N211 Gi Reading Notes

Front 1

Priority of care post-upper GI endoscopy:

Back 1

Aspiration

Front 2

Preventing aspiration post upper endoscopy:

Back 2

No fluids/food by mouth until gag reflex is intact

Front 3

Preparation for an EGD:

Back 3

NPO 6-8 hours before test
IV access for moderate sedation
Remove dentures
Ask about exposure to dye/contrast

Front 4

Nursing actions post-EGD:

Back 4

VS q15m
No fluids or food until gag reflex returns
Teach pt/family to report pain or fever

Front 5

Define peptic ulcer disease:

Back 5

Mucosal defenses are impaired and cannot protect epithelium from acid/pepsin

Front 6

Three types of GI ulcers:

Back 6

Gastric
Duodenal
Stress

Front 7

Three factors that play roles in development of gastric ulcers:

Back 7

Acid
Pepsin
H. pylori infection

Front 8

Protective factors in the stomach:

Back 8

Mucus and bicarbonate
Prostaglandins
Rich blood supply

Front 9

Describe gastric ulcers:

Back 9

Deep and penetrating

Front 10

Gastric ulcers usually occur where?

Back 10

On the lesser curvature of the stomach

Front 11

Where do most duodenal ulcers occur?

Back 11

Upper portion of the duodenum

Front 12

Describe duodenal ulcers:

Back 12

Deep, sharply demarcated lesions

Front 13

Main cause of duodenal ulcers:

Back 13

High gastric acid secretion

Front 14

Define stress ulcers:

Back 14

Gastric mucosal lesions occuring after medical crisis or trauma

Front 15

Main manifestation of stress ulcers:

Back 15

Bleeding from gastric erosion

Front 16

Signs of upper GI bleeding:

Back 16

Red or coffee-ground emesis
Tarry stools or frank blood in stool
Melena
Decreased BP, increased HR
Decreased H&H
Vertigo/dizziness/syncope
Confusion in older adults

Front 17

Most serious complication of PUD:

Back 17

Hemorrhage

Front 18

Melena is more common with which type of ulcer?

Back 18

Duodenal

Front 19

Manifestations of ulcer perforation:

Back 19

Sudden sharp pain in epigastric region that spreads
Tender, rigid, boardlike abdomen
Patient assumes knee-chest position

Front 20

Complications of ulcer perforation:

Back 20

Septicemia
Hypovolemic shock
Paralytic ileus
Death

Front 21

Manifestations of pyloric obstruction:

Back 21

Vomiting from stasis/gastric dilation
Bloating
Metabolic alkalosis
Hypokalemia

Front 22

Two factors associated with PUD development:

Back 22

NSAID use
H. pylori infection

Front 23

What makes NSAID ulcers difficult to treat?

Back 23

Tendency towards recurrence

Front 24

Gastritis/ulcer prevention:

Back 24

Avoid alcohol
Use caution with NSAIDs and steroids
Avoid large amounts of caffeine
Manage stress
Stop smoking

Front 25

Most commonly reported symptom with PUD:

Back 25

Dyspepsia

Front 26

Where is gastric ulcer pain located?

Back 26

Upper epigastrium with localization to left of midline

Front 27

Where is duodenal ulcer pain located?

Back 27

To the right of the epigastrium

Front 28

When does the pain of gastric ulcers occur?

Back 28

With/after eating

Front 29

When does the pain of duodenal ulcers occur?

Back 29

90 min - 3 hours after eating
Often at night

Front 30

GU vs. DU: stomach acid production

Back 30

GU normal or hyposecretion
DU hypersecretion

Front 31

GU vs. DU: pain related to food

Back 31

GU: worsened by ingestion of food
DU: relieved by ingestion of food

Front 32

Priority nursing dx for PUD:

Back 32

Acute/chronic pain

Front 33

Most important collaborative problem with PUD:

Back 33

Potential for GI bleeding

Front 34

Interventions to manage PUD pain:

Back 34

Drug therapy
Elimination of irritants

Front 35

Drug therapy for PUD:

Back 35

Triple therapy: PPI plus two antibiotics

Front 36

Interventions related to the potential for GI bleeding:

Back 36

Monitoring and early recognition!

Front 37

Interventions for upper GI bleeding emergency:

Back 37

Oxygen/ventilatory support
Large bore IVs for replacing fluids/blood
Monitor VS/crit/O2

Front 38

Procedure for gastric lavage:

Back 38

- Large-bore NG tube
- Patient on left side
- Room-temp solution, 200-300mL at a time
- Withdraw solution manually
- Repeat until returns are clear/light pink with no clots

Front 39

What aggressive treatment is used to prevent rebleeding in the upper GI?

Back 39

Acid suppression

Front 40

Types of cirrhosis:

Back 40

Alcoholic
Postnecrotic
Biliary
Cardiac

Front 41

What causes postnecrotic cirrhosis?

Back 41

Viral hepatitis, certain drugs/chemicals

Front 42

What causes biliary cirrhosis?

Back 42

Chronic biliary obstruction from gallbladder disease

Front 43

What causes cardiac cirrhosis?

Back 43

Heart failure (rare)

Front 44

Compensated vs. decompensated cirrhosis:

Back 44

Compensated: liver can still function without major symptoms
Decompensated: obvious manifestations of liver failure

Front 45

Define portal hypertension:

Back 45

Persistent increase in pressure within portal vein

Front 46

Sequelae of portal hypertension:

Back 46

Splenomegaly (blood backs into spleen)
Dilated veins in esophagus, stomach, intestines, abdomen, rectum
Ascites
Esophageal varices
Prominent abdominal veins (caput medusae)
Hemorrhoids

Front 47

What causes ascites?

Back 47

Increased hydrostatic pressure from portal hypertension --> collecting plasma protein in peritoneal fluid --> low albumin from liver failure --> colloid osmotic pressure is reduced and third spacing happens

Front 48

What is a complication of massive ascites?

Back 48

Renal vasoconstriction and RAA activation, which results in water/sodium retention and more ascites

Front 49

What are esophageal varices?

Back 49

Fragile esophageal veins become distended from blood backup

Front 50

Complications of esophageal varices:

Back 50

BLEEDING. Especially after activities that increase abdominal pressure, chest trauma, or dry/hard food.

Front 51

How does cirrhosis affect bleeding?

Back 51

Bile production is decreased
ADEK absorption decreased/prevented
No K = no clotting cascade = easy bleeding

Front 52

How does portal hypertension affect bleeding?

Back 52

Backup of blood into spleen causes splenomegaly; platelets are destroyed by enlarged spleen

Front 53

Symptoms of hepatic encephalopathy:

Back 53

EARLY:
Sleep and mood disturbance
Mental status changes
Speech problems

LATE:
Altered LOC
Impaired cognition
Neuromuscular problems

Front 54

Manifestations of hepatorenal syndrome:

Back 54

Sudden decrease in urinary flow
Elevated BUN/Cr with decreased urine sodium excretion
Increased urine osmolarity

Front 55

Prognosis of a patient who develops hepatorenal syndrome:

Back 55

Poor

Front 56

How does liver disease cause peritonitis?

Back 56

Low protein concentration means little protection
Bacteria migrate from bowel into ascitic fluid

Front 57

What is the leading cause of cirrhosis in the US?

Back 57

Hep C

Front 58

Important history to take for suspected cirrhosis:

Back 58

Employment history/exposure hx
Needle sticks
Sexual hx/preference
Alcohol/drug use
Tattoos
Military
Prison

Front 59

Early manifestations of cirrhosis:

Back 59

Fatigue
Weight change
GI symptoms
Abdominal pain/liver tenderness
Pruritis

Front 60

Clinical manifestations of liver dysfunction/failure:

Back 60

Jaundice/icterus
Dry skin, rashes
Rashes
Petechiae/ecchymosis
Palmar erythema
Spider angiomas on nose/cheeks/upper chest/shoulders
Dependent edema
Clubbing of nails

Front 61

Ascites can lead to:

Back 61

Dypnea/orthopnea
Balance/walking problems
Hernias

Front 62

Define fetor hepaticus:

Back 62

Distinctive breath odor of chronic liver disease and hepatic encephalopathy - fruity or musty odor

Front 63

Define asterixis:

Back 63

Coarse tremor; extension and flexions in wrists/fingers

Front 64

Most common nursing dx for pts with cirrhosis:

Back 64

Excess fluid volume r/t edema

Front 65

Primary collaborative dx for pts with cirrhosis:

Back 65

Potential for hemorrhage
Potential for hepatic encephalopathy

Front 66

Interventions for excess fluid volume related to ascites:

Back 66

Low-sodium diet
Vitamin supplements
Diuretic
Potassium supplement
Paracentesis
Respiratory support measures
I&O, daily weights, VS
Monitor LOC/neuro checks

Front 67

Interventions for prevention of bleeding in cirrhosis patients:

Back 67

Nonselective beta blocker to decrease HR and hepatic venous pressure
Vasoactive drugs (octreotide/terlipressin)
Endoscopic variceal ligration/sclerotherapy
TIPS

Front 68

What chemical likely causes hepatic encephalopathy?

Back 68

Ammonia

Front 69

Nutritional requirements of pts with cirrhosis:

Back 69

High carb
Moderate fat
High protein

Front 70

Changes in nutrition for cirrhosis pts with high ammonia:

Back 70

Moderate protein, fat, simple carbs

Front 71

Drug therapy for liver failure:

Back 71

Restriction of opioids, sedatives, and barbiturates
Lactulose for encephalopathy
Nonabsorbable antibiotics to kill normal flora and decrease ammonia production

Front 72

Define hepatitis:

Back 72

Widespread inflammation of liver cells

Front 73

Most common type of hepatitis:

Back 73

Viral

Front 74

How is HBV spread?

Back 74

Blood-borne (STD, needles, transfusions, dialysis, maternal-fetal)

Front 75

Sx of HBV:

Back 75

Anorexia/N/V
Fever
Fatigue
Right upper quadrant pain
Dark urine, light stool
Joint pain
Jaundice

Front 76

Prognosis for HBV:

Back 76

Most people recover & clear virus
Some become hepatitis carriers

Front 77

Spread of HCV:

Back 77

Blood/sex
Tattoos
Cocaine intranasal paraphernalia

Front 78

Sx of HCV:

Back 78

Often asymptomatic

Front 79

Prognosis for HCV:

Back 79

Most people become chronically infected

Front 80

Define fulminant hepatitis:

Back 80

Failure of the liver cells to regenerate; acute/fatal form of the illness

Front 81

Initial screening test for HCV:

Back 81

ELISA