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NUR2228 > Week 4 - GIT and Hepatic Nursing > Flashcards

Week 4 - GIT and Hepatic Nursing Flashcards

1
Q

Most common causes of an upper GI bleed:

A
  • Peptic ulcer disease
  • Erosive gastritis
  • Esophageal varices
  • Mallory-weiss syndrome
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2
Q

Most common causes of lower GI bleed:

A
  • Diverticulitis
  • Vascular ectasias
  • Ischaemic colitis
  • Infectious colitis
  • Inflammatory bowel disease
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3
Q

What is gastroesophageal reflux disease (GORD)?

A

A chronic digestive disease which occurs when stomach contents move up into the oesophagus (reflux)

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4
Q

What is the most common GIT disorder?

A

GORD

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5
Q

Risk factors of GORD:

A
  • Obesity
  • Male gender
  • Smoking
  • High alcohol intake
  • Age
  • Patients who are nursed in a supine position for long periods
  • Some surgeries can result in GORD (gastric bypass, gastric sleeve)
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6
Q

GORD complications:

A
  • Oesophagitis
  • Barrett’s Oesophagus
  • Oesophagus strictures from the build up of scar tissue in the oesophagus
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7
Q

How is GORD caused in infants?

A

Oesophageal sphincter, immaturity and fluid diet

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8
Q

What medications are used to manage GORD in children?

A
  • Proton pump inhibitors
  • H2 antagonists
  • Occasionally antacids
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9
Q

GORD pathophysiology:

A

Defective LOS → transient LOS relaxation → excessive acid exposure in the lower oesophagus → symptoms such as heartburn and regurgitation = reflux

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10
Q

Clinical manifestations of GORD:

A
  • Heartburn
  • Regurgitation
  • Painful swallowing
  • Haematesis
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11
Q

How is the diagnosis made for GORD?

A

Diagnosis is made when symptoms of heartburn and regurgitation consistently occur more than twice in one week

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12
Q

The main aim of treatment of GORD is to:

A
  • Prevent recurrences of symptoms
  • Relieve symptoms
  • Reduce the risk of complications and resolve complications such as mucosal lesions in the oesophagus
  • Improve quality of life
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13
Q

GORD nursing assessments:

A
  • Primary: ABCD
  • Secondary: general appearance, full set of vital signs and hydration assessment
  • Focused: abdominal assessment
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14
Q

What symptoms of a patient with GORD would require a gastroscopy to be performed?

A
  • Recurrent vomiting
  • Dysphagia
  • Unexplained weight loss
  • Evidence of gastrointestinal blood loss
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15
Q

Protein Pump Inhibitors action:

A
  • PPIs interfere with the release of hydrogen ions (H+) from the parietal cells in the stomach to decrease the secretion of gastric acid
  • Have a short half life but a long duration of action
  • Require an acidic environment to be active
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16
Q

Protein Pump Inhibitors indication:

A

Treatment of GORD and oesophagitis - most effective drug for suppressing the reflux of acidic gastric contents

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17
Q

Protein Pump Inhibitors side effects:

A
  • Dry mouth
  • GIT effects (diarrhoea, abdo pain, nausea, vomiting)
  • CNS effects (dizziness, headache)
  • Respiratory effects (cough, nasal congestion)
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18
Q

What are peptic ulcers?

A

Erosion of the mucosal lining of the stomach or duodenum leading to a break or ulcer

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19
Q

Peptic ulcer risk factors:

A
  • Regular use of NSAIDs
  • Infection of the gastric mucosa
  • Smoking
  • Advancing age
  • High alcohol/caffeine consumption
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20
Q

Peptic ulcer complications:

A
  • Haemorrhage from perforated ulcers → large perforations may be life threatening and require immediate surgical closure
  • Constipation → occurs due to dehydration and decreased diet intake secondary to anorexia
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21
Q

Peptic ulcer pathophysiology:

A

Alteration and breakdown in the cellular structure of the stomach’s protective mucosal layer → submucosal layer becomes exposed to acidic gastric secretions → development of an open lesion → secretions then penetrate to deeper tissue → damaged mucosa triggers histamine release as part of inflammatory response → further stimulation of acid production → damage to small vessels → haemorrhage

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22
Q

Where can peptic ulcers develop?

A

The ulcers can develop anywhere along the upper digestive tract, from the lower oesophagus, stomach & duodenum

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23
Q

How can peptic ulcers be diagnosed?

A
  • Clinical manifestations
  • Abdominal x-ray with barium study = will show depth of ulcer crater
  • Gastroscopy = performed to visualise the gastric mucosa, H.pylori can be tested for during the procedure and a biopsy can also be performed
  • Breath test = performed to determine if H.pylori is detected
  • Blood test = full blood count is used to detect anaemia secondary to bleeding from the ulcer
  • Faecal occult test = used to detect the presence of blood in faeces
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24
Q

Treatment of peptic ulcer can include:

A
  • Antisecretory therapy
  • Triple therapy for H.pylori infection
  • Endoscopy / gastroscopy
  • Breath testing
  • First line treatment is lifestyle modifications and medications
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25
Q

What does triple therapy consist of?

A

(Proton pump inhibitor, clarithromycin and amoxicillin or an imidazole)

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26
Q

Peptic ulcer nursing assessments:

A
  • Primary: ABCD
  • Secondary: general appearance, full set of vital signs and hydration assessment
  • Focused: abdominal assessment
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27
Q

Peptic ulcer clinical manifestations:

A
  • Intermittent epigastric pain
  • Feeling of fullness or abdo bloating
  • Heartburn
  • Nausea/vomiting
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28
Q

Histamine 2 (H2) Receptor Antagonists (H2 Blockers) actions:

A

Inhibit the action of histamine and the histamine-2 receptor sites on the parietal cells in the stomach, this blocking leads to a reduction in gastric acid secretion and reduction in overall pepsin production, which gives acid sensitive ulcers an opportunity to heal

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29
Q

Histamine 2 (H2) Receptor Antagonists (H2 Blockers) indications:

A
  • Short-term treatment of active peptic ulcers
  • Treatment of recurrent peptic ulcers
  • Prophylaxis of stress-induced ulcers and acute upper GIT bleeding in critically ill people
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30
Q

Histamine 2 (H2) Receptor Antagonists (H2 Blockers) side effects:

A
  • Headache
  • Diarrhoea, weight loss
  • Rash, hives,
  • Drowsiness/dizziness
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31
Q

Antacid actions:

A
  • Contains a jelly-like ingredient which floats on top of the stomach contents to form a barrier, preventing the contents of the stomach from entering the oesophagus
  • Neutralises the hydrochloric acid secreted by the stomach to provide relief from symptoms associated with hyperacidity
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32
Q

Antacid precautions:

A
  • Constipation
  • Diarrhoea
  • Renal failure
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33
Q

Antacid side effects:

A
  • Abdominal distension
  • Constipation
  • Diarrhoea
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34
Q

Antacid indications:

A
  • Symptomatic relief only of GIT disorders such as GORD and peptic ulcers
  • Recommended across the lifespan from infants to the elderly
  • Purchased over the counter (OTC)
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35
Q

What are the two types of Inflammatory Bowel Disease?

A

Ulcerative colitis and Crohn’s disease

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36
Q

Is bleeding more common in ulcerative colitis or crohn’s?

A

Ulcerative Colitis

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37
Q

Where is the location of inflammation in Ulcerative Colitis?

A

Limited to the large intestine/colon

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38
Q

Where is the location of inflammation in Crohn’s?

A

Anywhere in the GI tract

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39
Q

Signs and symptoms of inflammatory bowel disease:

A
  • Diarrhoea
  • Rectal bleeding
  • Abdominal pain
  • Fever
  • Weight loss
  • Vomiting
  • Cramps
  • Muscle spasms
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40
Q

Difference between ulcerative colitis and crohn’s disease

A

Crohn’s disease causes inflammation of the full thickness of the bowel wall, in any part of the digestive tract from the mouth to the anus. Ulcerative colitis is inflammation of the inner lining of the large bowel (colon and rectum).

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41
Q

What is ulcerative colitis?

A

Painful swelling, inflammation and ulceration of the mucosa of the large colon

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42
Q

Risk factors of ulcerative colitis:

A
  • Family history
  • Age - onset before the age of 30
  • Infections - viruses
  • Past bowel treatments such as radiation
  • Smoking
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43
Q

Ulcerative colitis complications:

A
  • Systemic inflammation - joints, skin, liver
  • Adverse effects of long term medication use such as steroids
  • Osteoporosis
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44
Q

Pathophysiology of ulcerative colitis:

A

Cellular changes of the mucosal lining → inflammation of the mucosal lining → oedema and thickening of the muscularis mucosa → small erosions develop on the mucosal lining → erosion form into ulcers and abscesses → leads to further inflammation, infection and development of pus → can result in necrosis of the muscularis mucosa cells (cellular death) → ragged ulceration develops → narrowing of the intestinal lumen → loss of absorptive mucosal surface and mucosal destruction → rapid colonic time, bleeding, cramping, pain, urge to defecate, frequent copious watery diarrhoea, passage of small amount of blood and purulent mucus.

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45
Q

Clinical manifestations of ulcerative colitis:

A
  • Moderate to severe abdominal pain / cramps
  • Bloody diarrhoea - often explosive
  • Mucous in the faeces
  • Fatigue
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46
Q

How is the diagnosis made for ulcerative colitis?

A
  • Blood path; crp, fbe, electrolytes
  • Stool specimen
  • Colonoscopy
  • Biopsy
47
Q

Treatment of ulcerative colitis:

A

Treatment is aimed at reducing symptoms, allowing the bowel to heal between relapses, preventing complications and improving quality of life and general well being. Pharmacological management and surgery may also be involved.

48
Q

Nursing assessment of ulcerative colitis:

A
  • Primary; abcd
  • Secondary; general appearance, full set of vital signs and hydration assessment
  • Focused; abdominal assessment
49
Q

What is Crohn’s disease?

A

Inflammation of the entire thickness of the bowel wall and can occur anywhere along the entire length of the GIT tract

50
Q

Crohn’s disease risk factors:

A
  • Family history: close relative
  • Caucasians
  • Bacterial infections can trigger an abnormal immune response
51
Q

Crohn’s disease complications:

A
  • Bowel obstruction: disease affects the thickness of the intestinal wall
  • Intestinal ulcers
  • Fistulas
  • Anal fissure
52
Q

Crohn’s disease pathophysiology:

A

Causative factor → inflammation of the submucosa → ↓mucin secretion → changes in mucosal layer of the GIT tract → ↑ permeability of the intestines → ↑ susceptibility of luminal inflammation → activates neutrophils and macrophages → tissue injury → ↑ inflammation and abscesses / ulcers in segments along GIT (called skip lesions) → mucosal lesions may develop into deep longitudinal and transverse ulcers with intervening mucosal oedema → tissue injury → creating a characteristic cobblestoned appearance to the bowel → results in fissures in intestinal wall (small tears), nodules of inflammation, fistulae, strictures, obstruction, nerve damage, bowel dysfunction → clinical manifestations such as pain, nausea, diarrhoea, urgency to defecate.

53
Q

Crohn’s disease clinical manifestations:

A
  • Diarrhoea/ Bloody / mucous stools
  • Weight loss
  • Cramping abdominal pain/epigastric pain or dysphagia
  • Fever
54
Q

Diagnosis of Crohn’s disease:

A
  • Blood path; crp, fbe, electrolytes
  • Stool specimen
  • Colonoscopy
  • Biopsy
55
Q

Treatment of Crohn’s disease:

A

Crohn’s disease is incurable so treatment aims to relieve symptoms, minimise flare ups, allow for periods of remission to allow the bowel to heal, improve quality of life and general well being. Most individuals will require surgery within 10 years of diagnosis and experience a disabling treatment course requiring frequent corticosteroids or escalation in immunosuppressive treatment.

56
Q

Nursing assessment of crohn’s disease:

A
  • Primary; abcd
  • Secondary; general appearance, full set of vital signs and hydration assessment
  • Focused; abdominal assessment
57
Q

What is diverticula?

A

A sac-like pocket that develops in the intestinal mucosa, mostly in the colon (singular)

58
Q

What is diverticulosis?

A

Multiple non-inflamed diverticula

59
Q

What is diverticulitis?

A

When the diverticula become inflamed or infected by bacteria → may perforate into the peritoneum

60
Q

Diverticulitis risk factors:

A
  • Main risk: low fibre diet → smaller, firm, compacted stool, constipation
  • Age > 40 years
  • Obesity
  • Sedentary lifestyle
  • Cigarette smoking
  • Medicines : corticosteroids, opioid medicines, and anti-inflammatory medicines
61
Q

Diverticulitis complications:

A
  • Gastrointestinal abscess
  • Perforation
  • Fistula
62
Q

Diverticulitis pathophysiology:

A

Diverticulosis → erosion of the intestinal wall → stool and bacteria get trapped in the diverticula → inflammation & infection → diverticulitis → clinical manifestations → complications such as perforation, sepsis and death

63
Q

Diverticulitis clinical manifestations:

A
  • Abdominal pain, mostly in the left lower quadrant
  • Fever
  • Nausea / vomiting / anorexia
  • Indigestion
  • Change in bowel habits - constipation, diarrhoea
  • Blood in stool
  • Flatulence
  • Bloating
64
Q

Diverticulitis diagnosis:

A
  • Presence of clinical manifestations
  • Examinations (abdominal xray, abdominal CT with oral contrast, abdominal ultrasound, sigmoidoscopy or colonoscopy
  • Pathology (FBC - elevated white cell count, inflammatory markers - elevated CRP)
65
Q

Diverticulitis treatment:

A

Treatment for uncomplicated diverticulitis focuses on:
- Antibiotics to clear the infection and inflammation
- Pain relief
- Bowel rest
- Liquid or high-fibre diet until resolved
Increased fluids - water

66
Q

What is a bowel obstruction?

A

Occurs when the intestinal contents can not pass through the GIT

67
Q

Partial bowel obstruction:

A

Intestine partially blocked, resolves with conservative treatment

68
Q

Complete bowel obstruction:

A

Intestines completely blocked, nothing can get through, requires surgery

69
Q

Closed loop bowel obstruction:

A

Strangulated - no blood supply, leads to an ischaemic gut

70
Q

Bowel obstruction causes (mechanical and non-mechanical):

A

Mechanical;

  • Detectable occlusion of the intestinal lumen
  • Occurs mostly in the small intestine
  • Examples include: surgical adhesions, birth defect, hernia strictures from for example Crohn’s disease, intussusception, cancer, diverticular disease, severe constipation

Non-mechanical;

  • Results from neuromuscular or vascular disorders, some medications, infection
  • Examples include paralytic ileus, pseudo-obstruction, vascular obstruction
71
Q

Bowel obstruction pathophysiology:

A

Obstruction occurs → fluid, gas and intestinal contents accumulate above the obstruction → bowel below the obstruction collapses → distension of the intestine → ↓absorption of fluids → stimulates intestinal secretions → ↑ distention → ↑ intraluminal pressure in bowel → ↑ capillary permeability → extravasation of fluids and electrolytes into peritoneal cavity → retention of fluids in intestines and peritoneal cavity (third spacing) → severe reduction in circulating blood volume → hypotension and hypovolemic shock → if blood flow ↓ → oedema to bowel → cyanosis → bowel ischaemia → gangrene / necrosis → perforated bowel → infection → sepsis → death

72
Q

Clinical manifestations of a small bowel obstruction:

A
  • Colicky abdominal pain
  • Nausea /vomiting (sometimes projectile)
  • Abdominal distension
  • Constipation and decreased flatus/bowel sounds
73
Q

Clinical manifestations of a large intestinal obstruction:

A
  • Colicky abdominal pain
  • Nausea and vomiting - usually gradual in onset
  • Foul/faecal smelling vomitus (indicates a long-standing obstruction and requires immediate surgery)
  • Abdominal distention
  • Constipation and decreased flatus/bowel sounds
  • Rigidity - late stage obstruction with associated peritonitis and perforation
74
Q

Bowel obstruction diagnosis:

A
  • Abdominal X-RAY, CT or MRI
  • Colonoscopy or sigmoidoscopy to allow visualisation of the bowel
  • Blood test - WBCs may indicate strangulation or perforation of bowel
75
Q

Bowel obstruction management:

A
  • Nil by mouth
  • Nasogastric tube insertion for decompression
  • Parenteral nutrition
  • IV fluids - normal saline or Hartmann’s solution
  • Occasionally potassium additive
  • Medications for symptom management - antiemetics, analgesia, antibiotics
76
Q

Common medications used in relation to the GIT (gastric motility medications):

A
  • Antiemetics/GI stimulants
  • Laxatives
  • Antidiarrhoeal
77
Q

What is a stoma?

A

A section of the bowel is brought to the surface of the abdominal wall, sutured in place and left open to form a stoma (colostomy = colon + ostomy)

78
Q

What would lead to someone to require a stoma?

A

Complications from a GIT disorder can result in the impairment of the elimination of faeces which may require surgery to create a new passage and opening (stoma) for waste removal.

79
Q

Stoma causative factors:

A
  • Trauma to the abdomen
  • Cancers e.g. colorectal cancer, cancers of the pelvic organs
  • Diseases such as diverticulitis, Crohn’s disease, ulcerative colitis
  • Congenital abnormalities
80
Q

What is a nasogastric tube?

A

A nasogastric tube (NGTs) is a long, thin polyurethane, silicone, or rubber tube that’s inserted into an individual’s nostril (or mouth) and down into the stomach

81
Q

How long is a NGT usually in place for?

A

> 6 weeks

82
Q

Indications to why someone would require a NGT?

A
  • To decompress the stomach in patients with a bowel obstruction that may prevent the stomach contents from moving down into the bowel
  • To allow removal of stomach contents (aspiration of gastric contents) such as vomitus
  • To administer medications, nutrients or hydration
  • To assess GI bleeding
  • Gastric lavage (irrigation) or aspiration of toxic substances
  • To collect a sample of gastric contents for analysis
  • Patients intubated / mechanically ventilated
  • Patients who have sustained a traumatic injury such as to their oral cavity
  • Comorbidities such as cancer, paralytic ileus
83
Q

2 types of NGTs:

A
  • Levin

- Salem sump

84
Q

What is a levin tube used for?

A

Used for the aspiration of gastric and intestinal contents and administration of tube feedings or medications. It has a single lumen.

85
Q

What is a salem sump tube used for?

A

Have a one-way anti-reflux valve that allows air to enter and prevents gastric contents from escaping. The second vent allows for suction and drainage for the tube. It has a double lumen.

86
Q

What size and length is an adult NGT?

A

12 to 18 fr

105-125cm

87
Q

Complications of NGTs:

A
  • NGT inserted into lungs
  • Patient may vomit / gag from the procedure
  • Tissue trauma = bleeding
  • Pressure area wounds at nostril from the tube with incorrect securing
88
Q

How to confirm NGT position:

A
  • Chest x-ray - this can only be requested by the doctor and is not a nursing action
  • Aspirate gastric contents by attaching a catheter tipped syringe to the end of the NGT and check acidity with pH paper. The result should be < 6 if acidic = in the stomach
  • Be aware: it is no longer a reliable practice to inject air into the tube whilst auscultating over the epigastrium to assess tube position
89
Q

Ongoing care of NGTs:

A
  • Ensure the NGT has no kinks
  • Ensure collection bag is attached - empty is needed
  • Assess drainage
  • Ensure the nose tape is secure: replace tape if soiled or lifting
  • If applicable, ensure the tube is secured to the patient’s gown or clothing securely and is not dragging or pulling
  • Document all assessments and cares in the patient’s clinical record.
90
Q

When should an NGT be flushed?

A

Flush the NGT as ordered, or at least every 4-6 hours or:

  • prior to bolus feed
  • on transfer from another clinical area
  • pre and post medication administration
  • as per dietician
91
Q

What to do when administering feeding via a NGT:

A 
- Check order for type of feeding
Collect equipment: 
- pump
- waterproof pad
- gloves
- feed as ordered
- syringe and pH strip to check position of tube
- Apply gloves
- Check position of tube
- Connect and prime tubing
- Set rate on pump and start
92
Q

NGT feed intolerance signs:

A
  • Nausea & vomiting
  • Stool frequency & consistency – diarrhoea & constipation
  • Complaints of bloating/fullness
  • Abdominal distension
  • Absent bowel sounds (not always reliable)
93
Q

What is hepatitis?

A

A diagnosis of hepatitis means there has been damage to, or necrosis of, the hepatocyte cells, which causes inflammation of the liver. This inflammation can lead to scarring (fibrosis) which impedes the function of the liver and can lead to liver failure or liver cancer. Acute hepatitis can last up to 4 - 6 months.

94
Q

What are the common causes of hepatitis?

A
  • Toxic substances (alcohol, drugs, medications)
  • Viral infections (Hepatitis A,B,C,D,E, cytomegalovirus (CMV), Epstein-Barr virus (EBV), herpesvirus, coxsackievirus and rubella).
  • Autoimmune diseases
  • Cancer or metastases
95
Q

What is Fulminant Hepatitis?

A

A type of acute liver failure that develops suddenly and can lead to massive hepatocellular necrosis.

96
Q

What does Fulminant Hepatitis develop from?

A
  • Paracetamol overdose
  • Viral hepatitis (A,B,C,D or E)
  • Epstein-Barr virus, Herpes Simplex
  • Autoimmune hepatitis
97
Q

Three phases of viral hepatitis:

A

Phase 1. Prodromal phase (also known as Pre-Icteric)
Phase 2. Icteric phase
Phase 3. Recovery phase:

98
Q

What is Phase 1. Prodromal phase of hepatitis?

A
  • Begins 2 weeks after exposure to the virus
  • The infected person may show signs of fatigue, anorexia, malaise, nausea, vomiting, headache, cough and low-grade fever
  • The infection is highly transmissible during this phase
  • Because there is no jaundice present during this stage, patients suffering from these general symptoms may appear to have influenza
99
Q

What is Phase 2. Icteric phase of hepatitis?

A
  • Begins 1–2 weeks after the prodromal phase and lasts 2–6 weeks
  • Patients can develop jaundice, which occurs when bilirubin metabolism or flow of bile into the hepatic or biliary duct systems is interrupted
  • This can also cause dark coloured urine and light-coloured stools
  • The liver is enlarged and tender, and percussion over the liver causes pain
100
Q

What is Phase 3. Recovery phase of hepatitis?

A
  • Commences 6 to 8 weeks after the initial exposure
  • The jaundice begins to resolve but it may take 12 or more weeks for liver function to return to normal as the liver cells regenerate
101
Q

What medications are used to cure hepatitis C?

A

Direct Acting Antiviral Medications: (DAAs)

102
Q

How do Direct Acting Antiviral Medications (DAAs) work?

A

DAAs act by interfering with the proteins in the hepatitis C virus to stop the virus replicating itself.

103
Q

Action of Direct Acting Antiviral Medications (DAAs):

A
  • Affects the viral replication cycle by binding to the receptors on the host cell to stops the virus from entering the cell
  • Standard Interferon has a short half life and requires administration three times per week
  • Pegylated interferon has a long half life and requires administration once per week.
104
Q

Side effects of Direct Acting Antiviral Medications (DAAs):

A

Fever, chills, muscle aches, malaise

105
Q

The nurse is teaching the patient and the family about possible causative factors for peptic ulcers. The nurse explains that ulcer formation is:

A

Promoted by a combination of possible factors that may result in erosion of the gastric mucosa, including certain drugs and alcohol.

106
Q

A patient with upper gastrointestinal bleeding is diagnosed with a peptic ulcer following an endoscopy. The nurse provides education for the patient by explaining that the risk factors for a peptic ulcer include:

A

Smoking, helicobacter pylori

107
Q

The nurse explains to the patient with gastro-oesophageal reflux disease (GORD) that this disorder:

A

Often involves relaxation of the lower oesophageal sphincter, allowing stomach contents to back up into the oesophagus.

108
Q

The nurse explains to the patient undergoing ostomy surgery that the procedure that maintains the most normal functioning of the bowel is:

A

A sigmoid colostomy.

109
Q

Signs or symptoms someone may have developed in the prodromal phase of viral hepatitis:

A

Signs of fatigue, anorexia, malaise, nausea, vomiting, headache, cough and low-grade fever. The infection is highly transmissible during this phase. Because there is no jaundice present during this stage, patients suffering from these general symptoms may appear like they have influenza.

110
Q

Pathophysiology of jaundice:

A

Jaundice is a yellowish discoloration of the skin that results from elevated serum bilirubin, which is caused by an abnormality of bilirubin metabolism or excretion. This can occur when the liver cells are damaged and are unable to conjugate bilirubin (make it fat soluble so that it can be used ). The bilirubin can be either unconjugated or conjugated.

111
Q

Clinical manifestations of jaundice:

A
  • Dark coloured urine and
  • Light-coloured stools,
  • Yellowing of the whites of the eyes (Sclera) .
  • Low-grade fever, joint pain and skin rashes/itchy skin (Pruritis).
  • Patients with impaired hepatic function will have elevated serum (AST & ALT) levels
112
Q

Why can someone with peptic ulcer disease not have NSAIDs?

A

NSAIDs block the Cox-1 enzyme and disrupt the production of prostaglandins in the stomach. A reduction of prostaglandin secretion effects in gastric mucosa, increasing the susceptibility to mucosal injury which can manifest as cause ulcers and bleeding.

113
Q

Oliver has been to the operating theatre to undergo a total colectomy and formation of a stoma. List four immediate nursing interventions you would undertake as part of your focused abdominal assessment:

A
  • Colour of the stoma
  • Drainage
  • Swelling to the abdomen/stoma site
  • Assess for bowel sounds
  • Pain assessment

NUR2228 (6 decks)

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