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Pharmacology Exam 1 > GI Pharmacology > Flashcards

GI Pharmacology Flashcards

1
Q

What is the product/function of Parietal Cells?

A

HCl for Protein Digestion, Sterilization, and Nutrient Absorption

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2
Q

What is the product/function of Superficial Epithelial/Neck Cells?

A

Mucus and Bicarbonate for gastroprotection

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3
Q

What is the product/function of ECL cells?

A

Histamine, which promotes HCl secretion

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4
Q

What is the product/function of G cells?

A

Gastrin, which promotes HCl secretion

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5
Q

What are the key regulatory of paracrine, endocrine, and neuronal acid seretion?

A

Paracrine –> Histamine

Endocrine –> Gastrin

Neuronal/Neurocrine –> Acetylcholine

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6
Q

What are the Direct/Indirect regulators of acid secretion from the parietal cells?

A

Gastrin and Acetylcholine

Directly stimulate the Parietal Cell

Indirectly stimulate the ECL Cells

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7
Q

What are the 3 key roles of prostaglandins?

A
  1. Mucus and Bicarbonate secretion
  2. Suppression of HCL secretion
  3. Increase gastric blood flow
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8
Q

What type of ulcer has the greatest frequency?

A

Duodenal Ulcers

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9
Q

Stress Ulcer (Definition)

A

Peptic ulcer caused by illness, systemic trauma, neuronal injury, emotions

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10
Q

Cushing Ulcer (Definition)

A

Stress ulcer associated with Head Trauma or Brain Surgery

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11
Q

Ischemic Ulcer (Definition)

A

Ulcer caused by hemorrhage, multi-system trauma, severe burns (Curling ulcer), heart failure, sepsis

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12
Q

What are the two most common causes of ulcers in the U.S.?

A

NSAIDs (COX inhibition) and H. pylori

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13
Q

Symptoms of an ulcer

A

1. Abdominal Pain (particularly after a meal)

  1. Nausea
  2. Vomiting, vomiting blood
  3. Bloody, tarry school
  4. Indigestion
  5. Weight loss
  6. Fatigue
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14
Q

Antacids (Therapeutic Goals)

A

Neutralize the acid in the stomach to a pH > 4

End products: Salt, Water (sometimes CO2)

No Target Receptor

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15
Q

Sodium Bicarbonate - NaHCO3 (Rate of Reactivity, Specific Adverse Effects)

A

Rate of Reactivity: FAST

Specific Adverse Effects: Metabolic acidosis, excessive NaCl absorption, Gas/Bloating (CO2__)

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16
Q

Calcium Carbonate - CaCO3 (Duration of Action, Rate of Reactivity, Specific Adverse Effects)

A

DoA: 1-2 hours

RoR: MODERATE

SAE: Acid Rebound (Feed forward mechanism causing INCREASED acid production after long-term use), Gas/Bloating (CO2), Hypercalcemia (large doses), Hypophosphatemia (Rare)

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17
Q

Magnesium Hydroxide - Mg(OH)2 (Rate of Reactivity, Specific Adverse Effects)

A

RoR: SLOW

Specific Adverse Effects: Osmotic Diarrhea (due to excess Salt in intestines), Hypermagnesemia (large doses over an extended period of time)

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18
Q

Aluminum Hydroxide - Al(OH)2 (Rate of Reactivity, Specific Adverse Effects)

A

RoR: SLOW

SAE: Constipation (slows down smooth muscle peristalsis), Aluminum toxicity (impaired RENAL FUNCTION), Hypophosphatemia, Bone Resorption, Hypercacelmia

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19
Q

Duration of Action of Antacids

A

Very SHORT (1-2 Hours)

***Have to take them very frequently, therefore, will see a Decrease in Compliance

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20
Q

Two common Adverse Effects of Anatacids

A
  1. Reduced Drug Bioavailability
  2. Enteric Infection
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21
Q

Therapeutic Uses of Antacids

A

GERD, Peptic Ulcers, Dyspepsia

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22
Q

Anatacids are used as adjunctive therapy with____

A

PPIs

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23
Q

Antacids are equally efficacious as _____ at treating GERD (heal rate = ___%) and Peptic Ulcers (heal rate = ___%)

A

Antacids are equally efficacious as H2-Receptor Antagonists at treating GERD (heal rate = 50%) and Peptic Ulcers (heal rate = 80%)

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24
Q

H2-receptor Antagonists

  1. Type of inhibition/Selectivity
  2. What is blocked?
A
  1. Competitive and Highly Selective
  2. Blocks Indirect action of Gastrin and Acetylcholine; Does not block direct action of Gastrin and Acetylcholine
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25
Q

What do all H2-receptor Antagonist names end in?

A

They all end in -tidine

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26
Q

H2-receptor Antagonists

Drug Names (4 of them)

A
  1. Cimetidine (Tagemet)
  2. Ranitidine (Zantac)
  3. Nizatidine (Axid)
  4. Famotidine (Pepcid)
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27
Q

H2-receptor Antagonists

  1. Duration of Action
  2. Common Adverse Effects
A

DoA: 10 hours or 6 hours OTC

CAE: Headache, diarrhea, fatigue, constipation, infection, drug kinetics, bradycardia (IV), hypotension (IV)

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28
Q

H2-receptor Antagonists

  1. Specific Considerations for Cimetidine
A
  1. CNS Effects (confusion, hallucinations, agitation)
  2. Endocrine Effects (inhibition of androgen receptors, inhibition of estradiol metabolism, increase prolactin levels)
  3. Inhibition of hepatic CYB metabolism (Inhibits cytochrome P450 activity, which leads to high potential of drug-drug interactions)
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29
Q

H2-receptor Antagonists

  1. Key Difference from Antacids
  2. Key Advantage compared to Antacids
A
  1. Must be absorbed into the BLOODSTREAM to take effect
  2. Have to be administered LESS often

(Equally efficacious as antacids at treating GERD and Peptic Ulcers and can additionally treat Gastritis)

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30
Q

Proton Pump Inhibitors (PPIs)

  1. Key Advantage over H2-receptor Antagonists
A
  1. Antagonizes the proton pump, so is able to block both Direct and Indirect actions of ACh, Histamine, and Gastrin
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31
Q

Proton Pump Inhibitors (PPIs)

  1. Mechanism of Action (5 things)
A
  1. Activated by low pH
  2. Acid-labile drug is absorbed into the BLOODSTREAM by GI
  3. Concentrates at the site of action (Parietal Cells)
  4. Irreversibly binds/inhibits proton pump
  5. Activation of pump requires new synthesis
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32
Q

What do all Proton Pump Inhibitors end in?

A

All PPIs end in -prazole

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33
Q

Proton Pump Inhibitors (PPIs)

  1. Drug Names
A
  1. Omeprazole (Prilosec)
  2. Lansoprazole (Prevacid)
  3. Rabeprazole (Aciphex)
  4. Esomeprazole (Nexium)
  5. Pantoprazole (Protonix)
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34
Q

Proton Pump Inhibitors (PPIs)

  1. Duration of Action
A

DoA: 24 hours (takes 3-4 days of dosing to reach max effect)

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35
Q

Proton Pump Inhibitors (PPIs)

  1. Common Adverse Effects
A

***Extremely SAFE***

  1. Decreased drug bioavailability
  2. Diarrhea, headache, abdominal pain (1-5%)
  3. Decreased nutrient absorption (Vitamin B12, Iron, Calcium, Zinc)
  4. Enteric and Respiratory infections
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36
Q

Why does it take 3-4 days for PPIs to reach maximum effect?

A

It takes 3-4 days for the body to exhaust its supply of proton pumps, which are waiting in the tubulovesicular network to be brought to the apical surface and inactivated by the PPI

***This is why you initially supplement w/ Antacids or H2-receptor Antagonists***

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37
Q

Proton Pump Inhibitors (PPIs)

  1. Therapeutic Uses
A

GERD

Peptic Ulcers

Dyspepsia

Gastritis

Hypersecretory Diseases

NSAID-associated Ulcers

H. pylori-associated Ulcers

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38
Q

Proton Pump Inhibitors (PPIs)

  1. Effectiveness
A
  1. Most Efficacious Inhibitors

(GERD Heal Rate = 90%)

(Peptic Ulcer Heal Rate = 90%)

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39
Q

Muscoal Protective Agents

  1. Drug Names
A

Sucralfate (Carafate)

Misoprostol (Cytotec)

Bismuth subsalicylate (Pepto-Bismol)

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40
Q

Mucosal Protective Agents

  1. Mechanism of Action
A

Sucralfate and Bismuth subsalicylate both create a physical barrier and stimulate mucus and HCO3- secretion from the gastric mucosa

Misoprostol (a prostaglandin derivative) stimulates mucus and HCO3- secretion from the gastric mucosa, but DOES NOT form a physical barrier

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41
Q

Mucosal Protective Agents

  1. Duration of Action
A

6 hours

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42
Q

Mucosal Protective Agents

  1. Common Adverse Effects - Sucralfate
  2. Other Adverse Effects
A
  1. Constipation, Impaired Drug Absorption
  2. Caution w/ Renal Insufficient Patients

***Constipation (inhibition of smooth muscle contraction) and Renal Toxicity due to presence of Aluminum***

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43
Q

Mucosal Protective Agents

  1. Common Adverse Effects - Misoprostol
  2. Other Adverse Effects
A
  1. Cramping, Diarrhea
  2. Abortificient (stimulates smooth muscle contractions, so could induce uterine contractions)
44
Q

Mucosal Protective Agents

  1. Common Adverse Effects - Bismuth subsalicylate
  2. Other Adverse Effects
A
  1. Blackening of Stool and Tongue
  2. High doses - Salicylate Toxicity
45
Q

Reasons to use Mucosal Protective Agents

A
  1. Generalyl 2nd line agents to PPIs
  2. Sucralfate –> prevents stress-related bleeding when you DO NOT want to prevent acid secretion (hospitalized patient who is at risk for infection)
  3. Misoprostol –> NSAID-associated ulcers
  4. Bismuth subsalicylate –> H. pylori-associated ulcers, Travelers diarrhea, Dyspepsia (indigestion)
46
Q

H. pylori and Gastric Ulcers

  1. 70 to 90% of patients with ________ are infected with H. pylori
  2. Transmission of H. pylori
A

70 to 90% of patients with Gastric or Duodenal Ulcers are infected with H. pylori

  1. Orally via Fecal Matter (tainted water) or transmitted from stomach to mouth from GERD or belching
47
Q

H. pylori and Gastric Ulcers

  1. Treatment of H. pylori (Triple Theory)
  2. Key of Treatment
A
  1. PPI –> Clarithromycin –> Amoxicillin

(Can used Metronidazole in place of Amoxicillin if there is a penicillin allergy)

  1. Two antibiotics given due to the high resistance of H.pylori ***Know***

MUST USE 3 drugs –> suppress acid secretion and two antibiotics

Old Triple Theory (Bismuth subsalicylate, Tetracycline, Metronidazole)

Quadruple Therapy –> New Triple Theory + Bismuth subsalicylte

48
Q

Summary of Antacids, H2-receptor Antagonists, PPIs, and Mucosal Protective Agents

49
Q

Serotonin (5-HT)

  1. Function in the GI System
A
  1. (Within the Enteric Nervous System) Stimulates gastric motility by inducing the release of Ach by neurons onto GI smooth muscle
50
Q

Acetylcholine

  1. Function in the GI System
  2. Regulation
A
  1. Binds to Muscarinic (M3) receptors and induces conraction of the GI smooth muscle
  2. Concentrations regulated at neuromuscular junction by Acetylcholine esterase (AchE)
51
Q

What is the function of Dopamine (D2) receptors in the GI system?

A

Pre-synaptic receptors involved in regulating the release of neurotransmitters:

Stimulate D2 receptor –> DECREASED** acetylcholine production –> **DECREASED motility/neuronal firing/smooth muscle contraction

52
Q

What is the function of the Motilin Receptor (MR) in the GI system?

A

Motilin is a hormone that is released and promotes motility in the UPPER GI tract (stomach, duodenum)

***Has less effect as you move lower

53
Q

Metoclopramide (Reglan)

  1. Mechanism of Action
  2. Used to Treat
  3. Adverse Effects
A

MoA: D2 Antagonist

***Promotes Motility***

Use: GERD, Impaired Gastric Emptying, Dyspepsia, Antiemetic

AE: CNS (restlessness, drowsiness, insomnia, anxiety), ***Altered Motor Function (Parkinsonian Symptoms)*** due to blocking of Dopamine

54
Q

Bethanechol (Urecholine)

  1. Mechanism of Action
  2. Used to Treat
  3. Adverse Effects
A

MoA: M3 Agonist

***Promotes Motility***

Use: GERD, Gastroparesis

AE: Cholinergic side effects

55
Q

Neostigmine (Prostigmin)

  1. Mechanism of Action
  2. Used to Treat
  3. Adverse Effects
A

MoA: AchE inhibitor

***Promotes Motility***

Use: Non-obstructive: urinary retation and abdominal distension

AE: Cholinergic side effects

56
Q

Erythromycin (Erythrocin)

  1. Mechanism of Action
  2. Used to Treat
  3. Adverse Effects
A

MoA: Motilin Receptor Agonist

***Promotes Motility***

Use: Gastroparesis

AE: Erythromycin-mediated side effects (alterations of the normal gut flora)

57
Q

Laxatives (Bulk-Forming)

e.g. Wheat Bran, Psyllium (Konsyl-D, Metamucil), Methycellulose (Citrucel), Polycarbophil

  1. Mechanism of Action
A
  1. Plant cell walls (fiber) that are RESISTANT to digestion by GI system –> forms gel-like substance that pushes on colonic wall and leads to mass peristaltic contractions

***Take with a lot of water***

58
Q

Laxatives (Stool Softener)

e.g. Glycerin and Mineral Oil

  1. Mechanism of Action
A
  1. Two Theories:
    a. Penetration of water/lipids into the stool
    b. “coats” the stool with oil
59
Q

Laxatives (Osmotic Agents)

e.g. Magnesium Hydroxide (Milk of Magnesia), Sorbitol, Lactulose, Polyethylene Glycol (PEG)

  1. Mechanism of Action
A
  1. Non-absorbable sugars and salts used to alter the osmotic pressure and pull water into the colon
60
Q

Laxatives (Stimulant)

e.g. Anthraquinone derivatives (Aloe & Senna), Castor Oil, Diphenylmethane derivatives (Phenophthalein)

  1. Mechanism of Action
A
  1. Three Theories:
    a. Stimulation of the ENS
    b. Inducing a leaky mucosa
    c. Inhibiting sodium uptake by the gut
61
Q

Methylcellulose (Citrucel)

  1. Mechanism of Action
  2. Absorption
  3. Use
  4. Adverse Effects
A

MoA: BULK-FORMING; Fiber –> adds bulk and retains water

Absorption: Poor

Use: Constipation, Minimize Straining, Prior to Surgical and Endoscopic Procedures

AE: Gas/Bloating

62
Q

Glycerin (Colace)

  1. Mechanism of Action
  2. Absorption
  3. Use
  4. Adverse Effects
A

MoA: SURFACTANT; Coats and Penetrates fecal material

Absorption: Poor

Use: Constipation, Minimize Straining, Prior to Surgical/Endoscopic Procedures

AE: Nutrient Malabsorption

63
Q

Laculose (Enulose)

  1. Mechanism of Action
  2. Absorption
  3. Use
  4. Adverse Effects
A

MoA: OSMOTIC; Change osmotic pressure

Absorption: Poor

Use: Constipation, Minimize Straining, Prior to Surgical/Endoscopic Procedures

AE: Gas, Electrolyte Flux

64
Q

Senna (Ex-Lax)

  1. Mechanism of Action
  2. Absorption
  3. Use
  4. Adverse Effects
A

MoA: STIMULANT; Stimulate ENS

Absorption: Poor

Use: Constipatio, Minimize Straining, Prior to Surgical/Endoscopic Procedures

AE: GI irritation

65
Q

Tegaserod (Zelnorm)

  1. Mechanism of Action
  2. Absorption
  3. Use
  4. Adverse Effects
A

MoA: SEROTONIN AGONIST

***STIMULATES***

Serotonin (5-HT) stimulates pre-synaptic 5-HT4 receptors –> release of NT (e.g. Ach) in ENS –> INCREASED motility** and **DECREASED** **pain (via decreased firing of extrinsic sensory neurons to the CNS)

Absorption: 10%

Use: Chronic idiopathic constipation

AE: GI, CV ***Not available for general use - a LAST DITCH EFFORT TYPE OF DRUG***

66
Q

Lubiprostone (Amitiza)

  1. Mechanism of Action
  2. Absorption
  3. Use
  4. Adverse Effects
A

MoA: CHLORIDE CHANNEL ACTIVATOR

Activates Chloride Ion Channel 2 (CIC-2) –> INCREASED** luminal concentration of **chloride in the gut –> accumulation of sodium and water –> motility

Absorption: Poor ***Accesses the apical/lumenal side, is NOT absorbed into the bloodsteram***

AE: Nausea/Vomiting, Diarrhea

67
Q

Methylnaltrexone (Relistor)

  1. Mechanism of Action
  2. Absorption
  3. Use
  4. Adverse Effects
A

MoA: Mu-OPIOID RECEPTOR ANTAGONIST

Blocks PERIPHERAL Mu-opioid receptors (normally activated by opioids (e.g. morphine) and lead to DELAYED intestinal motility) –> prevents pain treatment-associated/post-surgical constipation

Absorption: ***Poor CNS penetration allows pain management and prevention of constipation

Use: Opioid-induced constipation during palliative care

AE: Abdominal pain, Flatulence, Nausea, Diarrhea

68
Q

Alvimopan (Entereg)

  1. Mechanism of Action
  2. Absorption
  3. Use
  4. Adverse Effects
A

MoA: Mu-OPIOID RECEPTOR ANTAGONIST

Blocks PERIPHERAL Mu-opioid receptors (normally activated by opioids (e.g. morphine) and lead to DELAYED intestinal motility) –> prevents pain treatment-associated/post-surgical constipation

Absorption: ***Poor CNS penetration allows for pain management and prevention of constipation

Use: Postoperative Ileus in hospitalized patients with bowel resection

AE: GI similar to Methylnaltrexone

***Can cause Myocardial Infarction (so only short-term use, 7 days or less)

69
Q

Antidiarrheal Agents (Opioids)

  1. Mechanism of Action
A

Frequently administered Orally

MoA: only have peripheral effects (do not cross BBB/do not enter CNS) to minimize abuse potential

Alter GI Smooth Muscle by:

a. Decreasing peristalsic contractions
b. Increasing segmental (mixing) contractions
c. Increasing internal anal sphincter tone
d. Decreasing perception of GI distension

70
Q

Antidiarrheal Agents (Bismuth Subsalicylate)

  1. Mechanism of Action
A

Administered Orally

MoA: primarily mediated by salicylate inhibition of prostaglandin synthesis ***IN CONTRAST to what is occurring in the STOMACH

Also Bismuth compounds absorb bacterial toxins

71
Q

Antidiarrheal Agents (Bile Salt Binding Resins)

  1. Mechanism of Action
A

MoA: reduce the osmotic pressure in the lumen of the large intestine by binding the unabsorbed bile salts

72
Q

Antidiarrheal Agents (Octreotide)

  1. Mechanism of Action
A

Is a synthetic peptide (somatostatin analogue) so it has to be given IV or subcutaneously

MoA: activates somatostatin receptor, increasing fluid absorption and decreasing motility

73
Q

Loperamide (Imodium)

  1. Mechanism of Action
  2. Use
  3. Adverse Effects
A

MoA: OPIOID AGONIST

Use: Diarrhea (IBS)

AE: Constipation (VERY SAFE)

74
Q

Diphenoxylate (Lomotil)

  1. Mechanism of Action
  2. Use
  3. Adverse Effects
A

MoA: OPIOID AGONIST

Use: Diarrhea

AE: CNS Effects, Atropine Effects

***Given with Atropine to miniize abuse***

75
Q

Bismuth subsalicylate (Pepto-Bismol)

  1. Mechanism of Action
  2. Use
  3. Adverse Effects
A

MoA: Inhibit PG Synthesis (Intenstinal), Absorb Toxins

Use: Non-specific diarrhea, Travelers diarrhea

AE: Salicylate Toxicity

76
Q

Cholestyramine (Prevalite)

  1. Mechanism of Action
  2. Use
  3. Adverse Effects
A

MoA: Bind BILE ACIDS and SALTS

Use: Impaired bile salt absorption-mediated diarrhea

AE: Bloating, flatus, constipation; Fecal impaction; Impaired fat absorption/fat soluble vitamin absorption

77
Q

Octreotide (Sandostatin)

  1. Mechanism of Action
  2. Use
  3. Adverse Effects
A

MoA: Somatostatin receptor agonist

Use: Secretory diarrhea

AE: Impaired pancreatic secretion, Decreased GI motility (nausea, pain), Decreased gallbladder contraction, Glucose hemostasis

78
Q

What are the key receptors that regulate an emetic response in the Vestibular system?

A

Histamine (H1) and Muscarinic (M1)

79
Q

What are the receptors that are involved in an emetic response? (7 of them)

A

Histamine (H1)

Muscarinic (M1)

Dopamine (D2)

Neurokinin (NK1)

Serotonin (5-HT)

Chemoreceptors

Mechanoreceptors

80
Q

Ondansetron (Zofran)

  1. Mechanism of Action
  2. Adverse Effects
A

MoA: 5-HT3 (Serotonin) Antagonist

AE: Headache, Dizziness, Constipation, Prolonged QT Interval

81
Q

Scopolamine (Transderm Scop)

  1. Mechanism of Action
  2. Adverse Effects
  3. Use
A

MoA: M1 Antagonist (Vestibular System)

AE: Antimuscarinic Effects

Use: Motion Sickness

***Patch behind the ear***

82
Q

Metocloramide (Octamide)

A

MoA: D2 Antagonist

AE: Extrapyramidal (Parkinsonian Symptoms)

83
Q

Dimenhydrinate (Dramamine)

  1. Mechanism of Action
  2. Adverse Effects
  3. Use
A

MoA: H1 Antagonist (Vestibular System)

AE: Drowsiness

Use: Motion Sickness

84
Q

Aprepitant (Emend)

  1. Mechanism of Action
  2. Adverse Effects
A

MoA: NK1 Antagonist

AE: Fatigue, Dizziness, Diarrhea, CYP3A4 Interactions (leads to drug-drug interactions)

85
Q

Prochlorperazine (Compro)

  1. Mechanism of Action
  2. Adverse Effects
A

MoA: M1D2H1 Antagonist (***Last Resort***(severe conditions)–> knocks out all receptors)

AE: Extrapyramidal, Drowsiness, Anticholinergic

86
Q

Lorazepam (Ativan)

  1. Mechanism of Action
  2. Adverse Effects
  3. Uses
A

MoA: GABA Agonist

AE: Drowsiness

Uses: Indirect Antiemetic, Anxiety, Chemotherapy

87
Q

Nabilone (Cesamet)

  1. Mechanism of Action
  2. Adverse Effects
A

MoA: Cannabinoid Agonist

Uses: Indirect Antiemetic

AE: Dysphoria, Sedation, Increased Appetite

88
Q

Dexamethasone

  1. Mechanism of Action
  2. Adverse Effects
  3. Uses
A

MoA: Glucocorticoid Agonist (LAST RESORT (Extreme situations))

AE: Weight Gain, Water Retention, Other corticosteroid effects

Uses: Indirect Antiemetic, Chemotherapy, Post-operative

***Increases the effectiveness of 5-HT antagonists***

89
Q

How do aminosolicylates work?

A

Topical

***DO NOT want systemic absorption - will NOT work***

90
Q

Irritable Bowel Syndrome (IBS)

  1. Definition
  2. Cause
  3. Treatments
A
  1. Idiopathic chronic relapsing disorder charactereized by abdominal discomfort (pain, bloating, distension, or cramps) in association with alterations in bowel habits (diarrhea, constipation, or both)

Cause: Uncertain

Tx: Loperamide (reduces diarrhea), Osmotic laxatives (relieves constipation), as well as tricyclic antidepressants and antispasmodics/antimuscarinics (relieves pain)

91
Q

Tegaserod (Zelnorm) vs. Alosetron (Lotrenex)

  1. Mechanism of Action
  2. Use
  3. Adverse Effects
A

Tegaserod (Zelnorm)

MoA: 5-HT4 partial agonist

Use: IBS-constipation predominant

AE: GI (pain, dyspepsia, flatulence, nausea/vomiting, diarrhea), CV (0.01%, MI and Stroke) ***Not available for general use - EMERGENCY only***

Alosetron (Lotrenex)

MoA: 5-HT3 ANTagonist

Use: IBS-diarrhea predominant (works in WOMEN only)

AE: Constipation (29%), ***Ischemic colitis (fatal)***

92
Q

Inflammatory Bowel Disease (IBD)

  1. Key thing to think about
  2. Two specific diseases
A
  1. INFLAMMATION
  2. Crohn’s Disease and Ulcerative Colitis
93
Q

Crohn’s Disease vs. Ulcerative Colitis

A

Crohn’s Disease: an idiopathic inflammatory disorder that affects ANY PART of the GI tract

Ulcerative Colitis: a chronic inflammatory disease that causes ulcerations of the COLONIC/DISTAL mucosa of the GI tract

94
Q

Aminosalicylates (ASA)

  1. Mechanism of Action
A

MoA:

  1. Inhibition of COX production of prostaglandins
  2. Interfere with inflammatory cytokine production (i.e. IL-1)
  3. Inhibit NF-KB signaling
95
Q

How do 5-aminosalicylic acid (5-ASA) compounds work?

A

They are administered TOPICALLY to the GI site; they will not work if they are absorbed into the bloodstream

-Requires use of Proprietary Release Formulas (Jejunum, Ileum), Chemical Binding (Proximal Colon), and High Concentration Enemas (Distal Colon and Rectum)

96
Q

Which two 5-aminosalicylic acid (5-ASA) drugs are used to treat Inflammatory Bowel Disease (IBD)?

A

Sulfalazine

Mesalamine

97
Q

Which two Glucocorticoids treat IBD, and what is their general mechanism of action?

A

Prednisone

Hydrocortisone

MoA: Suppress inflammatory cytokines, signaling, etc.

98
Q

How do antimetabolites work to treat IBD, and what is an example of one?

A

MoA: Suppress cell proliferation of immune cells

Example: Methotrexate

99
Q

Anti-TNFa Therapy

  1. Mechanism of Action
  2. Example
A

MoA: TNFa monoclonal antibody (a protein) is administered IV or subQ –> binds and sequesters TNFa –> Inhibit TNFa-mediated immune response

Example: Infliximab

100
Q

Sulfsalazine (Azulfidine)

  1. Type of Agent
  2. Use
  3. Adverse Effects
A

Agent: Amicosalicylate (ASA)

Use: 1st line agent for mild to moderate ulcerative colitis

AE: Nausea, GI upset, headache, arthralgia, myalgia, bone marrow suppression, malaise (40% of patients cannot tolerate)

101
Q

Mesalamine (Pentasa)

  1. Type of Agent
  2. Use
  3. Adverse Effects
A

Agent: Aminosalicylate (ASA)

Use: 1st line agent for mild to moderate ulcerative colitis

AE: Headache, Dizzines, Abdominal Pain

102
Q

Prednisone (Predone)

  1. Type of Agent
  2. Use
  3. Adverse Effects
A

Agent: Glucocorticoid (STEROID)

Use: Moderate to Severe *ACTIVE* IBD

AE: Glucocorticoid adverse effects

103
Q

Azathioprine (Azasan)

  1. Type of Agent
  2. Use
  3. Adverse Effects
A

Agent: Antimetabolite

Use: Maintenance of REMISSION of IBD (onset 17 weeks)

AE: Nausea, vomiting, bone marrow suppression

104
Q

Methotrexate (Rheumatrex)

  1. Type of Agent
  2. Use
  3. Adverse Effects
A

Agent: Antimetabolite

Use: Maintenance of REMISSION of Crohn’s (onset 8-12 weeks)

AE: Low dose side effects uncommon, but include bone marrow depression and megaloblastic anemia

105
Q

Infliximab (Remicade)

  1. Type of Agent
  2. Use
  3. Adverse Effects
A

Agents: Anti TNFa antibody

Use: Will look at 5-ASA compounds and Steroids BEFORE LOOKING AT THIS

Consider this when moving into the Moderate to Severe IBD

AE: Infection

Pharmacology Exam 1 (3 decks)

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