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

1. Pharmacy Foundations Flashcards

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
Q

What kinds of compounds are most likely to oxidize?

A

Drugs with hydroxyl (-OH) groups directly bonded to a ring.
Ie. Epinephrine (catecholamines), phenylephrine (phenols), aldehydes

26
Q

How is oxidation catalyzed, and how do we prevent it?

A

Catalyzed by light, heat, and metal ions

Prevention: light, temp, pH controls, addition of antioxidants or chelating metal agents

27
Q

Describe hydrolysis and what groups are at highest risk of hydrolysis

A

When water causes cleavage of bonds in a molecule

Highest risk: esters, amides, lactams

28
Q

What are some methods to prevent hydrolysis?

A

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
Q

What drugs are most prone to photolysis?

A

Ascorbic acid (vitamin C)
Folic acid
Nitroprusside
Phytonadione (vitamin K)

30
Q

Define pharmacodynamics

A

The effect a DRUG has on the BODY

31
Q

Define pharmacokinetics

A

The effect the BODY has on the DRUG

32
Q

Describe additive effects of drugs at the SAME vs DIFFERENT binding sites

A

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
Q

What is drug SYNERGY?

A

When two drugs taken in combination have a greater effect than that the two individual effects together

34
Q

Why do polyvalent cations (antacids, multivitamins, sucralfate, bile acid resins, metals, phosphate binders) need to be separated from quinolones, tetracyclines, levothyroxine and PO bisphosphonates?

A

CHELATION may occur, where polyvalent cations prevent quinolones, tetracyclines, levothyroxine and PO bisphosphonates from getting absorbed

35
Q

Name one example of how GI acid suppression (increased pH) can decrease drug absorption?

A

H2RAs and PPIs decrease absorption of antifungal (ie. Itraconazole)

36
Q

Ritonavir “boosting” the effects of Darunavir in HIV is an example of what PK effect?

A

Inhibition of metabolism to increase time of drug in circulation

37
Q

Probenecid blocks the _____ ______ of penicillin, allowing for increased penicillin levels required to cross the BBB for neurosyphillis

A

Renal excretion

38
Q

How does sodium bicarb aid in the resolution of salicylate toxicity?

A

Bicarb binds to salicylate and ionizes the compound, allowing it to be more hydrophilic, be retained in the urine and be excreted

39
Q

Why are prodrugs used by drug manufacturers?

A

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
Q

What are the major CYP inhibitors?

A

G PACMAN

Grapefruit
Protease inhibitors (ritonavir)
Azoles
Cyclosporine, cobicistat
Macrolides (NOT Azithromycin)
Amiodarone
Non-DHP CCBs (Diltiazem, verapamil)

41
Q

What are the major CYP inducers?

A

PS CORPS

Phenytoin
Smoking
Carbamazepine
Oxcarbazepine
Rifampin
Phenobarbital
St. John’s Wort

42
Q

What is the role of P-glycoproteins (PGPs)? What happens when PGPs are inhibited?

A

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
Q

What are common PGP substrates?

A

DOACs
Cardiovascular drugs (digoxin, non-DHP CCBs)
HCV drugs
Transplant drugs (tacro/cyclosporine)
Colchicine

44
Q

What are common PGP inhibitors?

A

Uncommon Azoles (Itraconazole, posaconazole)
Cardiovascular drugs (Amiodarone, non-DHP. CCBs)
HCV drugs
HIV drugs (cobicistat, ritonavir)
Cyclosporine

45
Q

Define enterohepatic recycling

A

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
Q

What enzyme causes the interaction between amiodarone and warfarin? What is the resulting interaction?

A

CYP2C9 is inhibited by amiodarone, causing a decreased warfarin dose by 30-50% when amio is added to warfarin

47
Q

What causes the interaction between amiodarone and digoxin? What is the resulting interaction?

A

Amiodarone inhibits P-gp with synergy in increased bradycardia and decreased HR. Addition of amio decreases digoxin dose by 50%

48
Q

What is the interaction between digoxin and loop diuretics?

A

Loop diuretics decrease K+, Mg+2, Ca+2, Na+
Digoxin toxicity risk increases w decreased K and Mg levels

49
Q

What enzyme causes the interaction between statins and strong CYP3A4 inhibitors? What is the resulting interaction?

A

CYP3A4 - causes increased CYP3A4 SUBSTRATE (statins) LEVELS from inhibition

50
Q

What enzyme is warfarin a substrate of?
NOTE - This will cause changes in INR with inhibitors/inducers.

A

CYP2C9

51
Q

What is the interaction between valproate and lamotrigine?

A

Valproate inhibits lamotrigine metabolism, causing INCREASED LEVELS of lamotrigine!
This can lead to SJS/TENS

52
Q

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?

A

2 weeks between MAOIs and serotonergic drugs
*FLUOXETINE - long half life, wait 6 weeks\

Overlap = serotonin syndrome!

53
Q

What is the interaction between MAOIs and NE/Epi/Dopamine?

A

MAOIs intrinsically increase NE/Epi/dopamine; adding more can cause hypertensive crisis

54
Q

What class of foods should be avoided when on an MAOI?

A

Tyramine-rich foods
(Anything aged, pickled, fermented or smoked)
Ie. Cheeses, aged meats, sauerkraut, beers/wines

55
Q

What enzyme does SMOKING affect? Is it an inducer or inhibitor? What kinds of drugs does it affect?

A

CYP1A2 INDUCER
Affects some antipsychotics, antidepressants, hypnotics, anxiolytics, caffeine, theophylline, warfarin

56
Q

What drug classes have SEROTONERGIC properties and should be avoided together due to additive risk?

A

Antidepressants
MAOIs
Opioids
Triptans
St. John’s Wort
Buspirone, lithium

57
Q

What classes of drugs have the highest BLEED RISK and thus should be avoided together to prevent additive effect?

A

Anticoagulants (DOACs, warfarin)
Antiplatelets (salicylates, dipyrimadole, clopidogrel/prasugrel/ticagrelor)
NSAIDs
SSRI/SNRIs
Naturals (garlic, ginger, ginko, ginseng, glucosamine, etc)

58
Q

What drugs have the highest risk of HYPERKALEMIA and should be avoided together due to additive risk?

A

RAAS drugs (ACEi/ARBs, Entresto, MRA [spiro, eplerenon])
K-sparing diuretics (MRAs, amiloride, Triamterene)
CNIs (tacro, cyclo)
Bactrim
Canagliflozin
Drospirenone

59
Q

What drug classes have the highest QTc prolongation and should not be used together due to additive affects?

A

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
Q

What two drug classes have the highest risk for CNS depression when taken together?

A

Opioids + benzos

61
Q

What drugs are most likely to cause ototoxicity?

A

Aminoglycosides
Cisplatin
IV loop diuretics
Salicylates
Vancomycin

62
Q

What drugs are most likely to cause nephrotoxicity?

A

Antibiotics (aminoglycosides, vancomycin, amphoterecin B, polymixins)
Cisplatin
CNI
Loop diuretics
NSAIDs
Contrast dye

NAPLEX PREP (RxPrep) (7 decks)

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