GI 1

Question 1

If transition time is too slow or too fast, what can occur?

Answer 1

increased reabsorption of H2O —> constipation and obstruction

decreased reabsorption of H2O = diarrhea

Question 2

what is the active BMR for adults?

Answer 2

10cal/lb

Question 3

what situations can patients go NPO for?

Answer 3

unconsciousness, before/after surgery

Question 4

what is the average time it should take for patients to be no longer NPO?

Answer 4

usually after 24 hours

Question 5

is more than 5 days being NPO normal?

Answer 5

no, it is not normal to be NPO for >5 days

Question 6

what are the 3 main digestive functions

Answer 6

transport - (peristalsis)
absorption - villi in SI + water reabsorption in LI
digestive enzymes - HCl + enzymes, pancreatic juice, bile

Question 7

name the 2 main parts of the GI system

Answer 7

alimentary canal -> oral cavity -> rectum
accessory organs -> liver, gallbladder, pancreas, salivary glands

Question 8

what kind of digestion occurs in the stomach; name the structures that allow these to occur

Answer 8

mechanical digestion (gastric pits lines with mucous cells + specialized gastric cells) and chemical digestion (HCl)

Question 9

what is the pH range within the stomach?

Answer 9

pH = 1.5 to 3.5

Question 10

which type of cell is targeted when we want to decrease the acidity of the stomach and why?

Answer 10

the parietal cells are targeted as their main function is to synthesis HCl

Question 11

in what 2 populations does HCl production decrease?

Answer 11

in older adults and pregnant women

Question 12

which enzyme allows parietal cells to synthesize HCl?

Answer 12

sodium/potassium ATPase aka “proton pump”

Question 13

what are the 3 stimulus that are required for parietal cells to secrete HCl

Answer 13

gastrin from G cells
histamine from enteroendocrine (enterochromaffin) cells -> site of gastric histamine synthesis
acetylcholine from the parasympathetic nervous system = Ach receptors

Question 14

what do chief cells secrete and what is the function?

Answer 14

chief cells secrete pepsinogen which turns into pepsin in the presence of HCl; pepsin is used for protein digestion

Question 15

3 benefits of HCl

Answer 15

chemical digestion of food
destruction of pathogens (aka lowering numbers)
nutrient absorption (intrinsic factor synthesis for Vitamin B12 absorption; ferric iron -> ferrous iron GI absorption)

Question 16

Prostaglandin E2 stimulates what cells and what is the effect of NSAIDs on PGE2?

Answer 16

PGE2 stimulates mucous cells to secrete mucous to protect the stomach

NSAIDS can decrease PGE2 and this can lead to peptic ulcers due to less mucous production

Question 17

what is the pH of the duodenum + jejunum?

Answer 17

pH of 7, more alkaline than the stomach

Question 18

how much alkaline serous fluid is made by the intestinal mucosa

Answer 18

(2L/day)

Question 19

which NSAID drug is able to be absorbed by the gastric mucosa?

Answer 19

ASA

Question 20

what 2 conditions is HCl acid control required?

Answer 20

reflux and peptic ulcer disease (PUD)

Question 21

describe the 2 pathophysiological pathways that lead to reflux and GERD

Answer 21

reflux can occur when transient relaxations of the lower esophageal sphincter occurs, allowing stomach contents to enter the esophagus.

delayed gastric emptying d/t stress, immobility, over-eating, congenital syndromes

Question 22

name 4 examples of events that allow for reflux to happen

Answer 22

spicy food, caffeine, carbonated beverages, increased abdominal pressure (d/t obesity + pregnancy

Question 23

name 3 clinical presentations of reflux

Answer 23

pain (heartburn, chest pain), decreased appetite (d/t pain), bleeding (hematemesis)

Question 24

3 complications of reflux (more serious)

Answer 24

weight loss
reflux esophagitis —> GERD
respiratory/airway erosion

Question 25

what complication can GERD create and how

Answer 25

GERD can lead to Barrett’s esophagus which is a condition that can increase the risk of cancer. Repeated scarring esophageal tissue can lead to cell morphing.

Question 26

2 treatments for reflux

Answer 26

avoiding irritants decreasing acidity via medications

Question 27

3 drug classes used to treat reflux

Answer 27

antacids, proton pump inhibitors, H2 antagonists

Question 28

what is the effect of antacids?

Answer 28

increasing stomach pH, however, not by decreasing HCl secretions

Question 29

when should/shouldn’t you use antacids?

Answer 29

use for symptom relief do not use for chronic reflux or when taking other medications

Question 30

how long before/after should you wait to take other PO meds when taking antacids?

Answer 30

you should wait at least 2 hours before/after taking antacids to avoid affecting other drugs

Question 31

name 4 common minerals used in antacids and determine their side effects

Answer 31

aluminum can cause constipation magnesium can cause diarrhea calcium can cause kidney stones sodium can affect blood pressure

Question 32

what is the effect of proton pump inhibitors?

Answer 32

PPIs bind to sodium potassium ATPase to inhibit the proton pump -> decreasing HCl secretions

Question 33

name 3 PPI drugs and determine if it needs a prescription

Answer 33

Omeprazole (Losec) Lansoprazole (Prevacid) Pantoprazole (Pantoloc) PPIs require prescription d/t its high efficacy

Question 34

determine the effects of H2 receptor antagonists

Answer 34

they are selective (H2 specific) and decrease HCl by blocking the gastric histamine pathway

Question 35

determine the drug schedule of H2 receptor antagonist drugs

Answer 35

H2 receptor antagonist drugs are unscheduled

Question 36

name 3 H2 receptor antagonist drugs; which drug does not cross the BBB and why is it a benefit?

Answer 36

Ranitidine (Zantac) - does not cross BBB; those that cross BBB can bind to H1 receptors and cause side effects Cimetidine (Tegamet) Famotidine (Pepcid)

Question 37

surgery can be undertaken to reduce reflux and how does it help?

Answer 37

fundoplication is when the fundus of the stomach is wrapped around the LES to narrow the sphincter and decrease the risk of reflux.

Question 38

which is more efficacious in chronic reflux: PPIs or H2 receptor antagonists, and how?

Answer 38

PPIs are more efficacious because they are stronger, while H2 receptor antagonists are used for acute treatment/pain relief

Question 39

describe the pathophysiology of peptic ulcer disease

Answer 39

the failure of endogenous protection (tight mucosal cell junctions & mucous/bicarbonate layer) which causes mucosal inflammation and erosion of stomach/duodenum

Question 40

4 clinical presentations of PUD

Answer 40

pain anorexia d/t pain bleeding (emesis/stool) anemia

Question 41

3 common causes of PUD

Answer 41

stress d/t decreased mobility, increased HCl H. pylori infection d/t stress NSAID overuse (d/t decreased PGs = decreased mucosal barrier)

Question 42

individuals who have PUD are at risk for (3 serious complications)

Answer 42

perforation (into the peritoneal space), obstruction, and cancer

Question 43

which part of the GI is PUD more likely to occur?

Answer 43

more common in the duodenum (4x more likely) than the stomach

Question 44

Describe how H. pylori can cause GI issues

Answer 44

H. pylori makes an enzyme (urease) which makes surrounding are more alkaline by creating ammonia (increase pH); ammonia damages gastric mucosa

Question 45

how can we test for ammonia caused by H. pylori?

Answer 45

through a breathalyzer test or through stool culture

Question 46

percentage of presence of H. pylori in duodenal and gastric ulcers, respectively.

Answer 46

duodenal = 90% gastric = 75%

Question 47

how much time is needed for a patient to be off PPIs so that an H. pylori infection can be detected?

Answer 47

2 weeks prior

Question 48

what is the focus for PUD treatment?

Answer 48

decrease of acidity to kill H. pylori

Question 49

what is the 1st line therapy for PUD? (4 drugs)

Answer 49

PPIs, amoxicillin, clarithromycin, metronidazole