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GI week 2 > Fitz-antiulcerdrugs > Flashcards

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
Q

Muscarinic Receptor Antagonists MOA?

A

• comp. inhibitors of ACh

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26
Q

Which muscarininc receptor agonist is more selective?

A

pirenzipine

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27
Q

Side Effects of Anticholinergics?

A 
“ABCD’S”
o	Anorexia
o	Blurry Vision
o	Constipation
o	Dry Mouth
o	Sedation 
o	Stasis (urine)
28
Q

OVerdose of anticholiergic- higher doses?

A

o CNS→ hallunications/confusion
o Tachycardia
o Hot dry skin

29
Q

Are anticholingerics used to tx uclers

A

NO!

30
Q

Wha are the H2 Receptor Anatgonists:

A

CIMETIDINE, FAMOTIDINE, NIZATIDINE, RANITIDINE

31
Q

What is the MOA for H2-Receptor Antagonists?

A
  • Highly selective with no H1 activity

* Competititve antagonists of H2 receptors

32
Q

What are H2 receprots secondary effects?

A

o ↑ IC cAMP→ impact basal and nocturnal secretion due to other agents
o Known to ↓ meal-time stimulation

33
Q

What are the pharmacokinetics of H2-Receptor Antagonists

A
  • OTC→ 6 hours
  • Prescription→ 10 hours
  • Undergo extensive hepatic metabolism
  • Renal excretion
34
Q

Side effects of H-2 RA?

A

• 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
Q

What are the H2-RA drug-drug interactions?

A

• ↓ Ethanol metabolism ( in women)*
• Compete for tubular secretion with weak basics*
o metronidazole is a weak base*

36
Q

What’s special about cimetidine?

A

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
Q

Proton Pump Inhibitors (Block Acid Secretion) are?

A

ESOMEPRAZOLE/OMEPRAZOLE,LANSOPRAZOLE, PANTOPRAZOLE, RABEPRAZOLE
OMEPRAZOLE-racemic mix and esomeprazole-slowly metabolized

38
Q

What is the MOA of PPIs?

A

• IRREVERSIBLY block the final common pathway in acid secretion — the H+/K+ ATPase

39
Q

When do we prefer to use PPIs?

A
  • ZE syndrome and GERD*

* Very Effective for many purposes

40
Q

Pharmacokinetics of PPIs?

A

• 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
Q

What’s critical about Ppis?

A

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
Q

How many doses of PPI do you need to take a day?

A

1! They have a short ½ life, but they’re irreversible inhibitors, it takes 18 hours to make new pumps

43
Q

Full inhibition of all pumps takes how long?

A

3-4 days, and recovery takes 3-4 days as well., So take high initial dose and then taper as symptoms are controlled.

44
Q

How are PPIs broken down?

A

• Broken down by 1st pass metabolism

45
Q

Which PPI is not available via IV

A

omeprazole

46
Q

What are the PPI SE?

A
  • 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
Q

What if taking PPI long term?

A

↓ B12, Fe, Ca2+, Zinc absorption→↑Hip fractures*

↑Respiratory and Enteric Infections (d/t ↑ pH which normally is low in order to kill bugs)

48
Q

Why do you get ECL Hyperplasia (hypergastrinemia) with PPI?

A

Normally ↓ gastric pH: ↑Somatostatin release: ↓gastrin

but with Long-term PPI use, ↑↑ gastrin

49
Q

What are some weak bases to buffer acid?

A

ALUMINUM HYDROXIDE, CALCIUM CARBONATE, MAGNESIUM HYDROXIDE and SODIUM BICARBONATE)

50
Q

What are the factors affecting usefulness of base agents?

A
  • Systemic Absorption
  • Rate of dissociation (fast→faster effect→ shorter duration
  • Cation/Product effects
51
Q

What are the drug interactions of Buffer drugs?

A

↑ 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
Q

Side effect of ALUMINUM HYDROXIDE

A

constipation

53
Q

What is simethicone?

A
  • antifoaming agent: ↓gas pain
  • We add it to Sodium bicarbonate
  • also affects absorptions
54
Q

Why use antacids?

A

rapid onset but short duration of action; no prevention of ulcer recurrence → useful for intermittent dyspepsia

55
Q

why use H2 blocks?

A

relatively rapid onset, intermediate duration, some prevention → many uses

56
Q

Why use PPIs

A

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
Q

What is sucralfate?

A
  • Al(OH)3 and sulphated sucrose
  • Not an antacid
  • basically a band-aid, stress induced ulcers in the ICU
58
Q

MOA of sucralfate:

A
  • attaches to ulcer surface

* stress-induced gastritis (ICU)

59
Q

Pharmacokinetics of sucralfate

A

• Requires acidic environement

o cannot be given with PPI, H2 Blocker

60
Q

SE of sucralfate?

A
  • constipation

* binds other drugs

61
Q

Whewn is misoprostol used?

A
  • accounts for 5% of ulcer treatment (NSAID induced only)

* 15-25% of arthritis patients develop this though, so # maybe ↑

62
Q

Misoprostol MOA:

A
  • 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
Q

Pharmacokineteics of misoprostol?

A
  • rapid absorption and metabolism

* excreted in urine

64
Q

Misoprostol SE?

A

• diarrhea, nausea, cramping, abdominal pain
o 10-20% of patients which → ↓ compliance
• In preggers stimualtes uterine contractions→ abortifactant

65
Q

What do all combo therapy have?

A

pain and eradication!

66
Q

What form crosses more easily?

A

• Unionized, Increase in pH shifts right

67
Q

“net thing to worry about”

A

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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