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pharm 2 > immunosupressants and anticancer > Flashcards

immunosupressants and anticancer Flashcards

1
Q

Epidemiology of Cancer
 # associated disease processes
 leading cause of the death in the U.S.?
 Nearly ? deaths a day
 % of all deaths
 Many causes of cancer are mediated by ?
 theories on cancer pathophysiologic process?

A

 150+ associated disease processes
 Second leading cause of the death in the U.S.
 Nearly 1,500 deaths a day
 25% of all deaths
 Many causes of cancer are mediated by the environment
and lifestyle of a person
 Smoking
 Obesity
 Alcohol consumption
 Multitude of theories on cancer pathophysiologic process

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2
Q

 Neoplasia

A

 Process of altered cell differentiation and growth
 Uncoordinated
 Autonomous
 Lacks normal regulatory control

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3
Q

 Neoplasm

A

 New growth
 “Tumor”

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4
Q

Cancer

A

 Disease resulting from altered cell differentiation and growth

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5
Q

Review: Cell Growth & Proliferation

A
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6
Q

Cell Differentiation
 Proliferating cells become progressively?
 Cells have a specific set of?
 As cells differentiate, what deminishes?
 Undifferentiated cells are hallmark of?

A

 Proliferating cells become progressively more specialized
 Cells have a specific set of structural, functional, and life-expectancy characteristics
 As cells differentiate, their capacity or proliferation diminishes
 Undifferentiated cells are hallmark characteristic of cancer cells

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7
Q

Cell Growth Gone Wrong: Cancer

A

 Unchecked growth that progresses toward limitless expansion
 Abnormal and rapid proliferation
 Loss of differentiation> anaplasia
 Causation – genetic & external

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8
Q

Comparison of Characteristics: normal cells and cancer cells

A
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9
Q

Carcinoma

A

Carcinoma
 Arise from the cells that cover external and internal body surfaces such as lung,
pancreatic, breast, and colon

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10
Q

Sarcoma

A

 Arise from cells found in the supporting tissues of the body such as bone, cartilage,
fat, connective tissue, and muscle

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11
Q

Lymphoma

A

 Arise in lymph nodes and tissues of the body’s immune system

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12
Q

Leukemia

A

 Cancers of the immature blood cells that grow in the bone marrow

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13
Q

Invasion & Metastasis

A

 Solid tumors secrete enzymes that break down proteins and contribute to infiltration, invasion, and penetration of surrounding tissues
 Complete surgical removal difficult
 Cancer cells may travel and “seed” into different body cavities where they can proliferate and cause tumor growth (metastasis)
 Blood vessel and lymphatic spread
 Finely orchestrated; selected cells only
 Angiogenesis

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14
Q

Metastasis & Use of Bisphosphonates in Cancer

current tx guidelines

A
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15
Q

Metastasis & Use of Bisphosphonates in Cancer
 Bone health?
 bone pain?
 Reduction of ?

A

 Bone health maintenance
 Reduce bone pain due to hypercalcemia
 Reduction of bone metastasis (breast & prostate cancer)

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16
Q

bisphosphonates in prostate cancer

A

70% of breast and prostate cancer patients develop bone metastases
 15-30% of other common solid cancers

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17
Q

bisphophonates in breast cancer

early onset and when metatstisized

A
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18
Q

bisphosphonate names

A
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19
Q

Clodronate

moa, route, potentcy

A

BP
given oral/IV
10 potentcy factor

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20
Q

Pamidronate

moa, route, potentcy

A

BP, IV, 100

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21
Q

Alendronate

moa, route, potentcy

A

BP ,oral, 500

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22
Q

Ibandronate

moa, route, potentcy

A

BP , oral/IV, 1000

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23
Q

Risedronate

moa, route, potentcy

A

BP, oral, 2000

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24
Q

Zoledronate*

moa, route, potentcy

A

BP, IV, 10000

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25
Q

MOA: Bisphosphonates

A

 Inhibit osteoclast
 Attach to bony surfaces undergoing active resorption
 Bisphosphonates released during resorption by osteoclasts impairs ability of osteoclasts to form the ruffled border, to adhere to the bony surface
 Reduce osteoclast genesis and recruitment
 Promoting osteoclast apoptosis

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26
Q

Tumor Cell and Osteoclast Symbiotic Relationship
* tumor cell releases:

A
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27
Q

Tumor Cell and Osteoclast Symbiotic Relationship
* bone resobrtion releases:

A
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28
Q

Result of Tumor Cell and Osteoclast Symbiotic Relationship

A

Symbiotic relationship further increases bone destruction and
tumor growth.
[do not need to memorize hormones]

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29
Q

Tumor Cell and Osteoclast Symbiotic Relationship diagrammed

A
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30
Q

Dental Concerns: Bisphosphonates

associated with? mechanism? precipitated by?

A
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31
Q

risk factors of dental concerns for BP

A

 Hx of bisphosphonates especially IV
 Hx of Cancer
 Corticosteroid therapy
 Diabetes
 Smoking
 Alcohol use
 Poor oral hygiene
 Chemotherapuetic drugs

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32
Q

what often preceeds MRONJ

A

extractions

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33
Q

Study on ONJ Risk

A

increased incidence with increased duration of tx (1% per yr)

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34
Q

what bp has the highest risk for MRONJ

A

zolendronate

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35
Q

Non-Cancer pts on BP’s and dental tx

A

 Low-risk for osteoporosis dosed bisphosphonates – 0.1%
 ADA – “recommends that a patient with active dental or periodontal disease should
be treated despite the risk of developing ARONJ, because the risks and consequences
of no treatment likely outweigh the risks of developing ARONJ.”

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36
Q

Additional Considerations of BP’s
 Education
 drug holidays?
 chlorohexidine use?
 Prophylactic antibiotics?

A

 Education
 Avoid drug holidays
 0.2% Chlorhexidine: rinse for 1-minute prior to dental treatment and
continue rinsing twice daily for 7-days after treatment
 Prophylactic antibiotics: no specific dose/agent recommendations
 Amoxicillin (Amoxil) or amoxicillin/clavulanic acid (Augmentin) has been successful in studies

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37
Q

Retrospective analysis for prevention of ONJ in multiple myeloma pts using abx prophylaxis?

abx used and dose?

A
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38
Q

Prospective case series, for prevention of ONJ in patient requiring tooth
extraction and on IV bisphosphonate

abx/dose?

A
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39
Q

Cancer pts ADA/AAOMS dental tx and using BP’s

A

High-risk for oncologically dosed bisphosphonates – 2-18%
 ADA – does not address
 AAOMS – “procedures that involve direct osseous injury should be avoided.
Nonrestorable teeth may be treated by removal of the crown and endodontic
treatment of the remaining roots. Placement of dental implants should be avoided in
the oncologic patient receiving IV antiresorptive therapy”

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40
Q

BP duration and MRONJ

A

increased incicdence when used over longer times

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41
Q

Mechanism of Action: Denosumab (Xgeva, Prolia)

A

 Inhibit osteoclast activation
 RANKL is secreted by bone marrow cells and osteoblasts
 RANKL binds to the RANK receptor on osteoclasts and promotes osteoclast
differentiation and activity.
 Denosumab is a fully human monoclonal antibody that binds to RANKL
 Bound RANKL cannot attach to RANK receptors (i.e. inhibiting activation of
osteoclast)

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42
Q

Monocolonal Antibodies: Denosumab

production

A

Murine antibody that recognizes specific antigen

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43
Q

Murine Antibody:

A

 induce a human anti-mouse antibody immune response
 activate human immune effector mechanisms poorly
 short t1/2 in humans
Chimerized by substituting major portions of the human IgG molecule

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44
Q

Ab types and immunogenicity scale

A
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45
Q

Toxicities – Infusion Reactions with Ab’s
 Typical symptoms?
 time frame
 Premedication

A

 Typical include fever, chills, nausea, dyspnea, and rashes
 within 30 minutes to two hours of initiation of drug infusion, symptoms may be
delayed for up to 24 hours
 Premedication with diphenhydramine and acetaminophen is indicated

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46
Q

Denosumab Risk of MRONJ

high and low doses

A

 High Dose Denosumab : High prevalence (2-5% Osteonecrosis)

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47
Q

Mechanism of MRONJ

A

 Profound and prolonged inhibition of bone resorption with over-suppression of bone remodeling (ie, low bone turnover), and infection are the main mechanisms
 Postulated that MRONJ is a form of avascular necrosis, possibly caused by inhibition of angiogenesis.

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48
Q

MRONJ and inhibition of angiogenesis

A

 In vitro experiments consistently demonstrate inhibition of angiogenesis by zoledronic
acid, and cancer patients treated with this agent have decreased circulating VEGF levels
 Growing body of evidence linking MRONJ to antiangiogenic drugs, including
bevacizumab and orally active tyrosine kinase inhibitors.

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49
Q

Angiogenesis and Cancer
 Angiogenesis =
 Key factor in the?
 Solid tumors secrete ?
 stimulates?

A

 Angiogenesis = the development of new blood vessels
 Key factor in the growth and metastasis of certain solid tumors
 Solid tumors secrete proangiogenic factors, vascular endothelial growth factor (VEGF)
 stimulate new vessel development via downstream signaling pathways

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50
Q

inhibitors of angiogenesis introduced into oncology
practice

A

 monoclonal antibodies against VEGF (e.g., bevacizumab),
 tyrosine kinase inhibitors (e.g., sorafenib, sunitinib),
 mammalian target of rapamycin (mTOR) pathway inhibitors (e.g., everolimus)
 immunomodulatory agents (e.g., thalidomide, lenalidomide).

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51
Q

bevacizumab

A

monoclonal antibodies against VEGF

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52
Q

sorafenib

A

tyrosine kinase inhibitors

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53
Q

sunitinib

A

tyrosine kinase inhibitors

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54
Q

everolimus

A

mammalian target of rapamycin (mTOR) pathway inhibitors

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55
Q

thalidomide

A

immunomodulatory agents

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56
Q

lenalidomide

A

immunomodulatory agents

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57
Q

Bevacizumab moa

used in what cancers?

A

Bevacizumab (Avastin)- humanized; binds VEGF-A
 Used in solid tumor cancers
 Specifically recognize and bind to VEGF.
 Once bound, the complex is unable to activate the VEGF receptor.

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58
Q

Bevacizumab
 Most effective when?
 kills tumors? role?
 Reduces?
 possible adrs?

A

 Most effective when combined with additional
therapies, especially chemotherapy.
 Do not necessarily kill tumors; they instead may
prevent tumors from growing.
 Reduce formation of new blood vessels; reduce
nutrient delivery
 Increases in bleeding and reduced wound healing

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59
Q

Note on ONJ and antiangiogenic rx’s
 Association of ONJ with therapies that target angiogenesis is?
 Especially with?
 Risk for MRONJ when recieiving both antiabsorb and antiangio?

A

 Association of ONJ with therapies that target angiogenesis is more
controversial
 Especially monotherapy with an antiangiogenic agent
 Risk for MRONJ more clearly established for use of antiangiogenic
agents in patients ALSO receiving antiresorptive agents

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60
Q

International Task Force on Osteonecrosis of the Jaw

For patients whose cancer management includes treatment with denosumab or IV
bisphosphonates, recommends:

A

 “a thorough dental examination with dental radiographs should be ideally completed prior to the initiation of antiresorptive therapy in order to identify dental disease before drug therapy is initiated”
 “Any necessary invasive dental procedure including dental extractions or implants should ideally be completed prior to initiation of [bisphosphonate] or [denosumab] therapy.”

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61
Q

American Society of Clinical Oncology (ASCO) – 2017
 “All patients should have what before using a Bone-modifying agent (BMA).”
 “in the setting of invasive dental procedures, it is advisable, whenever possible to?
 “If an invasive manipulation of the bone underlying the teeth is clinically indicated
before starting BMA therapy…initiation of BMA therapy should be ideally delayed for?

A

 “All patients should have a dental examination and preventive dentistry before using a Bone-modifying agent (BMA).”
 “in the setting of invasive dental procedures, it is advisable, whenever possible to delay the starting of therapy with BMA until the initial bone healing process of the tooth socket bone has taken place”
 “If an invasive manipulation of the bone underlying the teeth is clinically indicated before starting BMA therapy…initiation of BMA therapy should be ideally delayed for 14 to 21 days to allow for wound healing, if the clinical situation permits.”

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62
Q

Cancer Treatment
 Goal of therapy based on severity of illness:
 Multiple modalities utilized:
 Supportive care for ?

A

 Goal of therapy based on severity of illness: Curative, Control, Palliative
 Multiple modalities utilized: Surgery, Radiation therapy, Chemotherapy, Hormonal therapy, Biotherapy
 Supportive care for clinical manifestations and/or treatment adverse reactions

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63
Q

Chemotherapy Agents
 forms?
 moa’s
 Reaches

A

 Adjuvant (given after therapy) vs. neoadjuvant (before tx to reduce size)
 Various mechanisms of action> slow/stop cell proliferation
 Reach ‘microscopic’ cancer cells
2 log kill desired

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64
Q

what limits chemotherapeutics use?

A

Adverse reactions limit use
 GI disturbances (N/V/D)
 Hair loss
 Bone marrow suppression
(anemia, increased infection risk)

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65
Q

Antineoplastic Medications forms

A
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66
Q

Alkylating Agents
 moa?
 cell cycle specific?
 Can be used in?

A

 Directly damage cell DNA
 Impairs replication & transcription= cell death
 Work in all phases of the cell cycle
 Can be used in many different cancers
* carbonium ion highly reactive>binds dna

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67
Q

alkylating agents ADRs/toxicity

A

oppurtunistic infections possible=thrush

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68
Q

alkylating agents classes

A

Nitrogen Mustards
Platinum Compounds
Nitrosoureas
Alkyl sulfonates
Triazines
Ethylenimines

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69
Q

Nitrogen Mustards:

A

 cyclophosphamide, chlorambucil, ifosfamide, melphalan

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70
Q

 cyclophosphamide class/moa

A

N mustard

akylarting agent

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71
Q

chlorambucil class/moa

A

N mustard

alk agent

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72
Q

ifosfamide class/moa

A

N mustard

alk agent

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73
Q

melphalan class/moa

A

N mustard

alk agent

74
Q

Platinum Compounds:

A

 cisplatin, carboplatin, oxaliplatin

75
Q

cisplatin class/moa

A

Plat compound, alk agent

76
Q

carboplatin class/moa

A

Plat compound, alk agent

77
Q

oxaliplatin class/moa

A

Plat compound, alk agent

78
Q

Nitrosoureas:

A

 streptozocin, carmustine and lomustine

79
Q

Nitrosoureas often used with?

A

brain tumors

80
Q

streptozocin class/moa

A

nistrosourea, alk agent

81
Q

carmustine class/,moa

A

nistrosourea, alk agent

82
Q

lomustine class/moa

A

nistrosourea, alk agent

83
Q

Alkyl sulfonates:

A

 busulfan

84
Q

busulfan class/moa

A

Alkyl sulfonates, alk agent

85
Q

Triazines:

A

 dacarbazine and temozolomide

86
Q

dacarbazine (DTIC) class/moa

A

triazine, alk agent

87
Q

temozolomide (Temodar®)

A

triazine, alk agent

88
Q

Ethylenimines:

A

 thiotepa and altretamine (hexamethylmelamine)

89
Q

thiotepa class/moa

A

Ethylenimines, alk agent

90
Q

altretamine (hexamethylmelamine) class/moa

A

Ethylenimines, alk agent

91
Q

platinum compounds nn adr

A

Neurotoxicity
 Drugs enter into the dorsal root ganglion and binds to DNA, causing apoptosis.

 Platinum compounds form intrastrand adducts and interstrand crosslinks altering tertiary structure of DNA. This promotes alterations in cell-cycle kinetics, leading to an attempt of differentiated postmitotic dorsal root ganglion neurons to re-enter cell cycle, which leads to the induction of apoptosis

Regardless of the mechanism, apoptosis results in secondary damage to peripheral nerves

92
Q

Oxaliplatin association with:
 Cold-induced?
 breathing?
 Mm?
 Jaw?
 swallowing?
 mm appearence?
 Voice?
 Ocular?

A

pain triggered by exposure to cold liquids
Cold-induced perioral paresthesias – 95%
 Cold-induced pharyngolaryngeal dysesthesia – 92%
 Dyspnea – 40%
 Muscle cramps – 34%
 Jaw stiffness – 34%
 Dysphagia – 30%
 Visible fasciculations – 30%
 Voice changes – 6%
 Ocular changes – 0.7%

93
Q

Antimetabolites:

A

 Antimetabolites are structurally related to normal compounds that exist
within the cell

94
Q

antimetabolites moa

A

Antimetabolites interfere with DNA and RNA growth by substituting for or competing with the normal building blocks of DNA and RNA
 i.e. the availability of normal purine or pyrimidine nucleotide precursors
 May either by inhibiting the synthesis of normal nucleotides or compete with them in the formation of DNA or RNA

95
Q

are antimetabolites cell phase specific

A

Their maximal cytotoxic effects are in S-phase
 Synthesis – DNA replicates, yielding two separate sets

96
Q

Antimetabolites types

A

 Folate antagonists
 Pyrimidine antagonists
 Purine antagonist

97
Q

Folate antagonists names

moa

A

methotrexate, pemetrexed
inhibit folate syn=no nucleic acids

98
Q

methotrexate

A

folate antagonist

99
Q

pemetrexed

A

folate antag

100
Q

Pyrimidine antagonists:

A

5-Fluorouracil (5FU), Cytarabine, gemcitabine

101
Q

5-Fluorouracil (5FU),

A

Pyrimidine antagonists:

102
Q

Cytarabine

A

Pyrimidine antagonists:

103
Q

gemcitabine

A

Pyrimidine antagonists:

104
Q

Purine antagonists

A

Mercaptopurine, Fludarabine

105
Q

Mercaptopurine

A

Purine antagonist:

106
Q

Fludarabine

A

Purine antagonist

107
Q

 Folate antagonists, Pyrimidine antagonists, Purine antagonist moa

A

Inhibit precursors to DNA synthesis

108
Q

Methotrexate
moa, used in? phase? affected tissues?

A

 Antineoplastic; immunosuppressant (psoriasis; RA)
 Target S-phase (DNA replication), inhibit rapid proliferating cells
 Bone marrow and intestinal epithelium
 Myelosuppression risk for hemorrhage and infection

109
Q

methotrexate dental note
 can cause?
 what agents are most stomatotoxic
 whiich rx known to be secreted into the saliva, result of this?

A

Dental Note: oral mucositis
 Oral pain; Erythema; Difficulty opening the mouth
 DNA cycle specific agents are most stomatotoxic
 Methotrexate, etoposide known to be secreted into the saliva
 further increasing stomato toxicity potential

110
Q

DNA cycle specific agents associated with oral mucositits

A

Methotrexate
5FU
Cytarabine
Doxorubicin
Etoposide
Bleomycin

111
Q

Cytotoxic Antibiotics moa

A

 Bind to and break DNA inside cancer cell to keep them from growing
and multiplying

produce radicals

112
Q

cytotoxic abx groups

A

 Anthracyclines: Doxorubicin, daunorubicin, epirubicin, idarubicin.
 Other: bleomycin, plicamycin, mitomycin

113
Q

Doxorubicin moa

A

Bind to and break DNA inside cancer cell to keep them from growing
and multiplying

Cytotoxic Antibiotics

114
Q

daunorubicin moa

A

Bind to and break DNA inside cancer cell to keep them from growing
and multiplying

Cytotoxic Antibiotics

115
Q

epirubicin moa

A

Bind to and break DNA inside cancer cell to keep them from growing
and multiplying

Cytotoxic Antibiotics

116
Q

idarubicin moa

A

Bind to and break DNA inside cancer cell to keep them from growing and multiplying (via radical production)

Cytotoxic Antibiotics

117
Q

bleomycin moa

A

Bind to and break DNA inside cancer cell to keep them from growing
and multiplying

Cytotoxic Antibiotics

118
Q

plicamycin moa

A

Bind to and break DNA inside cancer cell to keep them from growing
and multiplying

Cytotoxic Antibiotics

119
Q

mitomycin moa

A

Bind to and break DNA inside cancer cell to keep them from growing
and multiplying

Cytotoxic Antibiotics

120
Q

what can be seen orally with cytotoxic abx?

A

mucositis

121
Q

Mitotic Inhibitors

A

 Work in M-Phase to prevent cell division

122
Q

mitotic inhibitor groups include:

A

 Vinca Alkaloids: Vincristine, Vinblastine
 Taxanes: Paclitaxel, Docetaxel

123
Q

Vincristine moa
 Derived from ?

A

 Derived from Madagascar periwinkle
 MOA: bind β tubulin & block its polymerization with α tubulin into
microtubules
 Cell division arrests in metaphase
 Absence of intact mitotic spindle, chromosomes cannot align, disperse throughout the cytoplasm
 Apoptosis

124
Q

vinka alkloids/ vincristine toxicity

A

 Peripheral neuropathy-numbness, tingling
 Neurotoxicity may also be persistent, deep aching and burning pain that mimics a toothache

125
Q

Side Effects: Cell Replication Inhibition

A

 Primarily GI tract, Bone marrow, Oral cavity
 Mucositis painful inflammation along GI
 Develops within 1-week of chemotherapy initiation
 Stomatotoxic (toxic effects on the oral tissues)
 Impairment of bone marrow (myelosuppression)
 suppressing white blood cells, red blood cells, and platelets
 GET LABS THE DAY BEFORE ANY PROCEDURE
 WBC >2000
 ANC >2000
 Platelets >75,000

126
Q

Oral Complications Common to Chemotherapy & Radiation

A

Oral mucositis (20-40%)
Infection
Xerostomia/salivary gland dysfunction
Functional disabilities
Taste alterations
Nutritional compromise
Abnormal dental development

127
Q

Oral mucositis with Chemotherapy & Radiation

A

inflammation and ulceration of the mucous membranes
 can increase the risk for pain, oral and systemic infection, and nutritional compromise

128
Q

Infection with Chemotherapy & Radiation

A

viral, bacterial, and fungal
 from myelosuppression, xerostomia, and/or damage to mucosa from chemotherapy or radiotherapy

129
Q

Xerostomia/salivary gland dysfunction with Chemotherapy & Radiation

A

dry mouth d/t thickened, reduced, or absent salivary flow
 increases the risk of infection and compromises speaking, chewing, and swallowing
 persistent dry mouth increases the risk for dental caries

130
Q

Functional disabilities with Chemotherapy & Radiation

A

impaired ability to eat, taste, swallow, and speak
 due to mucositis, dry mouth, trismus, and infection

131
Q

Taste alterations with Chemotherapy & Radiation

A

changes in taste perception of foods, ranging from unpleasant to tasteless

132
Q

Nutritional compromise with Chemotherapy & Radiation

A

eating difficulties due to mucositis, dry mouth, dysphagia, and loss of taste

133
Q

Abnormal dental development with Chemotherapy & Radiation

A

altered tooth development, craniofacial growth, or skeletal
development in children secondary to radiotherapy and/or high doses of chemotherapy before age 9

134
Q

Taste Alterations - Chemotherapy

A

Common occurrence following
chemotherapy administration
 Lasts 3-4 weeks post-treatment

135
Q

common meds of taste of alterations

A

 Cisplatin
 Cyclophosphamide
 Doxorubicin
 5-Fluorouracil
 Methotrexate
 Paclitaxel
 Vincristine

136
Q

Neurotoxicity of chemo

side effects of what rx’s

A

Persistent, deep aching and burning pain that mimics a toothache, but no dental or mucosal source can be found.
 side effect of certain classes of drugs (vinca alkaloids; platinum compounds)

137
Q

Bleeding with chemo

A

oral bleeding from the decreased platelets and clotting factors

138
Q

Radiation caries:

A

Radiation caries: lifelong risk of rampant dental decay that may begin within
3 months of completing radiation treatment if changes in quality or quantity of saliva persist

139
Q

Osteonecrosis with radiation

A

blood vessel compromise and necrosis of bone exposed to high-dose radiation therapy; results in decreased ability to heal if traumatized

140
Q

Disease States for Immunosuppression

A

 Autoimmune, collagen, connective tissue and inflammatory disorders
 Systemic Lupus erythematosus
 Rheumatoid arthritis
 Chronic active hepatitis
 Inflammatory bowel disease
 Glomerulonephritis
 Nephrotic syndrome
 Myasthenia gravis
 …among others…

 Organ or tissue transplantation
 Prevent rejection

141
Q

Target of Immunosuppression

A

 Inhibit mononuclear cells
(lymph and blood cells)

142
Q

T-cell Inhibitors

A

 Cyclosporine (Sandimmune)
 Tacrolimus (Prograf; FK506)
 Sirolimus (Rapamune)
 Everolimus (Zortress)

143
Q

Cyclosporine (Sandimmune)

A

t cell inhib

144
Q

Tacrolimus (Prograf; FK506)

A

t cell inhib

145
Q

Sirolimus (Rapamune)

A

t cell inhib

146
Q

Everolimus (Zortress)

A

t cell inhib

147
Q

T-cell and B-cell inhibitors

A

 Azathioprine (Imuran)
 Leflunomide (Arava)
 Mycophenolate (Cellcept)

148
Q

 Azathioprine (Imuran)

A

b and t cell inhib

149
Q

Leflunomide (Arava)

A

b and t cell inhib

150
Q

Mycophenolate (Cellcept)

A

b and t cell inhib

151
Q

Corticosteroids

A

Corticosteroids = Glucocorticoids
 Prednisone, dexamethasone, prednisolone, et

152
Q

t cell inhibitors moa

used for?

A

Downstream inhibit helper and killer T-cell activation
 Actively attack/destroy any invading/invaded cell (each T-cell is specific to virus/bacteria/protein)
 To prevent and treat rejection of organ and bone marrow transplants; RA; Psoriasis

153
Q

Cyclosporine – Side Effects

suggested tx’s? avoid?

A
154
Q

Cyclosporine AND Tacrolimus DDIs

A

 Cimetidine (Tagamet)
 Clarithromycin (Biaxin)
 Erythromycin
 Corticosteroids
 Fluconazole (Diflucan)
 Itraconazole (Sporanox)
 Ketoconazole (Nizoral)

155
Q

Cyclosporine AND Tacrolimus Cimetidine DDI

A

Reports implicate cimetidine and
famotidine as increasing
cyclosporine concentrations and/or
decreasing cyclosporine clearance

156
Q

Clarithromycin and tarcolimus

A

One report describes 2 female patients (aged 37 and 69 years), who each experienced acute renal failure and more than a 2.3-fold increase in tacrolimus serum concentrations after 9 doses of clarithromycin therapy (250 mg daily)

157
Q

Corticosteroids and cyclosporine

A

Toxic effects of prednisone and/or
cyclosporine, if agents combined

158
Q

Azoles and cyclosporine concentrations

A

Serum cyclosporine concentrations have been reported to
increase as much as tenfold in transplant patients
following the initiation of azole antifungal agents

159
Q

T-Cell and B-Cell Inhibitors moa

used for?

A

 MOA: inhibit purine (azathioprine and mycophenolate) and pyrimidine (leflunomide) nucleotide synthesis for lymphocyte production (T and B)
 Prevent and treat rejection of organ and bone marrow transplants; RA

160
Q

b and t cell inhibitors dental notes:
 what rx’s? can reduce effectiveness of mycophenolate
 Risk for?

A

 Antacids and PPIs can reduce effectiveness of mycophenolate
 Risk for infection increased while taking

161
Q

 Directly damage cell DNA
 Impairs replication & transcription= cell death
 Work in all phases of the cell cycle
 Can be used in many different cancers

A

Alkylating Agents
 moa?
 cell cycle specific?
 Can be used in?

162
Q

Nitrogen Mustards
Platinum Compounds
Nitrosoureas
Alkyl sulfonates
Triazines
Ethylenimines

A

alkylating agents classes

163
Q

 cyclophosphamide (Cytoxan®), chlorambucil, ifosfamide, melphalan

A

Nitrogen Mustards:

164
Q

 cisplatin, carboplatin, oxaliplatin

A

Platinum Compounds:

165
Q

 streptozocin, carmustine (BCNU), and lomustine

A

Nitrosoureas:

166
Q

 dacarbazine (DTIC) and temozolomide (Temodar®)

A

Triazines:

167
Q

 thiotepa and altretamine (hexamethylmelamine)

A

Ethylenimines:

168
Q

interfere with DNA and RNA growth by substituting for or competing with the normal building blocks of DNA and RNA
 i.e. the availability of normal purine or pyrimidine nucleotide precursors
 May either by inhibiting the synthesis of normal nucleotides or compete with them in the formation of DNA or RNA

A

antimetabolites moa

169
Q

 Folate antagonists
 Pyrimidine antagonists
 Purine antagonist

A

Antimetabolites types

170
Q

methotrexate, pemetrexed

A

Folate antagonists names

171
Q

5-Fluorouracil (5FU), Cytarabine, gemcitabine

A

Pyrimidine antagonists:

172
Q

Mercaptopurine, Fludarabine

A

Purine antagonists

173
Q

Inhibit precursors to DNA synthesis

A

 Folate antagonists, Pyrimidine antagonists, Purine antagonist moa

174
Q

 Bind to and break DNA inside cancer cell to keep them from growing
and multiplying

A

Cytotoxic Antibiotics

175
Q

 Anthracyclines: Doxorubicin, daunorubicin, epirubicin, idarubicin.
 Other: bleomycin, plicamycin, mitomycin

A

cytotoxic abx groups

176
Q

 Work in M-Phase to prevent cell division

A

Mitotic Inhibitors

177
Q

 Vinca Alkaloids: Vincristine, Vinblastine
 Taxanes: Paclitaxel, Docetaxel

A

mitotic inhibitor groups include:

178
Q

 Cisplatin
 Cyclophosphamide
 Doxorubicin
 5-Fluorouracil
 Methotrexate
 Paclitaxel
 Vincristine

A

common meds of taste of alterations

179
Q

 Cyclosporine (Sandimmune)
 Tacrolimus (Prograf; FK506)
 Sirolimus (Rapamune)
 Everolimus (Zortress)

A

T-cell Inhibitors

180
Q

 Azathioprine (Imuran)
 Leflunomide (Arava)
 Mycophenolate (Cellcept)

A

T-cell and B-cell inhibitors

pharm 2 (20 decks)

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