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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
Q

What is sustained angiogenesis?

A

Growth of new blood vessels

Source of O2 & nutrients

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26
Q

What is the role of P53 (protein)?

A

A tumor suppressor

Triggers production of cell cycle inhibitor

Allows activation of DNA repair enzymes

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27
Q

When is p53 activated?

A

At G1 checkpoint which controls transition to S phase

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28
Q

Telomeres are

A

DNA end caps that prevents loss of genes as chromosome end

Shortened & losses related to cellular aging

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29
Q

What is telomerASE

A

Enzyme that extends telomeres

Reverses telomere shortening

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30
Q

Contemporary therapy aims to

A

Harness the power of intrinsic immune system actions

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31
Q

What is the target of chemotherapy?

A

Cells that are actively undergoing DNA synthesis or mitosis

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32
Q

4 anesthetic considerations of chemo

A

N/v or diarrhea
Kidney issues
Liver issues
Fluid balance

33
Q

What is CIPN

A

Common (chemo induced peripheral neuropathy) which can effect pain management & regional anesthesia

34
Q

Alkylating agents work where?

A

In all phases

35
Q

MOA for Alkylating agents

A

Form covalent alkyl bonds w/ nucleus acid (DNA) bases

Forms intra/interstrand DNA crosslinks

Impairs DNA structure

Inhibits replication & transcription

36
Q

Alkylating agents are indicated for

A

Hematologic malignancy

Solid tumors

37
Q

Alkylating agents adverse effects

A

Bone marrow suppression (lymphocytopenia w/in 24h & hemolytic anemia

Gonadal dysfunction

GI disturbance (hypertrophy & shedding)

38
Q

Alkylating agents effects on CNS

A

N/v

Muscle weakness

Seizure

39
Q

Alkylating agents can cause

A

Follicular damage (alopecia)

40
Q

Alkylating agents effects on pulmonary

A

Pneumonitis

Pulmonary fibrosis

Decreased diffusion capacity

41
Q

Alkylating agents effects on heart

A

Cardiotoxic

Pericarditis, pericardial effusion (tamponade)

Hemorrhagic myocarditis w/CHF

42
Q

Alkylating agents can cause

A

Hepatotoxic

New/secondary malignancy

Phlebitis & thrombophlebitis

43
Q

Alkylating agents can inhibit

A

Plasma cholinesterase for up to 2-3 weeks which can lead to a prolonged paralysis with Suxx

44
Q

Alkylating agents can cause this with the kidney

A

Nephropathy related to uric acid

(Allopurinol)

45
Q

Alkylating agents can have acquired

A

Resistance to alkylating therapy

Decreased cell permeability

Increased production of competitive substances

46
Q

Common Platinum Complexes

A

Cisplatin

Carboplatin

47
Q

Platinum Complexes are

A

Non cell specific and are alkylating like agents (Damaging all phases)

48
Q

MOA of Platinum Complexes

A

Crosslinks adjacent or opposing bases to disrupt DNA

Inhibit essential cellular processes

Inhibit enzyme involved in replication & division

49
Q

Which Platinum Complexes is mostly used?

A

Cisplatin for Solid tumors

50
Q

Adverse effects for Cisplantin, a Platinum Complex

A

Black box- nephrotoxic ( decreased GFR, increased creatinine)

Renal tubular necrosis leading to renal failure

51
Q

Effects of Cisplatin, a Platinum Complex on the ears

A

Ototoxic

Tinnitus

Hearing loss

52
Q

Effects of Cisplatin, a Platinum Complex on periphery

A

Black box- peripheral neuropathy

Sensory neuropathy

Paresthesia

Loss of vibratory & position sensation

All reversible

53
Q

Effects of Cisplatin, a Platinum Complex on bone

A

Myelosuppression

Leukopenia

Thrombocytopenia

54
Q

Effects of Cisplatin, a Platinum Complex on GIT

A

n/v- black box

55
Q

Effects of Cisplatin, a Platinum Complex, can cause hypersensitive reactions such as

A

Facial edema

Bronchoconstriction

Tachycardia

HOTN

56
Q

Antimetabolites is cell cycle specific with a MOA of

A

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
Q

Antimetabolites indications

A

Hematologic

Psoriasis (methotrexate)

RA

Solid tumors

58
Q

Antimetabolites effects

A

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
Q

Topoisomerase inhibitors are cell cycle specific with a MOA of

A

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
Q

Anthracycline anti tumors antibiotics

A

Create free radicals to break DNA strands

61
Q

Topoisomerase inhibitors indications

A

Solid tumors
Hematologic

62
Q

Topoisomerase inhibitors & antitumor adverse effects on CV

A

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
Q

Dexrazoxane is a

A

Free radical scavenger & protective against damage

64
Q

Topoisomerase inhibitors & antitumor adverse effects on lungs

A

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
Q

Topoisomerase inhibitors & antitumor anesthesia considerations

A

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
Q

Topoisomerase inhibitors & antitumor adverse effects

A

Myelosuppression

GI disturbances

Alopecia

67
Q

Microtubule inhibitors are cell specific & have a MOA of

A

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
Q

Microtubule inhibitors adverse effects

A

Myelosuppression

Autonomic neuropathy (ortho HOTN, decreased GI motility, laryngeal nerve paralysis-hoarseness, urinary retention, dry mouth, tachycardia

69
Q

The Microtubule inhibitors, Taxanes effects on the heart

A

Dysrhythmias

Ischemia

Edema

Effusion

70
Q

The neuromuscular effects of Microtubule inhibitors

A

Atonal demylenation

Sensory motor neuropathy

Areflexia

Paresthesia

Skeletal muscle pain weakness & ataxia

71
Q

Microtubule inhibitors effects of periphery

A

Peripheral neuropathy

Smirks of worsening neuropathy w/ regional & general

Use lowest concentration of local

AVOID EPI additives

Use nerve location technique

72
Q

Signal transduction modifiers (hormone) MOA

A

Variable

Normal cells require GF a/specific receptors

Hormonal tx disrupts growth factor- receptors interactions

Targets over expression

73
Q

Signal transduction modifiers are indicated for

A

Solid tumors

Autoimmune disease

74
Q

Signal transduction modifiers side effects

A

Thromboembolic events & stroke

Increased risk CV disease

Secondary malignancy (tamoxifen) leading to uterine CA

Hepatotoxic

Wt gain

Myalgia arthralgia fractures

75
Q

Signal transduction modifiers can cause

A

GI disturbances

Hormonal changes

76
Q

Immunomodylatory drugs

A

Treat multiple myeloma

Antiproliferative antiangiogenic imnunomodulatory effects

Thalidomide. Lenalidomide

Pomalidomide

77
Q

Cancer immunotherapies

A

Bind immune checkpoints proteins

Reprogram T cells to attack cancer cells

Inflammatory side effect tx with corticosteroids & immunosuppressants

78
Q

Adoptive cellular therapy autologous T cells

A

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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