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kol- Med Surg 320 Spring > GI- Gerd PUD Gastritis > Flashcards

GI- Gerd PUD Gastritis Flashcards

1
Q

Inflammation of the mucosal lining of the stomach=

A

gastritis

*may be part or all of the stomach

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2
Q

2 types of gastritis

A

acute and chronic

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3
Q

characteristics of acute gastritis

A
  • Occurs after exposure to local irritants or other causes
  • Sudden
  • Thickened, reddened mucous membrane with prominent rugae
  • Mild to severe
  • Can result in bleeding when muscle layer is involved
  • Usually resolves in several days
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4
Q

characteristics of chronic gastritis

A
  • Patchy diffuse inflammation of mucosal lining of stomach
  • Walls and lining of stomach will thin and atrophy
  • Parietal cell function decreased
  • Intrinsic factor production decreased
  • B12 absorption stops
  • Acid in stomach decreases
  • Results in intestinal metaplasia and Gastric Cancer
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5
Q

acute or chronic leads to intestinal metaplasia and gastric cancer?

A

chronic

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6
Q

acute or chronic gastritis: Patchy diffuse inflammation of mucosal lining of stomach

A

chronic

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7
Q

acute or chronic gastritis: Thickened, reddened mucous membrane with prominent rugae

A

acute

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8
Q

acute or chronic gastritis: Occurs after exposure to local irritants or other causes

A

acute

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9
Q

acute or chronic gastritis: Parietal cell function and Intrinsic factor production decreased

A

chronic

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10
Q

acute or chronic gastritis: Can result in bleeding when muscle layer is involved

A

acute

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11
Q

1 cause of chronic and acute gastritis

A 
chronic = H pylori 
acute= NSAIDs
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12
Q

True or false: H pylori will always cause gastritis

A

◦ Most people with H. Pylori do not have gastritis
◦ In some people, H. Pylori imbeds into the mucosal layer of stomach
–> Activates toxins and enzymes –>Inflammation of mucosa

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13
Q

Causes of gastritis

A 
H. Pylori (chronic)
NSAIDs (acute)
Alcohol Consumption (acute/chronic)
Severe Illness (acute)
Autoimmune disorders (chronic)
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14
Q

Reduce these things to help prevent gastritis and do these other things

A

REDUCE:

  • Caffeine
  • Spicy food
  • Chocolate
  • Alcohol
  • Tobacco
  • Aspirin
  • NSAIDS
  • Stress

DO:
Exercise
Balanced Diet

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15
Q

acute gastritis assessment - feels like, looks like:

A
  • Epigastric pain
  • Epigastric cramping
  • Indigestion
  • Anorexia
  • Nausea & Vomiting
  • Abdominal tenderness
  • Hematemesis
  • Melena
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16
Q

Chronic gastritis assessment- feels like, looks like:

A
  • Often Asymptomatic –> when starts to cause sxs seed PUD
  • Nausea & vomiting
  • Epigastric discomfort
  • Often after meal
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17
Q

Acute gastritis interventions

A 
• Self-limiting
• Support
	◦ Fluids
	◦ Blood products
	◦ Bland foods
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18
Q

Chronic gastritis interventions

A
  • Remove cause
  • Medications
  • Mucosal barrier
  • B12 replacement (IM)
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19
Q

what is the most common upper GI disorder in US that can strike at any age (most common in 40’s and older)

A

GERD

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20
Q

What is GERD?

A

• Backward flow of stomach contents into esophagus

◦ Highly acidic and irritating contents cause inflammation in esophagus

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21
Q

What causes GERD

A

• Lower esophageal sphincter is failing to prevent backflow from stomach to esophagus

Causes:
	◦ Excessive relaxation of LES
	◦ Increased abdominal pressure
	◦ Reduced emptying of stomach
	◦ Diabetes: gastric neuropathy
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22
Q

stomach pH vs esophagus pH

A

Stomach pH = 1.5-2

Esophagus pH = 6-7

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23
Q

What happens to ability to return food to stomach after coming up from GERD over time

A

> > Refluxed contents return to stomach via peristalsis and gravity… as esophagus becomes inflamed, it becomes more difficult to get contents back to stomach (reduced function)

  • -> Hyperemia
  • ->Erosion
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24
Q

Risk factors for GERD

A
  • Hiatal hernia
  • Alcohol use
  • Tube in nose or throat
  • Large spicy meals
  • Citrus food
  • Chocolate
  • Carbonated Beverages
  • Smoking
  • Pregnancy
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25
Q

Barrett’s epithelium is complication from what disease process? and what is it?

A

GERD

• Barrett’s epithelium
◦ Normal Squamaous cells of esophagus change to columnar epithelium which is precancerous but withstands acid better

26
Q

complications from GERD

A
  • Esophageal stricture (from scarring)
  • Asthma
  • Laryngitis
  • Dental Decay
  • Cardiac Disease
  • Aspiration pneumonia
  • Bleeding
  • Barrett’s epithelium
27
Q

GERD assessment- looks like/feels like:

A 
-Dyspepsia/ Indigestion (fullness, nausea, belching)
• Discomfort worsens with bending over, lying down
• Pain may radiate to neck or jaw
• May occur after eating for 20 mins- 2 hours
-Regurgitation
• Bitter taste
• Water brash may occur in response (reflexive saliva)
• Belching and flatulence
-Heartburn
-Asthma
-Morning Hoarseness
-Pneumonia
• Crackles in lungs? Wheezing?
• Coughing?
• Dysphagia
-Painful swallowing
28
Q

GERD diagnostics (2 main ones)

A
  • Barium Swallow Study (Esophagus)
  • **Upper endoscopy (EGD)- best definitive diagnosis
  • **pH exam ** - Ph capsule in esophagus reports pH , Gold standard but most don’t get it
  • Esophageal Manometry
  • Gastric emptying test

Diagnosis is often based sxs and how they respond to treatment –> if respond to treatment then assume its GERD

29
Q

Nutrition education for GERD- what not to eat, how should you eat?

A
  • Avoid irritating foods
  • Caffeine
  • Chocolate
  • Fried food
  • Fatty food
  • Citrus
  • Peppermint
  • Spicy foods
  • Eat small portions/ small meals more frequently
  • Avoid eating before bedtime
30
Q

lifestyle changes to manage GERD

A
  • Stop Smoking
  • Reduce Alcohol intake
  • Elevate head of bed 6-12 inches
  • Sleep on right side
  • Weight loss
  • Evaluation for obstructive sleep apnea
  • Avoid bending over
  • Sit upright after eating
  • Loose clothes
31
Q

• Medications that CAUSE LED relaxation/ contribute to GERD

A 
◦ Nitrates
	◦ NSAIDS
	◦ Oral contraceptives
	◦ CCB’s
	◦ sedatives 
		‣ Avoid these medications is not always possible!
32
Q

• Medications for TREATING GERD

A

◦ Antacids
◦ H2 antagonists
◦ PPI’s

(not meant for long term)

33
Q

Surgery for GERD

A

• Nissen fundoplication
◦ recreate tighter LED, make incisions in stomach to tighten it
◦ Standard surgical approach for GERD
◦ Continue taking meds/lifestylemod –> high rate of recurrence

34
Q

Peptic Ulcer Disease- what is it?

A

=Mucosal Lesion of the stomach or duodenum
• “PUD” occurs with impairment of mucosal defenses
◦ –> Acid and pepsin are able to destroy the epithelium tissue of stomach and duodenum

35
Q

Cause of many peptic ulcers is what? how does it cause damage?

A

H pylori

• May cause break in mucosal barrier >HCl can then injure epithelium of stomach and causes lesion

36
Q

gastric or duodenal : Ulcer caused by Delayed Stomach emptying

A

gastric

37
Q

gastric or duodenal: ulcer caused by increased stomach empyting

A

duodenal

38
Q

Increased, decreased or normal with gastric ulcer:
stomach empyting
acid secretion
diffusion of gastric acid into stomach tissue

A

Delayed Stomach emptying, normal acid secretion, increased diffusion of gastric acid into stomach tissue

39
Q

increased, decreased, or normal w/ duodenal ulcer?

Stomach emptying
acid secretion
diffusion of gastric acid into stomach tissue

A

=Increased stomach emptying, increased secretion of gastric acid, and normal diffusion of acid into stomach tissue

40
Q

onset of pain w/ gastric vs duodenal ulcer

A

gastric= pain occurs 30- 60 min after eating, occurs at night

duodenal= pain occur 1.5-3 hours after eating, occurs in middle of night

41
Q

Gastric vs duodenal ulcer: If bleeding occurs –> ?

A 
gastric = hematemesis
duodenal = melena
42
Q

Gastric vs duodenal ulcer- where is the pain?

A

gastric- • Upper epigastrium (and left)

duodenal- • Below epigastrium (and right)

43
Q

what is stress ulcer? what are some causes?

A 
=Occur after medical crisis or trauma
• Sepsis
• Head Injury
• Burns
• NPO for surgery
44
Q

why are we concerned about stress ulcers and what we gonna do about it?

A

> May cause bleeding (Increase death), develop very quickly
Lead to long hospital stays
give prophylactic PUD med in hospital to prevent

45
Q

Causes of peptic ulcers

A
  • **H. Pylori infection
  • **NSAIDS (COX-1 produces prostaglandins that promote inflammation AND protect the GI mucosal lining
  • Gastritis
  • Corticosteroids
  • Theophylline
  • Excessive alcohol intake
  • Smoking
  • Caffeine
  • Alcohol
  • Radiation therapy
  • Stress

—> same as gastritis!

46
Q

Assessment history for PUD

A
  • Risk Factors?
  • Medications?
  • What aggravates?
  • Past surgeries?
  • GI symptoms?
  • Relationship of GI symptoms to eating & sleep
  • Changes in GI symptoms
47
Q

Assessment for PUD- looks like/feels like:

A 
• INDIGESTION (Dyspepsia)
• Sharp, burning pain
• Abdominal fullness
• Epigastric tenderness
• Hyperactive bowel sounds (early)
• Hypoactive bowel sounds (late)
• Nausea & Vomiting
	◦  Vital Signs
• Appetite changes
48
Q

Diagnostics for PUD

A 
Urea Breath test- diagnose H. Pylori 
Stool Antigen test
Serum Antibody test
Hemoglobin and hematocrit
Fecal Occult test
CT scan
**Esophagogastroduodenoscopy **
Nuclear Medicine scan
49
Q

Goals of drug therapy for PUD

A
  • Provide pain relief
  • Eliminate H. pylori
  • Heal ulcers
  • Prevent recurrence
50
Q

Triple vs Quadruple therapy

A

-treat PUD:

Triple Therapy:
Proton pump inhibitor
2 antibiotics

Quadruple therapy:
Triple therapy + Pepto-Bismol

51
Q

Nutrition Ed for PUD

A
  • Avoid irritating foods
  • Bland foods (acute)
  • Avoid bedtime snacks
  • Avoid alcohol
  • Avoid smoking
52
Q

4 complications to consider for PUD

A
  • Hemorrhage
  • Perforation
  • Pyloric obstruction
  • Chronic & difficult to treat disease
53
Q

Hematemesis (UPPER) coloration?

A

bright red

coffee ground –> can be actively bleeding w/ this

54
Q

What is Melena a sign of related to PUD? What does it look like?

A

hemorrhage, dark tarry stool (digested blood)

55
Q

early detection interventions for GI hemorrhage

A
  • Vital signs
  • Hemoccult test for suspicious stool
  • H & H
  • Patient education
56
Q

nursing interventions for GI hemorrhage

A
  • Airway protection
  • Position (side)
  • Oxygen
  • Volume replacement (IV access)
  • Blood transfusion
  • Prepare patient for medical intervention
57
Q

Medical interventions for GI bleed

A 
-Endoscopic procedure
• Esophagogastroduodenoscopy
	◦ Inject chemicals into bleeding site
	◦ Treat bleed with heat source
	◦ Apply band or clip
	◦ IV sedation

-Interventional radiological procedure
• Catheter directed embolization of artery that is bleeding
• Emergency situation typically

-Acid Suppression
• To prevent re-bleeding
• IV Protonix
• IV Ocreotide: dhunts blood away from GI system

58
Q

what is a bowel perforation?

A

Allows contents of GI system to leak into peritoneal cavity

59
Q

s/s of bowel perforation- what we gonna do about it?

A

• Sudden, sharp mid -epigastric pain that radiates through abdomen
• TENDER, RIGID, BOARDLIKE ABDOMEN = Peritonitis
◦ + Rebound tenderness
◦ This is an emergency
—>SUPPORT AND GET TO SURGERY

60
Q

IV Ocreotide =

A

shunts blood away from GI system, admin during GI hemorrhage

61
Q

What happens during EGD?

A

◦ Inject chemicals into bleeding site
◦ Treat bleed with heat source
◦ Apply band or clip
◦ IV sedation

kol- Med Surg 320 Spring (43 decks)

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