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DEMS > GI Tract > Flashcards

GI Tract Flashcards

1
Q

Interstitial cells of Cajal

A

Pacemaker cells

Create the bioelectrical slow wave potential that leads to contraction of the smooth muscle

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2
Q

Odynophagia

A

Painful swallowing, in the mouth or esophagus

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3
Q

Ileus

A

Inability of the intestine (bowel) to contract normally and move waste out of the body

FAILURE OF PERISTALSIS

AKA GI atony

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4
Q

Which bacteria can cause renal failure?

A

Enterohemorrhagic E. coli

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5
Q

Mucosal scalloping is associated with?

A

Celiac disease

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6
Q

Hamartomatous polyps

A

A distinct subset of polyps, mostly occurring in childhood

“tumor-like” overgrowth / mature tissue / developing where it is NORMALLY present
= tissue that DOES belong there, but is overgrown and disorganized

Most arise in the presence of syndromes —> need regular screening

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7
Q

Urease breath test

A

Indicative of H. pylori infection in the setting of GERD, worsening pain

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8
Q

Tx for H. pylori infection?

A

Triple therapy:

1) amoxycillin
2) clarithromycin
3) PPI (omeprazole)

ACP!

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9
Q

Somatostatin

A

Inhibits the release of gastrointestinal and pancreatic enzymes (gastrin, CCK, insulin, glucagon, etc.)

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10
Q

Gastrin

A

Stimulates secretion of gastric acid (HCl) by parietal cells of the stomach

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11
Q

CCK

A

Stimulates release of bile, pancreatic enzymes in order to digest fats and proteins.
Mediates digestion in the small intestine by inhibiting gastric emptying and decreasing gastric acid secretion.

Synthesized by I-cells in the SI

Secreted by duodenum

Trypsin normally breaks down proteins. However, when protein level is low, trypsin acts on CCK/monitor peptide & inhibit CCK production, release. = self-regulating system

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12
Q

Secretin

A

Helps regulated the pH of the duodenum by stimulating the production of bicarb by the pancreas, inhibiting gastrin release from the stomach

Released by duodenum

Produced in S cells of the duodenum

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13
Q

G cells

A

Release gastrin

Present in pyloric antrum of stomach, duodenum, and pancreas

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14
Q

D cells

A

Somatostatin-producing cells

Found in the stomach, intestine and pancreas

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15
Q

What is the pathogenesis of cholesterol gall stones?

A
  • cholesterol supersaturation
  • phospholipid deficiency (acts as a detergent)
  • over-absorption of water in gall bladder
  • mucin plug or foreign body nidus (sand in oyster)
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16
Q

What are the risk factors for pigment gall stones?

A
  • bile duct obstruction
  • excess bilirubin (hemolysis)
  • East Asian ancestry
  • parasitic infxns
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17
Q

What are the risk factors for gall stones?

A

5 F’s!

  • forties
  • fat
  • female
  • fertile/fetus
  • family hx

Also, Latin American/Native American ancestry, rapid weight loss, or biliary obstruction

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18
Q

What is biliary colic?

A

Stone in the duct, obstructing gall bladder –> pain

Sx: intermittent pain in epigastrium, RUQ after meals (esp. fatty foods). Builds over an hour, remits 3-8 hrs later

Occurs with movement of stone into cystic duct or gall bladder neck

Tx: cholecystectomy; poss. bile acid supplement (UDCA)

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19
Q

What is ascending cholangitis?

A

A bacterial infxn of the bile duct
Usually a complication of choledocholithiasis

Sx: Charcot’s triad

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20
Q

Charcot’s triad

A

RUQ pain
Fever
Jaundice

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21
Q

Reynold’s pentad

A

Charcot’s triad (RUQ pain, fever, jaundice) + hypotension + altered mental status

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22
Q

Choluria

A

Bile in the urine - looks dark (Coca-Cola colored)

The presence of choluria is a useful symptom to distinguish if somebody presenting with jaundice has liver disease (direct hyperbilirubinemia) or hemolysis (indirect hyperbilirubinemia). In the first case, patients have choluria due to excess conjugated (“direct”) bilirubin in blood, which is eliminated by kidneys. Hemolysis, on the contrary, is characterized by unconjugated (“indirect”) bilirubin which is bound to albumin and thus not eliminated in urine.

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23
Q

What are the sx of biliary stricture?

A

Sx of cholestasis:

  • jaundice
  • dark urine
  • acholic stool
  • pruritis

RUQ pain
LFTs elevated in cholestatic pattern

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24
Q

What disease is associated with PSC?

A

UC

90% of PSC pts have UC

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25
Q

PSC

A

Strictures of the large and small bile ducts (intra- and extra-hepatic)

Males > Females

A/w UC

Risk of liver cirrhosis!
Increased risk of cholangiocarcinoma

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26
Q

Sphincter of Oddi dysfunction

A

Occurs mostly in young females

Mimics choledocholithiasis

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27
Q

How do gallstones cause acute pancreatitis?

A

Obstruction of pancreatic duct –> ↑ ductal pressure –> leakage of enzymatic fluids into pancreatic tissue –> tissue injury, inflammation, edema, ischemia due to auto-digestion of the pancreas

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28
Q

How does alcohol cause acute pancreatitis?

A

1) sphincter of Oddi contraction
2) stimulation of pancreatic secretion; premature release of enzymes
3) defective packaging of enzymes
4) proteinaceous plugs within pancreatic duct

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29
Q

Zollinger-Ellison Syndrome

A

Gastrin-secreting tumor in the pancreas

Pts p/w PUD

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30
Q

What is the most common pancreatic neuroendocrine tumor?

A

Insulinoma (42%)

Pts p/w fainting episodes due to hypoglycemia

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31
Q

What are the 6 main constituents of saliva?

A

1) water
2) bicarb (to buffer pH when vomiting)
3) mucins
4) amylase
5) lysozyme, lactoferrin, IgA (immune protection)
6) epidermal and nerve growth factors (mucosal growth/protection; dog licking a wound)

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32
Q

Structure of the salivary gland

A

1) myoepithelial cells help push secretions out
2) acinar cells secrete a hypertonic solution into the acinus
3) sol’n goes through intercalated duct
4) sol’n continues through striated duct, where ductal cells modify the content: adjust the level of solutes, water, etc.

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33
Q

Parasympathetic effect on salivary secretion

A

Increased acinar cell secretion; vasodilation of blood vessels surrounding the acini

Results in protein/fluid/ion rich solution = watery

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34
Q

Sympathetic effect on salivary secretion

A

Increased acinar cell secretion

High protein/low fluid solution = viscous

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35
Q

Fast vs. slow flow rate in salivary secretion

A

Fast flow = still get secretions, but don’t get time to reabsorb. Thus, much more Na, Cl present in secretions, much less K and HCO3

Slow flow = production in acinus, moves into striated duct, & because it has time, get a lot of reabsorption of Na, Cl; secretion of K and HCO3

SLOW = keep the SALT (NaCl)

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36
Q

List 3 stimuli that increase pancreatic secretion

A

1) Acetylcholine (ACh) - released from vagus and ENS systems; stimulates the release of digestive enzymes from ACINAR cells (mostly cephalic stage)
2) Secretin - released in the proximal SI in response to acid; stimulates the release of a bicarb sol’n from pancreatic DUCT cells
3) CCK - released from proximal SI in response to fats & proteins; stimulates the release of digestive enzymes from pancreatic ACINAR cells

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37
Q

What does CCK do, and where?

A

Gallbladder - stimulates contraction, bile secretion (for fat absorption)
Pancreas - stimulates acinar secretion of enzymes
Stomach - delayed emptying
Sphincter of Oddi - relaxation

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38
Q

What is the big compositional difference between salivary and pancreatic juices?

A

Saliva: KHCO3

Pancreas: NaHCO3

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39
Q

What are the 8 salivary gland diseases?

A
  1. Mumps
  2. CMV sialadenitis
  3. Bacterial sialadenitis
  4. Sarcoidosis
  5. Sjogren’s Syndrome
  6. Salivary Lymphoepithelial Lesion
  7. Xerostomia
  8. Halitosis
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40
Q

Pleomorphic adenoma

A

Diverse microscopic pattern

Cuboidal cells arranged in duct-like structures

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41
Q

Warthin’s tumor

A

Benign tumor of the parotid gland

Has both lymphoid and epithelial component

WHALE = Warthin’s Has Abundant Lymphoid and Epithelial components

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42
Q

Epigastric pain, radiating to the back is classic for?

A

Pancreatitis

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43
Q

What is the #1 cause of acute pancreatitis?

A

Gallstones

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44
Q

What are the etiologies of acute pancreatitis besides gallstones and alcohol?

A 
Iatrogenic (ERCP) 
Drug-induced
Hypertriglyceridemia 
Hypercalcemia
Pancreatic cancer
Pancreas divisum (cong. ductal abnormality)
Penetrating trauma
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45
Q

Serum lipase, amylase are elevated >3x normal. Dx?

A

Acute pancreatitis

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46
Q

What disease can occur in severe acute pancreatitis?

A

ARDS

A/w pancreatic necrosis. Fully reversible - tx: support.

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47
Q

What are causes of chronic pancreatitis besides alcohol?

A

CF, hereditary pancreatitis, and hyperlipidemia

20% are idiopathic

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48
Q

What are some sx of pancreatic insufficiency?

A

Weight loss, steatorrhea (fat malabsorption)

Bleeding problems (Vit K = fat-soluble = malabsorption)

Anemia (Vit B12)

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49
Q

Autoimmune pancreatitis

A

Diffuse or focal enlargement of pancreatic parenchyma

Infiltration by IgG, plasma cells, lymphocytes

Males, typically 40-70

A/w other autoimmune diseases

May masquerade as pancreatic cancer!

Sx: abdominal pain, jaundice, weight loss, (rarely) pancreatitis

Tx: PO steroids x 6 weeks

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50
Q

“Ringed” esophagus?

A

Eosinophilic esophagitis

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51
Q

Eosinophilic esophagitis

A

Esophageal STRUCTURAL disorder

Chronic immune/antigen-mediated dis.

Sx: vomiting, pain, dyspepsia, progressing to odynophagia and stenosis

Concentric rings in the esophagus

A/w food allergies, atopic sx

Tx: 3 D’s = drugs, diet, and dilation

Drugs = topical steroids that are swallowed 
Diet = 6 food elimination diet (milk, eggs, wheat, soy, seafood, nuts)
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52
Q

Zenker’s

A

Diverticulum in the uppermost portion of the esophagus

Sx: regurgitation, halitosis, aspiration

A/w reduced UES compliance

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53
Q

Which type of esophageal cancer is more common worldwide?

A

Squamous cell carcinoma

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54
Q

Dysphagia to both solids and liquids?

A

Sx of esophageal dsfxn - MOTILITY disorder

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55
Q

Achalasia

A

Esophageal propulsive/motility disorder

IMPAIRED RELAXATION of lower esophageal sphincter + absence of normal peristalsis

Etiology: selective loss of inhibitory neurons in myenteric plexus, resulting in unopposed excitatory (cholinergic) neurons –> hypertensive non-relaxed esophageal sphincter

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56
Q

Scleroderma in GI

A

Multi-system disorder characterized by:

  • obliterative small vessel vasculitis
  • CT proliferation w/ fibrosis of multiple organs

GI manifestations in 80-90%

Principally consist of smooth muscle atrophy & gut wall fibrosis –> weak peristalsis, weak LES –> dysphagia, GERD, esophageal strictures

Predominantly MYOPATHIC process

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57
Q

Dysphagia initially with solids, progressing to liquids

A

Esophageal STRUCTURAL disorder

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58
Q

Intrinsic factor

A

Secreted by parietal cells in the stomach

Necessary for the absorption of Vitamin B12 later in ileum

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59
Q

Stomach acid facilitates absorption of which nutrients?

A

Iron, calcium, and Vitamin B12

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60
Q

H. pylori

A

Microaerophilic GNR that produces abundant urease which produces ammonia and raises the local pH

Burrows through mucus layer of the stomach, colonizes gastric mucosa

Most people will never have any sx. Can cause thickened gastric folds.

Dx’ed via urea test (labeled urea ingested; if urease is present, labeled CO2 will be produced, analyzed by breath test machine)

ANTRAL infxns tend to have high levels of acid secretion, may develop duodenal ulcers

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61
Q

Tx for H. pylori infxn?

A

TRIPLE THERAPY

1) PPI (Abs work better at low pH)
2) Amoxicillin
3) Clarithromycin

“Classic” therapy = quadruple therapy

1) PPI
2) bismuth
3) tetracycline
4) metronidazole

Per the Kyoto guidelines, H. pylori infxn should be treated whenever diagnosed

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62
Q

Ethanol gastropathy

A

Similar to early NSAID-type injury

Increases acid secretions, disrupts mucosa

PUD with high concentration, high use, etc.

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63
Q

Effects of prostaglandins in the stomach

A
  • mucus layer thickness
  • cell membrane hydrophobicity
  • bicarb secretion
  • mucosal BF
  • epithelial cell proliferation

^^^All of this things are inhibited by NSAIDs!!!!!

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64
Q

Cushing’s ulcer

A

Seen in ICU pts w/ increased ICP, CNS injury

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65
Q

Curling’s ulcer

A

Burn victims

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66
Q

How do you treat PUD?

A

PPIs tx - ulcer(s) will heal in 4-8 weeks

H. pylori test & treat

Risk factor avoidance: NSAIDs, smoking

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67
Q

What is the 2nd most common cancer & cause of death from cancer worldwide?

A

Gastric adenocarcinoma

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68
Q

Menetrier Disease

A

Rare

Hypertrophic rugal folds

Histologically: massive foveolar hyperplasia with cystic dilation

Sx: abdominal pain, weight loss, & bleeding

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69
Q

GIST

A

Gastrointestinal stromal tumors

Most common mesenchymal tumor of the stomach

Cells of origin: interstitial cells of Cajal (pacemaker cells)

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70
Q

What mutation occurs in GISTs?

A

c-kit (CD117) mutation in transmembrane receptor tyrosine kinase

Treated with surgery, imatinib (small molecule RTK inhibitor)

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71
Q

Autoimmune atrophic gastritis

A

Autoimmune attack against parietal cells, IF

Achlorhydria (lose production of acid)

Pernicious anemia (B12 low, IF absent)

Atrophy seen (loss of rugae)

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72
Q

MALT

A

Mucosa Associated Lymphoid Tumor

A/w H. pylori infection

Eradication of H. pylori can sometimes induce regression of lymphoma

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73
Q

Pathophysiology of celiac disease?

A

Gluten digested by brush borders –> exposed to α-gliadin peptide –> auto-Ab formation –> inflammation, tissue damage, villous atrophy, etc.

Host factors: Class II HLA-DQ2 or HLA-DQ8 allele. These Class II MHC are uniquely able to present immunodominant peptides derived from gliadin (one of two kinds of gluten proteins) to Th1/Th17 cells. The dominant immunopathology is a “chronic frustrated immune response” against gliadin peptides, by Th1 and Th17 cells.

Autoimmune component:
TTG2 binds to gluten, tries to take off amino group, cleave gliadin –> gets “stuck” & becomes unable to release its substrate. Then, you have a foreign molecule linked essentially covalently to a self-molecule. As you remember, this is the setup for “illicit help.”
A B cell that’s anti-TTG2 (that never normally gets helped by Tfh) takes up the complex, and presents FOREIGN gliadin peptides to Tfh (specific for gliadin on DQ2 or DQ8), which then help the B cell make antibody to TTG2 (where it bound the complex).

As far as we know, the auto-antibody is not pathogenic. Useful as a diagnostic tool.

►Because this is happening in the gut, the class of antibody is IgA.

Eventual cross-rxn with TTG3 by epitope spreading –> dermatitis herpetiformis

A/w other autoimmune diseases (Type I DM, Sjögren’s Syndrome)

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74
Q

What is the test for celiac disease?

A

IgA to TTG

Need to check IgA levels concurrently

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75
Q

What are the 3 characteristic findings of celiac disease on tissue biopsy?

A

1) villous blunting
2) increased intraepithelial lymphocytes
3) lymphoplasmacytosis of the lamina propria

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76
Q

Whipple’s Disease

A

Cause by gram positive bacilli T. whippelii

Absorbed by WBCs, sit in lymph nodes –> lymphatic obstruction –> malabsorptive diarrhea

Clinical signs: fever, joint pain, diarrhea, abdominal pain, CNS/neurologic symptoms

Tx: 1 year of abx

77
Q

What causes pseudomembranous colitis?

A

C. diff

78
Q

What are the watershed areas for ischemic colitis?

A

Superior and inferior mesenteric arteries (at corner of transverse and descending colon aka splenic flexure)

Inferior mesenteric and hypogastric arteries (at corner of descending and sigmoid colon aka rectosigmoid)

79
Q

Etiology of IBD?

A

Combination of defects:

  • host interactions with intestinal microbiota
  • intestinal epithelial dysfunction
  • aberrant mucosal immune responses
80
Q

Features of Crohn’s

A
  • mouth to anus
  • skip lesions
  • transmural inflammation
  • 35% have granulomas
  • inflammatory strictures
  • fissuring ulcers, fistulae

Malabsorption –> steatorrhea

Sx: intermittent attacks of non-bloody diarrhea, fever, MID or LOWER abdominal pain

Extraintestinal manifestations: uveitis, ankylosing spondylitis, erythema nodosum

81
Q

Features of ulcerative colitis

A
  • ALWAYS rectal involvement
  • retrograde continuous diffuse disease
  • ONLY in the colon
  • mucosal inflammation only
  • no fissures, etc.

Sx: bloody diarrhea w/ LOWER abdominal pain, cramps, tenesmus

Associations: PSC

82
Q

Diverticular disease etiology

A

Results from decreased fiber in diet –> decreased stool bulk –> elevated intraluminal pressure –> mucosal herniation through focal defects in the bowel wall

83
Q

Diverticulosis

A

Presence of diverticula

NOT inflammation

84
Q

Diverticulitis

A

Inflammation of the diverticula, usually secondary to obstruction

Complications include perforation, abscess formation, bleeds, fistulae

Sx: LLQ pain, nausea, fever
Pts are usually very sick

85
Q

Tenesmus

A

Strong urge to defecate

86
Q

Pseudopolyps are a sign of what?

A

UC

87
Q

Microscopic colitis

A

Typically older females (50-80 yo)

Autoimmune; trigger unknown

Sx: chronic secretory diarrhea
Watery, non-bloody, 4-10 stools per day, minimal nocturnal sx

88
Q

What are the subtypes of microscopic colitis?

A

1) lymphocytic colitis
Chronic inflammation with lymphocytic infiltration

2) collagenous colitis
Thickened subepithelial collagen band, lymphocytic surface injury

89
Q

How do you diagnose microscopic colitis?

A

Biopsy is definitive:

  • lymphocytic infiltration of mucosa and SM (LC)
  • thickened collagenous band (CC)

Colonoscopy is usually normal

90
Q

What are some triggers for ischemic colitis?

A

Vasospasm, dehydration, hypotension, or cardiopulmonary insult (MI, PE, etc.)

90% of pts >60 yo

91
Q

What is the presentation for ischemic colitis?

A

Abrupt onset, crampy, lower abdominal pain

Urgent need to defecate

MILD diarrhea and/or hematochezia

92
Q

Diverticular hemorrhage

A

5% of patients with diverticulosis

Usually from R colon

Painless hematochezia, often heavy, typically stops within 2-3 days

Does NOT occur with diverticulitis

93
Q

Pt presents with N/V, abdominal distention, constipation or obstipation (change in bowel habits)

A

Colonic obstruction

Dx’ed by X-ray or CT

94
Q

Tumors of the appendix

A

Carcinoid (most common)

Benign (mucinous cystadenoma or villous adenoma), malignant adenocarcinoma or lymphoma, mets

95
Q

Clinical presentation & causes of fat malabsorption

A

Clinical signs: weight loss, steatorrhea, diarrhea, vitamin deficiencies

Causes:

  • surgery (gastric bypass, small bowel resection)
  • bacterial overgrowth
  • meds
  • pancreatic insufficiency
  • liver disease
  • intestinal inflammation/villus flattening
  • ulceration
  • ischemia
  • infiltration (amyloidosis)
96
Q

Small bowel bacterial overgrowth

A

Normal bacteria =

97
Q

What are some of the extra-intestinal manifestations of celiac disease?

A
  • iron deficiency anemia
  • dermatitis herpetiformis
  • AST/ALT elevation
  • cerebellar ataxia
  • osteoporosis
  • oral aphthous ulcers
98
Q

4 different types of diarrhea, based on stool characteristics

A

1) fatty (malabsorption; maldigestion)
2) water (osmotic, secretory)
3) inflammatory/exudative (blood in the stool)
4) functional

99
Q

Osmotic vs. secretory diarrhea

A

Measure stool Na + K

Normal serum osmolality is 290 mOsm

Osm gap = 290 - 2(stool Na + K)

If difference is >50 = osmotic
If difference is

100
Q

Inflammatory vs. non-inflammatory diarrhea

A

Non-inflammatory:

  • usually large volume
  • watery
  • small bowel

Inflammatory:

  • fever, fecal WBCs and RBCs
  • usually small voume, lots of times/day, feel better afterwards
  • colon
101
Q

Organisms that cause inflammatory diarrhea

A

Campylobacter jejuni, shigella, salmonella
+/- E. coli O157:H7, C. diff

Largely in your left colon

102
Q

Organisms that cause non-inflammatory diarrhea

A

Norwalk, rotavirus

Giardia, ETEC, cholera

103
Q

Leading cause of morbidity and death with diarrhea

A

Dehydration

Thus, rehydration is the mainstay of tx

104
Q

Which organism is the leading cause of death from diarrhea in the US and worldwide?

A

Rotavirus

Disease largely in children

105
Q

Basal electrical rhythm

A

Spontaneous contractions in smooth muscle , ~12/minute

Myogenic, or muscle-derived

Without external input = depolarization events fail to reach a membrane threshold sufficient to induce a contractile response.
In the presence of ACh, the membrane threshold is exceeded and contractions occur with the frequency of the BER.

106
Q

Migrating motor complexes

A

Between meals, MMCs sweep down the stomach and small intestine & clear out any remaining undigested material and bacteria

Every 90 min

107
Q

Haustrations vs. mass movement in colon

A

Haustrations: muscles of the colon wall contract intermittently to divide the colon into functional segments (haustra)

Mass movements: huge peristaltic waves 1-3x/day

108
Q

What happens with internal & external anal sphincters when rectum is filled –> defection occurs?

A

Filling of the rectum causes relaxation of the internal anal sphincter via release of VIP and NO from intrinsic nerves. At same time, the external anal sphincter contracts - rectoanal inhibitory reflex

Defecation occurs when the external anal sphincter is voluntarily relaxed and is enhanced by an increase in intra-abdominal pressure

109
Q

Parietal cells secrete what?

A

Acid (HCl) and IF (simultaneously)

110
Q

Phases of HCl secretion

A

1) Interdigestive (basal) phase - between meals. Highest HCl production in evening and lowest in morning prior to waking

2) Cephalic phase - neural regulation
Sight/smell/swallowing of food initiates release of ACh/histamine/etc. Accounts for 30% of acid production

3) Gastric phase - entry of food into stomach
Food distends gastric mucosa –> activates a vagovagal reflex as well as local ENS reflexes. Partially digested proteins stimulate antral gastrin (G) cells, which release gastrin. 50-60% of total acid secretion

4) Intestinal phase - mostly endocrine reg
Largely inhibitory - once your gastric contents pass into duodenum, stomach doesn’t need to produce HCl anymore.

111
Q

Effect of ACh on HCl secretion

A

ACh –> ↑ Ca2+ –> activates protein kinases –> phosphorylates H+/K+-ATPase = ↑ activity

112
Q

Effect of gastrin on HCl secretion

A

↑ in Ca2+ –> ↑ activity in H+/K+-ATPase

113
Q

Effect of histamine on HCl secretion

A

Histamine –> H2 receptor –> AC –> cAMP –> ↑ activity in H+/K+-ATPase

114
Q

What type of sugars can be absorbed?

A

Only simple monomeric sugars

115
Q

What are the 4 mechanisms of protein uptake?

A

1) Sodium-dependent cotransporters that utilize the N+/K+-ATPase gradient (major route)
2) Na-independent transporter of amino acids
3) Specific carriers for small peptides (di- and tri-) linked to H+ uptake
4) Pinocytosis of small peptides by enterocytes (infants). Intestines are so leaky that peptides can just wash across the cell barrier

116
Q

How is fat absorbed?

A

Bile salts + lipase + colipase

Lipase binds to colipase –> binds to bile salts –> binds to fat

Inside the enterocytes, triglycerides are re-synthesized from monoglycerides and fatty acids. They are then packaged into lipoprotein particles called chylomicrons. End up in the lacteals (lymphatic capillaries) –> thoracic duct

Bile acids are formed by liver from cholesterol; secondarily by bacteria in gut

Bile acids + glycine/taurine = bile salts

Bile salts are reuptaken in distal ileum = enterohepatic circulation

117
Q

What does Olestra do?

A

Inhibits normal lipase function –> prevent uptake of fat

Can eat normally fatty foods, take up less… however, you get steatorrhea :)

118
Q

Sitz marker

A

24 radioopaque markers given on Day 1

Plain abdominal x-ray on Day 5
5 markers in recto-sigmoid = defecatory disorder
>5 markers scattered through colon = slow transit

119
Q

Hirschsprung’s Disease

A

Congenital absence of myenteric neurons of the distal colon

No recto-anal inhibitory reflex - no ability to relax the internal sphincter. Difficult to mount enough pressure to bypass it.

If not treated, can lead to life-threatening megacolon

120
Q

H2 receptor antagonists

A

Bind H2 receptors in basolateral membrane of parietal cells

Better at blocking nocturnal (H2 mediated) than meal-stimulated acid secretion

Rapidly absorbed - advantage in ACUTE gastritis

121
Q

Examples of H2 receptor antagonists drugs

A

Ranitidine, Cimetidine, Famotidine, Nizatidine

122
Q

Misoprostol

A

Prostaglandin analogue

PGs in gastric parietal cells inhibit cAMP formation –> ↓ H+ secretion
Also stimulate acid neutralizing HCO3− formation and cytoprotective mucus formation

Major indication: NSAID-induced ulcers
BUT, rarely used because of 4-time daily dosing and adverse effects - diarrhea and/or uterine stimulation in 30%

Contra-indicated in pregnancy

123
Q

Sucralfate

A

Mucosal protective agent

Selectively binds to necrotic ulcer tissue to form protective barrier.

Activated by acid pH

124
Q

Antacids

A

CaCO3, Mg(OH)2, Al(OH)3, NaHCO3

Rapidly raise stomach pH to 4-5 (above the optimum of pepsin)

Constipation (Ca2+ and Al3+ antacids) or diarrhea (Mg2+ antacids) is common

125
Q

Metoclopramide

A

Antagonist (-) at presynaptic dopamine receptors (D2) that inhibit the release of acetycholine –> indirectly increases agonist activity at smooth muscle M3-receptors

Pro-kinetic agent –> will produce coordinated contractions that enhance transit of luminal contents

High doses used to treat nausea/vomiting of cancer chemotherapy

BLACK BOX WARNING: somnolence, dystonic reactions, tardive dyskinesias – EXTRA-PYRAMIDAL SE!!

126
Q

Ondansetron

A

MOA: Block of serotonin (5-HT3) receptors at chemoreceptor trigger zone (CTZ in CNS), solitary tract nucleus, and on visceral afferents (GI tract)

Clinical uses: Prevention and treatment of vomiting caused by chemo tx. Also used for nausea/vomiting a/w post-op use of opioid analgesics & used by pregnant women for morning sickness

AE: associated with QT prolongation!

127
Q

Prochloroperazine

A

MOA: Blockade of dopamine receptors in chemoreceptor trigger zone

Clinical uses: treatment of N/V

128
Q

Meclizine

A

Antihistamine

Primary use for motion sickness and postoperative emesis

129
Q

Diphenhydramine (dimenhydrinate, Dramamine)

A

Antihistamine

Primary use for motion sickness and postoperative emesis

130
Q

Scopolamine

A

Anticholinergic agent

Primary use is prevention and treatment of motion sickness; some efficacy in post-operative nausea and vomiting

Most commonly administered transdermally with duration of action of 72 hours

131
Q

AEs of an H2 receptor antagonist?

A

Cimetidine - gynecomastia with chronic high doses

Cimetidine also inhibits CYP450 metabolism

Annnnd causes CNS dysfxn in elderly in high doses

132
Q

Psyllium Seed (Metamucil®)

A

Fiber/bulk-forming

Recommended first - they approximate physiological mechanism (facilitate passage and stimulate peristalsis via absorption of water and subsequent bulk expansion)

Effective in 12-24 hrs to 3 days; always take with 8 oz water/juice

133
Q

Polyethylene glycols (Golytely®, Colyte®, Miralax®)

A

High volume solutions (4 liters of Golytely® or Colyte®) widely used for bowel cleansing prior to radiologic, surgical, or endoscopic procedures. Contain sodium and potassium salts to prevent net transfer of electrolytes into lumen.

Smaller volume solutions (250-500 ml of Miralax®) now used for difficult to treat constipation; given as daily dose for treatments of less than 2 weeks duration. Prolonged, frequent, or excessive use may lead to electrolyte depletion.

134
Q

Bisacodyl (Dulcolax®)

A

Thought to act via increase in peristaltic activity by inducing low-grade inflammation (local irritation) in bowel to promote accumulation of water and electrolytes and stimulation of intestinal motility

Effective, but potentially dangerous side effects (electrolyte / fluid deficiencies, severe cramping)

135
Q

Docusate

A

Stool-wetting agent

Acts as stool-softener (facilitates admixture of aqueous and fatty substances)

Role is primarily prevention. Used in patients with cardiovascular disease / hernia / postpartum patients. Often used in combination with stimulant laxative when initiating opioid analgesic therapy.

136
Q

Loperamide

A

Anti-diarrheal drug

MOA: several different mechanisms via opioid receptors, including effects on intestinal motility (μ), intestinal secretion (δ), and absorption (μ and δ)

Has anti-secretory activity against cholera toxin. Effective against traveler’s diarrhea +/- antimicrobials

137
Q

Polycarbophil

A

Anti-diarrheal

Marked capacity to bind to free fecal water

Useful in diarrhea (absorbs 60X weight in H2O) AND constipation (prevents fecal desiccation)

138
Q

Kaolin / Pectin (Kapectolin®)

A

Adsorbent

Take after each loose bowel movement until diarrhea controlled. Can usually manage mild to moderate diarrhea (promote “formed stools” and perception of decreased fluidity, but small effect on fluid volume excreted)

139
Q

Tegaserod (Zelnorm®)

A

Treatment of IBS with CONSTIPATION in women GO

Serotonin 5-HT4 agonists - leads to release of NTs involved in peristaltic reflex, promoting gastric emptying and intestinal motility

Approved for treatment of IBS patients with predominant constipation or chronic idiopathic constipation who haven’t responded to other treatments

140
Q

Alosetron (Lotronex®)

A

Treatment of severe IBS with DIARRHEA in women

–> STOP

Serotonin 5-HT3 antagonist - block of 5-HT3 receptors on sensory and motor neurons reduces pain and inhibits colonic motility

AEs: constipation in 30%, ischemic colitis in 3/1000 pts with some deaths

141
Q

Peutz-Jeghers syndrome

A

Presents usually 10-15 yo

Mutation: LKB1/STK11

GI lesions: arborizing polyps, SI > colon > stomach; colonic adenocarcinoma

Extra-GI: mucocutaneous pigmented lesions

142
Q

Juvenile polyposis

A

Presents usually

143
Q

Hyperplastic polyps

A

Location: L colon including rectum (90%)

Increase with age, small, sessile, SERRATED

Not dysplastic, but need to be distinguished from sessile serrated polyp/adenoma, which iS pre-malignant

144
Q

What are the first & second hits on the adenoma –> cancer pathway?

A

Loss of both copies of the APC gene (tumor suppressor)

When the APC protein is absent, the destruction of β-catenin (which requires an APC complex) cannot occur. Thus, cell is under constant stimulation by the WNT pathway –> promotes cell cycle progression

145
Q

What are the 3 main molecular pathways for developing colon cancer?

A

1) Wnt/APC/β-catenin (classical adenoma-carcinoma sequence)
2) K-ras/MAP kinase/PI3 kinase signaling pathways - activating mutations
3) Microsatellite instability - defects in mismatch repair proteins

146
Q

What chromosome is the APC gene located on?

A

Chr 5

“Polyp” has 5 letters :)

147
Q

Lynch Syndrome

A

AKA Hereditary non-polyposis colorectal cancer

= develop colon cancer at earlier age than sporadically; tend to be R sided

Inherited mutation of mismatch repair gene + lose 2nd allele over time –> microsatellite instability

148
Q

Infantile hypertrophic pyloric stenosis

A

Non-bilious projectile vomiting a/w upper abdominal mass (“olive-shaped mass”)

Usually presents around 3 weeks of life

149
Q

Meckel’s Diverticulum

A

Out-pouching of the intestine

Most common malformation of the small intestine. Abnormal remnant of vitelline duct, between yolk sac and intestine.

Rule of 2’s: 2 cm from ileocecal junction, 2% of population, presents around age 2

150
Q

Omphalocele

A

1/2000 live births

Failure of intestines to return to abdomen following physiologic herniation at weeks 6-10 of development. Peritoneal and amniotic covering.

30-50% associated with other congenital abnormalities

151
Q

Gastroschisis

A

Paraumbilical abdominal wall defect (rectus muscle) - no amniotic covering, no associated malformations

152
Q

What type of intestinal atresia is most common? What is the most common co-existing condition?

A

Duodenal atresia

40% have Down Syndrome

153
Q

Neonatal necrotizing enterocolitis

A

Typically occurs as a result of prematurity

PDA is a risk factor

154
Q

What is the etiology of ground glass-appearing cells on liver biopsy?

A

Viral inclusions

= hepatitis

155
Q

Which hepatitis viruses are fecal-oral?

A

A & E

156
Q

Which hepatitis virus is the only one that is DNA?

A

B

157
Q

What is the likelihood that Hep C infection will go on to be chronic?

A

80%

158
Q

What is the major cause of chronic liver disease worldwide?

A

Hepatitis B

159
Q

What is an important method of transmission of Hepatitis B?

A

Vertical

Also leads to a higher viral load

160
Q

Hepatitis D

A

Only occurs with coinfection w/ Hep B

Potentiates effects of HBV: increased risk of fulminant hepatitis, increased activity, and faster progression to end stage liver disease

161
Q

Hepatitis E

A

Very uncommon

Higher mortality in pregnant women

162
Q

Primary Biliary Cirrhosis (PBC)

A

Immune-mediated attack of intrahepatic SMALL CALIBER bile ducts

Most commonly affects: MIDDLE-AGED WOMEN

Insidious onset: pruritis, jaundice

Test: anti-microbial antibody (AMA) - 90%

25% with liver failure at 10 years

–> this disease is a risk factor for osteoporosis

Tx: UDCA (secondary bile acid made by bacteria; improves bile acid transport, “detoxifies” bile and provides cytoprotection)

163
Q

Primary Sclerosing Cholangitis (PSC)

A

Immune-mediated obliterative fibrosis of intra/extrahepatic LARGE CALIBER bile ducts

Men > women

70% will have UC

Asymptomic w/ persistent alk phos elevation; progressive fatigue/pruritus/jaundice

Dx: chlangiography shows alternating bile duct strictures & dilations (“beads on a string”)

Histology shows “onion skin” fibrosis around the bile duct

–> this disease is a major risk factor for cholangiocarcinoma

No effective medical tx; focused on stenting bile ducts to keep them open

164
Q

What are Mallory bodies?

A

Ropey inclusions in hepatocytes due to abnormal aggregation of cytoskeletal elements

Seen in alcoholic liver disease

165
Q

Hemangioma

A

Benign neoplasm of dilated vascular spaces

Most common primary hepatic tumor (2% of pop.)

F > M

Usually small and asymptomatic. Sx can include RUQ pain, early satiety, N/V

166
Q

Focal nodular hyperplasia

A

Benign mass-like proliferation of hepatocytes

Arises due to a local vascular flow anomaly

F > M

Usually asymptomatic

Central stellate scar is characteristic on biopsy/resection

167
Q

What do hepatocytes do with bilirubin?

A

They conjugate it into a water-soluble form

Conjugated bilirubin gets transported into the biliary drainage systems —> bile ducts —> duodenum

Undergoes enterohepatic circulation - gets recycled in GI tract

Also gets excreted in feces (gives them brownish color)

168
Q

Physiologic jaundice

A

Most infants have it

Onset is in first week, but NOT in first 24 hours

Increased unconjugated (indirect) bilirubin

Generally benign, resolving in 10 days to 1 month, although some cases may require phototherapy to prevent kernicterus (toxic accumulation of unconjugated bilirubin in neonatal brain)

169
Q

Pathological infantile jaundice

A

Onset in first 24 hours or >14 days after birth

Rapid increase in total bilirubin and DIRECT bilirubin = post-hepatic cause

170
Q

Crigler-Najjar Syndrome

A

Mutation in bilirubin-UDP-glucuronosyltransferase (UDP-GT), which conjugates bilirubin

Type I (AR): no functional enzyme; require phototherapy/transplantation (markedly elevated bilirubin levels in neonates result in neurotoxicity) = severe jaundice, neurologic impairment

Type II (AD): decreased enzyme activity; less severe = lower serum bili, no neurologic impairment

171
Q

Gilbert’s Disease

A

Mutation in promoter region of gene encoding for UDP-GT resulting in reduced activity –> recurrent, stress-induced hyperbilirubinemia

You get delay in moving unconjugated bili into the liver. Pts will have mildly elevated total bilirubin levels; mostly indirect bili. Indirect bili is an antioxidant; may protect against some cancers & heart disease

Common (5-10% of Western population homozygous for condition)

172
Q

Dubin-Johnson Syndrome

A

Mutation in multi-drug resistance protein 2 (MRP2), the protein responsible for transporting conjugated bilirubin from hepatocyte into bile canaliculus –> defect in excretion of conjugated bilirubin

Variable hyperbilirubinemia, esp in setting of stress

Benign, no rx needed

173
Q

What is the treatment for biliary atresia?

A

Kasai procedure - hepatoportoenterostomy

Better prognosis if performed before day of life 60

174
Q

Hepatoblastoma

A

90% present F

NOT associated with underlying liver disease

Sx: anorexia, weight loss, N/V, pain

90% have elevated serum alpha-fetoprotein levels (useful tumor marker)

175
Q

AST & ALT

A

Important in amino acid synthesis

When elevated, sign of hepatocellular damage

176
Q

Differences between AST & ALT

A

AST:

  • located in liver, heart, muscle, blood
  • in hepatocyte, located in cytosol and mitochondria
  • when elevated alone, not necessarily sign of liver damage

ALT:

  • located in liver only
  • in cytosol
  • when elevated, sign of liver damage ONLY
177
Q

AST:ALT ratio

A

Typically 1 seen in cirrhosis

Ratio >2 suggestive of alcoholic liver disease

178
Q

Etiology of severe (>15 nml) AST and ALT elevations

A
  • Acute viral hepatitis (A-E, herpes)
  • Meds/toxins (acetaminophen)
  • Ischemic hepatitis (found down)
  • Autoimmune hepatitis
  • Wilson’s disease
  • Acute Budd-Chiari Syndrome
  • Hepatic artery ligation or thrombosis
179
Q

Alkaline phosphatase

A

Present in liver, bone, placenta, intestines

Elevated during:

  • CHOLESTASIS
  • bone disease/mets
  • pregnancy
  • bowel perforation
180
Q

5’-nucleotidase

A

Significantly elevated only in liver disease

Highest levels in cholestatic disease

181
Q

γ-glutamyltransferase (GGT)

A

Elevated after alcohol consumption and almost all types of liver disease

182
Q

How do you calculate a MELD score?

A

6.4 + 9.8 x log(INR) + 11.2 x log(Cr) + 3.8 x log (t bilirubin)

183
Q

Octreotide

A

First-line immediate tx for someone who is having a massive variceal bleed

= inhibits release of vasodilator hormones such as glucagon causing splanchnic vasoconstriction –> reduces portal HTN –> brings down rate of variceal bleeding, temporarily

184
Q

Serum-ascites albumin gradient (SAAG)

A

Serum albumin - ascites albumin

Correlates with sinusoidal pressure. The higher above 1, the greater the HVPG

If SAAG > 1.1 and ascitic fluid total protein 1.1 and ascitic fluid total protein >2.5 = heart failure

SAAG

185
Q

Criteria in dx of hepatorenal syndrome?

A
  • advanced hepatic failure and portal HTN

- Cr > 1.5 or Cr clearance

186
Q

What are the two things that are always present in hepatorenal syndrome?

A

Ascites and hyponatremia (due to water retention)

187
Q

What is the tx for spontaneous bacterial peritonitis?

A

Abx + albumin

188
Q

How does lactulose treat hepatic encephalopathy?

A

Acidifies stool, makes ammonium which can’t be absorbed

Increases flow through colon - less time to reabsorb ammonia

DEMS (4 decks)

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