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Pharmacology > ALL DRUGS > Flashcards

ALL DRUGS Flashcards

1
Q

Fligastrim

A
  • stimulates proliferation in myeloid progenitor cells
  • activates PMNs
  • mobilizes hematopoetic stem cells to circulation
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2
Q

Oprelvekin

A
  • Stimulates myeloid, lymphoid and megarkaryocyte progenitor cells w/ growth factors
  • used for thrombocytopenia
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3
Q

Heparin

A
  • mixture sulfated mucopolysaccharides
  • enhances AT-III
    • inhibits activated clotting factors: thrombin IIa and Xa
  • uses:
    • acute anticoagulant, initial treatment of thrombosis and thromboemoblic disease
    • ONLY PREVENTS FORMATION OF THROMBUS
    • does not lyse
  • Toxicities
    • bleeding & thombocytopenia
      • can neautralize with *protamine sulfate *
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4
Q

Enoxaprin

A
  • from generic heparin
  • less toxicities
    • bleeding and thrombocytopenia
  • better heparin
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5
Q

Warfarin

A
  • oral anticoagulant vit K antagonst
    • reduce clotthing factors II, VII, IX, X
  • use as chronic prevention
    • administer with heparin
  • **Toxicity **
    • bleeding
    • vit k antagonist
    • can cross placenta
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6
Q

Aspirin

A
  • anti platelet drug
  • ONLY IRREVERSIBLE NSAID binding to COX1
  • prevents thrombus and re-thrombosis
  • Toxicity
    • GI ulcer
    • renal damage
    • bleeding tendencies
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7
Q

Clopridogrel

Ticlopidine

A
  • inhibits ADP synthesis
    • P2Y12 receptor antagonist
  • “prodrug” must be activated by liver
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8
Q

Abciximab

A
  • Fab frag antibody against IIb/IIIa receptor
    • glycoprotein IIb/IIIa once activated will anchor platelets and exposed matrix
  • **Toxicity **
    • bleeding tendencies
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9
Q

Tissue Plasminogen Activator (t-PA)

A
  • serine protease binding to fibrin
  • systemic plasmin activation
  • Toxicity
    • bleeding tendicies
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10
Q

vitamin K

A
  • confers growth factor II, VII, IX, X
  • requires bile salt for absorption
  • use
    • anticoagulant toxicity
    • vit k deficiency
    • hemorrhagic disease
  • types
    • K1 phytonadione (foods)
      • oral and parental use
      • IV for anaphylaxis
    • K2 menaquinon (GI bacteria)
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11
Q

Aminocaproic Acid

A
  • fibrinolytic inhibitor
  • blocks lysine binding site on fibrin (similar to lysine)
  • use
    • bleeding from fibrinolytic therapy
    • hemophiliacs
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12
Q

Desmopressin acetate

A
  • increase factor VIII in hemophilia A / Van Willbrand disease
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13
Q

Protamine Sulfate

A
  • for heparin OD
    • binds to heparin = neautralize
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14
Q

Erythropoetin

A
  • made in kidney response to hypoxia
    • prepared by recomb. technology
  • for chronic anemia from reduced EPO production in CRF
  • Toxicities:
    • hypertension and thrombosis
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15
Q

Statin

  • Levostatin
  • Simvastatin
A
  • most effective and best tolerted
    • can use with other drugs
  • use:
    • inhibit HMG-CoA = dec cholesterol
    • inc affinity LDL receptors in liver
      • inc LDL clearance and dec plasma LDLs
  • Toxicities:
    • possible increase in liver ezymes
    • teratogenic
    • interact with CYP450s
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16
Q

Niacin

A
  • act as vit B3 when converted to NAD
  • VLDL secretion inhibitor
  • use:
    • converted nicacin = inhibit VLDL production, secretion
    • inc lipoprotein lipase activity = increase clearance of VLDL
    • raise HDLs
  • Toxicities:
    • cutaneous flushing and itching
    • elevated liver enzyme
    • Gi distress and ulcers
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17
Q

Cholestryamine

Colestipol

A
  • bile acid sequestriants
  • oldest and safest drug
  • use:
    • large pos. charge -> bind bile acid in GI tract lumen = inhibition to reuptake in ileum/jejunum
    • dec bile = inc of bile production in liver = inc LDL uptake and clearance from plasma
    • use if statins don’t ineffective
  • Toxicities:
    • constipation/bloating
    • interaction with drug b/c charged
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18
Q

Gemfimbrozil

A
  • Fibrates (PPAR activator)
  • mechanism:
    • unclear
    • act on PPAR-a in liver
    • activate -> inc lipoprotein lipase -> dec VLDLs -> inc HDLs
  • Toxicities:
    • avoid with patients with liver disease
    • high cholesterol gallstones
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19
Q

Ezetimibe

A
  • sterol absorption inhibitor
  • excreted in bile -> absored -> metabolized
  • mechanism
    • inhibits intestinal absorption of phytosterols and cholestrol -> dec LDL
      • inhibit transport protein NPC1L1 in jejunal enterocytes for uptake cholesterol
      • liver LDL receptors inc -> removal of LDl from plasma
      • bile acid sequestriants will inhibit ezetimibe absorption
      • can use with statins
20
Q

Echinacea (Botanical)

  • purple coneflower
A
  • mechanism:
    • effects on immune system
      • stims cytokine
      • increases leukocyte phagocytosis
      • enhance immne function in flu or colds
  • antiinflam effects in vitro
    • inhibits COX, lipoxygenase
  • weak antimicrobial effects
  • Toxicities
    • unpleasant taste
    • GI upset
    • dizziness/headache (CNS)
    • allergic rxn
21
Q

Ginkgo

(Botanical)

A
  • from leaves of tree
  • active ingredients are glycosides and terpenoids
  • effects:
    • inc bl flow, tissue perfusion = aids circulation (vasodilator release)
    • antioxidant and free radical scavenging
    • produce changes to CNS NT (5HT, NE, Ach)
      • may benefit memory disorders (Alzheimers)
  • Toxicities:
    • epileptogenic; avoid with seizure
    • do not use with anticoagulants, can increase bleeding/antiplatelet effects
22
Q

St. John’s Wort

(Botanical)

A
  • found as shrub
  • from dried chopped flowers in methanol
  • uses:
    • inhibit monoamine oxidase enzymes, re-uptake of NE and 5HT
      • used for mild depression
    • photoactivation of hypericin by UV light - antiviral effect
      • may be beneficial in some tumors and HIV infections (unsure)
  • Toxicities
    • avoid antidepressent drugs, can potentiate effects
      • 5HT syndrome ! too much of 5HT enhancing the NT
    • may induce CYP450 enzymes -> accelerating metabolism of other drugs -> causing low plasma levels of another drug being metabolized by CYP450
23
Q

Saw Palmetto

(Botanical)

A
  • active ingredient of berries
    • phytosterols, flavinoids and aliphatic alcohols noted.
  • effects:
    • inhibition of 5-a-reductase; reduce testosterone to DHT in prostate
    • may block binding of DHT to andorgen receptor
    • main use for prostatic hyperplasia
    • inhibit growth factors
    • inhibit lipocygenases in protaste
  • Toxicities:
    • GI upset
    • Hypertension
    • decreased libido
24
Q

Coenzyme Q10

(nutraceutical)

A
  • acitive ingredient ubiquinon found in mitochondria of many tissue
  • use:
    • potent antioxidant
    • affects intracellular oxi-red rxn
    • can reduce bl. pressure in hypertension
    • affective in coronary art disease
    • beneficial to early parkinson’s
    • promotes ATP formation
  • Toxicities
    • similar in structure to Vit K; will block warfarin
    • adverse effects rare
25
Q

Glucosamine - can find at GNC

(Nutraceutical)

A
  • found in body in articular cartilage
  • amino sugar used as building block
  • from shellfish, shark cartilage etc
  • use:
    • precursor for GAGs
    • assist with repair and health of articular cartilage in OA
    • may have antiinflammatory effects
  • Toxicities:
    • allergies of glucosamine from shellfish
26
Q

Melatonin

A
  • use:
    • 5HT derivative by pineal gland
    • regulating sleep-wake cycles (circadian rhythm)
    • preventing/treating “jet lag”/insomia
  • Toxicities
    • decrease sperm quality
    • reduce LH, not advised for those trying to get pregnant
    • may inhibit prolactin release - avoid from nursing mothers.
27
Q

What are the steps to viral replication?

A
  1. attachment/entry
  2. uncoating
  3. early protein synthesis
  4. DNA/RNA replication
  5. Late protein synthesis
  6. Assembly/maturation
  7. Release
  • antiviral drugs will target these
28
Q

Oseltamivir

A

Use

  • prevent/treat early influenza A & B
  • H1N1 = subtype of influenza A

Mechanism

  • neuraminidase inhibitor
  • sialic acid analog
    • cleaves sialic acid of infected host cell -> release virus
  • prodrug to be metabolized by liver and GI tract

Adverse Effects

  • nausea, GI discomfort

Resistance

  • mutation in neuraminidase, however if there is a mutation virus is usually less virulent
29
Q

Amantadine

A

Use:

  • treat early influenza A
  • NOT H1N1

Mechanism:

  • inhibit proton ion channel M2 –> inhibit virus binding to endosome –> inhibits coating of virus.
  • distributed thoughou body, CNS, UNCHANGED BY KIDNEY

Adverse Effects

  • GI disturbances
  • CNS disturbance
  • renal damage w/ renal insufficiency

Resistance

  • mutation to M2
30
Q

acyclovir

A

Use:

  • herpes infection

Mechanism

  • guanosine analogy –> activcated by thymidine kinase –> infected cells susceptible tri-phosphate acyclovir that compete w/ dGTP during DNA synthesis = DNA termination
  • oral, IV or topical formulation distributed though body, CNS

Adverse Effects:

  • nausea, vomitting, diarrhea, headache, renal damage

Resistance:

  • altered or deficient thymidine kinase
31
Q

zidovudine (AZT)

A

Use:

  • HIV

Mechanism

  • nucleoside reverse transcriptase inhibitor
  • thymidine analogue –> phosphorylated by mammalian kinase viral reverse transcriptase –> compete with dTTP during DNA synthesis –> DNA termination
  • well distributed, CNS, metabolized in liver (glucoronidation)

Adverse Effects:

  • Bone marrow
    • anemia, netropenia
  • Heaptotoxicity
  • drug interactions
    • drugs competing with glucoronidation (acetaminophen, beznodiaszepines)

Resistance

  • reverse transcriptase mutation, inefficient kinase
32
Q

nevirapine

A

Use:

  • treatment of HIV

Mechanism:

  • Non-nucleoside reverse transcriptase inhibitor (NNRTIs)
  • binds to non-catalytic site inhibiting reverse transcriptase
  • well absored, CNS, fetus, tit milk, metabolized in liver –> glucoronidation

Adverse effects:

  • rash, psychiatric effects
  • heptatotoxicity
  • inc CYP3A4 –> inc metabolism of other drugs ex itselff, AZOLES, protease inhibitors

Resistance:

  • reverse transcriptase mutation
33
Q

ritonavir

A

Use

  • treat HIV

Mechanism:

  • Protease inhibitor
  • inhibit HIV aspartyl protease
  • inhibits CYP450, given as enhance of other PIs
  • give with choco MILK! or nutritional suppplement cause unpalatable!
  • metabolized by CYP3A4

Adverse effects:

  • nausea, vomiting, diarrhea, numbness, elevated liver enzymes
  • high bl glucose and lipid levels

Resistance

  • mutation in protease
34
Q

maraviroc

A

use:

  • treat HIV

Mechanism:

  • viral entry inhibitor
  • CCR5 reveptor antagonist blocks binding of viral gp120 to CCR5 –> prevent viral entry
  • dec viral load in patients

Adverse Effects

  • hepatotoxicity and cardriovascular
35
Q

raltegravir

A

Use:

  • treat HIV

Mechanism

  • Integrase inhibitor
  • dec transfer of viral DNA into host genome
36
Q

HAART

A

what is it

  • highly active antiretroviral therapy
  • First line treatment = combo of 3 antiviral drugs

HAART = 2 NRTIs + NNRTI or PI

37
Q

Cyclophosphamide

A
  • most commonly used alkylating agent
  • Oral / IV admin
  • non reactive prodrug
  • treat lyphomas, leukemias, neruoblastomas and breat ovarian carcinomas
  • Resistance
    • inc DNA repair, dec drug permeability, rxn w/ other cell constinuents = cross resistance
  • Adverse Effects
    • nausea and vomiting
    • bone marrow, immunosupression and alopecia
    • hemorrhagic cystitis, sterility, menopause and veno occulsive disease of liver
      • stop adverse effects by stop taking drug, platelet RBC transfusion
38
Q

Cisplatin

A
  • covalently binds N7 of guanine, also interacts with cystine and adenine
  • kills cells in all stages of cell cycle
  • IV or locally
  • testicular, ovarian and bladder
  • Adverse Effects
    • neuseaa, vomiting, nephrotoxicity and neurotoxicity
  • Resistance
    • inc DNA repair, reaction w/ other cellular constituents and dec cell uptake
39
Q

Bleomycin

A
  • non covalent dna binding agent
  • forms dna-bleomycin-Fe(II) complex
  • oxidation -> free radicals -> DNA strand breakage (cells stay in G2 phase)
  • treat squamous cell carcinomas, lymphomas and testicular tumours
  • **Adverse Effects: **
    • pulmonary fibrosis, pyrexia, anaphylaxis
  • Resistance:
    • inc DNA repair, inc drug efflux, inc expression of antioxidant enzymes or bleomycin hydrolase
40
Q

methotrexate

A
  • enters cell active transport
  • Folic Acid Inhibitor binding to dihydrofolate reductase (DHF)
  • reduce purine + pyrimidine synthesis -> affect RNA, DNA , protein synthesis
  • methotrexate polyglutamates: retained in cancer cells further inhibit RNA/DNA synthesis
  • treat leukemias, lymphomas and carcinomas
  • IV/oral
  • Adverse Effects
    • myelosuppresion, GI distress, alopecia, teratogenic, renal damage (high dose), liver damage (long term)
  • Resistance
    • Non proliferating cell, inc DHF reductase, dec binding to DHF, dec cell uptake
41
Q

Fluorouracil

A
  • carrier mediated transport
  • covnerted to ribosyl and deoxyrybosyl nucleotide metabolites
  • inhibit thymidylate synthetase -> dec thymidine -> dec DNA synthesis
  • primary use for breast and GI carcinomas
  • IV or topically
  • Adverse Effects
    • bone marrow, nausea, vomitting, diarrhea, oral and GI ulceration, anorexia, alopecia
  • Resistance:
    • inc fluorouracil metabolism, dec conversion nucleotide metabolite, inc thymidylate synthase activity.
42
Q

Topotecan

A
  • targets cells in S phase
  • binds to Topoisomerase I-DNA complex to prevent annealing of DNA breaks
    • Topoisomerase I assists w/ DNA replication and transcription
  • IV administration
  • ovarian cancers

Adverse Effects

  • bone marrow suppression
  • nausea
  • vomiting
  • diarrhea
  • alopecia
  • headache

Resistance

  • increase transport of drug out of cell
  • dec expression or a mutation in topoisomerase I
43
Q

Vincristine

(periwinkle plant)

A
  • Microtubule Inhibitors
    • decreases microtubule half-life -> spindle dissolves -> cell divides
  • block tubulin polymerization -> dysfunctional spindle
  • kills cell in M stage
  • IV admin
  • treat leukemias, lymphomas , rapid proliferating tumours

Adverse Effects

  • nausea, vomiting, alopecia, perhipheral neuropathy. antifungals slow metabolism. anticonvulsants accelerate metab

Resistance

  • altered tubulin structure, eeflux via P-glycoprotein in cell membrane
44
Q

Paclitaxel

A
  • microtubule inhibitor
    • decrease microtubule half-life -> spindle dissolves -> cell divides
  • promotes tubulin polymerization -> microtubules too stable = no dividing
  • advanced ovarian cancer, metastatic breast cancer - w/ cisplatin

Adverse Effects

  • nausea, vomiting, hypersensitivity, alopecia, myelosuppresion, peripheral neuropathy, pulmonary toxicity, heaptic function (CYP450)

Resistance

  • altered tubulin structure
  • eeflux via P-glycoprotein in cell membrane
45
Q

Prednisone

A
  • steroid sensitive tumours
    • mediating cell growth/proliferation
  • induce apoptosis of leukemia and lymphoid
  • for immune and inflammatory suppression - primarily lymphomas and leukemias

Adverse Effects

  • immunosuppression, hyperglycemia, ulcers, pancreatistis, weakening, osteoporosis, hypertension, mood swings

Resistance

  • absence or mutation of receptor
46
Q

Tamoxifen

A
  • ER partial agonist
  • estrogen sensitive tumour cells, bind ER mediating gene expression -> tumour growth
  • for estrogen dependent breast cancer
  • oral admin

Adverse Effects

  • hot flashes, nausea vomiting, irregular periods, blood clots, cataracts, uterine cancer

Resistance

  • absence or mutation of receptor

Pharmacology (13 decks)

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