pH or too many lipids make 3 things happen
|
|
|
Brief description of carbo digest
|
"salivary amylase begins breakdown
|
|
|
brief description of protein dig
|
"begins in stomach with pepsin
|
|
|
Brief summary of fat dig
|
"glycerol and fatty acid in stomach via lipase
|
|
|
Dyphagia is
|
Difficulty swallowing
|
|
|
odynophagia is
|
painful swallowing
|
|
|
Nutcracker esophagus
|
lack of cooridination
|
|
|
"Upper esophagus, dysphagia and foul smelling vomit"
|
Zenker
|
|
|
Midpoint diverticulum
|
Tracker
|
|
|
Lower esophagus diverticuli that can be do to inflammation or traction
|
epiphrenic
|
|
|
Complications of diverticuli
|
"Pneumonia
|
|
|
What causes esophageal stenosis
|
"fibrous thickening of the submucosa. congenital or from reflux, caustic agents, or radiation"
|
|
|
Plummer-Vinson Syndrome
|
"Iron deficient anemia
|
|
|
What pop are webs more common in
|
women over 50
|
|
|
A schatzki ring
|
"Distal esoph abover GE junction
|
|
|
B Schatzki ring
|
gastric cardia type mucosa
|
|
|
Primary cause of achalasia
|
inhibitor neuron issues
|
|
|
Secondary causes of achalasia
|
"Degenerative nerves
|
|
|
"Dysphagia, problems vomitting, chest pain"
|
Achalasia
|
|
|
Mallory Weis tears
|
longitudinal lacerations near GE junction
|
|
|
Boerhaave syndrome
|
"high mortality
|
|
|
Causes of esophagitis
|
"EtOH
|
|
|
"Esophagus with acute neutro infiltrates that can progess to necrosis, ulceration or granulation"
|
esophagitis
|
|
|
Infectious causes of esophagitis
|
"Candidiasis (#1)
|
|
|
Disease process of Barretts Esophagus
|
Metaplasia squamous-> columnar with goblet cells
|
|
|
Where is barretts common
|
white males 40-60 in developed countries
|
|
|
How can you identify barretts
|
"endoscope and biopsy
|
|
|
Squamous Cell esophageal carcinoma
|
"Males over 45
|
|
|
genetic factors in sq cell esoph cancer
|
p53 and p16/INK4a
|
|
|
where do you find sq cell esoph cancer
|
"middle and upper 1/3
|
|
|
genetics of adenocarcinoma of the esoph
|
"p53, rb, cERBB2, cyclinD1, cyclinE"
|
|
|
What area of the brain triggers hunger
|
hypothalamus
|
|
|
How does alpha amylase digest starches
|
"hydrolyzes the alpha 1,4 linkages"
|
|
|
what 3 digestive components are found in saliva
|
"Alpha amylase, lingual lipase, and carbonic anhydrase (neutralize pH)"
|
|
|
Are carbs digested in the stomach?
|
No
|
|
|
What enzymes does the pancreas release
|
"amylase, lipase, colipase, phospholipase, trypsin, elastase, and chemotrypsin"
|
|
|
Describe the digestion of protein in more detail
|
"begins in stomach with pepsin
|
|
|
How are proteins transported into the cell
|
"SGLT (Na/H+ cotransporters)
|
|
|
what enzymes are found on intestinal brush border
|
"endopeptidase
|
|
|
Describe in more detail carb digeston
|
"alpha amylase in mouth
|
|
|
how are sugars transported into the cells
|
"SGLT1 brings glucose and galactose in
|
|
|
What is important for the digestion and absorbtion of Vit A
|
pancreas
|
|
|
what is a good tx for GLUT1 deficiency syndrome
|
ketogenic diet
|
|
|
Hartnup disease
|
"tryptophan deficiency, pellagra like, affects niacin and seratonin"
|
|
|
What stimulates the secretion of gastrin
|
"Stretch receptors in the antrum of the stomach tell the G cells to release gastrin
|
|
|
What neurotransmitter is responsinle for relaxing the LES
|
VIP released from the vagus
|
|
|
What stimulates the ileocecal valve to open
|
vagal reflex and gastrin
|
|
|
What factors and neccessary for continence
|
"contraction of the puborectialis muscle
|
|
|
What factors are required for defecation
|
"relax puborectalis
|
|
|
What gases are found in flatus
|
"N2, CO2, H2, CH4, O2
|
|
|
What effect does progesterone have on the gut
|
slows down motility
|
|
|
What is the sequence of events in vommitting
|
"UES open, thrust out jaw, Antrum spasms, LES releaxes, Fundus and body are relaxed, abd muscles contract"
|
|
|
What class of drug is preferred for pts with PUD who are pregnant
|
H2 receptor blockers (cimetidine)
|
|
|
What is the main pharmacologic goal in treating PUD
|
"Controlling acid secretion, eliminate H. pylori"
|
|
|
H2 Blockers: better for gastric or duodenal ulcers
|
duodenal
|
|
|
Cimetidine ADR
|
"inhibits P450
|
|
|
MOA of PPI
|
irreversable H/K ATPase inhibitor
|
|
|
Use for PPI
|
"PUD, GERD, Zollinger-Ellison"
|
|
|
What GI drugs cause P450 inhibition
|
"Cimetidine, Omeprazole"
|
|
|
MOA sucralfate
|
"interacts with HCl and forms a paste that creates a barrier for mucosa, increases Prostaglandin synth"
|
|
|
What drugs interact with sucralfate
|
"Slows absorption of dioxin, anticoags, pheytoins, quinolones.
|
|
|
MOA of misoprostol
|
"increase Mucous, NO, PGD and decrease HCl"
|
|
|
When would you use misoprostol
|
Prevention of PUD with NSAID use
|
|
|
ADR misoprostol
|
"Diarrhea, gas, cramps, miscarriage/abortion"
|
|
|
MOA bismuth subsalicylate
|
"binds to mucous glycoproteins, protects against acid and bile
|
|
|
What are key Abx for H. pylori
|
"metranoidazole, tetracycline, amox, clarithromycin"
|
|
|
Drugs for use in GERD
|
"Prokinetics
|
|
|
3 prokinetics
|
"Metaclopramide- Blocks D2, inc Ach
|
|
|
aka sineropedic dysphagia"
|
"Webs, etrophic tongue, females, odynophagia"
|
|
|
Most common causes of dysphagia
|
"Achalasia, scleroderma, diffuse spasm"
|
|
|
what is a true (or traction) diverticulum
|
all layers are involved and sac is above the diverticulum
|
|
|
What is a zenker's diverticulum
|
"false diverticulum, only the mucosa is involved
|
|
|
Symptomatic Diffuse Esophageal Spasm
|
"Crushing substernal pain, dysphagia, vaso-vagal"
|
|
|
respiratory and atypical disorders associated with GERD
|
"Nocturnal coughing/wheezing
|
|
|
What causes projectile vomitting
|
pyloric stenosis
|
|
|
What genetic factors are associated with pyloric stenosis
|
"turner's syndrome
|
|
|
Breakdown of the mucosal barriers. mucous/acid mismatch
|
Acute hemorrhagic gastritis
|
|
|
What are the 2 types of ulcers from acute hemorrhagic gastritis
|
"Curling (severe stomach burns)
|
|
|
Macroscopic view of AHG
|
multiple ulcerations w no prediliction for any area. widespread petechial hemorrhaging
|
|
|
What dx is important to consider in a pt with hypochromic microcytic anemia
|
AHG
|
|
|
What blood results will show up in a pt with AHG
|
hypochromic microcytic anemia
|
|
|
What area does autoimmune gastritis tend to affect
|
"Body and fundus will atrophy
|
|
|
Sequelae of Autoimmune gastritis
|
"dec HCl production and dec IF
|
|
|
What is the pathogenesis of Autoimmune gastritis
|
CD4 Tcells attacking parietal cells and H/K ATPase
|
|
|
What diseases are linked to PUD
|
"chronic gastritis, smoking, ZE, hyperparathyroidism"
|
|
|
How often does PUD transform into a malignancy
|
very rare
|
|
|
Where are lesions found in D-PUD
|
"close to the pylorus, often paired lesions."
|
|
|
Describe a typical G-PUD ulcer
|
"single
|
|
|
When do the different types of PUD present with abd pain
|
"Gastric- after meals (result weight loss)
|
|
|
PUD microscopically
|
"fibropurulent exudate, necrosis, granulation, inflammation at base of ulcer
|
|
|
PUD complications
|
"Hemorrhage
|
|
|
What is the pathogenesis of H pylori
|
"inflammatory reaction inc cytokines, inc gastrin, suppress somatostatin, inc acid via histamine and IL receptors. can block inhibitory signals"
|
|
|
where is gastritis due to H pylori
|
"antral, high acid production"
|
|
|
H pylori increases the risk of what malignancy
|
adenocaricinoma
|
|
|
What chemicals does H pylori secrete
|
"Urease - elevates pH
|
|
|
what is the appearence of H pylori infected tissue
|
"erythematous, course/nodular, neutrophils, MALT, lymphoma"
|
|
|
Causes of reactive gastropathy
|
"chemical injury, NSAID, bile reflux, surgery"
|
|
|
what is GAVE
|
"gastric antral vascular ectasia
|
|
|
"Increased IgE leveles, parasites, H Pylori, collagen vascular disease are all associated with"
|
Eosinophilic gastritis
|
|
|
Causes of lymphocytic gastritis
|
"?
|
|
|
"crohns, sarcoid, mycobacterium, fungus, CMV, H pylori associated with"
|
granulmatous gastritis
|
|
|
Enlargement of rugal folds from hyperplasia with NO inflammation
|
"hypertrophic gastritis
|
|
|
Excessive tranforming growth factor alpha. protein losing enteropathy
|
Menetrier Disease
|
|
|
What happens to acid production in menetriers
|
"decreases
|
|
|
Zollinger Ellison
|
gastrin secreting tumors of SI or pancreas
|
|
|
MEN association with ZE
|
MEN1
|
|
|
Acid production in ZE
|
increases
|
|
|
"Common gastric polyp, single/multi, varied shape"
|
hyperplastic polyp
|
|
|
what are the benign polyps
|
"hyperplastic
|
|
|
"Large dilated glands, elongated branch crypts"
|
hyperplastic polyp
|
|
|
solitary velvety and lobulated appearance polyps in the antrum
|
adenomatous polyp
|
|
|
Smooth glassy sessile. can look like swiss cheese
|
Fundic Gland Polyp
|
|
|
when is the peak incidence for gastric carcinoma
|
50 esp in japan and chile
|
|
|
H pylori is strongly linked to what type of Gastric Ca
|
Diffuse
|
|
|
where is GC most commonly found
|
lesser curve of antrum and pre-pylorus
|
|
|
Polyploid type of GC
|
"solid mass projecting into lumen, may have ulceration"
|
|
|
Ulcerating type GC
|
"grows down, mimic peptic ulcer, ragged bases, punched out"
|
|
|
Diffuse adenocarcinoma
|
"no true mass, walls of stomach thickened (linitis plastica)"
|
|
|
Key microscopic finding for GC
|
signet ring cells (mucous pushes nucleus to the edge of cell)
|
|
|
what does it mean to be an early stage GC
|
"tumor limitted to the submucosa
|
|
|
"Dysphagia, weight loss, anorexia, abd/back pain, anemia"
|
Gastric carcinoma
|
|
|
CARC of carcinoid syndrome
|
"cardiac fibrotic lesions
|
|
|
"button like protrusions, yellow tan and firm, monomorphic"
|
"neuroendocrine tumors
|
|
|
prognosis- foregut carcinoid
|
very good
|
|
|
prognosis- midgut carcinoid
|
very poor
|
|
|
prognosis hindgut carcinoid
|
"incidental, almost never met"
|
|
|
Gastric Lymphoma
|
extra-nodal marginal zone B-cell lymphomas (MALToma) progress to more aggressive tumor
|
|
|
What mutations are associated w GL
|
"t(11:18) (q21;q21)
|
|
|
what is the net effect of the mutations in GL
|
"activate NF kappa B
|
|
|
how do you distinguish leiomyoma from leiomyosarcoma
|
sarcoma has more mitotic figures and will have abnormal morphology
|
|
|
whorls of smooth muscle cells
|
leiomyoma
|
|
|
From what do gastrointestinal stromal tumors come from
|
cells of cajal
|
|
|
most common mesenchymal tumor of the abd
|
GIST
|
|
|
GIST demographics
|
"males, 60 yo
|
|
|
Carney's triad
|
"women with GIST, paraganglioma, and pulmonary chondroma"
|
|
|
what marker is definitive for GIST
|
cKIT
|
|
|
Where does GIST metastasize
|
liver and peritoneum
|
|
|
where do you find gastric xanthomas
|
"lesser curve, antrum, and pre-pyloric areas"
|
|
|
Non inflammatory diarrhea is
|
"water, osmotic, enterotoxin mediated"
|
|
|
Inflammatory diarrhea is
|
hemorrhagic
|
|
|
Dysenteric diarrhea is
|
"mucous, blood, and debris (leukocytes, fibrin)"
|
|
|
What causes non inflammatory diarrhea
|
"viruses, parasites, V. cholerae, ETEC"
|
|
|
what risk factors enhance spread of diarrhea
|
"crowing, hygeine, flooding, fomites, contaminated water, animal slaughtering, raw milk"
|
|
|
what is the leading cause of gastroenteritis in children in the US
|
Rotovirus
|
|
|
What is the overall leading cause of GE in the US
|
Norovirus
|
|
|
Pathogenesis of viral mediated GE
|
"cytopathic, blunting of villi, results in malabsorption, get hypersecretion"
|
|
|
how does rotovirus affect cells that arent infected with the virus
|
produces and enterotoxin that causes Cl and H2O secretion
|
|
|
How can u distinguish bacterial and viral mediated GE
|
viral can have vommitting
|
|
|
how do you treat viral GE
|
maintain hydration and electrolytes
|
|
|
Rotavirus
|
"dsRNA
|
|
|
VP2
|
inner capsid
|
|
|
VP6
|
"middle capsid
|
|
|
VP7 and VP4
|
"G and P protein
|
|
|
What VP6 group causes illness in humans
|
group A
|
|
|
which is more virulent norovirus or rotavirus
|
norovirus (<100 particles for infection)
|
|
|
Important parts of hx when dealing with GE
|
"What, how well was it cooked, when, duration, vomitting vs diarrhea, pt population"
|
|
|
What pathogen is associated with petting farms
|
STEC
|
|
|
What pathogens are associated with vomitting
|
"norovirus, S. aureus, B. cereus (preformed toxins from bacteria)"
|
|
|
What are the causes of inflammatory diarrhea
|
"Shigella, campylobacter, C. difficile, STEC"
|
|
|
Heat stabile toxins
|
"S. aureus
|
|
|
What is the mean incubation of S. aureus
|
4 hrs
|
|
|
How long does Staph GE last
|
less than 24 hrs
|
|
|
Spore forming Gram+ bacillus that makes 2 toxins
|
Bacillus cereus
|
|
|
What are the 2 toxins made by B. cereus
|
"Heat stabile (rice)
|
|
|
Heat Stabile B. Cereus toxin
|
"<6 hrs incubation
|
|
|
Heat Labile B. cereus toxin
|
"Incubates >6 hrs
|
|
|
Anareobic spore forming bacillus
|
Clostridium
|
|
|
C. perfringes toxin
|
"heat labile, spores are heat resistant, affects ileum, watery diarrhea
|
|
|
quick hit: incubation vs heat
|
"shorter incubation- heat stabile
|
|
|
Highly motile gram negative curved rods
|
Vibrio
|
|
|
What species of vibrio are more common in the US
|
"parahemolyticus, vulnificus, and nontoxigenic cholera"
|
|
|
Differentiate parahaemolyticus from vlnificus
|
Vulnificus can infect wounds. parahaem cannot
|
|
|
"5-72 hr incubation and is cleared in 1-3 days, watery diarrhea"
|
parahaemolyticus
|
|
|
Mechanism of cholera toxin
|
"A and B subunits, activates cAMP, activates pumps secrete Na, Cl, K and carbonate"
|
|
|
Defining characteristics of enterobacteriaceae
|
"Gram neg
|
|
|
What bugs ferment lactose
|
Escherichia and Klebsiella
|
|
|
what does an H type designation mean for enterobacter
|
it is motile (flagellar antigen)
|
|
|
What is the nasty E coli strain
|
O157 H7
|
|
|
MOA of ETEC Heat Labile toxiin
|
"same as cholera, cAMP activated pumps"
|
|
|
MOA of ETEC Stabile toxin a
|
same as labile toxin but with cGMP
|
|
|
MOA of ETEC stabile toxin b
|
increases intracellular Ca and increases bicarb secretion
|
|
|
Mechanism of shiga-like toxin from STEC
|
dirupts protein synthesis at ribosome
|
|
|
HUS
|
"causes renal failure, morality low but kidney function reduced"
|
|
|
Clinical disease of STEC
|
"3-4 day incubate
|
|
|
Enteroinvasive E coli
|
"inflammatory, resembles shigella (ecoli ferments lactose)
|
|
|
"non motile non lactose fermenting, varied symtoms"
|
shigella
|
|
|
Which shigella causes watery diarrhea
|
sonnei
|
|
|
which shigella causes dysentary
|
"dysenteria, flexerni"
|
|
|
What is one of the most contagious causes of GE
|
"shigella
|
|
|
Pathogenesis of shigella
|
"invasive by phagocytosis, escapes lysosome, can make tails from actin like lysteria
|
|
|
What will stool of of pt with shigella be like
|
dysentary with high levels of leuks
|
|
|
Pathogenesis of salmonella
|
"enterotoxin much like cholera
|
|
|
Yersinia pathogenesis
|
"invasive can become systemic
|
|
|
what is the most common cause of inflammatory diarrhea in the US
|
campy
|
|
|
What does campy infection look like
|
"dysenteric, fever, 1 week duration
|
|
|
what growth medium can be used to find O157 ecoli
|
sorbitol macconkey agar
|
|
|
Diabetic with early satiety bloating and vomiting
|
Gastroporesis (delayed gastric emptying
|
|
|
how do you test for gastroporesis
|
"pt eats an egg with radioactive tracer, if 50% of tracer remains in stomach after 90 min, test is positive"
|
|
|
What needs to be ruled out when considering gastroporesis
|
"pyloric channel block, ulcer, anatomical blockage of pylorus"
|
|
|
Tx for gastroporesis
|
"metacopamid, erythromycin, last resort- pacer"
|
|
|
types of ulcer and liklihood of bleeding
|
"white based- less 1%
|
|
|
how do you treat an ulcer with a visible vessel
|
inject epi then cauterize
|
|
|
why do NSAIDs produce ulcers
|
mucosal protection is mediated by prostaglandins which are inhibited
|
|
|
Consquences of H pylori infection
|
"gastritis, peptic ulcers, gastric adenocarcinoma, MALToma"
|
|
|
in pts with G-PUD how many have H pylori
|
65-95%
|
|
|
how many pts with dypepsia have H pylori
|
20-60%
|
|
|
in pts with D PUD how many are infected w H pylori
|
80-95%
|
|
|
How many asymptomatic pts have H pylori
|
20-45%
|
|
|
DOC for H pylori
|
"Clarithromycin, amoxicillin, and any PPI"
|
|
|
3 Ps of MEN1
|
"parathryroid tumor
|
|
|
"what are the explainations if a pt has a nonhealing ulcer after PPI, H pylori tx, and no NSAIDS"
|
"pt is lying about nsaids
|
|
|
what is confirmatory lab test for gastrinoma
|
fasting serum gastrin level is over 1000
|
|
|
difference between gastritis and gastropathy
|
gastropathy doesnt have inflammation
|
|
|
organoaxial
|
stomach rotates over itself
|
|
|
mesoenteraxial
|
pylorus rotates anteriorly
|
|
|
Glisson's capsule is innervated by
|
"phrenic nerve
|
|
|
cholecystocoronary syndrome
|
gallbladder attack leading into an MI
|
|
|
if you see scar on abd what are you thinking
|
adhesions
|
|
|
Courvoisier's law
|
"large gallbladder, no jaundice, RUQ pain= stone in cystic duct
|
|
|
Boas Sign
|
"run fingers down back, hypersensitivity of skin T11-L1 positive sign for cholecystitis"
|
|
|
Cullen's sign
|
bluish discoloration around umbilicus. pancratic issue
|
|
|
Complications of chronic diarrhea
|
"dehydration
|
|
|
The trouble with celiac's
|
"gliadin (alcohol soluable part of gluten) induces proliferation of lymphocytes, esp CD8"
|
|
|
Mechanism of autoimmunity in celiac
|
the stim'd cd8 activate b cells to produce antibodies which kill the enterocytes
|
|
|
what antibodies are produced in celiac
|
"IgA class antitissue transglataminase (antitTG)
|
|
|
what HLA genes are involved in celiac
|
"HLA-DQ2, DQ8"
|
|
|
What 3 histological changes occur in celiac
|
"flattened villi
|
|
|
What interleukin is involved in celiac
|
IL-15
|
|
|
What receptor on the enterocytes is being attacked in celiac
|
MIC-A
|
|
|
Associated conditions with celiac
|
"Sjorgrens
|
|
|
what dermatological finding is found with celiac
|
Dermatitis herpetiformis- itchy blistering skin looks like herpes
|
|
|
Genetics of celiac
|
"CELIAC1= chromo 6
|
|
|
Histological staging of celiac
|
"Marsh 1- some lymphocyte infiltration, minor villi blunting
|
|
|
Tropical Sprue
|
"unrelated to gluten sensitivity
|
|
|
Autoimmune Enteropathy
|
"X linked, seen in children
|
|
|
Genes related to autoimmune enteropathy
|
"IPEX, FOXP12 (3)
|
|
|
Pathogenesis of autoimmune enteropathy
|
"antibodies against enterocytes and goblet cells
|
|
|
What kind of malabsorbtion is lactase deficiency
|
biochemical not mechanical/structural
|
|
|
Abetalipoproteinemia
|
"autosom recessive
|
|
|
Defect in abetalipoproteinemia
|
microsomal triglyceride transfer protein (MTP) cannot transport the lipoproteins
|
|
|
Presentation and sequelae of abetalipoproteinemia
|
"infant failure to thrive foul smelling greasy stool, lipid membrane defects (acantholytic RBCs), fat soluable vitamin deficiency"
|
|
|
Whipple's Disease
|
"white males 30-40
|
|
|
Presentation of whipples
|
"malabsorption, CNS symptoms, arthritis, hyperpigmentation"
|
|
|
Crohns
|
"mouth to anus
|
|
|
Ulcerative Colitis
|
"Only colon (usually distal beginning at rectum moving proximal)
|
|
|
genetic risk for crohns
|
"NOD2 (ineffective destruction of luminal microbes)
|
|
|
Pathogenesis in crohns
|
"exposed to bacteria
|
|
|
most common sites for crohns
|
"terminal ileum, ileocecal valve, cecum"
|
|
|
what are the early lesions in crohns
|
"aphtous ulcers, can progress into serpentine linear ulvers, can have strictures, and fistula"
|
|
|
When do you see creeping fat
|
increased mesenteric fat is found in crohns
|
|
|
crypt abscess
|
"acculmulation of neutros in crypts that can destroy the crypt
|
|
|
in which IBD do you find noncaseating granulomas
|
"Crohns
|
|
|
clinical presentation of Crohn
|
"diarrhea, fever, abd pain
|
|
|
Extraintestinal manifestations of Crohn
|
"Uveitis
|
|
|
(SBFT)"
|
"good for uppers (obsolete overall)
|
|
|
Gold standard for upper GI study
|
Esophagogastroduodenscopy
|
|
|
Push enteroscopy
|
only goes 2 ft past ligament of trietz. ligament of trietz is the border for having hematemasis
|
|
|
Problem with small bowl barium enema (entercolysis)
|
less sensitive in distal ileum (area w high incidence of crohns)
|
|
|
number 1 reason to order a capsule endoscopy
|
obscure GI bleed
|
|
|
what is CT enterography good for
|
"finding mural thickening,
|
|
|
what is MRI good for
|
distinguishing fibrosis from inflammation
|
|
|
what are the 4 immune patterns in crohns and what is their association
|
"Type I - ASCA
|
|
|
whats the most usefull lab test in detecting crohns
|
CRP
|
|
|
Why is a fecal lactoferrin test usefull
|
distinguish inflammatory bowel disease from IBS
|
|
|
differential for pt with celiac
|
"AMI, whipple, Tropical sprue, lymphoma, bacterial overgrowth, eosinophilic gastroenteritis, gastrinoma, giardia"
|
|
|
Gluten containing grains
|
"wheat, oats, barley, and rye"
|
|
|
sulfasalzine
|
"compound that breaks down to ASA in colon, reduces inflam"
|
|
|
Distinguishing feature of UC
|
continuous involvement beginning at rectum and moving proximally with abrubt transition to normal colon. pseudopolyps
|
|
|
what are pseudopolyps in UC
|
areas of regenerating epithelium in the lumen
|
|
|
what is the big complication in UC
|
toxic megacolon (damage to muscularis propria)
|
|
|
What does UC put you at risk for
|
Adenoma
|
|
|
what are the 3 catagories of polyp
|
"inflammatory
|
|
|
inflammatory polyp
|
"solitary rectal ulcer syndrome
|
|
|
Hamartomatous polyps are associated with
|
"peutz jegeher, cowden, bannayan ruvalcaba rileym, and cronkite-canada syndrome"
|
|
|
jeuvenile polyps
|
"hamartomatous polyps
|
|
|
What do the polyps in Juvenile polypolyposis look like
|
"less than 3 cm, pedunculated, smooth, cystic spaces"
|
|
|
Mutated genes in JP
|
SMAD4 BMPR1A
|
|
|
Peutz Jehger
|
"Autosom Dom
|
|
|
What malignancies are associated with Peutz jegers
|
"breast, colon, lung, ovaries, uterus, and testicle"
|
|
|
What is unique about adenocarcinoma in Peutz Jehgers
|
adenocarcinoma arises seperately from the polyps
|
|
|
SCAT
|
"sex chord tumor with annular tubules
|
|
|
Cowden syndrom
|
"macroencephaly
|
|
|
BRR syndrome
|
long ass name syndrom similar to cowdens with lower chance of neoplasm and higher mental changes
|
|
|
Conkite Canada
|
"nonhereditary, older peeps
|
|
|
when do you find hyperplastic polyps
|
60s-70s
|
|
|
where do you find hyperplastic polyps
|
left colon
|
|
|
what do hyperplastic polyps look like
|
"5 mm, smooth nodular, lots of goblet cells, serrated surface, looks like a christmas tree"
|
|
|
Gardner syndrome
|
"FAP
|
|
|
Turcot syndrome
|
"FAP
|
|
|
Tubular adenoma
|
"small on pedestel, cylindrical"
|
|
|
Villus adenoma
|
"large more sessile, slender villi, more dysplasia and invasion"
|
|
|
Tubulovillus adenoma
|
"mixed, villus component more at risk for malignancy"
|
|
|
Intramucosal Carcinoma
|
"dysplastic epithelium penetrates basement membrane invading lamina propria and muscularis mucosa
|
|
|
What genetic pathway does adenocarcinoma arrise from
|
APC/B catenin pathway and microsatellite instability with defects in DNA mismatch repair
|
|
|
traits of proximal tumors of the colon
|
"polyploid
|
|
|
traits of distal colon tumors
|
"annular, circumferential portions of bowel
|
|
|
Histological features or adenocarcinoma
|
"tall columnar, desmoplastic, abundant mucin production associated with worse prognosis"
|
|
|
sites of metastasis for adenocarcinoma
|
"local lymph nodes, bones, liver, lungs"
|
|
|
dimpled multiple creamy tan colored lesions
|
liver mets from colon
|
|
|
FAP
|
"autosomal dominant
|
|
|
Hereditary non polyposis colorectal cancer (lynch syndrome)
|
"Colorectum
|
|
|
Genetics assoc with lynch syndrome
|
MSH2 and MLH1
|
|
|
"basaloid pattern, squamous or mucinous differentiation"
|
Tumors of the anal canal
|
|
|
when is there pain in UC
|
predefecatory
|
|
|
hematochezia
|
bright red blood in stool
|
|
|
diagnosis of UC
|
"sigmoidoscopy, complete circumferential inflammation with ulceration. biopsy shows non specific inflammation"
|
|
|
morphology of pseudopolyps
|
smooth raised epithelium results from collagen depostiion and contraction during healing
|
|
|
what IBD has pseudopolyps
|
UC
|
|
|
what bile issues do people with crohns disease have
|
"bacteria deconjugate bile and is excreted as diarrhea, as a result more cholesterol is diverted to bilary tree to make more, but is over loased so get hypercholesterolemia of biliary tree: gallstones"
|
|
|
differential for rectal pain
|
"gonorrheal proctitis
|
|
|
collar button ulcerations
|
amebiasis
|
|
|
types of inflammatory bowel disease
|
"Idiopathic
|
|
|
highest chance of malignant polyp
|
"many, large and dysplastic"
|
|
|
cancer screening for pt with no fam hx
|
"annual fecal occult blood tests
|
|
|
causes of intestinal obstruction
|
"hernias
|
|
|
how do adhesions compromise bowel vasculature or create obstruction
|
bowel loops around the adhesion
|
|
|
what is volvulus
|
twisting of a loop of bowel around its mesenteric base of attachment
|
|
|
what is intussusception associated with
|
"infection in children
|
|
|
the compromising of what vasculature can result in ischemic bowel
|
"celiac, SMA, IMA"
|
|
|
"Patchy and segmental involvement, hemorrhagic, ulverated, dark red. edema that thickens bowel wall"
|
mucosal or mural infarction
|
|
|
mesenteric venous thrombosis
|
"atrophy of surface epithelium, acute inflam, abd pain and distention, vomitting, bloody stool."
|
|
|
angiodysplasia
|
"abnormal formation of blood vessels, presents in older pop, hyperemic, RLQ abd pain, blood in stool"
|
|
|
meckels diverticulum
|
"persistence of vitelline duct, solitary, more common in men, ectopic pancreatic tissue"
|
|
|
Colonic diverticulosis
|
"blind pouch lined by mucosa that communicates with the lumen
|
|
|
What can cause a diverticulosis to become diverticulitis
|
"diet including seeds, can progress into abscess, LLQ pain and fever"
|
|
|
4 kinds of appendix tumors
|
"carcinoids- most common
|
|
|
How does giardiasis present
|
"abdominal distention, malabsorb, failure to thrive, watery foul smelling stool"
|
|
|
tx for giardia
|
metronidazole
|
|
|
cryptosporidium
|
"acid fast, intracellular, extracytoplasmic"
|
|
|
what are the 3 AIDS defining parasites
|
"cryptosporidium, isospora, toxoplasmosis"
|
|
|
tx for cryptosporidium
|
notazoxanide
|
|
|
Ghost Cells
|
cyclosporiasis
|
|
|
Tx for cyclospora
|
trimethoprim
|
|
|
What is the unique virulence factor for microsporidiosis
|
"polar tubule, penetrates cell membrane"
|
|
|
tx for isospora belli
|
TMP SMZ or pyrimethamine
|
|
|
Entameba histolytica
|
"very virulent, disseminates to liver and lungs
|
|
|
what drugs are used against amebiasis
|
"metronidazole- disseminated inf
|
|
|
What is the space of disse
|
area between hepatocyte and a sinusoid
|
|
|
what is a stellate cell
|
"fat and vit a storing cells
|
|
|
why is regeneration a bad descriptor for the liver
|
more of a hyperplastic response to injury than regeneration
|
|
|
what parts of the liver are more susceptable to insult
|
the bare area
|
|
|
if there is an issue with the spleen or stomach what part of the liver should you place your attn
|
"to the left side, most of the blood flow from those organs enters the left lobe of the liver"
|
|
|
by what 3 methods does the liver regulate blood flow
|
"myogenic
|
|
|
Myogenic response
|
"have local control by releasing NO, CO2, H2S and endothelin"
|
|
|
Metabolic response
|
oxygen tension in the portal blood affects the pH
|
|
|
Hepatic arterial buffer response
|
"can release adenosine and when blood flow is slow the hepatic arterioles will dilate, when it is fast they stay constricted as the adenosine is washed away"
|
|
|
definition of choleresis
|
the production and secretion of bile
|
|
|
what stimulates choleresis
|
secretin
|
|
|
what stimulates bile release from gallbladder
|
CCK causes the sphincter of oddi to relax and the gallbladder to contract
|
|
|
how do bile salts return to the liver
|
they are carried by albumin
|
|
|
cholagogue
|
anything that contracts the gallbladder (CCK)
|
|
|
cholerectics
|
increase secretion of bile
|
|
|
cholestasis
|
"when everything is slowed down
|
|
|
describe the blood supply of the pancreas
|
"splenic artery suppiles neck and tail
|
|
|
what stimulates the production of pancreatic enzymes
|
"CCK
|
|
|
how do the centroacinar cells of the intercalated ducts produce bicarb
|
"H2O and CO2 and carbonic anhydrase. secrete H+ into the blood, get small acid tide but is buffered so no large pH shift"
|
|
|
what is the only pancreatic enzyme that is made in its active form
|
amylase
|
|
|
what enzyme is necessary for the conversion of zymogens to their active form
|
enterokinase found on the luminal epithelium
|
|
|
which enzyme can activate the rest of the zymogens
|
trypsin (from trypsinogen)
|
|
|
how does the pancrease protect itself from trypsin that gets spontaneously activated
|
has trypsin inhibitors produced alongside the other enzymes
|
|
|
What hepatic enzyme is more important in measuring liver function
|
ALT
|
|
|
ALT >15000
|
"extensive liver disease
|
|
|
ALT 10000- 15000
|
extreme cases of hepatitis
|
|
|
ALT 800-1200
|
HAV
|
|
|
ALT: 500-1000
|
Gallbladder (gallstones)
|
|
|
ALT <500
|
Cirrhosis and immunosupressed
|
|
|
ALT 250-300
|
Alcoholic liver disease
|
|
|
Normal LFT ranges
|
"AST 0-55
|
|
|
LFTs with intrahepatic disease
|
"AST 220
|
|
|
LFT Extrahepatic disease
|
"AST slight high
|
|
|
Pt has low albumin and prolonged protime
|
pt is going into liver disease (even wo jaundice)
|
|
|
LFTs showing active HAV infection
|
"if ALT is still rising, pt is infected
|
|
|
if pt has HBVab but no HBsAg
|
pt was exposed but is over it
|
|
|
indications for PTC
|
unknown cause of jaundice
|
|
|
what can cause painless jaundice
|
"pancreatic cancer (head)
|
|
|
difference between PTC and ERCP
|
"PTC evaulates the liver, bile ducts, gallbladder but no pancreas
|
|
|
"children, itchy butts"
|
enterobius vermicularis
|
|
|
rugby ball eggs
|
E. vermicularis
|
|
|
tx for E. vermicularis
|
"albendazole
|
|
|
myalgia"
|
trichonosis
|
|
|
moving rash
|
strongyloidiasis
|
|
|
strongyloiiasis tx
|
thiabendazole
|
|
|
complications with strongoloidiasis
|
gram neg sepsis
|
|
|
"tx for tapeworms (Taenia spp, E. granulosis, Neurocysticercosis)"
|
praziquantel
|
|
|
Lifecycle of malaria
|
"mosquito bites, injects sporozoites, they head to the liver to mature, merozoites are released and infect RBCs"
|
|
|
MOA of chloroquine CQ
|
"blocks the conversion of heme to hemazoin, heme kills plasmodium"
|
|
|
CQ toxicity
|
"hypotension
|
|
|
primaquine
|
"used for malaria relapse
|
|
|
drugs that target the hepatic stage
|
"atovaquone-proguanil
|
|
|
Drugs for blood stage
|
"atovaquone-proguanil
|
|
|
what drug should not be used in combo with an antidepressant
|
MQ
|
|
|
Definition of diarrhea
|
increase in daily stool weight over 200 g.
|
|
|
When should you order stool culture
|
only if diarrhea persists 2+ weeks
|
|
|
caution in using abx against diarrhea
|
"promote resistance, can cause HUS in 0157:H7 infected pts.
|
|
|
pathogenesis of c diff
|
"toxin a causes diffuse lymphocytic infiltrate in lamina propria leading to edema and bulging, epithelium seperates and creates malabsorption. pancolitis"
|
|
|
dx of c diff
|
"5-10 after abx tx
|
|
|
complications in c diff
|
"toxic megacolon, transverse volvulus, protein def"
|
|
|
tx of c diff
|
"Metronidazole, vanco if really bad (never IV)
|
|
|
"what parasite is treated with abx, and what abx"
|
cyclospora tx with bactrim
|
|
|
what is the most common hepatitis virus
|
Hep B
|
|
|
describe the HAV particle
|
"Picornavirus
|
|
|
describe the HBV particle
|
"Hepadnavirus
|
|
|
describe the HCV particle
|
"Flavivirus
|
|
|
what are the 3 forms of HBV found in the blood
|
"Small spherical- binds Ab but noninfectious
|
|
|
what antibody protects againts HBV
|
anti-HBsAg
|
|
|
What does the presence of HBeAg and no antibody mean about the patient
|
Person is infected with HBV and their blood is extremely infectious
|
|
|
HBV coinfection with HDV
|
"not too bad, pt can recover, pt is infected with both at the same time"
|
|
|
HBV and HDV superinfections
|
"pt was HBV infected previously and is infected with HDV, very bad prognosis"
|
|
|
how is HAV transmitted
|
Fecal oral
|
|
|
how is HBV transmitted
|
"Sexual contact, IVDA, (and technically blood)"
|
|
|
HCV transmission
|
"IVDA, Blood, sexual
|
|
|
what age group has the highest rate of HAV infection
|
early childhood
|
|
|
Symptoms of acute hepatitis
|
"fever, fatigue, nausea, abd discomfort, dark urine, jaundice lasting 1-3 weeks"
|
|
|
clinical definition of acute hepatitis
|
acute illness with discrete onset of symptoms and jaundice or elevated serum ALT
|
|
|
complications of HAV
|
"fulminant hepatitis
|
|
|
in what population is HEV infection more severe
|
preggos
|
|
|
when is someone considered immune tolerant for HBV
|
"exposed infants, HBeAg positive, no anti- HBeAg, normal ALT, no or minimal inflam"
|
|
|
how do you test for HAV
|
"AST ALT will be increased
|
|
|
what does an acute HBV infection appear serologically
|
"first thing that appears is HBsAg, shortly after get anti-HBc, around week 32 get Anti-HBs"
|
|
|
What occurs serologically in chronic HBV infections
|
never get anti-HBs. when person is especially infectious will not see anti-HBc. Anti-HBe is seen in inactive carriers
|
|
|
anti HBs -"
|
"susceptible, not exposed"
|
|
|
anti HBs +"
|
immune due to infection
|
|
|
anti HBs +"
|
Immune due to vaccine
|
|
|
anti HBs -"
|
accutely infected
|
|
|
anti HBs -"
|
Chronic infection
|
|
|
anti HBs -"
|
"recovering from accute infx
|
|
|
what will blood tests show in chronic HDV-HBV superinfection
|
"chronic levels of anti HDV
|
|
|
what receptor does the liver use to uptake glucose
|
"GLUT2
|
|
|
what type of amino acids does the liver not take up
|
branched chain AA
|
|
|
how does the liver interact with fats in the fasted state
|
"HSL is activated by glucagon, TG is carried to liver by albumin, broken down to FA and glycerol, converts them to acetyl coA and then into ketone bodies"
|
|
|
what tests measure liver integrity
|
"AST, ALT, LDH"
|
|
|
"BR, AP, GGT, 5' nucleotidase indicate"
|
biliary excretory function
|
|
|
what does AST:ALT ration tell you
|
"liver problem vs skeletal problem
|
|
|
10:1 AST:ALT
|
alcoholic liver disease
|
|
|
indirect bilirubin
|
"unconjugated
|
|
|
Direct bilirubin
|
"conjugated
|
|
|
what is feathery degeneration
|
"seen in cholestasis, bile accumulation within hepatocytes"
|
|
|
in a proliferation liver you will see
|
"mitoses, string like chords, disorganization, bile duct prolif"
|
|
|
pathogenesis of HBV
|
"not directly cytopathic
|
|
|
Macronodular cirrhosis is caused by
|
hepatitis virus (B or C)
|
|
|
Ground glass cytoplasm
|
HBV
|
|
|
where do you find HBsAg in the cell
|
cytoplasm
|
|
|
where do you find HBcAg in the cell
|
nucleus and cytoplasm
|
|
|
what is going on in fulminant hepatitis
|
"hepatic insufficiency
|
|
|
associations with hep C
|
"MPGN, lymphoma, Sicca syndrome, porpyria cutanea tarda"
|
|
|
histology of a HCV infection
|
predominant lymphocytic infiltration around the portal triad
|
|
|
autoimmune hepatitis
|
"females
|
|
|
Difference between type 1 and 2 autoimmune hepatitis
|
"1 is females with lots of autoimmune antibodies
|
|
|
micronodular cirrhosis
|
"Alcohol
|
|
|
pathogenesis of cirrhosis
|
"collagen I and III deposit in the lobules, liver may be enlarged at first but becomes contracted and shrunken
|
|
|
how does fibrosis/cirrhosis occur
|
stellate cells activated and transformed by alcohol into myofibroblast phenotypes
|
|
|
pt with limb wasting while maintaining trunk integrety
|
alcoholic cirrhosis
|
|
|
Steatosis
|
shunting of metabolic products away from catabolism and towards fat synthesis
|
|
|
how does alcohol enhance oxidative stress
|
"impairs methionine, decreases glutathione levels making liver more prone to oxidation
|
|
|
what is the cause of primary hemochromotosis
|
"defect on chromo 6 (hemochomotosis has 6 syllables)
|
|
|
what triad of symptoms will lead u to hemochromotosis as a dx
|
"liver abnormalities, hemoglobin problems, glucose intolerance
|
|
|
what are the 2 types of A1AT deficiency
|
"PiMM (good)
|
|
|
Primary Biliary Cirrhosis
|
"middle aged women
|
|
|
primary sclerosing cholangitis
|
"inflammation, fibrosis, dilation of obstructed bile ducts
|
|
|
population most affected by FNH
|
females 30-50
|
|
|
if a pt has multiple FNH lesions what does this suggest
|
high probability of vascular and neoplastic formations elsewhere in the body (brain)
|
|
|
What do FNH lesions look like
|
"clearly demarcated, central fibrosing scar (stellate)
|
|
|
"you have a liver sample in pathology and it tests positive for alpha 1 antitrypsin, what kind of lesion was removed from the pt"
|
FNH
|
|
|
FNH genetics
|
p21
|
|
|
Distinguish LCA from FNH
|
"LCA does not have a central scar, can look relatively normal. LCA can result in massive hemorrhage. LCA will also be encapsulated"
|
|
|
Presentation of HCC
|
"males with cirrhosis
|
|
|
What puts you at risk for HCC
|
"HBV
|
|
|
Gross appearance of HCC
|
"multiple, size varies, +/- capsule, necrosis, hemorrhage, heterogeneous "
|
|
|
Microscopic view of HCC
|
"trabecular growth pattern (solid or tubular), varied differentiation, mallory bodies, globules containing AFP, may have tumor islands"
|
|
|
genetics of HCC
|
"p53
|
|
|
Clear cell type
|
"females
|
|
|
Sclerosing type
|
"after therapy
|
|
|
Small cell type
|
"growing in broad nests
|
|
|
Lymphoepithelioma type
|
"resembles nasopharyngeal lesion
|
|
|
sarcomatoid cell type
|
"looks like sarcoma
|
|
|
Mixed hepatocarcinoma-cholangiocarcinoma type
|
duel differentiation into liver and bile duct lines
|
|
|
Fibrolamellar carcinoma
|
"young pts, no cirrhosis
|
|
|
How does HCC met
|
"via portal venous system
|
|
|
extrahepatic sequelae of HCC
|
"can invade portal vein, and create vena cava syndrome"
|
|
|
Hepatoblastoma
|
"infants
|
|
|
gross appearance of hepatoblastoma
|
"solid, well circumscribed, solitary"
|
|
|
microscopic hepatoblastoma
|
"immature hepatocytes, extramedullary hematopoeisis"
|
|
|
Genetics in hepatoblastoma
|
"WNT/B-catenin
|
|
|
what is the most common benign tumor of the liver
|
Hemangioma
|
|
|
complication of hemangioma of the liver
|
TTP (thrombocytopenic purpura)
|
|
|
Angiosarcoma
|
"free anastomosing vascular channels
|
|
|
Risk factors for angiosarcoma
|
"cirrhosis
|
|
|
Mets to liver
|
"Bowel, breast, lung, pancreas, kidney, stomach"
|
|
|
how do mets to liver appear
|
"discrete mass which raise capsule
|
|
|
Acute liver failure
|
"toxins
|
|
|
what is the most common cause worldwide of acute liver failure
|
viral hep
|
|
|
what major chemical changes are occuring in acute liver failure
|
"hypoalbuminemia-edema
|
|
|
life-threatening sequelae of liver failure
|
"encephalopathy
|
|
|
asterixis
|
hands flap when held out front
|
|
|
hepatorenal syndrome
|
"normal appearing kidneys, sodium retention, free water retention, dec GFR, dec renal perfusion"
|
|
|
hepatopulmonary triad
|
"hypoxemia
|
|
|
what course of action should be taken with a asymptomatic subacute hepatitis pt
|
watch pt closely and treat aggressively
|
|
|
what is the criteria for treatment of hepatitis
|
"Sig elevated LFT
|
|
|
Why do you need to continue to tx and monitor pts even when their LFTs return to normal and are asx
|
histology lags behind by 3-6 mo so liver hasnt been totally restored
|
|
|
how do you select pt with HCV to treat
|
"+ anti-HCV or + PCR-HCV (quant)
|
|
|
what are the causes of ascites
|
"portal htn
|
|
|
what do you look for in acscitic fluid
|
"color, clarity, cell count, chemistry, cytology"
|
|
|
causes:"
|
"Cirrhosis
|
|
|
causes:"
|
"Peritoneal carcinomatosis
|
|
|
what is the most common cause of portal htn
|
"western world- etoh and viral cirrhosis
|
|
|
Tx plan for varices
|
"Endoscope and cautery
|
|
|
Dx criteria for HPS
|
"Low GFR
|
|
|
Type 1 HPS
|
"Rapid
|
|
|
Type 2 HPS
|
"slower
|
|
|
Acalculous Cholecystitis
|
"high mortality
|
|
|
most common cause of acute cholecystits
|
cholelithiasis obstucting cystic duct
|
|
|
Murphy Sign
|
"arrest of inspiration with palpation of RUQ
|
|
|
what are the causes of acute pancreatitis
|
"gallstones
|
|
|
turners sign
|
blue-red-green-brown discoloration of flanks
|
|
|
diagnosis of pancreatitis
|
"lipase
|
|
|
difference in lipase and amylase
|
"amylase is less specific and normalizes first
|
|
|
difference in lipase and amylase in acute pancreatitis
|
"amylase is elevated first but normalizes first too
|
|
|
what is ranson imrie criteria
|
"how you make a decision on pt care for someone with acute pancreatitis, taken at admission and 48 hrs"
|
|
|
admission criterea
|
"age, cbc, glucose, ldh, ast
|
|
|
48 hr criterea
|
"Fall in Hct
|
|
|
complications of pancreatitis
|
"PE, ARDS, hypotension, DIC, ascites, death"
|
|
|
most common place to find diverticulosis
|
"sigmoid
|
|
|
uncomplicated diverticulosis
|
"bloated, flatulence, abd pain, constipation"
|
|
|
complicated diverticulosis
|
"diverticulitis ->abscess, peritonitis, obstruction
|
|
|
tx of diverticulitis
|
"fluid replacement
|
|
|
what is IBS
|
"altered bowel habits and abd pain in absence of detectable structural abnormalities
|
|
|
pathophy of IBS
|
exaggerated sensory response to visceral stimulation
|
|
|
Rome criteria
|
"dx of IBS
|
|
|
Tx for IBS
|
"elim aggrevating foods
|
|
|
gene mutations in pancreatitis
|
PRSS1 and SPINK1
|
|
|
what codes for trypsin inhibitor in the pancreas
|
SPINK1
|
|
|
Sequelae of pancreatitis
|
"microvascular leakage
|
|
|
what are the 3 paths of acute pancreatitis
|
"duct obstruction
|
|
|
metabolic complications with pancreatitis
|
"glycosuria
|
|
|
chronic pancreatitis
|
"begin to get fibrosis and destruction of exocrine, can eventually take out endocrine"
|
|
|
lymphoplasmacytic sclerosing pancreatitis
|
"autoimmune pancreatitis, lots of plasma cells"
|
|
|
tx for most worms
|
"albendazole
|
|
|
river blindness tx
|
ivermectin
|
|
|
tx for schistosoma
|
PZQ
|
|
|
bulk laxatives
|
"sound like plants cuz they are basically, absorb water and distend lumen to encourage peristalisis"
|
|
|
stool softeners
|
retard water absorption from stool
|
|
|
pancreatic pseudocyst
|
"accumulations of necrotic hemorrhagic material, no epithelial lining"
|
|
|
serous cystadenomas
|
"benign glandular tissue, clear straw colored fuild"
|
|
|
what pancreatic neoplasms are more common in women
|
"serous cystadenomas
|
|
|
where do mucinous cystic neoplasms grow
|
tail or body
|
|
|
intraductal papillary mucinous neoplasm
|
"men, head of pancreas, multifocal, benign/malig, large pancreatic duct"
|
|
|
solid pseudopapillary neoplasm
|
"well circumscribed masses, locally aggressive
|
|
|
precursor to pancreatic cancer
|
"pancreatic intraepithelial neoplasm
|
|
|
genes and pancreatic cancer
|
"k-ras
|
|
|
risk factors for pancreatic cancer
|
"smoking
|
|
|
morphology of pancreatic cancer
|
"head of pancreas
|
|
|
Trousseau sign
|
migratory thrombophlebitis
|
|
|
Sx of pancreatic cancer
|
"pain, obstructive jaundice, b symptoms, trousseasu sign"
|
|
|
acinar cell carcinoma
|
"zymogen granules, trypsin and lipase production (stains copper color)"
|
|
|
pancreatoblastoma
|
"rare, children
|
|
|
risks for cholelithiasis
|
"female, >40, obese, fertile
|
|
|
cholesterol stones
|
"bile saturated with cholesterol
|
|
|
pigment stones
|
"insoluble Ca salt and uncon bili
|
|
|
Charcot Triad
|
"RUQ, fever, jaundice
|
|
|
Acute Cholecystitis
|
"inflammation of GB
|
|
|
acute calculous cholecystitis
|
"chemical irritation and inflammation
|
|
|
acute acalculous cholecystitis
|
"insidious
|
|
|
cholesterolosis
|
"hypersecretion from liver
|
|
|
morphology of chronic cholecystitis
|
"gb wall may be thickened, gray, less flexible
|
|
|
porcelain GB
|
"dystrophic calcification
|
|
|
xanthogranulomatous cholecystitis
|
"shrunken, nodular, inflamed, necrosis, hemorrhage"
|
|
|
ascending cholangitis
|
"choledocholithiasis
|
|
|
"fever, chills, abd pain, jaundice, sepsis, reynolds pentad"
|
ascending cholangitis
|
|
|
reynolds pentad
|
"RUQ pain, Fever, jaundice, septic shock, CNS depression"
|
|
|
Biliary atresia
|
"fetal- abnormal organ dev
|
|
|
Cancer of extrahepatic bile ducts
|
"primary sclerosing cholangitis, UC, cystic liver, flukes
|
|
|
Osler weber rendu
|
"epistaxis
|
|
|
blue rubber blev nevus
|
"rubber nipple nodes
|
|
|
pseudooxantoma elasticum
|
"pt looks older than should
|
|
|
Dego disease
|
"GI ulcers
|
|
|
Scleroderma
|
"CREST
|
|
|
acanthosis nigricans
|
"hyperplastic, hyperpigmented, nonpuritic (dirty skin)
|
|
|
where are kayser fleisher rings located
|
descemets membrane (cornea)
|
