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DEMS > Unit 1 > Flashcards

Unit 1 Flashcards

1
Q

Be able to ID the 4 layers of the GI tract and describe why variations in those layers are important along the length of the tract

A

1) mucosa
- epithelial layer
- loose vascularized CT called lamina propria (contains lymphocytes, plasma cells, and macrophages)
- under is thin smooth muscle called muscularis mucosa

2) submucosa
- dense CT, larger blood vessels, nerve plexi, glands, and lymph nodes
- glands only in esophagus and duodenum (Brunner’s)

3) muscularis externa
- inner circle smooth muscle
- outer longitudinal smooth muscle
- nerve plexi between
- fcn in peristalsis and churning lumen contents

4) serosa/adventitia
- squamous epithelial cells separated from underlying muscular layers by thin CT

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2
Q

Describe how the major components of our food sources (proteins, nucleic acids, complex carbs, and lipids) are digested and absorbed. What components and conditions need to be secreted and met in order to do this?

A
  • enzymes secreted to digest
  • proteins –> AAs
  • carbs –> monosaccharides
  • fats –> fatty acids and monoglycerides

carb digestion

  • salivary amylase hydrolyzes alpha1,4 –> disaccharides maltose and alpha limit dextrans
  • pancreatic amylase hydrolyzes starch –> oligosaccharides and disaccharides
  • oligosaccharide hydryolases at BB produce monosaccharides (glucose, galactose, fructose)
  • SGLT1 takes up glucose and galactose (Na-dep)
  • GLUT5 takes up fructose (fac diff)
  • GLUT2 moves all to blood
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3
Q

What mechanisms are in place to avoid digesting ourselves?

A
  • proteases and amylases are released in pro-enzyme from that need to be activated in the proper environment first
  • mucus protects the inner layer of epithelium from acid and enzymes
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4
Q

ID the fundamental aspects of mucosal structures/functions that prevent bacterial infection along the GI tract? Describe the organization and role(s) of MALT in the GI tract

A
  • submucosa has a lot of lymphocytes and plasma cells
  • mucus provides protection
  • IgA
  • defensins and lysozymes from Paneth cells in SI
  • endogenous gut flora that is protective
  • serous epithelial cells of salivary glands secrete lysozyme and peroxidase
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5
Q

Describe the roles of smooth muscle and the enteric nervous system in gut motility, and the advantage of extrinsic control as well

A
  • smooth muscle acts as a unitary structure since the cells are held together by gap junctions and innervated by autonomic nerves
  • some cells can spontaneously depol –> APs w/o innervation –> tone at rest and innervation causes contraction or relaxation
  • can sustain contraction for a long time
  • enteric nervous system: resides in walls of GI tract
  • meissner’s and auerbach’s plexuses
  • meissner’s: submucosa, pregang para and postgang symp
  • auerbach’s: between muscle layers of GI tract, interneurons, sensory/motor neurons, pregang para, and postgang symp
  • exist outside of CNS and can control peristalsis without input
  • extrinsic parasympathetic NS promotes digestion and peristalsis
  • sympathetic NS on blood vessels and glands slows digestion to get blood to extremities
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6
Q

Delineate the requirements for pH control in different regions of the gut. Why in general do we have a much lower pH in the stomach?

A
  • low pH in stomach: activates pepsinogen –> pepsin
  • low pH kills bacteria, denatures proteins
  • neutralized in duodenum by pancreatic and duodenal enzymes
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7
Q

Describe some of the effects of key endocrine cells in the GI tract and understand their more general roles in regulation of GI coordination

A
  • G-cells: pylorus of stomach; secrete gastri
  • A-cells: secrete glucagon
  • EC-cells: secrete 5HT
  • D-cells: secrete somatostatin; widely dist, except mid stomach
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8
Q

ID the normal histology of the esophagus and be able to differentiate it from other regions of the GI tract

A
  • non-cornified squamous epithelium
  • upper is skeletal muscle
  • mid is mix of skeletal and smooth
  • lower 1/3 is smooth
  • see squamous epithelium, blood vessels, muscularis,
  • see change at GEJ
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9
Q

Describe the layers of the stomach, ID unique features of cells in these layers and be able to differentiate them from other regions of the GI tract

A
  • cardia: secretes mucus
  • fundus: secretes acid and digestive products
  • pyloris: secretes mucus and has endocrine cells that secrete gastrin
  • stem cells that renew epithelium
  • surface mucus cels release mucus and bicarb
  • chief cells secrete pepsinogen
  • parietal cells pump H ions; stim by gastrin and histamine; secrete intrinsic factor
  • have gastric pits
  • parietal cells with fried egg appearance
  • chief cells towards bottom
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10
Q

Understand the functional significance of rugae in the stomach and plicae circulares in the small intestine

A
  • longitudinal folds (rugae) and transverse folds (plicae circulares)
  • increase surface area a lot
  • PC are covered with villi which have microvilli
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11
Q

Be able to describe the layers of the small intestine, difference in the duodenum vs. other regions, and the cell types and specific functions in these layers

A
  • crypts of Lieberkuhn: simple tubular glands
  • paneth cells: large eosinophilic granules with densins and lysozymes and phospholipase
  • brunner’s glands: secrete bicarb into crypts
  • villi and microvilli
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12
Q

Describe and be able to recognize cellular structures of the exocrine pancreas. Define differences you would observe between pancreatic acini and acini of salivary glands. Describe the importance of zymogens and their activation

A
  • zymogens: precursor to enzymes that go to pancreatic duct and help in digestion; precursor form to prevent autodigestion of proteins/lipids on the way to ducts to the duodenum
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13
Q

Be able to ID normal histological features and differences among salivary glands

A
  • serous and mucus secretion
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14
Q

ID the layers of the colon, describe the cell types and their roles in the colon, and be able to differentiate the histology of the colon as compared to other regions of the GI tract

A
  • crypts and adipose tissue

- “rack of test tubes”

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15
Q

Achalasia

A
  • inflam destruction of neurons in myenteric plexus of esophagus
  • destroys NO prod inhib neurons –> smooth muscle LES cannot relax after swallowing
  • test with esophageal manometry
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16
Q

Scleroderma

A
  • fibrosis and smooth muscle atrophy
  • lower 2/3 of esophagus and LES –> difficulty swallowing and GERD
  • esophageal manometry shows no esophageal body peristalsis
  • weakened LES as opposed to hyperactive LES in achalasia
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17
Q

Spastic disorders of the esophagus

A
  • impairment of inhibitory innervation
  • chest pain and difficulty swallowing
  • inc vigor or rapid esophageal peristalsis while swallowing
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18
Q

Gastroparesis

A
  • delayed gastric emptying w/o obstruction
  • feeling full, bloating, nausea, anorexia, vomiting, abd pain, weight loss
  • caused by DM, meds, gastric surgery, post-viral, injury to vagus nerve
  • test with gastric emptying or wireless motility capsule
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19
Q

What is the MMC?

A
  • migrating motor complex
  • sweeps GI tract from stomach to bowel
  • 3 phases
  • requires intact enteric NS
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20
Q

Intestinal pseudo-obstruction

A
  • obstruction in small or large bowel w/o actual obstruction
  • see dilation of bowel on imaging
  • caused by degen neuropathies (parkinson’s, DM), chagas, paraneoplastic AI neuropathy
  • also by scleroderma, amyloidosis, eosinophilic gastroenteritis
  • see abd pain, bloating, distention
  • can test with wireless motility capsule or manometry
  • treat with antibiotics, nutrition, and prokinetic meds
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21
Q

Constipation

A
  • caused by meds, mechanical obstruction, metabolic disorders, pregnancy, immobility, functional disorders like IBS
  • myopathic causes: scleroderma, amyloidosis
  • neuropathic: parkinson’s spinal cord injury, MS, autonomic neuropathy, Hirschsprung’s
  • test with wireless motility capsule or sitz marker study
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22
Q

Hirschsprung’s disease

A
  • congenital absence of myenteric neurons of distal colon (involving internal anal sphincter) –> lack of reflex inhibition of internal anal sphincter
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23
Q

Dyssynergic defecation

A
  • disorder of coordination of pelvic floor muscles
  • contraction of pelvic floor and external anal sphincter during defecation
  • fix with biofeedback
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24
Q

Describe the 2 major types of motility in the GI tract, their fcn in digestion, and the differences between them

A
  • segmentation

- peristalsis

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25
Q

Explain how the symp and para systems communicate with intestinal smooth muscle

A
  • para: ACh mediates contraction

- symp: prevents digestion; move blood to extremities

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26
Q

Describe the characteristics of the BER of the SI and its relation to smooth muscle contractile activity

A
  • intrinsic/inherent to muscle (myogenic)
  • BER is not enough for contraction; need NT (ACh) input
  • ## BER inc as you move down tract
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27
Q

List the stimulus that initiates the swallowing sequence and the events that follow. ID the point at which the swallowing sequence switches from voluntary to involuntary

A
  • three stages: voluntary (bolus pushed by tongue to oropharynx), involuntary (glottis covers trachea, UES relax), involuntary (esophageal peristalsis)
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28
Q

Explain the mechanism of esophageal motility and peristalsis, and the role of the upper and lower esophageal sphincters in this process

A
  • muscle goes from skeletal to smooth as you go down esophagus
  • bolus distends wall of esophagus –> activates sensory neurons –> release ACh and substance P –> smooth muscle contracts at oral end of bolus –> force bolus down –> trigger relaxation distal to bolus with NO and VAP and ATP
  • LES: prevents backflow from stomach to esophagus
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29
Q

Describe the storage, digestion, and motility roles of the stomach

A
  • storage: stores 3-4L
  • digestion: forms gastric acid (disinfectant), digest proteins, produces intrinsic factor
  • chyme spurts into duodenum with pyloric sphincter as sieve
  • carbs leave stomach in a few hours; protein are slower; fat is slowest
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30
Q

List the phases of the MMC

A
  • every 90min; from stomach to ileocecal valve (doesn’t include LI); motilin activated and neural
  • sweeps food and material out

phase 1
- quiescence occurs for 50% of the 90min duration

phase 2

  • motility inc with irregular contractions
  • doesn’t propel luminal content
  • 25% of MMC

phase 3

  • 5-10min of intense contractions
  • stomach to ileocecal valve
  • pylorus fully opens
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31
Q

Compare and contrast the colonic motor activity during a “mass movement” with that during haustral shuttling and the consequence of each type of colonic motility

A

haustration:
- coordinated movements in both directions
- colon muscles contract intermittently to divide LI into functional segments (haustra)
- similar to segementation

mass movement:

  • strong peristaltic waves 1-3x/day
  • usually after a meal and lasts a while
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32
Q

Describe the sequence of events occurring during defecation, differentiating those that are under voluntary control from those under involuntary control

A
  • filling of rectum –> relaxation of internal anal sphincter via VIP and NO from intrinsic nerves –> external anal sphincter contracts (rectoanal inhibitory reflex)
  • defecation occurs with voluntary relaxation of EAS
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33
Q

What happens in emesis?

A
  • centrally regulated by vomiting center in brain
  • steps: salivate (bicarb secretion) and nausea, reverse peristalsis, abd muscle contract and UES and LES relax, gastric contents eject
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34
Q

List the functions of secreted gastric acid

A
  • kills bacteria
  • begins protein digestion
  • activates pepsinogen –> pepsin
  • parietal cells also secrete intrinsic factor for vitB12 abs
  • H/K ATPase pumps H across luminal surface against large gradient (uses up a ton of energy)
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35
Q

Describe the protective mechanisms in place to limit toxicity of gastric acid, including occasions where these processes might be disrupted

A
  • mucus and bicarb layer (PGs inc mucus production)
  • tight junctions b/w epithelial cells prevent acid from infiltrating layers of wall
  • rapid cell turnover maintains integrity
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36
Q

Discuss the modulation of gastric acid secretion throughout the day and night

A

Phases of HCl secretion:

  • interdigestive phase: between meals following circadian rhythms (high in evening, low in morning before waking)
  • cephalic phase: neural reg
  • gastric phase: neural –> endocrine/gastrin and neural reg
  • intestinal phase: mostly endocrine reg
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37
Q

In general terms describe how the 3 parietal cell secretagogues include acid secretion

A
  • muscarinic receptors (ACh), histamine receptors, and CCK receptors (gastrin)
  • Ca and cAMP –> rearrangement in cell –> secrete acid
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38
Q

Describe the mechanism of gastric acid generation and secretion, including the roles of K, Cl/bicarb, carbonic anhydrase, and H/K ATPase

A
  • H is actively transported across apical membrane with H/K exchanger ATPase
  • bicarb is transported into blood across BL membrane in exchange for Cl into cell
  • Cl accumulates in cell –> cross apical membrane
  • H2O follows HCl from blood to lumen –> pH of blood leaving the stomach is high due to bicarb (alkaline tide)
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39
Q

Describe the role of the stomach, if any, on the gastric digestion of carbs, proteins, and fats

A

Carbs:

  • amylase is major enzyme in saliva and pancreatic secretions
  • sucrose and lactose can be digested at surface of enterocyte
  • only simple monomeric sugars can be absorbed
  • isomaltase (alpha-limit dextrins –> glucose)
  • maltase (maltose and maltotriose –> glucose)
  • lactase (lactose –> glucose and galactose)
  • sucrase (sucrose –> glucose and fructose)
  • trehalase (trehalose –> glucose)
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40
Q

Describe the role of the stomach, if any, on the gastric digestion of carbs, proteins, and fats

A
  • acid denatures proteins
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41
Q

Explain where carb digestion occurs, what enzymes are required, and which sugars they target

A

Carbs:

  • amylase is major enzyme in saliva and pancreatic secretions
  • sucrose and lactose can be digested at surface of enterocyte
  • *only simple monomeric sugars can be absorbed
  • starch –> maltose, maltotriose, and alpha-limit dextrins

on surface of enterocyte:

  • isomaltase (alpha-limit dextrins –> glucose)
  • maltase (maltose and maltotriose –> glucose)
  • lactase (lactose –> glucose and galactose)
  • sucrase (sucrose –> glucose and fructose)
  • trehalase (trehalose –> glucose)
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42
Q

Predict the SI and colonic consequence of a deficiency in the enzyme lactase following the consumption of dairy products

A
  • lack of lactase (BB enzyme) causes gas and diarrhea due to colonic bacterial digestion of lactose –> osmotic and draws water (diarrhea)
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43
Q

Compare and contrast the carbohydrate uptake mechanisms in terms of location, ions involved, and specificity

A
  • Na/K ATPase causes electrochem gradient
  • SGLT1: Na and glucose/galactose come in (cotransport fac dif)
  • GLUT5: fructose comes across (Na-indep)
  • GLUT2: glucose, galactose, and fructose go into bloodstream through BL surface
  • SGLT1 is regulated by sugar; if you eat more carbs –> upreg transporters and inc uptake of simple sugars
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44
Q

List the 4 mechanisms of protein uptake

A

1) Na-dep cotransporters; H2O follows
2) Na-indep transporters
3) specific carriers for di and tri peptides linked to H ions (cotransporter PEPT1)
4) pinocytosis of small peptides by entereocytes in infants

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45
Q

Explain the roles of pancreatic lipase, colipase, and micelles. Discuss how fat soluble vitamins are absorbed and the consequence of fat malabsorption (steatorrhea) on their uptake

A
  • 1ary bile acids made in liver from cholesterol (cholic and chenodeoxycholic acid)
  • 2ary bile acids are formed by bacteria in intestines and colon
  • bile acids complex with glycine or taurine to make bile salts
  • fat is hydrophobic with low SA; lipase binds to colipase binds to bile salt penetrates fat; form micelles to be easily absorbed
  • bile is recycled through distal ileum
  • lingual and gastric lipase –> pancreatic lipase (triglyc –> FFAs) –> bile salts (fat into micelles; FFAs to enterocytes) –> triglyc –> chylomicrons into lacteal
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46
Q

Describe the composition and formation of chylomicrons, their movement across the enterocyte BL membrane, and the route of entry into the CV system

A
  • triglyc –> bile salts –> abs –> reform triglyc –> chylomicrons –> into thoracic duct/lacteal
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47
Q

Describe the abs of H2O-soluble vitamins, including the role of IF in the abs of vitB12

A
  • fat soluble vitamins (ADEK) abs along SI and in micelles into chylomicrons
  • H2O soluble vitamins through diffusion or specific transporters
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48
Q

Explain the physiological significance of the regulation of luminal H2O content and daily fluid balance. Understand the role of the intestinal epithelia in regulating fluid movement along with the pathways of secretion and absorption of major ions in the SI and LI

A
  • in 9L, out 100-200mL
  • H2O follows solutes
  • SI becomes iso-osmotic wrt blood
  • H2O can move between or through cells
  • net fluid secretion from cells in crypts
  • ## net fluid abs from enterocytes on villi
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49
Q

List the different classes of diarrhea and the mechanisms by which oral rehydration fluids are able to counter the loss of H2O and electrolytes

A
  • osmotic diarrhea: impaired abs capacity (lactase def, ileal resection so not abs bile salts, celiac disease)
  • secretory diarrhea: e.g. cholera; inc cAMP –> activate CFTR Cl channel –> Cl into lumen, Na and H2O follow
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50
Q

Cl absorption

A
  • passive in proximal intestines (loose TJs)

- distal ileum/colon: exchanged for bicarb

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51
Q

K absorption

A
  • passive
  • paracellular in jejunum (low K in intercellular space)
  • transcellular in colon
  • K is high in cells
  • diarrhea –> loss of K and hypokalemia
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52
Q

Ca and Mg absorption

A
  • inc in one is loss of other (compete for uptake)
  • enters enterocyte passively
  • store in intracellular Ca stores
  • vitamin D is important; synth in skin or abs in intestine; stim uptake of Ca
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53
Q

Fe absorption

A
  • regulated in proximal intestines
  • transport across apical membrane as heme or Fe++
  • either binds to apoferritin to form ferritin to stay in cell OR binds to transferrin and leaves cell to go into blood
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54
Q

Fe absorption

A
  • regulated in proximal intestines
  • transport across apical membrane as heme or Fe++
  • either binds to apoferritin to form ferritin to stay in cell OR binds to transferrin and leaves cell to go into blood
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55
Q

Oral rehydration for therapy

A
  • treat diarrhea
  • abx for bacteria
  • KHCO3 for hypokalemia and metabolic acidosis
  • glucose (Na-dep draws in Na and H2O)
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56
Q

List the tumors of the Appendix

A
  • carcinoid: neuroendocrine and most common
  • benign: mucinous cystadenoma (rare but can obstruct and rupture appendix); villous adenoma
  • malignant: adenocarcinoma, lymphoma
  • secondary tumors (mets)
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57
Q

Name 4 types of diarrhea based on stool characteristics and give examples of each

A

1) watery [gap = 290-2*(stool Na - stool K)]
- osmotic (gap>50): lactose intolerance, sorbitol, fructose, Mg laxatives
- secretory (gap <50): bacteria, neuroendocrine tumors, bile salt, stim laxatives, motility disorders

2) steatorrhea (fat in stool)
- malabsorption: celiac, whipple’s, SIBO, shortened bowel from surgery
- maldigestion: pancreatic insuff, biliary obstruction

3) inflam/exudative (bloody)
- crohn’s
- ischemia
- infection of colon: c diff, e coli, amebiasis, shigella

4) functional
- IBS

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58
Q

Describe the clinical presentation and causes of fat malabsorption

A
  • weight loss, diarrhea, steatorrhea, vitamin def
  • pale bulk malodorous stool
  • caused by surgery, bacterial overgrowth, meds, pancreatic insuff, liver disease, intestinal inflamm, ischemia, infiltration
  • check for fat in stool
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59
Q

Describe the pathogenesis, diagnosis, and treatment of celiac disease

A

Pathogenesis:

  • inflammatory of SI
  • autoimmune response to gluten –> loss of villi due to inc intraepithelial lymphocytes and crypt hyperplasia –> malabsorption of carbs, fats, protein, iron, and folate
  • diarrhea, weight loss, bloating, abd pain
  • can see dermatitis hepetiformis and iron def anemia

Diagnosis:

  • intestinal biopsy (see villi flattening, intraepi lymphocytes, crypt hyperplasia)
  • anti-tissue transglutaminase (tTg) IgA ABs

Treatment:
- gluten free diet

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60
Q

Describe the pathogenesis, diagnosis, and treatment of small bowel bacterial overgrowth

A

Pathogenesis:

  • bacterial overgrowth due to hypomotility in scleroderma or diabetes, partial obstruction, diverticula, dec gastric acid secretion
  • bacteria inactivate bile acids, catabolize disacch in microvilli, and dec effectiveness of enterokinases
  • see diarrhea, steatorrhea, and abd pain, flatulence, bloating, weight loss
  • def of vit ADEK and B12
  • normal to high folate
  • vitamin K normal

Diagnosis:

  • aspiration of duodenum with culture (not common anymore)
  • glucose-hydrogen breath test

Treatment:
- antibiotics empirically (ciprofloxacin)

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61
Q

Compare the clinical features, pathology, and endoscopic findings of UC and Crohn’s

A

UC:

  • lower abd pain
  • hematochezia
  • mucus in stool
  • tenesmus
  • urgency
  • affects just colon
  • diffuse
  • inflam in mucosa and SM
  • superficial ulcers
  • little fibrosis
  • no granulomas
  • potential for malignancy
  • toxic megacolon

Crohn’s:

  • mid or lower abd pain
  • N/V
  • steatorrhea
  • fistulas
  • affects entire GI tract
  • strictures are common
  • skip lesions
  • transmural inflam
  • deep ulcers
  • lots of fibrosis
  • lots of granulomas
  • obstruction
  • malabsorption
  • malignancy if colon involved
  • can recur after colectomy

Both:

  • chronic diarrhea
  • weight loss
  • fatigue
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62
Q

List the common extra intestinal manifestations of IBD

A
  • autoimmune conditions of eye, skin, bile ducts, and joints
  • more common in UC than Crohn’s
  • uveitis
  • pyoderma gangrenosum
  • erythema nodosum
  • ankylosing spondylitis
  • primary sclerosing cholangitis
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63
Q

Differentiate the clinical and pathologic features of ischemic colitis from those of other types of colitis

A

Ischemic colitis:

  • acute hypoxia from vasospasm
  • deydration, hypotension, CV insult
  • splenic flexure, rectosigmoid junction
  • abrupt lower abd pain
  • urgency to defecate
  • mild diarrhea +/- hematochezia
  • see inflam, ulceration on CT or endoscope
  • caused by vasculitis, SLE, PAN, HS, substance abuse, estrogens, mesenteric thrombosis
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64
Q

Diagnose a patient presenting with diverticulosis-related complications including lower GI bleeding or diverticulitis

A
  • diagnose with CT or MRI
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65
Q

Chronic abd pain and diarrhea

A

IBD

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66
Q

Diagnose a patient with colonic obstruction based on the history, physical exam, and xray findings

A

Causes:

  • tumor
  • strictures or volvulus
  • foreign body

Signs:

  • N/V
  • abd distention
  • constipation or obstipation

Diagnosis:

  • plain xray: air in colon, paucity of air in rectum, distended small bowel and colon
  • confirm with CT

Treatment:

  • admit to hospital
  • NG tube
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67
Q

Hematochezia after surgery or MI

A

Ischemic colitis

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68
Q

Acute dysentery, travel, ill contacts, or antibiotics use

A

Infectious diarrhea

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69
Q

Chronic, microcytic anemia

A

Neoplasia or AVMs

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70
Q

NSAIDs

A

Drug-induced colitis

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71
Q

History of pelvic radiation

A

Radiation proctitis

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72
Q

History of pelvic radiation

A

Radiation proctitis

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73
Q

Small bowel bacterial overgrowth

A
  • from hypomotility (diabetes, scleroderma)
  • presents with steatorrhea
  • diagnose with duodenal aspiration, glucose-hydrogen breath test
  • vit ADEK and B12 def
  • folate normal/high
  • treat with empirical abx (ciprofloxin)
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74
Q

Celiac disease

A
  • gluten (alpha-gliadin peptide) sensitive enteropathy
  • inflam of small intestine
  • autoimmune
  • HLA-DQ2, DQ8
  • enteropathy associated T-cell lymphoma and small intestinal adenocarcinoma
  • abd pain, diarrhea, weight loss, fatigue
  • steatorrhea
  • flatulence
  • dermatitis herpetiformis
  • biopsy small intestine is gold standard
  • loss of villi and scalloped duodenal folds on endoscopy
  • positive IgA antibodies to tissue transglutaminase
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75
Q

Celiac disease

A
  • gluten (alpha-gliadin peptide) sensitive enteropathy
  • inflam of small intestine
  • autoimmune
  • HLA-DQ2, DQ8
  • enteropathy associated T-cell lymphoma and small intestinal adenocarcinoma
  • abd pain, diarrhea, weight loss, fatigue
  • steatorrhea
  • flatulence
  • dermatitis herpetiformis
  • biopsy small intestine is gold standard
  • loss of villi and scalloped duodenal folds on endoscopy
  • positive IgA antibodies to tissue transglutaminase
  • tissue biopsy shows: villous blunting, intraepithelial lymphocytes, lymphoplasmacytosis of LP (crypt hyperplasia)
  • iron deficiency anemia
  • AST, ALT elevations
  • treat with gluten free diet
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76
Q

Celiac disease

A
  • gluten (alpha-gliadin peptide) sensitive enteropathy
  • inflam of small intestine
  • autoimmune
  • HLA-DQ2, DQ8
  • enteropathy associated T-cell lymphoma and small intestinal adenocarcinoma
  • abd pain, diarrhea, weight loss, fatigue
  • steatorrhea
  • flatulence
  • dermatitis herpetiformis
  • biopsy small intestine is gold standard
  • loss of villi and scalloped duodenal folds on endoscopy
  • positive IgA antibodies to tissue transglutaminase
  • tissue biopsy shows: villous blunting, intraepithelial lymphocytes, lymphoplasmacytosis of LP (crypt hyperplasia)
  • iron deficiency anemia
  • AST, ALT elevations
  • treat with gluten free diet
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77
Q

Tropical sprue

A
  • visiting tropical areas
  • bacterial toxins
  • macrocytic anemia from B12/folate def
  • villous flattening
  • give abx and B12/folate
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78
Q

Whipple’s

A
  • caused by T. whippelii
  • LP macrophages absorbed organism –> lymphatic obstruction –> malabs diarrhea
  • fever, joint pain, diarrhea, abd pain, CNS symptoms
  • PAS stain shows macrophages with whipple bacilli
  • villi distended by macrophages
  • one year of abx
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79
Q

Mesenteric ischemia

A
  • chronic: 2/3 major vessels occluded
  • acute: embolues/severe abd pain
  • post-prandial stomach pain, weight loss, diarrhea/malabs
  • fecal fat
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80
Q

SI tumors

A
  • most are adenocarcinomas
  • then carcinoid, sarcoma, lymphoma
  • symptoms of obstruction (abd pain, distention, dec stool)
  • get a biopsy
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81
Q

Appendicitis

A
  • inflammation of appendix
  • periumbilical pain that radiates to RLQ
  • fever, inc WBC, sever pain –> perforation
  • get an appendectomy
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82
Q

Inflammatory bowel disease

A
  • females in teens/20s and 80s
  • UC and Crohn’s
  • chronic diarrhea, abd pain, bleeding for >2wks
  • extraintestinal symptoms (uveitis, pyoderma gangrenosum, erythema nodosum, 1ary sclerosing cholangitis (UC), ankylosing spondilitis, osteoporosis)
  • screen for cancer
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83
Q

Ulcerative colitis

A
  • T helper type 2 mediated
  • bloody diarrhea, weight loss, fatigue
  • limited to colon, usually rectosigmoid –> surgery can cure
  • LLQ pain
  • hematochezia or mucus in stool
  • tenesmus (incomplete evacuation)
  • diffuse; from rectum more proximal
  • toxic megacolon
  • ulcer = mucosa+SM
  • crypt abscess
  • pseudopolyps and loss of haustra
  • assoc with 1ary sclerosing cholangitis
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84
Q

Crohn’s disease

A
  • T helper type 1 mediated
  • non-bloody diarrhea, weight loss, fatigue
  • anywhere but usually terminal ileum and right colon
  • periumbilical/mid abd pain
  • N/V
  • fistula
  • strictures
  • skip lesions
  • granulomas and lymphocytes
  • transmural ulcerations
  • full thickness inflammation
  • cobblestone mucosa
  • malabsorption
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85
Q

Microscopic colitis

A
  • 50-80yo females
  • lymphocytic and collagenous
  • assoc with celia, NSAIDs usually a cause
  • chronic mild secretory diarrhea non-bloody
  • no gross features, just on histology
  • lymphocytic infiltration of mucosa
  • thickened subepi collagenous band
  • treat with antidiarrheals
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86
Q

Ischemic colitis

A
  • usually >60yos
  • caused by vasospasms, dehydration, hypotension, MI, PE
  • affects splenic flexure and rectosigmoid (wateshed)
  • abrupt onset, crampy lower abd pain
  • loss of peristaltic sounds
  • mild diarrhea +/- hematochezia
  • get a colonoscopy and treat triggers
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87
Q

Irritable bowel syndrome

A
  • 20-40yo females
  • chronic recurrent abd pain, bloating
  • improve with defecation
  • get endoscopy and tissue biopsy
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88
Q

Infectious colitis (campylobacter spp)

A
  • from poultry, water, and unpast dairy
  • watery diarrhea +/- blood
  • friable colonic mucosa
  • treat with antibiotics
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89
Q

Infectious colitis (shigella)

A
  • highest infectivity rate
  • water contaminated with feces
  • severe watery or bloody diarrhea
  • hemorrhage, exudates, pseudomembranes
  • mimics IBD
  • treat with abx
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90
Q

Infectious colitis (salmonella)

A
  • food poisoning or traveler’s diarrhea
  • non-typhoid: mild gastroenteritis, diarrhea in 2nd week of infection
  • typhoid: pain, HA, fever, rash, leukopenia, perforation, toxic megacolon
  • mucosal redness, ulceration, exudates on endoscopy
  • treat with abx
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91
Q

Infectious colitis (e. coli)

A
  • enterotoxigenic: secretes toxin; diarrhea
  • enterovasive: similar to shigella; travelers’ diarrhea
  • enterohemorrhagic: contaminated meat –> renal failure; bloody diarrhea; necrosis and hemorrhage
  • ## enteroadherent: non-bloody diarrhea
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92
Q

Infectious colitis (pseudomembranous)

A
  • C diff after course of abx (3rd gen cephalosporins)
  • common in hospitalized patients
  • fever, leukocytosis, abd pain, cramps, non-bloody watery diarrhea
  • pseudomembrane formation; loss of crypts; volcano-like eruption of neutrophils
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93
Q

Infectious colitis (CMV)

A
  • affects anywhere in GI tract

- cytomegaly (large cells)

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94
Q

Infectious colitis (herpes virus)

A
  • usually esophagus and anorectum

- intranuclear inclusion

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95
Q

Infectious colitis (rotavirus)

A
  • most common cause of childhood diarrhea (now have 2 vaccines)
  • severe dehydration
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96
Q

Infectious colitis (adenovirus)

A
  • second most common cause of childhood diarrhea
  • in AIDS patients
  • diarrhea, dehydration
  • self resolves
  • villous atrophy
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97
Q

Infectious colitis (norovirus)

A
  • half of all gastroenteritis outbreaks
  • contaminated foods and person to person
  • diarrhea; SI affected
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98
Q

Infectious colitis (protozoan)

A

Entamoeba histolytica

  • dysentery-like fulminant colitis –> goes to liver and cecum
  • flask-shaped ulcers in mucosa

Giardia:

  • explosive watery diarrhea, abd pain, N/V
  • duodenum
  • schools of fish on histology

Cryptosporidium parvum:

  • usually in IC kids
  • diarrhea, weight loss, fever, pain; usually SI
  • mild erythema and mucosal granularity on endoscopy
  • basophilic ADD
  • treat all with anti-parasite therapy
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99
Q

Infectious colitis (helminthes)

A

Ascaris lumbricoides (roundworm)

  • soil infected with feces
  • obstruction, perforation, growth retardation

Strongyloides stercoralis (nematode):

  • penetrates skin –> lungs –> esophagus –> SI
  • diarrhea, pain, rash, pruritis

Schistosomiasis:

  • exposure to contaminated water and skin penetration
  • bloody diarrhea, anemia, weight loss
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100
Q

Drug-induced colitis

A
  • mimics IBD or ischemia
  • NSAIDs usually cause
  • pain and diarrhea
  • do colonoscopy to confirm and discont drug
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101
Q

Radiation colitis

A
  • radiation proctitis is most common (from pelvic radiation for treating cervical or prostate cancer)
  • hematochezia, diarrhea, painless rectal bleeding
  • see edema and telangiectasia on colonoscopy
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102
Q

Diverticulosis

A
  • outpouching of colon
  • usually in elderly
  • due to low fiber diet
  • hemorrhage (5%); usually right colon that is painless
  • get CT or MRI
  • no inflam cells
  • treat with high fiber diet
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103
Q

Acute diverticulitis

A
  • fecolith obstructs a diverticulum –> inflammation –> microperforation, abscess, or peritonitis
  • usually in sigmoid colon
  • acute LLQ pain, nausea, fever
  • not usually w/ diarrhea
  • can lead to obstruction, perforation, abscess formation, bleeding –> sepsis
  • get CT or MRI and see inflam cells
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104
Q

Zenker’s diverticulum

A
  • outpouching of oropharynx from muscle wall defect
  • above UES at esophagus and pharynx junction
  • dysphagia, obstruction, hal
  • treat with surgery
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105
Q

GERD

A
  • reflux of gastric acid into esophagus
  • more common in obese patients
  • RFs: high fat diet, caffeine or alcohol, tobacco, meds, age
  • inappropriate LES relaxation
  • hiatal hernias
  • ZES, Sjogrens, scleroderma
  • heartburn, especially postprandial and lying down
  • diagnose with 24hr pH study or just give PPI or antacids and evaluate
  • see inc eosinophils in distal esophagus
  • progresses to erosive esophagitis then to barret’s esophagus then to adenocarcinoma
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106
Q

Achalasia

A
  • no relaxation of LES
  • disorderly peristalsis
  • vagal input to LES is impaired or secondary to diabetic neuropathy
  • solid and liquid dysphagia
  • chest pain, regurg, weight loss, halitosis
  • diagnose with esophageal manometry
  • see bird’s beak on esophagram
  • EGD or CT to rule out cancer
  • absence of ganglia in distal esophagus and LES on pathology
  • treat with balloon dilation of LES, nitrates, CCBs, or botox injection into LES
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107
Q

Eosinophilic esophagitis

A
  • eosinophilic infiltration
  • diffuse narrowing of esophagus
  • males usually younger than 50yo
  • allergic causes (look for allergic history i.e. asthma, psoriasis, etc.)
  • dysphagia +/- food impaction (due to fibrosis and eventual stricture)
  • see concentric rings on endoscopy, nodular plaques, exudates
  • biopsy shows eosinophils in mid esophagus
  • treat with topical steroids
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108
Q

Barrett’s esophagus

A
  • consequence of GERD
  • can progress to adenocarcinoma
  • RFs: hiatus hernia, white, M>F, smoking, obesity (same as GERD)
  • asymptomatic or heartburn
  • metaplasia where squamous –> glandular columnar
  • salmon colored patch on endoscopy
  • alcian blue stain shows acidic mucus/goblet cells
  • treat GERD, inc screening, ablation, mucosal resection
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109
Q

Esophageal cancer

A
  • dysphagia, weight loss, sometimes hematemesis, chest pain, anemia

Adenocarcinoma:

  • GERD/Barrett’s
  • distal esophagus
  • resect, chemo, metal stent

SCC:

  • RFs: smoking, alcohol, caustic injury, really hot tea, poor oral health
  • upper/mid esophagus
  • resect, chemo, metal stent
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110
Q

Work up for esophageal disorders

A

Dysphagia:
- coughing, aspiration –> suspect NM disorder, benign obstruction, neoplasia –> do a barium swallow

Esophageal Motility Dysfunction:
- pain +/- dysphagia –> GERD, achalasia, esophageal spasm –> manometry

Benign Structural Disorder:
- painless +/- solid food dysphagia –> strictures, EoE –> EGD

Neoplasia:
- painless +/- solid food dysphagia + cancer symptoms (weight loss, fatigue, etc.) –> esophageal cancer –> endoscopy and biopsy

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111
Q

Infectious esophagitis

A

Herpes:

  • usually in IC patients
  • pain w/ swallowing, dysphagia, GI bleed
  • see punched out ulcers on endoscopy
  • multinuc cells, intranuclear viral inclusion on histo
  • give antiviral

Candida:

  • most frequent infection
  • in IC patients
  • pain with swallowing
  • white plaques on endoscopy and exudates
  • pseudohyphae and budding yeast on histology

CMV:

  • in IC patients
  • usually with candida
  • pain w/ swallowing
  • punched out ulcers in distal esophagus on endoscopy
  • cyto and nucleomegaly and intracytoplasmic inclusions on histology
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112
Q

Mallory-Weiss tear

A
  • longitudinal, linear superficial tears

- presents with alcoholics or bulemics

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113
Q

Describe the epidemiology, pathophysiology, and treatment of H pylori infection

A
  • HP produces urease which produces ammonia which raises local pH
  • virulence factors avoid destruction by gastric acid, colonize gastric epithelium, damage epithelial cells, cause inflam
  • injects CagA which can activate NFkB, dec cell adhesion assoc with gastric and duoenal ulcers
  • VacA: makes pores in membrane, inhibits T cells
  • can suppress Treg
  • epidemiology: age-dep in developed countries; crowded, low SE status; oral transmission
  • diagnosis: mucosal biopsies, CLO test; blood antibody; urea breath test; stool antigen test
  • treat with PPI, amoxicillin, clarithromycin
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114
Q

ID the causes of gastritis

A
  • infection usually by H pylori, but infectious gastritis in general is uncommon; can be syphilis, TB, candida, giardia, etc.
  • ## three types: mild/diffuse chronic and active, antral predominant (high acid secretion –> ulcer), multifocal atrophic gastritis
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115
Q

Describe PUD pathogenesis

A
  • gastroduodenal mucosa defenses are unable to protect epithelium from acid and proteases like pepsin –> disease of failed mucosal integrity, not acid hypersecretion
  • RFs: H pylori infection and NSAID use
  • may be asymptomatic, present with burning epigastric pain; relieved with food or antacids; pain comes and goes
  • complications are: bleeding (inc NSAID use among elderly –> HP infection), perforations (due to acute peritonitis), obstruction (not common; causes N/V)
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116
Q

Explain PUD treatment

A
  • anti-acid secretory meds
  • liquid antacids like Maalox
  • PPI and H pylori eradication
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117
Q

List the 5 most common types of gastric neoplasms

A

Adenocarcinoma:
- diffuse (signet ring, inc mucin) or intestinal (gland formation)

Gastric polyps:

  • hyperplastic: prolif of mucus producing cells from chronic inflam; seen in AI gastritis and H pylori infection with chronic atrophic gastritis; can lead to dysplasia or adenocarcinoma
  • adenoma: from dysplastic epithelial cells –> adenocarcinoma; FAP
  • fundic gland: dilated oxyntic glands lined by flattened parietal and mucus cells; most common polyp due to PPI long term

Stromal tumors/GISTs:

  • leiomyomas and lipomas
  • SM bulging into lumen, subserosal into lumen or both
  • usually asymptomatic, but if large –> abd pain and GI bleeiding
  • treat with resection
  • GISTs have different prognosis and treatment; express c-KIT (CD117) –> treat with imatinib

Neuroendocrine tumors:

  • carcinoid arise from enterochromaffin cells
  • 2 types of carcinoid tumors: sporadic (may metastasize, but try to resect) and achlorhydria due to atrophic gastritis (high levels of gastrin due to achlorhyria)

Lymphoma:

  • strong assoc with H pylori infection and 1ary gastric Bcell lymphoma
  • low grade clonal proliferation of Bcells in HP induced gastric MALT
  • eradicate HP, but if not may become high grade lymphoma
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118
Q

Eosinophilic gastritis

A
  • infiltration of gastric walls with eosinophils
  • mucosal ulceration or luminal obstruction
  • gastroparesis
  • rule out parasitic infestation
  • treat with corticosteroids and surgery
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119
Q

Menetrier diseas

A
  • hypertrophic rugal folds, spares the antrum, foveolar hyperplasia, cystic dilation into SM
  • abd pain, weight loss, bleeding
  • hypoalbumnemia
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120
Q

Zollinger-Elison syndrome

A
  • gastrin secreting neuroendocrine tumor stimulates parietal cells and increases acid secretion
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121
Q

Zollinger-Elison syndrome

A
  • gastrin secreting neuroendocrine tumor stimulates parietal cells and increases acid secretion
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122
Q

Gastritis

A
  • infection usually by H pylori, but also syphilis, TB, fungal, CMV, candida, etc.
  • HP is a gram neg rod
  • more common in developing countries in younger ages; older ages in developed countries
  • urease converts urea to ammonhia –> inc pH
  • abd pain, N/V, blood if ulcer
  • may progress to PUD and cancer
  • diagnose: endoscopy with mucosal biopsy, urease breath test
  • 3 forms: mild/diffuse, antral predom (high acid secretion), multifocal atrophic (low acid, but inc cancer risk)
  • treat: triple therapy (PPI, clarithro, amox for 2 weeks), or quad therapy (PPI, metro, tetrac, bismuth)
  • other causes: NSAIDs, autoimmune
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123
Q

Gastritis

A
  • infection usually by H pylori, but also syphilis, TB, fungal, CMV, candida, etc.
  • HP is a gram neg rod
  • more common in developing countries in younger ages; older ages in developed countries
  • urease converts urea to ammonia –> inc pH
  • abd pain, N/V, blood if ulcer
  • may progress to PUD and cancer
  • diagnose: endoscopy with mucosal biopsy, urease breath test
  • 3 forms: mild/diffuse, antral predom (high acid secretion), multifocal atrophic (low acid, but inc cancer risk)
  • treat: triple therapy (PPI, clarithro, amox for 2 weeks), or quad therapy (PPI, metro, tetrac, bismuth)
  • other causes: NSAIDs, autoimmune
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124
Q

Peptic Ulcer Disease

A
  • due to failed mucosal integrity not acid hypersecretion
  • NSAIDs and HP
  • burning epigastric pain
  • abd pain, anemia, acute bleeding, perforation, obstruction, subepi hemorrhage
  • treat with PPI/H2 blockers and eradicate HP
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125
Q

Peptic Ulcer Disease

A
  • due to failed mucosal integrity not acid hypersecretion
  • NSAIDs and HP
  • burning epigastric pain
  • abd pain, anemia, acute bleeding, perforation, obstruction, subepi hemorrhage
  • treat with PPI/H2 blockers and eradicate HP
  • treat bleeding with IV fluids, PPI, surgery if necesary
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126
Q

Hyperplastic gastric polyps

A
  • assoc with chronic gastritis
  • high gastrin –> inflammation
  • AI gastritis is common
  • prolif of foveolar epi and LP
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127
Q

Adenoma gastric polyps

A
  • assoc with chronic gastritis
  • intestinal metaplasia
  • high risk of malignancy
  • gastritis –> metaplasia –> adenoma (low grade) –> high grade –> adenocarcinoma
  • premalignant; assoc with FAP
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128
Q

Fundic gland polyps

A
  • assoc with chronic PPI and FAP

- cystic dilation of fundic glands

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129
Q

Gastric adenocarcinoma

A
  • assoc with HP, chronic gastritis
  • intestinal: RFS are age, male, tobacco, diet, smoked foods, salted fish, FAP; glad forming and assoc with atrophic gastritis
  • diffuse: younger, CDH1 mutation, worse prognosis; signet ring and inc mucin and linitis plastica
  • see weight loss, abd fullness, anemia
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130
Q

GISTs

A
  • benign gastric tumors from stroma
  • cells of Cajal
  • weight loss, anemia, dyspepsia
  • pain bleeding if large
  • submucosa
  • positive for c-kit (CD117)
  • give gleeva/imatinib or surgery
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131
Q

Carcinoid

A
  • neuroendocrine tumor
  • usually SI
  • AI gastritis, ZES, sporadic
  • gastrinoma, insulinoma, VIPoma,
  • prolif of endochromaffin cells of SI
  • resect
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132
Q

MALT lymphoma

A
  • low grade B cell lymphoma from HP
  • RFs are celiac, IBD, immunodeficiency
  • translocation of NFkB
  • HP infection –> low grade B cell prolif (BCell MALToma) –> high grade lymphoma
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133
Q

Describe the protective and damaging processes that are commonly deranged in gastric disease

A
  • surface mucosa secretion
  • bicarb secretion into mucus
  • mucosal blood flow
  • epithelium can regenerate
  • PGs

^^^these processes are damaged by HP, NSAIDs, etc.
- can also be by ischemia and shock

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134
Q

List the general features and causes of acute and stress-related gastritis

A
  • causes: NSAIDs, EtOH, tobacco, HP, bile, strong acids/bases
  • features: erythema, erosions

Acute:

  • destruction of mucosa
  • lots of inflmmatory infiltrate

Stress:

  • resembles acute gastritis
  • mediated by ischemia/vasoconst
  • erosion and ulceration widespread
  • common in critically ill patients
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135
Q

Describe the pathophysiology, epidemiology, and common sequelae of Helicobacter infection

A
  • gram negative bacillus, spiral shaped; flagella
  • resists acid through urease
  • adhesion binds to gastric foveolar cells
  • toxins to cause tissue damage
  • oral-oral, fecal-oral environmental spread
  • assoc w poverty, crowding, rural areas
  • histo shows HP in surface mucosa of cells; see neutrophils and lymphoctes and plasma cells into gastric mucosa
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136
Q

Describe the pathophysiology and common sequelae of AI gastritis

A
  • restricted to body
  • chronic
  • atrophic
  • CD4+ T-cells attack parietal cells
  • anti parietal cells and anti IF antibodies –> can be used for diagnosis
  • can lead to pernicious anemia
  • histo: lympocytes and plasma cells in body of stomach; atrophy of glands; intestinal metaplasia
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137
Q

Discuss the causes, appearance, and complications of PUD

A
  • acid mediated ulceration of stomach and duodenum
  • HP, cigarettes, NSAIDs, EtOH, stress
  • bleeding (black stools), perforation, obstruction
  • pathology: mucosa hangs over edge; ulcer has clean base; necrotic debris in ulcer bed
138
Q

Compare and contrast the appearance of the common types of gastric polyps, assoc conditions, and relationship to gastric cancer

A

Hyperplastic:

  • HP, chronic gastritis
  • antrum of stomach
  • inflam and edema
  • cystically dilated foveolae

Fundic gland:

  • assoc with PPI and FAP
  • protrustions in body or fundus
  • cystically dilated oxyntic glands
  • rarely progress to cancer

Adenoma:

  • FAP, HP, chronic gastritis
  • dysplasia, dark atypical cells
139
Q

Be acquainted with the RFs, epidemiology, assoc, and natural history of gastric adenocarcinoma

A
  • epithelia tumor derived from malignant gastric epithelium
  • assoc with chronic gastritis (HP)
  • most common gastric tumor
  • RFs: diet and HP
  • early signs: dyspepsia, dysphagia, nausea
  • late signs: weight loss, anorexia, early satiety, anemia
  • ulcerating pattern, heaped up edges (volcano); thickened wall
  • intestinal: malignant glands
  • diffuse: signet ring cells
  • wnt pathway activation –> intestinal type; loss of APC = FAP
  • loss of CDH1 –> diffuse type
  • amp of Her2/neu
140
Q

Describe the appearance, natural history, and molecular features of GI stromal tumors

A
  • derived from interstitial cells of Cajal
  • activating mutations in CKIT –> diagnostic and targeted therapy with imatinib
  • fibrous in appearance and firm
  • prolif of spindle cells; get CKIT immnohisto stain
141
Q

Hypertrophic pyloric stenosis

A
  • congenital abnormality
  • hyperplasia of pyloric MP –> gastric obstruction
  • M>F
  • 2-3rd week of life with regurg and persistent vomiting
  • feel a firm ovoid mass in abd
  • treat with surgical splitting
142
Q

List the causes of acute and chronic pancreatitis

A

Acute:

  • occurs when pancreatic duct becomes obstructed –> stagnation of pancreatic enzymes –> activation
  • ethanol is toxic to acinar cells and ductal epithelium
  • most common cause is gallstone that lodges in common bile duct or ampulla
  • other causes: tumor, procedures, congenital, hyperlipidemia, trauma, drugs, inc Ca, infections, CF

Chronic:

  • due to repeated acute pancreatitis and chronic EtOH abuse
  • cigarette smoking –> fibrosis
  • inherited causes
  • CFTR gene mutation/CF, trypsinogen or trypsin inhibitor mutations
143
Q

Pathophysiology, symptoms, diagnosis, treatment of acute pancreatitis

A

Acute:

  • obstruction of common bile duct leads to buildup of pancreatic enzymes which leads to inappropriate activation and pancreatic damage
  • symptoms: severe pain in upper abd that can radiate to back, N/V, fevers
  • lipase breaks down fat –> FFAs ppt with Ca –> saponification in severe pancreatitis
  • coagulation necrosis with neutrophilic infiltrate and apoptosis of epithelial cells
  • diagnose: typically a female, RFs of gallstone, EtOH, amylase and lipase elevated, CT or US of abd for gallstones
  • treat: hospitalization, NPO, IV pain meds, cholecystectomy
144
Q

Pathophysiology, symptoms, diagnosis, treatment of chronic pancreatitis

A
  • replace pancreatic cells with fibrosis
  • atrophy of gland
  • calcifications/stones in duct
  • lymphocytes and plasma cells
  • symptoms: malabsorption, abd pain that never disappears but gets worse or better and is epigastric that can radiate to the back, malnutrition
  • plugs in duct form due to changes in protein secretion or pH conditions of pancreatic duct
  • lipase secretion is normal or slightly less than normal
  • malabsorption –> weight loss, anemia, diarrhea, bleeding problems due to dec vit K
  • diabetes can manifest at endstage because insulin and glucagon secretion impacted by islet cell destruction
  • diagnosis: xray of abd showing calcifications scattered over epigastrium; stool fat; gold standard is secretin stimulation but rare
145
Q

Pseudocysts

A
  • pancreatic enzymes outside of duct that collect into liquefied/auto-digested pancreatic parenchyma comprised of pancreas juice and necrotic tissue
  • collections line a true epithelial lining characteristic of a cyst
  • resolved over time, but may grow in alcoholics
146
Q

Pancreatic adenocarcinoma

A
  • usually arise from ductal epithelial cells, but also acinar cells
  • normal –> atypia –> low grade dysplasia –> high grade dysplasia –> invasive cancer
  • cells from gland-like structures
  • fibrotic reaction called desmoplasia
  • RFs: family history, tobacco, chronic pancreatitis, obesity
  • difficult to image/screen –> late stage after onset of symptoms
  • symptoms: abd and back pain, weight loss, bile duct obstruction, jaundice, choluria, acholic stools, pruritus
  • diagnose: abd CT scan, biopsy or FNA, endoscopic ultrasound
  • treat: sometimes whipple’s resection (pancreas head, GB, bile duct, and duodenum), chemo, palliative care (ERCP with stent across bile duct)
147
Q

Neuroendocrine pancreatic tumors

A
  • from enterochromaffin cells of lung, GI tract, or islet cells
  • pain, or symptoms with inc in insulin, glucagon, gastrin, VIP, or somatostatin
  • diagnose: with CT or MRI, FNA, and resect
148
Q

Insulinoma

A

recurrent hypoglycemia

- can be treated with injection of concentrated alcohol under EUS guidance

149
Q

Glucagonoma

A

hyperglycemia/DM, weight loss, diarrhea

150
Q

Gastrinoma

A

GERD, PUD, diarrhea, steatorrhea

151
Q

VIPoma

A

severe, chronic, secretory type diarrhea with hypokalemia and weight loss

152
Q

Somatostatinoma

A
  • rare
  • weight loss
  • steatorrhea
  • acalculous cholecystitis by dec GI motility and exocrine secretion
153
Q

Autoimmune pancreatitis

A
  • chronic, inflam
  • IgG-4 and plasma cells and lymphocytes infiltrate pancreas and vessels –> localized or diffuse enlargement of pancreatic parenchyma and narrowing of pancreatic duct/bile duct
  • typically male 45-70yo with history of EtOH or hyperlipidemia and family history of pancreatitis
  • chronic epigastric or diffuse abdominal pain, cholestasis (jaundice, dark urine, itching)
  • assoc with RA, IBD, SLE, and sjogrens
  • elevated serum IgG-4
  • CT, MRI, US show enlarged pancreas with loss of lobular contour
  • can often see bile duct stricture
  • treat with 6wks of PO corticosteroids
154
Q

Antibiotics

A
  • acid suppression and antibiotic therapy
  • triple therapy: clarithromycin, amoxicllin or metronidazole, PPI
  • quad therapy: bismuth, metronidazole, tetracycline, PPI or H2 antagonist
  • sequential therapy: amoxicllin, PPI –> clarithromycin, tinidazole, PPI
155
Q

Proton Pump Inhibitors

A
  • omeprazole, lansoprazole
  • diffuses into parietal cells and irreversibly inactivates H/K ATPase
  • takes 2-5 days to reach steady state; PPIs work daily
  • rapidly absorbed, highly protein bound
  • best 1hr before meals
  • dosage reduction in pts w/ hepatic disease
  • treats: GERD, PUD, NSAID ulcers, stress gastritis prevention, ZES
  • omeprazole may inhibit activation of clopidogrel, which is an antiplatelet agent
156
Q

H2 Receptor Antagonists

A
  • ranitidine, cimetidine, famotidine, nizatidine
  • reversible competitive block at parietal cell H2 receptors on BL membrane
  • good at blocking nocturnal acid secretion
  • PPIs are better
  • rapidly absorbed
  • dosage reduction in pts w/ impaired renal function
  • treats: GERD, PUD, stress-related gastritis
  • side fx: well tolerated, but dizziness, diarrhea, HA, confusion
  • DDI: cimetidine inhibits cytochrome p450 –> inc toxicity of other drugs like warfarin and BDZs etc.
  • can dec ketoconazole abs by inc pH
157
Q

Mucosal Protective Agents

A
  • sucralfate
  • erosion caused by pepsin is inhibited by sulfated disaccharide aluminum salt that binds to necrotic ulcer tissue to make a protective barrier for 6hrs
  • dec back diffusion of H and binds to pepsin
  • activated by pH less than 4 –> don’t give with antacids, H2 blockers and is best 1hr before meals
  • side fx: constipation
  • not really used much, but adjunctive
158
Q

PGE1 analogs

A
  • misoprostol
  • inhibit cAMP in parietal cells –> dec H secretion
  • also stimulate bicarb and mucus formation
  • oral with rapid abs
  • helps with NSAID induced GI ulcers
  • side fx: diarrhea, uterine stimulation
  • contraind in pregnancy
159
Q

Gastric antacids

A
  • mylanta, maalox (OTC)
  • pain relief for PUD and acute gastritis
  • rapidly raises pH of stomach to 4-5 (if to 7, get rebound secretion with gastrin)
  • nonabsorbable
  • long-acting
  • side fx: constipation and diarrhea common
  • space drug dosing around antacid dosing
  • Ca (not good for chronic use), Al (chronic use –> CNS toxicity), Mg (osmotic diarrhea), NaHCO3 (avoid if pregnant, HTN, edema, renal failure)
160
Q

Antimuscarinic agents

A
  • adjunct with H2 blockers

- blurred vision, dry mouth, urinary hesitation, so not widely used

161
Q

What are the mechanisms for promotility drugs?

A
  • directly/indirectly inc agonist activity at smooth muscle M3 receptors in the gut
  • direct act = inc GI motility but not in a coordinated manner (no inc in propulsion, but inc in gastric and pancreatic secretions) so need upstream ACh inc in enteric NS for coordination
  • erythromycin: exc at neural and smooth muscle motilin receptors
  • cisapride: exc at 5HT4 receptors on enteric nervous system cholinergic motor neurons
  • metoclopramide: antagonist at presyn DA (D2) receptors that inhibit ACh release
  • neostigmine: inhibits hydrolysis of ACh by AChE
  • bethanechol: agonist at M3 smooth muscle receptors
162
Q

Metoclopramide

A
  • DA antagonist –> blocks presyn inhibition of ACh release at D2 receptors
  • coordinated contractions
  • relieves N/V by blocking DA receptors too
  • IV-IM, rapid abs
  • treats gastroparesis, GERD, constipation IBS
  • side fx: somnolence, dystonia, tardive dyskinesia
163
Q

5HT receptor antagonists

A
  • ondansetron
  • block 5HT receptors at chemoreceptor trigger zone in CNA, solitary tract nucleus, and visceral afferents of GI tract
  • well abs from GI
  • well tolerated, but QT prolongation
  • prevents vomiting due to cytotoxic drugs; treats N/V after post-op
164
Q

DA receptor antagonists

A
  • metoclopramide, phenothiazines, prochlorperazine
  • block DA receptors in CTZ; phenothiazines act on M and H1 (motion sickness) receptors
  • treats N/V
  • side fx: extrapyramidal symptoms - restless, fatigue, drowsy, diarrhea
165
Q

Antihistamines and anticholinergic agents

A
  • muscarinic receptor blocking actions
  • penetrates CNS
  • use for motion sickness and post op emesis
166
Q

Dronabinol

A
  • stim of CB1 cannabinoid receptors
  • highly lipid soluble and rapidly abs orally
  • prophylactic against emesis for cancer chemo patients
  • side fx: sympathomimetic - tachycardia, palpitations, hypotension, vasodilations, euphoria, somnolence, irritability
167
Q

Substance P receptor antagonists

A
  • blocks substance P (neurotransmitter) at neurokinin 1 receptor that are mediated via vagal afferent fibers to the STN and area postrema
  • oral, hepatic elimination; CYP3A4 metabolized
  • treats delayed phase emesis (2-5 days later) with cisplatin; 3d at start of therapy
168
Q

Anti-inflammatory glucocorticosteroids

A
  • possibly anti-emetic action via suppression of peritumoral inflammation and PG production
169
Q

BDZs

A
  • sedative, anti-anxiety, can reduce anticipatory N/V
170
Q

Treatment of N/V in pregnancy

A
  • ginger
  • pyridoxine: first line for moderate nausea, but doesn’t help vomiting; used with doxylamine
  • H1 antagonists: doxylamine is first line; acts on vestibular system; dry mouth, constipation, and lightheadedness; also diphenhydramine, dimenhydrinate, meclizine
  • DA antagonists: second line; prochlorperazine, metoclopramide, promethazine
  • 5HT3 antagonists: ondansetron
171
Q

List the RFs for gallstone formation

A
  • occur when too much cholesterol or too little water in bile
  • occur with genetic mutations in cholesterol side chains, bile acid hypersecretion, gallbladder stasis
  • RFs for cholesterol stones: obesity, rapid weight gain/loss, female, >30yo, latin american, native american, estrogen/contraceptive use
  • 5 Fs: Fat, Female, Forty, Fertile, Family history
172
Q

Compare and contrast the various gallstone-related complications (pancreatitis, choledocholithiasis, cholangitis) based on history, labs, and cross sectional imaging

A
  • biliary colic
  • acute cholecystitis
  • ascending cholangitis
  • gallstone pancreatitis
  • gallbladder carcinoma
  • choledocholithiasis
  • pancreatitis
173
Q

Compare and differentiate the various imaging studies of the biliary tree

A
  • best initial diagnostic study is ultrasound
  • CT can be considered if abd pain is unclear or need to look at other organs
  • MRI and ERCP are less common because there is a risk of pancreatitis and requires sedation
174
Q

Understand the causes, mechanism, presentation, and treatment of gallstones and their complications

A
  • lithogenic bile (genetics) + stasis + nucleation (mucin plug) = gallstone
  • gallbladder stasis, inflam, cholesterol hypersecretion by liver, overabs of water by GB
175
Q

Cholesterol stones

A
  • composed of cholesterol, bile acids, phospholipids, lecithin
  • white or yellow
  • soft and greasy
  • always develop in gallbladder
  • due to cholesterol and bile salt supersaturation (bile acid def)
176
Q

Pigment stones

A
  • made of Ca bilirubin salts around mucin
  • inc bilirubin in bile (like from hemolytic states)
  • black and hard
  • may develop with chronic inflammation in biliary tree, parasitic infections
  • RFs: biliary obstruction, asian ancestry
177
Q

Pure brown stones

A
  • de novo within bile duct due to bacterial infection in patients with tubes/stents
  • hybrid of cholesterol and pigment stone crystals
178
Q

Biliary colic

A
  • gallstone moves to gallbladder neck, cystic duct, or common bile duct –> when eats (and releases CCK) then have crampy pain in epigastrium or RUQ
  • epigastric or RUQ pain after meals
  • caused by movement of stone into cystic duct or gallbladder neck during eating
  • treat: cholecystectomy
179
Q

Cholecystitis

A
  • stone lodges in cystic duct and causes bacterial infection, inflammation, and ischemia
  • fever, nausea, and severe pain in RUQ that radiates to right flank or shoulder
  • murphy’s sign: stops exhaling when palpates RUQ during exhalation
  • treat with IV fluids and abx, NPO, and pain meds; surgically remove GB (perc drainage if can’t do surgery)
  • may lead to GB perforation or sepsis
  • acute: usually seen with obstruction of cystic duct; elevated alkaline phosphatase
  • chronic: repeated acute cholecystitis; inc risk of GB cancer
180
Q

Choledocholithiasis

A
  • gallstones migrate through cystic duct into common bile duct
  • may cause acute pancreatitis or bile duct obstruction
  • epigastric or RUQ pain, jaundice, dark urine
  • elevated liver chemistries
  • US then ERCP for diagnosis
181
Q

Ascending cholangitis

A
  • bacterial infection in bile duct above a stone
  • usually due to choledocholithiasis
  • life threatening and can progress to sepsis
  • Charcot’s triad: RUQ pain, jaundice, fever
  • Reynold’s pentad: confusion, hypotension, Charcot’s triad –> sign of sepsis
  • give IV abx and ERCP and stent placement
182
Q

Gallbladder cancer

A
  • adenocarcinoma
  • usually develops in patients with gallstones and chronic cholecystitis
  • late presentation typically because tumors do not obstruct a critical duct
  • treat with surgical resection of GB and lymph noes, maybe liver; palliative measures
183
Q

Benign biliary strictures

A
  • caused by edema and fibrosis
  • assoc w chronic choledocholithiasis
  • chronic inflam of the bile duct wall adjacent to a stone
  • can cause stone formation upstream due to stasis
  • can be cause iatrogenically during surgery or due to chronic pancreatitis which can cause narrowed CB duct due to severe fibrosis in pancreatic head
  • AIP can also cause it
  • symptoms: cholestasis leading to jaundice, dark urine, pruritis, and systemic retention of bile acids, acholic stools; RUQ pain or recurrent cholangitis, attacks of pain, fever, jaundice
  • diagnose: US or CT
  • treat: ERCP and stent placement
184
Q

Mirizzi’s syndrome

A
  • unusual cause of BBS where there is impacted stone in cystic duct or severe GB distention
185
Q

Primary sclerosing cholangitis

A
  • idiopathic inflam disorder that causes BBS throughout the biliary tree
  • white males 30-60yo
  • GB is spared
  • assoc w IBD, especially UC
  • 50% will developr liver fibrosis or cirrhosis
  • RUQ pain, jaundice, fevers
  • inc risk of cholangiocarcinoma
  • alk phos/GGT > AST/ALT
  • bilirubin rises late
  • diagnose with ERCP
  • no real treatment except liver transplant
186
Q

Malignant biliary strictures

A
  • adenocarcinoma of ampulla, pancreatic head cancer, cancer of biliary epithelium (cholangiocarcinoma), GB carcinoma, mets to liver, hepatocellular carcinoma
  • symptoms: cholestasis: jaundice, choluria, pruritis, acholic stools; abd pain
  • late presentation
  • early can be resected with Whipple’s surgery
  • ERCP otherwise and chemo
187
Q

Sphincter of Oddi dysfunction

A
  • SOD regulates opening and closing of biliary orifice
  • normally relaxes with NO and beta adrenergic control during fed state and contracts while fasting
  • usually females 20–55yo
  • symptoms: epigastric or RUQ pain, elevations in liver or pancreatic chemistries, recurrent pancreatitis, dilation of bile or pancreatic duct in imaging
  • mimics biliary colic
  • treat with ERCP guided biliary, pancreatic sphincterotomy
188
Q

List the clinical factors that inc risk for cholelithiasis, including major types of gallstones and clinical implications of each type

A
  • assoc w cholecystitis
  • cause pancreatitis
  • cholesterol stones: 5Fs, more common
  • pigment stones: asian, hemolytic syndromes, biliary infection, ileal disease
  • form due to cholesterol supersaturation (inc cholesterol output or dec bile acid synth) –> crystallization + hypomotility + mucus
189
Q

List at least 3 important complications of cholelithiasis

A
  • can cause gallstone ileus (SI obstruction after gallstone passes)
  • assoc w cholecystitis
  • can cause pancreatitis
190
Q

Compare and contrast the macroscopic and microscopic features of acute and chronic cholecystitis

A

Acute:

  • usually due to gallstone obstruction of neck/cystic duct
  • but can also be due to trauma, surgery, burns, postpartum

Chronic:

  • inflam and fibrosis of GB
  • usually assoc w gallstones
  • firm, rigid GB wall
  • histo: mononuc infiltrate; excess fibrous tissue in subserosa; thickened muscular tissue; herniations of muscular layer through muscular layer
191
Q

Describe the histopathologic features of GB cancer

A
  • RFs: gallstones, chronic cholecystitis
  • nearly all adenocarcinoma
  • histo: gland forming; lined with atypical epithelial cells
192
Q

Compare and contrast the histopathologic and clinical features of acute and chronic pancreatitis

A

Acute:

  • most caused by gallstones and alcohol
  • panc enzymes activated –> tissue injury, inflam, edema, ischemia –> more tissue injury
  • alcohol causes a defective packaging on enzymes, secretion of these enzymes, and contraction of SOD

Chronic:

  • usually EtOH abuse
  • also chronic duct obstruction and hereditary pancreatitis
  • acinar cell necrosis and replaced by fibrosis
  • histo: atrophic scarring, loss of acinar tissue and replaced with fibrosis
193
Q

Describe a pseudocyst and state the clinical settings where a pseudocyst sometimes occurs

A
  • digestive areas get walled off

- doesn’t have epithelial lining, has a fibrous wall and inside has fibrin, blood, and digested tissue

194
Q

Recognize the 2 common types of pancreatic neoplasms and compare and contrast the clinical syndromes and microscopic appearance of each type of lesion

A

1) ductal adenocarcinomas
- firm white mass with irregular borders
- can lead to obstruction
- painless jaundice
- histo: malignant gland forming tumor

2) endocrine neoplasms
- nonfcnl, well-differentiated usually
- can secrete insulin (see hypoglycemia), gastrin (see PUD), glucagon
- usually well-circumscribed
- histo: monomorphic, arranges itself in nests/strings of pearls

195
Q

State procedures that can help establish the diagnosis of cholelithiasis and ID under what conditions will one procedure not be informative

A
  • stones w/in biliary tree
  • major cause of ascending cholangitis
  • maybe caused by choledochal cyst: congenital dilatation of common bile duct
196
Q

Bile Duct Carcinoma

A
  • nearly all adenocarcinomas
  • very rare
  • RFs: choledochal cyst in older adults, PSC, infections (liver flukes), maybe cholelithiasis
197
Q

What drugs have constipation as a side effect?

A 
CCBs (verapamil)
Opioid analgesics
Antimuscarinic agents or drugs with antimuscarinic side fx (TCADs, 1st gen antihist, parkinsonian)
Al and Ca supplements
Chemo vinca alkaloids
198
Q

What are the different types of laxatives?

A 
Fiber/Bulk-forming
Saline cathartics
Stimulant/Irritant
Stool-wetting/Emollient
Glycerin suppository
Peripherally acting opioid antagonists
199
Q

Fiber/Bulk-forming

A
  • psyllium, methylcellulose
  • first line
  • facilitate passage and stimulate peristalsis via absorption of water –> bulk expansion
  • effective in 1-3 days; take with water
  • space dosing with other drugs
200
Q

Saline cathartics

A
  • nonabs ions –> cause osmotic retention of water in intestine –> inc peristalsis
  • added to fiber as second line
  • milk of magnesia, Mg citrate: most commonly used, avoid in renal dysfcn
  • phosphate enemas: reserved for fecal impaction
  • PEG: high vol –> bowel cleansing before operation; low vol –> treat constipation for less than 2wks
  • lactulose: nondigestable sugars –> disacch to LMW acids causing osmotic diarrhea and inc peristalsis
201
Q

Stimulant/Irritant

A
  • bisacodyl, senna, castor oil
  • try if fiber and saline fail
  • inc peristaltic activity by inducing inflammation in bowel –> accumulate water and electrolytes and stimulate intestinal motility
  • active w/in 6-10hrs orally, 1hr rectally
  • side fx: cramping, elec def, widely abused
202
Q

Stool-wetting agents and Emollients

A
  • surfactant: docusate
  • stool softener
  • primarily a preventive role; used in pts with CV disease, hernia, postpartum
  • lubricant: mineral oil
  • prevents colonic abs of fecal water
  • be careful of aspiration into lungs with young and elderly
203
Q

Glycerin suppositories

A
  • initiates defecation reflex

- used commonly in neonatal and pediatric patients

204
Q

Peripherally acting opioid antagonists

A
  • pts taking opioids for non cancer pain that laxatives don’t work
  • methylnaltrexone: SC, doesn’t cross BBB, expensive
  • naloxegol: naloxone form given orally; binds opioid receptors in GI tract only; inc spontaneous bowel movements w/o dec analgesia
205
Q

What are the antidiarrheal agents?

A
  • opioids
  • polycarbophil
  • adsorbents
  • probiotics
206
Q

Opioid antidiarrheal agents

A
  • mu receptors on intestinal motility, delta receptors on intestinal secretion, both on absorption
  • loperamide: treats traveler’s diarrhea; can be combined with abx; have anti-secretory against cholera
  • side fx: low addiction liability; can cause CNS dep and paralytic ileus; can worsen shigella infections
  • discont loperamide if no improvement in 48hrs
207
Q

Polycarbophil

A
  • binds free fecal water

- treats diarrhea and constipation

208
Q

Adsorbents

A
  • pepto bismol, kaopectate
  • adsorb toxins, drugs, nutrients, and digestive enzymes that cause irritation
  • take after each loose bowel movement until diarrhea is controlled
  • avoid using bismuth subsalicylate in kids under 12
209
Q

Probiotics

A
  • most common is lactobacillus species including rhamnosus CG
  • microorganism preparations suppress growth of pathogenic organisms and restore normal flora
  • can treat abx-assoc, viral, or traveler’s diarrhea
  • best benefit is with rhamnosus CG (Culturelle)
210
Q

What are treatments for IBS?

A
  • relieve abd pain and discomfort with low dose TCAD
  • improve bowel fcn with antidiarrheal agents (loperamide) or fiber supplements/osmotic laxatives if constipation
  • and then also add another agent specifically for IBS vvvv
  • 5HT3 antagonists (alosetron)
  • 5HT4 agonists (tegaserod)
211
Q

5HT3 antagonists

A
  • alosetron
  • block 5HT3 receptors on sensory and motor neurons –> dec pain and inhibit colonic motility
  • rapid oral abs
  • only treats severe IBS in women with diarrhea as prominent symptom that have not responded to conventional therapies
  • side fx: constipation, ischemic colitis
212
Q

5HT4 agonists

A
  • tegaserod
  • act of 5HT4 receptors –> stimulation of release of NTs involved in peristaltic reflex –> gastric emptying and intestinal motility
  • don’t take on empty stomach
  • don’t give to pts with severe renal or hepatic dysfcn
  • only treats women with IBS with predominant constipation or chronic idiopathic constipation who ave not responded to other treatments
  • side fx: diarrhea, MI, stroke, unstable angina –> restricted use
213
Q

ID the 2 leading causes of death from infectious diseases worldwide

A

pneumonia and diarrhea

214
Q

ID the age group preferentially affected by infectious disease syndromes

A

young and elderly

215
Q

ID the leading cause of morbidity and death with diarrhea

A
  • dehydration –> treat with rehydration
216
Q

State the most reversible cause of morbidity and death with diarrhea

A
  • dehydration
217
Q

Compare and contrast inflam and non-inflam diarrhea, both clinically and anatomically

A

Inflam:

  • colon
  • fever, fecal WBC, RBC

Non-inflam:

  • watery
  • in SI
218
Q

Name 3 organisms that cause inflam diarrhea and 3 that cause non-inflam diarrhea

A

Inflam:

  • colon
  • c. jejuni, shigella, salmonella, e. coli O156:H7, c. diff, e. histolytica

Non-inflam:

  • upper SI
  • cholera, ETEC, norovirus, rotavirus, giardia
219
Q

ID the leading cause of acute bacterial diarrhea in the US - all ages

A

campylobacter jejuni

220
Q

Describe the predominant cause of nosocomial diarrhea

A

c difficile

  • gram pos rod
  • assoc w abx use (resistant organism)
  • can cause mild diarrhea –> watery, bloody, fever, inc WBC, severe colitis
  • inflammatory
  • may cause pseudomembranus colitis
  • treat: give abx (metronidazole first, then vanc), but high recurrence; fecal transplant (inc microbial diversity)
221
Q

Cholera

A
  • A:5B structure
  • A is active part, B is binding
  • mechanism: stim cAMP –> stim CFTR –> secretory diarrhea
  • receptor: ganglioside GM1
  • similar to ETEC
  • presentation: rice water stool (mucinous); dehydration; abrupt diarrhea and vomiting
  • diagnose: non-inflam, no histo damage
  • treat with ORS
  • incubation: 1-5 days
222
Q

What are the signs of dehydration?

A
  • dec pulse vol
  • low BP
  • poor skin turgor
  • sunken eyes
  • dec urine
  • dec MS
  • metabolic acidosis (loss of perfusion and loss of bicarb in bowel)
  • hypoglycemia
  • hypokalemia
223
Q

How does ORS work?

A
  • in cholera, you open the CFTR channel and lose Cl –> lose Na and H2O
  • with glucose, open Na channel so Na comes back in and H2O comes with it
224
Q

ETEC

A
  • causes traveler’s diarrhea
  • non inflam
  • tolerated over time due to immune response and changes in behavior
  • treat with abx
225
Q

Rotavirus

A
  • most prominent non-viral diarrheal cause of death
  • leading cause of: prolonged diarrhea, dehydration from diarrhea, hospitalization from diarrhea, death from diarrhea
  • non-inflam
  • 2 oral vaccines: attenuated virus
  • sporadic cases
  • affects young
  • fecal-oral transmission
  • 1-3d incubation
  • 5-8d duration
226
Q

Norovirus

A
  • affects everyone (epidemics) in winter
  • older children/adults
  • transmission is fecal-oral and infected water and shellfish
  • non inflam
  • self limiting
  • 1-2d incubation
  • 1-2d duration
227
Q

Giardia lamblia

A
  • protozoan
  • diarrhea, fatigue, abd camps, bloating, flatulence, malodorous fatty stool
  • non-inflam
  • parasite in stool
  • give antiparasitic
228
Q

Campylobacter jejuni

A
  • found in poultry, water, and unpasteurized dairy
  • watery diarrhea +/- blood
  • inflammatory
  • fecal WBC
  • give abx
229
Q

E coli (O157:H7)

A
  • causes vast majority of hemorrhagic colitis and HUS
  • lasts 2-4days
  • highest in young and old
  • inflammatory diarrhea, but no fever and little WBCs instead bloody diarrhea
  • found in dairy and beef cattle –> uncooked beef
  • wide range of symptoms: asymptomatic, non-bloody diarrhea, hemorrhagic colitis, HUS, TTP (bloody diarrhea with low platelets)
  • shiga-like toxin binds to human renal endothelial cells –> inhibit protein synth
  • treat: don’t give abx esp bactrim (TMP/SMX) because can worsen; can give IVIG; but support, and prevent
230
Q

Salmonella typhi

A
  • gram neg rod
  • fecal contamination
  • typhoid fever
  • inflam
  • diagnose: get blood culture
  • treat: give abx
231
Q

Shigella

A
  • water contaminated with feces
  • highest infectivity rate
  • severe water or bloody diarrhea
  • inflam
  • give abx
232
Q

Review the systematic approach for interpreting abd radiographs

A

1) patient data: name, MRN, DOB
2) study/image data: projection, patient position, date and time, dept (ICU, trauma, etc.)
3) image quality and adequacy: is area of concern in study
4) detection of abnormalities: ABCDEs (alignment/airways, bone, cartilage/cardiac, diaphragm, everything else, soft tissue)
5) describe abnormality: size, shape, number, borders, location
6) DDx: correlate w patient history and exam findings
7) assess for change: compare with prior studies

233
Q

Recognize free intra-abd free air on abd radiographs and CT and describe how patient positioning affects sensitivity for its detection

A
  • usually supine (KUB)
  • 3way abd series = PA CXR, supine, and upright abdomen
  • upright PA CXR is most sensitive for free air
  • free air will be in the most non-dependent space
  • for an upright CXR: look under (right) diaphragm
  • for a cross table lateral: air anteriorly
234
Q

Explain the ACR Appropriateness Criteria to order appropriate imaging tests

A
  • RFs for pre-administration serum creatinine screening: >60yo, history of renal disease, HTN, DM, on metformin
  • ## get pregnancy test 72hrs before if suspected pregnancy
235
Q

CXR findings

A

Stones:

  • characteristic locations and distinct shadows
  • calcified stones are laminated and faceted
  • 10% of gallstones are calcified and visible on plain films

Calcifications:
- wall or capsule of an organ will have eggshell appearance and denser peripherally

Gas/air:

  • stomach air bubble: LUQ
  • supine –> air moves anteriorly
  • small bowel vs. colon: colon is more peripheral, but not too reliable
  • hallmark of obstruction is dilatation of the bowel
  • 3 6 9 rule –> 3cm (SI), 6cm (transverse colon), 9cm (cecum)
236
Q

Fluoroscopy

A
  • real time images
  • radiation is higher than xray
  • studies: barium swallow, esophogram, upper GI, small bowel follow through, enteroclysis, barium enema
  • don’t give barium upstream of a colonic obstruction –> impaction
  • avoid high osmolality Gastrografin and Gastroview in patients with proximal GI obstruction –> aspiration –> life threatening pulm edema
237
Q

Barium swallow

A
  • fluoroscopic-radiographic contrast exam of oral, pharyngeal, and/or esophageal swallowing
  • evaluates 3 phases of swallowing
  • evaluate oral, pharyngeal, and esophageal and structural and functional abnormalities of the oral cavity, pharynx, and esophagus
  • indicated for dysphagia, odynophagia, heartburn
  • caused by GERD, hiatal hernia, aspiration, neoplasm, esophagitis
238
Q

Upper GI

A
  • examines esophagus, stomach, and duodenum using single and double contrast
  • indicated for epigastric pain, hematemesis, N/V, guaiac positive stools
  • caused by gastritis/duodenitis, gastric or duodenal ulcers, diverticula, benign/malignant tumor
239
Q

Small bowel follow through

A
  • evaluate jejunum, ileum, and terminal ileum; combine with upper GI sometimes
  • obtained in timed intervals until barium reaches colon
  • indicated for IBD, malabs, diarrhea, partial SBO, unexplained GI bleed
  • caused by IBD, lymphoma, TB, sprue, adhesions, obstruction
240
Q

Enteroclysis

A
  • gold standard of SI imaging but not well tolerated, expensive, and high radiation
  • indicated and caused by same things as SBFT
241
Q

Barium enema

A
  • evaluates colon and rectum
  • do not perform immediately after endoscopic biopsy or in toxic megacolon –> perforation
  • replaced with CT
  • indicated for rectal bleeding, polyps, cancer, IBD, fistula, sinus tract, perforation, disimpaction
  • caused by UC, polyps, colorectal carcinoma, ulceration/strictures
242
Q

Ultrasound

A
  • evaluates abd organs and biliary system
  • not widely used in GI tract other than evaluation and suspected appendicitis and some peds conditions
  • no ionizing radiation –> safe in kids and pregnant women
243
Q

CT

A
  • evaluate causes of abd pain
  • barium exams are superior to CT and MRI for evaluating motility, intraluminal, and mucosal disease of GI tract
  • CT is better for evaluating intramural bowel and adjacent mesentery, omentum, retroperitoneum, peritoneal cavity, and viscera
  • risks: nephrotoxicity, allergic reaction, ionizing radiation, contraind in pregnancy
  • w/o IV contrast: detect renal stone or hemorrhage
  • w/ IV contrast: ischemic, infectious, or inflam disease, trauma, tumor
244
Q

IV contrast

A
  • improves evaluation of bowel wall, solid organs, and vasculature
  • ***important to provide radiologist with pertinent history and info about clinical question so study can be appropriately protocoled
  • IV contrast is nephrotoxic and can be allergic
  • get creatinine and GFR before contrast
245
Q

MRI

A
  • does not use ionizing radiation
  • mainly evaluates solid organs and biliary tract
  • contrast agents are gadolinium based –> no nephrotoxicity, but risk of nephrogenic systemic fibrosis
246
Q

Nuclear medicine

A
  • functional info
  • spatial resolution is not as good in comparison to others
  • HIDA: cholecystitis, bile leak, biliary atresia
  • gastric emptying: motility
  • tagged RBC scan: find GI bleed
  • tumor imaging
247
Q

List the 6 main constituents of saliva and their function

A

1) mucins: large glycoproteins that lubricate food and help swallowing
2) amylase (and lipase): digest starches and fats
3) bicarb: maintain optimal pH, dec Ca solubility
4) IgA, lysozyme (destroys bacterial cell walls), lactoferrin (chelates iron –> prevent growth of bacteria that require iron): antibacterial
5) water: solvent
6) epidermal and nerve growth factors: contributes to mucosal growth and protection

248
Q

Explain the structure and function of the salivary gland

A
  • acini of submax and subling have serous and mucous cells
  • serous: secrete fluid, electrolytes, and enzymes
  • mucous: secrete mucins
  • proteins exocytosed with inc in intracel Ca
  • saliva passes through short intercalated duct into striated duct
  • high flow in acini: slightly hypotonic, lots of bicarb
  • low flow in duct: really hypotonic because Na and Cl transported out and bicarb and K transported in
249
Q

Contrast the plasma and pancreatic concentration of Na, Cl, and bicarb at low secretion rates and at high secretion rates and the principal cell types involved in each secretion rate

A

Relative to plasma, pancreatic juice has:
- Virtually the same Na+ and K+ concentrations as plasma
- Much higher HCO3- than plasma to neutralize acidic
chyme in duodenum
- Much lower Cl- than plasma
- Isotonic at all flow rates

Composition of aqueous component of pancreatic secretion varies with
the flow rate
- At low flow rate the pancreas secretes an isotonic fluid composed of mainly Na+ & Cl- (secretion = NaCl) –> bicarb low, Cl high
- At high flow rate, secretes an isotonic fluid composed of mainly Na+ & HCO3-
(secretion = NaHCO3) –> bicarb high, Cl low

250
Q

List the major ionic and peptide/protein components secreted by the pancreas

A
  • each cell produces full complement of pancreatic enzymes
  • released by exocytosis
  • trypsinogen
  • chymotrypsinogen
  • proleastase
  • procarboxypeptidase A/B
  • RNAase, amylase, lipase
  • enterokinae (by SI mucosa) –> activate trypsin –> activates the rest
251
Q

State 3 types of stimuli that inc pancreatic secretion

A

1) ACh: from vagus and ENS nerves; stim release of digestive enzymes from acinar cells
2) secretin: from endocrine cells in proximal SI in response to acid; stim release of a bicarb rich solution from pancreatic duct cells
3) CCK: from endocrine cells in proximal SI in response to fats and proteins –> stim release of digestive enzymes from acinar cells

252
Q

Explain the function of CCK, where it is released from, what cells it works on and what the outcome of its actions are

A
  • chyme (fats and protein) arrives in SI –> stimulates release of CCK –> act pancreatic acinar cells –> secrete pancreatic digestive enzymes
  • CCK stim acinar cell secretion
  • CCK delays/dec gastric acid production and gastric emptying
  • contracts GB –> bile acid secretion
  • acinar secretion in pancreas
  • relax SOD
253
Q

List the 8 different infection/immunological salivary gland diseases

A

1) mumps
2) CMV sialadenitis
3) bacterial sialedenitis
4) sacroidosis
5) sjogrens
6) salivary lymphoepithelial lesion
7) xerostomia or dry mouth
8) halitosis

254
Q

Discuss characteristics of benign and malignant salivary neoplasia and be able to describe examples of both

A

Benign:

  • mixed tumor (pleomorphic adenoma): warthin’s tumor – bilateral, due to smoking, parotid gland, epithelial and lymphoid components
  • monomorphic adenomas: no mesenchymal stromal component, but similar to mixed tumor
  • ductal papilloma

Malignant:

  • mucoepidermoid carcinoma:
  • polymorphous low grade adenocarcinoma
  • adenoid cystic carcinoma: swiss cheese
  • clear cell carcinoma
  • acinic cell carcinoma
255
Q

List 8 forms of endocrine and 8 exocrine pancreatic cancers, ID their key features and how the TNM method of staging is used to grade them

A

Endocrine:

  • gastrinoma (ZES)
  • glucagonoma: large, mets
  • insulinoma: most common NE tumor
  • nonfunctional islet cell tumor
  • somatostatinoma: pancreas or duodenum
  • VIPoma: body or tail of pancreas

Exocrine:

  • acinar cell carcinoma: rare, inc in lipase
  • adenocarcinoma: start in duct
  • adenosquamous carcinoma: form glands, flattens
  • intraductal papillary-mucinous neoplasm: fingerlike projections into duct
  • mucinous cystadenocarcinoma: spongy cystic tumor
  • pancreatoblastoma: rare, kids
256
Q

What does bicarb in the pancreatic secretion do?

A
  • keeps enzymatic secretions moving down duct
  • neutralize gastric acid from stomach into SI
  • acid in SI –> secretion of secretin from duodenal endocrine cells
  • secretin stimulates bicarb production
  • secretin and CCK inhibit gastric acid/fluid production and delay gastric emptying
  • basically: secretin –> phos CFTR channel –> Cl into lumen –> bicarb into lumen with Cl/bicarb exchanger –> water and Na follow into lumen –> H ions formed pumped out via Na/H exchanger and Na/bicarb brings in Na and bicarb
257
Q

Tracheoesophageal fistula

A
  • see CV defects
  • distal esophagus and trachea connection –> proximal esophagus ends in blind pouch, distal esophagus open to trachea
  • prenatal: polyhydramnios
  • postnatal: choking with feeds
258
Q

Infantile Hypertrophic Pyloric Stenosis

A
  • M>F
  • hypertrophy and hyperplasia of pylorus –> obstruction and dilation of proximal stomach
  • non bilious projectile vomiting assoc w abdominal mass
  • usually 3wks of life
259
Q

Meckel diverticulum

A
  • remnant of vitelline duct –> blind pouch protrudes from ileum
  • rules of 2: 2% of pop, age 2, 2 inches long, 2 feet into small bowel, 2:1 M:F
  • usually asymptomatic
  • obstruction and bleeding and inflam
  • heterotrophic gastric or pancreatic tissue
  • 99Tc scan
260
Q

Omphalocele

A
  • failure of intestine to return to abdomen
  • defect in abd wall at umbilical cord site
  • large sac of amnionic membrane is filled with bowel
261
Q

Gastroschisis

A
  • similar to omphalocele superficially, but due to paraumbilical defect in abd wall
262
Q

Malrotation

A
  • LI doesn’t assume normal position
  • 10wks after gestation when intestines return to abd cavity
  • asymptomatic, but can have volvulus of LI
  • can have bilious vomiting
263
Q

Duplication/cysts

A
  • saccular bowel that present as cystic mass lesions leading to bowel obstruction
264
Q

Intestinal stenosis/atresia

A
  • usually with other malformations or with CF
  • duodenal atresia is most common
  • 40% have down
  • see polyhydramnios and bilious vomiting
  • only a segment is involved usually
  • usually caused by vascular insuff
265
Q

Imperforate anus/rectal agenesis

A
  • thin membrane of tissue covering anus to complete agenesis of rectum
  • assoc w fistula formation and cloacal or GU defects
266
Q

Hirschprung disease

A
  • congenital megacolon due to massive dilatation of intestinal lumen
  • failure to pass meconium
  • can lead to perforation
  • M>F
  • RET receptor mutation
  • failure of bowel nerve plexi (ENS) –> absence of ganglion cells that help with peristalsis
  • treat with resection
267
Q

Neonatal necrotizing enterocolitis

A
  • first 7-10days of life
  • complication of prematurity
  • abd distention and blood stools
  • assoc w hypoxemia (blood shunted away from intestine)
  • affects terminal ileum, cecum, and right colon
  • ischemic damage –> invasion of organisms, formation of gas gangrene –> peritonitis and perforation
  • treat with bowel rest and abx and surgical resection
268
Q

Esophagitis

A

1) reflux esophagitis:
- inadequate gastroesophageal sphincter fcn
- abnormal esophageal pH
- response to acid blocking drugs
- distal esophagus
- mild intraepithelial eos infiltrate

2) allergic/eosinophilic esophagitis:
- immune rxn to dietary allergens
- pH is normal
- no response to acid blockage
- treat with inhaled steroids
- total length of esophagus is affected

269
Q

Biliary Atresia

A
  • causes cholestasis
  • two forms: perinatal and embryonic/fetal form

Perinatal:

  • more common
  • extrahepatic biliary tree undergoes destruction after birth
  • late onset jaundice
  • acholic stools
  • atresia of entire extrahepatic biliary system
  • caused by infection, toxin, AI, genetics
  • histo: cholestasis in hepatocytes, canaliculi, and bile ducts; portal fibrosis with bile duct prolfi; inflam
  • diagnose: cholangiogram
  • treat: hepatoportoenterostomy (Kasai procedure) –> excise extrahepatic biliary system and small bowel is connected to hepatic hilum for bile drainage instead
  • progress to cirrhosis

Embryonic form:

  • less common
  • congenital anomaly of biliary tree
  • progressive jaundice
270
Q

Neonatal jaundice

A
  • abnormal deposition of bilirubin
  • DDx: physiologic jaundice (normal), infection, meds, TPN, obstruction, idiopathic, hyperbilirubinemia
  • unconj/conj bilirubinemia
271
Q

Physiologic jaundice

A
  • inc RBC turnover
  • immature conjugating system
  • deconjugating enzymes (beta-glucuronidases) in breast milk
  • w/in 1st week of life
  • inc unconjugated bilirubin
  • phototherapy, usually self resolves
272
Q

Idiopathic neonatal hepatitis

A
  • undiagnosed conjugated hyperbilirubinemia
  • hepatomegaly
  • see cholestasis, prominent giant cell transformation of hepatocytes, minimal inflam, normal bile ducts
  • give phototherapy
273
Q

Total parenteral nutrition hepatopathy

A
  • if TPN for a long time (GI disease of necrotizing enterocolitis)
  • discontinue TPN
274
Q

Crigler-Najjar syndrome

A
  • hereditary, unconj hyperbilirubinemia
  • type 1 (none) or type 2 (dec) of UGT1A1 which normally conjugates bilirubin to glucuronic acid –> have water-soluble bilirubin glucuronides excreted in bile
  • serum unconj bilirubin are really high
  • type 1 is fatal, type 2 is ok with jaundice
275
Q

Gilbert syndrome

A
  • hereditary unconj hyperbilirubinemia
  • mild fluctuating levels of serum bilirubin due to dec in UGT1A1 activity
  • episodic jaundice during stress
276
Q

Dublin-Johnson syndrome

A
  • hereditary conj hyperbilirubinemia
  • defect in excretion of bilirubin glucuronides across canaliculi due to absences of MRP2
  • stress induced
277
Q

Rotor syndrome

A
  • hereditary conj hyperbilirubinemia

- mechanism unknown

278
Q

Liver in genetic disease

A
  • alpha 1 antitrypsin disease
  • focal biliary cirrhosis in CF: patchy, irregular areas of fibrosis with bile duct prolif; centrilobular steatosis and chronic inflam
279
Q

Liver in metabolic disease

A
  • hematchromatosis: disease of Fe metabolism
  • Wilson’s: disease of Cu metabolism
  • glycogen storage disease: abnormal accumulation of glycogen
  • lysosomal storage diseases: lipid (wolman, defect in cholesterol ester storage), sphingolipdoses (niemann pick, sphingomyelin and gaucher, glucosyl ceramide), oligosaccharides (abnromal glycoprotein degradation, farber and fabry disease, ceramide accumulation)
  • defect in fatty acid oxidation –> rapid death from febrile illness (carnitine deficiency, defects in acyl-CoA-dehydrogenases)
280
Q

Choledochal cyst

A
  • congenital efect onf intra/extrahepatic bile ducts; ductal dilation and bile stasis
  • pain, direct jaundice, RUQ mass
281
Q

Hepatic neoplasms

A

Benign:

1) mesenchymal hamartoma:
- nontender abd enlargement
- vomiting, dec appetite, resp distress
- alpha fetoprotein levels not inc
- resect
- multicystic lesion composed of admixture of primitive, but histologically benign mesenchyme, bile dcuts, and cords of hepatocytes
2) teratoma
3) hepatocellular adenoma
4) focal nodular hyperplasia

Malignant:

1) Hepatoblastoma:
- 90% before 5yrs
- arises in normal liver
- enlarged abdomen, anorexia, weight loss, N/V, pain
- elevated alpha fetoprotein level, also bea-hCG
- treat with preop chemo and resection

2) hepatocellular carcinoma:
- usually adults
- background of chronic liver disease (congenital hep b or metabolic disease)
- serum alpha fetoprotein inc

3) undiff/embryonal sarcoma:
- aggressive
- serum alpha feroprotein not inc

282
Q

Inflammatory Polyps

A
  • present with bleeding
  • due to mucosal prolapse
  • injury and healing cycles –> polyp
283
Q

Hamartomatous polyp

A
  • disorganized tissue
  • tumor-like overgrowth
  • juvenile: sporadic or syndromic
  • peutz-jegers: syndromic
  • in lower GI
  • benign but foci of dysplasia
  • risk of future GI carcinoma
  • genetic counseling
284
Q

Hyperplastic polyps

A
  • left colon and rectum
  • inc with age
  • small (less than .5cm)
  • delayed maturation with overgrowth of superficial epithelium –> serrated architecture (neither tubular or villous)
  • no dysplasia
  • sessile
  • infoldings –> serrated
285
Q

Sessile serrated polyps/adenoma

A
  • alternative pathway to carcinoma rather than adenoma
  • goes through microsatellite instability pathway
  • usually right side
  • pre malignant
286
Q

Adenomas

A
  • variable size
  • throughout colon
  • cytologic dysplasia
  • villous are usually more invasive
  • size is most important indicator of malignancy
287
Q

RFs for CRC

A
  • advanced age
  • country of birth
  • FAP/HNPCC
  • long standing UC
  • red meat/fat diet
  • smoking
  • obesity
  • cholecystectomy
288
Q

CRC molecular pathways

A

1) WNT/APC/beta catenin - classic adenoma –> carcinoma
- w/o WNT signal: beta catenin destroyed
- w/ WNT signal: beta catenin is not phos and turns on genes
- mutation in APC –> basically beta catenin stays on and keeps activating genes –> stem cells do not differentiate and become cancer

2) K-Ras/MAP kinae/PI3 - activating mutations
- cetuximab does not help in mutated K-ras, but does help n wild type K-ras

3) microsatellite instability - defects in mismatch repair proteins

289
Q

HNPCC

A
  • earlier age
  • right sided
  • microsatellite instability
  • sessile serrated adenoma –> invasive carcinoma
  • mismatch repair gene mutation
290
Q

Neutrophils in hepatic parenchyma?

A

Steatohepatitis

291
Q

Eosinophils in hepatic parenchyma?

A

Drug reaction

292
Q

Plasma cells in hepatic parenchyma?

A

Autoimmune hepatitis

293
Q

Cholestasis

A
  • bile w/in hepatic parenchyma

- balloon degen

294
Q

Bile ductular reaction

A
  • obstructive cholestasis –> bile builds up in caniliculi of zone 1 hepatocytes –> metaplasia to be like bile ducts cells
  • edema and PMN inflam
295
Q

Fibrosis

A
  • end result of inflam/injury

- fibrosis from collagen deposition by activated stellate in space of Disse

296
Q

Acute hepatitis

A
  • less than 6mos
  • hepatocyte injury
  • inc in AST and ALT
  • causes: acute viral hepatitis (A and E), AI hepatitis, adverse drug rxn, idiopathic
  • lobular disarray and inflam
  • necrotic hepatocytes
  • cholestasis
  • not a lot of fibrosis
297
Q

Chronic hepatitis

A
  • hepatic injury/inflam >6mos
  • causes: viral (C»B>D), AI, drugs, idiopathic
  • less lobular disarray, less prominent inflam, rare single necroses, slow progression of fibrosis
298
Q

Cirrhosis

A
  • end stage chronic liver disease
  • bridging fibrous septa
  • distortion of architecture
  • regen nodules
  • portal HTN
  • poor synth fcn
  • inc risk for HCC
299
Q

Cholestatic liver disease

A
  • acute or chronic jaundice
  • inc in alk phos, GGT, and bilirubin
  • cholestasis, ductular reaction, edema, PMN inflam
300
Q

Hep A and E viruses

A
  • ssRNA
  • spread via fecal-oral
  • never lead to chronic disease
  • look for IgM and IgG specific antibodies (vaccine exists)
  • HEV has a high mortality in pregnant women (fulminant hepatitis)
301
Q

Hep C virus

A
  • 80% go onto chronic liver disease
  • transmit bia blood and fluids and vertically
  • antiHCV antibodies = exposure; in 97% of people exposed by 6mos
  • PCR for HCV RNA = ongoing infecton
  • rare presents as acute hepatitis
  • lobular and interface necroinflam and inc fibrosis
  • nodular aggregates of lymphocytes in portal areas
  • RFs: IV drug use, sex partners, surgery, needle stick, HCV contacts
  • see lymphoid aggregates
  • treat with pegIFN, ribavirin, (protease inhibitor) (no vaccine bc HCAb is not neutralizing)
302
Q

Hep B virus

A
  • DNA virus –> integrates into host genome –> tumor development
  • transmitted by blood and fluids and vertically
  • 10% do not clear virus, 5% progress to chronic hepatitis
  • ground glass hepatocytes and sanded nuclei
  • most adults recover
  • HBsAg = active infection
  • HBsAb = immunity to Hep B
  • HBcAb = active or prior infection
  • HBeAg = high viral load
  • HBeAb = lower viral load
  • HBV DNA = active viral replication
  • treat with IFN and tenofovir)
303
Q

Hep D virus

A
  • needs concurrent hep B virus

- can show inc plasma cells

304
Q

Autoimmune hepatitis

A
  • hepatic inflam
  • prominent plasma cells
  • acute flare –> chronic hepatitis
  • F>M
  • inc AST and ALT and normal alk phos
  • one positive antibody at least (ANA, ASMA, anti-LKMB)
  • inc IgG
  • treat with steroids
  • interface and centrolobular necroinflam
305
Q

Primary biliary cirrhosis

A
  • AI attack of intrahepatic bile ducts
  • usually middle aged women
  • insidious onset with pruritus before jaundice
  • inc alk phos, GGT, bilirubin
  • slightly inc AST and ALT
  • positive AMA
  • inc IgM
  • florid duct lesion:
    1) lymphohistiocytic and plasma cell rich inflam of portal areas
    2) active lymphocytic cholangitis
    3) bile duct destruction
  • granulomatous lymphocytic cholangitis
  • ductopenia
  • treat with ursodeoxycholic acid
306
Q

Primary sclerosing cholangitis

A
  • patchy inflam
  • obliterative fibrosis of bile ducts
  • usually affects extrahepatic bile ducts
  • persistently inc alk phos and no other signs
  • over time, see fatigue, pruritus, jaundice
  • M>F
  • strong assoc with UC
  • inc risk for cholangiocarcinoma
  • inc alk phos, GGT, bilirubin
  • diagnose with ERCP
  • string of pearls on cholangiography (strictures and dilations)
  • lymphocytic periductular inflam and fibrosis around larger bile ducts –> onion skin fibrosis
307
Q

Drug induced liver disease

A
  • can range from asymp elevations of LFTs to acute hepatitis to cholestasis
  • can see necrosis, cholestasis, biliary injury, AI hepatitis, acute hepatitis, or chronic hepatitis
  • acetaminophen: intrinsic hepatotoxin –> coagulative necrosis in zone 3 –> pan lobular necrosis
308
Q

Steatohepatitis

A
  • steatosis + lobular inflam + balloon degen = steatohepatitis
  • non-alcoholic (dec lipolysis): seen with DM, metabolic syndrome, obesity, or drug rxn
  • can lead to hepatic fibrosis and 20% risk of cirrhosis
  • alcoholic (block lipid clearance): AST:ALT >2, normal alk phos and inc GGT, mallory bodies, inc PMNs
309
Q

Hereditary hemochromatosis

A
  • iron overload due to HFE mutation
  • mutations are C282Y and H63D
  • AR inheritance
  • M>F
  • excess iron abs and deposition into tissues
  • liver disease + diabetes + heart failure
  • eventually leads to injury and fibrosis
  • primary: in hepatocytes
  • secondary: from excessive ingestion or transfusions or hemolysis and is in Kupffer cells
  • see joint stiffness, hyperpigmentation of skin, DM, hypothyroidism, hypogonadism, cardiomyopathy, cirrhosis
  • high ferritin, high transferritin saturation, high Fe sat
  • treat with phlebotomy until ferritin is 50
310
Q

Wilson’s disease

A
  • Cu overload
  • mutation in ATP7B gene
  • AR inheritance
  • low ceruloplasmin levels
  • KF rings in eyes
  • patchy Cu accumulation in hepatocytes
  • can see steatosis and acut/chronic hepatitis-like changes
  • treat with d-penacillinamine
311
Q

Alpha 1 antitrypsin

A
  • dec production of protease inhibitor
  • AR inheritance
  • normally prevents proteases released by neutrophils and limits tissue damage
  • mutation leads to emphysema
  • hyaline globules with progressive fibrosis
312
Q

Portal vein thrombosis

A
  • non-cirrhotic portal HTN
  • prominent congestion of sinusoids
  • hepatocyte atrophy
313
Q

Budd-Chiari syndrome

A
  • liver enlargement
  • pain
  • ascites
  • main hepatic vein occlusion
  • lead to fibrosis and cirrhosis
314
Q

Hepatocellular Carcinoma

A
  • in patients with HCV, HBV, NASH, alcohol (chronic) and cirrhosis
  • abnormally thickened hepatic plates (>3cells thick)
  • endothelialization of of the sinusoids, invasion of the fibrosis, unpaired arteries, and vascular invasion
  • treat with chemo
  • malignant
  • inc alpha fetoprotein
315
Q

Cholangiocarcinoma

A
  • malignant
  • neoplasm of bile ducts
  • RF is PSC
  • gland forming desmoplasia
316
Q

Hemangioma

A
  • benign
  • most common
  • F>M
  • small and asymptomatic
  • RUQ pain, early satiety, N/V
  • spongy hemorrhagic surface
  • dilated thin wall of vasculature
  • resect if large
317
Q

Focal nodular hyperplasia

A
  • benign
  • due to local vascular flow anomaly
  • F>M
  • small and asymptomatic
  • RUQ pain, early satiety,
    N/V
  • central stellate scar
  • enlarged arterioles
318
Q

Hepatocellular adenoma

A
  • benign
  • in women with oral contraceptive use
  • RUQ pain
  • risk of rupture with hemorrhage
319
Q

What can >15x normal inc in AST and ALT indicate?

A
  • acute viral hepatitis
  • meds/toxins
  • ischemic hepatitis
  • AI hepatitis
  • wilson’s disease
  • budd-chiari
  • hepatic artery ligation or thrombosis
320
Q

HBsAb > 6mos?

A
  • diagnosis of chronic HBV
321
Q

What criteria do people with chronic hepatitis need to meet for treatment?

A

1) HBsAg > 6mos
2) serum HBV DNA > 10^5
3) persistent inc in ALT and AST

  • if not then get liver biopsy
322
Q

What is the goal of HBV treatment?

A
  • HBeAg seroconversion (loss of HBeAg and development of HBeAb)
  • indicates negative HBV DNA
323
Q

HBsAg

A

HBsAg: Hepatitis B surface antigen
– Marker of active infection
– Presence for >6 months defines chronic hepatitis B infection

324
Q

HBsAb

A

HBsAb (or anti-HBs): Antibody to HBsAg

– Marker of immunity to hepatitis B

325
Q

HBcAb

A

HBcAb: Hepatitis B core antibody

– Marker of active or prior infection

326
Q

HBeAg

A

HBeAg: Hepatitis B “e” antigen

– Surrogate marker of high viral load

327
Q

HBeAb

A

HBeAb (or anti-Hbe): Antibody to hepatitis B “e” antigen

– Associated with lower viral load

328
Q

HBV DNA

A

HBV DNA: Presence means active viral replication

329
Q

How do you treat HBV?

A
  • pegylated interferon and nucleoside/tide analog (tenofovir)
  • IFN has side fx but last forever; don’t use in pts with advanced liver disease
  • tenofovir has fewer side fx
330
Q

How do you treat HCV?

A
  • pegIFN, ribavirin, NS3/4a protease inhibitor (boceprevir or telaprevir) for 24-48wks
  • then check to see if HCV RNA is negative 12wks after stopping
331
Q

How do you treat hereditary hemochromatosis?

A
  • phlebotomy
  • each 500mL removed contains 200-250mg Fe
  • one phlebotomy per week for one year
  • goal is serum ferritin of 50
332
Q

treatment for AI hepatitis

A
  • corticosteroids
  • azathioprine and/or prednisone
  • side fx: dec WBC, nausea, pancreatitis, weight gain, anxiety, osteoporosis, DM, HTN, cataracts
333
Q

treatment for PBC

A
  • usodiol (urosdeoxycholic acid)

- secondary bile acid –> improvement of bile acid transport

334
Q

treatment for PSC

A
  • management with stenting and ERCP
  • treat cholangitis with abx
  • liver transplant
335
Q

treatment for Wilson’s disease

A
  • chelators of copper
  • D-penicillamine and trientine
  • can also use zinc
336
Q

treatment for NASH

A
  • modify RFs for NASH:
    1) obesity
    2) type 2 DM
    3) dyslipidemia
337
Q

Th1 cells

A
  • attract macrophages
  • secrete IFNgamma
  • activates M1 macrophages (inflam, destructive)
  • secrete IL-2 –> activate CTL
338
Q

Th17 cells

A
  • cause focused inflam
  • resistance to listeria and candida
  • implicated in AI psoriasis
  • make IL-17
  • dendritic cells make IL-23 which differentiates cells to Th17
339
Q

Th2 cells

A
  • stim macrophages to become M2 –> wall off pathogens and promote healing
  • parasitic immunity
  • makes Il-4 which attracts macrophages and eosinophils
340
Q

Tfh cells

A
  • stim by Ag –> migrate from T cell areas to B cell follicles –> activate B cells –> make IgM, IgG, IgE, and IgA
341
Q

Treg

A
  • make IL-10, TGFbeta

- suppresses action of Th1, Th17, Th2

342
Q

CTL

A
  • destroy anything IDd as foreign or abnormal antigen on surface presented on Class I MHC
  • make IFNgamma to attract macrophages

DEMS (4 decks)

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