Weak 12: resp, immuno, GI Flashcards
Contraindications/nursing considerations with 1st gen H1 antagonists
Sedation more prevalant in first generation, means they should not be used concurrently with other CNS depressants and alcohol. Educate to use only as directed, many ODs because people see as “safe” and are more lax about dosing
Uses of H1 antagonists
mild allergy
adjunt to severe allergy
Motion sickness (some have antagonizing pathways to vestibular apparatus in inner ear responsible for motion sickness)
Insomnia (1st gen)
Caution/contraindications of theophylline
Slow IV admin to avoid fatal CV events
highly variable metabolism (CYP450), requires plasma monitoring
Caffeine (also a methylxanthine) – increase AE, compete for metabolizing enzymes
tobacco/marijuana – induces CYP450
CYP450 induces – subtherapeutic lvls
CYP450 inhibitors – supratherapeutic (even toxic levels)
Monoclonal antibody types
IgE antibody antagonist: omalizumab
IL-5 receptor antagonists
IL-4 receptor alpha antagonist
How does omalizumab work?
forms complex with IgE that prevents it binding to Mast cells
AE of omalizumab
viral infection, injection site reaction, hypersensitivity
Considerations of omalizumab
Long half life, after stops, takes about a yr to get back to pre-treatment levels
How do IL-5 receptor antagonists work?
inhibit IL-5, causing decreased eosinophils
AE of IL-5 receptor antagonists
HA, pharyngitis, fatigue, hypersensitivity rxns,
How do IL-4 receptor alpha antagonists work?
decreased cytokine-induced inflammation
AE of IL-4 receptor alpha antagonists?
injexn site rxns, oral herpes, conjunctivitis, antibody development against the drug
Montelukast is the most commonly prescribed leukotriene receptor blocker. In comparing its adverse effects with the other two leukotriene receptor blockers, why do you think it’s more highly prescribed?
Minimal side effects, no CYP450 inhibition or liver injury, only rare neuropsych effects
What is the purpose and mechanism of action of drugs to treat allergic rhinitis
Intranasal glucocorticoids: suppress immune response to allergens, prevention and treatment (not PRN)
Antihistamines: block histamine, less effective than intranasal glucocorticoids, can relieve some symptoms, but not nasal congestion
Sympathomimetics: cause local vasoconstriction, so less fluid can leak out to become snot, a1 agonism, only to relieve congestion
List three drugs used for cough (antitussives). Which can cause CNS depression? Which have abuse potential?
Codeine – small abuse potential when with something to deter abuse, CNS depression
Hydrocodone – CNS depression, small abuse potential when formulated with other drugs to deter abuse
Dextromethorphan – CNS actions, high doses can cause euphoria, thus abuse potential exists
How do all glaucoma drugs except prostaglandin analogs work?
decreased production of aqueous humor
AE of Beta blockers for glaucoma
systemic beta blockade
AE of Prostaglandin analogs for glaucoma
A2 agonists: dry mouth, ocular hyperemia
ocular hyperemia (enlarged vessels)
AE of A2 agonists for glaucoma
dry mouth, ocular hyperemia
Pt education for antibiotic treatment of H. Pylori
important to take all types and complete entire 10-14 days course, they should be taken 2-3 times a day and combined with an antisecretory agent (H2RA, PPI)
For each class of antiemetics, describe a patient you would NOT administer the drug to
Serotonin receptor antagonists: pt w/ a prolonged QT or on SSRIs
SubP/NK receptor antagonists: pt on warfarin, or on oral BC not using another method of contraception
Haloperidol: prolonged QT
Cannabinoids: psychiatric disease
Scopolamine: an elderly person who is particularly prone to disorientation
Discuss opioid use in diarrhea: how do they work? What drug category are they? Why are they not schedule II like many of the other opioids?
Loperamide, and other similar drugs agonize Opioid receptors, which decreases bowel motility, they are either schedule IV or unscheduled because they are poorly absorbed (no euphoria) and they are formulated with drugs (atropine) which create unpleasant side effects if the dose is increased
How does sulfasalazine work?
Sulfasalazine is metabolized by intestinal bacteria, and converted into 2 substances, one of which (5-ASA) suppresses prostaglandin synthesis and local inflammation, the other is sulfapyridine and causes the AE associated with the drug
What is Alosteron used for
IBS-D in women
AE of alosteron
well-tolerated to severe, including death d/t ischemic colitis
What are the differences in H1 and H2 receptor agonism? What drugs do we use for each?
H1 receptor agonism causes:
Vasodilation, increased vascular permeability,
Hypotension, reflex tachy
Bronchoconstriction
itching/pain (stim of nerves)
CNS: cognition, memory, sleep/wake
Drugs: diphenhydramine (benadryl), promethazine (phenergan)
H2: gastric secretion
Drugs H2RAs: cimetidine, famotidine
Pt education for immunosuppressants
Toxic: nephrotoxicity, hepatotoxicity
AE: bone marrow suppression, infection, depression, flu-like symptoms, injection site reactions, decrease vaccine effectiveness
Don’t use with other immunosuppressants
Encourage family members to get vaccinated, avoid live vaccinations
Avoid with other nephrotoxic drugs, metabolized by CYP450 – be careful with inducers and inhibitors
mTOR inhibitors with high fat foods → increased absorption and possible toxicity
Indication of Calcineurin inhibitors
prevent transplant rejection
Considerations for Calcineurin inhibitors
Unpredictable PO: must monitor plasma levels
hepatic metabolism: avoid CYP450 inducers and inhibitors
avoid with other nephrotoxic drugs