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Health, Wellness, & Disease > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Cancer definition

A

Uncontrolled cell growth and the abnormal spread of those cells

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2
Q

Causes of cancer

A

Internal- DNA mutation, hormones, genetics
External- chemicals, sunlight, viruses
VERY VARIED

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3
Q

Benign tumors

A

Abnormal growth

Cell growth slow, well differentiated and doesn’t invade or metastasize

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4
Q

Malignant (cancerous) tumors

A
  • persistent proliferation (uncontrolled growth): population of cells growing at unregulated rate, loss of cells ability to differentiate into functional cells, inability of cells to die properly
  • local invasive growth
  • metastatic spread- lymphatic (lymph nodes, spleen) or hematologic (lungs, brain, liver, bone)
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5
Q

Cancer treatment strategies

A

Radiation therapy, surgery (biopsy, palliative, cure), chemotherapy (toxic to both cancer and healthy cells, dosed by BSA)

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6
Q

Fractional cell chemotherapy

A

Chemo kills the same percentage (not same number) of cells

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7
Q

Classifications of combination chemotherapy

A

Cytotoxic agents
Hormones
Hormone antagonists
*Can be cell cycle specific (effective during specific phase of cell) OR cell cycle NON-specific (effective during any stage of cell cycle)

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8
Q

Chemotherapy timing strategies

A
  • avoid resistance: inherent (hard to treat); acquired after drug exposure (changes in cell, enzyme target, cell repair, uptake/excretion
  • use a drug with a different cell cycle stage, mechanism, or site of action
  • try to minimize overlapping toxicities
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9
Q

Examples of cell-cycle specific anti-neoplasm drugs

A 
Methotrexate (S-phase)
Vincristne (M-phase)
Paclitaxel (M-phase)
Hydroxyurea (S-phase)
Bleomycin (G2-phase)
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10
Q

Examples of cell-cycle non-specific anti-neoplasm drugs

A

DNA alkylating agents- cyclophosphamide, melphalan, chlorambucil
Anthracycline antibiotics- doxorubicin, Texans
Corticosteroids- prednisone
Interferons- INF-alpha
Vascular epithelial growth factors (VEGF) antagonists- bevacizumab, sunitinib

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11
Q

Pharmacists role in oncology team

A

Dosing, chemo prep, pain control, personalized medicines
Education/drug info- patients and families
Monitoring- outcomes, side effects, complications, drug interactions
Preventions and early detection

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12
Q

Epigenetics definition

A

Study of heritable changes in gene function that don’t directly involve changes in the DNA sequence

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13
Q

Allele definition

A

Variant form of a location on a chromosome, often a variant of a specific gene

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14
Q

Chromosome definition

A

Chunk of the genome that encodes specific genes (chapter of book)

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15
Q

Halotype definition

A

Group of continuous alleles on a chromosome that are inherited together

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16
Q

Single nucleotide polymorphisms (SNP’s)

A

Type of allele with variations in the nucleotide sequence at a specific position

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17
Q

Indels definition

A

Insertions/deletions of short sequences of nucleotides

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18
Q

Introns definition

A

Non coding regions- removed during sequencing

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19
Q

Exons define

A

Coding region- join together during sequencing

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20
Q

Untranslated regions (UTR’s)

A

Sections on each side of the coding sequence

-carry info on what to do with RNA

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21
Q

Promoter definition

A

Initiates transcription of gene (DNA to RNA)

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22
Q

CpG methylation

A
  • most commonly studied epigenetic marker: methylation of cytosine
  • clusters of CpG sites can be found in gene promoters and regulate expression
  • site-specific dynamics: most stable, some changes in response to environment
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23
Q

Histone modifications

A

Characteristic signatures of promoters, enhancers, depressors found on modified residues of specific histone tails

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24
Q

Imprinting definition

A

Only one working copy of gene was inherited (instead of 2)

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25
Examples of cell-cycle non-specific anti-neoplasm drugs
DNA alkylating agents- cyclophosphamide, melphalan, chlorambucil Anthracycline antibiotics- doxorubicin, Texans Corticosteroids- prednisone Interferons- INF-alpha Vascular epithelial growth factors (VEGF) antagonists- bevacizumab, sunitinib
26
Pharmacists role in oncology team
Dosing, chemo prep, pain control, personalized medicines Education/drug info- patients and families Monitoring- outcomes, side effects, complications, drug interactions Preventions and early detection
27
Epigenetics definition
Study of heritable changes in gene function that don’t directly involve changes in the DNA sequence
28
Allele definition
Variant form of a location on a chromosome, often a variant of a specific gene
29
Chromosome definition
Chunk of the genome that encodes specific genes (chapter of book)
30
Halotype definition
Group of continuous alleles on a chromosome that are inherited together
31
Single nucleotide polymorphisms (SNP’s)
Type of allele with variations in the nucleotide sequence at a specific position
32
Indels definition
Insertions/deletions of short sequences of nucleotides
33
Introns definition
Non coding regions- removed during sequencing
34
Exons define
Coding region- join together during sequencing
35
Untranslated regions (UTR’s)
Sections on each side of the coding sequence | -carry info on what to do with RNA
36
Promoter definition
Initiates transcription of gene (DNA to RNA)
37
CpG methylation
- most commonly studied epigenetic marker: methylation of cytosine - clusters of CpG sites can be found in gene promoters and regulate expression - site-specific dynamics: most stable, some changes in response to environment
38
Histone modifications
Characteristic signatures of promoters, enhancers, depressors found on modified residues of specific histone tails
39
Imprinting definition
Only one working copy of gene was inherited (instead of 2)
40
Phenotype define
Observable trait of an individual
41
Penetrance define
Determines the probability that a person is carrying mutation A exhibits trait X -common genetic variants have low penetrate such as schizophrenia
42
What does PGx study?
Phenotypes AND drug responses, side effects, tailoring biomarkers, pharmacodynamic measures, pharmacokinetic profiles
43
What is the purpose of PGx?
PGx tests guide* treatment - less scientific rigor compared to clinical trials for new drugs * *exceptions- companion diagnostics which provide essential info used to select/exclude specific individuals for treatment. These tests are included in FDA drug labels and usually co-developed with therapeutic drug
44
PGx phenotypes: PK profiles
What is body doing to drug? - level of drug/metabolite; measured in circulation or other parts of body; elimination Level of drug reaching the desired target, or undesired target, drive response and side effects
45
Tell me about CYP’s and transporters
- cytochrome P450 family of drug- metabolizing enzymes (CYPs) [metabolism] - UGT’s- metabolism - solute carrier families (SLCs, OAT, OCTs)- absorption, distribution, excretion - ATP binding cassette families (ABCs, Pgp-1, MDR-1) absorption, distribution,excretion
46
Pharmacodynamic (PD) responses
Biochemical or physiological effect of drug on the body | Ex- what functional impact is the drug having
47
What are PD responses used for?
Used to measure pharmacologic activity- is your drug doing what it should be to the extent it should? - ideally measured adjacent to target and in same body compartment - ex: activity of receptor, enzyme behavior
48
Drug response define
Does subject show desired clinical response to drug? | Ex- 50% reduction in migraine headaches a month
49
PGx outcomes (side effects and serious adverse effects)
Most side effects and ADRs caught by FDA before approval but some require post-approval PGx studies Drawbacks- inconsistent side effect characterization, low sample numbers, difficulty merging results
50
How to measure genotypes
Low thorough-put: PCR based methods used to measure one genotype and get small amount of info from it- have to know what you’re looking for High thorough-put: SNP array methods; whole genome sequencing (WGS) can detect unknown/complex mutations genome-wide, but more expensive and laborious. LOTS of info provided from test
51
Where does PGx guidance come from
FDA- drug label | CPIC (clinical pharmacogenetics implementation committee)- what clinicians should be aware of, beyond the label
52
Models of stress
Stimulus-based: outcome is result of outside stress manipulation (ex- divorce) may leave out certain circumstances or emotions Response-based: stress defined by pattern of responses (ex- how we think/act) variables include those coming within Transactional: interaction between environment and individual (emphasize role of individuals appraisal of situations in shaping their responses)
53
Arousal/Activation Theory
Too much or little arousal degrades performance (either too much going on or not enough to do) -need little bit of stress to adapt and grow- reach “optimal” stress
54
General adaptation syndrome
Alarm phase- initial shock of stressor (excitability, increased adrenaline) countershock phase (defensive processes start) Resistance stage- alarm reaction disappears, organism has adapted to stressor, resistance to other stressors decrease Exhaustion stage- organism can no longer adapt, alarm symptoms appear again (resistance no longer possible, irreversible damage appears, organism dies) Limitations- appraisal important, lacks coping mechanisms, individual responses influences personality, perceptions (anticipation of stress) (not all responses to stress are uniform- assumes uncertainty and non-specificity)
55
Appraisal-coping method
Appraisal- explains individual differences in quality, intensity, duration of elicited emotion (Factors- motivational dispositions, goals, values, generalized expectancies) Coping- cognitive and behavioral efforts made to master, tolerate or reduce, tolerate or reduce external/internal demands and conflicts -primary: having to do with a persons well-being -Secondary: coping options
56
Allostatic load model
Physiological systems activated by stress cant only protect and restore, but can also damage the body Allostatic load- cumulative wear and tear that results of chronic over-activity (chronic stress) or under-activity (stressors happening over and over, we can only handle so much) 4 conditions- repeated hits of stress, failure to habituate to repeated stressors of the same kind, failure to turn off each stressor response in timely manner due to delayed shut down, inadequate responses that leads to compensatory hyperactivity of other mediators
57
Social readjustment rating scale
Identified events that force people to make changes in their lives -modest correlation between number of life-changing events in previous year to outcomes
58
Trait-oriented coping strategy
Views coping styles as personality dispositions that transcend the influence of situational context; emphasizes stability in coping vs change
59
State-oriented coping strategy
Actual coping by an individual and investigation of outcome - defense mechanisms: unconscious mechanisms such as denial, regression, projection, displacement - Appraisal-focused: directed towards challenging ones assumptions (adaptive cognitive) - problem-focused: directed towards reducing or eliminating a stressor (adaptive behavior- info seeking, taking control, evaluate pros/cons) - emotion-focused: directed towards changing ones own emotional reaction (imagining, blaming, socializing)
60
Monitoring and blunting
Individuals react with arousal according to the amount of attention they give the stressor Blunting- arousal levels lowered when person employs avoidant cognitive strategies Monitoring- focus on monitoring if event is controllable (seek more adaptive coping strategy)
61
Model of coping modes (MCM)
Most stressful situations characterized by vigilance and cognitive avoidance -arousal to stressor should stimulate the tendency to cognitively avoid further processing of cues related to encountere
62
Stress management techniques
- manage time, practice relaxation, exercise, eat right - spheres of influence- focus on what you CAN control - tend and befriend- female fight or flight oxytocin response where women tend to be nurturing after a stressful day while men tend to withdraw

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