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
Why are two antibiotics used in tx of PUD?
so resistance doesn't develop to one (?)- says on slides
26
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?
More effective at reducing gastric secretions
27
Why does a patient routinely receive an H2 antagonist or PPI post-op or while in hospital with an acute medical problem?
Decrease risk of stress ulcers