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Drug Action II > Block 1: PUD, GERD, IBD Med Chem > Flashcards

Block 1: PUD, GERD, IBD Med Chem Flashcards

1
Q

What is the primary mechanism of antacids?

A

As an antacids that neutralizes stomach acid, but doesn’t prevent acid over-production

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2
Q

What is the secondary mechanism of antacids?

A

Promotes gastric mucosal defense:
1. Secretion of mucus → protective barrier against HCl
2. Secretion of bicarb: buffer
3. Secretion of PG: prevent activation of proton pumps

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3
Q

Raising gastric pH from 1.3 to 1.6 neutralizes how much of gastric acid?

A

50%

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4
Q

Raising gastric pH from 1.3 to 2.3 neutralizes how much of gastric acid?

A

90%

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5
Q

Describe the interaction between sodium bicarb with H-Cl?

A

May cause gas and burps

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6
Q

Describe the interaction between aluminum hydroxide with H-Cl?

A
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7
Q

How does sodium bicarb and aluminum hydroxide differ?

A

Sodium: mono valent
Al: tri valent has DI due to chelation

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8
Q

What are the forms of Mg2+ salts?

A

Carbonate, hydroxide, oxide, trisilicate

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9
Q

What is the use of Mg2+ salts?

A

Laxative and commonly combined with aluminum antacids to counter

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10
Q

What are the CI of Mg2?

A

Renal failure

Failing kidneys can’t excrete Mg2+ → accumulation

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11
Q

What are the ADRs of calcium salts?

A

Constipation

Kidney stones

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12
Q

What are the products of mg antacids?

A

Maalox, Mylanta

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13
Q

What are the types of antacid?

A
  1. Mg
  2. Ca
  3. Na bicarb
  4. Alumin
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14
Q

ADRs and CI of sodium bicarb?

A
  1. Metabolic alkalosis
  2. CI: renul failure, HTN (Na overload)
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15
Q

ADRs and info about Aluminum?

A
  1. Constipation
  2. Used with Mg
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16
Q

What is bismuth subsalicylate?

A
  1. Mild antacid
  2. Anti-inflammatory
  3. Prevetn N/diarrhea
  4. Black stool/tongue -> Reyes syndrome (children)
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17
Q

How is gastric acid secreted?

A
  1. Gastin and Ach
  2. PG
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18
Q

What are the indication of H2RA?

A
  1. DU
  2. GERD
  3. Hypersensitivity
  4. Upper GI bleeding
  5. Acid reflux
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19
Q

What is the MOA of H2RAs?

A

Inverse agonist that blocks basal activity H2 receptors that inhibit cAMP and stimulation of PPI, however, gastin and Ach can still stimulate PPI

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20
Q

Describe the MOA of H2 receptors?

A

Gs -> increase cAMP

PG that inhibit this ppathway

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21
Q

What are the binding site of Histamine to receptor?

A

2 Aspartate (98 and 186) and Threonine 190

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22
Q

Describe the original SAR of H2RA and how it differs from modern? How did manufacturing improve?

A

Metiamide;
1. Thioester
2. Imidazole ring
3. Guanidine
4. 4 atom spacer

Failed: agranulocytosis and thiorea

To make better, they attached a EWG to guanidine to convert into N-CG -> CImetidine (Tagamet) (selective H2)

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23
Q

Is Cimetidine an inhibitor or inducer?

A

Cimetidine is CYP450 inhibitor: Imidazole replaces histidine that is used as a ligand to porphyrin iron

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24
Q

MOA of PPI?

A

Irreversiblly inhibit PP irrespective of the stimulation process

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25
Q

Describe the dosage form of PPIs?

A
  1. Acid-stable in order to be released in the duodenum and avoid activation in stomach
  2. Absorbed in canaliculus -> secreted from parietal cell -> disulfide binding to pump
  3. Add Na bicarb to raise gastric pH
  4. Spinocyclic intermediate -> sulfuric acid -> bind to CYS813 or CYS822
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26
Q

What is the most critical residue in inhibiting PPIs?

A

CYS813 in the luminal vestibule of the ATPase (most accessible)

PPIs that slowly activate may react with CYS822

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27
Q

Should PPIs be considered prodrugs?

A

Not true prodrugs since activation in pH driven not enzymatically induced

2 protonation is required

benzimadazole (EDG on R1-4) -> sulfemic acid analog -> sulfenamide analogue

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28
Q

What are the benefits of using a pyridine ring in PPI?

A

pKa: 3.83-4.53
Ensures that PPI will mostly be ionized at low pH 1.3 of the parietal cells

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29
Q

Rank the stability of the PPIs?

A

Pantoprazole (less reactive) > Omeprazole > lansorazole > rabeprazole (more reactive)

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30
Q

Describe the different binding of PPIs?

A

CYS813 (surface) or CYS 822
GSH regenerates inactivated enzymes can only reach 813
1. Omeprazole/lansoprazole only react with Cys813
2. Pantoprazole can react with Cys822
3. Rabeprazole pyridine nitrogen has highest pKa-> much more reactive – faster onset of action

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31
Q

CYP enzymes important for PPI metabolism

A

2C19
3A4

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32
Q

CYP enzymes inhibited by omeprazole/esomeprazole

A

2C19
2C8

33
Q

How does esomeprazole metabolism differ from omeprazole?

A

Lower dependenct on CYP2C19 and more reliant on CYP3A4 biotransofrmation

better bioavailability in extensive metabolizers and less variation between extensive and slow metabolizers

34
Q

What PPI is not commonly metabolized by CYP?

A

Rabeprazole

35
Q

PPI with the greatest risk for toxicity due to CYP inhibition of 2C19?

A

Omeprazole and esomeprazole

Poor metabolizers will have a greater response vs extensive metabolizers

36
Q

2C19 polymorphism effects of PPI?

A

Polymorphism

Esomeprazole better F and less variation

Dexlansoprazole: consistent

DDI: Clopidogrel

37
Q

What are prostaglandins?

A

20C molecules from Omega 3 FA that have anti-secretory effects on gastric acid and stimulates bicarb and mucous secretion

38
Q

Example of PG analogue?

A

Misoprostol (Cytotec)

39
Q

Misoprostol? MOA? Structure? Indication?

A
  1. Synthetic analogue of PGE1 -> Prodrug
  2. C15-16 changes to prevent rapid metabolism
  3. Allylic secondary alcohol shift from C15 to 16 as a tert alcohol

Indication: Non-NSAID GU and bleeding prevention

40
Q

ADRs and CI od Misoprostol?

A

ADRs: Diarrhea, abdominal cramping
CI: Pregnancy and not for DU

41
Q

MOA of sucralfate?

A
  1. Sulfuric acid ester complex of sucrose and aluminim hydroxide
  2. Anionic (-) sulfate esters bind to (+) charged edges on ulcers - procting from erosion
  3. Stimulate PG, Bicarb, and epidermal and fibroblast GF
42
Q

CI and ADRs of Sucralfate?

A

CI: Renal impairment (aluminum)
ADRs: H2RA, quinolone, Pheytoin, Warfarin, Anatacids (di or tri)

Aluminum can cause chelation on the absorption of other drugs

43
Q

What is the precation of using prokinetics like Cisapride?

A

Can cause arrhythmias because it mimic procainamide

Long QT syndrome

43
Q

What is the MOA of prokinetic agents?

A
  1. Increase LES pressure (tone)
  2. 5-HT4 partial agonists (seratonin)
44
Q

What is mesalamine?

A
  1. 5ASA anti-inflammatory drug that treat CD and mild-moderate UC
  2. Antioxidant by trapping ROS
45
Q

What is the MOA of sulfasalazine?

A

5ASA -> IBD and RA
1. Reducing synthesis of inflammatory mediators
2. Reduced inflammatory cytokine
3. No immunosuppressant activity

Sulfonamide protion contributes to antimicrobial activity

46
Q

What is a pruine RNi? MOA?

A

Mercaptopurine is an immunosuppressive drug that treats leukemia and Pediatric non-Hodgkin’s lymphoma

Inhibitons de novo purine nucleotide biosynthesis

47
Q

Azothioprine MOA?

A

Immunosuppresant prodrug used in organ transplantation, RA, IBD, pemphigus

47
Q

MOA of Cyclosporin A?

A

Binds to Protein cyclophillin of immunocompetant lymphocytes: inhibits calcineurin and lymphokine production -> reducted effector T cell function

48
Q

SAR of H1 antihistamine?

A

Ar1- aryl (cis)
Ar2- aryl or arylmethyl (tras)
Chain can be part of another ring
x- several atoms/functionalities N or C

49
Q

Difference between C2 and C4 substituents on aromatic ring?

A

C2: direct activity towards anticholinergic activity
C4: direct activity towards antihistaminic activity

Increasing alkyl group size (tBu>iPr>Et>Me)

50
Q

Common anti-H1 for N?

A
  1. Meclizine
  2. Demenhydrinate
  3. Promethazine
51
Q

What is dimenhydrinate?

A

8-chlorotheophyllinate salt of Benydryl

  1. Lowers potency
  2. chlorotheophylline added -> sedation than Benydryl
  3. Anticholinergic ADRs, sedation
52
Q

MOA of prmethazine? Why is it better than Dimenhydrinate?

A

Phenergan

Phenothiazine: branched 3 carbon side chain between R10, opposed to unbranched found on antipsychotics

Longer DOA, higher sedative

53
Q

MOA of meclizine?

A

Bonine and Antivert: Cyclic ethylenediamine

Block H1 and muscarinic
Chloro -> Blcoks aromatic hydroxylation (Longer DOA) -> drug distribution

54
Q

ADRs of antimuscarinics?

A
  1. Blurred vision
  2. Dry mouth
  3. Tachycardia
  4. Uriranry retention
  5. HA
55
Q

SARA of anticholinergics?

A

N-tert: CNS activity (not as potent)
N-quat: more potent antagonist, ANS (bicyclic)
X: ester (prone to breakdown), ether (stable), C (rare)
A: 1-phenyl group
B: aromotic ricg
C: -OH, -CH2OH, -CONH2

56
Q

Products that are +/-Hyoscyamine Solanaceous alkaloids?

A

Atropine (Tropin, Eumydrin, Atropisol)

57
Q

Products that are -Hyoscyamine Solanaceous alkaloids?

A
  1. Levisin
  2. Symax
  3. Anaspaz
  4. Cytospaz
58
Q

Indication of Hyoscyamine? ADRs?

A
  1. Mydriatic, antispasmodic

Dry mouth, urine retention, blurred vision, constipation

59
Q

Brand name of scopolamine? Indications

A

Scop/Scopderm: antiemetic (motion sickness), mydriatic, antispasmotic, preanesthetic medicant

60
Q

Brandname Methscopolamine? Indication?

A

Pamine

GI antispasmotic and adjuct tx for DU

61
Q

Types of synthetic anticholinerigcs?

A
  1. Propantheline
  2. Dicyclomine
  3. Isopropamide
62
Q

Indication for propantheline?

A

Pantheline
2. 1. hyperhidrosis
2. Cramps and spasm of GI and bladder
3. Enuresis
4. IBD

63
Q

Indication of dicyclomine?

A

(Bentyl, Procyclomin, Wyovin)

GIT spams, dysmenorrhea and biliary dysfunction

Decreased side effects compared to atropine

64
Q

Incidaction of Isopropamide?ADRs? CI?

A

PU and GI hypermotility and acidity
Long DOA

ADRs: dry mouth, mydriasis, urinary difficulty

CI: glaucoma

65
Q

Example of selective seratonin antagonist?

A
  1. Dolasetron (Anzemet)
  2. Ondansetron (Zofran)
  3. Granisetron (Kytril)
66
Q

MOA of 5-HT3 receptor antagonists?

A
  1. Blocks receptors on nerve terminals of vagus in P and C in the CTZ -> postema
  2. Modied cocaine
  3. Little or no affinity for other serotonin receptors
67
Q

Medication for bacterial diarrea?

A

E. coli, Shigella sp., Salmonella sp: Fluoroquinolone (ciprofloxacin) or TMP-SMX

Campylobacter sp. : macrolide (erythromycin)

C. difficile: Fidaxomicin, Metronidazole, Vanc

68
Q

Medications for parasitic diarrhea?

A

Metronidazole, Tinidazole, Nitazoxanide

69
Q

MOA of opioid antidiarrheals?

A

µ and 𝛿 receptors have strong inhibitory action on the peristaltic reflex of the intestine

µ: abuse potential and constipating effects

Combos of meperidine and methadone

70
Q

MOA of diphenoxylate?

A

Difenoxin: low µ-agonist
1. Rapidly metabolized by ester hydrolysis 2. Zwitterion is 5x more potent (active form) -> prevent CNS
2. Atropine to block the block of ACh-induced peristalsis (synergistic)

71
Q

MOA of loperamide?

A
  1. Potent opioid agonist
  2. Highly lipophilic but no CNS activity (first pass, slow dissolution, P-gp efflux)
72
Q

MOA of octreotide? Indication?

A

Sandostatin
1. Mimic somatostatin and inhibits gastrin, secretion, cholecystokinin, glucagon, growth hormone, insulin, secretin, pancreatic polypeptide, TSH, and vasoactive intestinal peptide
2. Analgesic effect at µ

Tx of diarrea in VIPomas

73
Q

MOA of polycarbophil?

A

Stool stabilizer for constipation, diarrhea, and abdominal discomfort

Absorbs liquid in intestine and sweel -> solft bulky stool

Stimulates the intestinal muscles, speeding stool transit time through the colon

74
Q

INdications of Linaclotide?

A

Linzess (IBS-C, chronic C)

  1. Mimic of guanylin and uroguanylin
  2. Increases cGMP stimulate secretion of chloride, bicarb, and water in lumen
  3. increases intestinal fluid and accelerated transit
75
Q

BBW of Linzess?

A

CI in children under 6
Avoid people 6-18 -> severe dehydration

76
Q

MOA of docute?

A

Colace

Anionic surfactant that lower ST at oil-water interace of feces (more fat and water combo): easy pass

Systemic action as well

Drug Action II (28 decks)

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