Exam 1 Flashcards

1
Q

Cancer definition

A

Uncontrolled cell growth and the abnormal spread of those cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Causes of cancer

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Benign tumors

A

Abnormal growth

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Cancer treatment strategies

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Fractional cell chemotherapy

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Epigenetics definition

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Allele definition

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Chromosome definition

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Halotype definition

A

Group of continuous alleles on a chromosome that are inherited together

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Single nucleotide polymorphisms (SNP’s)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Indels definition

A

Insertions/deletions of short sequences of nucleotides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Introns definition

A

Non coding regions- removed during sequencing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Exons define

A

Coding region- join together during sequencing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Untranslated regions (UTR’s)

A

Sections on each side of the coding sequence

-carry info on what to do with RNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Promoter definition

A

Initiates transcription of gene (DNA to RNA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Histone modifications

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Imprinting definition

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
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

26
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

27
Q

Epigenetics definition

A

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

28
Q

Allele definition

A

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

29
Q

Chromosome definition

A

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

30
Q

Halotype definition

A

Group of continuous alleles on a chromosome that are inherited together

31
Q

Single nucleotide polymorphisms (SNP’s)

A

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

32
Q

Indels definition

A

Insertions/deletions of short sequences of nucleotides

33
Q

Introns definition

A

Non coding regions- removed during sequencing

34
Q

Exons define

A

Coding region- join together during sequencing

35
Q

Untranslated regions (UTR’s)

A

Sections on each side of the coding sequence

-carry info on what to do with RNA

36
Q

Promoter definition

A

Initiates transcription of gene (DNA to RNA)

37
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
38
Q

Histone modifications

A

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

39
Q

Imprinting definition

A

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

40
Q

Phenotype define

A

Observable trait of an individual

41
Q

Penetrance define

A

Determines the probability that a person is carrying mutation A exhibits trait X
-common genetic variants have low penetrate such as schizophrenia

42
Q

What does PGx study?

A

Phenotypes AND drug responses, side effects, tailoring biomarkers, pharmacodynamic measures, pharmacokinetic profiles

43
Q

What is the purpose of PGx?

A

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
Q

PGx phenotypes: PK profiles

A

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
Q

Tell me about CYP’s and transporters

A
  • 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
Q

Pharmacodynamic (PD) responses

A

Biochemical or physiological effect of drug on the body

Ex- what functional impact is the drug having

47
Q

What are PD responses used for?

A

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
Q

Drug response define

A

Does subject show desired clinical response to drug?

Ex- 50% reduction in migraine headaches a month

49
Q

PGx outcomes (side effects and serious adverse effects)

A

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
Q

How to measure genotypes

A

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
Q

Where does PGx guidance come from

A

FDA- drug label

CPIC (clinical pharmacogenetics implementation committee)- what clinicians should be aware of, beyond the label

52
Q

Models of stress

A

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
Q

Arousal/Activation Theory

A

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
Q

General adaptation syndrome

A

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
Q

Appraisal-coping method

A

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
Q

Allostatic load model

A

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
Q

Social readjustment rating scale

A

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
Q

Trait-oriented coping strategy

A

Views coping styles as personality dispositions that transcend the influence of situational context; emphasizes stability in coping vs change

59
Q

State-oriented coping strategy

A

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
Q

Monitoring and blunting

A

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
Q

Model of coping modes (MCM)

A

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
Q

Stress management techniques

A
  • 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