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Clinical 2 (Part B) > 14 - Dyspepsia > Flashcards

14 - Dyspepsia Flashcards

1
Q

What 2 things cover the stomach from the esophagus?

A

diaphragm and LES

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2
Q

Define dyspepsia

A
  • bad digestion
  • “predominant epigastric pain lasting at least 1 month”
  • “can be associated with any other upper GI symptom such as epigastric fullness, n/v, heartburn, provided epigastric pain is the patient’s primary concern”
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3
Q

What are the 2 categories of dyspepsia?

A
  • Organic
  • Functional (non-ulcer)

Functional = no cause that we can find

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4
Q

Describe the categories of Organic Dyspepsia

A

Organic:

  • PUD
  • GERD
  • BE (Barrett’s esophagus)
  • Cancer
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5
Q

What are some other causes of dyspepsia?

A
  • Gastritis: bile reflux, viral infection
  • Parasites
  • Pancreatitis or other abdominal cancers
  • Carb malabsorption
  • Systemic diseases: diabetes, thyroid, connective tissue
  • Drugs: antibiotics, iron, NSAIDs
  • Herbs: saw palmetto, garlic, feverfew
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6
Q

What is PUD?

A

-a group of ulcerative disorders that are dependent on BOTH acid AND pepsin for their production

ACID and PEPSIN

-common symptomatology include episodic epigastric pain, and heartburn

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7
Q

What are the 2 types of PUD?

A
  • gastric ulcers (GU)

- duodenal ulcers (DU)

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8
Q

What is the PUD pathology?

A

imbalance between mechanisms of injury and protection/repair

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9
Q

What are some sources of injury of PUD ?

A

acid, enzymes and toxins (ex. bacteria, viruses, drugs)

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10
Q

What are some complications of PUD?

A
  • perforation
  • penetration
  • hemorrhage
  • gastric outlet obstruction
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11
Q

What are some risk factors for PUD ? (there are 2 main ones !!)

A

Main:

  • *H pylori
  • *NSAIDs

Other:

  • zollinger ellison
  • genetic
  • smoking?
  • alcohol?
  • caffeine?
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12
Q

Describe the diagnosis of PUD

A
  • Endoscopy and (much less commonly) diagnostic imaging (ex. CT)
  • Barium swallow (almost never now) - it will see big ulcers but not small ulcers
  • H. pylori: Test & Treat
  • PPI Test

**most common is PPI test. Give them one and see if they improve

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13
Q

Treatment goals of PUD ?

A
  • Symptom relief
  • Accelerate healing
  • Prevent and treat complications (such as perforation, penetration, hemorrhage, gastric outlet obstruction)
  • Prevent recurrence
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14
Q

Non-pharms for PUD

3 categories

A

1) Nutrition:
- Avoid large HS meals (increases acid production)

2) Avoid precipitations and factors affecting healing:
- Drugs (NSAIDs, ASA)
- Smoking, alcohol, excess caffeine

3) Surgery: rarely needed
- acute treatment (primarily endoscopic)
- secondary prevention with selective gastric vagotomy almost never done now

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15
Q

Antacids for PUD:

Place of therapy?

A

for symptomatic relief due to compliance issues

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16
Q

Antacids for PUD:

Equivalence based on ?

A

acid neutralizing capacity

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17
Q

Antacids for PUD:

When do you give them?

A

Give 1 & 3 hour post meals & at HS

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18
Q

Antacids for PUD:

SE ?

A
  • constipation or diarrhea (calcium or magnesium)

- drug interactions

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19
Q

Antacids for PUD:

List 2 things you need to watch for

A
  • Na Bicarb content in CHF/Cirrhosis patients

- Magnesium based salts in dialysis patients

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20
Q

H2 Blockers for PUD:

Decrease acid production by ____

A

50-75%

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21
Q

H2 Blockers for PUD:

Describe the healing rate for GU and DU

A

DU:

  • 80% are healed in 4 weeks
  • 90% are healed in 8 weeks

GU:
-ulcers need min 8 week therapy

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22
Q

H2 Blockers for PUD:

Equivalence amongst agents?

A

All the same at appropriate dosage.

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23
Q

H2 Blockers for PUD:

How often are they given?

A

1-2 times per day

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24
Q

H2 Blockers for PUD:

Side effects ?

A

very low SE except for drug interactions with cimetidine

  • cimetidine is hardly used due to drug interactions
  • won’t have sedation from H1 blockade bc these are specific to H2
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25
Q

PPIs for PUD:

How much do they decrease acid?

How long do the effects last?

A
  • 80% at 2 hr
  • 50% at 24 hours

-effects last 3 days

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26
Q

PPIs for PUD:

Will doubling the dose of omeprazole help a lot (ex. 20mg to 40mg) ?

A

only decreases acid by further 6%

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27
Q

PPIs for PUD:

They are ___ ______

A

gold standard !!!

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28
Q

PPIs for PUD:

Heals ulcer quicker than _________

A

H2 blockers

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29
Q

PPIs for PUD:

PPI’s also have a key role in _____ eradication regimens

A

H. pylori

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30
Q

PPIs for PUD:

Best suited for ?

A

Serious upper GI bleeding, refractory PUD.

In reality, these are the only agents used to treat active ulcers

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31
Q

PPIs for PUD:

Are they all equivalent?

A

likely all the same

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32
Q

Describe the PUD recurrence

A

With H2 Blocker:

  • 20% of ulcers are unhealed at 4 weeks
  • <10% of ulcers are unhealed at 8 weeks
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33
Q

When is treatment considered refractory for ulcers?

A

DU: If fail 8 week therapy

GU: If fail 12 week therapy

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34
Q

What do most people use for recurrence of PUD ?

A

twice daily PPI

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35
Q

What are some reasons for recurrence of PUD ?

A
  • Non-adherence
  • H. pylori (re-test all serious bleeders to ensure eradication)
  • NSAIDs
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36
Q

For H. pylori eradication, who should get triple therapy and who should get quadruple therapy ?

How long is Tx ?

A

For those with low risk for clarithromycin resistance (<15%) or proven high local eradication rates (>85%): use triple therapy

For all others: use quadruple therapy

14 day Tx

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37
Q

For Manitoba, how are our clarithromycin resistance rates?

A

> 15% threshold

HENCE recommend quadruple therapy

*this was based on a very limited sample size

38
Q

Up to __% of patients with complications cured of HP will have an ulcer recurrence in 6 months

A

20

39
Q

What type of patients require chronic therapy for prophylaxis of ulcers?

A

Those with a severe PUD complication or significant co morbidity, a case can be made for placing these on a once daily PPI indefinitely

ex. dialysis patient with a PUD bleed that required hospitalization

40
Q

PPI Chronic use:

Increases ____ level by 2-4 fold

A

gastrin

41
Q

PPI Chronic use:

What effects does gastrin have? What fear does this result in?

A

Proliferative effects on:

  • ECL cells
  • parietal cells

These effects can result in hyperplasia and/or hypertrophy (rebound hypersecretion)

Leads to a fear of cancers but has not been seen in humans

42
Q

List SE of PPI (3)

A

1) Infections:
- CAP
- C. dif

2) Fractures

3) Interaction with clopidogrel (increases cardiac events)
* Prospective data does not support this view

43
Q

When should PPI therapy be stopped?

A

If it is no longer providing benefit and patients should not have long-term PPI therapy without attempts to withdraw it every 6-12 months

44
Q

Define GERD

A
  • Retrograde spilling of gastric contents into the esophagus
  • Occurs in everyone but is pathogenic only in some
  • Both structural and symptomatic pathology which often do not coincide with each other
45
Q

List classical symptoms of GERD

A
  • Regurgitation
  • Heartburn
  • Dysphagia (trouble swallowing)
  • Odynophagia (painful swallowing)
46
Q

List atypical symptoms of GERD

A
  • Coughing
  • Wheezing (asthma)
  • Globus sensation
  • Laryngitis
  • Chest pain
  • Dental erosions
47
Q

What are some risk factors for GERD?

A
  • Pregnancy or obesity
  • Increased age (poor acid clearance)
  • Disease states (ex. Sjogren’s)
  • Hiatus Hernia ?
48
Q

What is a Hiatus Hernia (HH) ?

A

Normally, the LES and diaphragm work together to seal off stomach from esophagus

In HH, the LES move sup and they aren’t working together and the seal is not as tight.

49
Q

Complications of GERD (4)

A
  • Esophagitis and much less commonly esophageal bleeding
  • Esophageal stricture (chronic inflammation can cause fibrosis and cause esophageal stricture and then you can’t swallow as easily)
  • Barrett’s Esophagus
  • Esophageal Cancer
50
Q

How is GERD diagnosed?

A
  • Endoscopy
  • Barium swallow
  • pH monitoring
  • Impedance monitoring
  • Antisecretory therapy (PPI Test) *just give them a PPI and see if their symptoms improve
51
Q

GERD is a ____-driven disease

A

symptom

52
Q

What are the subgroups of GERD?

A

1) NERD: non-erosive reflux disease
2) EE: erosive esophagitis
3) BE: barrett’s esophagus (and esophageal cancer)

53
Q

Goals of GERD?

same as for PUD

A
  • symptom relief
  • accelerate healing
  • prevent and treat complications (esophagitis, esophageal bleeding, esophageal stricture, BE, esophageal cancer)
  • prevent recurrence
54
Q

Lifestyle mods/ non-pharms for GERD

A
  • smaller, more frequent meals
  • avoid foods that precipitate events
  • avoid smoking
  • reduce alcohol & caffeine
  • obtain ideal weight
  • stress reduction
  • reassurance
55
Q

There are ____ and ____ types of surgery to treat ulcers.

A

open and laproscopic

56
Q

Who is surgery revered for ?

A

mostly reserved for those with severe LES problems or reluctance to use medications

57
Q

What drug was the best at treating erosive esophagitis ?

A

PPI

58
Q

Antacids in GERD:

place in therapy?

A

provides symptom relief

59
Q

Antacids in GERD:

When should they be given?

A

Give 1 & 3 hr post meals & at HS or PRN

60
Q

H2 Blockers in GERD:

Dose compared to PUD?

A

Can go up to twice the PUD dose (ex. ranitidine 300mg BID)

  • Bc of cost this is rarely done now
  • If you’re going up on dose, might as well go to PPI
61
Q

H2 Blockers in GERD:

place in therapy?

A

commonly employed for OTC use, step out and step down GERD regimens

62
Q

List some examples of Prokinetics

A
  • cisapride
  • comperidone
  • metoclopramide
63
Q

MOA of prokinetics

A
  • increase LESP

- accelerate gastric emptying

64
Q

Best agent of prokinetics ?

A

cisapride - but it’s very difficult to get now due to risk of cardiac arrhythmias

65
Q

SE of cisapride

A

risk of cardiac arrhythmias

66
Q

SE of metoclopramide

A

CNS adverse events but it is an excellent antiemetic

67
Q

Overall efficacy of prokinetics ?

A

probably near H2 blockers though lacking clinical studies

*not good long term as there are bad adverse effects so only for episodic use

68
Q

PPI for GERD:

They are ____ _____

A

gold standard

69
Q

PPI for GERD:

Heals EE quicker than _____ ____

A

H2 blockers

70
Q

PPIs have a key role in _______ ______

A

barrett’s esophagus (BE)

71
Q

Everyone with BE gets what for life?

A

high dose PPI

though this is not proven to decrease rates of esophageal cancer

72
Q

Describe the recurrence of GERD

A
  • considered a chronic disease or chronically relapsing disorder
  • questions remain on who requires continuous (daily) therapy
73
Q

Define functional dyspepsia

A

-defined as dyspepsia of at least 3 months with no clearly identifiable pathology (structural or biochemical)

74
Q

Functional Dyspepsia:

postulated mechanisms?

A
  • both motor and sensitivity changes in the GI tract are postulated mechanisms
  • increase sensitivity to organ distension
  • poor correlation between actual delayed gastric emptying, patient symptoms and response to prokinetics
  • contribution of psychosocial issues in the prevalence and severity of FD is considerable debate
75
Q

What are symptom subgroups of FD ?

A

Symptom subgroups can include:

  • ulcer-like dyspepsia
  • dysmotility-like dyspepsia
  • reflux-like dyspepsia
76
Q

Goals of therapy for FD?

A
  • symptom relief
  • prevent recurrence

*there’s no damage so we’re just treating symptoms

77
Q

What is the approach for treating functional dyspepsia ?

A

-H. pylori test and treat

For H. pylori negative patients:

  • Endoscopy vs PPI
  • PPI vs H2B
  • PPI vs Prokinetics
  • TCAs/SSRIs
  • CBt and other psychological approaches (IBS lecture)
78
Q

Lifestyle mods for FD?

A
  • smaller, more frequent meals
  • avoid foods that precipitate events
  • avoid smoking
  • reduce alcohol
  • reduce caffeine
  • obtain ideal weight
  • stress reduction
  • reassurance
79
Q

Are antacids beneficial in FD?

A

-appear to be of limited to no benefit

80
Q

OTC H2 blockers are more used for _____ and ____ than for dyspepsia

A

GERD and PUD

81
Q

Are PPIs beneficial in FD ?

A
  • significant benefit over placebo but it is less than overwhelming
  • PPIs much more beneficial for ulcer and reflux like symptoms
82
Q

dose of PPIs in FD ?

A

limit PPI to once daily - don’t increase to BID for FD

*don’t confuse this recommendation with GERD (may increase PPI to BID for GERD and we use for OD and BID PPI for active treatment of peptic ulcers)

Do not use BID PPI for PUD prophylaxis though

83
Q

Describe alternative therapies in FD

A
  • theory that the symptoms may be related to psychiatric disorders (depression, anxiety, somatic, etc)
  • SSRIs and anxiolytics = no benefit (best to avoid)
  • Best evidence is with TCAs (amitriptyline and imipramine)
84
Q

When do we recommend TCA for FD?

A

when patients get no symptom relief from PPI (TCA over pro kinetic)

85
Q

When does the TCA over pro kinetic not apply ?

A

to other indications such as diabetic gastroparesis

86
Q

Prokinetics:

How long do we limit metoclopramide use?

A

12 weeks

87
Q

Prokinetics:

Daily dose of domperidone ?

A

max of 30 mg daily (10mg TID)

88
Q

Few trials indicated that any therapy is proven very effective for ___. Despite this up to 98% of ppl who seek medical help for ___ will get a drug prescribed

(same blank)

A

FD

89
Q

___ weeks should be more than enough time to determine benefits of therapy for FD

A

4

90
Q

Describe the relapses of FD

A

commonly relapses with up to 2/3 of patients have the same symptoms 3 years later

91
Q

Dyspepsia encompasses both _____ and _____ disorders

A

organic and functional

92
Q

Dx and Tx goals are dependent on the _____ of dyspepsia

A

cause

Clinical 2 (Part B) (30 decks)

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