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EXAM 2 - NUR 228 > EXAM 2 - UGI > Flashcards

EXAM 2 - UGI Flashcards

1
Q

Which cells secrete HCl in the stomach to help with digestion?

A

Parietal cells

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2
Q

Two esophageal disorders

A

GERD, hiatal hernia

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3
Q

Three inflammatory disorders of the stomach

A

gastritis, actue gastroenteritis, PUD

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4
Q

What is Dysphagia?

A

difficulty swallowing; begins with solids and progresses to liquids; concerned with aspiration

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5
Q

What can cause Dysphagia?

A

mechanical obstruction (stenosis, stricture, diverticula, tumors)
neuromuscular dysfunction (CVA, achalasia)

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6
Q

What is GERD?

A

gastroesophageal reflux disease
backflow from the stomach into esophagus; occurs via the LES; highly acidic material

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7
Q

What can GERD result in?

A

inflammation, pain, ulceration, scarring, strictures, Barrett’s esophagus

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8
Q

What is the cause of GERD?

A

anything that alters closure strength of LES or increases abdominal pressure (fatty foods, caffeine, alcohol, smoking, sleep flat on back)

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9
Q

What are the clinical manifestations of GERD?

A

heartburn (pyrosis), dyspepsia, regurgitation, chest pain, dysphagia, pulmonary symptoms

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10
Q

What are the causes of esophagitis?

A

other than GERD… infection, chemical ingestion, drugs, frequent emesis

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11
Q

What is a hiatal hernia?

A

a defect in the diaphragm that allows part of the stomach to pass into the thorax

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12
Q

Two main types of hiatal hernias

A

sliding hernia
paraesophageal hernia

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13
Q

What are the risk factors for a hiatal hernia?

A

age, anything that loosens the muscular band around the gastroesophageal junction

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14
Q

What are the clinical manifestations of a hiatal hernia?

A

asymptomatic, or the same as GERD

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15
Q

What is acute gastritis?

A

temporary inflammation of the stomach lining

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16
Q

What causes acute gastritis?

A

irritating substances (alcohol), drugs (NSAIDs), infection

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17
Q

What is chronic gastritis?

A

a progressive disorder with chronic inflammation in the stomach

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18
Q

What causes chronic gastritis?

A

autoimmune (attack parietal cells), H. Pylori

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19
Q

What is Helicobacter pylori?

A

a bacteria that grows in an acidic environment, produces urease that neutralizes stomach acid

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20
Q

What can H. pylori cause?

A

persistent inflammation, chronic gastritis, PUD, stomach cancer

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21
Q

How is H. pylori transmitted?

A

orally (food)

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22
Q

What are the clinical manifestations for acute or chronic gastritis?

A

sometimes none, anorexia, N/V, postprandial discomfort, hematemesis, anemia

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23
Q

What is acute gastroenteritis?

A

inflammation of the stomach and small intestine

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24
Q

What are the clinical manifestations of acute gastroenteritis?

A

diarrhea, abdominal pain, N/V, fever, malaise

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25
Q

What is the complication of acute gastroenteritis?

A

fluid volume deficit = increase HR

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26
Q

What is peptic ulcer disease?

A

upper GI tract ulcerative disorders (esophagus, stomach, duodenum)
develops when GIT is exposed to acid and pepsin

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27
Q

What are aggressive factors r/t ulcers?

A

H. pylori, NSAIDs, acid, pepsin, smoking

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28
Q

What are defensive factors r/t ulcers?

A

mucus, bicarbonate, blood flow, prostaglandins

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29
Q

What are the causes of peptic ulcer disease PUD?

A

H. pylori, NSAIDs, ASA, alcohol, excess secretion of acid, stress, smoking, family history

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30
Q

How does H. pylori cause PUD?

A

it sets up a colony and grows in the lining causing gastritis

31
Q

How do NSAIDs cause PUD?

A

they decrease the secretion of COX-1 and COX-2 (COX-1 protects gastric mucosa by secreting prostaglandin E)

32
Q

What are the risk factor for NSAID-induced PUD?

A

age, higher does of NSAIDs, history of PUD, use of corticosteroids and anticoagulants, serious systemic disorders, H. pylori

33
Q

What is the pathogenesis of PUD?

A

mucosa is damaged, histamine is secreted resulting in increase acid and pepsin secretion (causes further tissue damage) and vasodilation (edema)

34
Q

Duodenal Ulcer

A

most common type, any age/early adulthood

35
Q

Gastric Ulcer

A

peak 50-70 year olds d/t NSAID use

36
Q

What are the clinical manifestations of PUD?

A

sometimes none, N/V, anorexia, weight loss, bleeding, pain

37
Q

What kind of pain is associated with a gastric ulcer?

A

burning, cramping, gas-like, epigastrium and back, 1-2 hours after eating

38
Q

What kind of pain is associated with a duodenal ulcer?

A

burning, cramping, gas-like, epigastrium and back, 2-4 hours after eating

39
Q

What are the complications of PUD? (HOP)

A

H - hemorrhage
O - obstruction
P - perforation and peritonitis

40
Q

What kind of drugs increase protective factors in the UGI?

A

antacids, sucralfate

41
Q

What kind of drugs decrease aggressive factors in the UGI?

A

treat H. pylori, H2 blockers, proton pump inhibitors

42
Q

MOA of antacids

A

Large doses: neutralizes acid - 50%
Small doses: increased secretion of mucous, PGE, HCO3

43
Q

Indication of antacids

A

PUD (healing)
GERD (symptoms)
Stress ulcers (prophylaxis)

44
Q

Major forms of antacids

A

Aluminum (Al) - Basajel
Calcium (Ca) - Tums
Magnesium (Mg) - Milk of Magnesia
Al+Mg - Maalox, Mylanta

45
Q

AE of antacids

A

diarrhea or constipation, acid rebound

46
Q

Interactions with antacids

A

chelation = altered gastric absorption of other meds

47
Q

What is sucralfate composed of?

A

sucrose base and aluminum hydroxide

48
Q

MOA of sucralfate

A

alters when exposed to gastric acid, forms a sticky/thick gel for protective barrier

49
Q

Indication of sucralfate

A

duodenal ulcers, gastric ulcers

50
Q

Mode of delivery of sucralfate

A

PO- tablet or suspension

51
Q

AE of sucralfate

A

No major AE

52
Q

Interactions with sucralfate

A

decreased drug absorption, if PO take drugs 2 hours apart, DO NOT take with antacids

53
Q

What kind of drugs do you use to treat H. pylori?

A

several antibiotics + gastric acid inhibitor
metronidazole, tetracycline, bismuth, PPI or H2 blocker

54
Q

Why use combination therapy when treating H. pylori?

A

to minimize resistance, H. pylori likes acidic environments so try to decrease the acid

55
Q

Length of Rx for H. pylori?

A

10-14 days

56
Q

How is adherence to treatment for H. pylori?

A

not good
expensive - $200
up to 12 pills over 2 weeks

57
Q

H2RA Prototypes

A

cimetidine
famotidine

58
Q

MOA of H2RA

A

block H2 receptor
reduces gastric acid secretion

59
Q

Indication for H2RA

A

GERD - relieves symptoms
PUD - promotes healing, prophylaxis

60
Q

AE of H2RA

A

well tolerated, CNS effects in elderly, slight increased risk for pneumonia in elderly

61
Q

Interactions with H2RA

A

inhibits CYP 450 enzymes (but newer generation H2RAs do not have this problem)

62
Q

Proton Pump Inhibitors (PPI) prototypes

A

omeprazole
pantoprazole

63
Q

MOA of PPIs

A

binds to proton pump
irreversibly inhibits the secretion of HCl

64
Q

Indication for PPIs

A

short term treatment of PUD and GERD

65
Q

AE of PPIs

A

short term: safe, few AEs
long term: pneumonia, hip fracture, stomach cancer

66
Q

Interactions with PPIs

A

a few interactions - works very well

67
Q

prototype of pro kinetic agent

A

metoclopramide

68
Q

MOA of pro kinetic agent

A

increases upper GI motility, suppresses emesis

69
Q

indications for pro kinetic agent

A

GERD
chemo-induced N/V or post-op N/V

70
Q

AE of metoclopramide

A

many AE
neuron: sedation or restlessness
extrapyramidal reactions

71
Q

interactions with metoclopramide

A

there are many, use cautiously

72
Q

Extrapyramidal Reactions

A

the extrapyramidal system (EPS) is a network of neurons in the brain that coordinate movement
EP reactions can occur in response to drugs
symptoms: akinesia, akathesis, tardive dyskinesias

73
Q

Relationship between V B12 and Intrinsic Factor

A
  1. acid degrades meat, releasing B12
  2. parietal cells secrete intrinsic factor
  3. in duodenum, B12 binds to IF
  4. IF shuttles B12 into cells of ileum
  5. B12 helps produce hemoglobin
74
Q

What is the cause pernicious anemia?

A

IF and B12 deficiency

EXAM 2 - NUR 228 (6 decks)

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