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MDCN 350: Course 1 > PPIs and NSAIDs Continued > Flashcards

PPIs and NSAIDs Continued Flashcards

1
Q

What’re the likely causes in the esophagus, stomach, and duodenum that could be the reason behind a GI UGIB?

A

esophageal: ulcer, tear, varices
stomach: ulcer, varices, vascular abnormality
duodenum: ulcer

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2
Q

Differential Diagnosis for UGIB of the esophagus

A

esophagitis
ulcer
varices
malignancy

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3
Q

DDx for UGIB in the stomach

A 
Mallory Weiss Tear
Ulcer
Erosions/inflammation
GAVE
Portal hypertensive gastropathy
varices
vascular abnormalities (AVM, vascular ectasia, dieulafoy)
malignancy
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4
Q

DDx for UGIB in duodenum

A

ulcers
erosion/inflammation
varices
maligancy

*also biliary or aortoenteric fistula

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5
Q

Peptic ulcer complications if left untreated

A

Bleeding

  • acute bleeding
  • chronic bleeding

Stricture/Obstruction

Perforation

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6
Q

Types of GI bleeding that could be a sign of UGIB

A
  • coffee ground emesis
  • hematemesis
  • melena
  • hematochezia
  • fecal occult blood/fit positive (no actual blood seen,and not for an actually acute situation)
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7
Q

what type of presentation of an UGIB impacts mortality the most?

A

fresh hematemesis and hematochezia has a 29% mortality rate.

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8
Q

rank the types of ulcer on best prognosis

A
  1. clean base (prev 42%, 2% mortality)
  2. flat spot (prev 20, morality 3)
  3. adherent clot (prev 17, mortality 7)
  4. visible vessel (prev 17, mortality 11)
  5. active bleeding (prevalence 18%, mortality 11%)
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9
Q

4 types of endoscopic therapy for UGIB

A
  1. injection therapy (epinephrine or saline)
  2. thermal (cautery or argon plasma coagulation)
  3. mechanical (hemoclips)
  4. Foam (hemospray)

endoscopic therapy reduces risk of re-bleeding and reduces mortality.

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10
Q

Medical, angiography, and surgical management/treatment of PUD

A

medical:

  • Treat the cause: NSAIDS, H. Pylori antibiotics (PBMT etc)
  • PPI

Angiography (when endoscopy fails)
- foam, coils

Surgical Management
- oversew the ulcer

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11
Q

Anti-Ulcer drugs

A

Antacids
H2 receptor antagonists (H2RA)
PPI

Others:
- octreotid (for variceal bleeding)
PGE/prostaglandin E, misoprostol
-sulcrate

HPylori antibiotics
Endoscopic therapy (washing with saline, foam, hemoclips, cautery)
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12
Q

Drugs that specifically target acid reduction in Acute bleeding during PUD

A

PPI: decreases re-bleeding, need for surgery etc.
IC PPI: faster increase in pH. Good for acute. Give 800mg bolus. Less variable.

H2RA has shoqn no reduction in re-bleeding, urgent surgery rates or mortality.

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13
Q

OVERALL: what’s the contemporary treatment of bleeding in PUD

A 
PPI
H Pylori Treatment
Stop provoking etiologies
endoscopic injections
thermal cautery
mechanical hemoclips
foam
angiography (coils)
surgery
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14
Q

Name some PPI options and what is the most financially realistic?

A

omeprazole, pantoprazole Na, rabeprozole, esomeprazole, lansoprazole, pantoprazole Mg, dexlansoprazole

dexlansoprazole is super expensive for its dose of 30mg.
pantoprazole Mg is the best for price. 40mg for 30.

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15
Q

When is the best time to take PPIs and why?

A

most effective if taken before meals.
- PPIs bind to proton pumps actively secreting acid. At fasting state, onl 5% of stomachs proton pumps are active. during meal stimulation, 60-70% of the proton pumps actively secrete acid.

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16
Q

choosing wisely suggests that PPI should be attempted to be stopped at least once a year. What are the exceptions?

A

dont attempt to reduce the amount of PPI if:

  1. barretts esophagus
  2. severe esophagitis
  3. GI bleeding
  4. High risk of bleeding (NSAIDS, antiplatelet therapy)
  5. ZEs
17
Q

general approach to GI bleeding

A
  1. resuscitation: 2 large bore IVs with ringers lactate or saline. endoscopy, make sure BP is stabe, type and transufse if shock symptoms are present, if decrease urine output, or if Hb under 80.
  2. determine site or cause of bleeding. Done via thorough history of NSAID/Hpylori/Mallory Weiss tear etc, and localized via endoscopy
  3. definitive treatment. Also treat HPylori
  4. prevent recurrence
    - PPI management, life style change.
18
Q

Why are NSAIDS typically used?

A

antiinflammatory agents to combat aginst arthritis, connective tissue disases, but can cause GU. Might also be used to alleviate the paid of GU.
- also used as an analgesic

19
Q

explain the pathway of how arachidonic acid normally helps to make prostoglandins in the GI mucosa, kidneys, and cardiovascular structures.

A

In the GI mucosa
- arachidonic acid interacts with COX1 to create PGE2, which is involved in gastric protection– it helps to increase mucus secretion, bicarbonate, mucosal blood flow

In the kidneys
-AA interacts with COX2 and COX 1, to produce PGI2 and PGE2. this promotes afferent arteriolar vasodilation, and increased sodium and water excretion.

in the heart
- AA intreracts with COX 1 and COX 2 to create PGI2 and TXA2. PGI2 promotes vasodilation and inhibits platelet aggregationg., whereas TXA2 facilitates vasoconstriction.

20
Q

What happens if you block COX1 in the GI mucosa?

A

peptic ulcers, GI bleeding

21
Q

what happens if you block COX 1 and 2 in the kidneys

A
  • sodium and water retention
  • hypertension
  • hemodynamic state
  • kidney injury
22
Q

What happens if NSAIDS are localized in the heart

A

causes COX2>COX1 inhibition. may lead to stroke of MI

23
Q

How do COX inhibitors (NSAIDS) Cause PUD

A

NSAID can block COX1: results in reduced mucosal blood flow (PGE2), reduced mucus and bicarb secretion, and impaired platelet aggregation. this causes impaired defenses and thus mucosal injury and bleeding
NSAIDS can block COX2 which results in reduced angiogenesis, and increased leukocyte adherence whch results in leukocyte activation and then further mucosal injury and bleeding.

Without the interactions with COX, NSAIDS can also cause general epithelial damage (esp if swallowed without water and can cause esophagitis), results in acid diffusion and impaired platelet aggregation and then mucosal injury and bleeding.

See slide 94 for diagram.

24
Q

which lab result may point to hidden NSAID over use

A

Anemia, low albumin

25
Q

Both COX1 and COX2 inhibition affect the mucosa, but which one is more involved in the GI tract?

A

COX1. we gotta start making NSAIDS that only afect COX2 so that we maintain PGE2 activity and the integrity of the GI mucosal layer

26
Q

T/F: PPIs may make NSAID injury worse

A

true, possible due to the changing microbiome

27
Q

Demographics of people at risk for GI Complications that can exacerbate NSAID use

A 
age 60-75
history of UGI symptpoms
history of UGIB
history of peptic ulcer
high dose NSAID
multiple NSAID
COncomitant low-dose ASA
concomitant anticoagulants
concomitant corticosteroids
concomitant selective serotonin reuptake inhibitors
severe rhematoid arthritis disability
history of CVD
HPylori positive
28
Q

fenoprofen, ibuprofen, tolemtin, naproxen, aspirin, indomethacin, ketoprofen, and flurboprofen are all ___ selective NSAIDS

A

COX1 selective. these can really cause GI disturbance.

29
Q

most people take NAIDS to treat arthritis. What are the alternatives in the treatment of arthritis if a person is experiencing UGIB/Gi problems

A 
acetominophen for an analgesic
immunosuppresicces
glucocorticoids
biologic agens
safer use of NSAIDS
Selective COX2 inhibitor nsaids like lumiracoxib, rofecoxib, etodolac, diclofenac
30
Q

Coxibs. What are the “cons”?

A

COX2 inhibitors. theres a bunch that are made, and they account for 60% of all NSAID costs.theyre effective with similar efficacy as traiditonal NSAID use, and have a lower rate of GU/DU versus NSAIDS, BUT THIS EFFECT IS LOST WITH LOW DOSE ASA

CONS: increased risk of MI and other CV events, therefore only one is currently marketed (Celecoxib). Vioxx (anotehr type of coxib) has been shown to have an incidence of serious thromboembolic edverse events

31
Q

Medications for preventing and treating NSAID induced ulcers

A
  • misoproblem reduces ulcers but also causes GI side effects. H2ra blockers, PPI, significantly reduce ulcers.
32
Q

What to do if NSAIDS are needed:
Low CV risk pt
high CV risk pt (Low dose asprin required)

A

Low CV risk:
WIth Low GI Risk: NSAID alone but hte least ulcerogenic one at lowest effective dose
With MOderate GI risk: NSAID and PPI/Misoprostol
High GI Risk: Alternative therapy if possible, or COX2 inhibitor + PPI/misoprostol

High CV Risk:
Low I risk: NAPROXEN and PPI/misoprostal
Moderate GI risk: same
High GI risk: Avoid NSAIDS or COX2 inhibitors. Use alternative therapy

remember that GI risk factors include
Age
High dose NSAID therapy
a previous history with uncomplicated ulcer
concurent use of aspirin, corticosteroids or anticoaulants.

MDCN 350: Course 1 (48 decks)

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