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
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)
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
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
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
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
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
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
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
10
Q
streptokinase
A
- drug class: fibrinolytic
- synthesized by Streptococci
- MOA: binds to plasminogen to activate it to promote fibrinolysis
- indication: MI, PE
11
Q
urokinase
A
- drug class: fibrinolytic
- synthesized by the kidney
- MOA: lyses the thrombus from within
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
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
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)
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
16
Q
fresh frozen plasma (FFP)
A
drug class: factor replenishment
target: multiple
result: normal clotting cascade
indications: hemophilia
17
Q
desmopressin
A
- increased factor VIII activity
- indications: mild hemophilia A, von-willebrand disease
18
Q
aminocaproic acid
A
drug class: fibrinolytic inhibitor
MOA: competitively inhibits plasminogen activation
result: stablized clot
indication: post-op
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
20
Q
lispro, aspart, glulisine
A
rapid acting insulins
bolus insulin
21
Q
novolin, humulin
A
short acting (regular) insulin
acts fast; leaves fast (longer acting than RA)
22
Q
NPH
neutral protamine Hagedorn
A
intermediate acting
23
Q
glargine, detemir
A
long acting insulin
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
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
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
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
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
29
Q
amylin
A
- amylin is released by beta cells
+suppresses glucagon release - decreases circulating glucose
- concomitant with insulin
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
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
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
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
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
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)
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
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?)
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
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»_space;»»> COX-1)
40
Q
meloxicam
A
- drug class: COX-2 inhibitor»_space; COX-1
- not as selective as other COXIBs
- fewer GI effects
- tox effects similar to other NSAIDs
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
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
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
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
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
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)
47
Q
morphine
A
- phenanthrene structure
- strong opioid
48
Q
dilaudid
A
- phenanthrene structure
- 5x more potent than morphine
- strong opioid
49
Q
codeine
A
- phenanthrene structure
- 1/10th as potent as morphine
- moderate agonist
50
Q
oxycodone
A
- phenanthrene structure
- more effective as a combination med
- 2x more potent than morphine
- moderate agonist
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)
