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Fitz-antiulcerdrugs Flashcards

1
Q

What are these drugs used for?

A
  1. Peptic Acid Disease
    a. H. Pylori (95%)
    b. NSAID-Induced
    c. Other
  2. GERD/NERD Treatment (non-erosive reflux disease)
  3. Hypersecretory states
    a. Hyperacidity → dyspepsia
    b. Stress ulcers
    c. Gastrinoma (Zollinger-Ellison Syndrome)
    d. Systemic Mastocytosis
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2
Q

What are the management objectives

A
  1. Heal Lesion
  2. Relieve Pain
  3. Removing reoccurance possibilities
  4. Avoid Complications→ avoid drug interactions
  5. Eliminate need to take maintenance
  6. H. pylori→ prevent development of resistance
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3
Q

Treatment strageties?

A
  1. Eliminate H. pyloric
  2. Reduce Pain (↓H+ secretion)
    a. ↓ Stimulation (anticholin, H2 blockers)
    b. ↓ Secretion (PPIs)
    c. Buffer Acid (Antiacids)
    d. Protect Surfaces
    e. Replace Prostaglandins (unique to NSAID-Induced)
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4
Q

What antimicrobials are most effective for H. pylori and preventing peptic ulcer disease?

A

AMOXICILLIN, CLARITHROMYCIN, METRON-IDAZOLE, RIFABUTIN and TETRACYCLINE

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5
Q

What factors influence the choice of specific antimicrobial agents for treatment of H. pylori infection:

A
  • Susceptability to drug: measured by MIC 50/90
  • Pharmacokinetics: Esp. distribution→ where it is in the stomach- through the stomach cells or needs to be acid stable
  • Drug Resistence
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6
Q

Why use amoxocillin the choice?

A

Needs to be effective against gram neg (3), orally available (3), acid stable (3)

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7
Q

What kind of drugs are penicillin?

A
  • Cidal
  • Cell Wall Inhibitors
  • Major toxicity of penicillins are hypersensitivities
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8
Q

How do you end up with clarithroymycin?

A

has the lowest MIC50 and is more acid stabile.,

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9
Q

Why not azithryomcyin?

A

decrease dosing, decrease Gi effectsm

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10
Q

Macrolydes side effects (clartthydromycin)

A

bacteriostatic drugs
Inhibit protein synthesis via 50s RNA
-GI Irritation
-Drug interactions-CYP 3A4

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11
Q

Why does tetracycline good?

A
  • It is incompletely absorbed which is good when it’s isolated to stomach
  • Give with Food (opposite of normal)
  • Don’t give with anything that has metal ions (antiacids) since chelation will occur
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12
Q

Tetracyline MOA and toxicity

A
  • Static
  • Protein Synthesis inhibitors on 30S
  • GI Irritation
  • Photosensitiity
  • Teeth Discoloration (in pregnant women and children)
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13
Q

When all else fails what drug do you use?

A

Rifabutin (rifamycin)

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14
Q

Why do we use Rifabutin

A
  • It’s more effective than other Rifamycins
  • It is CIDAL
  • MOA: Inhibits bacterial DNA dependent RNA polymerase
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15
Q

Toxicity of rifabutin

A

o HS
o Liver problems
o CYP450 inhibitor*
o Orange pee/secretions *

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16
Q

What s tinidazole?

A

• newer drug which requires less administration, less dosing
• MOA is unknow but:
o May cause DNA Damage
• 35-65% of H. pylori infections are resistant, so use is decreasing

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17
Q

Side effects of tinidzole

A

CNS Toxicitity*
Produce Disulfarum rxn*
GI
Teratogenic
Inhibit CYP2C9*
↑Warfarin’s Actions..shit if someone has a bleeding ulcer*
↓ Clearance of H2 Blockers (that’s actually good though)*
↑Effectiveness, ↑ Side Effects of H2 Blockers*

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18
Q

MOA of Bismuth?

A

Antimicrobial action via cell wall disruption or preventing adhesion or my inhibiting urease
It protects the surface
o Coats the Surface (think bandaid)
o Stimulates secretion of mucous prostaglandins and HCO3-

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19
Q

What is the active ingrideint?

A

bismuth in stomach, not the lower GI

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20
Q

Sx of bismuth?

A

Caused by the subsalicylate
o Turns tongue black (not harmful, hideous)
o Turns stool black which makes it hard to visualize blood
o Vomiting
o Tinnitus*
o Confusion/CNS*
o Hyperthermia
o Respiratory Alkalosis→ can cause metabolic acidosis via correction

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21
Q

Tx failure of H pylori reasons?

A
  1. Resistance to the drugs given
    (35-65% occurs) Metronidazole, 5-10% (may now be 35-50%) for clarithromycin, rarely H. pylori is resistent to tetracycline, amoxiciliin, and rifabutin
  2. Treatment Compliance
    Too many pills for too long. Damn.
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22
Q

Why dont we use muscarinc receptors anatgonstis anymore?

A

• Very rarely (not used) because they slow emptying and prolong exposure of ulcer to acid

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23
Q

How do muscarinic receptors work again?

A

M1 and M3 are G-proetein linked

Activate phospholiapse C: ↑ IP3: ↑ Ca2+ release

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24
Q

What are the Muscarinic Receptor Antagonists

A
  • Atropine

* Pirenzipine

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25
Muscarinic Receptor Antagonists MOA?
• comp. inhibitors of ACh
26
Which muscarininc receptor agonist is more selective?
pirenzipine
27
Side Effects of Anticholinergics?
``` “ABCD’S” o Anorexia o Blurry Vision o Constipation o Dry Mouth o Sedation o Stasis (urine) ```
28
OVerdose of anticholiergic- higher doses?
o CNS→ hallunications/confusion o Tachycardia o Hot dry skin
29
Are anticholingerics used to tx uclers
NO!
30
Wha are the H2 Receptor Anatgonists:
CIMETIDINE, FAMOTIDINE, NIZATIDINE, RANITIDINE
31
What is the MOA for H2-Receptor Antagonists?
* Highly selective with no H1 activity | * Competititve antagonists of H2 receptors
32
What are H2 receprots secondary effects?
o ↑ IC cAMP→ impact basal and nocturnal secretion due to other agents o Known to ↓ meal-time stimulation
33
What are the pharmacokinetics of H2-Receptor Antagonists
* OTC→ 6 hours * Prescription→ 10 hours * Undergo extensive hepatic metabolism * Renal excretion
34
Side effects of H-2 RA?
• None when given orally to healthy patients except… o Rapid IV infusion may result in bradycardia and hypotension* o H2-receptors in heart→ give slow infusion* • Unknown pregnancy effects so not recommended
35
What are the H2-RA drug-drug interactions?
• ↓ Ethanol metabolism ( in women)* • Compete for tubular secretion with weak basics* o metronidazole is a weak base*
36
What’s special about cimetidine?
has side effects at high doses- o Decreased binding of dihydrotestosterone (DHT) to androgen receptors o ↓ estrogen metabolism o ↑ prolactin excretion o Results in gynecomastia and impotence in males* o galactorrhea in females* Cimetidine is an inhibitor of CYP450 ↑effects of other drugs (boosts concentrations), It is an isozyme of a lot of drugs
37
Proton Pump Inhibitors (Block Acid Secretion) are?
ESOMEPRAZOLE/OMEPRAZOLE,LANSOPRAZOLE, PANTOPRAZOLE, RABEPRAZOLE OMEPRAZOLE-racemic mix and esomeprazole-slowly metabolized
38
What is the MOA of PPIs?
• IRREVERSIBLY block the final common pathway in acid secretion --- the H+/K+ ATPase
39
When do we prefer to use PPIs?
* ZE syndrome and GERD* | * Very Effective for many purposes
40
Pharmacokinetics of PPIs?
• They are prodrugs and acid-labile* o they must pass through stomach to be absorbed (they have a special coating on them) • Absorbed into the small intestine→circulate throughout body • They are attracted to acidic compartments o they are protonated and converted to activated form o require and acidic environment to function*
41
What’s critical about Ppis?
o Give in a fasting state so that motility is low, preventing the pills getting crushed o The drug only inhibits active pumps (in fasting state only 10% of PP are active) o SO! Take the drug ½ hour before the meal allowing the drug concentration to be highest (when pump activity is highest)
42
How many doses of PPI do you need to take a day?
1! They have a short ½ life, but they’re irreversible inhibitors, it takes 18 hours to make new pumps
43
Full inhibition of all pumps takes how long?
3-4 days, and recovery takes 3-4 days as well., So take high initial dose and then taper as symptoms are controlled.
44
How are PPIs broken down?
• Broken down by 1st pass metabolism
45
Which PPI is not available via IV
omeprazole
46
What are the PPI SE?
* None, that’s why they’re OTC * 1-5% of patients report headache/diarrhea/nausea * When the patient stops taking drug, there is significant hypersecretion-rebound effect*
47
What if taking PPI long term?
↓ B12, Fe, Ca2+, Zinc absorption→↑Hip fractures* | ↑Respiratory and Enteric Infections (d/t ↑ pH which normally is low in order to kill bugs)
48
Why do you get ECL Hyperplasia (hypergastrinemia) with PPI?
Normally ↓ gastric pH: ↑Somatostatin release: ↓gastrin | but with Long-term PPI use, ↑↑ gastrin
49
What are some weak bases to buffer acid?
ALUMINUM HYDROXIDE, CALCIUM CARBONATE, MAGNESIUM HYDROXIDE and SODIUM BICARBONATE)
50
What are the factors affecting usefulness of base agents?
* Systemic Absorption * Rate of dissociation (fast→faster effect→ shorter duration * Cation/Product effects
51
What are the drug interactions of Buffer drugs?
↑ gastric pH: ↑/↓ absorption of other drugs bind drugs: ↓ absoprtion Bulky: ↑ Gastric Emptying: ↓Absorption Systemically absorbed will alkalinize urine: ↓ elimination o You need to be extremely careful with tetracycline *
52
Side effect of ALUMINUM HYDROXIDE
constipation
53
What is simethicone?
* antifoaming agent: ↓gas pain * We add it to Sodium bicarbonate * also affects absorptions
54
Why use antacids?
rapid onset but short duration of action; no prevention of ulcer recurrence → useful for intermittent dyspepsia
55
why use H2 blocks?
relatively rapid onset, intermediate duration, some prevention → many uses
56
Why use PPIs
slow onset of action, very long duration of action, excellent prevention → drugs of choice for Zollinger-Ellison syndrome and GERD, as well as ulcer treatment
57
What is sucralfate?
* Al(OH)3 and sulphated sucrose * Not an antacid * basically a band-aid, stress induced ulcers in the ICU
58
MOA of sucralfate:
* attaches to ulcer surface | * stress-induced gastritis (ICU)
59
Pharmacokinetics of sucralfate
• Requires acidic environement | o cannot be given with PPI, H2 Blocker
60
SE of sucralfate?
* constipation | * binds other drugs
61
Whewn is misoprostol used?
* accounts for 5% of ulcer treatment (NSAID induced only) | * 15-25% of arthritis patients develop this though, so # maybe ↑
62
Misoprostol MOA:
* You’re replacing PGE1 to reactivate PG→ GI pathway to inhibit cAMP, and reduce H+ * Works because PGE1 is not that involved in inflammation compared to other prostaglandins * Misoprostol has a short ½ life compared to NSAIDS (around 2 hours)
63
Pharmacokineteics of misoprostol?
* rapid absorption and metabolism | * excreted in urine
64
Misoprostol SE?
• diarrhea*, nausea, cramping, abdominal pain o 10-20% of patients which → ↓ compliance • In preggers stimualtes uterine contractions→ abortifactant*
65
What do all combo therapy have?
pain and eradication!
66
What form crosses more easily?
• Unionized, Increase in pH shifts right
67
“net thing to worry about”
o anything like PPI, H2 Blockers, Antiacids→ affect absorption o systemically absorbed antiacids will affect excretion of other drugs

GI week 2 (8 decks)

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