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Pharmacology Exam 3 > Chemotherapeutics > Flashcards

Chemotherapeutics Flashcards

1
Q

Which interphases do cell spend most of their time

A

G1
S
G2

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2
Q

In interphase, cells will

A

Double; cytoplasm synthesis DNA

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3
Q

What happens is G0 phase?

A

Performing normal functions; not going through process of dividing

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4
Q

When is G0 phase signaled?

A

Signaled to progress through cell cycle by presence of growth factors & other signals

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5
Q

In G0 phase, mutated cells are

A

Permanent (avoids replication which is a good thing)

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6
Q

What happens in G1 phase

A

Cells recruited into the growth faction start G1

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7
Q

Which phase starts prior to DNA synthesis?

A

G1

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8
Q

Cell characteristics in G1 phase

A

Cells increase in mass & organelles in preparation for cell division; diploid w/2 sets of chromosomes

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9
Q

What happens in the S (synthesis) phase?

A

DNA synthesis

Duplication of chromosomes

Continued cell growth

DNA check point

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10
Q

Normally, if an error is found, what happens to the cell?

A

Either repaired or cellular apoptosis

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11
Q

When does G2 phase begin

A

Between DNA replication & start of miosis

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12
Q

Characteristics of cells in G2 phase

A

Synthesis of additional proteins & cellular mitotic materials

Continued cell growth

Additional DNA checkpoint

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13
Q

What happens in M phase

A

Cell divided into 2 daughter cells (4 phases)

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14
Q

In mitosis (M phase), prophase is when

A

Chromatin condenses into distinct chromosomes

Chromosomes migrate to center of cell

Nuclear envelope breaks down & spindle fibers form

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15
Q

In mitosis (M phase), metaphase includes

A

Nuclear membrane disappears

Spindle develops

Chromosomes align

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16
Q

In mitosis (M phase), anaphase involves

A

Paired chromosomes separate

Spindle fibers lengthen the cell

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17
Q

In mitosis (M phase) l, telophase involves

A

Chromosomes sectioned off into distinct new nuclei

Genetic content distributed equally

Cytokinesis begins

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18
Q

Cytokinesis involves

A

Division of cytoplasm in o form 2 new cells

Begins after anaphase & finishes after telophase

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19
Q

How are males giant cells characterized

A

Rapid division & synthesis of DNA

Multiply without growth factor

Genetic mutations (oncogenes)- overactive ; CA promoting

Problems with encoding regulator proteins

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20
Q

Mutations promote

A

Increased cell growth & division

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21
Q

Mutations escape

A

Internal & external division controls

Avoids programmed cell death (apoptosis)

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22
Q

Additional mutations are often required in

A

Tumor progression

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23
Q

Malignant tumors are insensitive to

A

Anti-growth signaling

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24
Q

Malignant tumors are

A

Groups of cells that divide excessively (self-sufficient)

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25
What is sustained angiogenesis?
Growth of new blood vessels Source of O2 & nutrients
26
What is the role of P53 (protein)?
A tumor suppressor Triggers production of cell cycle inhibitor Allows activation of DNA repair enzymes
27
When is p53 activated?
At G1 checkpoint which controls transition to S phase
28
Telomeres are
DNA end caps that prevents loss of genes as chromosome end Shortened & losses related to cellular aging
29
What is telomerASE
Enzyme that extends telomeres Reverses telomere shortening
30
Contemporary therapy aims to
Harness the power of intrinsic immune system actions
31
What is the target of chemotherapy?
Cells that are actively undergoing DNA synthesis or mitosis
32
4 anesthetic considerations of chemo
N/v or diarrhea Kidney issues Liver issues Fluid balance
33
What is CIPN
Common (chemo induced peripheral neuropathy) which can effect pain management & regional anesthesia
34
Alkylating agents work where?
In all phases
35
MOA for Alkylating agents
Form covalent alkyl bonds w/ nucleus acid (DNA) bases Forms intra/interstrand DNA crosslinks Impairs DNA structure Inhibits replication & transcription
36
Alkylating agents are indicated for
Hematologic malignancy Solid tumors
37
Alkylating agents adverse effects
Bone marrow suppression (lymphocytopenia w/in 24h & hemolytic anemia Gonadal dysfunction GI disturbance (hypertrophy & shedding)
38
Alkylating agents effects on CNS
N/v Muscle weakness Seizure
39
Alkylating agents can cause
Follicular damage (alopecia)
40
Alkylating agents effects on pulmonary
Pneumonitis Pulmonary fibrosis Decreased diffusion capacity
41
Alkylating agents effects on heart
Cardiotoxic Pericarditis, pericardial effusion (tamponade) Hemorrhagic myocarditis w/CHF
42
Alkylating agents can cause
Hepatotoxic New/secondary malignancy Phlebitis & thrombophlebitis
43
Alkylating agents can inhibit
Plasma cholinesterase for up to 2-3 weeks which can lead to a prolonged paralysis with Suxx
44
Alkylating agents can cause this with the kidney
Nephropathy related to uric acid (Allopurinol)
45
Alkylating agents can have acquired
Resistance to alkylating therapy Decreased cell permeability Increased production of competitive substances
46
Common Platinum Complexes
Cisplatin Carboplatin
47
Platinum Complexes are
Non cell specific and are alkylating like agents (Damaging all phases)
48
MOA of Platinum Complexes
Crosslinks adjacent or opposing bases to disrupt DNA Inhibit essential cellular processes Inhibit enzyme involved in replication & division
49
Which Platinum Complexes is mostly used?
Cisplatin for Solid tumors
50
Adverse effects for Cisplantin, a Platinum Complex
Black box- nephrotoxic ( decreased GFR, increased creatinine) Renal tubular necrosis leading to renal failure
51
Effects of Cisplatin, a Platinum Complex on the ears
Ototoxic Tinnitus Hearing loss
52
Effects of Cisplatin, a Platinum Complex on periphery
Black box- peripheral neuropathy Sensory neuropathy Paresthesia Loss of vibratory & position sensation All reversible
53
Effects of Cisplatin, a Platinum Complex on bone
Myelosuppression Leukopenia Thrombocytopenia
54
Effects of Cisplatin, a Platinum Complex on GIT
n/v- black box
55
Effects of Cisplatin, a Platinum Complex, can cause hypersensitive reactions such as
Facial edema Bronchoconstriction Tachycardia HOTN
56
Antimetabolites is cell cycle specific with a MOA of
Prevent synthesis of complementary DNA in S phase which acts as a FALSE nutrient (mimics folic acid) Enzyme inhibition Mimics nucleobases Stops DNA replication & cell proliferation
57
Antimetabolites indications
Hematologic Psoriasis (methotrexate) RA Solid tumors
58
Antimetabolites effects
High alert Resistance to therapy risks Bone marrow suppression (megaloblastic anemia) Pulmonary toxicity GI toxic Nephrotoxic Hepatotoxic Caution with nasal ‘ oral airway Ataxia Drowsiness Dermatological toxicity (photosensitive)
59
Topoisomerase inhibitors are cell cycle specific with a MOA of
Corrects DNA alterations during replication & transcription Inhibits topoisomerase 1 or 2 Inhibits uncoiling of DNA during replication Most active during S & early G 2 phase
60
Anthracycline anti tumors antibiotics
Create free radicals to break DNA strands
61
Topoisomerase inhibitors indications
Solid tumors Hematologic
62
Topoisomerase inhibitors & antitumor adverse effects on CV
Cardiotoxic (doxorubicin & daunorubicin) Free radicals disrupt cardiac protein & cell membrane components Increased troponin T CHF w/ impaired LV function Acute myopathy w/arrhythmias Fatal form associated w/ bronchitis & progressive ventricular failure
63
Dexrazoxane is a
Free radical scavenger & protective against damage
64
Topoisomerase inhibitors & antitumor adverse effects on lungs
Pulmonary toxic-Bleomycin Free radical production in presence of O2 ‘ iron/copper Capillary endothelial’ alveolar damage Pulmonary fibrosis Hypoxia dyspnea pneumonitis Pulmonary lesions & infiltrates Decreased pulmonary diffusion capacity
65
Topoisomerase inhibitors & antitumor anesthesia considerations
Post-op respiratory failure in bleomycin Risk w/ excessive crystalloid (use colloid & minimize fluids) Risk in presence of hyperoxia Keep inhaled 02 concentration below 30% Risk factors include pre-existing pulmonary damage or renal dysfunction
66
Topoisomerase inhibitors & antitumor adverse effects
Myelosuppression GI disturbances Alopecia
67
Microtubule inhibitors are cell specific & have a MOA of
Microtubules create cellular architecture & mediate cellular functions Vinca alkaloids (bind & inhibit microtubule formation) Taxanes (bind & inhibit microtubule breakdown) Active in M phase Mitosis phase fails & cell does w/o replicating
68
Microtubule inhibitors adverse effects
Myelosuppression Autonomic neuropathy (ortho HOTN, decreased GI motility, laryngeal nerve paralysis-hoarseness, urinary retention, dry mouth, tachycardia
69
The Microtubule inhibitors, Taxanes effects on the heart
Dysrhythmias Ischemia Edema Effusion
70
The neuromuscular effects of Microtubule inhibitors
Atonal demylenation Sensory motor neuropathy Areflexia Paresthesia Skeletal muscle pain weakness & ataxia
71
Microtubule inhibitors effects of periphery
Peripheral neuropathy Smirks of worsening neuropathy w/ regional & general Use lowest concentration of local AVOID EPI additives Use nerve location technique
72
Signal transduction modifiers (hormone) MOA
Variable Normal cells require GF a/specific receptors Hormonal tx disrupts growth factor- receptors interactions Targets over expression
73
Signal transduction modifiers are indicated for
Solid tumors Autoimmune disease
74
Signal transduction modifiers side effects
Thromboembolic events & stroke Increased risk CV disease Secondary malignancy (tamoxifen) leading to uterine CA Hepatotoxic Wt gain Myalgia arthralgia fractures
75
Signal transduction modifiers can cause
GI disturbances Hormonal changes
76
Immunomodylatory drugs
Treat multiple myeloma Antiproliferative antiangiogenic imnunomodulatory effects Thalidomide. Lenalidomide Pomalidomide
77
Cancer immunotherapies
Bind immune checkpoints proteins Reprogram T cells to attack cancer cells Inflammatory side effect tx with corticosteroids & immunosuppressants
78
Adoptive cellular therapy autologous T cells
Genetically engineered to recognize & attack tumor cells Risk for life threatening side effects such as release of cytokines & systemic inflammation

Pharmacology Exam 3 (3 decks)

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