Week 10-12: Gastrointestinal Tract Flashcards

Question

Barrett's esophagus: what it is and how it may progress

Answer 1

= distal squamous mucosa of esophagus is replaced by metaplastic columnar epithelium. A response to prolonged injury, columnar epithelium may be more resistance to acid. ## Footnote Barrett's esophagus is a complication of GERD that may progress to esophageal adenocarcinoma. Premalignant dysplasia does not invade lamina propria. Graded based on histologic assessment.

Answer 2

= abnormal protrusion of a segment of the stomach above the diaphragm. Can be (a) sliding or (b) paraesophageal/nonaxial Usually asymptomatic, can have reflux or heartburn.

Answer 3

= inflammation/irritation of the gastric mucosa ACUTE: sudden onset; often with erosions or ulcer. Often caused by NSAIDs, alcohol, cocaine, stress, trauma. CHRONIC: Ongoing. Often multifactorial and often combined with acute. Due to infection, autoimmunity, reactive. CHRONIC ACTIVE: persistent inflammation of the gastric mucosa related to **h pylori**. Typically affects antrum of stomach and may extend to body. Increased risk of gastric carcinoma and gastric lymphoma.

Answer 4

= acid-induced ulceration of the mucosa and wall of the stomach or duodenum often associated with h. pylori. Complications: perforation, hemorrahage, obstruction (stenosis), penetration

Answer 5

didn't find this in lecture but it is an objective so check CBL research from the week.

Answer 6

= abnormal growth of tissue projecting from a membrane in the stomach Can be neoplastic (benign or malignant) or non-neoplastic (hyperplastic or fundic gland polyp)

Answer 7

= malignant neoplasm of gastric epithelium - **adenocarcinoma** * Prevalence: more common in certain countries (i.e., Japan and less common in north america) * Appearance: intestinal-type epithelium with signet ring cells, ulcerating.

Answer 8

= a type of esophagitis characterized by numerous eosinophils within the squamous mucosa and associated with _dysphagia_ may present as difficulty swallowing, food impaction, heartburn Looks like rings in the trachea on endoscopy. Biopsy needed to confirm eosinophils. Must exclude GERD.

Answer 9

- low resting tone in lower esophageal sphincter - delayed esophageal clearance - delayed gastric emptying - increased abdominal pressure - increased acid production

Answer 10

Variable - heartburn, water brash, belching, retrosternal pain

Answer 11

Clinically - history and relief with medication (PPI) Endoscopy warranted if... * heartburn presents with alarm symptoms (bleeding, weight loss) * Persistent reflux or previous severe erosive esophagitis * History of esophageal stricture with persistent dysphagia

Answer 12

- stricture (scarring) - ulceration - bleeding - barrett's esophagus - adenocarcinoma

Answer 13

- increased inflammatory cells in the epithelial layer (eosinophils, neutrophils, excess T lymphocytes) - basal cell hyperplasia - elongation of lamina propria

Answer 14

- PPI to decrease acid production - Antacids - Diet modifications - Weight loss

Answer 15

Endoscopy: - red vevety GI type mucosa between pale squamous mucosa. Tongues extend upward from gastroesophageal junction or may be a broad band moving the who junction up. Histology: - squamous epithelium replaced by columnar epithelium or intestinal type and may see other types of glandular epithelium.

Answer 16

- anti-reflux therapy - endoscopy every 1-2 years to assess for dysplasia, carcinoma

Answer 17

Serology urea breath test stool antigen test biopsy

Answer 18

## Footnote - Water - Organic compounds (Intrinsic Factor, Pepsinogen, Lipase, Mucus) - Ions (Na+, K+, H+, Cl-, HCO3-)

Answer 19

Early * Abnormal oral glucose tolerance test (OGTT) but normal fasting glucose * Treat with diet and exercise Overt, but mild T2D * Moderate fasting hyperglycemia develops (~7 mM) * Treat with diet and exercise and add oral hypoglycemic agents (sulfonylureas), insulin-sensitizing drugs (metformin), DPP-4 inhibitors, and/or GLP-1 analogues. Advanced: * Severe fasting hyperglycemia (\>9 mM) * Insulin dependence often required

Answer 20

* Involves genetic and/or acquired defects in insulin action. Can arise as part of other syndromes (i.e., PCOS) or rare gene mutations. * Associated with obesity (especially central obesity)/BMI * Associated with inflammation in adopose tissue (macorphages produce TNFalpha)

Answer 21

* Impaired glucose-induced insulin secretion from B cells * Impaired proinsulin processing --\> manifests as hyperproinsulinemia * B cells become unable to compensate for increasing insulin resistance and produce decreasing amounts of insulin

Answer 22

1. Glucose and lipid toxicity to beta cells 2. Increased # islet macrophages that make pro-inflammatory cytokines 3. Toxic amyloid deposits build up in pancreas

Answer 23

Mature onset diabetes of the young (MODY) Neonatal diabetes mellitus

Answer 24

Mature Onset Diabetes of the Young ~2-5% of all type 2 diabetes. All associated with renes that regulate B cell mass or function

Answer 25

Rare: born with type 2 diabetes; a single gene type Formerly diagnosed as type 1 diabetes, which influences the efficacy of treatment. Now treated with sulfonylureas

Answer 26

Appears during pregnancy and disappears following birth. Pregnant women become insulin resistant and insulin secretion increases. \>50% of GDM women later develop T2D. Carries risk for the infant (increased size, dificult birth)

Answer 27

lifestyle modifications are very effective for slowing progression of diabetes. Metformin is also effective but not actually as much as lifestyle changes!

Answer 28

They are located in oxyntic glands of stomach body and they produce HCl and Intrinsic factor

Answer 29

pepsinogen (turned to pepsin by HCl) and lipase

Answer 30

somatostatin

Answer 31

Gastrin is released into the blood stream (endocrine) from G cells in the pyloric glands of the stomach. It acts on parietal cells to increase HCl secretion and on Chief Cells to increase pepsinogen secretion. It also increases contractions of the stomach.

Answer 32

* Stimulation of the stomach stimulates the tubulovesicles to fuse with the canaliculi of parietal cells to form long microvilli * H+/K+ ATPase proton pump in tubulovesicle membranes is now on microvilli surface and facilitates production of HCl * The cell received CO2 from blood, which is is taken with water by Carbonic Anhydrase to make HCO3- + H+. * H+ from this reaction is exported out of the cell into the stomach by the **H+/K+ ATPase** * Cl moves from the blood, through the cell, and to the stomach down its concentration gradient, where it combines with H+ int he stomach to make HCl

Answer 33

Pepsinogen is produced by chief cells in the stomach. Pensinogen is cleaved by acid (HCl) to its active form (i.e., pepsinogen is a zymogen), pepsin. Pepsin can also activate more pepsinogen directly - this is called autocatalysis

Answer 34

Mucus (sticky secretions containing mucin and glycoproteins) and bicarbonate

Answer 35

Protects the luminal epithelium from acid and pepsin-based hydrolysis as well as microorganisms.

Answer 36

**Mucus neck cells** of gastric glands secrete clear mucus in response to several stimuli (e.g., mechanical/vagal stimulation, ACh, PGs, bacterial toxins) **Surface epithelial cells** continuously secrete viscous mucus with high [HCO3-] via exocytosis. Mucus is held in place by the surfacephosopholipids on the luminal membrane f the cells to lubricate and protect against damage.

Answer 37

Involved in the protection of the stomach. * inhibit acid secretion * prevent exfoliation of epithelial cells * increase mucosal blood flow * stimulate mucus and bicarbonate secretion * enhance synthesis of surface-active phsopholipids that line the gastric mucosa and hold mucus in place.

Answer 38

Comes from G cells in the pyloric glands in the antrum of the stomach; Secreted in response to the peptide NT GRP (gastrin releasing peptide) from enteric neurons and in response to digested protein in the gastric lumen; Binds to CCK receptors on the basal surface of parietal cells and chief cells to activate them, thus upregulating their products.

Answer 39

HCl is produced by parietal cells, which have receptors for gastrin (CCK receptor), histamine (H2 receptor), and ACh (M3 receptor). Gastrin is released by G cells in the pyloric glands of the stomach in response to presence of digested protein or in reposnse to GRP released by enteric neurons. Histamine is released by ECL cells in response to gastrin and in response to ACh stimulation from neurons. ACh action on the parietal cells is the product of direct stimulation from neurons.

Answer 40

There is thought to be continuous background release of histamine in gastric interstitial fluid to maintain basal acid secretion. Gastrin and ACh can act both via stimulation of histamine and synergistically with histamine direclty on the parietal cell.

Answer 41

cephalic (psychic), gastric, and intestinal

Answer 42

The cephalic phase is responsibel for preparing the stimach for an incoming meal. COnscious thought, smell, and taste stimulate the hypothalamus, which activates parasympathetic outflow from the vagus nerve. This stimulated chief cells and G cells to release acid and pepsin in the stimach before food even arrives in there. _Inhibition_: Stomach filling and feelings of satiety result in sympathetic discharge.

Answer 43

Rate of secretion is maximal during the gastric phase. There are two components: ## Footnote _Non-neuronal_: Food entering the stomach increases pH, stimulating gastrin release and stimulating parietal cells directly. _Neuronal:_ Food entering the stomach causes distension, which activates a **vago-vagal reflex** via mechanoreceptors in the gastric wall. This results in stimulation of acid and pepsinogen release and indirect stimulation of gastrin release. _Inhibition_: pH drop in the antrum stimulated D cells in pyloric glands to release somatostatin, which acts locally to inhibit G cell production of gastrin.

Answer 44

Nutrients (peptones) in the duodenum stimulate G cells to secrete more gastrin, which then acts on parietal cells and chief cells in gastric glands. _Inhibition_: Passage of chyme into duodenum and its breakdown inthe jejunum stimulates the **enterogastric reflex arc**, leading to production of enterogastrones. Enterogastrones feedback to inhibit G cell, parietal cell, and chief cell activity as well as smooth uscle contraction in the stomach.

Answer 45

Somatostatin is released from D cells in the pyloric glands in response to pH drop in the antrum. It acts to inhibit the gastric phase of acid secretion by locally inhibiting G cell production of meal-stimulated gastrin.

Answer 46

Entrogastrones include secretin (stimulated my acid), SSK (stimulated by AAs and fat), GIP and GLP-1 peptides (stimulated by fat and glucose). They are all hormones produced as a response to chyme passage to duodenum ad jejunum. They act to inhibit the intestinal phase of acid secretion by feeding back to inhibit G cell, parietal cell, and chief cell activity as well as smooth muscle contraction in the stomach.

Answer 47

They inhibit the production of PGs. PGs' role int hes tomach is to inhibit acid secretion, increase mucosal flow/production, enhance synthesis of surphase phospholipids, and prevent exfoliation of epithelial cells. Inhibiting PGs inhibits this important protective mechanism for the gastric mucosa.

Answer 48

* Mechanism of damage: Inject viruluence factors into epithelial cells, causing them to release nutrients and urea to nourish the bacteria. This damage the epithelial cells and their tight junctions, resulting in inflammation. Cytokines related to inflammation stimulate G cells (++gastrin) and inhibit D cells (--somatostatin), increasing acididty and furthering injury. * Adapted to survive in the stomach: Flagellated and motile with chemotaxis toward high pH areas of stomach (mucus). Adhesive to epithelial cells. Produces a potent urease, which converts NH3 and CO2 to protect itself from gastric acid and promote further gastrin secretion.

Answer 49

Standard triple therapyy combined PPI and 2 antibiotics (clarithromycin and amoxicillin or metronidazole)

Answer 50

worsens heart burn

Answer 51

worsens heartburn

Answer 52

post-prandial, retrosternal pain of varying duration and severity. May experience water brash, sour taste, odynophagia (pain with swallowing) aggravating - supin position, caffeine and peppermint (foods that relax upper esophageal sphincter), fat and protein (foods that delay emptying) alleviating - antacids

Answer 53

peppermint, caffeine, opioids, smoking, alcohol

Answer 54

gastroesophageal reflux disease. Retrograde movement of gastric contents into the esophagus with symptoms AND/OR complications.

Answer 55

Acid damage to esophagus. A common complication of GERD. Caused by increased abdominal pressure, increased volume in stomach, or decreased esophageal clearance.

Answer 56

1. Correct underlying cause 2. Lifestyle changes (remove exacerbating factors such as smoking, alcohol, weight) 1. Medications: antacids, H2 antagonist (OTC), PPI (slower onset but more effective). Usually stopped after symptoms resolve and relief maintained with lifestyle modification. 3. Surgery: Fundoplication - wrapping stop of stomach around the esophagus (rarely performed)

Answer 57

Pain/bleeding Stricture Barrett's esophagus (progresses to adenocarcinoma)

Answer 58

* _Infection_ (HSV, CMV, candida): typically in immunosuppressed and v painful (odynophagia) * _Inflammatory (eosinophilic)_: rings form in trachea, exudate produced; can be treated with elimination diet * _Trauma (pill):_ causes painful swallowing, common in elderly (impaired esophageal clearance) * Reflux

Answer 59

"stomach ache" **Rome III definition =** one or more of... * post-prandial fullness * epigastric pain or burning * early satiety Sometimes associated with nausea, bloating, anorexia

Answer 60

* Usually no obvious cause: ulcer-like symptoms or dysmotility-like symptoms

Answer 61

Gastritis = inflammation of gastric mucosa associated with injury (h pyloria, autoimmune, alcohol) Gastropathy = epithelial cell damage and regeneration _without inflammation_ (NSAIDs, bile reflux, congestion)

Answer 62

Acute (alcohol, early h pylori) Chronic (autoimmune, late h ylori)

Answer 63

**Antral-based gastritis** - infection increases gastrin secretion, which increases parietal cell acid production, causing duodenal damage. May eventually cause metaplasia in stomach or duodenum or produce ulcers in stomach or duodenum. **Corpus-predominant atrophic gastritis or pangastritis** - caused by genetically lower acid output, predisposing the body for h pylori infection. Increased risk for ulcers, metaplasia, and gastric CA.

Answer 64

test for h pylori by investigating the presence of urease enzyme which braeks down uria into ammonia and carbon diaoxis. Pt swallows radiolabelled urea and radiolabelled CO2 is measured in breath. Diagnostic for dyspepsia.

Answer 65

damage to the mucosal lining of the intestinal surface where acid is implicated in pathogenesis. May vary from normal mucosal to erosive (damage restricted to superficial mucosa) to ulcerative (damage extends to muscularis mucosa).

Answer 66

* correct underlying cause * Lifestyle changes * Medication: PPI * Endoscopic: injection around ulcers to stop blood leak coagulation of vessels if ulcer is shallow, place clips to hold ulcer shut, embolizaation (obstruct problem blood vessel), omental patch, other surgical approaches.

Answer 67

= dysfunctional swallowing. May be progressive (i.e., cancer) or longstanding (physical difference)

Answer 68

Where is the issue? transfer (oropharyngeal vs esophageal) What is the issue? SCC \> adenomacarcinoma \> pepstic stricture

Answer 69

Easy to get, cheap Won't show mild inflammatory bowel disease

Answer 70

Easy and cheap Low sensitivity and specificity Good for testing dysphagia

Answer 71

3D information, very sensitive and specific. Expensive Exposure to ionizing radiation Best test for severe abdominal pain

Answer 72

Same as a CT abdomen, but with negative PO contrast and another IV contrast. ## Footnote Good for showing strictures, intraluminal fillinf defects. Better than plain CT if you are suspecting Crohn's disease

Answer 73

Similar to a CT but non-ionizing. Not affected by bones so it can image with high resolution close to bony structures. All are better resolution than CT. MR enterography is analogous to CT enterography with contrast added. MRCP is magnetic resonance cholangiopanreatoagraphy - excellent for viewing liver, biliary tree, and pancreas. Best first test in pelvis and pt \< 25 years old.

Answer 74

* Most sensitive and specific test for intraluminal lesions, BUT not able to detect lesions outside of the lumen * Able to diagnose, take biopsies, and perform interventions all during the same procedure, BUT it's invasive and ofter requires sedation

Answer 75

Can be done in upper or lower GIT, producing highly detailed images of internal organs. Can take biopsies and perform injections during the procedure.

Answer 76

Patient swallows to map out pressure points (i.e., achalsia stricture). Detects abnormalities earlier in disease process than imaging (more sensitive). Accurate for distinguishing between mobility disorders or esophagus (fairly specific). BUT Invasive and very expensive, plus need a specialized lab and person to perform the investigation

Answer 77

Ingestion - pills, food (stuck) Infection - CMV, HSV (candida dysphagia \> odynopagia) Inflammation - radiation, Crohn disease

Answer 78

Inflammation and epithelial damage of colon (colitis) and/or rectum (proctitis) mucosa

Answer 79

infection, inflammatory bowel disease, ischemic colitis, or other

Answer 80

Diarrhea containing red cells and white cells and debris. Requires microscopic evaluation and usually associated with inflammation of the colorectum.

Answer 81

Two seperate diseases (Crohn Disease and Ulcerative Colitis) of uncertain etiology characterized by inflammation in the GIT. May be 'indeterminant type' IBD, which means unable to differentiate between UC & CD. Etiology is poorly understood - genetic and environmental factors.

Answer 82

* Any part of GIT ('gum to bum') * Patchy distribution * Transmural inflammation with associated serositis * Granulomas * - Cobblestone appearance of mucosal surface due to linear ulceration * - Thickened walls, narrowed lumen * - Abscess * Radiology: string sign

Answer 83

Granuloma of the colon, may be Crohn Disease

Answer 84

Crohn Disease

Answer 85

* - Colon only (starts in rectum) * Continuous involvement * - Inflammation limited to mucosa * No granulomas * - Affects mucosal layer only * - Absence of goblet cells * Crypt distortions and abscesses

Answer 86

- Fistula tracts - Stenosis and obstruction - Dysplasia and carcinoma - Extraintestinal features (arthritis, eye lesions, skin lesions)

Answer 87

- Toxic megacolon (rare today) - Dysplasia and carcinoma - Extraintestinal features (arthritis, eye lesions, skin lesions)

Answer 88

Presents with chronic, water, non-bloody diarrhea. Colonoscopy is normal but mucosal biopsy is abnormal.

Answer 89

= multiple diverticula, usually on the left side of the colon that may be associated with normal function. Risk factors include lifestyle (low fibre diet, inactivity, obesity) and muscle weakness. Caused by high intraluminal pressure. Complications: Diverticulitis (infalmmation of a diverticulum - could leed to abscess), bleeding, associated colitis

Answer 90

Polyps are abnormal tissue growth projecting from a mucous membrane. **Sessile polyp** has a broad base **Pedunculated polyp** has a stalk Polyps can be neoplastic (premalignant, malignant) or non-neoplastic

Answer 91

epithelial neoplasma that have potential to progrss to carcinoma. Should be considered a premalignant neoplasm.

Answer 92

Tubular, villous, or tubulovillous

Answer 93

Malignant epithelial neoplasm of the colorectum that has invaded through the muscularis mucosae. One of the most common malignant neoplasma and a leading cause of cancer death in mean and women.

Answer 94

Genetics (FAP, Lynch) and environmental (diet)

Answer 95

The vast majority are adenocarcinomas, often preceded by non-invasive pre-malignant adenomas (a type of colon polyp). Staging by TNM * Tumor size/depth/invasion through submucosa * Lymph Node spread * Metastasis to distant sites Grading by appearance and histological differentiation/rate of growth/division.

Answer 96

Acute inflammation of the appendix usually secondary to obstruction of appendiceal lumen. obstruction of lumen --\> bacterial overgrowth --\> inflammation --\> increased pressure --\> local ischemia --\> perforation --\> peritonitis or abscess

Answer 97

Neuroendocrine (carcinoid) tumour is the most common neoplasm of the appendix. A carcinoid tumour is a neuroendocrine tumour that produces serotonin. Typically benign, but can metastasize. **Carcinoid syndrome:** symptoms such as flushing, diarrhea, and wheezing may occur if the tumour metastasizes to the liver or serotonin is released into systemic circulation.

Answer 98

The major components of the diet - sugars, proteins, and lipids. Often in polymer forms that must be broken down before they may be absorbed. The daily requirement for protein is fixed, but carb and lipid amounts may vary. Proteins: 9 of 20 AAs must be obtained from diet (i.e., are essential) Fats: 2 FAs are essential (linoleate and linolenate)

Answer 99

Micronutrients are the minor components of diet that are functionally critical. They include **vitamins** (fat and water soluble) and **minerals**. Water-soluble vitamins are essential because they are co-factors for enzyme function. Functions of fat-soluble vitamins vary. Some micronutrients may be absorbed directly, but some must be modified before they may be absorbed (i.e., B12, folate, iron).

Answer 100

* Small intestine lined by _simple columnar (absorptive) epithelium_. Little EC matrix bt cells, cells linked by cell-cell junctions. Cells form epical villi.

Answer 101

The enterocytes of the simple columnar epithelium of the intestinal mucosa are bound together by apical tight junctions and their microvilli have a glycocalyx brush border. Tight junctions present 'transepithelial resistance' that is lower is the small intestine, where small, charged ions can move down the conc grad through tight junctions between cells - **paracellular transport.** Beyond the enterocytes themselves, there is a basolateral plasma membrane, and a basement membrane before contacting the blood or lypmhatic capillary.

Answer 102

Apical tight junctions between enterocytes present 'transepithelial resistance' that is lower is the small intestine, where small, charged ions can move down the conc grad through tight junctions between cells - **paracellular transport**. On the contrary, **transcellular transport** is transport across the plasma membrane of enterocytes. Material moves through cells by diffusion, facitiated transport, active transport, or micropinocytosis/endocytosis.

Answer 103

most carbs and proteins are absorbed in the first 50% of small intestine (duodenum and jejunum) and lipids (as well as lipid soluble vitamins) are delayed because they take longer to digest.

Answer 104

Fat breakdown is initiated in the stomach (gastric hydrolysis) where fats start otbe dispersed and emulsified. Further fat hydrolyces and micelle formation takes place in the small intestine. After complete digestion/breakdown of fates, absorption is normally 98% efficient. SOme complex fats (i.e., TGs, and phospholipids) are resynthesized within enterocytes. Absorbed fats may then be packaged into chylomicrons and taken away in the lymph. Fats packaged as glycerol and some free FAs will also be taken up into portal blood.

Answer 105

Contributes to early dispersion of large fats, with preference for breaking the third Fa off of a TG. Efficient at low pH.

Answer 106

The release of free FAs, mixing and interaction with protein breakdown products, resultin gin disperion of large fat globules into small lipid droplets in the chyme.

Answer 107

Generate lipids with polar head groups that faciltiate further emulsification. Colipase helps anchor lipase to emulsification droplets once they are coated with bile salts. Very small droplets mean large SA to volume ratio

Answer 108

Form a shell around FAs and monoglycerides - a micelle - in partnership with other lipid breakdown molecules (lipase and colipase). Micelles may then move through the aqueous 'unstirred water layer' to reach the apical'luminal surface of enterocytes.

Answer 109

_Absorption of short/medium length FAs_ occurs primarily via (a) directly partitioning into microvillus membrane. But also occurs via (b) carrier mediate, facilitated diffusion with protein transporters. Does not require solubilization of the micelle as most of these lipids are on the micelle surface. _Absorption of long chain FAs, monoglycerides and cholesterol_ usually requires dissociation/breakdown of the micelle as these less soluble lipids are often buried inside. Most require binding proteins in the microvillar membranes of the enterocytes.

Answer 110

Small and medium chain FAs are released baslaterally and diffuse into capillaries that drain into the hepatic portal vein (--\> liver). Long chain FAs and monoglycerides are re-esterified with glycerol to form TGs int he enterocyte. **TGs, cholesterol, phospholipids, fat soluble vitamines are packaged by apolipoproteins in the Golgi and secreted by exocytosis as chylomicrons basolaterally.** Chylomicrons are exocytosed, pass through basement membrane and enter the **central lacteals** (discontinuous with lymphatic capillaries). They bypass th eliver and enter the bloodstream at the thoracic duct. They can then be broken down in the blood by lipoprotein lipase to free FAs, glycerol and cholesterol. Cholesterol may then travel to the liver to be incoporated into LDL. Intestinal cells can also produce and secrete cholesterol-rich, VLDL, which can pass into the blood. VLDL is a prominent route of cholesterol management when fasting.

Answer 111

1. starch - long chains of sugars (digestible) 2. dietary fibre - long chains of sugars (non-digestible) 3. Dietary disaccharaides (digestible) 4. dietary monosaccharaides (fully digested)

Answer 112

alpha amylose has alpha 1:4 bonds amylopectin has alpha 1:4 bonds and alpha 1:6 bonds

Answer 113

* amylase hydrolyzes 1:4 and 1:6 linkages, thereby initiating the breakdown of both linear and branched starch molecules. Amylase is broken down by gastric acid and then pancreatic amylase completes initial carb digestion in the duodenum. * Pancreatic amylase digestion generates di- and trisaccharaides * Enzymes in duodenal and jejunal brush border membrane fully break down dugars to monosaccharaides (galactose, glucose, fuctose) * Monosaccharaide transporters in the apical microcvillar membranes bring sugars into enterocytes and another group of tranpsorters expels them basolaterally into the interstitial fluid. SGLT1 brings in glucose/galactose paired with Na+ (Na+ expelled by Na/K ATPase to maintain gradient) and GLUT5 brings in fructose. Glucose, galactose, and fructose all expelled basolaterally by GLUT2 into the interstitial fluid where they may be transported into the blood.

Answer 114

* Stomach: Protein digestion is initiated in the stomach. Pepsinogen is cleaved to pepsin by HCl and then pepsin can perform autocatalysis on pepsinogen to further increase pepsin levels. * Duodenum: Pancreatic trypsinogen is cleaved to trypsin by enterokinase from enterocyte brush borders in the duodenum. Activated trypsin activates other pancreatic proteases and some lipases in the duodenum, which free up AAs, di- and tripeptides, and some slightly longer polypeptides. * AAs, di- and tripeptides brought across enterocytes by **direct transport** via the **peptide transporter** or **amino acid transporter**, which uses cotransport with a H+. The The H+ gradient is maintained by the **Na+/H+ exchanger.** transporters and released into the interstitial fluid for uptake into blood. * Longer polypeptides can be further hydrolyzed by brush border hydrolases. After uptake some peptides can be further hydrolyzed inta AAs intercellularly.

Answer 115

Gut-associated lymphoid tissue is important for immunity in the gut. Microfold (M)-cells are responsible for uptake of intact protein antigens.

Answer 116

Most often absorbed passibled from icelles and transported out of the cells into chylomicrons as part of the lipid transport process

Answer 117

Water soluble vitamins are transported across the intestinal epithelium by a number of mechanisms, including facilitated diffusion, active transport, endocytosis (B12/coalbumin), and deconjugation followed by faciltiated diffusion (folate)

Answer 118

Minerals are transported across the intestinal epithelium by a number of mechanisms, including active transport (Mg), facilitated diffusion (Ca), and alternate transport mechanisms based on the form of the mineral (Fe)

Answer 119

distal small intestine (ileum)

Answer 120

* coalbamin = VitB12 * COBALAMIN (CBL) is ingest bound to proteins in food. Gastric acid and pepsin release it during protein digestion. * CBL is acid sensitive, so it binds to glycoprotein **haptocorrin,** which is produced by salivary and gastric glands and acts to protect CBL. * Pancreatic proteases digest haptacorrin in the duodenum, liberating CBL * **Intrinsic Factor** is secreted by parietal cells in gastric glands. Intrinsic factor complexes with CBL in the jejunum where pH is more neutral. * The CBL/IF complex binds a receptor on the apical membrane of ileal enterocytes (free CBL will not bind), which triggers receptor-mediated endocytosis. * CBL is liberated in the lysosome, then it complexes with **transcoalbamin II** and the complex is secrete basolaterally, where it may enter the intestinal capillaries. It will be delivered to the liver by the portal venous system

Answer 121

* Calcium undergoes passive absorption both paracellularly and transcelluarly in the jejunum and ileum * Transcellular transport begins in duodenum. Ca diffuses down concentration gradient through the apical brush border via **Ca Channels** * **Calbindin** is a protein syntehsized in response to the transcriptional activation of **Vitamin D**. Calbindin complexes with Ca to buffer levels of free Ca in the cytoplasm. * Finally, Ca is actively transported against its concentration gradient acorss the basolateral membrane of duodenal enterocytes.

Answer 122

KADE these are transported in micelles passively

Answer 123

**Paracellular** - between cells, down gradient through tirght junctions. Tight junctions most receptive in small intestine. Resistance increases as you move down the large intestine. **Trancellular** - crossing the membranes. Genearlly, at least one membrane passage is active, in order to push agains the gradient.

Answer 124

Paracellular in early small intestine and transcellular for whole intestine (large and small). In the proximal small intestine, Na enters enterocytes via Glucose/Na cotransporter (SGLT1) and AA/Na cotransporter. Na leaves enterocyte by Na/K ATPase. This process is not cAMP sensitive so it isn't affected by bost enterotoxins that cause diarrhea. Na can also enter via Na/H exchangers (NHE3) in response to high pH in the lumen. In the ileum and proximal colon, Na enteres enterocytes via Na/H exchanger (NHE3) just like before, but now it's coupled with a Cl/HCO3- exchanger, therefore the process is electrocially neutral. This process is inhibited by a number of signallying cascade and therefore may be a cause of diarrhea. In the distal colon and rectum, Na enters enterocytes via facilitated diffusion through **ENaC**, coupled to the Na/K ATPase, which maintains the concentration gradient. ENaC transport is upregulated by aldosterone (increases channel opening, channel transportation, channel synthesis, and Na/K ATPase synthesis)

Answer 125

7. 5 - 12 L in duodenum and jejunum 1. 3-4.6 L in ileum and colon

Answer 126

Crypts responsible for secretion and surface responsible for absorption

Answer 127

(a) Passive, voltage-gates Cl absorption (following the movement of Na+) occurs in both the small and large intestine (transcellular). (b) It can also occur paracellularly. (c) Electroneutral exchange of Cl- and HCO3- in the ileum and colon (can occur in both the presence or absence of parallel Na/H exchange). Driven by movement of Na and a charge gradient heightened by negatively charged AAs and carbs in the lumen. This modality can be disrupted by signalling cascades and lead to diarrhea.

Answer 128

Water follows movement of Na and Cl. It is absorbed passively, driven by the osmotic gradient. It can be absorbed paracellularly (tight junctions) or transcellularly (directly, or via aquaporins or SGLT1). Assistance from aquaporins or co-transporters increases efficiency significantly. For every 1 glucose moved through SGLT1, 2 Na and 260 H20 go across, so this is the most efficient mode of H20 transport (responsible for 5 L absorption/day).

Answer 129

1) propel substances out of the crypts 2) maintain the fluidity of intraluminal contents 3) maintain osmotic equilibrium 4) dilute potentially injurious substances

Answer 130

* Duodenum * _Crypt enterocytes_ secrete HCO3 rich fluid, related to the HCO3/Cl exchange at apical membrane * _Glands_ secrete mucinous fluid (contains lysozyme, Igs) by secretory exocytosis at slow rate that increases after feeding. * Jejunum and Ileum * _Crypt enterocytes_ secrete isotonic NaCl solution, driven in part by active secretion of Cl through CFTR channel. Na follows paracellularly down the gradient and water follows them both. CFTR channels are upregulated in response to Ca2+, cAMP, cGMP, which are all hormone regulated.

Answer 131

1) hormones and paracrines produced by mucosal cells in response to luminal stimuli 2) NTs produced by enteric neurons 3) chemicals released by immune cells and fibroblasts in lamina propria 4) changes in capillary blood and lymphatic flow 5) smooth muscle contraction

Answer 132

1) decreased absorption of fluid and electrolytes 2) increased secretion of fluid and electrolytes

Answer 133

1. Inhibited ion transport (ex: e coli's enterotoxin inhibits NaCl absorption) 2. Increased osmotic pressure in lumen prohibits absorption of water (osmolar gap) (ex: production of short chain FAs and hydrogen in lactase deficiency results in diarrhea with acid pH) 3. Increased propulsive activity resulting in decreased contact time for absorption (ex: irritable bowel syndrome)

Answer 134

1. Stimulated anion secretion (ex: cholera bacterial toxins) 2. Secretion from hyperplastic crypts (ex: chronic inflammation characteristic of celiac sprue)

Answer 135

* Gluten triggers an inflammatory response * Decreased brush border hydrolases results in unabsorbed osmoles * Villus atrophy (fluid, nutrient, and electrolyte malabsorption) * Crypt hyperplasia (increased endogenous secretion) * Inflammatory cells --\> inflammation-induced hyper-secretion by crypt enterocytes * * ULTIMATE RESULT: diarrhea

Answer 136

* Cholera lives in feces and is contracted by contaminated food/water - cocurs in places lacking proper sanitation/clean water * Stream of events leading to elevation of cAMP, which inhibits neutral NaCl absorption and stimulates Cl- secretion. BUT nutrient-coupled Na absorption is not affected. * Treat by taking advantage of the fact that Na-nutrient uptake isn't affected. Administer Na/glucose solutions to replenish Na and minimize dehydration.

Answer 137

Maldigestion - defective hydrolysis of nutrients Malabsorption - defective mucosal absorption

Answer 138

In orer for iron to be absorbed, it has to be in the Fe2+ state. Most ingested iron is Fe3+ or Fe4+ and requires interaction with acid to facilitate its absorption --\> so take it with orange juice.

Answer 139

* Colon may adapt to better absorb certain nutrients * Villi can elongate and in crease in number (i.e., in small bowel resection) * Increased pancreatic enzyme production *

Answer 140

Crude assessment of weight and body type to assess malnutrition. Includes BMI (kg/m2), weight, weight, hip/waist ratio, skinfold (fat), and general muscle bulk

Answer 141

**Subjective global assessment** : includes a physical exam (subcutaneous fat, edema, muscle bulk). Identifies pts who are malnourished. **Mini-nutritional assessment:** more often used in elderly patients; includes food intake, weight loss, mobility, psycholgical, BMI or SC fat

Answer 142

Well nourished = eating well and gaining weight; may still have weight loss and muscle wasting mild/moderate malnutrition = 5-10% weight loss, compromised food intake, continued weight loss, progressive functional impairment, moderate physiological stress severe malnutrition = \>10% weight loss, poor nutrient intake, progressive functional impairement, muscle wasting.

Answer 143

Assesses carb absorption. Administer a carbohydrate (i.e., lactose) and test breath at baseline and 2 h later. Diagnose lactose intolerance.

Answer 144

identify B12 deficiency/malabsorption. 1. Give a small dose radiolabelled B12 --\> absorbed by small intestine 2. Give large dose IM non-labelled B12 --\> saturate B12 carriers 3. Measure radiolabelled B12 in urine; malabsorption if \<7-10% of oral dose is recovered 4. Confirm site of malabsorption by administering intrinsic factor, then pancreatic enzyme, then antibiotic and see if the issue resolves. (antibiotic to see if SIBO is consuming gut B12)

Answer 145

Identify pancreatic insufficiency

Answer 146

Quantitative fecal fat, fecal elastase/chymotrypsin

Answer 147

* **Classic**: abnormal histology, IgA EMA or tTG Ig positive | symptoms * **Atypical:** abnormal histology, IgA EMA or tTG Ig positive | normal and extraintestinal symptoms * **Silent:** abnormal histology, IgA EMA or tTG Ig positive | asymptomatic * **Latent**: Genetic susceptibility HLA-DQ2 or -DQ8 | lack of histological changes but current symptoms or will develop symptoms * **Refractory**: Symptomatic, severe histology, does not respond to gluten free diet for at least 6 mo

Answer 148

Gluten/gliaden exposure triggers an inflammatory response • Villus atrophy (fluid, nutrient, and electrolyte malabsorption) • Crypt hyperplasia (increased endogenous secretion) • Enterocyte disarray • Inflammatory infiltrates --\> inflammation-induced hyper-secretion by crypt enterocytes • Decreased brush border hydrolases results in unabsorbed osmoles Results in: increased osmotic load, luminal electrolytes, FA production by colon bacteria, decreased release of bile acids and pancreatic enzymes in response to meals, unabsorbed bile salts in colon  DIARRHEA

Answer 149

Serology: Anti-tTG IgA\*\*\*\*\*; OR Anti-Endomysial Ig; OR Anti-gliadin IgA, IgG Endoscopy & small bowel biopsy: marbelizatin of duodenum

Answer 150

villus atrophy, crypt hyperplasia, enterocyte disarray, inflammatory infiltrates

Answer 151

HLA DQ2 or HLA DQ8

Answer 152

Autoimmune response. Gliaden is taken into interstitium by an Ig, recognized by tTG, and presented on APCs via HLA DQ2 or HLA DQ8 (upregulated in celiac) to T cells. T cells mediate inflammation and B cells to make anti-gliaden and anti-tTG antibodies. Killer T cells come over and destroy enterocytes affected by inflammation. Summary: exposure results in **inflammation**, **heightened sensitivity (new Igs)**, and tissue destruction

Answer 153

Rome IV Criteria: recurrent abdominal pain at least 1 day/week in the last 3 months associated with 2 or more of: - related to defecation - onset associated with a change in stool frequency - onset associated with a change in form (appearance) of stool

Answer 154

* Weight loss * Onset after 50y * Family history of colorectal cancer or celiac disease * Joint pain, skin rashes * Malnourishment * Presence of a mass, obstruction * FOBT +ve (fecal blood) * Abnormal CBC, CRP, thyroid, electrolytes

Answer 155

Crohn involves the whole mucosal layer - big deep ulcers. Ulcerative colitis only involves the superficial mucosa.

Answer 156

- eyes: uveitis (more in UC) - mouth: aphthous stomatitis (more in UC) - shins: e nodosum [rash] - ankles: pyoderma [ulcer-appearing] - feet - bones: arthritis (more in UC)

Answer 157

Montreal classification considers the E(xtent) and S(everity) of disease.

Answer 158

Number and extent of lesions and inflammation viewed in monitoring endoscopy informs how aggressive treatment needs to be.

Answer 159

1. _Mild Disease_: topical treatment * Budenoside and aminosalicylates to bring down inflammation 2. _Moderate Disease_: * Biologics: infliximab * Systemic corticosteroids * Oral steroids * Azathioprine/6-MP or methotrexate 3. _Severe Disease_: * Surgery * Biologics: infliximab * Azathioprine/6-MP or methotrexate

Answer 160

Often the first pharm therapy used in crohn disease. An antiinflammatory. Good to use this instead of using corticosteroids. Available in multiple forms (pH dependent, timed release, bacterial cleavage).

Answer 161

Less than 50% of patients with CD require corticosteroid therapy. Reserve for more complicated disease courses. These drugs are effective at obtaining remission, but they have significant side effects (i.e., adrenal insufficiency, osteoporosis, more). Budenoside - a topically-acting steroid - has incrased the options for steriod use though. Can use corticosteroid to achieve remission and then maintain remission using Azathioprine.

Answer 162

Azathioprine can be used to maintain remission in CD patients who achieved remission using corticosteroids and need to be tapered off.

Answer 163

Anti-TNFs have proven effective at healing the gut. Infliximab. May cause some immunogenic-related side effects. Use in tandem with an immunosuppressant.

Answer 164

Surgery for relief of symptoms or complications of the disease. IT's an effective treatment option when medical therapy has failed or complications arise. It should be considered very carefully.

Answer 165

Start with topical --\> oral --\> steroids --\> immunosuppressants --\> biologic

Answer 166

Failure of medical therapy, cancer risk, perforation, hemorrhage, stricture

Answer 167

formation of a J pouch? more?

Answer 168

upt o 20% risk after 30 years of disease. _Risk factors_: Duration of disease, extent of disease, presence of primary sclerosing cholangitis, FHx, dysplasia, endoscopic appearance, severity of inflammation

Answer 169

C-HAND Colitis (infectious, inflammatory, ischemic) Hemorrhoids Angiodysplasia Neoplastic Diverticulsis

Answer 170

separates the rectal columnar epithelium from the anal squamous epithelium

Answer 171

Most common cause of GI bleeding in patients under 50. Usually minor and painless with hemorrhoids, but may be painful with fissures (little cuts). Pts present with fresh blood, often dripping into the toilet or streaked on their stool. Diagnosis by history, digital rectal exam, endoscopy.

Answer 172

Lifestyle: high fibre, fluid, don't strain on toilet Medications: hydrocortisone ointments, sitz bath, fissues can be treated with nitroglycerin or other mode of dilating anal canal so it can heal Surgery: rarely indicated; banding, removal, injection of botox into sphincter or sphincterotomy for fissures

Answer 173

= sac-like protrustions from colon wall. Common with older age; associated with western diet. Mostly in sigmoid colon, however R sided in Asian pts.

Answer 174

Usually large volume, painless. Usually stops spontaneously, but recurrent bleeds are common.

Answer 175

Infection of diverticulosis. Presents with pain, fevers, high WBC, **not typically bleeding.**

Answer 176

* _Resuscitation_: ABCs * _Colonoscopy_: can be challenging; requires clean bowel and active bleeding * _Angiography_: contrast injected into a major artery to find the vessel that is bleeding. Use CT scan. Only detects bleeding at rates \>0.5mL/min. Can embolize (cauterize) the bleed once it is identified. * _Surgery_: Segmental resection may be warranted if bleeding is persistent. recurrent (3+ episodes annually), or pt is unstable despite recussitation.

Answer 177

Inject with epinephrine

Answer 178

Reduction of blood flow from the mesenteric vasculature. Some areas - rectosigmoid junction & splenic flexture - are more prone to ischemia due to less collateral blood supply. If colonic infarction develops, it can lead to peritonitis, sepsis, gangrene. Present with _acute abdominal pain_ followed by diarrhea and mild rectal bleeding. Patients are often elderly and have CV risk factors. Diagnosis by labs (anemia, high serum lactate, high WBC), CT, colonoscopy

Answer 179

Supportive: most cases improve in 1-2 days Antibiotics: when ischemia is severe or has culminated in peritonitis. Gereal Surgery may then become involved. Address underlying CV risk factors

Answer 180

Organisms contaminating food and water, common in developed countries. Manifest in _acute onset_ bloody diarrhea, nausea, vomiting, fever Diagnosis: stool for infectious workup; endoscopy (rarely) Treatment: hydration, antibiotics *if diarrhea is severe*

Answer 181

Dilated, tortuous submucosal bleeds, spider-like appearance. Associated with end-stage renal disease, aortic stenosis, and advanced age. Common in the cecum and right colon. Does not typically manifest in bleeding, but if it is does, bleed is slow and occult. Treatment: endoscopy with argon plasma coagulation

Answer 182

Responsible for 10% of lower GI bleeds in patients over 50 yrs. Presents as a low grade chronic bleed. May be bright red blood if lesion is left sided or maroon stools/melena if right sided. Most commonly presents with _occult iron deficiency_. Patients may experience altered bowel habits. May lead to bowel obstruction or metastasis. _Management_: Surgery. Endoscopic treatment not ideal because tumours are highly friable (will just bleed)

Answer 183

1. ABCs: airway, breathing, circulation 2. IV setup 3. Monitory closely 4. Fluid resucitation and prepare blood for transfusion in case it is needed evaluation of cause: * History: symptoms, type of bleed, medications, liver disease, upper GI bleed * Vitals: assess level of blood loss * Assess mental status * Digital rectal exam

Answer 184

elevated blood urea to creatinine ratio (ACR) because of elevated urea.

Answer 185

Can investigate and treat at same time. But patient needs to be stable and have their bowel prepped (polyethylene glycol). Enema only cleanses left colon and refluxes blood up, making it hard to identify source. If a brisk bleed is expect, EGD can be done as well (microclips applied that are pooped out later).

Answer 186

Can diagnose bleeding throughout the GIT. Quick and no need for bowel prep. A better option for patients who are unstable or the bleed wasn't foudn on colonoscopy. Options: RBC scan, CT angiography, angiography

Answer 187

Technetium tagged RBCs or sulfur colloid injected and then repeat XR taken for up to 24 hr. Non-invasive, sensitive for bleeding 0.1mL-0.5mL/min. Disadvantage: requires active bleeding and not good at localizing source due to persitalsis. High false positive rate that leads to unnecessary surgeries.

Answer 188

Contrast enhanced CT scan. Widely available, fast, non-invasive. Sensitive - detects bleeds of 0.3-0.5mL/min. Disadvantages: IV contrast, radiation exposure, lack of therapeutic capability.

Answer 189

Performed by an interventional rediologist. For pt who can't do endoscopy or it wasn't diagnostic. Requires active bleeding of 0.5-1mL/min. Can stop bleed during the test. No need for bowel prep. May cause complications such as bowel ischemia, renal failure, rebleeding, not widely available. Need general surgery involved

Answer 190

* May be present in 15-20% of adults (only 20% present to health care) * More common in women and middle aged * Accounts for 12% of primary care visits and 25-40% of GE referrals. * Huge impact on pt due to investigations, interventions, psychosocial distress * Huge burden on health care and economy due to missed work and disbaility

Answer 191

* huge variability in presentation * constipation, pain, diarrhea * Extraintestinal manifestations: * Gynecologic: dymenorrhea, dyspareunia * Urologic: dysuria, frequent urination * MSK: fibromyalgia * Psychological: depression, anxiety, abuse (risk factor)

Answer 192

* *Motility disturbance _and_* *Visceral hypersensitivity* * **Normal perception of abnormal motility OR abnormal perception of normal motility * *dysregulation in **gut-brain axis*** : increased perception of visceral pain and altered secretomotor function * Multifactorial etiology * Microbiome imbalance * Psychological stress, smoking, diet * Genetics * Often psychological comorbities (anxiety, depression, somatization)

Answer 193

- new onset over age 50 - significant wt loss - GI bleeding - Fever - Nocturnal bowel movements

Answer 194

Normally, fibre acts to bulk stool and accelerate transit time. In IBS, fibre may be fermented into short-chain FAs and gas. Gas causes pain, bloating and flatulence. FAs result in increased osmotic load, decreased pH, changes to microbiome and possible inflammation and permeability of gut.

Answer 195

1. Dialogue 2. DIet * Regular meals, time time and eat slow, good fluid intake * Limit fats, fizzy drinks, caffeine, sugar-free sweets, fruits * Specific food avoidances when specific intolerance is identified (lactose, gluten, fructose) 3. Drugs (variable, based on symptoms)

Answer 196

Fermentable Oligosaccharaides DIsacharaides Monosaccharaides and Polyols Fermented by gut bacteria to produce gas and short chain FAs, leading to distension and diarrhea.

Answer 197

Chosen based on symptoms * _Diarrhea_ * absorbants * GI relaxants * _Constipation_ * Fibre supplements, Osmotic laxatives, GI stimulants, Pro-secretory * _Pain/Bloating_ * __Anxiolytics, antispasmodics, anti-gas, SSRIs, TCA, pro-secretory * Others... ***CBT/psychotherapy very effective but expensive***

Answer 198

Bulk Osmotic Stimulant (contact)

Answer 199

Dietary fibre through altered intake (food or supplement). Introduce indigestible, water-absorbing molecules that pull water into the gut, therbey bulking up stool. Intestinal distension leads to ENS stimulation of peristalsis. Used to treat constipation. Do not use if GI blockage is suspected - could exacerbate the problem. SE: flatulence/hypersensitivity

Answer 200

Osmotic laxatives are poorly absorbed salts and sugars that ast to retain or draw back waterinto the colon by osmosis. Increased distension leads to stimulation of peristalsis. Some (lactulose, glycerin) have additional effectiveness as stool softeners.

Answer 201

Indicated in constipation or for bowel evaculation prior to a GI examination. Contraindicated in case of known or suspected GI blockage

Answer 202

Electrolyte imbalance (salts only) bloating and/or flatulence, abdominal cramps, and/or diarrhea

Answer 203

Ex: Sennosides aka Senna MOA: Direct stimulation of myenteric plexuses in ENS resulting in smooth muscle motility and evacuation of contents. Pharmacokinetics: Minimal systemic absorption. May require enteric coating to get through stomach. Side effects: Craming and/or diarrhea; pigmentation of the colon (=melanosis coli)

Answer 204

Indications: Constipation Contraindications: Known or suspected GI blockage. Other cotnact laxatives unsafe in pregnancy.

Answer 205

Also known as emollients (i.e., glycerin, docusate). Oral and rectal formulations. MOA: Increase lubrication of feces. Mostly lubricates surface, some core penetration. Soften fecal matter to reduce effort of excretion. SE: rectal irritation Contraindications: known or suspects GI blockage

Answer 206

Selective competitive block of mu-pioid receptors (ex: methynaltrexone). Re-establish GI mobility that may have been blocked by opioid use. Indicated for pt experiencing opioid-related constipation. Administered subcutaneously. Does not readily fross BBB, so minimal effect on opioid-induced analgesia. May cause abdominal pain or cramping, diarrhea/flatulence, or nausea. Contraindicated in case of known or suspected GI blockage.

Answer 207

Try laxatives and stool softeners first, followed by peripherally-active, mu-opioid receptor antagonists if the first line treatment doesn't work.

Answer 208

Depends on severity of contition, the cause, and the pt nutritional/health status. Non-pharm therapy: diet changes and supportive management until resolution (fluid and electrolyte supplementation) Pharmacological: Antimotility agents (Loperamide)

Answer 209

A selective mu-opioid receptor agonist (antimotility agent). MOA: inhibits ENS activity, increasing colonic transport time, allowing more time for water absorption. Pharmacokinetics: Doesn't readily cross BBB, and that which does has high affinity for P-glycoprotein transporter, which swiftly effluxes the drug. Does not appear to produce tolerance with chronic use. SE: constipation Indicated for use in acute, non-infectious diarrhea, chronic diarrhea. Contraindicated if use of the drug results in worsened diarrhea

Answer 210

Pepto Bismol! Can treat diarrhea by reducing intestinal PGs, resulting in reduced smooth muscle contraction (motility) and reduced chloride secretion (decrease liquid). Also antimicrobial effects.

Answer 211

* symptomatic relief (pain, diarrhea) * nutrient supplementation * reduce inflammatory response

Answer 212

* Reduce inflammatory activity * aminosalicylates * glucocorticoids * immunosuppressants * anti-TNF alpha therapy * anti-integrin therapy treat according to severity of disease, responsiveness to each line of treatment and induction or maintenance of remission.

Answer 213

An aminosalicylate: Anti-inflammatory – NSAID-like inhibition of PGs, interference with cytokine production, reduced leukocyte activity

Answer 214

All glucocorticoids should be avoided in pt with peptic ulcer disease, heart disease, HTN with heart failure, or osteoporosis

Answer 215

ENaC in the distal colon and rectum

Week 10-12: Gastrointestinal Tract Flashcards

(245 cards)