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E&E > pharm (davis) > Flashcards

pharm (davis) Flashcards

1
Q

What 3 receptors and antiporter lie on the basal side of a gastric parietal cell?

basal side = blood vessel side

A

Histamine, gastrin, AcH; HCO3+/Cl- antiporter

Cl goes in, bicarb goes out

bicarb-chloride antiporter
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2
Q

What pump lies on the luminal side of a gastric parietal cell?

A

H+/K+ ATPase pump (in most animals, is inactive inside the parietal cell)

K+ goes in, H+ goes out (into stomach)

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3
Q

How is HCl- formed in stomach?

A

H+ and Cl- leaving the gastric parietal cell on luminal side

(H+ gets pumped out via H+/K+ ATPase pump; Cl- diffuses passively out of the cell)

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4
Q

Suppression of gastric acid production

H2 receptor antagonists

Histamine receptor

A

Ranitidine, famotidine
- reversible, competitive inhibitors
- reduce amt. of gastric acid present in gastric secretions -> increase gastric pH
- less efficacious w/ chronic dosing; rare ADEs

Famotidine does not have cancer-causing agent that’s found in ranitidine

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5
Q

Suppression of gastric acid production

Proton pump inhibitors

H+/K+ ATPase pump

A

Omeprazole, Pantoprazole
- irreversibly inhibit -> no H+ to combine with Cl- to form gastric adic –> decrease gastric acid // increase gastric pH by 95%
- Omeprazole: given in an inactive form –> ionized and activated intracellularly (therefore, [plasma] do not relate to effect

have replaced most of H2-receptor antagonists, but can be used adjunctively b/c PPIs take a couple days for full effect

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6
Q

Suppression of gastric acid production

Mucosal protectants

A

Sucralfate (complex of sucrose & AlOH)
- Works at bicarb border inside of stomach to help heal gastric ulcers (AlOH binds to damaged GI epithelial cell membranes)
- binds to/inactivates bile acids
- stimulates PGEs –> increased mucosal blood flow (which aids with ulcer repair), negative feedback on acid production
- adjunctive tx only - not strong enough for monotherapy
- give 2 hours apart from other drugs!!

gastroduodenal ulvers, esophageal ulcers, colon ulcers

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7
Q

Suppression of gastric acid production

Prostaglandin analogue

synthetic prostaglandin E1 (PGE1)

A

Misoprostol
- Suppresses gastric secretion & improves mucosal bloow flow
- Use for NSAID-induced ulcers, and equine glandular ulcers
- Abortifacient!!! Owner education & safety!!
- has been shown to decrease pruritus by 30% in atopic dermatitis dogs (anti-inflamm. effects)

negative feedback (activate PGE receptor -> suppression)

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8
Q

Suppression of gastric acid production

Antacids

A
  • Work in lumen to break apart HCl- bonds
  • require q2h dosings (large volumes, frequently)
  • contain AlOH (chelate other drugs like fluroquinolones)
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9
Q

Which H2-receptor antagonist is most potent?

A

Famotidine (> ramitidine = nizaditine > cimetidine)

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10
Q

What is the only FDA-approved drug in vetmed for treating gastric ulcers?

A

Omeprazole; only in horses (all other uses = off-label use)

Ulcergard; Gastrogard — both exact same thing, only difference = dosage

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11
Q

Omeprazole vs Pantoprazole regarding clinical uses

A

twice daily dosing is likely needed for dogs/cats

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12
Q

Why must omeprazole be administered in a buffered form?

A

To reach and be absorbed in the SI

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13
Q

Hay diets in horses & omeprazole

A

Omeprazole should be administered on an empty stomach//30 mins before a meal (all species).

All-hay diets blunt effects of omeprazole (during tx) but are recommended in horses with hx ulcers (prevention– want hay in the stomach as a buffer)

develop a proper dosing schedule for treatment
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14
Q

Why does omperazole absorption increase with dosing?

A

B/c there is less acid available to break down the omeprazole

less acid b/c omperazole is breaking that down

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15
Q

Describe proper dosing scheduling of ABX (tetracyclines, fluoroquinolones) with sucralfate

A

Give abx, wait 2h, then give sucralfate

Not following this regimen can cause decrease in therapeutic concentrations of the antibiotic and therefore increase risk of microbial resistance devleoping!!!

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16
Q

Why are antibiotics never a first-line tx for gastric ulcerations in veterinary species?

A

Helicobacter spp. not significantly found to be associated with gastric ulceration in veterinary species

only found in gastric ulcers of foals and non-healing ulcers in horses

17
Q

What receptors do drugs that induce emesis work at?

A

D2, NK1, 5-HT

18
Q

Which species do not/rarely vomit?

A

Horses cannot vomit; cows/swine rarely do

19
Q

Ropinirole

Clevor

A
  • dopamine agonists (affinity for D2) in CRTZ in brain
  • rapid absorption across conjunctival mucosa, highly metabolized and rapidly eliminated via urine
20
Q

Apomorphine

A
  • derivative of morphine (NOT an opioid)
  • D2 agonist
21
Q

When should you use Ropinirole over Apomorphine 100% of cases?

A

MDR1-mutation dogs
- apomorphine causes more severe v+ (# & duration) and more severe CNS depression
- Ropinirole is NOT a substrate for p-glycoprotein

MDR-1 mutation: these dogs are homozygous for the mutation, where they LACK P-GLYCOPROTEIN EFFLUX PUMPS @ BBB

22
Q

What drug class is used to induce v+ in cats

A

Alpha-2 agonists (cats have more alpha-2 receptors in CRTZ. dogs have more dopamine receptors).

23
Q

Thiazine-derivative anti-emetics

A
  1. Acepromazine
  2. Chlorpromazine - PO drug
    - acts on emetic center, CRTZ and peripheral receptors
    - not used often anymore
    - long-term sedation, but can have idiosyncratic effect of hyperness/somewhat aggressiveness
24
Q

Prokinetic Agent: Metoclopramide Mechanism and effects

A

Central dopaminergic antagonist (@ CRTZ), also works at peripheral serotonin receptors => CNS & GI effects
- CNS effects: b/c it crosses the BBB (CRTZ signals to the emetic center, which is within BBB), it can cause extrapyramidal signs (Parkinsons-like = uncontrollable muscle tremors/spasms)
- GI effects: stimulates parasymp. activity, stimulates/coordinates esoph, gastric, pylorc and duodenal motor activity

25
Q

Clinical uses of metoclopramide

A
  • mainly in dogs (sometimes for cats) for anti-emetic effects
  • particularly useful in dz with decreased GI motility (parvo; megaE)
  • post-operative ileus in horses

Erythromycin used more frequently for abomasal emptying in cattle compared to Metoclopramide

26
Q

Why is metoclopramide always given as a CRI in horses?

A

Slower admin @ lower concentrations b/c the drug causes intense CNS effects (crazy+++ and aggressiveness)

also never give in conjunction w/ chlorpromazine

27
Q

Maropitant citrate

A

Cerenia
- inhibits binding of substance P to NK-1 receptors (substance P stimulates emesis –is an emetogen) in CRTZ, emetic zone, peripheral vagal receptors in GIT
- PO and inj (dogs) – PO: small amt of non-fatty foods (fatty foods delay dissolution)
- Inj only (cats)

pre-op maropitant may lower anesthetic requirements and provide additional analgesia for GI and reproductive procedures

100% of patients administered cerenia 45 mins before opiod admin for surgery experienced NO pre-op v+

PO has higher does than SC b/c PO has greater first-pass metabolism

28
Q

Ondansetron

A

Peripheral & Central action:

  • Peripheral = reduces vagal n. activity
  • Central = 5-HT3 antagonist at CRTZ
  • short half life
  • ADE: prolonged QT intervals
29
Q

Mirtazapine

A
  • Alpha-2 antagonist
  • serotonin and histamine receptor antagonist
  • renal/liver disease cats: drug when given PO has prolonged clearance/half life -> Adjust dose!
  • no increase in ADE when administered at label doses transdermally

ADE: vocalization, restlessness, agitation, tremors/trembling, vomiting, hypersalivation, tachypnea, tachycardia, lethargy, ataxia, abnormal gait

30
Q

Capromorelin

A

Entyce (dogs); Elura (cats)
- mimics “hunger hormone” = ghrelin (makes your stomach go Ghrrrrrr…elin)

bitter taste; use in hospital

31
Q

What 2 GI drug/drug classes chelate other classes like fluoroquinolones and tetracylines?

A

Mucosal protectant (sucralfate) & Anatacids

Contain AlOH

E&E (30 decks)

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