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NAPLEX PREP (RxPrep) > 1. Pharmacy Foundations > Flashcards

1. Pharmacy Foundations Flashcards

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1
Q

Define substrate/ligand

A

A substance that creates a signal/produces an effect by binding to a receptor, enzyme or transporter

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2
Q

Define “endogenous”

A

Substance produced naturally by the body

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3
Q

Define “exogenous”

A

Substance produced outside the body (ie. Drugs)

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4
Q

Define “agonist”

A

A substance that binds to a receptor to initiate an action

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5
Q

Define “antagonist”

A

A substance that reduces or blocks a reaction

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6
Q

Define “induction”

A

When a substance INCREASES the metabolism of an enzyme (faster metabolism)

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7
Q

Define “inhibition”

A

When a substance decreases/blocks the metabolism of an enzyme (SLOWED metabolism)

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8
Q

The peripheral nervous system controls the rest of the body aside from the CNS. What are the two branches of the PNS?

A

Somatic nervous system
Autonomic nervous system

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9
Q

What is the difference between the somatic and autonomic nervous systems?

A

Somatic = VOLUNTARY, controls muscle movements
Autonomic = INVOLUNTARY, controls bodily functions (ie. Digestion), cardiac output and BP

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10
Q

What is a neurotransmitter?

A

The body’s chemical messengers
Released from presynaptic neuron to postsynaptic neuron/other parts of the body to create an effect

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11
Q

Name 5 neurotransmitters

A

Acetylcholine (ACh)
Epinephrine (Epi)
Norepinephrine (NE)
Dopamine (DA)
Serotonin (5-HT)

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12
Q

What is the primary neurotransmitter in the somatic nervous system? What is its mechanism in the somatic NS?

A

Acetylcholine
Binds to nicotine c receptors in skeletal muscles to cause movement

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13
Q

What are the two branches of the autonomic nervous system? What are they known for?

A

Sympathetic (“fight or flight”) - releases Epi and NE, activating the adrenergic receptors (alpha and beta) in the cardiovascular and respiratory systems. Affects BP, HR, bronchodilation.

Parasympathetic (“rest and digest”) - releases ACh that binds to muscarinic receptors, causing movement in SLUDD (salivation, lacrimation, urination, defamation, digestion)

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14
Q

Define SLUDD (parasympathetic nervous system)

A

Salivation
Lacrimation
Urination
Defecation
Digestion
(All increased w parasympathetic activation)

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15
Q

What is the difference between competitive and non-competitive inhibition?

A

Competitive - antagonist binds to SAME binding site as an endogenous substrate, preventing reaction
Non-competitive - antagonist binds at an ALLOSTERIC site that changes the shape of the active site, preventing endogenous binding

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16
Q

Define structure-activity relationship

A

When the structure of a drug affects its activity. Ie. The functional groups on a drug will affect not only its therapeutic affects but also its adverse effects

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17
Q

NSAIDs contain what functional group?

A

An acidic CARBOXYL group

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18
Q

What functional group is featured in Aztreonam?

A

One standalone LACTAM ring (thus, the class “monobactam”)

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19
Q

What functional groups are featured in aminoglycosides?

A

An AMINE group and a SUGAR (GLYCOSIDE) (thus, aminoglycoside)

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20
Q

What functional group is featured in levothyroxine?

A

T4 - so 4 IODINES
(Note, T3 is when an iodine is removed)

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21
Q

What is the featured functional group in tricyclic antidepressants?

A

Three ring structure (thus, tricyclic)

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22
Q

What is drug stability?

A

The extent which a product retains its original properties throughout its period of storage and use (SHELF LIFE)

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23
Q

Drug degradation can make a drug ineffective, unpalatable, or even toxic. Name 3 reactions that cause drug degradation:

A

Oxidation-reduction
Hydrolysis
Photolysis

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24
Q

What is oxidation-reduction (degradation)? What happens to a compound when it is oxidized?

A

When a compound is oxidized = loses electrons or reduced = gains electrons (recall OIL RIG [oxidative is lose, reduce is gain])
Oxidized compounds often have a VISIBLE COLOR change (yellow, orange, pink)

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25
What kinds of compounds are most likely to oxidize?
Drugs with hydroxyl (-OH) groups directly bonded to a ring. Ie. Epinephrine (catecholamines), phenylephrine (phenols), aldehydes
26
How is oxidation catalyzed, and how do we prevent it?
Catalyzed by **light, heat**, and **metal ions** Prevention: light, temp, pH controls, addition of antioxidants or chelating metal agents
27
Describe hydrolysis and what groups are at highest risk of hydrolysis
When water causes cleavage of bonds in a molecule Highest risk: esters, amides, lactams
28
What are some methods to prevent hydrolysis?
Addition of adsorbents (absorbs moisture), lyophilized powders (freeze dried), hygroscopic salt (water absorbing) and other agents for prevention of oxidation (chelating agents, temp control, pH controls, light protection)
29
What drugs are most prone to photolysis?
Ascorbic acid (vitamin C) Folic acid Nitroprusside Phytonadione (vitamin K)
30
Define pharmacodynamics
The effect a DRUG has on the BODY
31
Define pharmacokinetics
The effect the BODY has on the DRUG
32
Describe additive effects of drugs at the SAME vs DIFFERENT binding sites
SAME binding site = increased AEs and direct additive effects DIFFERENT binding sites = drugs that have similar end effects through different receptors causing additive effects (ie. Benzos enhance GABA effects, may increase risk of opioid overdose in combo w opioids)
33
What is drug SYNERGY?
When two drugs taken in combination have a greater effect than that the two individual effects together
34
Why do polyvalent cations (antacids, multivitamins, sucralfate, bile acid resins, metals, phosphate binders) need to be separated from quinolones, tetracyclines, levothyroxine and PO bisphosphonates?
CHELATION may occur, where polyvalent cations prevent quinolones, tetracyclines, levothyroxine and PO bisphosphonates from getting absorbed
35
Name one example of how GI acid suppression (increased pH) can decrease drug absorption?
H2RAs and PPIs **decrease** absorption of antifungal (ie. Itraconazole)
36
Ritonavir “boosting” the effects of Darunavir in HIV is an example of what PK effect?
Inhibition of metabolism to increase time of drug in circulation
37
Probenecid blocks the _____ ______ of penicillin, allowing for increased penicillin levels required to cross the BBB for neurosyphillis
Renal excretion
38
How does sodium bicarb aid in the resolution of salicylate toxicity?
Bicarb binds to salicylate and ionizes the compound, allowing it to be more hydrophilic, be retained in the urine and be excreted
39
Why are prodrugs used by drug manufacturers?
Increased bioavailability (prevents excessive loss during first-pass) Prevent drug abuse (ie. Vyvanse [lisdexamfetamine] formulated so amphetamine is not released until lysine is detached only by enzymatic cleavage)
40
What are the major CYP inhibitors?
G PACMAN Grapefruit Protease inhibitors (ritonavir) Azoles Cyclosporine, cobicistat Macrolides (NOT Azithromycin) Amiodarone Non-DHP CCBs (Diltiazem, verapamil)
41
What are the major CYP inducers?
PS CORPS Phenytoin Smoking Carbamazepine Oxcarbazepine Rifampin Phenobarbital St. John’s Wort
42
What is the role of P-glycoproteins (PGPs)? What happens when PGPs are inhibited?
Efflux pumps that protects the body against foreign substances by pumping into the GI tract for excretion. When PGPs are inhibited, drug levels INCREASE (less excretion)
43
What are common PGP substrates?
DOACs Cardiovascular drugs (digoxin, non-DHP CCBs) HCV drugs Transplant drugs (tacro/cyclosporine) Colchicine
44
What are common PGP inhibitors?
Uncommon Azoles (Itraconazole, posaconazole) Cardiovascular drugs (Amiodarone, non-DHP. CCBs) HCV drugs HIV drugs (cobicistat, ritonavir) Cyclosporine
45
Define enterohepatic recycling
When a drug is metabolized by the liver, dropped into the GI, reabsorbed via the small intestine and re-entering the portal vein. Increases duration of action of the drug
46
What enzyme causes the interaction between **amiodarone** and **warfarin**? What is the resulting interaction?
**CYP2C9** is inhibited by amiodarone, causing a *decreased warfarin dose by 30-50%* when amio is added to warfarin
47
What causes the interaction between **amiodarone** and **digoxin**? What is the resulting interaction?
Amiodarone inhibits **P-gp** with synergy in increased bradycardia and decreased HR. Addition of amio decreases digoxin dose *by 50%*
48
What is the interaction between **digoxin** and **loop diuretics**?
Loop diuretics *decrease K+, Mg+2, Ca+2, Na+* Digoxin toxicity risk increases w decreased K and Mg levels
49
What enzyme causes the interaction between **statins** and **strong CYP3A4 inhibitors**? What is the resulting interaction?
**CYP3A4** - causes increased CYP3A4 SUBSTRATE (statins) LEVELS from inhibition
50
What enzyme is warfarin a **substrate** of? NOTE - This will cause changes in INR with inhibitors/inducers.
CYP2C9
51
What is the interaction between **valproate** and **lamotrigine**?
Valproate inhibits lamotrigine metabolism, causing INCREASED LEVELS of lamotrigine! This can lead to **SJS/TENS**
52
How long should be waited between switching from an MAOI to a serotonergic drug? (What is the one exception?) What is the AE of overlapping the two classes?
**2 weeks** between MAOIs and serotonergic drugs *FLUOXETINE - long half life, wait *6 weeks*\ Overlap = serotonin syndrome!
53
What is the interaction between MAOIs and NE/Epi/Dopamine?
MAOIs intrinsically increase NE/Epi/dopamine; adding more can cause **hypertensive crisis**
54
What class of foods should be avoided when on an MAOI?
**Tyramine-rich** foods (Anything aged, pickled, fermented or smoked) Ie. Cheeses, aged meats, sauerkraut, beers/wines
55
What enzyme does SMOKING affect? Is it an inducer or inhibitor? What kinds of drugs does it affect?
**CYP1A2** INDUCER Affects some antipsychotics, antidepressants, hypnotics, anxiolytics, caffeine, theophylline, warfarin
56
What drug classes have SEROTONERGIC properties and should be avoided together due to additive risk?
Antidepressants MAOIs Opioids Triptans St. John’s Wort Buspirone, lithium
57
What classes of drugs have the highest BLEED RISK and thus should be avoided together to prevent additive effect?
Anticoagulants (DOACs, warfarin) Antiplatelets (salicylates, dipyrimadole, clopidogrel/prasugrel/ticagrelor) NSAIDs SSRI/SNRIs Naturals (garlic, ginger, ginko, ginseng, glucosamine, etc)
58
What drugs have the highest risk of HYPERKALEMIA and should be avoided together due to additive risk?
**RAAS drugs** (ACEi/ARBs, Entresto, MRA [spiro, eplerenon]) **K-sparing diuretics** (MRAs, amiloride, Triamterene) CNIs (tacro, cyclo) Bactrim Canagliflozin Drospirenone
59
What drug classes have the highest **QTc prolongation** and should not be used together due to additive affects?
**Antiarrhythmics Antimalarials Azoles Macrolides Quinolones Antidepressants** (SSRIs [escitalopram/citalopram], TCAs, trazodone, mirtazapine) **Antipsychotics** (1st gen, plus ziprasidone) **Antiemetics** (5-HT3 antagonists [ondansetron], metoclopramide, promethazine, droperidol) **Onco meds** (leuprolide, TKIs, arsenic) Methadone Loperamide Donepezil Hydroxyzine Ranolazine Solifenacin
60
What two drug classes have the highest risk for CNS depression when taken together?
Opioids + benzos
61
What drugs are most likely to cause *ototoxicity*?
Aminoglycosides Cisplatin IV loop diuretics Salicylates Vancomycin
62
What drugs are most likely to cause *nephrotoxicity*?
Antibiotics (aminoglycosides, vancomycin, amphoterecin B, polymixins) Cisplatin CNI Loop diuretics NSAIDs Contrast dye

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