SUMMARY - Questions Flashcards
(292 cards)
1
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What are the primary objectives of cancer screening?
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2
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How are the validity of screening and the validity of a screening program evaluated?
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3
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What are some common cancer screening methods mentioned, including the target age ranges and frequencies?
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4
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Explain the role of Circulating Tumor Cells (CTC) and Circulating Tumor DNA (CTDNA) as metastatic cancer biomarkers.
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5
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What are the clinical implications associated with detecting CTC and CTDNA?
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6
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What is a biomarker defined as?
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7
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What are some pros and cons of using liquid biopsy (blood sample) as an alternative to solid biopsy?
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8
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Describe the different types of biomarkers based on their clinical application (e.g., predictive, prognostic, diagnostic) and provide an example for each.
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9
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List some of the molecular markers that can be detected in blood, urine, or saliva.
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10
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Discuss the challenges associated with using blood/serum and urine for biomarker detection.
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11
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What are some of the technologies used for the detection of biomarkers?
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12
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Define and differentiate between Genomic, Genetics, Pharmacogenetics, and Pharmacogenomics (Pgx).
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13
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What is Functional genomics, and how can it guide personalized medicine?
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14
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Explain Comparative genomics.
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15
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Distinguish between Germline and Somatic genomic variants and provide an example of how each can arise.
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16
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How is Genome instability and mutation linked to the Hallmarks of cancer?
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17
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Why might different metastatic sites show different DNA variations compared to the primary tumour?
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18
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What are the different types of genomic testing described?
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19
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How is monitoring a tumour’s genomic profile clinically applied at various stages?
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20
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What might the detection of DNA variants prompt in terms of further investigation?
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21
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Describe the characteristics of familial/inherited cancers with genetic pre-disposition compared to rare familial cancer syndrome with a distinct phenotype.
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22
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Explain Knudson’s 2 hit hypothesis and how it applies to hereditary vs sporadic cancer cases.
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23
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What types of screening are mentioned for individuals with a genetic predisposition to cancer?
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24
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How is Lynch syndrome diagnosed, and what is a preferred treatment approach based on diagnosis?
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25
How does germline data inform treatment decisions in pharmacogenomics?
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26
Why is pharmacogenomics considered better than a standard approach in some cases?
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27
Explain the allele category and diplotypes system used to describe enzyme metaboliser status.
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28
Provide examples of how prodrugs (like codeine) and specific enzymes (like CYP2D6 and UGT1A1in Gilbert syndrome) are affected by genetic variation, and the clinical implications.
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29
What inherited variants in the DPYD gene are mentioned, and why is DPYD testing important for patients receiving Fluoropyrimidines?
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30
Discuss the importance of diversity in genomic variation for treatment decisions and the existing gap in genomic data.
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31
Provide examples of how pharmacogenomics can personalize healthcare for specific drugs like Clopidogrel, Carbamazepine, and Statins.
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32
Name some genes and the drugs for which PGx guidelines are available from CPIC.
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33
What are some key challenges in the field of personalized medicine omics?
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34
Define Proteomics, Clinical proteomics, and Translational proteomics.
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35
What is the primary technology/tool used for proteomic detection and analysis?
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36
Describe the Ionization techniques used in mass spectrometry (Electrospray and MALDI).
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37
Define Metabolomics and explain how metabolites can act as a chemical "fingerprint".
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38
What are the main challenges in Metabolomics?
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39
Explain the difference between Untargeted and Targeted Metabolomics techniques.
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40
What technologies are used for metabolomic detection and analysis?
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41
Outline the strategies for drug target discovery using omics techniques.
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42
How does Multi-omics provide a comprehensive view in drug discovery?
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43
What is the clinical relevance of omics, particularly in understanding the need for precise, molecularly targeted therapies?
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44
Differentiate between Targeted therapy and Chemotherapy.
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45
How do techniques like Next generation sequencing, gene expression analysis, and the Human epigenome project (HEP) contribute to understanding cancer biology and guiding treatment?
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46
How do Epigenetic Drugs that target chromatin work, and how are they used in combination therapies?
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47
Compare Traditional cancer drugs with Chromatin-targeted drugs in terms of their mechanisms and toxicity.
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48
How can molecular profiling and companion diagnostics help direct the use of targeted agents beyond standard of care?
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49
What is the role of patient selection in ensuring effective treatment and minimizing harm with targeted therapies?
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50
What are the updated hallmarks and enabling characteristics of cancer, and how do they form the basis for targeted therapies?
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51
Identify the hallmarks considered REQUIRED for a cell to become cancerous vs those that are NOT REQUIRED but contribute to cancer progression.
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52
How does the inflammatory microenvironment support cancer?
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53
Explain how Obesity increases cancer risk based on the information provided.
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54
Describe how cancer cells Deregulate cellular metabolism to meet their high energy and biosynthesis demands.
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55
Explain the Warburg effect and how cancer cells adapt to its toxic byproduct.
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56
How do Genetic and Epigenetic changes influence gene expression in cancer cells?
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57
How do the Tissue origin and the Tumor microenvironment influence cancer cell metabolism?
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58
List and briefly explain some of the key evasion strategies cancer cells use for Avoiding immune destruction.
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59
How do cancer cells hijack inflammation for their benefit?
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60
Explain how Genome instability and mutation arise in cancer cells and lead to tumour heterogeneity and metastasis.
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61
What is Non-mutational epigenetic reprogramming, and what are its key mechanisms?
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62
How does DNA Methylation (hypermethylation and hypomethylation) impact gene expression in cancer?
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63
What are Histone Modifications, and how do they affect chromatin structure and gene expression?
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64
In which cancer types are abnormal methylation patterns commonly found?
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65
Provide examples of methylation-based biomarkers and their prognostic or diagnostic roles in specific cancers.
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66
How do Polymorphic microbiomes around tumors influence cancer?
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67
How do kinases, particularly receptor tyrosine kinases (RTKs), function in normal cell signaling?
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68
What are some mechanisms by which dysregulated RTKs contribute to cancer?
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69
Describe the intracellular kinase pathways mentioned (e.g., RAF-MEK-ERK) and their role in cancer.
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70
How do EGFR inhibitors work, and what are some common resistance mechanisms to them?
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71
Explain the mechanism of Vemurafenib as a BRAF inhibitor and why resistance often occurs.
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72
How does radiation damage DNA through direct and indirect mechanisms?
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73
Why are hypoxic tumors resistant to radiotherapy?
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74
Describe the difference between External beam radiotherapy (X-ray/MRI vs Proton beam).
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75
Explain the mechanisms of Internal radiotherapy (Brachytherapy and Radiopharmaceutical therapy) using examples like Radium-223 and Lutetium isotopes.
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76
How does combining Radiotherapy with chemotherapy enhance the response, using Cisplatin, 5-Fluorouracil (5-FU), and Gemcitabine as examples?
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77
What is the role of the MGMT enzyme in the response to Temozolomide in glioblastoma, and how is its methylation status used as a predictive biomarker?
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78
Explain the mechanism of Immune checkpoint inhibitors, such as those targeting PD1/PDL1.
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79
How can radiotherapy and chemotherapy potentially influence PDL1 expression?
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80
What is the concept of Therapeutic ratio when combining chemo and radiotherapy?
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81
What are some key challenges related to emerging resistance in highly targeted therapies?
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82
Using ALK inhibitors as an example, describe the mechanism, initial effectiveness, resistance mechanisms, and strategies to overcome resistance.
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83
Why do cancers with a high mutation burden often respond better to immunotherapy?
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84
Explain the role of KRAS in signaling pathways and the strategies attempted to target it, including the new approach using Storasil for the KRAS G12C mutation.
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85
Compare using SiRNA and CRISPR as genetic tools to block protein production like KRAS.
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86
Explain the concept and mechanism of PROTACs (PROteolysis TArgeting Chimera), drawing on the ubiquitin proteosome system.
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87
How can PROTACs be attached to antibodies?
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88
Describe the evolution of PROTACs from the Ovacillin example to small molecule PROTACs, highlighting the key improvements and advantages.
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89
Using ARV-110 and ARV-471 as examples, explain how small molecule PROTACs target specific receptors (Androgen Receptor and Estrogen Receptor).
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Why are PROTACs considered better than traditional endocrine therapies like Tamoxifen or Fulvestrant?
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91
Summarize the key Advantages and Challenges of using PROTACs.
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92
What are Antibody Drug Conjugates (ADCs), and how are they designed to deliver chemotherapy more safely?
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Describe the different regions of an antibody (FAB and FC) and their roles in ADC function.
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Explain the mechanism of action for ADCs.
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What are the different types of linkers used in ADCs, and what are the potential issues if the linker breaks prematurely?
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96
List the different types of payloads (cytotoxic drugs) used in ADCs.
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97
What is the Drug to antibody ratio (DAR)?
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98
Using Kadcyla (TDM1) and ENHERTU (TDX2) as examples, explain how ADCs are structured and why one might be considered better than the other.
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99
What are the main drawbacks and problems associated with ADCs, including off-target toxicityand poor tumor penetration?
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100
Despite the drawbacks, what is a noted advantage of ADCs?
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101
Explain the concept of Peptide drug conjugates (PDCs) using the CMML example and targeting CCR2 receptors.
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102
Why might chemotherapy not be suitable for CMML cells based on the source?
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103
What are the potential benefits of PDCs?
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104
Compare the potential advantages and disadvantages of Antibody Drug Conjugates, Antibody Degrader Conjugates, and Peptide Drug Conjugates.
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105
How can the concept of mRNA vaccines used for viruses be applied to cancer targeting?
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106
Describe the different ways mRNA can be delivered, including the use of lipid-based nanoparticles.
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107
Explain the Mechanism of Action for formulated mRNA delivered via lipid nanoparticles, and how it can reactivate the immune response against tumors.
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108
What are lipid nanoparticles made of, and what is the role of each component?
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How do lipid nanoparticles release mRNA inside the cell?
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110
Summarize the Advantages and Disadvantages of mRNA vaccines.
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What are some future considerations for mRNA cancer vaccines, particularly regarding personalization and manufacturing?
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112
Define Advanced Therapy Medicinal Products (ATMPs).
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113
Define Gene Therapy, Somatic Cell and Tissue Engineering.
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114
Explain the different types of viral vectors used for gene therapy (Adenovirus, AAV, Retrovirus, Lentivirus) and their characteristics (in vivo vs ex vivo, integration, immunogenicity, size capacity).
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115
Outline the process of creating and using CAR T cells.
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116
Provide examples of approved CAR T cell products and the types of cancers they are used for.
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117
Describe the specific process for Kymriah, including how the cells are obtained, modified, and stored.
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118
What are some examples of Somatic cell therapy and Tissue Engineering products?
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119
Describe the common toxicities of CAR-T therapy, including Cytokine release syndrome and Immune effector cells associated neurotoxicity (ICANS), and their management.
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120
What are the key implications of ATMPs for pharmacy, including governance, regulation, handling, storage, toxicity management, and patient monitoring?
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121
What is lymphodepletion chemo and bridging therapy in the context of CAR-T administration?
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122
Name some monoclonal antibodies (Mabs) used in Acute Leukaemia and the targets they bind to.
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123
How do these Mabs kill cancer cells compared to chemotherapy?
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124
What are Targeted Therapies (TKIs), and when are they used in haematological malignancies?
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125
Provide an example of an Antibody-Drug Conjugate used in AML.
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126
Explain how Bispecific Mabs (BiTEs) work, using Blinatumomab as an example.
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127
Why might some cancers, like lung cancer and melanoma, respond better to immunotherapy?
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128
List common symptoms of acute leukaemia.
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129
What are some risk factors for acute leukaemia?
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How is acute leukaemia typically diagnosed?
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131
Describe the main types of Acute Leukaemia (AML, ALL, APL).
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Outline the treatment approaches for AML, including intensive/non-intensive chemo, advanced therapies, and molecular targets.
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Describe Acute Promyelocytic Leukaemia (APL), its cause, treatment, and prognosis.
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134
What are the key characteristics of ALL, including commonality, types, and the need for CNS prophylaxis?
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135
List treatment options for ALL, including chemotherapy, Mabs, TKIs, and approaches for relapsed disease.
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136
Describe the causes, features, and diagnostic markers of Chronic Myeloid Leukaemia (CML).
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137
How do TKIs work in treating CML, and why were second-generation TKIs developed?
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What are some side effects and management considerations for TKIs in CML?
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139
Describe Chronic Lymphocytic Leukaemia (CLL), including its cause and how gene testing informs prognosis and treatment.
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Compare Chemoimmunotherapy and Targeted therapies for CLL.
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141
Explain the mechanisms of Small molecule inhibitors used in CLL, such as BTKis (Ibrutinib, Acalabrutinib, Zanubrutinib) and BCL2is (Venetoclax).
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142
What are the main side effects and management considerations for BTKis and BCL2is, particularly regarding cardiovascular risk and tumour lysis syndrome?
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143
Compare the pros and cons of Continuous therapy with BTK inhibitor monotherapy vs Fixed duration venetoclax-based treatment for CLL.
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144
Describe the general characteristics and diagnosis of Lymphoma.
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145
Outline the treatment approach for DLBCL using R-CHOP, including the components, common side effects, and supportive drugs.
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146
Explain the mechanism of Rituximab in treating Lymphoma.
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147
What is used for relapsed/refractory DLBCL?
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148
What is the first-line treatment for Hodgkin lymphoma?
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149
Name and describe the mechanism of some drugs used for relapsed/refractory Hodgkin lymphoma.
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150
What is Multiple myeloma, and what are its common clinical features?
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151
How is multiple myeloma diagnosed, including the role of immunoglobulins, free light chain test, paraproteinaemia, electrophoresis, and immunofixation test?
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152
Distinguish between MGUS and Symptomatic/active myeloma.
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153
What are the key criteria for diagnosing active myeloma, including bone marrow findings and the CRAB features?
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154
List the main treatment approaches for multiple myeloma, including transplant, immunomodulatory drugs, Mabs, proteosome inhibitors, ADCs, BiTEs, and conventional chemotherapy.
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Explain the mechanisms of some specific treatments like Thalidomide, anti-CD38 Mabs, Proteosome inhibitors, Bilantumab mafadotin (ADC), and BiTEs.
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156
What factors influence drug choice in the setting of relapsed myeloma?
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157
When is Stem Cell Transplantation used, and what is its goal?
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Describe the different types of Stem Cell Transplants (Autologous vs Allogeneic) and when each is typically used.
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Explain the process for Autologous Stem Cell Transplant, highlighting the goal of rescuing bone marrow after high-dose chemotherapy.
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Outline the process for Allogeneic Stem Cell Transplant, including conditioning and ongoing immunosuppression.
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What is the Graft-versus-malignancy (GvM) effect in allogeneic transplant?
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What are some key considerations for donor matching in allogeneic transplant?
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Describe the major complications of stem cell transplant, such as Graft Failure, Graft-versus-Host Disease (GvHD), Veno-Occlusive Disease, and Infections.
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How is GvHD typically managed, and what is the challenge in balancing immunosuppression?
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What factors are assessed for Patient Selection for stem cell transplant?
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166
How do viruses infect host cells?
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167
Explain the key molecular mechanisms through which viral infections can lead to cancer, including Viral Oncoproteins, Signalling Mimicry, Disruption of DDR, Chronic Inflammation, DNA Integration, and Epigenetic Changes.
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168
What are some co-factors that contribute to cancer development alongside viral infections?
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169
Explain how EBV causes Burkitt lymphoma, mentioning the role of viral proteins (EBNA2, EBNA3C, LMP1, LMP2, EBNA1, HBZ) and CMYC translocation.
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170
How does HPV lead to cervical cancer, specifically mentioning the role of E6 and E7 proteins.
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171
Explain how Hepatitis B virus (HBV) infection leads to HCC, including the role of the HBx protein.
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172
How does Hepatitis C (HCV) lead to HCC, mentioning the role of viral proteins, ROS, and cancer stemness.
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173
Explain how Human T lymphotropic virus-1 (HTLV-1) induces Adult T Cell Leukemia/Lymphoma, highlighting the roles of TAX and HBZ proteins.
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174
What are the molecular mechanisms through which bacterial infections can induce carcinogenesis?
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175
How do bacteria evade the immune system (evade complement, avoid phagocytosis, bypass antigen presentation)?
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176
Explain the concept of using anaerobic bacteria for precise targeting to a tumour for delivering anti-cancer agents.
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177
How do parasite infections lead to human malignancies, including their mechanisms of infecting and evading the immune system?
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178
Provide examples of parasites linked to specific cancers and the mechanisms involved (ROS, inflammation, DNA damage, oncogene activation).
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179
How does the immune system fight viruses?
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180
Explain how vaccines, specifically the HPV vaccine, are developed based on viral mechanisms.
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181
What is Oncolytic virotherapy, how does it work, and how does it relate to turning cold tumours into hot tumours?
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182
How can targeting CD47 on cancer cells enhance the immune response?
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183
Define PK (Pharmacokinetics) and PD (Pharmacodynamics), and explain their relationship (PK/PD).
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184
Why does the relationship between concentration and effect matter in cancer therapy, especially for drugs with narrow therapeutic windows?
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185
Explain the concept of variability in drug response, including predictable (intrinsic) and unpredictable (unexplained) variability.
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186
Using 5-Fluorouracil (5-FU) as an example, discuss its narrow therapeutic window, variable PK, concentration-dependent toxicity, metabolism by the DPD enzyme, and the importance of DPYD polymorphism and genetic testing for dosing.
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187
Differentiate between Stratified dosing and Individualised/personalised precision dosing.
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188
How is Gentamicin dosing stratified for specific patient populations?
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189
Explain the biotransformation of 6-MP and the role of the TPMT enzyme.
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190
Describe the link between TPMT enzyme activity (including polymorphism and genotype/phenotype testing) and the efficacy and toxicity of thiopurine drugs.
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191
How do Virtual Twins & Precision Dosing approaches work, and what types of data are captured for individualization?
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192
What tools are used in precision dosing, such as AI and QSP models?
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193
List some clinical applications of these advanced precision dosing strategies.
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194
Understand how cancer therapies cause toxicity and how patient factors (like genetics, age, polypharmacy) influence risk.
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195
Describe the different types of Nausea and vomiting associated with chemotherapy and their underlying pathways.
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196
Explain the causes of Diarrhoea and Mucositis induced by chemotherapy.
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197
How does the immune response contribute to Mucositis?
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198
What are the main patient factors affecting toxicities (Intrinsic and Extrinsic)?
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199
Explain the mechanism of Peripheral Neuropathy caused by platinum compounds.
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200
What are the patient factors that affect the risk of chemo-induced peripheral neuropathy?
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201
Describe the mechanism of Cardiotoxicity induced by Doxorubicin, including the role of ROS and iron.
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202
How is late-onset Doxorubicin cardiotoxicity managed or prevented?
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203
What are the patient factors and co-medications that affect the risk of doxorubicin-induced cardiotoxicity?
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204
Explain the mechanism of Immune checkpoint inhibitor induced colitis.
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205
What are the patient factors affecting the risk of ICI-induced colitis?
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206
Explain the mechanism of BRAF and MEK inhibitors and how the BRAF V600E mutation drives uncontrolled proliferation in melanoma.
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207
How do BRAF + MEK inhibitors cause skin effects?
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208
What are the key challenges in traditional cancer chemotherapy and drug delivery?
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209
Describe the structural and functional abnormalities of tumor vasculature.
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210
Explain the Enhanced Permeability and Retention (EPR) effect and its role in passive targeting with nanomedicine.
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What are some factors that affect the EPR effect?
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How can the EPR effect be improved or enhanced through physical and pharmacological strategies?
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Differentiate between passive and active targeting strategies in nanomedicine delivery.
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What are the potential pros and cons of Active vs Passive targeting?
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How are nanomedicines typically cleared from the body based on their size?
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216
Using Doxil as an example, describe how nanomedicine can be formulated (liposome encapsulation, PEGylation) to improve drug delivery and reduce side effects.
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217
Explain the challenges associated with formulating Paclitaxel and how the development of Abraxane (Nab-Paclitaxel) overcame these issues.
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218
Describe the mechanism of cellular uptake for Nab-Paclitaxel, specifically mentioning Caveolin-Dependent Endocytosis and organelle targeting.
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219
What are the main Biological Barriers to Drug Delivery, and how do strategies like PEGylationhelp overcome the vasculature barrier?
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220
Explain the components of a Targeted Drug Delivery Strategy, including ligands, linkers, and cargo.
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221
Using the SGT-53 clinical trial example, explain how liposome delivery and a transferrin ligandare used for cell targeting of a large gene.
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222
Describe the concept of Organelle Targeting Strategies, particularly for Lysosomes, and the methods used for Lysosomal Escape.
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223
How is Nucleus Targeting achieved, given the barrier presented by the nuclear envelope?
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224
Explain the strategies for Mitochondria Targeting (passive and active).
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225
What are some strategies for targeting the ER & Golgi Apparatus?
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226
Describe different Advanced responsiveness strategies to improve targeted delivery based on the tumour microenvironment, such as pH-Responsive, Enzyme/MMP2 responsive, and Redox responsive drug delivery.
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227
Explain the mechanisms of Magnetic hyperthermia and Light photothermal nanomaterial as stimuli-responsive strategies.
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228
What are some key translational barriers in developing nanomedicine?
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229
Differentiate between Supportive care and Holistic care.
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230
What are some increasing complexity factors that influence patient care?
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231
List the different causes of Cancer Pain.
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232
Describe the general Pain Treatment Approach for cancer pain, including the use of non-opioids, weak opioids, and strong opioids.
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233
Define Breakthrough Cancer Pain (BTcP) and how it is typically managed.
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234
What are the common analgesics mentioned for cancer pain?
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235
Summarize key considerations for Opioid Safety and potential side effects.
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236
What are the criteria for referring a patient to Specialist Supportive Care for pain management?
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237
Explain the concept of Psychedelic therapy for depression and anxiety in cancer patients and why they might be considered better than traditional antipsychotics.
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238
What are some caveats or challenges associated with conducting clinical trials for psychedelics?
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239
Describe the general pharmacology and brain effects of psilocybin.
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240
Define Therapeutic Drug Monitoring (TDM) and explain its purpose and importance in clinical practice.
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241
What are the main indications for TDM?
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242
Explain the relationship between the Therapeutic Window, Narrow Therapeutic Index, and Target Concentration Strategies.
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243
How is TDM typically performed, including sample types, lab techniques, and influencing factors?
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244
Using Methotrexate and Warfarin as examples, explain why TDM is clinically indicated and what is monitored.
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245
Apply TDM principles to IV antibiotics like Vancomycin and Gentamicin, including target levels, dosing strategies (intermittent vs continuous/once-daily), and considerations for renal impairment.
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246
How is clinical decision-making guided by TDM results?
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247
Summarize how emerging trends and technologies like pharmacogenomics, point-of-care testing, and AI are changing the landscape of personalised medicine.
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248
Know the underpinning principles of the prescribing framework for healthcare professionals.
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249
Outline how the perspectives, attributes, and attitudes of patients and prescribers influence prescribing decisions.
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250
Name some modifiable and non-modifiable influences on prescribing practice.
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251
Explain how intersecting influences shape prescribing practice.
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252
Discuss the importance of context and setting, using the prison setting as an example to illustrate unique influences and challenges in prescribing.
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253
Define scope of practice and explain its relationship to scope of competence.
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254
Identify the factors that determine an individual's scope of practice.
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255
Suggest possible scopes of prescribing practice for newly qualified pharmacists and how their scope might expand.
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256
Why is it important to evaluate our practice?
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257
What are some structured tools and methods used for evaluating practice?
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258
When should we evaluate our practice?
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259
Describe the types of concerns that the GPhC can investigate regarding fitness to practise.
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260
Outline the four stages the GPhC follows for managing concerns.
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261
Explain the two limbs of the Real Prospect Test applied by the Investigating Committee.
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262
What are the possible outcomes from the GPhC's Investigating Committee and Fitness to Practise Committee?
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263
Describe the actions that should be taken following a dispensing error.
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264
What are the key responsibilities of Safeguarding Adult Boards?
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265
List some relevant legislation related to safeguarding.
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266
Name the different types of abuse recognized in safeguarding.
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267
What actions should be taken when you are concerned about a vulnerable adult?
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268
Describe the key principles to follow when managing safeguarding concerns, including what to avoid.
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269
What is the process for a safeguarding referral from community pharmacy or a GP?
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270
What steps are taken if the at-risk adult denies all abuse?
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271
Explain how causality of ADRs is assessed, mentioning the TRIP acronym.
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272
What are some strategies for preventing ADRs?
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273
How are ADRs managed?
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274
Describe the role and scope of the Yellow Card scheme.
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275
What types of suspected adverse events should be reported to the Yellow Card scheme?
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276
What are the main consequences of polypharmacy?
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277
What are some solutions or interventions for managing polypharmacy, including deprescribing tools and the person-centred approach?
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278
Describe the different models and phenotypes of Frailty.
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279
What are the key assessment tools for frailty, such as the Comprehensive Geriatric Assessment (CGA) and the G8 Screening Tool?
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280
Explain the components and process of a CGA.
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281
List the components of the G8 screening tool.
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282
Describe the common bone conditions found in the elderly.
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283
Explain the process of bone ageing and pathophysiology.
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284
What are the modifiable and non-modifiable risk factors for poor bone health?
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285
How is Bone Health linked to Cancer and its treatments?
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286
What are some Fall Risk Assessment Tools, their risk factors, and who should be assessed?
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287
How is poor bone health diagnosed and screened for, including the use of DXA scans and lab tests?
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288
What are the key Falls Prevention Strategies (Exercise, Lifestyle, Nutrition)?
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289
How is Frailty managed?
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290
What are the first-line and alternative treatments for poor bone health?
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291
Explain the importance of co-management and starting osteoporosis treatment in post-fracture care.
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292
What is involved in the monitoring and follow-up of patients receiving treatment for poor bone health?
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