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Pharm 2 > Anticancer Drugs & Immunosuppressants > Flashcards

Anticancer Drugs & Immunosuppressants 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 the environment
and lifestyle of a person
(3)
 Multitude of theories on cancer pathophysiologic process

A

150
Second
1,500
25

 Smoking
 Obesity
 Alcohol consumption

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2
Q

Neoplasia
(4)

A

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

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3
Q

Neoplasm
(2)

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

Normal tissue renewal and repair
involves 2 components

A

 Proliferation
 Differentiation

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6
Q

Cell cycle is orderly chain of events
(3)

A

 Duplicate contents & divide
 Genetic information is distributed to
“daughter cells”
 Checkpoints for pauses or arrests in
proliferation

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7
Q

— is hallmark characteristic of
cancer cells

A

Abnormal and rapid proliferation of
cells

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8
Q

Cell Differentiation
 Proliferating cells become
progressively more —
 Cells have a specific set of …
 As cells differentiate, their capacity
for — diminishes
 — cells are hallmark
characteristic of cancer cells

A

specialized
structural,
functional, and life-expectancy
characteristics
proliferation
Undifferentiated

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9
Q

Cell Growth Gone Wrong: Cancer
 Unchecked growth that progresses toward limitless expansion
(3)
 Causation – (2)

A

 Abnormal and rapid proliferation
 Loss of differentiation
anaplasia

genetic & external

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10
Q

Carcinoma

A

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

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11
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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12
Q

Lymphoma

A

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

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13
Q

Leukemia

A

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

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14
Q

Invasion & Metastasis
 Solid tumors secrete enzymes that …
 Complete surgical removal difficult
 Cancer cells may travel and “seed” into different body cavities
where they can …

A

break down proteins and
contribute to infiltration, invasion, and penetration of
surrounding tissues

proliferate and cause tumor growth (metastasis)

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15
Q

Cancer cells may travel and “seed” into different body cavities
where they can proliferate and cause tumor growth (metastasis)
(3)

A

 Blood vessel and lymphatic spread
 Finely orchestrated; selected cells only
 Angiogenesis

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16
Q

–% o f b r e a s t c a n c e r p a t i e n t s d e v e l o p b o n e m e t a s t a s e s

A

7 0

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17
Q

C u r r e n t b r e a s t c a n c e r t r e a t m e n t g u i d e l i n e s r e c o m m e n d
p o s t m e n o p a u s a l w o m e n w h o r e c e i v e c h e m o t h e r a p y a f t e r s u r g e r y f o r
e a r l y - s t a g e b r e a s t c a n c e r w i t h a h i g h r i s k o f r e c u r r e n c e s h o u l d a l s o
r e c e i v e

A

b i s p h o s p h o n a t e t r e a t m e n t a f t e r s u r g e r y

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18
Q

a l s o i n d i c a t e d f o r t h e m a n a g e m e n t o f — f o r
m o s t p a t i e n t s w i t h s o l i d t u m o r s

A

m e t a s t a t i c b o n e d i s e a s e

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19
Q

Metastasis & Use of Bisphosphonates in Cancer
(3)

A

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

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20
Q

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

A

70

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21
Q

in women with early — cancer
 reduce the risk of bone metastases and provide an overall survival benefit compared to
placebo or no bisphosphonates

A

breast

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22
Q

n women with metastatic breast cancer and bone metastases
 reduce the risk of developing (3)

A

skeletal-related events (SRE), delay the median time to an
SRE, and appear to reduce bone pain compared to placebo or no bisphosphonat

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23
Q

MOA: Bisphosphonates
(3)

A

 Inhibit osteoclast
 Reduce osteoclast genesis and
recruitment
 Promoting osteoclast apoptosis

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24
Q

 Inhibit osteoclast
(2)

A

 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

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25
Q

Tumor cells secrete:

A

 parathyroid hormone related peptide (PTHrP) as the primary
stimulator of osteoclastogenesis
 interleukin-6 (IL-6), prostaglandin E2 (PGE2), tumor necrosis
factor (TNF), and macrophage colony-stimulating factor (M-CSF)
 increase RANK ligand expression, which directly acts on osteoclast
precursors to induce osteoclast formation and bone resorption

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26
Q

bone resorption process releases:

A

 transforming growth factor-beta (TGF-β), which increase PTHrP
production by tumor cells as well as growth factors (eg, insulin-
like growth factors [IGFs], fibroblast growth factors [FGFs],
platelet-derived growth factor [PDGF], bone morphogenetic
proteins [BMPs]) increasing tumor growth

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27
Q

Symbiotic relationship further increases (2)

A

bone destruction and
tumor growth

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28
Q

Dental Concerns: Bisphosphonates
(3)

A

 AntiResorptive-associated
OsteoNecrosis of the Jaw (ARONJ)
 Medication Related ONJ (MRONJ)
 Precipitated by extractions or
periodontal and implant procedures

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29
Q

 AntiResorptive-associated
OsteoNecrosis of the Jaw (ARONJ)
 —% on IV bisphosphonates

A

1-10

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30
Q

 Medication Related ONJ (MRONJ)
(4)

A

 Reduced levels of osteoclast
- Necrotic bone is maintained
- New bone deposited on necrotic bone
 Includes Denosumab (Xgeva) &
Antiangiogenic Medications

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31
Q

Dental Concerns: Bisphosphonates
Risk factors:

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

Median time to onset of MRONJ
was 15 to 16 months
 63 (1.9%) on denosumab and 44
(1.3%) on zoledronic acid
developed MRONJ
 Cumulative incidence increased
with longer duration of exposure
 Dental extraction preceded
MRONJ event in –% of cases

A

63

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33
Q

Study on ONJ Risk
 Prospective observational study assessed cumulative incidence of ONJ at 3 years in
metastatic bone disease pts from any malignancy receiving zoledronic acid
 3,491 evaluable pts (breast 1,120; myeloma 580; prostate 702, lung 666, other 423)
between 2009-2013
 2/3 of pts had a baseline dental exam
 87 pts developed confirmed ONJ
 cumulative incidence of ONJ –% at year 1, –% at year 2, and –% at year 3
 Rates of 3-year confirmed ONJ highest in myeloma pts (4.3%)
 Fewer total number of teeth, presence of dentures and any oral surgery at baseline were all
associated with a higher rate of ONJ
 Conclusion: 1 in 40 patients on zoledronate for metastatic bone disease developed ONJ
 Cancer type, and oral health effect risk

A

0.8
2.0
2.8

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34
Q

Non-Cancer Versus Cancer Indication
 Low-risk for osteoporosis dosed bisphosphonates – 0.1%
 ADA – “recommends that a patient with active dental or periodontal disease …

A

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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35
Q

Additional Considerations
(4)

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)

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36
Q

Non-Cancer Versus Cancer Indication
 High-risk for oncologically dosed bisphosphonates – 2-18%
 ADA – does not address
 AAOMS – “…

A

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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37
Q

Monocolonal Antibodies: Denosumab

A

 Murine antibody that recognizes specific antigen

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38
Q

Humanised’
Murine Antibody:
(3)

A

 induce a human anti-mouse antibody immune response
 activate human immune effector mechanisms poorly
 short t1/2 in humans

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39
Q

Toxicities – Infusion Reactions
 Typical include (5)
 within 30 minutes to two hours of initiation of drug infusion, symptoms may be
delayed for up to 24 hours
 Premedication with (2) is indicated

A

fever, chills, nausea, dyspnea, and rashes

diphenhydramine and acetaminophen

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40
Q

Denosumab Risk of MRONJ
 High Dose Denosumab :
 Xgeva :

A

High prevalence (2-5% Osteonecrosis)

Bone cancer treatment - same prevalence as bisphosphonate
 120mg every 4weeks

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41
Q

 Low Dose Denosumab:
 Prolia :

A

Rare Osteonecrosis
 Weak evidence (case reports)

Osteoporosis treatment
 60mg every 6months

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42
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

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43
Q

Postulated that MRONJ is a form of avascular necrosis, possibly caused
by 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.

44
Q

Angiogenesis =

A

the development of new blood vessels

45
Q

Angiogenesis = the development of new blood vessels
(3)

A

 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
 Various inhibitors of angiogenesis have been developed and introduced into oncology
practice

46
Q

Various inhibitors of angiogenesis have been developed and introduced into oncology
practice
(4)

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).

47
Q

Angiogenesis Inhibitor: Bevacizumab
 Bevacizumab (Avastin)- humanized;
binds VEGF-A
(5)

A

 Used in solid tumor cancers
 Specifically recognize and bind to VEGF.
- Once bound, the complex is unable to activate the
VEGF receptor.
 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

48
Q

Note:
 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

A

antiangiogenic
agents in patients ALSO receiving antiresorptive agents

49
Q

International Task Force on Osteonecrosis of the Jaw

A

 2015 systematic review and international consensus paper
 For patients whose cancer management includes treatment with denosumab or IV
bisphosphonates, recommends
 “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.”

50
Q

American Society of Clinical Oncology (ASCO) – 2017

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.”

51
Q

Cancer Treatment
 Goal of therapy based on severity of illness
(3)

A

 Curative
 Control
 Palliative

52
Q

Multiple modalities utilized
(5)

A

 Surgery
 Radiation therapy
 Chemotherapy
 Hormonal therapy
 Biotherapy

53
Q

— care for clinical manifestations and/or treatment adverse reactions

A

Supportive

54
Q

Chemotherapy Agents
 Multiple cancer chemotherapeutic agents
(4)

A

 Adjuvant vs. neoadjuvant
 Various mechanisms of action
 slow/stop cell proliferation
 Reach ‘microscopic’ cancer cells

55
Q

Adverse reactions limit use
(3)

A

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

56
Q

Antineoplastic Medications
(5)

A

 Cytotoxic drugs
 Hormones
 Monoclonal antibodies (MABs)
 Protein Kinase Inhibitors
 Miscellaneous

> 100 various agents

57
Q

 Cytotoxic drugs
(4)

A

 Alkylating agents
 Antimetabolites
 Cytotoxic antibiotics
 Plant derivatives

58
Q

Alkylating Agents
(4)

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
 Due to affect on DNA, big impact on bone marrow
- Bone Marrow Suppression – reduce blood cell
production
- Highly immunosuppressant
 Toxicity related to cumulative dose
- Mucosal damage – oral mucosal ulceration
- GI disturbance
- Sterility
- Acute non-lymphocytic leukemia

59
Q

Alkylating Agents
(6)

A

 Nitrogen Mustards:
 Platinum Compounds:
 Nitrosoureas: (brain tumors)
 Alkyl sulfonates:
 Triazines:
 Ethylenimines:

60
Q

 Nitrogen Mustards:

A

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

61
Q

 Platinum Compounds:

A

 cisplatin, carboplatin, oxaliplatin

62
Q

 Nitrosoureas: (brain tumors)

A

 streptozocin, carmustine (BCNU), and lomustine

63
Q

 Alkyl sulfonates:

A

 busulfan

64
Q

 Triazines:

A

 dacarbazine (DTIC) and temozolomide (Temodar®)

65
Q

 Ethylenimines:

A

 thiotepa and altretamine (hexamethylmelamine)

66
Q

Noteworthy: Platinum Compounds – Cisplatin, Oxaliplatin
 Neurotoxicity

A

 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

67
Q

Oxaliplatin associated:

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%

68
Q

Antimetabolites are structurally related to

A

normal compounds that exist
within the cell

69
Q

Antimetabolites interfere with DNA and RNA growth by

A

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

70
Q

Their maximal cytotoxic effects are in

A

S-phase
 Synthesis – DNA replicates, yielding two separate sets

71
Q

Antimetabolites
 Folate antagonists:
 Pyrimidine antagonists:
 Purine antagonist:
=== Inhibit precursors to DNA synthesis

A

methotrexate, pemetrexed
5-Fluorouracil (5FU), Cytarabine, gemcitabine
Mercaptopurine, Fludarabine

72
Q

Methotrexate
(2)

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

73
Q

Methotrexate
Dental Note: oral mucositis
(3)

A

 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

74
Q

Cytotoxic Antibiotics
(2)

A

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

75
Q

Cytotoxic Antibiotics
 Groups:
 Anthracyclines: (4)
 Other: (3)

A

Doxorubicin, daunorubicin, epirubicin, idarubicin.

bleomycin, plicamycin, mitomycin.

76
Q

Mitotic Inhibitors

 Groups include:
 Vinca Alkaloids: (2)
 Taxanes: (2)

A

Work in M-Phase to prevent cell division

Vincristine, Vinblastine
Paclitaxel, Docetaxel

77
Q

Example: Vincristine

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

78
Q

Side Effects: Cell Replication Inhibition
(4)

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)

79
Q

 Impairment of bone marrow (myelosuppression)

A

 suppressing white blood cells, red blood cells, and platelets
 GET LABS THE DAY BEFORE ANY PROCEDURE
 WBC >2000
 ANC >2000
 Platelets >75,000

80
Q

Oral Complications Common to Chemotherapy & Radiation
(7)

A

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

81
Q

 Oral mucositis (20-40%):

A

inflammation and ulceration of the mucous membranes

 can increase the risk for pain, oral and systemic infection, and nutritional compromise.

82
Q

 Infection: viral, bacterial, and fungal

A

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

83
Q

 Xerostomia/salivary gland dysfunction: dry mouth d/t thickened, reduced, or absent salivary flow
(2)

A

 increases the risk of infection and compromises speaking, chewing, and swallowing
 persistent dry mouth increases the risk for dental caries

84
Q

 Functional disabilities: impaired ability to eat, taste, swallow, and speak

A

 due to mucositis, dry mouth, trismus, and infection.

85
Q

 Taste alterations:

A

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

86
Q

 Nutritional compromise:

A

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

87
Q

 Abnormal dental development:

A

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

88
Q

Taste Alterations - Chemotherapy
 Common occurrence following
chemotherapy administration
 Lasts 3-4 weeks post-treatment
 Commonly associated with:
(7)

A

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

89
Q

—% of the patients reported taste alterations during
at least one assessment time, and 14.6% reported at all
assessment times during the study period

A

69.9%

90
Q

Other Complications
 Neurotoxicity:

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)

91
Q

 Bleeding:

A

oral bleeding from the decreased platelets and clotting factors

92
Q

 Radiation caries:

A

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

93
Q

 Osteonecrosis:

A

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

94
Q

Disease States for Immunosuppression
 Autoimmune, collagen, connective tissue and inflammatory disorders

A

 Systemic Lupus erythematosus
 Rheumatoid arthritis
 Chronic active hepatitis
 Inflammatory bowel disease
 Glomerulonephritis
 Nephrotic syndrome
 Myasthenia gravis
 …among others…
 Organ or tissue transplantation
 Prevent rejection

95
Q

Target of Immunosuppression

A

 Inhibit mononuclear cells
(lymph and blood cells)

96
Q

Immunosuppressants
(3)

A

 T-cell Inhibitors
 T-cell and B-cell inhibitors
 Corticosteroids = Glucocorticoids

97
Q

 T-cell Inhibitors
(4)

A

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

98
Q

 T-cell and B-cell inhibitors
(3)

A

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

99
Q

 Corticosteroids = Glucocorticoids
(2)

A

 Prednisone, dexamethasone, prednisolone, etc
 Will cover – 4/19 – Adrenal Cortex – Dr. Knell

100
Q

T-Cell Inhibitors
(3)

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

101
Q

Cyclosporine – Side Effects
(4)

A

 Gingival hypertrophy
 Infection risk
(immunosuppressant)
 Hypertension/Kidney Impairment
- Avoid NSAIDs and Bactrim
 DRUG INTERACTIONS!!!

102
Q

 Gingival hypertrophy
(2)

A

 May be additive with CCBs (nifedipine,
amlodipine)
 Case reports suggest tx’d with 2-week
course metronidazole (750mg po TID)
while cyclosporine continued

103
Q

Drug Interactions
(7)

A

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

104
Q

T-Cell and B-Cell Inhibitors
 MOA:

A

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

105
Q

T-Cell and B-Cell Inhibitors
 Dental Notes
(2)

A

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

Pharm 2 (13 decks)

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