Unit I, week 1 Flashcards

Question

How does detection of food in the duodenum effect rate of emptying?

Answer 1

Detection of food in duodenum → reflex inhibition of gastric peristalsis and increase in pyloric tone

Answer 2

Cholecystokinin: secreted by enteric endocrine cells in response to arrival of fats in duodenum → inhibit gastric motility

Answer 3

Centrally regulated by vomiting center in brain Steps involved: 1) Salivation (HCO3-) and sensation of nausea 2) Reverse peristalsis from upper small intestine to stomach 3) Abdominal muscles contract and UES and LES relax 4) Gastric contents are ejected

Answer 4

sweep down gastric antrum and along small intestines between meals (every 90 minutes) Housekeeping role = remove bacteria and indigestible material Peristaltic wave begins in stomach → ileocecal sphincter → repeat Wave initiated by motilin hormone released from small intestine Eating terminates MMC DO NOT HAPPEN IN LARGE INTESTINE

Answer 5

Phase I: quiescence, occurs 40-60% of 90 min duration Phase II: motility increases but contractions are irregular - Fails to propel luminal content - Lasts 20-30% of MMC duration Phase III: 5-10 minutes of intense contractions -From body off stomach to pylorus to duodenum to ileocecal valve - (pylorus fully opens)

Answer 6

Segmentation: chyme mixed with digestive enzymes and continually exposes surface to new contents for absorption Peristalsis: propels chyme 1 cm/min

Answer 7

stomach activity stimulates movement of chyme through the ileocecal sphincter

Answer 8

normally closed (to prevent reflux of bacteria from colon into ileum) Opened by distention of end of ileum (local reflex) Closed by distension of proximal colon (local reflex)

Answer 9

food in stomach stimulates mass movement in colon

Answer 10

Distension in ileum → relaxation of ileocecal sphincter → contents pass into cecum of large intestine

Answer 11

Haustration | Mass movement

Answer 12

muscles of colon wall contracted intermittently to divide colon into functional segments known as haustra

Answer 13

giant migrating contraction 1-3X/day does forward propulsion Intense and prolonged peristaltic contraction that strips an area of large intestine clear of contents Segmental activity temporarily ceases, loss of haustration

Answer 14

1) Mass movements push feces into rectum which is usually empty * *Gastrocolic reflex stimulates this 2) Feces enter rectum → distension of rectum → stimulate defecation reflex * *Spinal mediated via pelvic nerves - Reflex relaxation of internal anal sphincter and voluntary relaxation of external anal sphincter → defecation

Answer 15

HCl Kills bacteria (disinfects food at pH 1.0) Begins protein digestion - denatures proteins and activates pepsinogen → pepsin Acid producing parietal cells also secrete IF when secreting acid

Answer 16

mucus layer and alkaline (HCO3-) layer at cell surface (surface mucus cells) protects stomach lining Prostaglandins can increase mucus production Tight junctions between cells prevent acid from infiltrating layers of wall Rapid turnover maintains surface integrity

Answer 17

1) Basal interdigestive phase 2) Cephalic phase 3) Gastric phase 4) Intestinal phase

Answer 18

follows circadian rhythm Rate of acid secretion lowest in morning before awakening, highest in evening

Answer 19

initiated by smell, sight, taste, and swallowing of food Mediated by vagus nerve Accounts for 30% of total acid secretion

Answer 20

stimulated by entry of food into stomach Food distends gastric mucosa → activate vagovagal reflex and local ENS reflex Partially digested proteins stimulate antral gastrin G-cell→release gastrin Responsible for 50-60% of total acid secretion

Answer 21

presence of amino acid and partially digested peptides in proximal portion of small intestine stimulates acid secretion Stimulate duodenal gastrin G-cells → secrete gastrin Accounts for 5-10% of total acid secretion

Answer 22

1) ACh release 2) Histamine release from ECL cells 3) Release of gastrin-releasing peptide from vagal enteric neurons 4) Inhibition of somatostatin release from delta cells in stomach

Answer 23

secrete HCl and Intrinsic Factor into stomach Stimulation of parietal cells causes them to significantly increase their secreting surface area → prodigious HCl output → Luminal pH of 2 Have lots of mitochondria: use lots of ATP to pump H+ against big gradient

Answer 24

acid secretion stimulated by ACh, Gastrin hormone, and pancreas substance histamine → increase in Ca2+ and cAMP in cell → activation of distinct protein kinases that phosphorylate and increase activity of H+/K+ ATPase

Answer 25

from vagus nerve stimulation, binds muscarinic receptors on basolateral membrane → activate G-protein → increase [Ca2+] in cell --> increase activity of H+/K+ ATPase in parietal cells

Answer 26

bind gastrin receptors, also increases intracellular Ca2+ --> increase activity of H+/K+ ATPase in parietal cells

Answer 27

binds H2 receptors → activate G-protein → turn on AC → increase cAMP in cell --> increase activity of H+/K+ ATPase in parietal cells

Answer 28

ACh, gastrin, and histamine directly stimulate parietal cell, triggering secretion of H+ into lumen

Answer 29

ACh and gastrin stimulate histamine release from enterochromaffin-like cells (ECL) → histamine acts on parietal cell

Answer 30

H+ transported across apical membrane via H+/K+ ATPase Primary active transport Also drives Cl- and H2O movement into cell

Answer 31

HCO3- transported across basolateral membrane in exchange for Cl- via Cl-/HCO3- anion exchanger Downhill movement of HCO3- drives Cl- into cell against gradient When H+ transported out of cell → increase [HCO3-] in cell via CARBONIC ANHYDRASE activity Secondary active transport

Answer 32

Cl- accumulation in cell due to Cl-/HCO3- exchanger, transported across apical membrane by Cl- facilitated diffusion = passive transport, CFTR channel Cholera toxin → constitutively activate this channel

Answer 33

H2O follow HCl from blood into lumen via transcellular pathway

Answer 34

high pH of venous blood leaving stomach due to HCO3- transport

Answer 35

Epithelial cells, mucous, and bicarbonate provide barrier to dissipation of massive pH gradient and harmful effect of acid Mucous secreted by Goblet Cells and Mucous Neck Cells of the gland - Mucous forms an unstirred gel layer in which H2O is trapped - Serves as neutralization zone, so acid is neutralized

Answer 36

Only simple monomeric sugars can be absorbed! Amylase is the major enzyme in saliva and pancreatic secretions Other dietary sugars like sucrose and lactose can be digested at the surface of enterocyte Plant starch amylopectin is largest single source of carbs in our diet

Answer 37

Venule → other nutrients (not fat) enter venule and portal vein Central lymphatic lacteal vessel → products of fat digestion enter lacteal and blood stream at thoracic duct

Answer 38

First secreted as inactive precursors (zymogens, proenzymes) → Prevent enzymes from digesting pancreatic membranes and each other before they are needed

Answer 39

In stomach: pepsinogen (proenzyme) → pepsin by stomach acid In duodenum: trypsinogen → trypsin by brush border (microvillar) enzyme called enteropeptidase/enterokinase *Trypsin → more active trypsin produced from trypsinogen and converts all other zymogens to active enzymes

Answer 40

catalyzes hydrolysis of internal a-1,4 linkages, converts amylose and amylopectin → maltose, maltotriose, and a-limit dextrin Free glucose is NEVER the product of amylase digestion Cellulose = B-1,4 linked polymer → cannot be digested = “fiber”

Answer 41

last stage of small intestinal digestion of branch points of starch to glucose, breaks 1,6 linkages Convert a-limit dextran → glucose

Answer 42

inal step in small intestinal digestion of linear forms of starch to glucose Convert maltotriose → glucose

Answer 43

converts sucrose → glucose and fructose

Answer 44

converts trehalose → glucose

Answer 45

lactose intolerance due to deficiency of lactase enzyme that converts lactose to glucose and galactose Absence of brush border enzyme lactase Unabsorbed lactose draws water into intestinal lumen → osmotic diarrhea Gut bacteria flora metabolize unabsorbed lactose → gases

Answer 46

intestinal sugar transportes transport monosaccharides (glucose, galactose, and fructose) from intestinal lumen to blood

Answer 47

brush border/apical membrane of enterocytes, transports glucose and galactose with Na+ from lumen → cytosol Requires sodium as a co-transporter

Answer 48

glucose-galactose malabsorption → diarrhea upon sugar ingestion due to reduced small intestine Na+ fluid absorption and fluid secretion secondary to osmotic effect of non-absorbed monosaccharide Potentially fatal

Answer 49

apical transporter, transports fructose from lumen into cytosol

Answer 50

basolateral and transports all three monosaccharides from cytosol to blood

Answer 51

begins in stomach - Pepsin breaks down 15% of proteins to small peptides ends in small intestine

Answer 52

pancreatic proteases like trypsin, chymotrypsin, carboxypeptidase and elastase break down proteins to oligopeptides di/tri peptides and amino acids

Answer 53

Endopeptidases: secreted, hydrolyze interior peptide bonds Exopeptidases: secreted, hydrolyze one AA at a time from carboxy (C)-terminus of proteins and peptides

Answer 54

Trypsin Chymotrypsin Elastase *all secreted as zymogens

Answer 55

Carboxypeptidases A and B (secreted as zymogen, Pro-Carboxypeptidase A and B)

Answer 56

peptidases break down oligopeptides into amino acids, dipeptides, and tripeptides 1) Aminopeptidase 2) Dipeptidyl aminopeptidase 3) Dipeptidase

Answer 57

peptidases in enterocyte can break down di/tri peptides into amino acids

Answer 58

1) Activation of trypsinogen→ trypsin by brush border enterokinase 2) Activation of all other precursors by trypsin 3) Trypsin, chymotrypsin, elastase, carboxypeptidase A and B, all hydrolyze protein to amino acids and di-, tri-, and oligopeptides 4) Brush border proteases hydrolyze oligopeptides to amino acids 5) Pancreatic proteases digest themselves and each other

Answer 59

1) Na+-dependent cotransport 2) Sodium independent transporters of amino acids 3) Specific carriers for small peptides (di/tri) linked to H+ uptake (cotransporter) 4) Pinocytosis of small peptides by enterocytes (infants)

Answer 60

di and tripeptides are absorbed intact Cotransporters utilize the N+/K+ ATPase gradient are major route for different classes of amino acids, water follows Broken down into AAs by cytoplasmic peptidases in the enterocyte AAs exit basolateral membrane of enterocyte by facilitated diffusion and enter blood capillaries

Answer 61

Primary bile acids are produced in the liver from cholesterol Secondary bile acids are formed by bacteria in the intestine and colon Bile acids are complexed with glycine or taurine to make bile salts Bile is recycled during a meal by uptake in distal ileum = enterohepatic circulation

Answer 62

Converts triglyceride (unabsorbable) into a 2-monoglyceride and two free fatty acids (absorbable) Fat droplets emulsified by bile salts and lecithin to form 1 um particles → increase surface area for digestion by lipase and colipase

Answer 63

protein that anchors lipase to surface of droplets

Answer 64

products of lipase digestion (2’-monoglycerides and fatty acids) are solubilized in bile-salt micelles Cylindrical structure, hydrophilic groups pointing out, hydrophobic part inward Required to transport products of fat digestion through “unstirred” water layer near surface of enterocytes

Answer 65

1) products of lipase digestion (2' monoglycerides and fatty acids) solubilized in bile salt micelles 2) Bile salt micelles allow transport through "unstirred water" 3) When lipids strike cell surface → diffuse passively into enterocyte 4) → packaged into chylomicrons (triglycerides, phospholipids, cholesterol, apolipoproteins) 5) → incorporated into secretory vesicles in golgi 6) → vesicles migrate to basolateral membrane and released into interstitial space by exocytosis 7) → enter lacteals (too large for capillaries)

Answer 66

(A, D, E, K): absorbed same as fat and cholesterol

Answer 67

excessive loss of fat in stool as well as lipid soluble vitamins

Answer 68

B vitamins, C vitamins, Niacin, Folic acid, Pantothenic acid, and Biotin Absorbed by cotransport with Na+ or by passive diffusion Absorption complete in upper small intestine except for B12

Answer 69

B12 absorption in distal ileum in complex with IF Dietary proteins contain B12 (cobalamin) - important for RBC production 1) B12 binds salivary R protein in stomach 2) Pancreatic proteases remove R protein in duodenum 3) IF from stomach then binds B12 in duodenum 4) IF/B12 complex binds specific B12-IF receptor in terminal ileum enterocyte membrane Impairment of B12 absorption → pernicious anemia

Answer 70

absorption of sugars and amino acids in cotransport with Na+ causes Cl- to follow, and H2O to follow for osmotic reasons = PARACELLULAR pathway Osmotic gradient due to solute deposition in confined regions between cells → driving force for H2O absorption

Answer 71

Crypts = net fluid secretion from cells | Villi: net fluid absorption, vill surface area > crypt surface area

Answer 72

most nutrients already absorbed → continues to absorb H2O Cl- absorbed by TRANSCELLULAR pathway involving Cl-/HCO3- exchange in apical membrane and facilitated diffusion across basolateral membrane

Answer 73

Na absorption via apical Na+ channels (epithelial sodium channel, ENaC) Aldosterone promotes ENaC water reabsorption and K+ secretion

Answer 74

passive process Paracellular movement in jejunum (due to low [K+] in intercellular space from Na+/K+ ATPase) but transcellular in colon In severe diarrhea, when fluid loss is substantial, can cause hypokalemia -Give K+ with oral rehydration fluids

Answer 75

Ca2+ and Mg2+ compete for uptake by cells - ONE OR THE OTHER Ca2+ enters enterocyte passively down its electrochemical gradient in proximal intestines Uptake of Ca2+ in intracellular calcium stores maintains the gradient Ca2+ ATPase pumps calcium out to the blood

Answer 76

- synthesized in skin, or absorbed by intestine - 25-hydroxylated in liver - 25-OH VitD is 1-hydroxylated in kidney in presence of PTH - VitD binds to cytoplasmic receptor, activating transcription/translation **VitD stimulates uptake if Ca2+ by increasing Ca2+ binding proteins and Ca2+ ATPase molecules

Answer 77

regulated absorption in proximal intestines Transported across apical membranes as either heme or Fe2+ (Receptor mediated) Two possible fates: 1) Binds apoferritin → ferritin stays in cell and is lost when cell dies 2) Binds transferrin (carrier protein) → leaves cell and goes into blood

Answer 78

caused by impaired digestion or defects in absorption Causes: Lactase deficiency, ileal resection (bile salts not absorbed), Celiac disease (gluten sensitivity with gliadin-induced destruction of villi)

Answer 79

may be caused by vibrio cholerae Increases cAMP levels in cells and activates CFTR chloride channel → water into lumen

Answer 80

Loperamide will have NO impact on someone who has cholera induced diarrhea

Answer 81

antibiotics plus KHCO3 to prevent hypokalemia and metabolic acidosis, glucose or amino acids with NaCl to facilitate the absorption of electrolytes and water

Answer 82

Teeth + lips → biting and grinding Mastication, saliva → conversion of bite into small, soft, lubricated bolus Tongue → push bolus into pharynx Pharynx → move bolus from mouth to upper esophagus

Answer 83

Transport: conduit for food and water from oropharynx to stomach Barrier: protection of mediastinum and lungs from ingested food/water 1-way system → prevent reflux of gastric contents into pharynx or airway

Answer 84

Symptoms: **dysphagia to BOTH solids/liquids chest pain DX: Exclude structural lesion (upper endoscopy, barium esophagram) Esophageal manometry

Answer 85

luminal narrowing/obstruction Symptoms: Dysphagia to solids → liquids much later, Weight loss, heartburn

Answer 86

1) Achalasia: abnormal peristalsis, failure of LES relaxation 2) Spastic disorders of esophagus 3) Scleroderma (weak peristalsis)

Answer 87

1) Esophageal strictures 2) Extrinsic compression 3) Eosinophilic Esophagitis (EoE) 4) Esophageal rings

Answer 88

pathologic reflux of gastric juice (acid) into esophagus due to reduced LES tone Acid in esophagus or airway → symptoms and/or esophageal damage Esophagus lacks defenses (mucous secretion, alkalinity) against acid

Answer 89

Inappropriate LES relaxation **hiatal hernia Risk factors: alcohol, tobacco, pregnancy, obesity, fat-rich diet Rare: Zollinger-Ellison, Sjogren’s, Scleroderma

Answer 90

* *Heartburn: burning sensation, substernal or epigastric, rises in chest - May be positional (lying down) - Often postprandial (After meals) **Regurgitation with acidic taste Cough, throat clearing, hoarseness Damage to enamel of teeth

Answer 91

antacids, anti-secretory medications (PPI)

Answer 92

Barrett’s esophagus, ulceration with stricture

Answer 93

usually by symptoms response to acid suppressive therapy (PPIs) Endoscopy: usually for refractory symptoms **Vast majority normal -Ambulatory pH testing Transnasal catheter or wireless capsule

Answer 94

cardinal motility disorder of esophagus

Answer 95

damage to myenteric plexus ganglion cells (between inner circular and outer longitudinal muscle of the muscularis propria layer) 1) Idiopathic - affects both genders, all races, adults - VAST MAJORITY 2) Pseudoachalasia (secondary achalasia) - Direct mechanical obstruction of LES - Infiltrative submucosal invasion - Paraneoplastic → ab to myenteric plexus * *Chagas disease

Answer 96

1) Impaired relaxation of lower esophageal sphincter - Due to selective loss of inhibitory neurons in myenteric plexus → unopposed excitatory (ACh) neurons → hypertensive, non relaxed esophageal sphincter 2) Absence of normal peristalsis in distal esophagus

Answer 97

**Dysphagia to solids AND liquids ``` Weight loss Regurgitation Chest pain Difficulty belching Heartburn Hiccups ```

Answer 98

Esophageal manometry Barium swallow study ("bird beak sign" due to buildup and distention of esophagus)

Answer 99

Medical therapy: 1) Nitrates (stimulate intracellular Ca2+ → SMC relaxation) 2) Ca2+ channel blockers 3) Sildenafil Endoscopic therapy: 1) GE junction botulinum toxin injections → inhibit ACh release from nerve endings 2) Pneumatic balloon dilation → tear LES muscle fibers 3) POEM: Per-Oral Endoscopic myotomy Surgical: Surgical Myotomy

Answer 100

metaplasia of lower esophageal mucosa from stratified squamous epithelium → nonciliated columnar epithelium with goblet cells

Answer 101

Consequence of GERD, response of lower esophageal stem cells to acidic stress Significant risk of developing dysplasia to esophageal adenocarcinoma Endoscopy with biopsies every 3-5 years to assess for dysplasia Dysplasia → much greater risk for esophageal cancer development

Answer 102

Esophagectomy Endoscopic treatment for HGD and early esophageal adenocarcinomas - Ablation of Barrett’s tissue - Endoscopic resection of lesions

Answer 103

malignant proliferation of glands in LOWER ⅓ of esophagus Risk factors: old age, smoking, obesity, GERD, BARRETT’S ESOPHAGUS, radiation exposure -More common in men Rising incidence in US and Europe - most common type in West

Answer 104

squamous cell epithelial malignancy in UPPER or MIDDLE third of esophagus Risk factors = IRRITATION: - Old age, alcohol/tobacco use, hot tea, achalasia (rotting food in esophagus), esophageal web (traps rotting food), esophageal injury (e.g. lye ingestion) - More common in men and african americans Declining incidence in US/Europe, more common worldwide

Answer 105

weight loss, hemoptysis, chest pain, anemia Progressive dysphagia to solids → liquids Does not cause sx until advanced

Answer 106

benign or malignant Cardinal symptom = dysphagia to solids -Painless, symptoms on regular/daily basis, progressive, weight loss

Answer 107

GERD, radiation, caustic ingestion, congenital *Rule out cancer with biopsy during EGD Malignant: squamous cell carcinoma, adenocarcinoma

Answer 108

Chronic immune/antigen mediated esophageal disease Diagnosis: - Symptoms of esophageal dysfunction and dysphagia - Vomiting, pain, dyspepsia, progressing to odynophagia and stenosis - Eosinophilic infiltrate in esophagus - Absence of other potential causes of esophageal eosinophilia - Can cause esophageal strictures → ringed appearance

Answer 109

Most common less than 40 years of age White males classic Commonly associated with other allergic diseases (asthma, atopic dermatitis, seasonal allergies, food allergies)

Answer 110

3 D’s Drugs: steroids (topical >>> systemic), swallowed topical steroids Diet: elemental diet (allergen-free) Dilation

Answer 111

History, physical exam = MOST helpful Barium swallow

Answer 112

xray video of mouth and throat under direct observation while patient chews and swallows various consistencies of radio-opaque barium

Answer 113

inflammation and injury to esophageal mucosa 1) Chemical injury: - Reflux of gastric contents** most common - Acids, alkalis, alcohol, tobacco 2) Medications 3) Infection: - Fungal (Candida) → white plaques - Viral (HSV, CMV, adenovirus) → punched out ulcers, viral inclusions 4) Immune related: - Eosinophilic esophagitis - Dermatologic diseases (lichen planus) 5) Radiation, trauma 6) Graft-versus-host disease

Answer 114

Clinical features: heartburn and regurgitation If left untreated → severe ulcerations, strictures, Barrett’s esophagus, and adenocarcinoma may develop

Answer 115

``` transient LES relaxation decreased LES tone hiatal hernia increased intraabdominal pressure delayed gastric emptying ```

Answer 116

GERD-Barrett Esophagus (metaplasia)-Dysplasia-Esophageal Adenocarcinoma

Answer 117

outpouching of pharyngeal mucosa through an acquired defect in muscular wall (false diverticulum) Uppermost esophagus, above esophageal sphincter Regurgitation, halitosis, and aspiration Associated with reduced UES compliance

Answer 118

protrusion of esophageal mucosa Often in UPPER esophagus Presents with dysphagia for poorly chewed food Increased risk for esophageal squamous cell carcinoma

Answer 119

Dilated submucosal veins in LOWER esophagus Due to PORTAL HTN and shunting of blood from portal to system venous system Left gastric vein backs up into esophageal vein Presentation: PAINLESS hematemesis Associated with cirrhosis - most common cause of death in cirrhosis

Answer 120

Longitudinal laceration of mucosa at gastroesophageal junction Caused by vomiting usually due to alcoholism of bulimia Presents with PAINFUL hematemesis

Answer 121

congenital defect resulting in a connection between the esophagus and trachea Most common variant = proximal esophageal atresia with distal esophagus arising from trachea Presents with vomiting, polyhydramnios (baby can’t swallow amniotic fluid), abdominal distension (breathing into stomach), and aspiration

Answer 122

Anomaly demonstrates significant narrowing of mid-esophagus → Esophageal web/rings, muscular hypertrophy, inflammation

Answer 123

Gastric pits contain mucous cells that secrete mucus and small amount of pepsinogen

Answer 124

Contain gastric pits with OXYNTIC glands = mucous cells, parietal cells, chief cells, endocrine cells, and enterochromaffin cells

Answer 125

Contains PYLORIC glands = mucous cells, endocrine cells, G cells (produce gastrin), and D cells (produce somatostatin)

Answer 126

1) Receptive relaxation 2) Digestion/mixing 3) Slow release of chyme into duodenum 4) Parietal cells secrete HCl to disinfect food, and IF for B12 absorption

Answer 127

Liquids rapidly emptied from proximal stomach to duodenum Solids initially stored in proximal stomach and then move to antrum - -> Vagally mediated segmented contractions originating in mid-body of greater curve mix food - -> When food particles 1 mm or less, it empties into pylorus Inhibitory mechanisms in small intestine prevent it from being overwhelmed by rapid entry of nutrients from stomach -CCK, secretin, GIP, pH receptors, osmoreceptors, etc. in duodenum reflexively inhibit gastric emptying

Answer 128

Prostaglandin E2 and Prostacyclin → stimulate bicarb secretion, mucus, and mucosal blood flow

Answer 129

most common cause of gastritis, typically in ANTRUM - adult prevalence of H. pylori correlates with crowded living conditions and socioeconomic status during childhood - Transmission occurs person-to-person, especially among children - fecal-oral and environmental spread

Answer 130

gram-negative spiral produces abundant urease which produces ammonia and raises local pH → escape acidic gastric juice and burrow through mucus layer to colonize surface epithelium of gastric mucosa Elicits robust inflammatory response → active/chronic gastritis

Answer 131

1) Flagella to maneuver through gastric mucous 2) Adhesion molecules bind to gastric foveolar cells 3) Acid resistance with urease 4) CagA protein: decreased cell adhesion-associated with both gastric and duodenal ulcers and cancer 5) VacA: exotoxin → pores in membrane 6) Minimization and evasion of immune response

Answer 132

Mucosal biopsies indicate presence of urease (CLO) - use pH sensitive test medium Shows infiltration of gastric mucosa with neutrophils (active gastritis) or lymphocytes (chronic gastritis)

Answer 133

1) Mucosal biopsy 2) Culture (least sensitive) 3) Blood antibody test 4) Urea breath test 5) Stool antigen test

Answer 134

H. pylori produces circulating antibody that can be detected on ELISA - BUT can’t be used acutely to determine effect of abx

Answer 135

urea radiolabeled ingested with liquid meal, if urease present, can be detected by analysis of expired breath Virtually 100% PPV and 95% NPV PPI can result in false negative test

Answer 136

similar performance characteristics of UBT, most commonly used test in outpatient setting to confirm eradication

Answer 137

Asymptomatic Gastritis Peptic ulcer disease - both duodenal and gastric ulcers Neoplasia (gastric cancer, lymphoma)

Answer 138

course for 7-14 days Triple therapy: Proton pump inhibitor + Amoxicillin + Clarithromycin Quadruple therapy = PPI + bismuth + tetracycline + metronidazole Confirm eradication (stool antigen)

Answer 139

Gastritis, gastritic and duodenal ulcers, gastric adenocarcinoma, gastric lymphoma

Answer 140

- infiltration of gastric wall with eosinophils - Allergic disease (e.g. cow’s milk) and parasitic infection Symptoms: delayed gastric emptying, associated peripheral eosinophilia TX: corticosteroids, surgery

Answer 141

Associated with Crohn’s, sarcoidosis, and infection

Answer 142

**CD4+ T cells against parietal cells Anti-parietal cell and anti-Intrinsic Factor antibodies +/- pernicious anemia Most common in scandinavian / N. Euro descent Can develop intestinal metaplasia → higher risk of gastric cancer Histology: lymphocyte and plasma cell infiltrate in the body of stomach and glandular atrophy

Answer 143

gastroduodenal injury with little or no inflammation associated with lesion

Answer 144

Gastropathy Cause: prostaglandin depletion Increased risk: elderly, prior ulcer disease Treatment: PPIs - healing usually occurs even if NSAID is continued

Answer 145

Ulceration = > 5mm in diameter, depth breaches muscularis mucosa - Often gastric ulcers but can also be in duodenum - Increased risk for GI bleed Erosion = not below mucosa

Answer 146

lesion similar to NSAID induced lesions, can occasionally cause serious bleeding, but rare

Answer 147

hemorrhages and erosions of stomach and duodenum in patients under “physiologic stress” Morphologically resembles acute gastritis Patients with CNS injury, prolonged mechanical ventilation, coagulopathy, and burns - NOT pts in coronary care units

Answer 148

Trauma, shock, sepsis → stress ulcers Burns → Curling's ulcers -Due to hypovolemia and decreased blood supply Intracranial disease → Cushing ulcers -Increased ICP → increased vagal stimulation → increase ACh → increased acid production by parietal cell

Answer 149

most patients not acid hypersecreters but due to mucosal ischemia/vasoconstriction

Answer 150

acid mediated ulceration of distal stomach or proximal duodenum

Answer 151

gastroduodenal mucosal defenses unable to protect epithelium from corrosive effects of acid and proteases (pepsin) Primarily disease of failed mucosal integrity, NOT excess acid/pepsin secretion

Answer 152

gastric ulcer: H pylori infection, NSAID use duodenal ulcer: H. pylori and ZE syndrome

Answer 153

Asymptomatic, or burning epigastric pain relieved by food or antacids, may awaken patient from sleep “Nocturnal pain relieved with antacids” = most specific sxs

Answer 154

Bleeding (15%) Perforations/Penetration (5%) → acute development of peritonitis Obstruction (2%) → nausea, vomiting, early satiety Due to repeated ulceration and formation of scar tissue

Answer 155

PPI and H.pylori eradication are cornerstones of therapy Severe acute bleeds → PPI drips used in ICU to tightly control pH

Answer 156

1) Acanthosis nigricans 2) Leser-Trelat sign (seborrheic keratoses) 3) Spread to left supraclavicular node (Virchow's node) Distant mets: 4) Sister Mary Joseph nodule: periumbilical region (intestinal type) 5) Bilateral ovary mets = Krukenberg tumor (diffuse type)

Answer 157

1) diffuse type | 2) intestinal type

Answer 158

signet ring cells, diffusely infiltrate gastric wall Can cause desmoplasia = thickening of stomach wall (linitis plastica)

Answer 159

large, irregular ulcer with heaped up margins Most common in lesser curvature of antrum Associated with H. pylori, autoimmune gastritis, nitrosamines (smoked food, Japan), blood type A

Answer 160

90% of all malignant gastric tumors | 2nd most common malignancy in the world (but not USE)

Answer 161

related to depth of invasion (worse if in muscular layer) High mortality unless disease detected early 5-year survival = 30% (90% for early cancer)

Answer 162

Early: dyspepsia, dysphagia, nausea Late: weight loss, anorexia, early satiety, anemia

Answer 163

1) Wnt signalling pathway activation (can occur with loss of APC as in FAP) 2) Loss of CDH1 (mutation or methylation) - Common in diffuse type cancers 3) Amplification of Her2/neu → TX with trastuzumab (TKI)

Answer 164

1) Hyperplastic polyps 2) Gastric adenomas 3) Fundic gland polyps

Answer 165

proliferation of gastric foveolar cells (mucus producing) Arise from chronic inflammation Found in gastric body autoimmune gastritis and H. pylori infection with chronic atrophic gastritis *Rare malignant potential > 1 cm → increased risk of dysplasia or adenocarcinoma

Answer 166

Histology: inflammation and edema, cystically dilated foveolae typically in antrum of stomach

Answer 167

arise from dysplastic epithelial cells, risk progression to adenocarcinoma Premalignant - Should be removed endoscopically Familial adenomatous polyposis (FAP) → multiple polyps and adenomas

Answer 168

dark, atypical cells

Answer 169

dilated oxyntic glands lined by flattened parietal and mucous cells (most common type of gastric polyp) Unrelated to H. pylori infection Typically due to PPI use Benign - No malignant potential Increased incidence with FAP

Answer 170

cystically dilated oxyntic gland

Answer 171

benign gastric tumors arising from supporting tissues Leiomyomas and Lipomas → malignant leiomyosarcoma, liposarcoma Usually asymptomatic, but larger ones can present with abdominal pain and GI bleeding TX = surgical resection

Answer 172

subtype of stromal tumor Express c-KIT (CD117) transmembrane receptor tyrosine kinase → TX with imatinib (receptor tyrosine kinase inhibitor) and surgical resection Mesenchymal neoplasms derived from interstitial cells of Cajal (pacemaker cells)

Answer 173

arise from enterochromaffin or enterochromaffin-like cells in intestinal tract Well-differentiated endocrine neoplasm Can be associated with MEN1 Histology: Nests and trabeculae of monomorphic cells Sporadic type → higher rate of malignant behavior Atrophy associated → typically indolent

Answer 174

Strong association between H. pylori infection and primary gastric B-cell lymphoma Low grade clonal proliferation of B-cells in H. pylori induced gastric MALT → lesion may progress to high-grade lymphoma → require surgical resection and chemo/radiation

Answer 175

hyperplasia of pyloric muscularis propria → obstructs gastric outflow Presents in 2-3rd week of life with regurgitation and persistent projectile, nonbilious vomiting (DEVELOPS AFTER YOU ARE BORN) More common in boys Presents as firm ovoid abdominal mass TX: surgical splitting of muscularis propria (“myotomy”)

Answer 176

very rare Mucous cell hyperplasia Gastric acid secretion low-normal Signs/symptoms: abdominal pain, weight loss, N/V, hypoalbuminemia

Answer 177

neuroendocrine tumor in pancreas or duodenum Gastrin secreted leading to hyperplasia of parietal cells Signs/symptoms: chronic diarrhea, abdominal pain, peptic ulcers

Answer 178

1. mucosa 2. submucods 3. muscularis externa 4. Serosa adventitia

Answer 179

epithelial layer + lamina propria (underlying loose, vascularized CT) + muscularis mucosae (thin layer of smooth muscle underlying this)

Answer 180

contains enteroendocrine cells (secrete into blood) and M cells (immune sampling cells) Contain IgA receptor that are ingested and transported into lumen → first defense layer

Answer 181

underlying epithelial cells, specialized to allow molecules across epithelium of gut

Answer 182

contains capillaries and WBCs (including MALT) Lymphocytes, plasma cells, and macrophages scattered throughout lamina propria

Answer 183

connective tissue (more dense than mucosa), larger blood vessels, nerve plexes, glands, lymphatic nodules

Answer 184

Meissner's nerve plexus

Answer 185

inner circular and outer longitudinal smooth muscle layers

Answer 186

Peristalsis and churning of lumenal contents

Answer 187

Auerbach’s plexus between inner circular and outer longitudinal smooth muscle

Answer 188

1. inner circular 2. outer longitudinal 3. oblique smooth muscle (churning)

Answer 189

outer covering of squamous epithelial cells separated from underlying muscular layer by thin CT layer - Adventitia = above diaphragm (esophagus), no outer squamous layer - Contains large blood vessels and nerves

Answer 190

- Mucosae lining the tube creates a microenvironment at surface of the tube that is resistant to proteolytic digestion - Mucin = heavily glycosylated, heavily hydrated, resistant to proteolysis → prevent digestion and protective layer from bacteria

Answer 191

Lymphoid tissue present as scattered individual cells and as lymphatic nodules Peyer’s patch: group of lymphatic nodules M-cells: specialized epithelial cells, function in antigen-uptake - Phagocytose luminal contents and present antigens to underlying lymphocytes and macrophages Plasma cells in nodules release IgA immunoglobulins that bind to receptors on epithelial cells and are transcytosed to lumenal surface → antibacterial agents Prevents pathogenic colonization and adherence

Answer 192

1) Enteric neurons: lie outside CNS, produce local gut motility 2) Parasympathetic and sympathetic fibers: directed by CNS, enables coordinated input → coordinated peristalsis and effects on blood vessels (PS) and glands (S)

Answer 193

convey ingested material from pharynx to stomach (no digestion)

Answer 194

posterior to stomach, anterior to thoracic spine/ribs in retroperitoneum

Answer 195

superior pancreaticoduodenal and splenic arteries (branch off celiac axis) and inferior pancreaticoduodenal artery (branch off the SMA)

Answer 196

made up of epithelial cells with acinar glands (Acinar cells) 1) Secrete digestive enzymes as pro-enzymes/zymogens and amylase/lipase as active enzymes in response to cholecystokinin 2) Produce large amounts of bicarb and water in response to secretin→ maintain flow throughout ducts, keep zymogens inactive with low pH, protect pancreas and duodenum/ileum from low pH 3) Trypsin inhibitor in pancreas deactivates any trypsin prematurely activated

Answer 197

enzymes secreted across apical cell membrane into tiny ductule at center of each acinus → ductules coalesce into larger exocrine duct system of pancreas → main (ventral) duct and ampulla of Vater

Answer 198

pancreatic islet cells produce insulin, somatostatin, VIP, glucagon, and others

Answer 199

when pancreatic enzymes are inappropriately and prematurely activated resulting in autolysis of the gland → severe inflammation and necrosis of pancreatic tissue

Answer 200

serum amylase and lipase elevated > 3x upper limit of normal Lipase more specific for pancreatitis - rises within 1-2 hrs, remains high for 1 week Amylase - rises and falls within 24-48 hrs - can be high due to other etiologies (mumps, Sjogrens, penetrating peptic ulcer, ectopic pregnancy, intestinal ischemia/trauma, etc.)

Answer 201

contrast CT or ultrasound US: best for gallbladder stones CT: detects edema, calcifications, fluid collections (complications of acute pancreatitis)

Answer 202

caused by obstruction of pancreatic duct → stagnation of pancreas enzymes within duct lumen and activation of enzyme cascade Lipase released from dying acinar cells → break down fats → fatty acids precipitate with calcium and form insoluble soaps → Coagulation necrosis of gland and hemorrhage into retroperitoneum → Intense infiltrates of neutrophils and apoptosis of epithelial cells

Answer 203

1) Gallstone: most common cause of pancreatitis in US** 2) Ethanol 3) Other causes: tumors, surgical, congenital ductal abnormalities, Sphincter of Oddi dysfunction types 2 and 3, hyperlipidemia, blunt/penetrating trauma, drugs, hypercalcemia, infection, CF

Answer 204

direct toxic effect on pancreatic acinar cells and ductal epithelium → premature release/activation of trypsinogen and stagnant flow of pancreas juice

Answer 205

Stone lodges in distal common bile and/or ampulla → obstructing ventral duct and causing bile reflux into pancreas → zymogen activation

Answer 206

1) sudden onset severe pain in upper abdomen, radiating to back 2) Nausea/vomiting 3) Low grade fevers * Self-limited Elevated pancreatic enzymes in serum

Answer 207

1) admission, NPO, IV pain meds, IV fluids, time - supportive only usually 2) Consider ERCP for bile duct stone removal - If persistent bile duct stone → requires extraction 3) Cholecystectomy to remove source of stones in some cases 4) Avoidance of alcohol is KEY

Answer 208

1) Ileus (paralysis of gut) 2) Intra-abdominal hemorrhage (digestion through artery) 3) Pseudocyst formation 4) Severe pancreatitis → bowel/bile duct obstruction, shock, respiratory distress/failure/renal failure, death 5) Pancreatic necrosis → increases mortality significantly

Answer 209

develops after repeated bouts of acute pancreatitis, permanent destruction of pancreatic parenchyma with replacement by fibrosis

Answer 210

1) Ductal strictures/stones → pain, exocrine failure - NOT seen in acute pancreatitis ** 2) Pancreatic pseudocysts → pain, nausea, vomiting 3) Acinar destruction → exocrine failure 4) Diabetes → endocrine failure (late)

Answer 211

1) History and physical 2) Plan abd xray 3) CT 4) Endoscopic US 5) Rapid fat stool stain 6) 72 hour quantitative stool collection 7) Secretin stimulation test

Answer 212

CT → dilated duct, atrophy, calcifications, pseudocysts | Mainstay of diagnosis

Answer 213

tube in stomach and duodenum - duodenal bicarb response to secretin [HCO3-] less that 80 mEq/L after 2 hours = diagnostic of pancreatic exocrine failure -Secretin should stimulate bicarb and water secretion from pancreas in normal patient

Answer 214

typically chronic alcohol abuse +/- smoking ALCOHOL = most common cause Genetic conditions: CF, mutations in trypsinogen (PRSS), or trypsin inhibitor genes (SPINK), familial hypertriglyceridemia

Answer 215

Replacement of healthy pancreatic tissue by hard, fibrous tissue, and possible atrophy of the gland Pancreas juice becomes viscous and calcifications develop within duct Fibrous tissue → strictures of duct

Answer 216

broad bands of scar tissue replace lost tubular tissue Moderate numbers of lymphocytes/plasma cells present Relative sparing of islet cells

Answer 217

1) Malabsorption 2) Pain (chronic, waxes/wanes, never disappears) - epigastric, radiates to back, worse after meals 3) Malnutrition

Answer 218

1) Dominant malabsorbed nutrient is lipid = steatorrhea 2 )B12 malabsorption (pancreatic enzymes cleage R-bond) 3) Can eventually get diabetes due to glucagon/insulin secretion 4) Vitamin K malabsorption → bleeding

Answer 219

Dominant malabsorbed nutrient is lipid = steatorrhea (oily, foul smelling, and/or buoyant stools), flatulence, weight loss Due to decreased lipase and colipase in duodenum and decreased duodenal pH Malabsorption occurs in later stages since only 10-20% of acinar cells required for maintaining lipase reserve

Answer 220

1) Pseudocyst | 2) **Ductal obstruction due to strictures or stones (NOT in acute pancreatitis)

Answer 221

fluid collection of liquefied/auto-digested pancreatic parenchyma containing a mixture of pancreas juice and clumps of semi-solid, necrotic tissue surrounded by granulation tissue Resolve as pancreatitis improves, but if they persist, may grow/push on adjacent structures and require drainage

Answer 222

1) ETOH avoidance ** = Mainstay of treatment 2) Pancreas enzyme replacement for steatorrhea 3) ERCP and dilation, stent placement, or stone removal for duct obstruction 4) Celiac nerve block for pain 5) Surgical resection if refractory and severe

Answer 223

endoscopic retrograde cholangiopancreatography= visusalization and palliative stent placement across bile duct stricture to relieve cholestasis symptoms

Answer 224

Adenocarcinoma → Refer in patients to ERCP with stent if they have metastases, recurrent disease, or high surgical risk Autoimmune pancreatitis → ERCP with placement of biliary stent effective in patients with jaundice or pruritus Acute pancreatitis → consider ERCP for bile duct stone removal if it doesn’t pass on its own

Answer 225

IgG-4 + Plasma cells and lymphocytes infiltrate pancreas and its vessels → localized or diffuse enlargement of pancreatic parenchyma and narrowing of pancreatic duct and/or bile duct Glandular atrophy, ductal dilation **calcifications and steatorrhea are NOT features of AIP (features of chronic pancreatitis)

Answer 226

- chronic epigastric or diffuse abdominal pain +/- cholestasis (jaundice, dark urine, itching) - Typically males in ages 40-70 **Can masquerade as pancreatic cancer

Answer 227

Elevated serum IgG-4 Elevated total IgG, ANA, and RF CT, US, or MRI → focally or diffusely enlarged pancreas with decreased enhancement and loss of lobular contour

Answer 228

6-week corticosteroid course (MUCH more treatable than cancer) ERCP with placement of biliary stent effective in patients with jaundice or pruritus

Answer 229

aka carcinoids Histology: arise from enterochromaffin cells of lung, GI tract, or pancreatic islets Presentation: 1) Most are clinically silent and detected on routine imaging 2) Larger ones cause pain 3) Symptoms of hormone excess (insulin, glucagon, gastrin, VIP, somatostatin)

Answer 230

Diagnosis: imaging studies, FNA Treatment: surgical resection or close observation in high surgical risk patients

Answer 231

4th leading cause of cancer mortality in men and women in US 5-year survival only 5%

Answer 232

typically arise from ductal epithelial cells (acinar cells 5-10% of time) Form primitive mucin-positive gland-like structures Elicit strong fibrotic reaction (desmoplasia) → hard to penetrate with chemo

Answer 233

family history, tobacco use, chronic pancreatitis, obesity, genetic syndromes (VHL, Peutz-Jeghers)

Answer 234

usually present late, with locally advanced/metastatic disease 1) Weight loss, abdominal/back pain (late symptom) 2) **Symptoms of bile duct obstruction → jaundice, dark urine, pruritus - Due to bile duct obstruction at head of pancreas 3) Hypercoagulable state (Trousseau’s syndrome)

Answer 235

Diagnosis: contrast abdominal CT, fine needle aspiration (FNA), biopsy -Endoscopic ultrasound is test of choice to stage pancreatic cancer Treatment: surgical resection

Answer 236

Lansoprazole, Omeprazole, Esomeprazole, Lansoprazole

Answer 237

prodrug → systemic circulation → diffuses into parietal cells → activated in canaliculi to sulfenamide → then “trapped”

Answer 238

Irreversibly inactivates H+-K+-ATPase ONLY inactivates ACTIVE pumps → 2-5 days for steady state effect Must take PPI before a meal so Cp max coincides with maximal pump secretion Inactive pumps stored inside cell, put on membrane when active Acid suppression for > 18 hours

Answer 239

1) GERD (#1 agent) 2) Peptic ulcer disease - Used in triple therapy in order to increase gastric pH and promote healing with H. pylori associated PUD 3) NSAID induced ulcers (prevention and treatment) 4) Prevention of stress gastritis (IV infusion) 5) Zollinger-Ellison Syndrome

Answer 240

Dosage reduction required for HEPATIC disease (not renal) Remarkably safe drug, minimal side effects (headache, GI pain, nausea, diarrhea, constipation) Acid rebound upon discontinuation (taper dose) -Gastrin levels are increased due to decreased acidity, but proton pump is blocked so pH stays high → remove PPI → rebound acidity Chronic use → increased fracture risk (decreased Ca2+ absorption), decreased Mg2+ absorption

Answer 241

Prostaglandin analog → acts on epithelial cells to decrease H+ secretion and increase mucus bicarbonate Indicated for NSAID induced ulcers - not first line (PPIs are)

Answer 242

diarrhea uterine cramping, contraindicated in pregnancy

Answer 243

Sulfated disaccharide Al+++ salt → binds necrotic tissue forming protective barrier Activated by acidic pH → give on empty stomach Not absorbed → few side effects (constipation)

Answer 244

Cimetidine, Famotidine, Ranitidine

Answer 245

competitive reversible block of H2 receptors on basolateral membrane

Answer 246

GERD PUD (usually PPIs used instead) Stress related gastritis (IV H2 antagonist)

Answer 247

Less efficacious than PPIs More rapid onset of action than PPIs → better for acute gastritis Better at blocking nocturnal H2 than meal stimulated (ACh-gastrin) acid secretion, but PPIs are still more effective

Answer 248

Generally well tolerated 1) CNS dysfunction (mental status change) in elderly or renally impaired 2) Gynecomastia (chronic high dose cimetidine) 3) Tolerance possible with continued use

Answer 249

DDIs: Cimetidine inhibition of CYP450 metabolism** Renal excretion - dosage reduction with renal dysfunction

Answer 250

used to eradicate H. pylori infection that damages epithelial cells and increases susceptibility to ulceration (associated with 85% of duodenal ulcers) **Confirm eradication (stool antigen test)

Answer 251

Clarithromycin-Amoxicillin/Metronidazole-PPI

Answer 252

bismuth subsalicylate-Metronidazole-Tetracycline-PPI (or H2 Antagonist)

Answer 253

amoxicillin-PPI x 5 days, THEN clarithromycin-Tinidazole / Metronidazole-PPI x 5 days

Answer 254

rapidly raise pH (to pH=4) nonabsorbable long acting, no adverse effects no drug-drug interactions

Answer 255

Rapid, prolonged neutralization → rebound secretion Safe, but NOT for chronic use (except when used as Ca2+ supplement) Side effects: Constipation, hypercalcemia, renal calculi

Answer 256

Widely used Binds phosphate in gut (used in CKD) Side effect: constipation, CNS toxicity with chronic intake

Answer 257

osmotic diarrhea

Answer 258

Metoclopramide (Reglan) Tegaserod, Cisapride

Answer 259

dopamine antagonist → block presynaptic inhibition of ACh release → increase in coordinated contractions → enhance transit Weak 5-HT antagonist at chemoreceptor trigger zone → relieve n/v

Answer 260

somnolence, dystonic reactions, tardive dyskinesias (EPSEs)

Answer 261

5HT4 receptor agonists → direct stimulation of ACh release → increase coordinated contractions and transit in esophagus and stomach

Answer 262

reduces bloating of irritable bowel syndrome (IBS)

Answer 263

Cisapride → LIFE THREATENING ARRHYTHMIAS (increase QT) Tegaserod → linked to strokes, MI, angina

Answer 264

non-cornified squamous epithelium

Answer 265

Upper portion → skeletal muscle, midway → mix skeletal/smooth, lower ⅓ → solely smooth muscle

Answer 266

present in dermis → lubrication, assist in swallowing

Answer 267

contains small incomplete sphincter with maintained muscular contraction to prevent reflux of stomach contents

Answer 268

small area with mucus secreting glands around entry of esophagus

Answer 269

main body of stomach, secretes acid, peptic digestive products, and mucus

Answer 270

secretes mucous, contains endocrine cells that secrete gastrin hormone

Answer 271

- face cavity of stomach, arranged in folds along underlying lamina propria 1. Contain large vesicles with mucins and bicarbonate → local discharge onto surface to provide viscous protective layer - Shelter epithelial cells against stomach acid and abrasion from churning chime 2. Have short microvilli on surface with glycoprotein/glycolax covering

Answer 272

spaces between epithelial folds, continue deep into mucosa as one or more tubular gastric glands

Answer 273

- contain differentiated epithelial cells crucial for function of stomach (digestion of food at acidic pH) - Stomach lumen extends to very body of gastric glands

Answer 274

Enable constant renewal of gastric epithelium (every 3-5 days) 1. Deep in glands, turn over every 6-12 months 2. Located in upper neck region, undifferentiated → downward to specialized cells on gastric glands → upward mucous-secreting cells

Answer 275

protein secretors with apical granules and elaborate basal RER 1. Secrete pepsinogen → converted to pepsin in presence of acid 2. Pepsin: protease, optimal function at low pH 3. Derived directly from stem cells

Answer 276

unique acid producing cells 1. H+/K+ ATPase pumps H+ ions into lumen of gastric glands against high concentration gradient pH of gastric juice = 1-1.5 2. Extensive microvilli bordering canaliculi → enormous surface area for pumping H+ into lumen 3. Lots of mitochondria 4. Stimulated to produce acid by gastrin and histamine 5. Secrete intrinsic factor

Answer 277

excessive secretion of gastrin → overproduction of HCl by parietal cells → duodenal ulcers

Answer 278

APUD cells (amine precursor uptake decarboxylation), typically oriented toward vascular side to release into bloodstream

Answer 279

1. G-cells: secrete gastrin, located in pylorus 2. A-cells: secrete glucagon 3. EC-cells: secrete serotonin (serotonin also taken up and stored by platelets) 4. D-Cells: secrete somatostatin, widely distributed in middle portion of stomach

Answer 280

Stomach - longitudinal folds in stomach wall - Disappear upon distension

Answer 281

(small intestine) - permanent transverse-oriented folds covered with villi - Increase surface area of small intestine 8x

Answer 282

- low pH chyme from stomach enters duodenum upon relaxation of pyloric sphincter - Digestion continues in duodenum at higher pH and with enzymes released from pancreas and present at surface of intestinal mucosa - Absorption also occurs due to high surface area here

Answer 283

Duodenum: Present Jejunum: Absent Ileum: Absent

Answer 284

Duodenum: + Jejunum: ++ Ileum: +++

Answer 285

Duodenum: + Jejunum: ++ Ileum: ++++

Answer 286

Duodenum: + Jejunum: Best developed Ileum: +

Answer 287

Duodenum: Most numerous Jejunum: decreased distally Ileum: least abundant

Answer 288

1. Enterocytes 2. Goblet mucous cells 3. Enteroendocrine cells 4. Intestinal glands 5. Intestinal villi

Answer 289

- epithelial cells, also contain microvilli on their surface, - increase surface area 30x - Glycolax and glycoproteins cover microvilli → digestive processes within glycolax due to digestive enzymes found in matrix

Answer 290

scattered between absorptive/digestive cells - Produce mucus for protection/lubrication - Least abundant in duodenum

Answer 291

also in SI, secrete different stuff than stomach ones

Answer 292

1. Crypts of lieberkuhn 2. Paneth cells 3. Brunner's glands

Answer 293

simple tubular glands, penetrate from base of villi deeper into mucosa - Continuous with surface epithelium - Stem cells most abundant in lower third of crypts → give rise to other cells (mucous cells, enterocytes, Paneth cells)

Answer 294

contain large eosinophilic granules with lysozyme, phospholipase, and antibacterial peptides called defensins

Answer 295

only in duodenum, release contents into crypts - Secrete large amounts of mucins and bicarb to neutralize acid arriving in pyloric sphincter

Answer 296

highly structured 1. Loose lamina propria core containing small blood vessels, lymphocytes, and lymphatic spaces that joint at the lacteal 2. Contains lacteals: larger lymphatic vessel in center of intestinal villa-> larger lymphatics and proceed to bloodstream via thoracic duct

Answer 297

1. Passage for fluid entering lumen of intestine | 2. Transport for lipoprotein droplets (chylomicrons) exocytosed by enterocytes on side facing lamina propria

Answer 298

take up fatty acids and monoglycerides form lumen of gut, and resynthesize them to di- and triglycerides → release them by exocytosis on opposite side Nutrient taken up by capillaries via hepatic portal system of liver

Answer 299

- Chyme neutralized → enzymes produced by pancreas and enterocytes digest proteins to AAs, complex carbs to single monomers (glucose, galactose), and lipids to fatty acids and monoglycerides - Muscularis externa: inner circular and outer longitudinal layers in intestine → movement of luminal contents by peristalsis - Segmented movement with alternate contraction and relaxation of segments → back and forth movements that agitates luminal contents

Answer 300

Main pancreatic duct joins common bile duct near its entry to duodenum - Sphincter of Oddi (hepatopancreatic sphincter)

Answer 301

Organized into cluster of pancreatic acinar cells arranged at end of common duct

Answer 302

full of RER, synthesis of proteins for secretion

Answer 303

secretory granules (zymogen granules) with packaged product that gets secreted into ducts - Most secreted enzymes initially inactive (zymogens) - Prevents autodigestion of proteins/lipids of pancreas en route via ducts to duodenum

Answer 304

trypsin, chymotrypsin, elastase, carboxypeptidase, triacylglycerol lipase

Answer 305

enterokinase Not secreted by pancreas, membrane anchored enzyme in apical plasma membrane of duodenal digestive/absorptive cells (epithelial enterocytes)

Answer 306

Activates other zymogens by proteolysis

Answer 307

degrades starch to glucose and maltose | Synthesized in active form in pancreas

Answer 308

cleaves RNA | Synthesized in active form in pancreas

Answer 309

cells in acini, represent beginning of duct system Secrete much of the volume of pancreatic juice (water, bicarb) - Help Brunner’s glands neutralize acid - Secretion under control of secretin and cholecystokinin

Answer 310

have complex glycolax at their surface Some of final digestive processes occur in this layer just outside cell

Answer 311

amylase (from pancreas) digestion → maltose and isomaltose → broken down by maltase and isomaltase (membrane-anchored enzymes in apical plasma membrane of enterocytes) → glucose Glucose absorbed via nearby glucose transporters = most effective absorption instead of being consumed by bacteria

Answer 312

Lactase → on enterocyte surface, cleaves lactose → glucose + galactose Absence of lactase → lactose intolerance because bacteria utilizes undigested lactose

Answer 313

1. serous 2. Mucous 3. Mixed

Answer 314

1. submandibular 2. sublingual 3. parotid

Answer 315

mucous (lubricative and protective)

Answer 316

serous (watery, contain enxymes- amylase, RNAse, DNAse) Serous epithelial cells also transport IgA class Ig that together with lysozyme and peroxidase provide antibacterial action

Answer 317

Organized in acinar design: | Contraction of myoepithelial cells propel salivary secretions form acini

Answer 318

cecum, appendix, transverse colon, descending colon, and rectum - Smooth, lacks plicae and villi - Contains numerous straight tubular glands/crypts - Epithelial layer: abundant mucous-producing cells and absorptive cells

Answer 319

recovery of water and salt during concentration of fecal material

Answer 320

longitudinal structural folds of mucosa located near distal portion of rectum

Answer 321

Lymphocytes

Answer 322

- Large band of circular smooth muscle - Muscular specializations in longitudinal layer: 1. Taeniae: bands in this layer - segmented contraction → sacculation of bowel which compresses and segments fecal material 2. Anus: where circular layer is thickened to form internal anal sphincter - External anal sphincter is circular striated muscle

Answer 323

1. Thick mucosa, glands that branch deep into mucosa with acini at end of branches 2. Acinar/Chief cells at end running down to muscularis mucosa 3. pH = 1-2 → kill bacteria, and denature proteins

Answer 324

1. Villi on surface specialized for absorption, lined by epithelium 2. Small crypts at end of folded epithelium

Answer 325

thick mucosa with linear, highly regular crypts filled with mucous secreting cells

Answer 326

Requires complicated coordination between CNS (SNS and PNS) and enteric nervous system with the gastric musculature Gastric pacemaker cells: drive baseline motility of stomach (not well understood) - Interstitial cell of cajal

Answer 327

area relaxes upon ingestion of food = Receptive relaxation Main role of proximal stomach is storage with minimal pressure increase

Answer 328

controls mechanical (grinding) and enzymatic digestion and processing → liquid chyme sent in small amounts to SI Contraction of distal stomach → gastric emptying into duodenum

Answer 329

1. Receptive relaxation (vagally mediated inhibition of body tone) - Swallowing induced vagal response - Gastric Accommodation: smooth muscle relaxation elicited by mechanical distention of stomach (gastric mechanoreceptors) - -Vasovagal response 2. Liquid emptying by tonic pressure gradient 3. Solid emptying by vagally-mediated contractions 4. Residual solids emptied during non-fed state by MMC (migrating motor complex) every 90-120 minutes

Answer 330

1. chemical substances (inside and outside body) = NEUROPATHIC 2. Diseased GI muscles: genetic defect (muscular dystrophy) or acquired (progressive systemic sclerosis) = MYOPATHIC 3. Abnormalities of interstitial cells of Cajal - pacemaker cells 4. CNS disorders (input for SNS and PNS)

Answer 331

transport, store, and expel stool after absorbing majority of luminal fluid

Answer 332

1. Low amplitude tonic and phasic contractions for mixing luminal contents (Haustra) 2. High amplitude propagated contractions (HAPCs) for propelling

Answer 333

Colonic motility increases after meal (gastrocolonic response) and on awakening

Answer 334

1. Drugs, mechanical 2. Metabolic: DM, hypoK, hyperCa, hypoMg, hypothyroid 3. Myopathy: amyloid, scleroderma 4. Neurogenic: Parkinson’s spinal cord injury, MS, autonomic neuropathy, Hirschsprung’s 5. Other: pregnancy, immobility 6. IBS-C 7. Normal transit, slow transit, dyssynergic defecation

Answer 335

esophageal motility disorder due to inflammatory destruction of neurons in myenteric plexus of esophagus - Predominant destruction of inhibitory neurons that affect relaxation of esophageal smooth muscle → failure of appropriate LES relaxation after swallowing → esophagogastric junction outflow obstruction - Spares cholinergic neurons that contribute to LES tone - Absence of peristalsis

Answer 336

dysphagia to solids and liquids, regurgitation of undigested food

Answer 337

esophageal manometry → incomplete relaxation of LES, aperistalsis in smooth muscle esophagus

Answer 338

multi-system disorder, skin and GI involvement mostly | Small vessel vasculitis → vascular derangement and resultant smooth muscle atrophy and fibrosis of multiple organs

Answer 339

Myopathic process 1. Atrophy of smooth muscle → weak peristalsis → dysphagia 2. Atrophy of smooth muscle → weak LES → GERD 3. Unrepentant GERD → esophagitis → stricture

Answer 340

delayed gastric emptying

Answer 341

esophageal manometry → weak/absent esophageal body peristalsis Differentiate from achalasia due to weakened LES pressure

Answer 342

conditions of uncertain etiology, peristalsis preserved

Answer 343

chest pain and dysphagia

Answer 344

related to overactivity of excitatory nerves, and impairment of inhibitory innervation or overreactivity of smooth muscle response EX) Jackhammer esophagus = lots of red on esophageal manometry, with high pressure and long contraction time

Answer 345

“Stomach paralysis”, delayed gastric emptying in absence of mechanical obstruction Impaired transit of food from stomach to duodenum

Answer 346

nausea, vomiting, bloating, early satiety, postprandial abdominal distension and pai

Answer 347

1. Idiopathic, post-infection 2. Post-surgical (vagal nerve injury) or myenteric plexus injury COMMON with thoracic surgical procedures (lung transplant) 3. Diabetic (autonomic neuropathy), medication related (opiates) 4. Others: paraneoplastic, rheumatologic, neurologic, myopathic (scleroderma)

Answer 348

scintigraphic gastric emptying (gastric emptying study)

Answer 349

1. Lifestyle and dietary measures: small and infrequent meals, low-fat and low-residue diet, glucose control in diabetics 2. Medications: prokinetic agents, antiemetics 3. Gastric electric stimulation 4. Surgery (removal of stomach) - last resort

Answer 350

Signs and symptoms of mechanical obstruction of small bowel without a lesion obstructing flow of intestinal contents - Characterized by presence of dilation of bowel on imaging - Major manifestation of small intestinal dysmotility

Answer 351

small intestinal bacterial overgrowth: stasis → bacterial overgrowth → fermentation and malabsorption

Answer 352

1. Underlying neuropathic disorder involving enteric nervous system or extrinsic nervous system (Parkinson’s Shy-Drager syndrome, Diabetes) 2. Infectious (Chagas) 3. Myopathic disorder (involving smooth muscle) EX) Scleroderma, amyloidosis, eosinophilic gastroenteririts 4. Or abnormality in interstitial cells of Cajal

Answer 353

mostly congenital, mostly primar conditions, absent MMC predicts need for IV nutrition, ⅓ of infants born die in 1st year of life

Answer 354

Congenital absence of myenteric neurons of distal colon (neuropathic motility disorder) No reflex inhibition of the IAS following rectal distention (No Recto-anal inhibitory reflex)

Answer 355

Disorder in coordination of pelvic floor musculature - paradoxical contraction of pelvic floor and external anal sphincter with attempts at defecation

Answer 356

anorectal manometry

Answer 357

Biofeedback therapy is effective

Answer 358

assessment of esophageal body peristalsis and upper and lower esophageal sphincter function - Transnasal, intraluminal manometry catheter containing pressure sensors → from nares into stomach, assess esophageal motility as patient swallows repeated small boluses of water - UES relaxation (red color) → esophageal peristalsis from top to bottom (proximal peristalsis of striated muscle and distal peristalsis of smooth muscle) → post-deglutitive LES relaxation

Answer 359

Aka gastric scintigraphy Low fat EggBeaters radiolabeled with 1 mCi Technetium 99, measure percentage remaining after certain amount of time

Answer 360

retention >60% at 2hr or >10% at 4hrs

Answer 361

used to assess for gastroparesis and motility disorders of small intestine and colon - Measures pressure, temperature, and pH as it traverses GI tract

Answer 362

1. Measure motility of SI with pressure sensors 2. Measure pressure waves that result from phasic contractions of circular muscle layer 3. Neuropathic process: discoordinated infrequent contractions 4. Myopathic process: nothing happening even though nerves stimulating SI tract intact

Answer 363

Colonic transit study Swallow 24 capsules containing radiopaque markers on Day 1 → plain abdominal xray on Day 5 - Less than 5 markers = normal - > 5 markers in recto-sigmoid suggests defecatory disorder - > 5 markers scattered throughout colon = slow transit

Answer 364

1. Primary means of assessing defecation disorders 2. Catheter with pressure sensors placed in anus and rectum 3. Resting pressure, stimulated defecation, rectal sensation testing, and recto-anal inhibitory reflex testing are all tested

Answer 365

achalasia, scleroderma

Answer 366

scleroderma

Answer 367

gastroparesis, functional dyspepsia

Answer 368

slow transit constipation (scleroderma)

Answer 369

Hirschsprung’s, dyssynergic defecation