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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
What is the complication of acute gastroenteritis?
fluid volume deficit = increase HR
26
What is peptic ulcer disease?
upper GI tract ulcerative disorders (esophagus, stomach, duodenum) develops when GIT is exposed to acid and pepsin
27
What are aggressive factors r/t ulcers?
H. pylori, NSAIDs, acid, pepsin, smoking
28
What are defensive factors r/t ulcers?
mucus, bicarbonate, blood flow, prostaglandins
29
What are the causes of peptic ulcer disease PUD?
H. pylori, NSAIDs, ASA, alcohol, excess secretion of acid, stress, smoking, family history
30
How does H. pylori cause PUD?
it sets up a colony and grows in the lining causing gastritis
31
How do NSAIDs cause PUD?
they decrease the secretion of COX-1 and COX-2 (COX-1 protects gastric mucosa by secreting prostaglandin E)
32
What are the risk factor for NSAID-induced PUD?
age, higher does of NSAIDs, history of PUD, use of corticosteroids and anticoagulants, serious systemic disorders, H. pylori
33
What is the pathogenesis of PUD?
mucosa is damaged, histamine is secreted resulting in increase acid and pepsin secretion (causes further tissue damage) and vasodilation (edema)
34
Duodenal Ulcer
most common type, any age/early adulthood
35
Gastric Ulcer
peak 50-70 year olds d/t NSAID use
36
What are the clinical manifestations of PUD?
sometimes none, N/V, anorexia, weight loss, bleeding, pain
37
What kind of pain is associated with a gastric ulcer?
burning, cramping, gas-like, epigastrium and back, 1-2 hours after eating
38
What kind of pain is associated with a duodenal ulcer?
burning, cramping, gas-like, epigastrium and back, 2-4 hours after eating
39
What are the complications of PUD? (HOP)
H - hemorrhage O - obstruction P - perforation and peritonitis
40
What kind of drugs increase protective factors in the UGI?
antacids, sucralfate
41
What kind of drugs decrease aggressive factors in the UGI?
treat H. pylori, H2 blockers, proton pump inhibitors
42
MOA of antacids
Large doses: neutralizes acid - 50% Small doses: increased secretion of mucous, PGE, HCO3
43
Indication of antacids
PUD (healing) GERD (symptoms) Stress ulcers (prophylaxis)
44
Major forms of antacids
Aluminum (Al) - Basajel Calcium (Ca) - Tums Magnesium (Mg) - Milk of Magnesia Al+Mg - Maalox, Mylanta
45
AE of antacids
diarrhea or constipation, acid rebound
46
Interactions with antacids
chelation = altered gastric absorption of other meds
47
What is sucralfate composed of?
sucrose base and aluminum hydroxide
48
MOA of sucralfate
alters when exposed to gastric acid, forms a sticky/thick gel for protective barrier
49
Indication of sucralfate
duodenal ulcers, gastric ulcers
50
Mode of delivery of sucralfate
PO- tablet or suspension
51
AE of sucralfate
No major AE
52
Interactions with sucralfate
decreased drug absorption, if PO take drugs 2 hours apart, DO NOT take with antacids
53
What kind of drugs do you use to treat H. pylori?
several antibiotics + gastric acid inhibitor metronidazole, tetracycline, bismuth, PPI or H2 blocker
54
Why use combination therapy when treating H. pylori?
to minimize resistance, H. pylori likes acidic environments so try to decrease the acid
55
Length of Rx for H. pylori?
10-14 days
56
How is adherence to treatment for H. pylori?
not good expensive - $200 up to 12 pills over 2 weeks
57
H2RA Prototypes
cimetidine famotidine
58
MOA of H2RA
block H2 receptor reduces gastric acid secretion
59
Indication for H2RA
GERD - relieves symptoms PUD - promotes healing, prophylaxis
60
AE of H2RA
well tolerated, CNS effects in elderly, slight increased risk for pneumonia in elderly
61
Interactions with H2RA
inhibits CYP 450 enzymes (but newer generation H2RAs do not have this problem)
62
Proton Pump Inhibitors (PPI) prototypes
omeprazole pantoprazole
63
MOA of PPIs
binds to proton pump irreversibly inhibits the secretion of HCl
64
Indication for PPIs
short term treatment of PUD and GERD
65
AE of PPIs
short term: safe, few AEs long term: pneumonia, hip fracture, stomach cancer
66
Interactions with PPIs
a few interactions - works very well
67
prototype of pro kinetic agent
metoclopramide
68
MOA of pro kinetic agent
increases upper GI motility, suppresses emesis
69
indications for pro kinetic agent
GERD chemo-induced N/V or post-op N/V
70
AE of metoclopramide
many AE neuron: sedation or restlessness extrapyramidal reactions
71
interactions with metoclopramide
there are many, use cautiously
72
Extrapyramidal Reactions
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
Relationship between V B12 and Intrinsic Factor
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
What is the cause pernicious anemia?
IF and B12 deficiency

EXAM 2 - NUR 228 (6 decks)

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