PUD (Class) Flashcards

1
Q

Causes/risk factors for PUD?

A
  • Infection from Helicobacter pylori
  • Excessive secretion of HCL (r/t stress (life, hospitilization, sepsis), milk, caffinated beverages, smoking, ETOH
Chronic use of:
     -NSAID’s
     -ETOH
     -Excessive smoking
? Familial tendency
? People with Type O blood
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2
Q

In which population does PUD NOT generally occur?

A

Women of childbearing age

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3
Q

How does NSAIDs contribute to formation of PUD?

A

-NSAID inhibit the secretion of mucous to protect the gastric mucosal layer.

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4
Q

How is H pylori spread?

A

Food + water

-Can also be caused through person-person transmission of the bacteria (close contact and exposure to emesis)

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5
Q

Do all of those infected with H Pylori get ulcers?

A

NO

  • more than 50% of the worlds’ population harbor H. Pylori in their upper GI tract
    • 80% of people are asymptomatic (?may play a role in natural stomach ecology)
  • It is not known why HP infection does not cause ulcers in all people
    • most likely, predisposition to ulcer formation depends on certain factors like type of HP
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6
Q

WHere in the world is infection with H pylori more prevalent?

A

in developing countries

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7
Q

How does a urea breath test work?

A

-based upon the ability of HP to convert urea to ammonia and CO2; pt swallow urea labelled with an uncommon isotope (radioactive carbon-14 or non-radioactive carbon-13  10-30 minutes: detection of isotope-labelled CO2 in breath indicates the urea was split  indicates that urease (enzyme that HP uses to metabolize urea) is present in the stomach  HP bacteria are present

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8
Q

How is PUD treated?

A

Treatment: one week “triple therapy” consisting of PPI (omeprazole); and antibiotics clarithromycin and amoxicillin (or metronidazole for pen allergies)

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9
Q

Clinical manifestations of PUD?

A
  • Symptoms may differ depending on the location of the ulcer (duodenal vs gastric)
  • Pain (or not, dull or burning)
  • Pyrosis (heartburn)
  • Eructation (burping)
  • Vomiting
  • Constipation
  • Diarrhea
  • Bleeding (occult and/or melena)
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10
Q

Assessments for pt with PUD?

A

Does the patient have any history of potential causes/risk factors? RQRST related to pain? Medications (prescribed and OTC)

  • describe pain and methods to relieve pain
  • characteristics of vomitus (?red; ?coffee grounds)
  • 24hour diet record/food habits
  • lifestyle habits (?smoking; ?NSAID’s; ?stress)
  • palpate for localized tenderness
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11
Q

What would you potentially find or not during the physical assessment?

A

-Episgastric tenderness, abdo distention; tachycardia/hypotension (?anemia from GI bleeding)

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12
Q

Labs important in PUD?

A

Hgb for bleeding (platelets, ptt PTINR)

Na, K, renal function for vomiting/diarrhea ,decreased oral intake, medication use

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13
Q

Key aspects of medical management of PUD?

What meds, lifestyle changes, sx

A

Medications: antibiotics, proton pump inhibitors, bismuth salts, histamine 2 receptor antagonists (adherence to regime important)

Lifestyle changes: stress reduction, dietary changes, smoking cessation

Surgical intervention: for intractable ulcers, life threatening haemorrhage, perforation or obstruction

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14
Q

4 main potential problems for PUD?

A

hemmorrhage

  • perforation
  • penetration
  • pyloric obstruction
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15
Q

Key planning/goals for nursing intervention in PUD?

A
  • relief of pain
  • reduce anxiety
  • maintenance of nutritional requirements
  • knowledge about management and prevention of ulcer recurrence
  • absence of complications
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16
Q

Goals in changing diet with pUD?

A
  • Avoid over-secretion of acid

- Minimize hypermotility

17
Q

What ending indicates a proton pump inhibitor?

A

-prazole

Pantoprazole (Pantoloc)
Esomeprazole (Nexium)
Lansoprazole (Prevacid)
Omeprazole (Losec)
Rabeprazole (Pariet EC)
18
Q

PPIs
New or old?
What are they used for?
What do they do?

A

Relatively new

Widely used for the treatment of PUD and GERD

Block the gastric proton pump found in the gastric parietal cells  targets the terminal step in acid production

Example: Omeprazole (Losec)

19
Q

H2RA

How do they work?
When are they used?

A

H2 receptors are responsible for increasing acid secretion in the stomach

Effective at suppressing the volume/acidity of stomach acid

Also used pre-operatively

Example: Ranitidine (Zantac)

20
Q

H2RA
What kind of dietary consideration is required for these drugs?
Other adverse effects?

A

can cause Vitamin B12 deficiency (stomach acid helpful in absorption)

  • MS changes in elderly
  • can also cause UTOX to come back positive for amphetamines!
21
Q

Antacids
What are they made from?
Examples?

A

Made from: aluminum/magnesium/calcium/potassium/sodium hydroxide or bicarbonate

Example: Maalox; MOM; TUMS
Maalox = Aluminum bicarbonate
MOM = Magnesium hydroxide
Tums = Calcium carbonate

22
Q

Pink Lady – Maalox and viscous xylocaine Why use it?

A

used for GERD in an acute pain episode, not given routinely.

xylocaine = lidocaine = anesthetic

23
Q

Who are antacids contraindicated in? Which are less harmful in this regard?

A

-contraindicated for people with renal failure (aluminum may accumulate to toxic levels)
–calcium based formulas pose less risk

24
Q

What antibiotics are used in PUD?

A

Carithromycin and amoxicillin (or metronidazole for penicillin allergies)

25
Q

Why are two antibiotics used in tx of PUD?

A

so resistance doesn’t develop to one (?)- says on slides

26
Q

Your patient tells you that his previous medication, ranitidine (Zantac) is cheaper than what the doctor has prescribed. What is the advantage of PPI over H2 Antagonists?

A

More effective at reducing gastric secretions

27
Q

Why does a patient routinely receive an H2 antagonist or PPI post-op or while in hospital with an acute medical problem?

A

Decrease risk of stress ulcers