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Pharm > Cancer > Flashcards

Cancer Flashcards

1
Q

most common causes of death in US

A

1st: heart disease
2nd: cancer

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2
Q

most common sites of cancer in men

A
  1. prostate
  2. lung and bronchus
  3. colon and rectum
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3
Q

most common sites of cancer in women

A
  1. breast
  2. lung and bronchus
  3. colon and rectum
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4
Q

What is cancer?

A
  • A collection of diseases which share
    common characteristics:
  • Uncontrolled cell proliferation
  • Insensitivity to anti-growth signals
  • Prevention of cells to self-destruct through apoptosis
  • Limitless replicative potential
  • Sustained angiogenesis
  • Tissue invasion and metastasis
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5
Q

Cancer develops when…

A

a normal cell becomes abnormal

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6
Q

cancer often involved the malfunction of what?

A
  • genes that control cell growth, cell division, or
    cell death
  • Activation of proto-oncogene
  • down-regulation of tumor-suppressor gene
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7
Q

What do Onco-genes do?

A

essentially put the “brakes” on apoptosis and cause normal cells to reproduce relatively unchecked

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8
Q

What does tumor suppressor gene provide?

A
  • inhibitory signals that lead to the cessation of cell division and DNA transcription
  • Mutations in these genes are considered a loss of function –> genomic instability and the
    potential for cancer initiation
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9
Q

Sequence of events necessary for successful metastatic spread:

A
  • Detachment and escape from primary tumor site
  • Invasion of surrounding tissues and penetration into circulatory or lymphatic channels and survival without detection
  • Invasion and colonization at a distant site.
  • Once invasion of a new site occurs, persistent survival in this environment, and subsequent angiogenesis for further proliferation, require additional mechanisms and capabilities
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10
Q

Cancer causes - risk factors?

A
  • Genetic factors
  • physical carcinogens
  • chemical carcinogens
  • biological carcinogens
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11
Q

Genetic factors

A

up to 10% of all cancers can be caused by inherited genetic changes

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12
Q

physical carcinogens

A

UV and ionizing radiation

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13
Q

chemical carcinogens

A

asbestos, tobacco smoke, arsenic, aflatoxin

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14
Q

biological carcinogens

A
  • Infections from certain viruses, bacteria, and parasites
  • Human papilloma virus (HPV), Hepatitis B virus (HBV), Hepatitis C virus (HCV), and Helicobacter
    pylori (H. pylori)
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15
Q

Categories of drugs used to treat cancer

A
  • Chemotherapy
  • Immunotherapy
  • Target therapy
  • Anti-hormonals
  • Often used in combinations and come in the form of liquid or pills
  • Each has a diverse target with a distinct mechanism of action (MOA)
  • Many have a narrow therapeutic index (TI)
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16
Q

Main goal of chemotherapy

A
  • Eliminate the cancer cells without affecting normal tissues
  • Cytotoxic drugs affect both normal and cancerous cells
  • Aim for a favorable therapeutic index
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17
Q

cost of chemotherapy

A
  • one of the most expensive medical conditions
  • patents and survivors of cancer are more likely to have financial toxicity than those without cancer
  • CAR-T cell therapy is $475,000 for one treatment
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18
Q

What can limit the dose of chemotherapy

A
  • Toxicity
  • Poor selectivity of drugs for cancer cells versus normal cells means both healthy and cancerous cells are affected
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19
Q

Which tissues are often the cause of dose-limited toxicities

A
  • Bone marrow
  • GI tract (primarily the mucosal lining)
  • Skin
  • Germinal cells (sperm & ova)
  • Hair follicles
    (tissues with high growth rates)
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20
Q

Implications for physical therapy

A
  • A clear understanding of the complex and ever-changing use of chemotherapeutics and supportive medications is one of the most challenging parts of working with people with cancer
  • Important to understand the clinical aims, MOA, and adverse effects of antineoplastic agents to provide optimal care
  • A comprehensive rehabilitation program can improve a person’s ability to tolerate
    a more aggressive treatment regimen
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21
Q

Common Toxicities - Myelosupression

A
  • inhibition of bone marrow cells resulting in fewer red blood cells, white cells, and/or platelets
  • Neutropenia, Thrombocytopenia, Anemia
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22
Q

Neutropenia

A
  • Low white bloods cell count
  • Increased risk of infection
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23
Q

Thrombocytopenia

A
  • Low platelet count
  • Bruising, nosebleeds, and/or bleeding gums
  • Malaise, fatigue, and weakness
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24
Q

Anemia

A
  • Low red blood cell count
  • Vague symptoms: tiredness, weakness, SOB, decreased activity tolerance
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25
Q

Common toxicities: GI system

A
  • Diarrhea
  • Nausea, vomiting
  • Stomatitis –> Inflammation and ulceration of the oral mucosa
  • Mucositis –> Painful inflammation or ulceration of the mucus membranes anywhere in the GI tract
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26
Q

Common Toxicities: Integumentary

A

Hand Foot Syndrome

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27
Q

What is hand foot syndrome

A
  • Pain, redness, peeling of the skin on palms and/or soles of the feet
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28
Q

Treatment for hand-foot syndrome

A
  • Adjusting does of chemotherapy or changing the drug
  • May reduce efficacy of cancer treatment
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29
Q

Integumentary - Management

A
  • Corticosteroid creams
  • Skin moisturizers
  • Pain relievers: oral or topical
  • Avoid activities that cause friction on palms
    or soles
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30
Q

Common Toxicities: Nervous System

A
  • Chemotherapy-Induced Peripheral Neuropathy (CIPN)
  • Common, potentially debilitating and dose-limiting side effect of cancer treatment that
    may occur when chemotherapeutic agents damage the peripheral nerves
  • Pathophysiology is poorly understood
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31
Q

Symptoms of chemotherapy-induced peripheral neuropathy

A
  • Begin in the hands and feet and move proximally
  • Pain, burning, tingling, numbness, electric shock, pins and needles, temperature sensitivity
  • Affect ADLs and QoL
  • Can persist months to years after completion of chemotherapy
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32
Q

Chemotherapy- Induced Peripheral Neuropathy results in ….

A
  • Deficits in sensory, motor and/or autonomic functions
  • Sensory symptoms develop first – “glove and stocking” distribution –> Numbness, tingling, altered touch sensation, impaired vibration, paresthesias, dysesthesias induced by touch and warm or cool temperatures, painful sensations including spontaneous burning, shooting or electric-like pain
  • Motor symptoms – less frequent than sensory –> Distal weakness, gait and balance disturbances, impaired movements
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33
Q

Chemotherapy- Induced Peripheral Neuropathy results in ….

A
  • Deficits in sensory, motor and/or autonomic functions
  • Sensory symptoms develop first – “glove and stocking” distribution –> Numbness, tingling, altered touch sensation, impaired vibration, paresthesias, dysesthesias induced by touch and warm or cool temperatures, painful sensations including spontaneous burning, shooting or electric-like pain
  • Motor symptoms – less frequent than sensory –> Distal weakness, gait and balance disturbances, impaired movements
33
Q

Chemotherapy- Induced Peripheral Neuropathy results in ….

A
  • Deficits in sensory, motor and/or autonomic functions
  • Sensory symptoms develop first – “glove and stocking” distribution –> Numbness, tingling, altered touch sensation, impaired vibration, paresthesias, dysesthesias induced by touch and warm or cool temperatures, painful sensations including spontaneous burning, shooting or electric-like pain
  • Motor symptoms – less frequent than sensory –> Distal weakness, gait and balance disturbances, impaired movements
34
Q

CIPN - PT Management

A
  • Balance training
  • Strength training
  • Interactive sensory-based activities
  • Endurance training
35
Q

CIPN PT Management Outcomes

A

improved static and dynamic balance, reduction in CIPN symptoms, decreased postural sway, increased QOL, decreased pain, increased lower
extremity strength, improved TUG and BB

36
Q

Common Toxicities: Cancer-Related Fatigue

A
  • An unusual, persistent, subjective sense of tiredness related to cancer or cancer treatment that interferes with usual functioning
  • Likely the result of many causes
37
Q

What is PT most effective with?

A

Treating fatigue

38
Q

Diagnostic criteria for Cancer related fatigue

A
  • Period of 2 weeks or longer within the preceding month during which significant CRF or diminished energy was experienced each day along with additional CRF-related symptoms
  • Results in significant distress or impairment of function
  • Clinical evidence suggesting CRF = consequence of cancer or cancer therapy
  • CRF is not primarily a consequence of a concurrent psychiatric condition (major
    depression)
39
Q

Cancer Related Fatigue PT management

A
  • Nonpharmacological Interventions = EXERCISE
  • Aerobic, resistance, multimodal with higher intensity
  • Timing: safe and effective during treatment, post-treatment and survivorship
40
Q

General principles for treating CRF

A
  • 60% to 85% of maximal HR
  • At least 30 minutes, 3 times per week working up to a least 150 minutes of moderate or 75
    minutes of vigorous activity (ACSM guidelines for patients with cancer)
41
Q

How do Alkylating Agents work?

A
  • Cause cell death through transfer of their alkyl groups to various cellular constituents
  • May cause inhibition of DNA replication and transcription, mispairing of DNA, or DNA strand breakage.
  • Work in all phases of the cell cycle
42
Q

Dose limiting side effect of alkylating agents

A

myelosupression

43
Q

other side effects of alkylating agents

A

nausea/vomiting, alopecia, infertility, leukemia (!)

44
Q

What are platinum analogs?

A
  • Commonly classified as alkylating agents, but do
    not technically alkylate DNA
  • Activated forms of these drugs react with
    nucleophilic sites on DNA to form cross-links and
    decrease replication
45
Q

How do platinum analogs work?

A
  • Covalently binds to DNA and produce
    intrastrand (>90%) and interstrand (<5%) cross-links –> inhibition of DNA synthesis and inhibition of transcription
  • Tend to cause a variety of neurologic
    complications
46
Q

Antimetabolites

A
  • Structural analogs of naturally occurring substances in the body
47
Q

How do Antimetabolites exert damage?

A
  • Incorporating directly into DNA or RNA
  • Competing for binding sites on enzymes
  • Inhibit cell growth and proliferation in S phase of the cell cycle
48
Q

How do Topoisomerase Inhibitors work?

A
  • Topoisomerase family of enzymes alter the supercoiling of double-stranded DNA
  • A transient cut is formed in one or both strands of the DNA, allowing the supercoiled DNA to relax ahead of the replication fork as replication progresses
  • Regulation of DNA supercoiling is essential to transcription and replication.
  • Topoisomerase inhibitors bind to topoisomerase I or topoisomerase II and limit the ability of DNA to repair itself resulting in cell death
49
Q

Who does colorectal cancer often affect?

A
  • Affects men and women of all racial and ethnic groups
  • Most frequently diagnosed in individuals >50 years old
  • ~ 1:24 men and 1:25 women will develop colorectal cancer in the US
50
Q

Patients with chemotherapy for colorectal cancer often receive multiple drugs with what advantages?

A
  • Suppression of drug resistance
  • Increased cancer cell death rates
  • Reduced systemic toxicity
51
Q

How do anthracyclines

A
  • Multiple mechanisms of action
  • Inhibit topoisomerase II and prevent repair of DNA during replication causing DNA strand breaks
  • High affinity for binding to DNA and insert themselves between DNA base pairs causing additional DNA breaks.
  • Metabolized in the liver to form reactive oxygen species (e.g., oxygen free radicals), adding to both the cytotoxicity and adverse effect profile
52
Q

How do plant alkaloids work?

A

Cell cycle specific (active in M phase of the cell cycle)

53
Q

How do taxanes work?

A
  • Interfere with the G2 phase of the cell cycle
  • Arrest the cells that are in mitosis
54
Q

What are receptor tyrosine kinases?

A

proteins responsible for the activation of
signaling cascades important for many cellular functions, such as cell signaling and growth –> in some cases, RTKs become dysregulated and lead to cancer

55
Q

What are Tyrosine Kinase Inhibitors and how do they work? (targeted therapy)

A
  • TKI block the actions of RTKs to help in the management of certain types of
    cancer –> Small molecule drugs and can more easily enter the cell to reach their target
  • NOT cell cycle dependent
56
Q

how do Monoclonal Antibodies work? (targeted therapy)

A
  • Not cell cycle dependent
  • Make the cancer cell more visible to the immune system
  • Neutralize growth factors that are required by cancer cells thereby inhibiting tumor
    expansion
  • Deliver “toxic cargo” to the cancer cells
57
Q

how do monoclonal antibodies make the cancer cell more visible to the immune system

A
  • The immune system doesn’t always recognize cancer cells, mAbs can be directed to attach to
    cancer cells in order to “mark” them for destruction via antibody-dependent cell-mediated cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC)
58
Q

How do monoclonal antibodies deliver “toxic cargo” to the cancer cells?

A
  • mAbs can be conjugated or linked to anticancer drugs, radioisotopes, or biologic response
    modifiers so that when the antibodies bind with antigen-bearing cells, they deliver their load directly to the tumor
  • Activate the immune system to fight cancer by targeting Cytotoxic T- Lymphocyte Antigen
    4 (CTLA-4) or PD-1
59
Q

Women have a BLANK risk of developing breast cancer

A

1 in 8 lifetime risk

60
Q

what is present in the majority of breast cancers

A
  • estrogen receptors
61
Q

what plays in an important role in many treatment regimens

A
  • The modulation of estrogen levels
  • Direct – anti-estrogens
  • Indirect –aromatase inhibitors
  • Most ER+ breast cancers don’t overexpress HER2
62
Q

What works by blocking the estrogen receptor

A

tamoxifen
(typically pre menopausal, after you’ve gone through chemo)

63
Q

What inhibits the production of aromatase thereby reducing estrogen levels?

A

Exemestane

64
Q

How are estrogens synthesized

A
  • From cholesterol
  • Secreted primarily by the ovaries
  • Contributions from placenta, adipose tissue, and adrenal glands
65
Q

What does estrogen stimulate?

A
  • Stimulates development and maintenance of female characteristics and sexual reproduction
  • The breast and uterus, which play central roles in sexual reproduction, are two of the main targets of estrogen, but estrogen also acts on the brain, bone, liver, and heart
66
Q

How do aromatase inhibitors work?

A
  • Block growth of “estrogen sensitive“ tumors by lowering estrogen levels
  • Premenopausal Women –> AIs unable to effectively block the larger amounts of estrogen produced by the ovaries
  • Postmenopausal Women –> Almost complete suppression of estradiol secretion by adipose and breast tissue
67
Q

what are aromatase inhibitors associated with?

A
  • Majority of side effects are mild to moderate
  • Compared to tamoxifen, AIs are associated with a decreased risk of endometrial cancer and thromboembolic events and increased rates of fractures (osteoporosis)
68
Q

things about prostate cancer

A
  • Prostate cancer is the most common cancer in men; 2nd leading cause of cancer- related deaths in American men
  • A man’s lifetime risk of prostate cancer is 1:8
69
Q

What increases the risk of prostate cancer

A
  • Family History increases risk (1st degree relatives) –> BRCA1 and BRCA2 increase risk, but these account for a very small percentage of
    prostate cancer
  • When prostate cancer develops, the PSA level > 4
70
Q

Does prostate cancer typically cause symptoms?

A
  • not initially
  • By the time symptoms occur, the disease may have spread
  • Symptoms include decreased urinary stream, increased urinary frequency, hematuria,
    bladder/bowel incontinence, bone pain
71
Q

Androgen Production

A
  • Androgens are often necessary for prostate cancers to grow
  • Testosterone and dihydrotestosterone (DHT) are the most abundant androgens in men
  • Testosterone sources: testes (80-90%) and adrenal glands (10-20%)
  • Treatment of advanced prostate cancers usually involves some form of surgical or chemical castration to lower androgen levels
72
Q

how do anti-androgens work?

A

Inhibit testosterone from binding to its receptor –> blocking its effects in the body and preventing the stimulation of cell growth in prostate cancer

73
Q

Lifetime risks of developing lung cancer

A

1:16 men
1:17 women

74
Q

what accounts for most lung cancer cases and deaths

A
  • Cigarette smoking: about 80%
  • Second hand smoke is the 3rd most common cause of lung cancer
75
Q

What is epidermal growth factor receptor

A
  • Belongs to the HER family that includes
    EGFR (HER 1), HER2, HER3, and HER4
  • EGFR – 1st receptor proposed as a target
    for cancer therapy
76
Q

How is epidermal growth factor receptor activated?

A

through genetic mutations, genetic amplification, or both –> Changes are closely related to the
occurrence, progression, and prognosis of non-small cell lung cancer (NSCLC)

77
Q

Common EGFR mutations in NSCLC

A
  • 10 - 35% of patients with NSCLC have somatic changes in the kinase domain of their EGFR gene
  • The most common EGFR mutations include short in-frame deletions in exon 19 and a point mutation in exon 21 at codon 858 –> Together these account for 86% of the EGFR mutations detected
  • Activating EGFR mutations in NSCLC pts are more common in women, nonsmokers, and those of Asian ethnicity
78
Q

What do patients harboring activation EGFR mutations have?

A

an increased response to some EGFR TKIs

79
Q

initial overall response to EGFR TKIs

A
  • initially high for patients with EGFR mutations but almost all pts develop resistance

Pharm (12 decks)

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