Hehi Test #3 - Care Of Clients With Upper Gastrointestinal Disorders

Front 1

GI assessment

Back 1

History:
- Current health status
- Previous health state
- Family Hx
- Lifestyle patterns (diet - frequency and types of food, alcohol?)

Physical Exam:
- Inspect
- Auscultate
- Percuss
- Palpate

Front 2

Signs of GI emergency

Back 2

ABDOMINAL PAIN
emesis and stools
abdominal tenderness

Other signs: fever, tachycardia, hypotension, dehydration

Front 3

Lower GI scopes and Patient instructions

Back 3

1. Colonoscopy
2. Protosigmoidoscopy

Pt. Instructions:
- Go off anticoagulants for about 4 days prior
- Don't eat anything with seeds (get stuck on colon wall)
- GoLYLELY
- Someone to drive them home (post anesthesia)

Front 4

Upper GI scopes and Patient instructions

Back 4

1. Esophagogastroduodenoscopy

Pt. Instructions:
- NPO 8-12 hours prior
- Someone to drive them home (post anesthesia)

Front 5

Bilirubin

Back 5

Normal - none in urine

Presence: biliary obstruction

Front 6

Colostridium difficile toxin assay

Back 6

Presence of C. diff. Sign of Pseudomembranous colitis

Front 7

Fecal Lipid

Back 7

Normal: < 7 g./24 hrs

Increased fat in stool if malabsorption is suspected

Could mean insufficient pancreatic enzyme secretion

Front 8

Fecal occult blood

Back 8

Measures concealed blood in stool

Positive: signifies GI bleed

Front 9

Fecal Urobilinogen

Back 9

Normal: Males - 0.3-2.1; Females - 0.1-1.1 Ehrich units/ 2 hrs.

Detects impaired liver function


elevated: Impaired liver function
Lowered: total biliary obstruction

Front 10

Stool Culture

Back 10

Normal: no pathogens

Presence: bacterial, viral, or fungal GI infection

Front 11

Ova & Parasite

Back 11

Normal: none

Confirms or rules out intestinal parasitic infestation and disease

Possible infection

Front 12

GERD symptoms

Back 12

Gastroesophageal Reflux Disease

1. Heartburn (pyrosis)
2. Water brash (increased salivary secretion - response to peptic esophagitis
3. Laryngitis
4. Aspiration (passage of gastric fluid up the esophagus and down into the lungs)
5. Wheezing
6. Night tiem awakening with choking

Front 13

Pharmacological Management of GERD

Back 13

Pharmacologic:
- Histamine receptor antagonists - inhibit parietal cell activity increasing pH and decreasing gastric volume
- Antacids
- PPI - Prilosec: inhibits parietal cell H+, K+, and ATPase

Front 14

Nonpharmacological Management of GERD

Back 14

1. Reduce pressure on abdomen (includes tight clothing and belts)
2. Reduce pH of gastric contents
3. Reduce large colume contents in stomach

Surgicla: Fundoplication

Front 15

Bright red of coffee ground vomit or black stools

Back 15

Bleeding in esophagus

possibly due to: ulcer, varices, liver disease

Bleeding in stomach

Possibly due to: ulcer, gastritis, carices, Mallory-Weiss

Front 16

Bright Red/ Maroon bleeding

Back 16

Bleeding in small intestine

Possibly due to: ulcer or tumor

Front 17

Blood in stool

Back 17

Bleeding in colon

Possibly due to: colon cancer, polyps, colitis, diverticulosis

Front 18

Bright red blood in stool

Back 18

Bleeding in rectum

Possibly due to: hemorrhoids, deverticulosis, tumor

Front 19

Nursing Assessment r/t GI bleeds

Back 19

1. Assess severity of blood loss:
- Direct measures - visually seen in vomit/ stool & VS
- Indirect measures: labs (Hgb & Hct)

Laboratory Data:
- Type and cross
- CBC

Radiographic Studies - Barium enema

Front 20

Esophageal varices Physiology

Back 20

1. Portal Hypertension (liver)
2. Vessel dilation - HTN

Front 21

Esophageal Varice - Rupture

Back 21

- 40% of those who have varices will bleed
- 40-70% of those will die with the first bleeding event due to:
- Exsanguinatiaon (blood loss)
- Liver failure
- Sepsis
- Cerebral Edema (due to rapid liver cirrhosis)
- Anemia

Front 22

Sclerotherapy

Back 22

Treatment for esophageal varice

- A sclerosant solution is injected into the bleedin varix or the overlying mucosa
- Obliterates teh lumen by forming thrombosis whereas injection into the submucosa poduces inflammation followed by fibrosis
- Controls bleeding in 80% of cases

Front 23

Esophageal banding

Back 23

Therapy used to treat esophageal varices - cuts of blood flow through the vein and elliminates the change for a bleed

Front 24

Balloon Tamponade

Back 24

Treatment for esophageal varices:
- a tube with balloon is utilized to exert pressure ont eh varix area in an effort to control bleeding
* Sengstaken-Blakemore tube - it is important to note placement, time fram for deflation and sequence of balloon deflation

Front 25

Divertici

Back 25

Tunnel fomations in the mucosa of the esophagus or bowel in which food or stool can become trapped causing infection

Front 26

Mallory-Weiss

Back 26

Mucosal laceration caused by teh force of vomiting or severe coughing
- Generally at or just below the esophagogastric junction

Front 27

PUD

Back 27

Peptic Ulcer Disease

Lesions of the lower esophagus, stomach, duodenum, or jujenum

Contact with HCl and pepsin

Causes:
1. H. pylori
2. Use of NSAIDS
3. Inadequate protection of mucous membranes
4. Pathologic hypersecretory disorders

Front 28

Pharmacological Treatment of PUD

Back 28

1. Antibiotics - target H. pylori bacteria (Metronidazole, tetracycline, clarithromycin, amoxicillin)
2. H2 blockers: prevent secretion of HCl (cimetidine, ranitidine, famotidine, mizatidine)
3. Proton Pump Inhibitors (omeprazole, lansoprazole, rabeprazole, esomeprazole, pantoprozole)
4. Stomach lining protector (bismuth, subsalicylate, carafate)

Front 29

Treatmet of PUD

Back 29

1. Gastric lavage with ice water and norepinephrine (causes vascular contriction)
2. Gastroscopy with cautery or laser
3. Surgery

Front 30

Common Gastric Surgeries

Back 30

1. Vagotomy with gastroenterostomy (cut vagal nerve to stomach inhibiting production of HCl and pyloric acid)
2. Vagotomy with antrectomy (removal of the lower part of the stomach)
3. Vagotomy with pyloroplasty
4. Billroth I
5. Billroth II

Side Effect: Dumping sydrome (diarrhea due to decreased digestion. absorption of water)

Front 31

Patient Considerations regarding gastric surgery

Back 31

1. Preparation
2. Monitoring aftercare:
- Bowel sounds - NPO until BS present, clear liquids - advance as tolerated
- Turn, cough, deep breath (encourages diaphramatic breathing and prevents pneumonia)
- Asses for complications (dumping syndrome, B12 deficiency)

Front 32

Pancreatitis

Back 32

Enzymes intended for digestion of proteins, fats, and lipids are activated inside the pancreas itself and breakdown the proteins that form it

Front 33

Acute Pancreatitis

Back 33

1. Usually sudden onset of nausea, vomiting, and a knife-like pain in the upper abdomen which seems to pass straight through to the back and which is partially relieved by leaning forward
2. Precipitated by passage of gallstone, drinking alcohol, or taking certain medications (diuretics or some antibiotics)
3. Acure pancreatitis can develop for no obvious reason - idopathic pancreatitis

Front 34

S/S of acute pancreatits

Back 34

1. Elevated blood amylase or lipase levels (exzymes leak into surrounding tissues if unable to be secreted in to the small intestine - absorbed by general circulation)
2. sometimes liver function tests are abnormal and jaudice is present
3. CT scan
4. Low grade fever, hyperglycemia, abdominal tenderness and rigidity

Front 35

Whipple Procedure

Back 35

Pancreaticoduodenectomy - operation to remoce the head of the pancreas and reattach the tail to the duedenum

Performed for:
- tumor of the pancreas
- tumor of the bile duct
- Inflammation of the pancreas chronic pancreatitis

Front 36

Cholecystitis

Back 36

Blockage of cyctic duct by gall stone (cholesterol stone)

S/S - N/V, anorexia, elevated WBC, RUQ pain

Front 37

Functions of Liver

Back 37

1. Detoxify blood of hormones, drugs, and chemicals (individuals with impaired liver function can easily reach toxic drug levels)
2. Add prothrombin and fibrinogen to blood (liver impairmend presents risk of hemorrhage)
3. Secrete bile
4. Metabolize carbohydrates, fats, and proteins
5. Make glucose available
6. Store Vitamins A, D, E, K, B12, copper and iron
7. Convery ammonia to urea (one product of protein metabolism is a component of ammonia)
8. Form keton bodies, acetate, lipproteins cholesterol, and phosphlipids

Front 38

Hepatitis

Back 38

- Can be acute or chronic
- Hep A, B, C, D, and E are known
- Cytomegalovirus and Epstein-Barr may cause hepatitis
- Alcohol abuse, certain drugs/ chemicals, and autoimmune disorders, Amebic dysentery and malaria may also inflame the liver

Front 39

Hep A & Hep B Stage

Back 39

1. Incubation tim 6-24 weeks the prodromal preicteric phase commences with lethargy, anorexia, commonly nausea, vomiting and RUQ pain
- After 2 days - 2 weeks of prodrome the icteric phase begins with dark urine (ice tea) pale stools (claylike), jaundice, and RUQ pain
- Convalescent phase may be long and drawn out over several weeks with fatigue and malaise

Front 40

Treatment of Acute Hepatitis

Back 40

1. Bedrest until initial phase passes - then resume activity
*Total isolation is NOT necessary
2. Precautions depend of type of Hepatitis:
HepA - feces and urine must be carefully disposed of
Hep B, C, & D it is necessary to avoid contaminationby blood or other body fluids

Front 41

Treatment for acute hepatitis

Back 41

1. For persons who have been in close and prolonged contact with patient with HepA, gamma globulin may be gicen
- HepA vaccine may be gicen to those who are at increased risk of exposure
- Persons exposed to blood containing B virus may receive hepatitis B immune globulin

Front 42

S/S of chronic hepatitis

Back 42

Defined as liver inflammation lasting longer than 6 months
1. Nausea
2. Fatigue
3. Jaundice
- condition may be mild or lead to cirrhosis and concer of the liver

Front 43

Fulminant Failure

Back 43

Progression for jaundice to encephalopathy in less than one week

Brain exhibits cytotoxic edema

- encephalopathy is seen in chronic cirrhosis, slowly progressive liver failure does not produce cerebral edema or neurologic death
- these latter complications are seen only in patients suffering the fulminant course and greatly complicate their management. The etiology of cerebral edema is unclear

Front 44

Cirrhosis

Back 44

- 8th leading cause of death by disease

S/S of cirrhosis - many people with cirrhosis have no symptoms in the early stages of the disease. however as scar tissue replaces healthy cells, liver function starts to fail and a person may experience the following symptoms:
- Exhaustion Fatigue
- Loss of appetite
- Nausea
- Weakness
- Weight loss

As the disease progresses complications may develop. In some people these may be the first signs of disease

Front 45

Complications caused by cirrhosis

Back 45

1. Edema
2. Ascites
3. Bruising and bleeding
4. Itching
5. Jaundice
6. Gallstones
7. Toxins in the blood or brain
8. Sensitivity to medications
9. Portal hypertension
10. Varices
11. Impact on other organs

Front 46

Treatment of Cirrhosis

Back 46

1. Liver damage from cirrhosis CANNOT be reversed
2. Treatment cay stop or delay further progression and reduce complications
3. Treatment depends on the cause ocirrhosis and any complications a person is experiencing
4. Treatment for hepatitis related cirrhosis involves medications used to treat the different types of hepatitis

Front 47

Ascites

Back 47

Abnormal (pathologic) build up of fluid in peritoneal cavity

Front 48

Reasons that ascites occurs

Back 48

1. There is a diseas in the peritoneal cavity that is producing excessive fluid (infection or cancer)
2. There is fluid back up from the liver or large blood vessels into the peritoneal cavity -- known as portal hypertension
3. Low sodium state in the body
4. Miscellaneous

Front 49

Treatment of Ascites

Back 49

1. Monitoring:
- fluid
- diet (sodium restriction)
- weight
2. Medication - diuretics

*Only 10% do not respond to medical approach (diuretics + dietary restriction of sodium) and in those who do respond, there is no other treatment needed

Front 50

Diuretic-Resistant Ascites

Back 50

1. Therapeutic Paracentesis - remove fluid
2. LeVeen or Denver shunt
3. Liver transplant
4. Extracorporeal ultrafiltration of ascitic fluid with reinfusion
5. Transjugular intrahepatic portosystemic stent shunt (TIPPS)