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GI First half > pharm - GI drugs > Flashcards

pharm - GI drugs Flashcards

1
Q

what stimulates chief cells ? result?

A

ACh, CCK, gastrin –> release of pepsinogen

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2
Q

prostaglandins in the stomach

A

are protective! stimulate mucous cell secretion (reduce inflammation)

vs rest of body where they cause inflammation

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3
Q

ECL cell secrete

A

histamine

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4
Q

major stimulatory mechanism for HCl secretion from parietal cells?

A

paracrine - histamine from ECL cells –> H2 receptor

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5
Q

imbalance between aggressive and defensive stomach mechanisms

A

peptic ulcer disease

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6
Q

antacids

A

neutralization of the HCl

4 –> aluminum hydroxide, magnesium hydroxide, calcium carbonate, and sodium bicarbonate

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7
Q

tums

A

sodium bicarbonate/ca carbonate

may increase gassiness and bloating due to CO2 product

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8
Q

antacids w effects on gastric motility

A

aluminum hydroxide –> DECREASE motility
magnesium hydroxide –> INCREASE motility
tums –> no effect

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9
Q

which antacid INCREASES gastric motility?

A

mg hydroxide

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10
Q

mucosal protective drugs

A

sucralfate (aluminum sucrose sulfate)
and
bismuth-subsalicylate

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11
Q

sucralfate

A

aluminum sucrose sulfate
forms a water insoluble viscous layer over ulcer tissue - maintenance therapy
**give on empty stomach!
-few side effects (constipation/dry mouth)

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12
Q

bismuth-subsalicylate

A

(pepto) does NOT neutralize acid –> binds to ulcer and
1) absorbs bile acids
2) stimulates mucous secretion
3) antibacterial effect on H pylori
* *aspirin sensitive people might be sensitive
* *turns stool black

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13
Q

what drug forms a viscous water insoluble layer over ulcer; non curative just maintenance

A

sucralfate

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14
Q

antimuscarinic agents?

A

dicyclomine and hycosamine

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15
Q

dicyclomine and hycosamine use?

A

antimuscarinic agents —-UNPLEASANT, bad side effects, rarely used to treat PUD

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16
Q

H2 receptor antagonists

and mechanism?

A

cimetidine, ranitidine

  • used to treat ulcers
    mech: structural analogs to histamine –> competitively inhibit histamine binding to H2 receptors
  • —REDUCE ACID SECRETION
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17
Q

Do H2 receptor antagonists have CNS side effects?

A

**they are hydrophilic so NO CNS side effects

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18
Q

H2 receptor antagonists have a ____ half life.

why is this not an issue?

A

short (2-3 hrs)

lack of significant side effects allow high/multiple dosages

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19
Q

which H2 receptor antagonist is the least ideal (most side effects)?
what are its negative effects?

A

cimetidine

  • enhances prolactin and binds androgen receptos leading to gynecomastia, impotence and lactation issues
  • inhbits cyt P450s –> prolongs half life of other drugs
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20
Q

PPIs

A

proton pump inhibitors - used to treat ulcers
omeprazole, esomeprazole, lansoprezole, pantoprazole
mech: inhibit the H K ATPase of gastric parietal cells with an irreversible covalent bond(kills the pump)

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21
Q

how PPIs get to the ATPase

A

prodrug as delayed release/enteric coated capsules–> absorbed as prodrug in duodenum –> circulation –> reaches parietal cell and is pumped into the acidic caniculi –> protonated by low pH –> active drug –> inactivates that same atpase

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22
Q

PPIs are most effective when…

how long is the effect?

A

–>taken 30-60 minbefore eating
when you are hungry the pumps begin pumping
they have half life of 1 hr, but since the ATPases are irreversibly inhibited, effect lasts days until new ones can be made

23
Q

treatment of choice for zollinger ellison syndrome?

A

PPI

omeprazole

24
Q

what is more effective for GERD: PPI or H2 antagonists?

A

PPI

25
Q

do PPIs have CNS effects?

A

yes

26
Q

PPIs side effects

A
  • CNS, nausea, diarrhea
  • prolonged suppression of acid secretion may increase c dificile colonization in stomach –> risk of pneumonia
  • risk of spinal/hip fracture
  • inhibits clopidrogel activation
27
Q

Misoprostol

A

prostaglandin analog that inhibits gastric acid secretion and stimulates mucin secretion (protective just like PGE2)

28
Q

why is misoprostol not used often?

A

1) PPIs are more effective and getting cheaper

2) potential abortifacient –> doesnt allow/aborts pregnancies

29
Q

antimicrobial therapy for peptic ulcers

A

many ulcers have H pylori infection
Quadruple therapy - PPI + 2 antibiotics (tetracycline and metronidazole) + busmuth-subsalicylate
Concomittant therapy - PPI + 3 antibiotics (clarithromycin, metronadizole/tinidazole, and amoxicillin)

30
Q

concommittant antimicrobial therapy

A

PPI + 3 antibiotics

clarithromycin. amoxicillin, and metronidazole/tinidazole

31
Q

quadruple antimicrobial therapy

A

PPI + bismuth-subsalicylate + 2 antibiotics (tetracycline and metronidazole)

32
Q

metoclopramide

A

increases gastric motility
D2 antagonist, 5HT3 antagonist, 5HT4 agonist
*binding to 5HT4 increases motility in 3 ways = 1) increase LES pressure, 2) increases rate of gastric emptying, and 3) decreases small bowel transit time
—-treats nausea associated with cancer treatment

33
Q

why is metoclopramide not used alot?

A

central D2 side effects!
hyperprolactinemia, galactorrhea, parkinsonism, tardive dyskinesia
RISKY drug

34
Q

cholinergic activity _____ motility

receptors?

A

increases
D2 antagonists
5HT3 antagonists
5HT4 agonists

35
Q

adrenergic activity ____ motility

receptors?

A

decreases
opioid Mu receptor
5HT3 antagonists

36
Q

emesis center

A

is the medulla - receives input from higher and lower areas and from area postrema (half in and half out of the BBB so good sensory)
receptor trigger zone has 5HT3, D2, and M1 receptors

37
Q

treatment choice for cytotoxic (chemotherapy) drug emesis/nausea

A

1) 5HT3 antagonists are best (ondansetron or palonosetron)
2) NK1 antagonist - aprepitant
3) metoclorpramide (D2/5HT3 antagonist) - last option due to bad side effects

38
Q

aprepitant

A

nk1 antagonist

treats CINV from cytotoxic/chemo

39
Q

ondansetron vs palonosetron

A

both are 5HT3 antagonists
O - centrally acting - blocks peripheral and central emetic serotonin input
P - better for CINV

40
Q

treatment for severe IBD?

A

TNF inhibitors, monoclonal Ab (-mab) –> INFLIXIMAB or etanercept

41
Q

treatment for mild/moderate IBD?

A

salazines
they are converted to the active drug mesalamine (5-ASA)
anti-inflammatory and aspirin analog (aspirin sensitive ppl watch out!)

42
Q

what is used to treat gut after antibiotic treatments?

A

probiotics to repopulate gut

43
Q

what drugs can cause increased h pylori populatiion?

A

PPIs

44
Q

treatment options for diarrhea?

A

loperamide
or
alosetron

45
Q

loperamide

A

an opioid mu agonist (doesnt penetrate CNS so low abuse potential)
**DO NOT use with ulcerative colitis; can cause constipation and toxic megacolon

46
Q

alosetron

A

5HT3 antagonist that blocks motility
usually 5ht3 antagonists promote motility BUT this is an exception
**ONLY use for diarrhea-predominant IBS

47
Q

linaclotide

A

increases cGMP –> increased Cl/bicarb secretions in intestine
treats constipation predominant IBS

48
Q

lubiprostone

A

bicyclic FA that opens Cl channel

treats opioid induced constipation

49
Q

naloxegol

A

opioid antagonist that doesnt enter CNS

treats opioid induced constipation

50
Q

two drugs to treat opioid induced constipation

A

lubiprostone
and
naloxegol

51
Q

bulk laxatives

A

mild and slow acting that add fiber and water to gut

bran, psyllium, and methylcellulose

52
Q

osmotically active agents

A

promote water retention in distal ileum/colon
sodium phosphate/bisphosphate (oral)
polyethylene glycol

53
Q

stimulant laxatives

A

promote accumulation of water and salts in the colonic lumen and stimulate motility –> POTENT AND QUICK
(bisacodyl, senna)

GI First half (8 decks)

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