CPPS 304 ACTUAL 2026 EXAM SCRIPT QUESTIONS AND
SOLUTIONS RATED A+
✔✔What are microtubules composed from? - ✔✔a and B tubulin
polymerization of tubulin allows it to grow
✔✔How do microtubule inhibitors work? - ✔✔taxanes bind to B tubulin, preventing the
microtubule from growing or shortening
prevents mitosis = prevents cell division
✔✔General negative effect of cytotoxic chemotherapy - ✔✔affects all tissue with rapid
cell turnover
✔✔Cytotoxic chemotherapy main toxicities (2) - ✔✔bone marrow suppression
GI effects
✔✔Cytotoxic chemotherapy - bone marrow suppression - ✔✔neutropenia - increased
risk of infection
thrombocytopenia - increased risk of bleeding
✔✔Cytotoxic chemotherapy - GI effects - ✔✔direct effect on GI tract - irritation
increased serotonin (5HT) levels
- leads to nausea and vominting
✔✔Other cytotoxic chemotherapy effects (5) - ✔✔- hair loss
- inflammation/irritation of the mouth (mucositis)
- fatigue
- infertility
✔✔Cytotoxic chemotherapy - cardio toxicity - ✔✔free-radical mediated - irreversible,
fatal
late onset
ex. anthracyclines
✔✔Cytotoxicity - neurotoxicity - ✔✔microtubules facilitate neuron al function
microtubule inhibitors are a problem
✔✔Cytotoxic chemotherapy - pulmonary toxicity - ✔✔can be acute or chronic
✔✔Cytotoxic chemotherapy - ototoxicity - ✔✔can result in hearing loss
genetic profiling may help reduce the risk
✔✔Cytotoxicity - malignancies - ✔✔thought to be mainly due to DNA damage
,✔✔Newer and alternative method of drugs - ✔✔inhibiting cell growth rather than killing
them
✔✔Targeted therapies vs cytotoxic drugs - ✔✔targeted therapies - have specific target
(receptor) to inhibit growth
cytotoxic drugs - target is to destroy
✔✔Osimertinib - ✔✔epidermal growth factor receptor (EGFR) antagonist
EGFR plays an important role in the development of many cancers (ex. lung)
✔✔Tumour genotyping - ✔✔pharmacogenetics application
based on EGFR
therapies can be chosen accordingly
increased specificity/efficacy
✔✔Intention of growth factor inhibitors - ✔✔extend life rather than curative
can sometimes be tolerated and can be used chronically
✔✔Example of angiogenesis inhibitor - ✔✔bevizicumab
vascular endothelial growth factor (VEGF) inhibitor
✔✔How do cancer cells avoid cell death despite DNA damage? (2) - ✔✔inhibiting
apoptosis
repairing DNA
✔✔How can cancer cells avoid apoptosis? - ✔✔increasing expression of anti-apoptotic
proteins
ex. bcl-2 (b-cell leukaemia/lymphoma 2)
✔✔How does bcl-2 work? - ✔✔works by binding pro-apoptotic proteins (ex. bax)
prevents them from acting
✔✔BH3 mimetics - ✔✔BH3 proteins are a family of proteins that facilitate apoptosis
BH3 mimetics bind bcl-2 and prevent it from inactivation pro-apoptotic proteins like bax
✔✔Example of BH3 mimetics - ✔✔venetoclax
✔✔PARP inhibitors - ✔✔poly (ADP-ribose) polymerase (PARP) senses DNA damage
and facilitates repair
PARP inhibitors prevent DNA repair from occurring and promotes instability and cell
death
✔✔Example of PARP inhibitor - ✔✔olaparib
, ✔✔How can immunotherapy be used to treat cancer? - ✔✔empowers the body to fight
cancer
cancer cells have a way of turning off the immune response
✔✔How does cancer turn off the immune system off? - ✔✔proteins expressed by
tumours that turn off immune response
ex. programmed cell death protein (PD) expressed on tumour cells
the PD-1 receptor is expressed on activated T-cells
PD on tumours binds to the PD-1 receptor
turns off T-cell response to the tumour
✔✔Example of immunotherapy and effects - ✔✔pembrolizumab
targets the PD-1 receptor
prevents PD from binding to the receptor
T-cells remain activated to attack tumour cells
✔✔Major issue facing all chemotherapy drugs? - ✔✔resistance (bacteria, viruses, fungi,
parasites, and cancer)
✔✔What mechanisms of resistance affect enzyme inhibitors? (2) - ✔✔- creates more
enzyme
- changes shape of enzyme target
✔✔What mechanisms of resistance affect ribosomal inhibitors? (1) - ✔✔alter shape of
binding site
✔✔What mechanisms of resistance affect intracellular drugs? (2) - ✔✔prevent entry into
the cell
pump drug out of cell
✔✔Beta-lactamases - ✔✔disrupt beta-lactam ring of penicillin
example of how bacteria can produce enzymes that break down the chemical structure
of certain drugs
✔✔Why is clavilunate useful when administered alongside penicillin/amoxicillin? -
✔✔has similar structure to beta-lactam ring - acts as decoy
beta-lactamase attacks clavulanate instead of antibiotic
✔✔Cloxacillin - ✔✔larger molecule with chemical groups that block beta-lactamases
✔✔Pan-drug resistance - ✔✔microorganism is resistant to all available antibiotics
✔✔When was the last major antibiotic class developed? - ✔✔1962
SOLUTIONS RATED A+
✔✔What are microtubules composed from? - ✔✔a and B tubulin
polymerization of tubulin allows it to grow
✔✔How do microtubule inhibitors work? - ✔✔taxanes bind to B tubulin, preventing the
microtubule from growing or shortening
prevents mitosis = prevents cell division
✔✔General negative effect of cytotoxic chemotherapy - ✔✔affects all tissue with rapid
cell turnover
✔✔Cytotoxic chemotherapy main toxicities (2) - ✔✔bone marrow suppression
GI effects
✔✔Cytotoxic chemotherapy - bone marrow suppression - ✔✔neutropenia - increased
risk of infection
thrombocytopenia - increased risk of bleeding
✔✔Cytotoxic chemotherapy - GI effects - ✔✔direct effect on GI tract - irritation
increased serotonin (5HT) levels
- leads to nausea and vominting
✔✔Other cytotoxic chemotherapy effects (5) - ✔✔- hair loss
- inflammation/irritation of the mouth (mucositis)
- fatigue
- infertility
✔✔Cytotoxic chemotherapy - cardio toxicity - ✔✔free-radical mediated - irreversible,
fatal
late onset
ex. anthracyclines
✔✔Cytotoxicity - neurotoxicity - ✔✔microtubules facilitate neuron al function
microtubule inhibitors are a problem
✔✔Cytotoxic chemotherapy - pulmonary toxicity - ✔✔can be acute or chronic
✔✔Cytotoxic chemotherapy - ototoxicity - ✔✔can result in hearing loss
genetic profiling may help reduce the risk
✔✔Cytotoxicity - malignancies - ✔✔thought to be mainly due to DNA damage
,✔✔Newer and alternative method of drugs - ✔✔inhibiting cell growth rather than killing
them
✔✔Targeted therapies vs cytotoxic drugs - ✔✔targeted therapies - have specific target
(receptor) to inhibit growth
cytotoxic drugs - target is to destroy
✔✔Osimertinib - ✔✔epidermal growth factor receptor (EGFR) antagonist
EGFR plays an important role in the development of many cancers (ex. lung)
✔✔Tumour genotyping - ✔✔pharmacogenetics application
based on EGFR
therapies can be chosen accordingly
increased specificity/efficacy
✔✔Intention of growth factor inhibitors - ✔✔extend life rather than curative
can sometimes be tolerated and can be used chronically
✔✔Example of angiogenesis inhibitor - ✔✔bevizicumab
vascular endothelial growth factor (VEGF) inhibitor
✔✔How do cancer cells avoid cell death despite DNA damage? (2) - ✔✔inhibiting
apoptosis
repairing DNA
✔✔How can cancer cells avoid apoptosis? - ✔✔increasing expression of anti-apoptotic
proteins
ex. bcl-2 (b-cell leukaemia/lymphoma 2)
✔✔How does bcl-2 work? - ✔✔works by binding pro-apoptotic proteins (ex. bax)
prevents them from acting
✔✔BH3 mimetics - ✔✔BH3 proteins are a family of proteins that facilitate apoptosis
BH3 mimetics bind bcl-2 and prevent it from inactivation pro-apoptotic proteins like bax
✔✔Example of BH3 mimetics - ✔✔venetoclax
✔✔PARP inhibitors - ✔✔poly (ADP-ribose) polymerase (PARP) senses DNA damage
and facilitates repair
PARP inhibitors prevent DNA repair from occurring and promotes instability and cell
death
✔✔Example of PARP inhibitor - ✔✔olaparib
, ✔✔How can immunotherapy be used to treat cancer? - ✔✔empowers the body to fight
cancer
cancer cells have a way of turning off the immune response
✔✔How does cancer turn off the immune system off? - ✔✔proteins expressed by
tumours that turn off immune response
ex. programmed cell death protein (PD) expressed on tumour cells
the PD-1 receptor is expressed on activated T-cells
PD on tumours binds to the PD-1 receptor
turns off T-cell response to the tumour
✔✔Example of immunotherapy and effects - ✔✔pembrolizumab
targets the PD-1 receptor
prevents PD from binding to the receptor
T-cells remain activated to attack tumour cells
✔✔Major issue facing all chemotherapy drugs? - ✔✔resistance (bacteria, viruses, fungi,
parasites, and cancer)
✔✔What mechanisms of resistance affect enzyme inhibitors? (2) - ✔✔- creates more
enzyme
- changes shape of enzyme target
✔✔What mechanisms of resistance affect ribosomal inhibitors? (1) - ✔✔alter shape of
binding site
✔✔What mechanisms of resistance affect intracellular drugs? (2) - ✔✔prevent entry into
the cell
pump drug out of cell
✔✔Beta-lactamases - ✔✔disrupt beta-lactam ring of penicillin
example of how bacteria can produce enzymes that break down the chemical structure
of certain drugs
✔✔Why is clavilunate useful when administered alongside penicillin/amoxicillin? -
✔✔has similar structure to beta-lactam ring - acts as decoy
beta-lactamase attacks clavulanate instead of antibiotic
✔✔Cloxacillin - ✔✔larger molecule with chemical groups that block beta-lactamases
✔✔Pan-drug resistance - ✔✔microorganism is resistant to all available antibiotics
✔✔When was the last major antibiotic class developed? - ✔✔1962
