Week 1

Question 1

What is the GALT (gastrointestinal-associated lymphoid tissue)? (where is it found and its purpose)

Answer 1

1. GALT is a general term used to refer to all of the organized lymphoid tissues found in the small intestine. It is found in the mucosa and submucosa of small intestine lining.
2. Function is to protect the body from foreign antigens and pathogens, while allowing tolerance to commensal bacteria and dietary antigens

Question 2

What is the difference between MALT and GALT?

Answer 2

GALT is a subdivision of MALT and specifically located to the GI tract (small intestine)

Question 3

1. Location of lymphoid follicles?
2. What is the purpose of lymphoid follicles found within the GALT and in between villi of small intestine?

Answer 3

1. These lymphoid follicles are in mucosa and protrude into the lumen of the gut.
2. It is the site where adaptive immune response is activated (T cells and B cells)

Question 4

1. What are Peyer’s patches?

Answer 4

1. Clusters of lymphoid follicles found in the lining of small intestine

Question 5

1. What are M cells (microfold cells)
2. What aspects of these cells allow it do its job (basolateral and apical surface)

Answer 5

1. Microfold (M) cells are located in Peyer’s patches (PPs) of the small intestine. M cells actively transport luminal antigens to the underlying lymphoid follicles to initiate an immune response
2. Basolateral surface forms fold around follicle (easy transport to APCs / lymphocytes) —> Apical surface lacks thick glycocalyx layer (easy uptake of antigens)

Question 6

1. Describe the Tolerogenic environment found in mucosal immunity.
2. What happens when this tolerogenic environment is interrupted?

Answer 6

1. This is general immune tolerance to the many antigens presented in gut. When non-harmful antigen is presented to M cell and lymphoid follicles then regulatory T-cells secrete TGF-beta and IL-10. These two signal molecules suppress T cell responses so there is no immune reaction to these non-harmful antigens.
2. loss of tolerance is what causes food allergies, celiac disease, IBD, etc

Question 7

1. What is the secretory, Dimeric IgA immunity?
2. where is found?
3. Its purpose?
4. Why does it not cause inflammation

Answer 7

1. This is a type of primary antibody defense –> IgA antibody on surface of intestinal lining NEUTRALIZES pathogens instead of causing inflammatory response. Meant to prevent bacteria from crossing the intestinal lining.
   - -> Neutralization occurs bc IgA lacks Fc receptor which prevents complement activation

Question 8

What causes secretion of IgA in small intestine? (4 steps)

Answer 8

1. IgA can be produced by naïve B cells in GALT in response to stimulation by commensal microbes, microbial pathogens, or after vaccination.
2. Regulatory T cells release TGF-beta and IL-10 which cause differentiation of plasma B cells to class switch and make IgA.
3. Plasma B cells secrete dimeric IgA in lamina propria and dimeric IgA bind to poly-Ig receptor on basolateral surface of mucosal epithelial cells
4. When on the apical side - poly-Ig receptor is cleaved and released IgA into lumen. IgA is tethered within mucosal layer and stays there to neutralize toxins/microbes

Question 9

1. When is fluoroscopy utilized?
2. When is barium swallow (esophogram) used?
3. When is video swallow test used?

Answer 9

1. evaluates morphology and motility of internal organs using real time X-rays
2. Evaluates upper GI tract (pharynx and esophagus)
3. Modified barium swallow - used to evaluate swallow reflex after CNS injury

Question 10

What does hiatal hernia look like in imaging?

Answer 10

image

Question 11

What does reflux esophagitis look like in imaging?

Answer 11

1. Reflux esophagitis is defined as inflammation of the esophageal mucosa secondary to gastroesophageal reflux disease (GERD)
2. image

Question 12

What does barrett’s esophagus look like in imaging?

Answer 12

1. Barrett’s esophagus is a condition in which the flat pink lining of the swallowing tube that connects the mouth to the stomach (esophagus) becomes damaged by acid reflux, which causes the lining to thicken and become red
2. image

Question 13

What does esophageal carcinoma look like in imaging?

Answer 13

1. looks like bitten apple - showing apple core

Question 14

Function of these papillae in tongue

1. filiform papillae
2. foliate papillae
3. Fungiform papillae
4. Circumvallate papillae

Answer 14

1. break up foods and move food towards throat
2. have taste buds
3. have taste buds
4. have taste buds + has salivary glands that help flush taste buds

Question 15

Differentiate how the filiform, foliate, fungiform, and circumvallate papillae of tongue look like under microscopy

Description: rounded/very large+rounded/columnar/spiky+keratinized

Answer 15

image

Question 16

1. What is the difference between serous and mucous glands?
2. how do they look differently under microscopy?

Answer 16

1. serous glands secrete a protein-containing solution, which is involved in digesting starch and protecting oral cavity from pathogens like bacteria - stain darker (blue arrow)
2. mucous glands secrete a thick solution with mucus, which is involved in lubricating food and oral cavity - stain lighter

Question 17

label the layer of the GI wall

Answer 17

1. mucosa - blue bracket (closest to lumen)
2. submucosa - black bracket
3. muscularis externa - dotted bracket (closer to lumen - circular muscle that can create sphincters → then Myenteric/Auerbach plexus → then outer longitudinal muscle)
4. Adventitia/serosa -brown bracket

Question 18

1. What layers/structures are found within the mucosa?
2. Function of each

Answer 18

1. Epithelium, lamina propria, muscularis mucosa
2. epithelium protects - lamina propria is loose connective tissue with blood vessels, nerve fibers, lymphatics, immune cells, etc - muscularis mucosa is thin strip of smooth muscle

Question 19

1. What important plexus is found in submucosa?
2. What important plexus is found in muscularis externa?

Answer 19

1. Meissner’s nerve plexus- controls GI secretions and local blood flow
2. Auerbach’s/Myenteric plexus - coordinates peristalsis

Question 20

1. Function of submucosa
2. Function of muscularis externa
3. Function of adventitia and serosa

Answer 20

1. more connective tissue with glands, vasculature, and lymphatics - has meissner’s plexus to regulate secretions and blood flow
2. help with peristalsis
3. Adventitia- attaches organs to body wall and contains blood vessels, lymphatics, and nerves — serosa - produces lubricant to prevent friction

• organs can have adventitia and serosa or just one

Question 21

1. where are parotid, sublingual, and submandibular glands found?
2. What does each secrete (serous acini vs mucous acini)

Answer 21

1. image
2. Parotid - serous acini only
3. Sublingual - mucous acini only
4. Submandibular - both serous and mucous acini

Question 22

1. What are the types of cells that line the esophagus epithelium?
2. identify the structure pointed out by blue arrow

Answer 22

1. non-keratinized stratified squamous epithelium
2. esophageal glands that secrete lubricating mucus

Question 23

Differentiate between these cells of the stomach

1. surface mucous cells
2. parietal cells
3. mucous neck cells
4. chief cells
5. diffuse neuroendocrine (DNES) cells

Answer 23

1. produce thick ALKALINE mucus to prevent autodigestion
2. produce HCl and Intrinsic factor
3. secrete fluid mucus for lubrication
4. secrete pepsinogen and lipase
5. secretes hormones like (gastrin, serotonin, ghrelin, somatostatin)

Question 24

Indicate what cells are found in these parts of the stomach

1. Cardia
2. Fundus (body)
3. Pylorus
   4.

Answer 24

1. high number of mucous cells - no chief cells
2. mix of every cell type - very thick mucosa
3. high number of mucous cells - no chief cells

gastric glands are found throughout stomach but what cells they have within can depend on the area of the stomach (for example cardia has gastric glands but there are no chief cells found within

Question 25

1. Describe where the gastric pit, neck, and gastric gland is 2. Describe what cells are typically found within each region

Answer 25

1. image 2. Gastric pit- has surface mucous cells 3. Neck - parietal, DNES, Stem, and Mucous neck cells (4) 4. Gastric gland (at the base) - chief cells and G cells

Question 26

1. What hormones/signal induce the parietal cells to secrete HCl and intrinsic factor? (3)

Answer 26

1. Gastrin, Histamine, and Parasympathetic activity (ACh)

Question 27

The small intestine has villus and crypts. when the epithelial cells slough off how do you regenerate epithelium?

Answer 27

At bottom of crypt you have undifferentiated stem cells - these regenerate villous epithelial cells

Question 28

GI regulatory substances: GASTRIN 1. what cells secrete this? Where are these cells found? 2. Action of this substance? 3. Direct and indirect effects of gastrin?

Answer 28

1. G cells in the stomach antrum and duodenum 2. increase gastric H+ secretion ( plus increase in growth of gastric mucosa and gastric motility) 3. direct- gastrin directly stimulates parietal cells to secrete substances 4. Indirect - gastrin stimulates ECL cells in stomach to release histamine which also stimulates parietal cells

Question 29

GI regulatory substances: CCK (cholecystokinin) 1. what cells secrete this? Where are these cells found? 2. released in response to what? 3. Action of this substance?

Answer 29

1. I cells of duodenum and jejunum 2. a meal rich in fat and lipids 3. increased pancreatic secretion, increased gallbladder contraction and relaxation of sphincter of Oddi PLUS decrease gastric emptying (all in the effort to metabolize food in small intestine)

Question 30

GI regulatory substances: Somatostatin 1. what cells secrete this? Where are these cells found? 2. Action of this substance? 3. In what instances is this used therapeutically?

Answer 30

1. D cells in pancreatic islets and GI mucosa 2. DECREASE HCl and pepsinogen secretion, decrease pancreatic and small intestine secretion, decrease gallbladder contraction, decrease insulin and glucagon release [INHIBITS MOST GI HORMONES] 3. Used to reduce overactive GI system (in carcinoid serotonin secreting tumor/diarrhea)

Question 31

GI regulatory substances: SECRETIN 1. what cells secrete this? Where are these cells found? 2. Action of this substance?

Answer 31

1. S cells in duodenum 2. INCREASED pancreatic bicarbonate (HCO3-) secretion, increase bile secretion + DECREASED gastric acid secretion

Question 32

GI regulatory substances: Glucose dependent insulinotropic peptide (GIP) - type of incretin 1. what cells secrete this? Where are these cells found? 2. Action of this substance?

Answer 32

1. K cells in duodenum and jejunum 2. decreases H+ secretion and increases insulin release

Question 33

GI regulatory substances: MOTILIN 1. Where are these cells found? 2. Action of this substance? 3. What disorder is it typically used in therapeutically?

Answer 33

1. stomach and small intestine - increased in fasting state 2. produces migrating motor complexes (MMCs) -a cyclic, recurring motility pattern that occurs in the stomach and small bowel during fasting 3. Gastroparesis (delayed gastric emptying)

Question 34

GI regulatory substances: Vasoactive intestinal peptide (VIP) 1. Where are these cells found? 2. Action of this substance?

Answer 34

1. parasympathetic ganglia in sphincters, gallbladder, and small intestine 2. increases intestinal water and electrolyte secretion + increases relaxation of intestinal smooth muscle and sphincters, limiting intestinal muscle contractions -can cause diarrhea

Question 35

GI regulatory substances: Peptide YY 1. what cells secrete this? Where are these cells found? 2. Action of this substance?

Answer 35

1. L cells in terminal ileum and colon 2. decreases intestinal motility - this is bc fat reaches terminal ileum after not being efficiently absorbed - meal will be retained longer to allow for more digestion+absorption

Question 36

GI regulatory substances: Glucagon like peptide (GLP-1/GLP-2) - type of incretin 1. what cells secrete this? Where are these cells found? 2. Action of this substance? 3. What disorders is GLP1 or GLP2 used for as therapeutic?

Answer 36

1. L cells in terminal ileum and colon 2. stimulates insulin secretion (GLP1) and epithelial proliferation (GLP2) 3. GLP1 - used for diabetes ;;; GLP2 is used for short bowel syndrome to increase absorptive capacity

Question 37

GI regulatory substances: Serotonin 1. what cells secrete this? Where are these cells found? 2. Action of this substance?

Answer 37

1. EC cells (in intestinal lining) 2. Stimulates gastric motility (reduces appetite) *99% of body serotonin is made in GI tract*

Question 38

Small intestine epithelium Small intestine has villi and crypts. 1. What cells are found in the crypt, neck, and tip of villi?

Answer 38

1. bottom of crypt- has undifferentiated stem cells and paneth cells 2. neck has absorptive cells, goblet cells, enteroendocrine cells (EEC) 3. tip of villi have absorptive cells and goblet cells

Question 39

How are the linings of colon different than in small intestine?

Answer 39

1. small intestine has villi and crypts but colon has surface cells and crypts (image is of colon)

Question 40

1. What is crypt of Lieberkuhn? 2. What is the purpose of paneth cells in small intestine?

Answer 40

1. crypt between villi in small intestine 2. secrete **antimicrobial peptides, called defensins**, thereby contributing to host defense against microbes in the small intestine

Question 41

What is each of the salivary glands innervated by? 1. parotid gland 2. submandibular gland 3. sublingual gland

Answer 41

1. IX - glossopharyngeal (parasympathethic) 2. VII - facial (parasympathetic) 3. VII - facial (parasympathetic)

Question 42

what is in the composition of saliva? (6)

Answer 42

* water * mucin - for lubrication * glycoproteins - solubilization of food which allows for taste * salivary amylase - for carb digestion * lingual lipase - for lipid digestion * electrolytes including bicarbonate (for neutralization of gastric secretions in esophagus) * and more

Question 43

In salivary glands what are the different roles of acinar cells vs ductal cells?

Answer 43

1. Acinar cells - these are at the base of salivary glands and produce initial form of salivary fluid (isotonic solution) (can be serous or mucus) 2. Ductal cells - line the salivary glands and do secretion or absorption of ions to make saliva a hypotonic solution

Question 44

1. What are the functions of the ductal cells to make saliva a hypotonic solution? (4 movements) (think of Na, K, HCO3-, Cl, Water, H+)

Answer 44

1. NaCl are taken out of saliva (this occurs with Na/H and Cl/HCO3- exchanger protein - absorption) 2. K and HCO3- are put into saliva (this occurs with Cl/HCO3- exchanger protein AND H/K exchanger - excretion) 3. water is impermeable in ductal epithelium so none is reabsorbed or secreted

Question 45

What happens to saliva concn with high flow rate and low flow rate through the salivary glands?

Answer 45

1. With high flow rate you get concn closer to the original isotonic solution because there is less time to change concn within gland 2. With low flow rate you get greater modification (very hypotonic saliva) because more time is spent in gland

Question 46

How does sympathetic vs parasympathetic input affect saliva secretion?

Answer 46

1. sympathetic - induces scant amylase rich saliva 2. parasympathetic - leads to voluminous saliva secretion (parasympathetic is mainly regulatory system) → Muscarinic antagonists = dry mouth, muscarinic agonists = drooling / salivation

Question 47

What salivary gland is responsible for most of the saliva we make?

Answer 47

submandibular gland (makes both serous and mucus saliva)

Question 48

What are the steps to swallowing (5)

Answer 48

Image For step 2: pharyngeal mechanoreceptors are activated when food is pushed back and this sends afferents to swallowing center in medulla which sends efferent impulses via cranial nerves and vagus nerve to finish swallowing reflex

Question 49

what is primary peristalsis vs secondary peristalsis

Answer 49

1. moves bolus down into stomach- after food passes through UES 2. initiated by distention of esophagus - this is meant to clear esophagus from remaining bolus and refluxed acid

Question 50

What is the receptive relaxation reflex?

Answer 50

* This is when bolus is pushed through to the stomach. The stomach has to dilate and there is relaxation of lower esophageal sphincter and proximal part of the stomach. * To receive the bolus more easily * This uses extrinsic innervation of the stomach (vagal fibers)

Question 51

What are the different functions of the proximal and distal parts of the stomach?

Answer 51

1. proximal - storing food 2. distal - mixing and grinding food

Question 52

Describe the different patterns of gastric motility (indicate special cells or hormones or molecules that are involved in the steps) 1. Accommodation (reservoir) 2. Segmentation (mixing) 3. Propulsion (peristalsis)

Answer 52

1. proximal stretch of stomach - relaxation when food is entering from esophagus (**release of NO and VIP cause relaxation**) 2. some regions of stomach contract and some relax in distal stomach to mix - **does this via interstitial cells of Cajal** that generate slow waves of spontaneous depolarization 3. pushes food down close to pyloric sphincter by contracting stomach and relaxing pyloric sphincter - **(decreased CCK from duodenum allows for gastric emptying)**

Question 53

What is gastric accommodation reflex?

Answer 53

When the stretching of the stomach body due to food and presence of nutrients in duodenum induces relaxation of stomach → this causes food to be stored in stomach and slow down passage of any more food since there is already food present that needs to be digested

Question 54

When proximal stomach contracts and pyloric sphincter relaxes what happens?

Answer 54

gastric emptying

Question 55

What is found within gastric juice and their functions (4)

Answer 55

1. HCl - initiates digestion, activates pepsin 2. Pepsinogen - aids in protein digestion 3. Intrinsic factor - for B12 absorption 4. Mucus - protects gastric mucosa from HCl and gastric contents

Question 56

How does parietal cells secrete H+ (HCl) when originally they have H2CO3?

Answer 56

Has H2CO3 then split into HCO3- and H+. HCO3- goes into blood but H+ goes into stomach lumen (along with Cl- to make HCl)

Question 57

low intra-gastric pH leads to what changes in the stomach?

Answer 57

inhibits the secretion of gastric juices because inside of stomach is already very acidic and pH is just going lower. → does so via somatostatin (which inhibits all GI hormones)

Question 58

What is the zollinger-ellison syndrome?

Answer 58

Ulcers of the DUODENUM produced by excessive gastric acid secretions

Question 59

How does H pylori cause ulcers?

Answer 59

H. pylori bacterium that reside in GI tract can produce ulcers because it inhibits somatostatin release (which is responsible for inhibiting secretion of all GI hormones and gastric acid secretion)

Question 60

ACHALASIA 1. What is it? 2. What causes it? (3 reasons) 3. How it looks on imaging? 4. Clinical presentation (3)

Answer 60

1. distention of esophagus and constriction of LES. Constriction of LES bc there is increased LES tone. 2. first cause: Idiopathic (ganglion cell degeneration resulting in failure of inhibitory neurons responsible for LES relaxation) ----- second and 3rd cause: Chaga's disease and diabetic neuropathy 3. Birds beak (look at image) 4. chest pain, regurgitation that leads to aspiration pneumonia, difficulty belching

Question 61

Mallory-Weiss Syndrome 1. What is it? 2. What causes it? 3. Clinical presentation (2)

Answer 61

1. partial thickness, longitudinal lacerations at the gastroesophageal junction 2. violent coughing or vomitting 3. hematemesis, severe vomiting/retching

Question 62

BOERHAAVE SYNDROME 1. What is it? 2. What causes it? 3. Clinical presentation (3)

Answer 62

1. severe transmural (across an entire organ or blood vessel) tears of esophagus associated with mediastinitis (swelling of mediastinum) → mediastinitis happens because contents of esophagus fall out and into surrounding area causing pain 2. forceful vomiting or straining 3. chest pain, tachypnea, shock [HEMATEMESIS IS NOT A FREQUENT SYMPTOM WHICH IS WHAT DIFFERENTIATES THIS FROM MALLORY-WEISS) +requires surgery

Question 63

1. What are esophageal varices? 2. Often seen with what disorder?

Answer 63

1. abnormal, enlarged veins in the esophagus. Can be small ruptures where patient bleeds out from 2. cirrhosis/portal hypertension - move blood back and one place it increases tension is esophagus vessels

Question 64

1. What is Barrett's Esophagus a complication of? 2. Clinical presentations?

Answer 64

1. GERD - this results in metaplasia of esophageal lining → transforms into lining that is seen in intestine (columnar epithelium and goblet cells) 2. may be asymptomatic or just GERD symptoms

Question 65

1. What is a complication of barrett's esophagus? 2. What type of cancer can this develop into

Answer 65

1. dysplasia (abnormal looking cells) - this is a step before cells turn cancerous. This is treated as a pre-invasive lesion 2. Adenocarcinoma

Question 66

Esophageal adenocarcinoma 1. What does it develop from? 2. Where is it found in esophagus? 3. What should you look for in microscopic imaging to know its adenocarcinoma?

Answer 66

1. Barrett's esophagus 2. In the distal third of esophagus bc that is where reflux is which causes barrett's 3. glandular formation

Question 67

Esophageal Squamous Cell Carcinoma 1. Risk factors for this? 2. Where is it found in esophagus? 3. What should you look for in microscopic imaging to know its adenocarcinoma?

Answer 67

1. squamous dysplasia can lead to this. Alcohol, tobacco, esophageal injury, achalasia 2. anywhere in esophagus (early on it has a small gray-white plaque thickening and later becomes a mass that obstructs lumen) 3. Keratin pearls

Question 68

Erosion vs ulceration

Answer 68

1. Erosion - shedding of the superficial mucosa - no deeper than muscularis mucosa (still mucosa) 2. Ulcer - loss of entire mucosal thickness

Question 69

What is reflux esophagitis?

Answer 69

this is also know as GERD - inflammation of epithelial layer

Question 70

1. What is infectious esophagitis 2. What is eosinophilic esophagitis

Answer 70

1. Commonly caused be candida/HSV-1/CMV - inflammation of esophagus epithelium 2. immune mediated allergic reaction with eosinophilic inflammation. Eosinophils on biopsy

Question 71

Acute gastritis 1. What is it? Chronic gastritis 1. What is it 2. What causes it?

Answer 71

Acute gastritis 1. mucosal damage from too much acid or loss of protection leads to inflammation which has neutrophils Chronic gastritis 1. same as acute but because it is chronic can show atrophy, metaplasia, dysplasia, carcinoma 2. Chronic NSAID use, autoimmune gastritis, H. Pylor

Question 72

Difference between gastritis and gastropathy

Answer 72

Gastritis and gastropathy are conditions that affect the stomach lining, also known as the mucosa. In gastritis, the stomach lining is inflamed. In gastropathy, the stomach lining is damaged, but little or no inflammation is present.

Question 73

1. What is Cushing ulcers 2. What is Curling's ulcers

Answer 73

1. Cushing ulcers: a gastro-duodenal ulcer produced by elevated intracranial pressure caused by an intracranial tumor or head injury. increased intracranial pressure leads to overstimulation of the vagus nerve. As a result, increased secretion of gastric acid may occur which leads to gastro-duodenal ulcer formation known as Cushing's ulcer. 2. Curling's ulcers: a stress-induced ulcer of the stomach or duodenum that occurs in relation to extreme physical stress, such as major surgery

Question 74

What are Type A Chronic Gastritis and Type B Chronic Gastritis?

Answer 74

1. Type A Chronic Gastritis - Pernicious Anemia ;; autoimmune destruction of gastric parietal cells leads to loss of intrinsic factor. You get chronic inflammation in the gastric body/fundus. 2. Type B Chronic Gastritis - H. Pylori Infection ;; infection that can lead to imbalances in mucosal defenses cause ulcers and leads to chronic inflammation in antrum. H.Pylori is associated with MALT lymphoma and gastric adenocarcinoma

Question 75

What is in the therapy for H. Pylori infection? (4)

Answer 75

1. Proton pump inhibitor 2. Clarithromycin 3. Amoxicillin 4. metronidazole

Question 76

1. What is peptic ulcer disease 2. Where is peptic ulcer disease most likely to occur? 3. Symptoms

Answer 76

1. development of solitary ulcer 2. Duodenum (as a result of H. Pylori infection) 3. epigastric pain that improves with eating/food and worse at night. Can should upper GI bleeding. -→ for peptic ulcer disease complications include hemorrhage and obstruction

Question 77

1. If Peptic Ulcer Disease occurs in stomach (gastric ulcer)…where in the stomach is it most likely to occur? 2. How to differentiate from duodenal ulcer

Answer 77

1. lesser curvature of stomach 2. gastric ulcer has epigastric pain that WORSENS with meal and has risk of malignancy (duodenal is usually benign)

Question 78

Gastric carcinoma - Intestinal type 1. What type of cancer? 2. Results due to what? 3. Ulcer description and location 4. Risk factors

Answer 78

1. adenocarcinoma 2. from intestinal metaplasia (as a result of H. Pylori autoimmune/chronic gastritis) - gastritis meaning stomach, particularly antrum of stomach 3. large ulcer with irregular margins found in antrum of stomach 4. Older men, smoking, H. Pylori

Question 79

Gastric carcinoma - Diffuse type 1. What type of cancer? 2. Arises from what cells? 3. Histology shows what feature? 4. Risk factors

Answer 79

1. Adenocarcinoma 2. Thickening of stomach - presents with early satiety. Derived from gastric mucosa cells 3. signet ring cells 4. CDH1 mutation, loss of E-Cadherin, TP53 mutation

Question 80

Gastrointestinal Stromal Tumor (GIST) 1. What is this 2. What cells does it arise from 3. mutations in what gene leads to this

Answer 80

1. a type of cancer that begins in the digestive system. GISTs happen most often in the stomach and small intestine (submucosal lesion). 2. arises from interstitial cells of Cajal (pacemaker cells meant for mixing/stomach movement) 3. c-KIT gene activating mutation

Question 81

Proton pump inhibitors 1. mechanism of action 2. end in what suffix? 3. disorders it is used in?

Answer 81

1. inhibit the H+/K+ ATPase pump in parietal cells resulting in reduced gastric acid secretion → this is irreversible inactivation of proton pumps (for 24-48 hrs) 2. end in -prazole 3. GERD, gastric and duodenal ulcers, in H. Pylori treatment

Question 82

H2 receptor antagonists 1. mechanism of action 2. end in what suffix? 3. disorders it is used in? 4. adverse effects

Answer 82

1. prevent histamine from binding to H2 receptor on gastric parietal cell which prevents gastric acid secretion 2. end in -tidine 3. Mild GERD, gastric reflux that is not chronic 4. confusion and headache; can lead to vitamin B12 deficiency

Question 83

Acid neutralizers (Antacids) 1. mechanism of action 2. Drug names

Answer 83

1. Neutralizes H+ released intro gastric lumen to decrease acid concn 2. Al(OH)3, milk of magnesium, alka seltzer, tums

Question 84

How does pancreatic juices from from acini to main pancreatic duct? (4 steps)

Answer 84

1. Acini (many acini together make a lobule) - Acini contain zymogen granules containing pancreatic enzymes. Acini synthesize and secrete almost all the digestive enzymes active in the lumen of the small intestine 2. Acini drain these juices into intercalated ducts 3. Intercalated ducts drain into intralobar ducts 4. Intralobar ducts drain into main pancreatic duct

Question 85

Pancreatic secretion 1. High or low bicarb? 2. High or low Chloride? 3. Hypo/Hyper/Iso -tonic?

Answer 85

1. High carbohydrate concn - bicarb neutralizes acidic fluid from stomach and allows pancreatic enzymes to function? 2. Low chloride in pancreatic secretion 3. Isotonic

Question 86

What are the functions of the enzymes found in pancreatic secretions? 1. alpha amylase 2. pancreatic lipase 3. phospholipase A2 4. Trypsin/chymotrypsin/elastase/carboxypeptidase

Answer 86

1. hydrolyzes alpha (1,4) linkages between glucose monomers in starch (secreted in active form so don't have to be altered) 2. hydrolyzes 1 and 3 bond triglycerides (fatty acids) 3. hydrolyzes phospholipids (secreted in inactive for so needs to be activated by trypsin) 4. protein digestion enzymes (secreted in inactive form and activated by trypsin)

Question 87

Explain the mechanism of bicarbonate secretion form pancreatic ductal cells (remember bicarb is PRESENT in pancreatic secretions- so it is excreted)

Answer 87

1. bicarb enters into ductal epithelial cells on basolateral side via Na/HCO3 cotransporter + along with diffusion of CO2 into ductal epithelial cells 2. On apical/luminal side of ductal epithelial cells;;; HCO3- is exchanged for Cl- (which is what makes there be bicarb in secretions and less Cl-)

Question 88

What are the 2 functions of bile? (bile is secreted from liver)

Answer 88

1. promote digestion and absorption of dietary lipid and cholesterol 2. Elimination of waste products

Question 89

How do bile salts hep digestion of lipids?

Answer 89

Bile salts act like detergents. They emulsify lipid particles, dissolving particles in water and allowing digestion.

Question 90

1. What is cholestasis (pay attention to the “stasis” part) 2. What symptoms are seen (some symptoms indicate how urine and stool look like)

Answer 90

1. Disrupted bile flow to intestines. 2. Retaining too much bile acids/bile salts - you get hapatocyte injury and pruritus 3. Retaining too much bilirubin - you get jaundice 4. Retaining too much cholesterol - you get xanthomas

Question 91

1. What is cholelithiasis? 2. What are the two types

Answer 91

1. Gallstones 2. Cholesterol (supersaturation of cholesterol in bile) and pigment (excess bilirubin production due to hemolytic anemia or excess recycling of bilirubin)

Question 92

What are esophageal webs?

Answer 92

An esophageal web is a thin (2-3 mm), eccentric, smooth extension of normal esophageal tissue consisting of mucosa and submucosa that can occur anywhere along the length of the esophagus. Cause is unknown.

Question 93

1. What is plummer-vinson syndrome? (classic triad)

Answer 93

***Plummer***-***Vinson syndrome*** (PVS) is a rare condition characterized by the classic triad of dysphagia, iron-deficiency anemia, and esophageal web. Plummer-Vinson syndrome is **a condition that can occur in people with long-term (chronic) iron deficiency anemia**. People with this condition have problems swallowing due to small, thin growths of tissue that partially block the upper food pipe (esophagus).

Question 94

1. What is oropharyngeal dysphagia? 2. What is esophageal dysphagia?

Answer 94

1. Difficulty initiating the swallowing process 2. Difficulty passing food bolus from upper esophagus to stomach. Food sticks after swallowing.

Question 95

1. What general issue is occurring if person has esophageal dysphagia with solid foods only? 2. What general issue is occurring if person has esophageal dysphagia with solid AND liquids?

Answer 95

1. mechanical obstruction 2. neuromuscular disorder

Question 96

Fill in the blank (3 different disorders)

Answer 96

image esophageal rings- a ring of tissue that forms where esophagus and stomach meet

Question 97

Fill in the blank (3 disorders)

Answer 97

image

Question 98

1. What is scleroderma esophagus 2. What is herpes esophagitis

Answer 98

1. In the GI tract, scleroderma can affect the smooth muscle of the esophagus, damaging healthy tissue and replacing it with scar tissue. Scleroderma **causes strictures, or narrowing, of the esophagus and makes the muscle tissue weaker** 2. Esophagitis is inflammation and irritation of the esophagus, and ***herpes esophagitis*** is a rare type that results from an HSV infection. **causing inflammation and ulcers of the esophagus**

Question 99

When a physician makes a mistake what is the framework for best practice disclosure?

Answer 99

1. acknowledgement, explanation, remorse, reparation

Question 99

What is the difference between invasive and non-invasive bacterial diarrhea?

Answer 99

Invasive causes bleeding in the diarrhea (hematochezia) - there is blood and leukocytes due to direct damage to the GI tract. You also get fever.

Question 100

Secretory vs osmotic diarrhea?

Answer 100

1. Secretory - when the body secretes electrolytes into your intestines and this causes water to build up in the intestines 2. Osmotic - involves unabsorbed substances in the intestines that draws water out from plasma and into intestinal lumen.

Question 101

What bacteria cause food borne illness that manifests mainly in vomiting?

Answer 101

1. Staph aureus (enterotoxin producing) 2. B. Cereus *both do not show person to person spread*

Question 102

What bacteria cause food borne illness that manifests mainly in diarrhea?

Answer 102

1. C. perfringens (watery diarrhea)

Question 103

Humans are the only host of what parasite?

Answer 103

pinworm (E. Vermicularis)

Question 104

1. What is the life cycle of the pinworm? 2. What test is done to check for pinworm infestation?

Answer 104

* Eggs laid by adult female worms at night in the perianal area. * These eggs are spread after hosts touches perianal area and then other person ingests this * Then larvae hatch in small intestine and migrate to perianal region, lay eggs, and cycle repeats * Scotch tape test - seeing eggs on tape laid in perianal area at night and removed in morning

Question 105

Describe the pathogenic strain of E. Coli (EPEC) 1. presentation 2. method of infecting

Answer 105

1. shows with pediatric diarrhea in developing countries. 2. Pili/adhesions allow bacterial attachment to small intestine epithelial cells. (not toxin)

Question 106

Describe the enteroinvasive strain of E. Coli (EIEC) 1. presentation 2. method of infecting

Answer 106

1. Dysentery 2. Penetrates intestinal epithelium through M cells to gain access to submucosa (like shigella)

Question 107

Describe the Toxigenic strain of E. Coli (ETEC) - “traveler's diarrhea” 1. presentation 2. method of infecting (hint: toxins) 3. Treatment

Answer 107

1. watery diarrhea w/o inflammation 2. LT (heat labile toxin) - increases cAMP and leads to increased H2O secretion ----- ST (heat stabile toxin) - increases cGMP and leads to increased H2O secretion 3. azithromycin/ciprofloxacin

Question 108

Describe the Hemorrhagic strain of E. Coli (EHEC) 1. presentation 2. method of infecting 3. tx 4. O:H ratio?

Answer 108

1. shiga-toxin producing e.coli - bloody diarrhea (dysentery) 2. attach to mucosa of large intestine similar to EPEC (M cells) 3. ANTIBIOTICS are CONTRAINDICATED - just do supportive tx 4. O157:H7 ratio

Question 109

Protozoal Diarrhea Giardia Intestinalis 1. presentation 2. treatment

Answer 109

1. foul smelling fatty diarrhea 2. metronidazole

Question 110

Protozoal Diarrhea Entamoeba Histolytica 1. presentation 2. treatment

Answer 110

1. dysentery, liver abscesses – Trophozoites with RBCs in cytoplasm 2. metronidazole

Question 111

Protozoal Diarrhea Cryptosporidium 1. presentation

Answer 111

1. water, self limited diarrhea in immunocompetent patients → acid fast oocysts

Question 112

Protozoal Diarrhea Balantidum coli 1. presentation

Answer 112

1. diarrhea - largest protozoan that infects humans

Question 113

Protozoal Diarrhea Cyclospora 1. presentation

Answer 113

1. diarrhea in traveler's or from contaminated imported foods - more severe in immunocompromised

Question 114

Intestinal Nematodes Taenia Solium 1. presentation

Answer 114

1. neurocysticercosis (a preventable parasitic infection of the central nervous system)

Question 115

Differentiate between 1. Ascaris lumbricoides 2. Trichinella spiralis 3. Enterobius Vermicularis

Answer 115

1. thick-shelled eggs that creates very long worms. These long worms can obstruct ileocecal valve 2. Trichinella spiralis - cause fever, vomiting, MYALGIAS - encyst in striated muscle cells 3. Remember scotch tape taste - worms migrate to perianal region

Question 116

Viral Diarrhea Norovirus (A calicivirus) 1. presentation 2. How is it spread/infectious dose needed 3. duration

Answer 116

1. epidemics of diarrhea and vomiting - most common cause of epidemic gastroenteritis worldwide 2. Low infectious dose - highly infectious 3. 1-3 days

Question 117

Viral Diarrhea Rotavirus (A Reovirus) 1. presentation 2. prevention?

Answer 117

1. PEDIATRIC (\<4 years old) vomiting and fever (uncommon in adults) 2. vaccine given to kids

Question 118

Viral Diarrhea Adenovirus 1. presentation 2. duration/season of presentation

Answer 118

1. conjunctivitis, hemorrhagic cystitis, pediatric gastroenteritis in summer 2. peak is during summer

Question 119

Viral Diarrhea ECHO (enteric cytopathic human orphan) virus 1. presentation

Answer 119

1. can cause mild gastroenteritis but most manifestations are extraintestinal (like aseptic meningitis)

Question 120

What are the two toxins of clostridium difficile and what do they each do?

Answer 120

1. Toxin A (enterotoxin) - binds to brush border of gut and disrupts normal flora of large intestine 2. Toxin B (cytotoxin) - cytoskeletal disruption via actin depolymerization → leads to pseudomembranous colitis (swelling or inflammation of the large intestine (colon) due to an overgrowth of C diff bacteria)

Question 121

Clostridium difficile 1. how is it treated? 2. symptoms

Answer 121

1. oral vancomycin (MAIN ONE)….fecal transplant 2. Mild to severe diarrhea that can lead to sepsis or death – antibiotic associated or hospital acquired diarrhea

Question 122

Bacterial Diarrhea Salmonella spp 1. How is it transmitted usually 2. What are the types 3. unique agar finding

Answer 122

1. Both types are transmitted via contaminated food (poultry or dairy) and also person to person spread 2. Salmonella typhi and salmonella enteritidis 3. only on salmonella enteritidis: black colonies on Hektoen agar bc it makes H2S

Question 123

Salmonella typhi vs enteritidis Differences in symptoms

Answer 123

1. Typhi - constipation then diarrhea but symptoms start 5-21 days after ingestion and improve over weeks or months. Can show fever, rose spots, abdominal pain, intestinal bleeding 2. Enteritidis - Watery Diarrhea, sometimes bloody (don't give antibiotics bc this typically prolongs excretion of salmonella)

Question 124

Salmonella typhi 1. prevention methods? 2. tx?

Answer 124

1. preventative vaccines against the virulence factors 2. azithromycin if uncomplicated but ceftriaxone if severe

Question 125

Bacterial Diarrhea Shigella 1. presentation

Answer 125

1. watery diarrhea followed by dysentery

Question 126

Bacterial Diarrhea Vibrio cholera (cholera) 1. presentation 2. pathogenesis 3. tx

Answer 126

1. rice water stools w/no blood or WBCs 2. overactivation of cAMP which leads to extreme H2O secretion 3. oral rehydration

Question 127

Bacterial Diarrhea Vibrio parahaemolyticus 1. what does it cause? 2. from what source?

Answer 127

1. gastroenteritis 2. raw shellfish

Question 128

Bacterial Diarrhea Campylobacter Jejuni 1. presentation 2. how is it spread 3. complications from this?

Answer 128

1. Bloody diarrhea (#1 cause in USA) 2. spread via poultry 3. Guillain-barre syndrome, reactive arthritis

Question 129

Bacterial Diarrhea Yersinia Enterocolitica 1. presentation 2. how is it spread

Answer 129

1. diarrhea, pseudoappendicitis pain 2. pet feces and pork

Question 130

H pylori 1. how is it diagnosed?

Answer 130

1. Urea breath test - H. pylori produces an enzyme called urease, which **breaks urea down into ammonia and carbon dioxide**. During the test, a tablet containing urea is swallowed and the amount of exhaled carbon dioxide is measured.

Question 131

1. How do chief cells look differently to parietal cells and DNES cells in histology 2. what do you stain DNES cells with?

Answer 131

1. silver stain

Question 132

What do mucous cells look like - histology?

Answer 132

Question 133

The left gastric artery branches directly from the celiac trunk - after which it splits again - one part continues to lesser curvature of the stomach while the other part ascends towards the (Blank)

Answer 133

1. abdominal esophagus

Question 134

omeprazole and esomeprazole (PPI) inhibit CYP2C19 and increases serum concn. of (3)

Answer 134

1. diazepam 2. citalopram 3. phenytoin

Question 135

1. What change to ionic composition of saliva would be achieved with vagal stimulation? 2. What structure in the esophagus is controlled by efferents from the dorsal motor nucleus? 3. What pressure change happens immediately after the UES opens during swallowing?

Answer 135

1. High HCO3- content 2. lower esophagus 3. a decrease in gastric pressure

Question 136

1. Vagal stimulation causes what gastric motility pattern? 2. How does acute gastritis cause excessive acid production?

Answer 136

1. gastric accomodation reflex 2. increased ECL cell (**endocrine cells of the stomach - release histamine)** stimulation

Question 137

What is the best way to distinguish between inflammatory and secretory diarrhea with a bacterial etiology?

Answer 137

Fecal lactoferrin is a marker of white blood cell presence. released from PMNs. Therefore, presence or absence of fecal indicative of fecal white blood cells and an inflammatory mechanism