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Drugs Flashcards

1
Q

How do antiacids work?

A

act as buffers, neutralize acid, thus raise pH

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2
Q

Examples of antiacids?

A

CaCO3 - calcium carbonate - TUMS
AlOH - aluminum hydroxide - Alu-Cap, Alu-Tab, etc
MgOH - magnesium hydroxide - milk of magnesia
Maalox - M(g)aALox (Mg+Al)

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3
Q

how are antiacids absorbed and eliminated?

A

poorly absorbed

eliminated through kidneys - watch with poor renal function

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4
Q

how do antiacids interact with other drugs?

A

bi- and tri-valent Al3+, Mg2+, Ca2+
can chelate other drugs and interfere with absorption
try to give 2 hrs apart from others

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5
Q

indications for antiacids?

A

heartburn
dyspepsia = indigestion
dys = difficult pepsia = digestion

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6
Q

Side effects for Mg antiacids (like milk of magnesia)?

A

Mg - think Mugst go to the bathroom

diarrhea, b/c Mg creates osmotic gradient in the gut

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7
Q

Side effect for Al antiacid (like Alu-Tab)?

A

Constipation
AluMINIMUM amount of feces
Al3+ is good at chelating P in GI, so can lead to hypophosphatemia

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8
Q

Side effects of Ca antiacids (like TUMS)?

A

Constipation
hypercalcemia (b/c intake of Ca+ increases)
can chelate drugs like Al
can cause bloating, flatulence, belching, nausea - CaCO3 -> CO2 released

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9
Q

Why are Al and Mg given together (like MaALox)?

A

perfect together b/c Mg causes diarrhea and Al constipation - at the end only antiacid effect left

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10
Q

What is sodium bicarb? (NaHCO3)

A

Used in some 3rd world countries - baking soda-like, but concerns of bad effect of Na+ on CV health, and creates alkalosis (b/c HCO3- is a base, makes everything more basic)

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11
Q

What do H2 antagonists do?

A

by definition, block H2 receptors
H2 receptors are on parietal cells (which make HCl and IF in stomach = remember PARents provide Home for InFants)
parietal cells can be stimulated by:
* gastrin secretions from G cells
* histamine secretions from ECL cells - enterochromaffin like cells - inside GI, look like chromaffin cells on staining - > neuroregulated endocrine cells in stomach, which release histamine -> histamine binds to H2 receptors and gets parietal cells to produce HCl
* block H2 receptors, block HCl production
* but since parietal cells can also be stimulated by G cells (gastrin in blood) and neural stimulus (ACh), H2 antagonists do not fully block HCl production

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12
Q

Do H2 blockers/antagonists block reversibly or irreversibly?

A

reversibly

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13
Q

What are some names of H2 blockers?

A

raniTIDINE - “run to dine” = ranitidine = Zantac, over the counter
cimeTIDINE = “see me to dine” - many side effects, prescription only
famoTIDINE - pepsid = “famous dining”
nizaTIDINE

think ToDINE - when you dine and have a good meal, you need H2 antagonist to deal with all that acid

available oral, IV, IM

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14
Q

is H2 more effective during day or night?

A

Day: parietal cells stimulated by Ach, gastrin and histamine
Night: stimulated to release HCl mainly by histamine
better nocturnal coverage

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15
Q

Side effects of H2?

A

attentuates ability of gastrin and Ach to stimulate the activity of parietal cells (proton pumps)
all eliminated by kidneys (like antiacids)
diarrhea, drowsiness, fatigue, constipation, etc common
some H2 drugs = TIDINES = can dine on your brain = can cross blood brain barrier, extremely rare, usually in IV in elderly = confusion, delirium, hallucinations due to antagonism of H2 in CNS
* cimetidine-only* = very strong inhibitor of CYP450 = MULTIPLE DRUG INTERACTIONS
* cimetidine-only* = antiandrogenic effects - gynecomastia in males (increased breast tissue), galactorrhea (milk production, sometimes in males), decreased libido in males;

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16
Q

Indications for H2 antagonists?

A

GERD
dyspepsia
gastritis - prevention of bleeds from stress related gastritis esp.
peptic ulcer

17
Q

Whats the difference btwn H2 and PPIs? advantages to use?

A

PPIs way more effective than H2, but H2 is cheaper and also increase H+ by 6-70% so many resort to them first (but tolerance can develop)
H2 antagonists reversible, PPIs irreversible

18
Q

proton pump inhibitors, reversible or irreversible?

A

irreversible

19
Q

What are some of the names of PPIs?

A

think #1 in pump inhibition, like president! PRAZZOLE
omeprazole = omm (feel good) for the stomach + president = Losec (do not confuse with Lasix)
esomeprazole = isomer “esomer” of omeprazole
pantoprazole = pants + president
lansoprazole

20
Q

MOA of PPI?

A

rather than blocking receptors on parietal cell like H2, block proton pumps directly and irreversibly (H+/K+ ATPase in parietal cells) - > dramatically reducles H+ in the stomach
but block only active pumps, so take a few days to achieve maximum effectiveness

21
Q

absorption? and intake timing?

A

must be absorbed through circulation (enteric coating -> circulation via small intestine -> activated by low pH of parietal cells), so must be taken 30-60 mins before food so has time to reach parietal cells and block H+ pumps

22
Q

how are PPIs metabolized?

A

hepatic metabolism! CYP450 inhibitors - worrya bout drug interactions, especially with CLOPIDOGREL - antiplatelet agent that is also very common
also increase pH, and some drugs need low pH to be metabolized

23
Q

indications for PPIs?

A

gastric and duodenal ulcers
GERD
hypersecretory conditions like Zollinger-Ellison (non beta cells in pancreas producing gastrin -> stimulates parietal cells to produce a lot of HCl -> H+ in stomach high!)
NSAID-induced gastric ulcers
used in H.Pylori regiments b/c seem to enhance antimicrobial action of other drugs in cocktail

24
Q

S/E of PPIs?

A

nausea, abdo pain, constipation, diarrhea, flatulence
increased risk of osteoporosis and infection (b/c change flora)
gastrin is released when pH in stomach higher and stimulates ECL cells (the ones that produce histamine) and mucosal proliferation - with PPIs gastrin overstimulated b/c pH high, so worry about potential to stimulate growth of gastric tumours

25
what do gastric cytoprotectants do? | what are indications for their use?
protect stomach lining prostaglandins: use to prevent NSAID-induced gastric ulcer (NSAIDs do bad acts mostly in stomach not duodenum) sucralfate: treatment of duodenal and gastric ulcer (can coat both); prevention of duodenal ulcer recurrence bismuth: adjuct to H.pylori eradication; in acute diarrhea (think pepto ads)
26
what are some prototypes of GI cytoprotectants?
prostaglandin analogue: misoprostol (like prostaglandins in COX, stimulates mucous and bicarb secretion, reduces gastric acid secretion, enhances mucosal blood flow) think miso soup - relief for the stomach, much better than aspirin = here counteracts aspirin coating agents: sucralfate, bismuth - physically coat ulcerations to protect cell lining, short-acting, can induce secretion of mucous and bicarbonate; bismuth can reduce H.pylori binding to gastric mucosa
27
How does misoprostol work (PGE-2 analogue)?
in COX pathway (largely COX1), PGE-2 binds to receptors on proton pump (EP3 receptors), reducing its activity and thus secretion of gastric acid. it also helps to maintain mucosal barrier by stimulating secretion of mucin and bicarb and enhancing mucosal blood flow
28
How do NSAIDS and misoprostol come together?
NSAIDS block COX 1 and reduce PGE-2 (reducing mucous in stomach and increasing acid production). PGE-1 analogues such as misoprostol restores PGE lost b/c of NSAIDs, reducing stomach irritation
29
How does sucralfate and bismuth work?
sucralfate has sucrose and aluminium hydroxide (negative charge) - sticks to positively charged proteins exposed by ulcer - protective barrier formed. can also indirectly stimulate prostaglandin synthesis - mucous and bicarb secretions. bismuth - similar coating action around ulcer, also enhances production of prostaglandins (against what NSAIDs do) - prostaglandins increase mucous secretions and bicarb secretions. bismuth also used in H.pylori treatment because they inhibit their growth and prevent their binding to gastric mucosa (think pepto bismol is good for ulcers :P )
30
indications for prostaglandin (misoprostol) use?
prevention of NSAID-induced gastric ulcers
31
contraindications of misoprostol? bismuth?
THINK SMOOTH MUSCLE CONTRACTIONS DO NOT USE IN PREGNANCY - stimulates uterine contractions - used to terminate pregnancies prostaglandins stimulate smooth muscle contractions ! - > uterine contractions - > GI smooth muscle contractions -> cramps and diarrhea (sometimes very severe) =TAKE WITH FOOD - > IBD patients at increased risk (already sensitive lining ) - > recommended to take with food to reduce smooth muscle irritation BISMUTH CAN CAUSE BLACK TARRY STOOLS THAT LOOK LIKE BLOOD IN STOOL, also can discolour tongue (also black) -> think pink to black :P Bismuth subsalicylates have salicylic acid (same as in ASA) - do not give to people sensitive to ASA or children (fear of Reyer's syndrome)
32
Whats this confusion about PGE1 and PGE2
misoprostol is PGE1 analogue COX 1 works mainly through PGE2 (prostaglandin), they are similar and misoprostol induces COX (mainly COX1), whereas NSAIDs block it
33
How do prokinetic GI drugs work?
Dopamine blocks ACh release from axon terminals by binding to D2 receptors and initiating downstream actions. Prokinetic drugs are dopamine antagonists - they block dopamine receptors so dopamine cannot bind to D2. Thus, ACh works on smooth muscles of GI causing: Lower Esophageal Muscle contraction (increased tone) and increased motility in upper GI (like stomach) (does not do much in lower GI) also somehow act to inhibit vomiting centres: anti-nauseants
34
Name 2 examples of prokinetics?
Domperidone and metoclopramide (think drinking champagne with large (meta) clops (fleas) around)
35
What are indications for prokinetics like domperidone and metoclopramide?
because increases lower esophageal sphincter tone: GERD gastroparesis (gastro = "stomach" paresis = "partial paralysis") => partial weakness of stomach muscles nausea and vomiting (because inhibits vomiting centres in the brain)
36
When not to use prokinetics such as domperidone and metoclopramide?
when extra motility harmful, like in obstruction of perforation - can obstruct or perforate more!
37
What are side effects of prokinetics?
hypermotility: GI cramping and diarrhea Galactorrhea, gynecomastia, dysmenorrhea metoclopramide: CROSSES BRAIN BLOOD BARRIER parkingson-like symptoms tardive dyskinesia drowsiness, restlessness, insomnia, anxiety, etc domperidone: DOES NOT CROSS BB Barrier, but can still reach vomiting centres (which are outside of the barrier), considered better antiemetic than prokinetic (metoclopramide much stronger as prokinetic) take domperidone 15-30 mins before food b/c low oral availability - better absorbed with food, but if taken exactly with food it takes a long time to reach its peak concentration
38
Treatment for H.pylori ulcers?
Eradication regiment *Twice daily* PPI +2 antibiotics: lansoprazole, omeprazole, pantoprazole or esomeprazole (PPI) amoxicillin (1gx2/day) + clarithromycin (500gx2/day) for 2 weeks 2x2x2 2 antibiotics 2 day for 2 weeks put a CAP on H.Pyrori = Clarithromycin, Amoxicillin, PPI

Gastroenterology (8 decks)

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