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NUR 326 Exam 3 > Upper GI Disorders > Flashcards

Upper GI Disorders Flashcards

1
Q

Upper GI problems are composed of what organs? (3)

A

esophagus
stomach
BEGINNING of small intestines

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2
Q

Lower GI problems are composed of what organs? (3)

A

small intestines
colon (large intestines)
rectum/anus

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3
Q

What are the esophageal disorders? (2)

A

GERD (Gastroesophageal reflux disease)
Hiatal Hernia

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4
Q

What are the inflammatory disorders of the stomach? (3)

A

Gastritis
Acute Gastroenteritis
PUD (peptic ulcer disease)

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5
Q

Dysphagia: Definition

A

difficulty swallowing
(begins with solids and progresses to liquids)

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6
Q

Dysphagia: Causes

A
  1. Mechanical obstruction
    Stenosis or stricture
    Diverticula (w/in esophagus)
    Tumors
  2. Neuromuscular dysfunction
    CVA
    Achalasia (LES can’t open properly
    People with trachs or that were intubated (can get better)
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7
Q

GERD: Definition

A

AKA “heartburn”
Backflow of gastric acid from the stomach into the esophagus
Occurs via the lower esophageal sphincter (LES): doesn’t close properly
Highly acidic material

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8
Q

GERD: Etiology

A

Anything that alters closure strength of LES
OR
increases abdominal pressure

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9
Q

GERD: Etiology Examples (11)

A

fatty foods
spicy foods
tomato based foods
citrus foods
caffeine
large amounts of alcohol
cigarette smoking
sleep position
obesity
pregnancy
pharmacologic agents

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10
Q

GERD: Clinical Manifestations (CM) (6)

A

heartburn (pyrosis)
dyspepsia
regurgitation
chest pain
dysphagia
pulmonary symptoms

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11
Q

GERD: Mouth CM (3)

A

tooth decay
gingivitis
bad breath

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12
Q

GERD: Ears CM (1)

A

earache

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13
Q

GERD: Chest CM (3)

A

chronic cough
worsening asthma
recurrent pneumonias

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14
Q

GERD: Throat CM (6)

A

hoarseness
chronic sore throat
throat clearing
laryngitis
lump in throat
post nasal drip

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15
Q

GERD: Complications

A

ulceration
scarring
strictures
Barrett esophagus

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16
Q

GERD: Barrett esophagus

A

development of abnormal metaplastic tissue- premalignant
3-fold increased risk of developing adenocarcinoma of the esophagus
over all survival only 17%

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17
Q

Hiatal Hernia: Definition

A

A defect in the diaphragm that allows part of the STOMACH to pass INTO the THORAX

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18
Q

Hiatal Hernia: Main Types (2)

A
  1. Sliding hernia
  2. Paraesophageal hernia
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19
Q

Type 1: Sliding Hernia

A

usually small and often does not need treatment

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20
Q

Type 2: Paraesophageal Hernia

A

part of the stomach pushes through the diaphragm and stays there

21
Q

Hiatal Hernia: Pathophysiology

A

Exact cause is unknown
Age related
Injury or other damage may weaken the diaphragm muscle
Repeatedly putting too much pressure on the muscles around the stomach (severe coughing, vomiting, constipation and straining to have a BM)

22
Q

Hiatal Hernia: Risk Factors (3)

A

age
obesity
smoking

23
Q

Hiatal Hernia: CM (5*)

A

asymptomatic
belching
dysphagia
chest or epigastric pain
*common for GERD and Hiatal Hernia to coexist

24
Q

Hiatal Hernia: Treatment

A

Mostly a conservative treatment:
Teaching: small,
frequent meals, avoid
lying down after eating
Avoid tight clothing and
abdominal supports
Weight control for
obese individuals
Antacids for the
GERD/esophagitis
symptoms
Surgery if the conservative treatments don’t work

25
Q

Gastritis: Definition

A

inflammatory condition of the stomach

26
Q

ACUTE Gastritis: Definition

A

Temporary inflammation of the stomach lining ONLY (intestines NOT affected)
Generally last from 2-10 days

27
Q

ACUTE Gastritis: Etiology (3)

A

irritating substance (alcohol)
drugs (NSAIDs)
infectious agents

28
Q

CHRONIC Gastritis

A

Progressive disorder with chronic inflammation in the stomach
Can last weeks to years

29
Q

CHRONIC Gastritis: Complications (4)

A

PUD
bleeding ulcers
anemia
gastric cancers

30
Q

CHRONIC Gastritis: Main Etiologies (2)

A

Autoimmune: attacks parietal cells
H. pylori infection

31
Q

What is H. pylori?

A

Helicobacter pylori bacterium
Gram negative spiral bacteria that thrives in an ACIDIC environment
When it becomes overgrown, causes destructive pattern of persistent inflammation
Can cause chronic gastritis, PUD, and stomach cancer

32
Q

How is H. pylori transmitted?

A

person to person via: saliva, fecal matter, or vomit
OR
contaminated food or water

33
Q

Acute OR Chronic Gastritis CM (10)

A

sometimes none
anorexia
N/V
stomach burn
upset stomach
postprandial discomfort (symptoms soon after you eat)
intestinal gas
hematemesis (blood in vomit)
tarry stools
anemia

34
Q

Acute Gastroenteritis: Definition

A

inflammation of stomach AND small intestine
Usually lasts 1-3 days but may last as long as 10 days

35
Q

Acute Gastroenteritis: Etiology (3)

A

Viral infections: Norovirus and rotavirus
Bacterial infections: E. coli, salmonella, and campylobacter
Parasitic infections

36
Q

Acute Gastroenteritis: CM (4)

A

watery diarrhea (may be bloody if bacterial)
abdominal pain
N/V
Fever, malaise

37
Q

Acute Gastroenteritis: Complication (1)

A

fluid volume deficits (worried about dehydration)

38
Q

Peptic Ulcer Disease (PUD): Definition

A

Ulcerative disorder of the upper GI tract
ulcer in esophagus:
esophageal ulcer
ulcer in stomach:
gastric ulcer
ulcer in duodenum:
peptic ulcer
Develops when the GI tract is exposed to acid and H. pylori

39
Q

Aggressive Factors for Developing Ulcers? (5)

A

H. pylori
NSAIDs
Too much acid secretion
Pepsin
Smoking

40
Q

Defensive Factors to help GI Tract? (4)

A

Mucus
Bicarbonate
Increase blood Flow
Prostaglandins

41
Q

PUD: Etiology (6)

A

H. pylori
injury causing substances (NSAIDs, ASA, alcohol)
excess secretion of acid
smoking
family history
stress (increased gastric acid secreted with the stress response)

42
Q

Risk factors: NSAID-Induced PUD (6)

A

age
higher doses of NSAIDs
history of PUD
use of corticosteroids and anticoags
serious systemic disorders
H. pylori infection

43
Q

PUD: Pathogenesis

A

Mucosa is damaged
Histamine is secreted resulting in:
increase in acid and
pepsin secretion- causes
further tissue damage
vasodilation- causes
edema
If blood vessels are destroyed, this results in BLEEDING

44
Q

PUD: Classification

A

DUODENAL Ulcer: most common type, age- any; early adulthood

Gastric/peptic ulcer: age- peak 50-70;
why?
increased use of NSAIDs, corticosteroids, anticoags, and more likely to have serious systemic illnesses

45
Q

PUD: CM (6)

A

sometimes none
N/V
anorexia
weight loss
bleeding
burning pain- in middle of abdomen that is usually when the stomach is empty

46
Q

Gastric Ulcer: Pain characterisitcs, location, timing

A

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

47
Q

Duodenal Ulcer: Pain characterisitcs, location, timing

A

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

48
Q

PUD: Complications (3)

A

“HOP”
H- hemorrhage
O- obstruction
P- perforation and peritonitis

NUR 326 Exam 3 (11 decks)

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