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Advanced Pharm > Exam 4 Drugs > Flashcards

Exam 4 Drugs Flashcards

1
Q

heparin

A
  • drug class: indirect thrombin inhibitor
  • indications: prevent venous thrombosis
  • MOA: target - anti-thrombin III
    +binds an activates antithrombin (conformational change)
    +enhances activity 1000x
    +catalyzes rxns without being consumed
  • tox:
    +bleeding, HIT
  • monitoring: aPTT
  • reversal agent: protamine sulfate - highly positively charged and binds heparin and inactivates it
  • contraindications: active bleeding, hemophilia, thrombocytopenia, severe hypertension, ICH, infective endocarditis, active TB, GI ulcers, advanced hepatic disease
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2
Q

lmw heparin

A
  • more specific for factor Xa (less effect on thrombin)
  • less effective on coagulation in general
  • more predictable plasma levels for monitoring
  • examples include: enoxaparin, dalteparin, tinzaparin (-parin drugs)
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3
Q

fondaparinux (arixtra)

A
  • pentasaccharide molecule of heparin
  • synthetic
  • not as effective; selective for factor X
  • less bleeding risks involved
  • indications: anticoagulation for people with HIT
  • indirect thrombin inhibitor
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4
Q

protamine sulfate

A

* reversal agent for heparin
* highly positively charged; binds heparin and inactivates
* excess protamine is also anticoagulant
* less effect on LMW heparins
* does not affect fondaparinux

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5
Q

leprudin (hirudin) or bivalirudin (angiomax)

A
  • drug class: direct thrombin inhibitors
  • MOA: bind to both active and subtrate recognition sites of thrombin; prevents fibrin clot from forming
  • hirudin - leech therapy
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6
Q

argatroban, dabigatran (pradaxa)

A
  • drug class: direct thrombin inhibtor
  • MOA: binds only to thrombin active sites (from biological sources); prevents fibrin clot from forming
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7
Q

warfarin

A
  • drug class: direct thrombin inhibitor
  • MOA: blocks the gamma-carboxylation of several glutamate residues (vitamin k dependent)
  • onset: 8-12 hour delay in onset (heparin weaned off to warfarin)
  • tox:
    +hemorrhagic disorder in the fetus
    +birth defects
    +cutaneous necrosis
  • measured with INR (normal 0.8-1.2; target 2-3)
  • reversal:
    +d/c drug
    +vitamin K
    +FFP
    +factor IX concentrates
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8
Q

rivaroxaban (xarelto), apixaban (eliquis)

A
  • drug class: factor Xa inhibitors
  • MOA: targets factor Xa
  • indication: clot prevention
  • no reversal agent
  • effects: less bleeding issue d/t Xa specificity
  • indication: CVA, VTE
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9
Q

tissue plasminogen activator (tPA)

A
  • drug class: fibrinolytic
  • recombinant forms: alteplase
  • MOA:
    +plasminogen activates to plasmin
    +t-PA activates plasminogen that is bound to fibrin
    +confines fibrinolysis to the formed thrombus and avoids systemic activation
  • indication: MI, PE
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10
Q

streptokinase

A
  • drug class: fibrinolytic
  • synthesized by Streptococci
  • MOA: binds to plasminogen to activate it to promote fibrinolysis
  • indication: MI, PE
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11
Q

urokinase

A
  • drug class: fibrinolytic
  • synthesized by the kidney
  • MOA: lyses the thrombus from within
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12
Q

ASA

A
  • drug class: COX-1 selective antiplatelet drug (effects both COX-1 and COX-2, but more selective for COX-1)
  • MOA:
    +TXA2 normally causes: PLT shape change, granule release, and aggregation
    +ASA inhibits TXA2 synthesis, which will cause antiplatelet activity
    +irreversibly binds to COX-1; this means that it inhibits the enzyme activity for the lifetime of the enzyme (8-10 days).
  • indication: arterial thrombosus
  • adverse effects:
    +GI upset
    +buffering may decrease (d/t irritation of gastric mucosa and inhibition of GI protective PGG)
    +increase in GI ulcers
    +salicylate poisoning
    +reye syndrome: hepatic injury and encephalopathy in children treated with ASA after a viral infection
  • can be used for colon/breast/prostate CA for anti-inflammatory properties & prevention

ASA toxicity graph:
mild: N/V, dizziness
moderate: N/V, tinnitus, HA, confusion, hyperventilation, tachycardia, fever
severe: delerium, hallucinations, seizures, coma, respiratory arrest

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13
Q

clopidogrel (plavix), ticlopidine (ticlid)

A
  • drug class: antiplatelet aggregation
  • MOA: irreversibly inhibits ADP receptors on PLTs; no effects on PGG metabolism
  • can be released from drug-eluting stents with polymer coating
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14
Q

abiciximab

A
  • drug class: IIb/IIIa receptor blocker
  • MOA: antiplatelet aggregation by targeting IIb/IIIa-R complex (this receptor normally gets activated in the final common pathway)
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15
Q

vitamin k

A

drug class: factor replenisher
target: oxidation/reduction
MOA: carboxylation & 2 reductions will activate vitamin k to active form (hydroquinone
+confers activity on prothrombin (II), VII, IX, and X
indications: warfarin OD, vit K deficiency

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16
Q

fresh frozen plasma (FFP)

A

drug class: factor replenishment
target: multiple
result: normal clotting cascade
indications: hemophilia

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17
Q

desmopressin

A
  • increased factor VIII activity
  • indications: mild hemophilia A, von-willebrand disease
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18
Q

aminocaproic acid

A

drug class: fibrinolytic inhibitor
MOA: competitively inhibits plasminogen activation
result: stablized clot
indication: post-op

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19
Q

tranexamic acid (TXA)

A

drug class: fibrinolytic inhibitor
MOA: inhibits plasminogen conversion to plasmin
indication: trauma, heavy menstrual bleeding, postpartum, epistaxis
decreased risk of death in major bleeding

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20
Q

lispro, aspart, glulisine

A

rapid acting insulins

bolus insulin

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21
Q

novolin, humulin

A

short acting (regular) insulin

acts fast; leaves fast (longer acting than RA)

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22
Q

NPH

neutral protamine Hagedorn

A

intermediate acting

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23
Q

glargine, detemir

A

long acting insulin

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24
Q

metformin

A
  • drug class: biguanide (two guanine molecules)
  • fist line therapy for NIDDM (type II)
  • MOA: **reduces hepatic glucose production **
  • 500 mg prandial
  • GI toxicities
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25
Q

sulfonylurea

ex) glipizide (2nd gen)

A
  • drug class: insulin secretagogue
  • MOA: binds to K+ channel, K+ channel closes causing depolarization
  • 1st gen vs 2nd gen
    +2nd gen requires a lower dose for same efficacy
  • increased CV mortality
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26
Q

thiazolidinediones (TZDs)

A
  • MOA: decrease insulin resistance (PPAR mediated)
    +drug binds to receptors and increases likelihood of cellular responsiveness to insulin
    +increases insulin signal transduction
  • risk of MI, increased with insulin and nitrates
  • Avandia-Rosiglitazone Medicine Access Program - only certain physicians had access to Rx it

*PPAR: peroxisome proliferator-activated receptor

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27
Q

acarbose

A
  • drug class: alpha-glucosidase inhibitor
  • MOA: blocks digestion of complex carbs
  • beneficial in pre-diabetics
  • SE: GI upset
    +flatulence
    +diarrhea
    +bd pain
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28
Q

bile acid binding resin

A
  • large cation exchange resins - not absorbed
  • also good for dyslipidemia
  • binds bile acids - prevents reabsorption
    +must be taken with food
  • GI upset
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29
Q

amylin

A
  • amylin is released by beta cells
    +suppresses glucagon release
  • decreases circulating glucose
  • concomitant with insulin
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30
Q

semaglutide (ozempic)

A
  • drug class: GLP-1 agonist//incretin-based therapuetic agent
  • GLP-1 agonism:
    +stimulates insulin release
    +inhibits glucagon release
    +both leads to effect of lowering blood glucose
    pancreatic CA risk

GLP: gluagon-like peptide

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31
Q

sitagliptin (januvia)

A
  • drug class: DPP-4 antagonist
  • MOA: blocks DPP-4, which increases GLP-1 agonism and incretin hormones leading to decreased glucose

DPP-4: dipeptidyl peptidase-4

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32
Q

gliflozins

AKA SGLT-2 inhibitors

A
  • MOA: prevents glucose reaborption in PCT
  • SE: glucosuria
    +osmotic diuretic - BP reduction
    +wt. loss
    +dehydration
  • ex) Jardiance, Invokana
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33
Q

statins

A
  • MOA: HMG-CoA reductase inhibitors
  • decreases overall cellular cholesterol synthesis
  • increases LDL receptors
    +scavenge LDL from blood
    +major effect on liver (raises liver enzymes)
  • modest decrease in triglycerides
  • small increase in HDL
  • SE/tox: muscle pain/increased CK
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34
Q

niacin

vitamin B3

A
  • decreases VLDL and LDL (reduces VLDL secretion from liver)
  • increases HDL
  • incorporated into NAD - ETC glycolysis/energy producing pathway
  • dosing 2-6g daily
  • main tox: flushing
  • other tox: pruritic, dry skin, nausea, abd pain, elevation of liver enzymes
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35
Q

gemfibrozil

A
  • drug class: fibrate
  • MOA: decreases VLDL, moderate decrease in LDL
  • tox: GI upset (rare)
  • increaes lipolysis in the liver (PPAR mediated)
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36
Q

BABR

bile acid binding resins

A
  • MOA: cationic bile acid binding (positively charged drug binds to negatively charged bile)
  • prevents reuptake from the bile
  • SE: constipation, bloating, steatorrhea, oral drug absorption impairment
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37
Q

ezetimibe

A
  • drug class: absorption inhibitors
  • MOA: inhibits cholesterol absorption; NPCL-1 antagonist
  • tox: possible hepatic, ENHANCE trial (reduced LDL, promoted arterial wall thickening?)
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38
Q

evolocumab

A
  • drug class: PCSK9 inhibitor
  • MOA:
    +inhibits protein PCSK9 (this protein normally binds to LDL + LDL receptors on the liver and promotes their degradation)
    +by PCSK9 binding to PCSK9, LDL can bind to LDL-Rs & the number of LDL receptors are increased and available to clear cholesterol from the blood, therefore, lowering LDL levels
  • these drugs are not usually given by themselves - they’re usually given with statins
  • statins upregulate serum PCSK9 levels
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39
Q

celecoxib

A
  • drug class: COX-2 selective inhibitor
  • less effects on “housekeeping” COX-1
    +**fewer GI effects, **no impact on PLT aggregation, absorption increased by food
  • indication: arthritis
  • effects: analgesia, antipyretic, anti-inflammatory
  • adverse effects: CV BB warning (inhibition of PGI2 production - pro clot!)
  • is a sulfonamide - allergy warning

(COX-2&raquo_space;»»> COX-1)

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40
Q

meloxicam

A
  • drug class: COX-2 inhibitor&raquo_space; COX-1
  • not as selective as other COXIBs
  • fewer GI effects
  • tox effects similar to other NSAIDs
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41
Q

diclofenac (voltaren)

A
  • drug class: non-selective COX inhibitor
  • anti-inflammatory, analgesic, antipyretic
  • 20% of pts have adverse GI effects (decreased with misoprostol AKA cytotec)
  • also comes as a topical gel
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42
Q

ibuprofen

A
  • drug class: NSAID (non-selective COX inhibitor)
  • less GI upset than ASA (equal in efficacy as an anti-inflammatory/analgesic drug)
  • OTC
  • PO, cream, gel, IV
  • adverse effects: like all other NSAIDs
    +agranulocytosis and aplastic anemia is rare
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43
Q

indomethacin

A
  • potent COX inhibitor (inhibits COX and LOX synthesis)
  • MOA: may also inhibit PLA/PLC
  • reduces PMN migration
  • decrease T&B cell proliferation
  • indications: rheumatism, gout, patent ductus arteriosus - open duct that allows arterial/venous blood to mix between the aorta/PA
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44
Q

ketorolac (toradol)

A
  • drug class: NSAID (COX1=COX2 inhibition)
  • indication: post-op pain, ER/sports medicine (IV/PO/IM/IN)
  • short-term use
  • NSAID but primarily used for pain
  • can be used in conjunction with opioids
  • typically use 25-50% lower dose of opioids
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45
Q

acetaminophen

A
  • drug class: NOT AN NSAID//selective COX-2 inhibitor in the CNS
  • weak PG inhibitor in peripheral tissues
  • PO or PR (newer IV formulation)
  • metabolized by hepatic enzymes (toxic to both kidneys/liver)
  • it does not affect inflammation
  • while it is an analgesic and an antipyretic, it doesn’t inhibit the COX enzymes in peripheral tissues to the same extent as NSAIDs, which limits its anti-inflammatory effects
  • adverse effects:
    +mild increase in hepatic enzymes
    +larger doses: dizziness, excitement, disorientation
    +FATAL: 15 grams, hepatotoxicity, acute renal tubular necrosis
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46
Q

glucocorticoids

A
  • bind to glucocorticoid response elements (which increase gene expression that decreases inflammation)
  • annexin-1 (lipocortin-1) is increased
    +this suppresses PLA-2; also inhibits leukocyte response
  • SLPI is increased (secretory luekoprotease inhibitor)
  • IL-10 is increased (decreases WBCs rushing to area)
  • INh-NFK B is decreased (this is pro-inflammatory, so inhibiting this makes it anti-inflammatory)
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47
Q

morphine

A
  • phenanthrene structure
  • strong opioid
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48
Q

dilaudid

A
  • phenanthrene structure
  • 5x more potent than morphine
  • strong opioid
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49
Q

codeine

A
  • phenanthrene structure
  • 1/10th as potent as morphine
  • moderate agonist
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50
Q

oxycodone

A
  • phenanthrene structure
  • more effective as a combination med
  • 2x more potent than morphine
  • moderate agonist
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51
Q

percadan/percocet

A
  • oxy + tylenol = percocet
  • oxy + ASA = percodan
  • moderate agonists
52
Q

methadone

A
  • phenylheptylamine structure
  • 10x more potent than morphine
  • strong opioid agonist
  • indications: chronic pain (with morphine tolerance)
  • “less problematic drug” - typically used for people with drug abuse
  • duration of analgesia: 4-6 hours
  • long half-life (25-50 hrs)
  • CYP3A4 metabolism
53
Q

fentanyl

A
  • phenylpiperidine structure
  • strong opioid agonist
  • 100x more potent than morphine
  • carfentanil: 10,000x more potent (drugs laced with this can be fatal)
54
Q

meperidine (demerol)

A
  • phenylpiperidine structure
  • strong opioid agonist
  • antimuscarinic effects: tachycardia
  • negative inotrope
  • can potentiate seizures to someone who is already predisposed
  • indications: post-op shivering
    +increased kappa opioid receptor agonism; some serotinergic effects
55
Q

tramadol

A
  • phenylpiperidine structure
  • moderate agonist
  • also has SNRI activity
  • racemic mixture
  • *safer alternative
56
Q

buprenorphine (buprenex)

A
  • indication: opioid abuse/dependency
  • partial agonist
57
Q

butorphanol (stadol)

A
  • partial agonist
  • indication: post-op shivering
58
Q

dextromethorphan

A
  • indication: cough
  • effect: antisussive
59
Q

naloxone

A
  • derivative of morphine
  • opioid reversal agent (1-3 mins)
  • short duration; effects may return
  • little effect in absence of agonist
60
Q

naltrexone

A
  • derivative of morphine
  • indication: opioid & ETOH abuse
61
Q

naloxegol

A
  • derivative of morphine
  • indication: treatment of opioid induced constipation
  • only goes into enteric nervous system
  • suppresses enteric response
62
Q

PCN, ampicillin, amoxicillin

A
  • beta-lactam abx
  • MOA: inhibition of cell wall synthesis
    +beta lactam ring attaches to enzymes that cross link peptidoglycans and prevent cell wall synthesis
    +these abx inhibit cell wall synthesis of bacterial cell walls by binding to and inactivating PCN binding proteins (PBPs)
    +this prevents the cross-linking of petidoglycan chains, leading to cell lysis and death
  • PCN is a 5 ring structure
  • effective against gram (+) bacteria and some gram (-) cocci
  • indications: strep throat, syphillis, meningitis
  • adverse effects: allergic reactions (rash to anaphylaxis), GI upset, neurotoxicity (rare)

prototype: PCN G

63
Q

cephalosporin

A
  • beta-lactam abx
  • inhibits cell wall synthesis by binding to and inactivating PCBs
  • prevents cross-linking of peptidoglycan chains
  • cell lysis/death
  • more resistant to beta-lactamase
  • broader spectrum than PCNs and is used for respiratory tract infections, skin infections, & UTIs
  • first generation: better gram (+) activity
  • adverse effects: allergic rxns (cross-reactivity with PCNs), GI upset, and potential nephrotoxicity

prototype: cephalexin

64
Q

vancomycin

A
  • MOA: inhibits cell wall synthesis
    • glycopeptide
  • useful for gram (+) bacteria
  • resistant to beta-lactamase
  • alternative to PCN resistant bacteria (MRSA)
  • drug of last resort
  • adverse reactions: 10%
    +irritant to tissues
    +ototoxicity
    +nephrotoxicity
    +chills/fever
    +“red neck” syndrome
65
Q

polymyxin

A
  • polypeptide antibiotic
  • MOA: disruption of cell membrane function
    +binds to phospholipids to cause cell death
    +effective against gram-negative bacteria, which have an outer membrane
66
Q

daptomycin

A
  • MOA: disruption of cell membrane function
    +binds to phospholipids to cause cell death
  • better against gram (+) bacteria
  • indications: skin infections, bacteremia
67
Q

tetracyclines

A
  • MOA: inhibits protein synthesis
  • bacteriostatic
  • pharmacoK: readily absorbed, widely distributed
  • have the widest spectrum of activity on any abx
  • destroys normal intestinal microbiota, and often produce severe GI disorders (bone deposition disorder)
  • can lead to c. diff
  • adverse reactions:
    +GI (N/V/D), bone, neurotoxicity, allergies, neprho/ototox
68
Q

erythromycin

A
  • drug class: macrolide
  • spectrum: gram + and -
  • this is the prototype drug
  • MOA: inhibits protein synthesis
69
Q

azithromycin (zithromax)

A
  • drug class: macrolide
  • MOA: inhibits protein synthesis
  • semi-synthetic derivative
70
Q

neomycin

A
  • MOA: inhibition of protein synthesis
  • can be topical
71
Q

rifamycin

A
  • MOA: DNA/RNA synthesis
  • binds to a bacterial RNA polymerase
72
Q

ciprofloxacin (cipro)

A
  • drug class: floroquinolone
  • MOA: targets DNA/RNA synthesis
    +inhibits DNA gyrase (bacterial)
    +this is an enzyme crucial for DNA synthesis
  • excellent gram (-) activity
  • also good for gram (+)
  • routes: PO, IV, opthalmic injections,
  • indications: respiratory, inhaled anthrax, tuberculosis, GI/abd infections, prostatitis, UTIs, STDs (chlamydia), bone/soft tissue/joint infections
73
Q

sulfonamide

A
  • MOA: inhibition of folic acid synthesis
    structurally similar to PABA (precursor to folic acid production)
    +competitively binds to block synthesis of folic acid
  • indications: pneumocystis, taxoplasmosis
  • often combined with trimethoprim to enhance effectiveness
  • combo: bactrim, septra
  • tox:
    +allergenic
    +may precipitate in urine
    +hematopoietic distrubances
74
Q

trimethoprim

A
  • MOA: inhibition of folic acid synthesis
    +inhibits the enzyme dihydrofolate reductase
    +blocks bacterial growth
  • often combined with trimethoprim to enhance effectiveness
  • combo: bactrim, septra
75
Q

ketoconazole

A

antifungal

76
Q

lamisil

A

antifungal

77
Q

hydroxychloroquine

A

antiprotozoal agent
indication: malaria

78
Q

metronidazole

A

antiprotozoal
adverse effect: black, hairy tongue

79
Q

niclosamide

A

indication: parasitic worms

80
Q

ivermectin

A

indication: parasitic worms

81
Q

permethrin

A

indication: parasitic worms

82
Q

acyclovir

A
  • MOA:
  • inhibits viral DNA synthesis
  • converted into acyclovir triphosphate inside infected cells, then competes with deoxyguanosine triphosphate for incorporation into viral DNA
  • once incorporated, acyclovir triphosphate acts as a chain terminator - it lacks a 3’-OH group, preventing further elongation of the DNA chain
  • indications: HSV1, HSV2, VZV infections
  • safe in pregnant women, can reduce shedding in c-section rate when given in last trimester of pregnancy
83
Q

azidothymidine (AZT)

A
  • drug class: antiretroviral nucleoside/nucleotide analog
  • MOA:
    +combined with other antivirals in HAART (highly active antiretroviral therapy)
    +inhibitor of reverse transcriptase
84
Q

lamivudine

A
  • MOA: inhibits HBV DNA polymerase and HIV reverse transcriptase
85
Q

cabotegrovir

AKA PrEP

A
  • Pre-exposure preventative
  • blocks integration
86
Q

interferon

A
  • naturally occuring in human cells
  • used with some success in preventing and treating viral infections
87
Q

oseltamivir phosphate (tamiflu)

A
  • influenza antiviral
  • early treatment of flu (FDA approved)
88
Q

zanamivir (relenza)

A
  • must be taken BEFORE sx occur
  • not rec for ppl with asthma or COPD
89
Q

baloxivir marboxil (xofluza)

A
  • polymerase inhibitor
  • not rec for pregnant women, breastfeeding mothers, outpatients with progressive or complicated illness or hospitalized pts
  • may reduce duration of flu by 1 day
  • one-time pill dose
90
Q

paxlovid

A
  • COVID tx
  • 2 antivirals, emergency use authorization (PO)
91
Q

remdesivir

A
  • FDA approved COVID tx
  • chain terminator
  • IV
92
Q

COVID MABs

A
  • COVID tx
  • (3)
  • block covid entry into cells
  • IV
93
Q

dexamethasone

A
  • COVID tx
  • cytokines
94
Q

levodopa/carbidopa

A
  • L-isomer of dopamine
  • crosses the BBB (dopamine does not)
  • improved uptake with carbidopa and COMT inhibitors (tolcapone)
  • decreased toxicity (hallucinations) with pimavanserin (nuplazid)
  • MOA: restores dopa levels
95
Q

pimavanserin (nuplazid)

A
  • drug class: a-typical antipsychotic
  • inverse agonist ast 5-HT2A (visual cortex)
  • interacts with the thalamus, which interacts with the substantia nigra
  • combats hallucinations associated with parkinson’s
96
Q

pramipexole

A
  • drug class: dopamine receptor agonist
  • less effective than L-Dopa
  • decreased SE
97
Q

selegeline

A
  • drug class: MAO-B antagonist
  • minor effects alone
  • increases dopamine levels
98
Q

tolcapone

A
  • drug class: COMT inhibitor
  • catecholamines are inactivated by oral admin
  • catecholamines are inactivated by catechol-O-methyltransferase (COMT)
  • by inhibiting COMT, tolcapone increases circulating dopamine
99
Q

apomorphine

A
  • drug class: dopamine agonist
  • useful to treat “off” periods of parkinson’s
  • decreases akinesia symptoms
100
Q

baclofen

A
  • drug class: muscle relaxant
  • indication: cerebral palsy
  • MOA: relaxes muscle movements associated with CP (hyper/hypotonia)
101
Q

tetrabenazine

A
  • drug class: VMAT2-inhibitor
  • MOA: depletes dopamine (dopamine stimulates ACh receptors, leading to Chorea associated with Huntington’s Disease)
102
Q

haloperidol (haldol)

A
  • drug class: antipsychotic
  • MOA: dopamine receptor blocker
  • treats Chorea symptoms associated with Huntington’s Disease
103
Q

riluzole

A
  • drug class: sodium channel blocker
  • MOA: blocks sodium channel binding
  • extends quality of life in ALS patients
104
Q

tacrine

A
  • drug class: AChE-inhibitor
  • MOA: inhibits the breakdown of AChE in the synapse to help with Alzheimer’s Disease sx
105
Q

ASA OD treatment

A
  • activated charcoal
  • IV fluids
  • hemodialysis
106
Q

memantine

A
  • drug class: NMDA-R antagonist
  • useful in the treatment of Alzheimer’s Disease
107
Q

echinacea

A
  • sitmulation of immune system, anti-inflammatory
108
Q

garlic

A
  • HMG CoA reductase inhibitor
  • “inhibits cholesterol synthesis”
109
Q

ginko

A
  • improved blood flow
  • free radical scavenger
  • “dementia: memory”
110
Q

st. john’s wort

A
  • antidepressant
  • CYP450
  • not to be used with MAO-i’s and SSRI’s
111
Q

ginseng

A
  • memory
  • immune system
  • analgesia
112
Q

milk thistle

A
  • reduction in hepatotoxicity
113
Q

saw palmetto

A
  • BPH
114
Q

kava kava

A
  • anxiety, muscle relaxant, sedative
115
Q

kombucha

A
  • BP
  • CA
  • GI health
116
Q

aloe

A
  • laxative
  • burn ointment
117
Q

black cohosh

A
  • menstrual discomfort
118
Q

cyclophosphamide

A

drug class: alkylating agent - nitrogen mustard
* most common alkylating agent
* MOA:
1. forms highly reactive carbonium ion
2. transfers alkyl groups to nucleophilic sites on DNA bases
3. results in:
+cross linkage
+abnormal base pairing (cell cycle arrests)
+DNA strand breakage
+decreased cell proliferation
also damages RNA and proteins

119
Q

chlorambucil

A
  • least toxic nitrogen mustard alkylating agent
120
Q

nitrosoureas

A
  • alkylating agent that crosses BBB (useful in brain tumors)
121
Q

cisplatin

A
  • highly bound to plasma proteins
  • concentrates in kidney, intestine, and testes
  • poorly penetrates BBB
  • slowly excreted in urine
  • indications:
    +testicular CA (85-95%)
    +ovarian CA
    +other solid tumors: lung, esophagus, gastric
  • MOA:
    1. cisplatin enters cell
    2. Cl- ions released
    3. forms highly reactive platinum (Pt) complexes
    4. instra strand/interstrand x-linkage
    5. DNA damage
    6. inhibits cell proliferation
  • adverse effects: emesis, nephrotox, peripheral neuropathy, ototox
122
Q

methotrexate

A
  • anti-metabolite drug
  • inhibits dihydrofolate reductase (DHFR) and interferes with DNA/RNA synthesis by inhibiting folate synthesis
  • cytotoxic actions:
    +predominant on bone marrow
    +ulceration of intestinal mucosa
    +crosses placenta intereferes with embryogenesis (fetal malformations and death)
  • immunosuppresive actions:
    +prevents clonal expansion of B & T lymphocytes
  • anti-inflammatory action
    +interferes with release of inflammatory cytokines
123
Q

antimetabolites

A
  • 6-mercaptopurine (6-MP)
  • 5-fluorouracil (5-FU)
124
Q

vincristine, paclitaxel (taxol)

A

antineoplastic: plant based

125
Q

dactinomycin, doxorubicin, bleomycin

A

antineoplastic: anti-tumor abx

126
Q

corticosteroids, tamoxifen, fulvestrant

A

antineoplastics: hormonal agents

127
Q

Imatinib, Trastuzuman, Rituximab

A

antineoplastics: miscellanous -MABs & -ibs (growth factor inhibitors)

Advanced Pharm (8 decks)

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