Drugs Flashcards
cyclosporine-GIVE ON EMPTY STOMACH & FREEZE
Side effects
Side effects:
1. GI upset:In dogs, vomiting, anorexia, diarrhea*
2) gingival hyperplasia*
3)hepatotoxicity + NEPHROTOXICITY
4)thromboembolic events
5) altered glucose metabolism/diabetes mellitus, 6)hypertrichosis/excessive shedding
7)psoriasiform lichenoid-like dermatosis
8) papillomatosis–>FREEZE THEM!!
9)One case series of 6 dogs describes the development of Burkholderia cepacia complex deep skin infections while receiving oral cyclosporine.
10) Bacteriuria and urinary tract infections may occur.
Cyclosporine effects on lactating /pregnant queen/bitches
cyclosporine has been shown to be fetotoxic and embryotoxic in rats and rabbits at doses 2 to 5 times the recommended dose.65 Reduced fetal weight and growth, skeletal retardation, and premature birth have occurred. The manufacturer does not recommend use in pregnant or breeding dogs or cats. Use during pregnancy only when the risks outweigh the benefits.
Cyclosporine is distributed into maternal milk; the manufacturer does not recommend use in lactating queens or bitches.
Because safety has not been established in animals, this drug should only be used when the maternal benefits outweigh the potential risks to offspring.
Cyclosporine dog with treatment for skin infection
In one appraisal study, the prevalence of bacterial infections in 828 dogs with atopic dermatitis receiving anti-allergic dosages of oral cyclosporine was 11%, most commonly affecting the cutaneous and urinary systems and not multiple systems.55 In 95 dogs receiving higher dosages of cyclosporine for other diseases, the prevalence of bacterial infection was 17%, occurring most often in the GI, urinary, and respiratory systems. The prevalence of bacterial infections in atopic dogs treated with cyclosporine appears to be low and occur most often in the skin. However, when given for immunosuppression, the prevalence of bacterial infections appears to be higher and to affect 1 or more body systems
Cyclosporine side effects in cats:
1) GI effects (including vomiting, diarrhea, hypersalivation, decreased appetite, and anorexia) are often reported during the first month of therapy.56,57 Resulting weight loss may lead to hepatic lipidosis in this species (rare)
2) Lethargy, malaise, behavior changes
3) increased hair growth
4) acute bullous keratopathy
5) gingival hyperplasia, and flares of latent viral infections have also been noted in cats receiving cyclosporine
6) Hemolytic uremic syndrome has been reported after renal transplant.
7) Cats developing fatal systemic toxoplasmosis while on cyclosporine therapy have been reported
Cyclosporine MOA
a calcineurin inhibitor, is an immunosuppressive agent that focuses on cell-mediated immune responses, with some humoral immunosuppressive action. Cyclosporine binds to T-cell cyclophilin and blocks calcineurin-mediated T-cell activation.
-T-helper lymphocytes are the primary target, but T-suppressor cells are also affected. Cyclosporine can also inhibit cytokine production and release (including IL-2 and interferon-gamma in dogs20–22 and IL-3, IL-4), thereby affecting the function of eosinophils, mast cells, granulocytes, and macrophages.
-It may also inhibit antigen-presenting functions of the dermal immune system.
- It is not considered myelosuppressive. One study suggests that cyclosporine therapy does not affect circulating lymphocyte CD4/CD8 ratio.
-Cyclosporine appears to increase thromboxane production in dogs,25,26 and low-dose aspirin inhibits this effect
omeprazole-MOA:
metabolized and extreted via which organs? and which diseases will prolong half life and need to be adjusted?
concentration dependent?
IMP considerations- what not to give with and taper or not:
MOA: PPI
In an acidic environment, omeprazole is activated to a sulfenamide derivative that binds irreversibly at the secretory surface of parietal cells to the active enzyme H+/K+ ATPase, where it inhibits the transport of hydrogen ions into the stomach by 90% to 99%. Omeprazole can reduce acid secretion during both basal and stimulated conditions.
In dogs, ≈3 to 5 days are required for maximum gastric acid reduction. The drug has no effect on gastric emptying time or secretion of intrinsic factor.*****
metabolized and extreted via which organs? and which diseases will prolong half life and need to be adjusted?
-renal and liver disease..
Omeprazole is extensively metabolized in the liver ; these are excreted principally in the urine but also via the bile into feces.
In patients with hepatic or renal disease, the drug’s elimination half-life may be prolonged, and dose adjustment may be necessary if the disease is severe.
Discontinue omeprazole administration in patients with interstitial nephritis
[ ] dependent?:
Omeprazole’s effects on acid secretion are independent of its drug concentrations.
considerations:
-When administered to patients for longer than 4 weeks, omeprazole should be gradually tapered to avoid rebound gastric acid hypersecretion; consider a decrease in the dose by 50% each week, with cessation of the evening dosing during the first week
SE of omeprazole
-GI distress (eg, anorexia, colic, nausea, vomiting, flatulence, diarrhea-most common in dogs)
-hematologic abnormalities
-proteinuria
- and CNS disturbances can potentially occur.
SE:
-Omeprazole will increase serum gastrin levels early in therapy. A study reported that a 7-day withdrawal from short-term administration of omeprazole is sufficient for serum gastrin to return to the baseline concentration, +/- gastric dysbiosis
-IV administration of omeprazole, a reduction in CSF production has been noted. Although this effect could be useful in the treatment of conditions causing intracranial hypertension (eg, hydrocephalus, syringomyelia), this effect has not been confirmed in healthy dogs after oral administration.Omeprazole can also be considered as one of the possible drugs used for medical management of decreasing CSF production in diseases such as hydrocephalus and Chiari-like malformation
cisapride- indications/ MOA/SE
indications:
-GERD
-reflux esophagitis
-primary GI disorders
-constipation in cats with megacolon
-enhance detrusor contractility in dogs with micrurition disorders*****(IMP))
MOA:
-5-HT4 receptor agonist–enhances release of Ach at the myenteric plexus without stimulating nicotinic or muscarinic receptors or inhibiting aceytelcholinesterase activity
-direct 5-HT2 alpha receptor AGONIST on colonic smooth muscle
5-HT1 & 5-HT3 receptor- ANTAGONIST of the enteric cholinergic neurons
-The drug stimulates smooth muscle contraction (thus increasing lower esophahageal peristalsis and sphincter pressure)
-increases gastric contractions
-accelerates gastric emptying
-promotes SI and LI motility
-it stimulates distal esophageal smooth muscle and is considered INEFFECTIVE for distal esophageal dysmotility in dogs due to the striated muscle of that species’ distal esophagus; only stimulates distal esophageal motility in cat(?????)
cisapride -pharmacokinetics-
plasma protein binding how much %?
where is it metabolized (organ?)
eliminated which way?
95%
liver-
eliminated in urine 25%, 70% feces
cisapride- contraindications
-in which GI motility could be harmful (FB, GI obstruction, GI hemorrhage or GI perforation)
-Liver disease **
-CORRECT Hypokalemia and hypomagnesemia prior to use; use in caution in P that experience a low plasma K+ (????))
cisapride SE:
-V+, D+, abdominal disomcofort
-prolonged QT intervals or cardiac arrhytmia possible but not reported (**)
-excreted in milk dams()
Misoprostal
MOA
SE
extreted how?-urine
harmful to humans how? EQ
PGE analog (class of drug)
-MOA:
Misoprostol is a synthetic prostaglandin E1 analog. It has 2 main pharmacologic effects that make it a potentially useful agent in prevention of upper GI ulceration.
1) It acts via direct action on parietal cells to inhibit basal (acid release without food present) and nocturnal gastric acid secretion as well as gastric acid secretions stimulated by food, pentagastrin, or histamine—pepsin secretion is decreased under basal conditions, but not when stimulated by histamine.
2) Misoprostol also has a cytoprotective effect on gastric mucosa, likely by increasing production of gastric mucosa and bicarbonate ***
and increasing turnover and blood supply of gastric mucosal cells.
indications:
treatment of gastroduodenal ulcers by NSAIDs but not steroids..
SE: GI distress (diarrhea, abdominal pain, vomiting, flatulence) and potentially uterine contractions and vaginal bleeding in female dog
contraindicated:
pregnant animals and nursing dams (Causes diarrhea in neonates)–causes abortion AND IN HUMANS THAT ARE PREGNANT
:remature birth, uterine rupture, or birth defects
Sucralfate-class of drug:
MOA
SE
erythromycin
MOA
SE
famotidine
ranitidine/nizatidine
cimetidine
