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Pharmacology B > Lecture 11 - GI > Flashcards

Lecture 11 - GI Flashcards

1
Q

Where is gastric mucosa secreted from?

A

mucosal epithelial cells

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2
Q

Why is the gastric mucous layer important?

A

This mucous layer protects from the cells of the stomach from the acid and enzymes in the lumen of the stomach (otherwise the stomach would eat itself)

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3
Q

What can loss of the mucous layer lead to?

A

It can allow acid to reach the cells and cause an ulcer

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4
Q

Parietal cells in the stomach make _____ (one of the strong acids known)

A

HCl

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5
Q

What is the purpose of HCl in the stomach?

A

This acid is primarily to kill bacteria, viruses and other parasites, not for digestion

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6
Q

What can overproduction of the acid (hyperacidity) lead to?

A

It can overwhelm the mucous layer and buffer systems and lead to ulcers

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7
Q

What is a systemic antacid?

A

NaHCO3

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8
Q

NaHCO3 dissociates into?

A

Na+ and HCO3- (bicarbonate)

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9
Q

What effect does the bicarbonate ion have on the stomach?

A

The bicarbonate ion isn absorbed into the blood and slightly increases pH (alkalosis)

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10
Q

NaHCO3 is quick, easy, and effective in the ____ term to reduce stomach acid

A

short

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11
Q

Problems with NaHCO3 antacids?

A
  • Alkalotic urine can increase the deposition of calcium and phosphate to form a kidney stone (cranberry juice does the opposite)
  • This increases blood sodium, thus exacerbating HTN
  • Acid rebound due to feedback regulation
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12
Q

List some non-systemic antacids

A

CaCO3
Al(OH)3
Mg(OH)2

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13
Q

Do non-systemic antacids affect extracellular or blood pH?

A

No

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14
Q

Aluminum and calcium antacids are _______, thus they are often combined with magnesium

A

constipating

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15
Q

______ ____ receptors in parietal cells stimulate HCl secretion from these cells

A

Muscarinic Ach

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16
Q

Inhibiton of Muscarinic Ach receptors reduces ____ _______

A

acid secretion (but not by much)

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17
Q

List an example of a Muscarinic type 1 ACh Receptor blocker

A

Pirenzipine

*can reduce acid by up to 40%

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18
Q

SE of anticholinergics?

A

dry mouth, dry eyes, sedation, etc.

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19
Q

Are anticholinergics a good choice?

A

Not really

-Since they are very non-selective and therefore will cause lots of side effects and limited acid reduction

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20
Q

What are Cytoprotectives?

A

Drugs which protect cells from acidic damage, either directly or through stimulation of mucous

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21
Q

What are two major Cytoprotective drugs?

A
  • Sucralfate

- Misoprotol

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22
Q

Sucralfate is an ______-based salt

A

aluminum

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23
Q

Describe Sucralfate

A

Aluminum base salt:

  • Binds to hydrogen ions to form a gooey paste, increasing pH (decreasing acidity)
  • Also binds to degenerating cells, forming a protective layer
  • “Artificial” mucous
  • It is not absorbed into the bloodstream, but can inhibit absorption of other drugs
  • Works for 8-12 hours, specifically protects damaged tissue as well as reducing acidity
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24
Q

Describe Misoprostol

A

Misoprostol is a prostaglandin analogue which stimulates production of the mucosal layer
*Often given with Diclofenac (NSAID) to counteract stomach issues

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25
Q

What does stimulation of H2 receptors in parietal cells cause?

A

increases HCl production

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26
Q

______ of H2 receptors are highly effective in a number of acid-related disorders

A

Inhibition

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27
Q

H2 blockers are very _____ to the organ, to the receptor type (do not cross to PGE) and no adverse effect on mucosa

A

specific

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28
Q

List 3 H2 blockers

A
  • Cimetidine
  • Ranitidine
  • Famotidine
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29
Q

Cimetidine (H2 blocker):

Causes ____% reduction in acidity

A

50-60 (moderate)

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30
Q

Cimetidine (H2 blocker):

Binds to Cyt ___ to cause DI

A

P450

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31
Q

Cimetidine (H2 blocker):

Binds to androgen receptors - so what adverse effects can it cause?

A
  • gynecomastia
  • reduced libido
  • impotence
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32
Q

Ranitidine (H2 blocker):

Causes _____% reduction in acidity

A

65-70 (more effective than cimetidine)

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33
Q

Ranitidine (H2 blocker):

Why does it cause less drug interactions than cimetidine?

A

Only binds P450 at high doses

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34
Q

Ranitidine (H2 blocker):

Does it bind to androgen receptors?

A

No

**Therefore less side effects

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35
Q

Brand name of Cimetidine?

A

Tagamet

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36
Q

Brand name of Ranitidine?

A

Zantac

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37
Q

Brand name of Famotidine?

A

Pepcid

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38
Q

Famotidine (H2 blocker):

Why is it the most effective?

A
  • Doesn’t bind to P450 at all
  • Very few adverse side effects
  • Famotidine is the most effective at reducing acid secretion and has the best safety profile
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39
Q

Proton Pump Inhibitors (PPI):

MOA

A

Inhibit gastric H+/K+ ATPase Proton Pump

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40
Q

Proton Pump Inhibitors (PPI):

Are especially good for ____ reduction of acid

A

rapid

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41
Q

Proton Pump Inhibitors (PPI):

Where do they bind to?

A

Bind to H+ extrusion sites and block the release of H+ and Cl-

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42
Q

Proton Pump Inhibitors (PPI):

_____ effective

A

fairly

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43
Q

Proton pump inhibitors all end in _____

A

prazole

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44
Q

List some PPI’s

A 
Omeprazole
Esomeprazole
Lansoprazole
Pantoprazole
Rabeprazole
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45
Q

PPI’s are especially good for ____

A

GERD (as well as other acid-dependent disorders)

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46
Q

Proton Pump Inhibitors (PPI):

Are generally ____ and ____

A

safe and cheap

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47
Q

Describe in detail the MOA of Proton Pump Inhibitors (PPI)

A
  • PPI’s enter the secretory canaliculus of the parietal cell which opens when acid secretion occurs
  • The pro drug is converted to the active drug here
  • PPI’s bind very tightly to the channel, thus have a long half-life

*Rabeprazole also increases mucous secretion

48
Q

In the early 1980’s, what was found to be the major cause of ulcers?

A

H. Pylori infection

49
Q

H.Pylori is present is ___% of duodenal ulcers and ____% of gastric ulcers

A

95

80

50
Q

How does H. Pylori cause an ulcer?

A
  • To escape gastric acid, H P burrows into the gastric mucosa
  • HP then produces urease, the enzyme that converts urea to ammonia and CO2
  • This kills mucosal epithelial cells, leaving the gut unprotected
51
Q

List some ways that we can test for H. Pylori infection

A
  • Breath test for urea
  • Serological
  • Culture
  • Histology
52
Q

What treatment do we recommend for H. Pylori infection?

A

Combination of anti secretory or antibiotic treatments as it is more effective than either alone

53
Q

What is defined as triple therapy for an H. pylori infection?

A

-A PPI to control acid and 2 effective antibiotics to kill the HP

54
Q

What is defined as quadruple therapy for an H. pylori infection?

A
  • A PPI to control acid and 2 effective antibiotics to kill the HP
  • Add bismuth
55
Q

What is GERD?

A

Gastroesophageal Reflux Disease:

  • The most prevalent type of ulceration-5X more common that gastric ulcers
  • Lower esophageal sphincter (LES) defect allows acidic contents to contact the esophageal lining
56
Q

What kind of drugs can contribute to GERD by reduces LES pressure and allowing reflux?

A
  • B blockers
  • Ca channel blockers
  • Nicotine
57
Q

Treatment of GERD?

A

Pharmacological treatments (PPI) are not nearly as effective as behavioural changes:

  • Avoid fat, caffeine, chocolate, peppermint, and alcohol
  • Avoid large meals, especially right before bed, stop smoking
58
Q

What is Ulcerative Colitis?

A
  • Inflammation of the submucosa

- Ulcerations may cover the entire surface of the colon

59
Q

Symptoms of Ulcerative Colitis?

A

-Diarrhea, bleeding, severe pain

60
Q

What can Ulcerative Colitis cause?

A
  • loss of nutrition
  • anemia
  • starvation is a risk

*can cause colon to be come “stiff” from scarring and burst, leading to peritonitis

61
Q

What is Crohn’s disease?

A
  • Inflammatory disease which can cover the entire digestive system
  • Tends to be separate, isolated regions of inflammation
  • Unlike UC, fistulas may form
  • Unlike UC, the intestinal wall may be breached
  • CD may also be associated with severe skin inflammation
62
Q

IBD = ??

A

Irritable Bowel Disease

63
Q

IBD:

Is there a cure ?

A

No - only treatments which are variably effective

64
Q

Surgical removal of the colon can eliminate ______ ______

A

ulcerative colitis

*surgery cannot always eliminate CD

65
Q

3 goals of treatment for these disorders (UC, CD, IBD)?

A

1 - Treat the acute outbreak
2 - Induce and retain remission
3 - Treat complications

66
Q

UC:

What is the first line treatment?

A

5-ASA
(5 - Amino Salycilic Acid)
(Mesalamine)

  • It is effective for mild to moderate UC
  • It is less useful in severe UC and in CD.
67
Q

5-ASA for Ulcerative Colitis:

MOA

A
  • Unknown method of action

- Does not work by COX inhibition (NSAIDs exacerbate the disease)

68
Q

5-ASA for Ulcerative Colitis:

Response rate:

A

60-80%

69
Q

How is 5-ASA released in large intestine?

A

5-ASA is only released in large intestine in sulfasalzine by bacteria (N=N)

??? WTF

70
Q

5-ASA linked to _____

A

sulfapyridine

71
Q

The non-therapeutic ______ causes most side effects (nausea, headaches)

A

sulfapyridine

72
Q

If formulated with a pH coating, 5-ASA may be released through entire _____

A

intestine

73
Q

Glucocorticoids:

Describe “Steroid-responsive” patients

A

In these patients (~4-%) symptoms improve over 1-2 weeks, and the disease remains in remission as the steroids are tapered off

74
Q

Glucocorticoids:

Describe “Steroid-dependent” patients

A

These patients (30-40%) responds to steroids well, but experience relapse of the disease with tapering of the steroids

75
Q

Glucocorticoids:

Describe “Steroid-unresponsive” patients

A

As indicated, these patients (15-20%) do not respond to steroid treatment

76
Q

What are Glucocorticoids used for?

A

Used for acute treatment of moderate to severe bowel issues

77
Q

Are Glucocorticoids useful in maintaining remission?

A

No way jose

78
Q

SE of Glucocorticoids?

A
  • Weight gain, moon-face, stress and emotional responses
  • Steroid-dependent diabetes
  • Increased risk of infection
79
Q

What are immunosuppressants?

A

Drugs usually developed for tissue rejection or cancer

80
Q

Immunosuppressants are ____ derivatives: DNA synthesis inhibitors (used in cancer work)

A

thiopurine

81
Q

List some immunosuppressants

A
  • Mercaptopurine

- Azothiopurine

82
Q

How long may it take Immunosuppressants to work?

A

may take weeks to months (immune cell lifespan)

83
Q

What kind of patients are thiopurines reserved for?

A

Steroid-resistant or steroid-dependent patients

84
Q

What are thiopurines useful in?

A

Remission and reduction of relapse (UC and CD)

85
Q

Are thiopurines useful in acute attacks?

A

NO - as they have a long onset time

86
Q

Thiopurines have a small risk of major _____, especially in cotreatment with steroids.

A

infection

87
Q

Methotrexate is a ?

A

Dihydrofolate reductase inhibitor

*Blocks DNA synthesis

88
Q

What kind of patients is Methotrexate reserved for?

A

steroid-resistant or steroid-dependent patients

89
Q

What is Cyclosporine?

A

Calcineurin inhibitor (tissue transplantation)

90
Q

What is Cyclosporine used for?

A

Only used for the most serious cases of UC and CD as it has serious side-effects (severe immune suppression)

91
Q

Cyclosporine is used right before ______

A

surgery

92
Q

_____% of severe UC patients respond to cyclosporin

**Levels must be constantly monitored **

A

50-80

93
Q

What is TNF alpha?

A

a major pro-inflammatory ligand

94
Q

What are TNF alpha inhibitors used for?

A

used to treat other inflammatory diseases, such as eczema and RA

95
Q

Give an example of a TNF alpha inhibitor

A

Infliximab (Remicade)

96
Q

Describe Infliximab (Remicade)

A
  • It is an engineered antibody
  • It may kill the cell to which it attaches
  • Has very prolonged effects
97
Q

________ also reduces TNF alpha but is NOT effective as a UC treatment

A

Etanercept

98
Q

TNF alpha inhibitor:

Prolonged effect may be due to the ??

A

long half life of the drug (8-10 days)

99
Q

TNF alpha inhibitor:

If this drug kills the immune cells, then _____ in the submucosa is required

A

repopulation

100
Q

TNF alpha inhibitor:

are very _____

A

expensive

101
Q

TNF alpha inhibitor:

Increases chances of serious ___ infection, especially tuberculosis

A

lung

102
Q

UC and CD may be due to changes in ??

A

intestinal bacteria

103
Q

______ and _______ are drugs that are investigated that may change the proportions of different bacteria

A

antibiotics

probiotics

104
Q

______ = frequent liquid stool due to an intestinal disorder

A

diarrhea

105
Q

List some causes of diarrhea

A 
foods
bacteria
virus
drug side effect
laxative abuse
malabsorption syndrome
stress
bowl tumor

*diarrhea can be very mild or cause life-threatening dehydration

106
Q

Treatment for diarrhea

A
  • clear liquids
  • pedialyte
  • BRAT diet (Bananas, Rice, Applesauce, Toast)
107
Q

How do antidiarrheals work?

A
  • Decrease hypermotility

- Opiates, opiate-related agents, adsorbents antidiarrheal combos

108
Q

Describe Opiates

A
  • Decrease intestinal motility

- Tincture of opium, paregoric, codeine

109
Q

SE of Opiates

A

CNS depression

constipation

110
Q

Duration of opiates

A

2 hours

111
Q

List some Opiate-Related Agents

A

diphenoxylate (Lomotil)
loperamide (Imodium)

*these are synthetic drugs chemically related to the opioid meperidine

112
Q

SE of Opiate-Related Agents

A

drowsiness

distention

113
Q

Adsorbents are another type of _______

A

antidiarrheal

114
Q

How do Adsorbents work?

A

coat the wall of the GI tract and adsorb the bacteria or toxins causing diarrhea (the substance takes in toxin)

115
Q

List some examples of Adsorbents

A
  • Kaopectate (kaoline and pectin)

- Pepto-bismol adsorbs bacterial toxin & for GI discomfort

Pharmacology B (21 decks)

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