Chapter 1: Pharmacy Foundation Flashcards
(rapid fire!)
m
What are the key components of the central nervous system (CNS) and how does it control bodily functions?
The CNS, comprising the brain and spinal cord, regulates body functions by sending signals to the PNS. Neurotransmitters are chemical messengers facilitating signal transmission. They’re released from presynaptic neurons into the synaptic cleft, reaching postsynaptic neurons or other body parts. The PNS includes the somatic (voluntary) and autonomic (involuntary) systems. The somatic system controls muscle movement through the release of acetylcholine (ACh) acting on nicotinic receptors in skeletal muscles. Meanwhile, the autonomic system regulates functions like digestion, cardiac output, and blood pressure
AUTONOMIC NERVOUS SYSTEM: What are the main divisions of the autonomic nervous system (ANS), and how do they differ in their functions and neurotransmitter actions?
The autonomic nervous system (ANS) consists of the parasympathetic and sympathetic divisions. The parasympathetic nervous system (PSNS) facilitates “rest and digest” activities, employing acetylcholine (ACh) on muscarinic receptors, leading to responses like salivation and urination. Conversely, the sympathetic nervous system (SNS) triggers the “fight or flight” response through epinephrine (Epi) and norepinephrine (NE), acting on adrenergic receptors (alpha-1, beta-1, and beta-2), causing increased blood pressure, heart rate, and bronchodilation, while suppressing digestion and urination.
.
Be familar with where the alpha and beta receptors are located! (see pic)
Common Receptor, Substrates, and Drug Example
Receptor: Muscarinic
- Endogenous substrate
- Agonist action
- Drug agonist
- Antagonist action
- Drug antagonist
Receptor: Muscarinic
- Endogenous substrate: Acethylcholine
- Agonist action: Increase salivation, lacrimation, urination, diarrhea, digestion (“wetness”)
- Drug agonist: Pilocarpine, Bethanechol
- Antagonist action: Decrease Wetness
- Drug antagonist: Atropine, Oxybutynin
What is metabolized by monoamine oxidase
serotonin
Common Receptor, Substrates, and Drug Example
Receptor: Alpha 1
- Endogenous substrate
- Agonist action
- Drug agonist
- Antagonist action
- Drug antagonist
Receptor: Alpha 1 (mainly in peripheral)
- Endogenous substrate: Epin/ norpei
- Agonist action: smooth muscle vasoconstriction = Increase BP
- Drug agonist: phenyleprine, dopamine (dose dependent)
- Antagonist action: vasodilation, decrease BP
- Drug antagonist: Alpha 1 blocker (doxazosin, carvedilol)
Common Receptor, Substrates, and Drug Example
Receptor: Alpha 2 (mainly in the brain)
- Endogenous substrate
- Agonist action
- Drug agonist
- Antagonist action
- Drug antagonist
Receptor: Alpha 2
- Endogenous substrate: Epi/norepi
- Agonist action: decrease release of Epi/Norepi = decrease BP/ HR
- Drug agonist: Clonidine, Brimonidine
- Antagonist action: increase HR, BP
- Drug antagonist: Ergot alkaloids
Common Receptor, Substrates, and Drug Example
Receptor: Beta 1 (mainly in heart)
- Endogenous substrate
- Agonist action
- Drug agonist
- Antagonist action
- Drug antagonist
Receptor: Beta 1
- Endogenous substrate: Increase myocardial contractility, and increase CO, HR
- Drug agonist: Dobutamine, isoproterenol, dopamine (dose dependent)
- Antagonist action: Decrease CO, HR
- Drug antagonist: Beta 1 selective blocker: metoprolol; non selective beta blocker: propanolol, carvedilol
Common Receptor, Substrates, and Drug Example
Receptor: Beta 2 (mainly in lungs)
- Endogenous substrate
- Agonist action
- Drug agonist
- Antagonist action
- Drug antagonist
Receptor: Beta 2
- Endogenous substrate: Epi
- Agonist action: bronchodilation
- Drug agonist: albuterol, isproterenol
- Antagonist action: Bronchoconstriction
- Drug antagonist: Non selective beta blockers (propanolol, carvedilol)
Pharmacodynamic VS Pharmacokinetics
Pharmacokinetics pertains to the absorption, distribution, metabolism, and elimination of drugs within the body, while pharmacodynamics involves the study of a drug’s effects on the body and its mechanisms of action.
Common CYP Inhibitors
Think of G-PACMAN for inhibitors!
- Grapefruit
- Protease Inhibitors
- Azoles
- Cyclosporine, Cobicistat
- Macrolides (not azithro tho)
- Aminodarone
- Non-DHP CCBs (diltizem, verapamil)
.
Inhibitors = decrease drug metabolism = INCREASE drug levels! = supratheraputic
Common CYP Inducer
Think of PS PORCS for inducers
- Phenytoin
- Smoking
- Phenobarb
- Oxcarbazepine
- Rifampin
- Carbamazepine
- St. Johns Wort
.
Inducer = increase metabolism = Decrease drug concentration = subtheraputicn
Pgp Efflux pump…what is it?
Permeability glycoprotein efflux pumps are located in many tissue membrane where they protect agaisnt foreign substrate. When a drug blocks (or inhibits) P-gp, a drug that is a P-gp substrate will have increased absorption (less drug is pumped into the gut) and the substrate drug level will increase.
P-gp Common Substrate, Inducers, and Inhibitors
Substrate: Anticoag (DOACs), Digoxin, diltizem, verapamil, immunosuppresents (cyclophos), colchicine
.
Inducer: Carbamazepine, pheobarb, phenytoin, St John, Rifampin
.
Inhibitor: PI boosters, certain azole, amino, diltizem, verapamil
Common Cardio DDI
Amiodarone + Warfarin
Risk: Amio inhibits mutiple CYP including CYP2C9 which metabolizes warfarin! = decreased warfarin metabo = increase levels/ INR/ bleed risk
Common Cardio DDI
Amiodarone + Digoxin
Amio inhibits P-gp and Digoxin is a P-gp substrate = decrease digoxin metabo = increased Digoxin levels = bradycardia!!!
Common Cardio DDI
Digoxin + Loop Diuretic
Loop diuretic decrease K/Mg/Ca/Na…Digoxin toxicity is increased with low K/ Mg and high Ca - need monitoring
Drugs with Additive Risk/ SEs
Serotonergic Toxicity: Drugs that can contribute, what’s the effects?
- Antidepressants: SSRI, SNRI, TCA
- MAO Inhibitors: isocarboxzid, phenelizine, linezolid, selegiline, rasagiline
- Opioids: Fent, tramadol, methadone
- Triptans
- Natural Stuff: St John
.
Serotonin syndrome risk increases with two or more drugs that affect serotonin are used together: autonomic dysfunction (N/V, hyperthermia), altered mental status (anxiety/ agitation), neuromuscular excitation (tremors, rigidity, tonic-clonic sz)
Drugs with Additive Risk/ SEs
Bleeding: Drugs that can contribute, what’s the effects?
- Anticoag
- Antiplatelet
- NSAIDs: Ibu, ASA, naproxen, diclofenac
- SSRI/SNRI: “prams” and “ine”
- Natural products: 5 G’s - garlic, ginger, ginko, glucosamine, ginseng
.
Increase bleeding risk!
Drugs with Additive Risk/ SEs
Hyperkalemia: Drugs that can contribute, what’s the effects?
- ACEi and ARBs
- Sprinolactone, eplerenone
- K+ sparing diuretics: Amiloride, Triamterene
- Others: Bactrim, Tac/cyclophos
.
Hyperkalemia: weakness, heart palp, arrhythimia
Drugs with Additive Risk/ SEs
QT Prolongation: Drugs that can contribute, what’s the effects?
- Antiarrhy: Calss 1a, 1c and III
- Anti Infectives: hydroxycholoroquine, Azole, Marcolides, Quinolones
- Antidepressents: SSRI, TCA, mirtazipine, trazodone
- Antipsycho: 1st and 2nd gen
- Antiemetics: 5HT3 (ondansetron), promethazine, droperiol
- Oncology medication: tyrosine kinase inhibitors, androgen therapy
- Other: tac, methadone, hydroxyzine
.
QT prolongation = increase risk of torsades de pointes = a fatal arrhythmia
Drugs with Additive Risk/ SEs
Ototoxicity: Drugs that can contribute, what’s the effects?
- Aminoglycoside (tobramycin, gentamicin, etc)
- Salicylates: ASA
- Vancomycin
- Cisplatin
- Loop diuretic (more so IV)
.
Can lead to hearing loss, vertigo, tinnitus
Drugs with Additive Risk/ SEs
Nephrotoxic: Drugs that can contribute, what’s the effects?
- Antiinfectives: vancomycin, animoglycoside, AmpB
- Cisplatin
- Calcineurin inhibitors (tac/cyclophos)
- Loop diuretic (furosimide, torsemide, bumetianide)
- NSAIDs
- Contrast Dye
.
Worsening renal function (increase Scr/ BUN)
Drugs with Additive Risk/ SEs
Anticholinergic Drugs that can contribute, what’s the effects?
- Antidepressant/ antipycho
- Sedating antihis: Diphenhydramine, brompheniramine, meclizine
- Muscle relaxants: cyclobenzaprine, baclofen
- Centerally acting anticholingerics: Benztropine
- Antimusc: oxybutynin, darfenacin
- Other: atropine, Belladonna
.
Anticholinergic symp: CNS depression (sedation), dry mouth, dry eyes, constipation, urinary retention, blurry vision, agitation…high risk in elderly
Drugs with Additive Risk/ SEs
Hypotension/ Orthostasis: Drugs that can contribute, what’s the effects?
- PDE-5 inhibitors: Sildenafil, tadalafil + CYP3A4 inhibitors OR Nitrates OR Alpha 1 blocker (nonselctive: doxazosin) or selective (tamsulosin)
.
Increase risk of vasodilation, falls, decreased BP
Common CYP450 Enzyme, Substrate, Inducer, Inhibitors
CYP3A4: Substrates, Inducers, Inhibitors
Substrates:
- Analgesics - fent, methadone, hydrocodone, oxy
- Anticoag - apix, riva, warfarin R (less potent form)
- Cardio drugs: amio, amlodipine, diltizem, verapamil
- Statins: Ator, Lova, Sim
- HIV drugs: NNRTI
- PDE5- Inhibitors
- Others: ethinyl estradiol, etc..many
.
Inducer:
- Carbamazepine. oxcarbazepine, phenytoin, phenobarb, rifampin, smoking, St johns
.
Inhibitors: G PACMAN
Common CYP450 Enzyme, Substrate, Inducer, Inhibitors
CYP2C9: Substrates, Inducers, Inhibitors
Substrates
- many but just know important one: WARFARIN-S (potent form), carvadilol, diltizem, tamoxifen, phenytoin
.
Inducers
- Carbamazepine, phenobarb, phenytoin, rifampin, smoking, st john
.
Inhibitors
- Amiodarone, fluconazole, metronidazole, bactrim
Basic Counseling
Nasal Spray Counseling
Before use
■ Shake the bottle gently and remove the cap.
■ Prime the pump before the first use or when you have not used it recently (7-14 days on average).
■ Blow your nose to clear your nostrils.
.
Using the spray
■ Close one nostril and insert the nasal applicator into theother nostril.
■ Start to breathe in through your nose, and press firmly and quickly down once on the applicator to release the spray.
■ Breathe out through your mouth.
■ If a second spray is needed in that nostril, repeat the above
steps. Repeat the above steps in the other nostril.
■ Wipe the nasal applicator with a clean tissue and replace cap.
■ Do not blow your nose right after using the nasal spray.
Basic Counseling
Eye Drop Counseling
- Wash hands before and after use.
- Shake bottle before opening; invert gels once for proper dispersion.
- Tilt head back, pull down lower eyelid, use a mirror if needed.
- Administer one drop without touching eye or eyelid; avoid squeezing excess drops to prevent wastage.
- Close your eye after applying the drop. Use a tissue to blot any excess solution from the eyelid.
- If using more than one eye drop:
If administering two drops of the same medication, wait five minutes between drops.
Wait 5-10 minutes before applying a second medication. For ointments, wait 10 minutes after using other eye medications. - If your eye drop contains benzalkonium chloride (BAK) and you wear soft contact lenses, remove the lenses before application and wait 15 minutes before reinserting them
Basic Counseling
Ear Drop Counseling
-Warm the solution by gently shaking or rolling the bottle in hands for 1-2 minutes; avoid dropping cold medication into the ear to prevent discomfort and dizziness.
-Lie down or tilt the head so the affected ear faces up.
For adults, gently pull the earlobe up and back; for children under 3, pull down and back to straighten the ear canal.
-Administer the prescribed drops into the ear canal and keep the ear facing up for about five minutes to allow the medication to coat the canal.
-Avoid touching the dropper tip to any surface; clean by wiping with a tissue.
Lab Values And What Can Effect Them
Calcium
- if albumin is low make sure you correct level
- High: Vitamin D, Thiazides
- Low: Heparin, loop diuretic, bisphosphonates, cinacalcet, steroids
Lab Values And What Can Effect Them
Magnesium
- High: supplements
- Low: PPIs, Diuretics, AmpB
