Cancer Chemotherapy In Clinical Practice

Cancer Chemotherapy In Clinical Practice

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Cancer Chemotherapy In Clinical Practice

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Cancer Chemotherapy In Clinical Practice

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Mr BT is 47-year-old man admitted to hospital with prostate hypertrophy requiring a transurethral resection of the prostate (TURP). The procedure is completed without complication and Mr BT returns to the ward with an indwelling catheter in place, it remains in situ for three days.
After the catheter is removed, Mr BT experiences urinary frequency and a burning sensation during micturition. A urine sample is taken and sent to the psychology laboratory for analysis. The microbiology report shows the following:

Microscopy: white blood cells ++, Gram-negative rods
Culture: Pseudomonas aeruginosa
Sensitivity: amoxicillin-resistant, cephalexin-sensitive, trimethoprim-resistant, gentamicin-sensitive

His medical history indicates hypersensitivity to penicillin.

Which antibacterial agent(s) would be effective in the therapy of Mr BT’s urinary tract infection? (4 marks)

State the mechanisms of action of each of these agents. (4 marks)

Ciprofloxacin is known to correlate with two related but different targets within the cell of the bacteria, enzyme topoisomerase II (DNA gyrase) and topoisomerase IV. DNA gyrase and topoisomerase IV are required for the negative supercoiling of the DNA which is essential for the replication of the DNA in the cell. Inhibition of the topoisomerase enzyme II and topoisomerase IV is fatal to the cells of the bacteria (Baldo & Pham, 2013).
Research by Morgan (2013), states that trimethoprim employs antimicrobial activity by blocking the reduction of the dihydrofolate to tetrahydrofolate which is the active form of folic acid. Tetrahydrofolic acid is a precursor in the pathway of thymidine synthesis and interference with the thymidine synthesis pathway inhibits the synthesis of DNA. The affinity of trimethoprim to the dihydrofolate reductase of the bacteria is much higher compared to its affinity for the human dihydrofolate reductase (Bullock & Manias, 2013).
Outline the pathophysiology underlying Mr BT’s hypersensitivity to penicillin (4 marks)
According to Bullock & Manias (2013), hypersensitivity to penicillin may lead to anaphylaxis which is characterized by symptomatic hypotension. Anaphylaxis is the most severe exhibition of IgE- mediated drug allergy which results when antigen-specific IgE is existing on mast cells and an occurrence of a systemic exposure links the IgE. This leads in the concurrent degradation of great numbers of mast cells containing histamine and several other vasoactive mediators. The sudden release the mast cells due to either an IgE mediated anaphylactic reaction or a similar non-IgE mediated reaction result in a sudden drop of blood pressure, probable compromise of the respiratory system, edema of the bowel and potential cell death (Bullock & Manias, 2013)
Given the fact that Mr BT is allergic to penicillins, is cephalexin therapy contraindicated here? (3 marks)
Baldo & Pham (2013), argues that cephalexin therapy is contraindicated because it is a beta-lactam antibiotic. Penicillin belongs to the same class of beta-lactams. Incidences of cross-reactivity to cephalexin in patients allergic to penicillin, therefore, may probably occur (Baldo & Pham, 2013)
KY is a 12-year-old boy who has been diagnosed recently with acute lymphoblastic leukemia (ALL). He has been admitted to hospital for treatment.
 KY’s initial therapy will comprise the corticosteroid dexamethasone, as well as the cytotoxic agent’s vincristine, L-asparaginase, daunorubicin, methotrexate and cytarabine. He experiences gastrointestinal upset but responds well to therapy; economics, he does require close monitoring of his condition. KY receives adjunct therapy with the colony stimulating factor filgrastim.
KY’s four siblings are tissue-typed for bone marrow transplant. One of the children is considered a good match. While awaiting transplantation, KY develops a fever. He receives intravenous therapy with doxycycline to reduce the risk of sepsis. This crisis passes. After bone marrow transplant, KY makes good progress and moves into remission.

Describe the mechanism of action of the corticosteroids and indicate the adverse effects that require monitoring during treatment with these drugs. (6 marks)

Mechanism of action
According to Vora (2017), when corticosteroids get into the cytoplasm of the cell, they form a steroid receptor complex by reacting with receptor proteins that are in the cytoplasm. The receptor complex then goes to the nucleus and binds to the DNA. The binding process of the DNA and the receptor complex leads to change in the transcription of the messenger RNA. Vora, (2017) states that since corticosteroids act as protein synthesis template, corticosteroids can either inhibit or stimulate the synthesis of definite proteins. However, the corticosteroids are recognized to stimulate the production of lipocortin, a glycoprotein, which inhibits the activity of phospholipase A2. Phospholipase A2 produces arachidonic acid which is a precursor for leukotrienes and proteinoids. On the other hand, corticosteroids inhibit the formation of interleukin-1. These activities of corticosteroids on interleukin-1 and the metabolism of arachidonic acid leads to anti-inflammatory and immunosuppressive responses ((Bullock & Manias, 2013).
Adverse effects of corticosteroids that require monitoring

Difficulty in breathing or shortness of breath
High blood pressure which may be due to blurred vision, severe headache,
The severe allergic reaction which may be manifested through symptoms such as fever
Low potassium levels which may show symptoms such as irregular heartbeats, leg cramps, and constipation.
Bloody or tarry stools
Confusion, numbness or tingly feeling around the mouth
Pancreas disorder
To which cytotoxic drug groups do each of the drugs in the case study belong?(5 marks)

Cytotoxic group of each drug
Vincristine- plant alkaloids or inhibitors of mitosis
L-asparaginase- enzymes
Daunorubicin- alkylating agents
Cytarabine- antimetabolites (Priestman, 2012)
Describe the mechanism of action of each of the drug groups identified in question two
Mechanism of action


Vincristine binds to tubulin thereby inhibiting the polymerization of tubulins to microtubules. Microtubules are responsible for the pulling apart of the cell when it divides. Therefore, when vincristine binds to tubulin, mitosis of the cell is inhibited since microtubules are absent. Like other vinca alkaloids, vincristine may also interfere with amino acid, cyclic AMP, glutathione metabolism, calmodulin-dependent calcium ions transport ATPase activity, cellular respiration and nucleic acid and lipid biosynthesis (Cancer Drug Design and Discovery, 2013)


Bullock & Manias (2013) found out that L-asparaginase is an enzyme that hydrolyzes asparagine resulting in the production of ammonia and asparagine acid. This leads to depletion of L-asparagine from the cell plasma causing an inhibition of the synthesis of RNA and DNA with consequent apoptosis of the blastic cell. Healthy cells are able to produce their own asparagine but cancer cells are not able to make their own asparagine. Therefore, the depletion of the asparagine by the asparaginase enzyme kills cancer cells while healthy cells are not affected. (Bullock & Manias, 2013).


Daunorubicin has antimitotic and cytotoxic activity through various ways of the mechanism of action. It acts by forming DNA complexes by intercalating between base pairs. Daunorubicin also leads to the inhibition of the activity of the topoisomerase II enzyme by stabilizing the DNA- topoisomerase II complex. (Bullock & Manias, 2013). The stabilizing of the complex consequently results to the preclusion of the relegation portion of the ligation relegation reaction that is catalyzed by the enzyme topoisomerase II


Methotrexate acts by inhibiting the synthesis of pyrimidine and purine, the building blocks of DNA thereby inhibiting normal cell division and development (Cancer Drug Design and Discovery, 2013). Methotrexate looks like folic acid to the folic acid reductase enzyme consequently binding to it strongly and inhibits the activities of the enzyme. Subsequently, DNA synthesis is halted because the coenzymes required for the reactions of one-carbon transfer are absent because tetrahydrofolic acid is missing (Bullock & Manias, 2013).


Research by the Cancer Drug Design and Discovery (2013), concludes that the activity of cytarabine is as a result of the inhibition of the DNA polymerase. Cytarabine acts by damaging the DNA incorporating into the DNA. Cytarabine exhibits the specificity of the cell phase principally killing the cells undergoing DNA synthesis. Under certain circumstances, cytarabine blocks the progression of cells from the G1 phase to the S phase.
What are the common immediate and delayed adverse reactions associated with cytotoxic drugs? (4 marks)
Immediate adverse reactions
Nausea and vomiting
Damage to the mucosa of the pharynx and mouth
Delayed adverse reactions
Alopecia (hair loss)
Suppression of bone marrow cells
Describe the clinical management of a client with increased susceptibility to infection. (5 marks)
Nijkamp and Parnham (2011), argues that infections of patients with increased susceptibility to infections pose a serious clinical challenge because the disease-causing organisms are always unfamiliar. Therefore, necessary treatment should begin early during the period of the illness. These patients should also be given the maximum tolerated doses of antimicrobial agents and for prolonged periods of time. Prophylactic drugs should also be administered depending on the pathogens that are likely to be reactivated at the period of more severe immunosuppression (Nijkamp and Parnham 2011).
To which antimicrobial drug group does doxycycline belong? Is it considered a bactericidal or bacteriostatic agent? Explain.(3 marks)
Doxycycline drugs are considered bacteriostatic. Research by Bullock & Manias (2013)., shows that doxycycline is lipophilic and hence can pass through the lipid bilayer of the bacterial cell. Doxycycline acts by binding to the 30S ribosome subunits and possibly to the 50S ribosomal subunits reversibly, consequently blocking the binging of the amino acetyl tRNA to mRNA thereby inhibiting the protein synthesis of the bacteria. Therefore, doxycycline drugs act by limiting the growth of bacteria by interfering with DNA replication, protein synthesis and other characteristics of metabolism of the bacterial cells (Bullock & Manias, 2013).
Define the term ‘antimicrobial drug spectrum of activity’. What is the spectrum of activity of doxycycline? Why choose a drug with this spectrum of activity? (2 marks)
According to Bryan (2012), antimicrobial drug spectrum of activity is the range of target microbes against which an antimicrobial drug is clinically active. Doxycycline is a broad-spectrum antimicrobial. Drugs that have a broad spectrum of activity are active against a wide range of microbes, both gram negative and gram positive (Piscitelli, Rodvold & Pai, 2011).
In the ambulance, a paramedic initiates oxygen therapy and administers morphine to SA (patient) for pain relief, as well as a low dose of aspirin. After SA arrives at the hospital, investigations confirm that he is suffering from an acute myocardial infarction. SA receives an intravenous infusion of the fibrinolytic agent streptokinase, as well as the anti-dysrhythmic amiodarone for ventricular tachycardia. Cardiac enzyme level test indicates that the damage to the myocardium is extensive.
During his hospital stay, he receives treatment with subcutaneous heparin and the B-blocker atenolol. Acute heart failure develops, which requires treatment with the ACE inhibitor enalapril and the loop diuretic frusemide. The diuretic is for the treatment of SA’s pulmonary edema.
After prolonged hospital stay, SA is discharged. He goes on to develop chronic heart failure, which is managed with an ACE inhibitor, a diuretic, and a peripheral vasodilator.
What is the rationale for the use of fibrinolytic drugs in acute myocardial infarction (AMI)?  Are there any constraints regarding the timing of administration of these drugs in AMI? (4 marks)
Research by El-Sherif & Ramana Reddy (2013), shows that fibrinolytic agents are necessary for the lysis of the intracoronary thrombi and the decrease of the mortality related to myocardial infarction. There are constraints in the administration of fibrinolytic drugs in AMI. This is because the drugs should be administered immediately after the thrombotic incident. Any delay in instituting the therapy decreases the probability for optimum efficiency of the drug (El-Sherif & Ramana Reddy, 2013).
Compare and contrast the mechanisms of action of the fibrinolytic drugs streptokinase and aspirin. (3 marks)
Mechanism of action of both streptokinase and aspirin lead to the degradation of blood clots.
Streptokinase works by forming a highly enzymatic complex with plasminogen which converts inactive plasminogen into active plasmin. Plasmin consequently degrades fibrin clots as well as fibrinogen resulting into the degradation of blood clots. On the other hand, aspirin works by inhibiting platelets activation and aggregation. Bullock & Manias (2013), explains that aspirin achieves this by causing an irreversible inhibition of the cyclooxygenase enzyme that is platelet-dependent thereby preventing the synthesis of prostaglandins. Aspirin, by inhibiting platelet activation, irreversibly inactivates COX-1 thereby blocking the generation of thromboxane A2 leading to a probable antiplatelet effect (Bullock & Manias, 2013).
What adverse reactions should be monitored during and after fibrinolytic drug therapy? (3 marks)
During fibrinolytic therapy
Migration of the clot to another part of the vascular system
Damage to the blood cell
Bleeding at the access site
After fibrinolytic therapy
Intracranial bleeding
Kidney damage to patients with diabetes
Nose bleeding
Describe the mechanism of action of the antidysrhythmic agent amiodarone. 
To which Vaughan Williams antidysrhythmic drug class does it belong? (4 marks)
According to the research by Bullock & Manias (2013), amiodarone works by prolonging the repolarization of the cardiac myocyte by blocking the swiftly activating delayed rectifier potassium channels. Amiodarone may also block inactivated L-type calcium channels and sodium channels.
Amiodarone belongs to class III drugs according to Vaughan Williams classification. (Bullock & Manias, 2013).
Compare and contrast the actions of heparin and streptokinase(3 marks)
El- Sherif & Ramana Reddy (2013), explains that both heparin and streptokinase are indicated for the prevention of clotting of blood. However, the actions of heparin and streptokinase differ significantly. Heparin acts by averting the progression of existing clots by inhibiting further clotting while streptokinase acts by degrading the blood clots (El-Sherif & Ramana Reddy, 2013).
Outline the pathophysiology of heart failure (4 marks)
According to Bullock & Manias (2013), heart failure is as a result of an injury to the myocardium from several causes such as ischemia, diabetes, and hypertension. Other causative agents may include; myocarditis, systemic toxins, cardiomyopathies, and cardiotoxic drugs. Symptoms that are caused as the heart fails are dyspnea from the congestion of the pulmonary, ascites from the venous return that are impaired, and peripheral edema. Symptoms such as loss of appetite, fatigue, and nausea are also common (McDonagh, 2011).
As the heart fails, several compensatory mechanisms occur to sustain adequate function of the heart. These mechanisms include; an increment of the cardiac output, the addition of the volume of the ventricle and thickness of the wall, and maintenance of the perfusion of the tissue with the increased pressure of the artery. These mechanisms are usually helpful at the early periods of heart failure but consequently, the mechanisms result into a vicious cycle of heart failure worsening ( McDonagh, 2011).
Describe the mechanism of action of ACE inhibitors and indicate why they are a drug of choice in heart failure (4 marks)
Mechanism of action of ACE inhibitors
Bullock & Manias (2013), explains that ACE inhibitors induce vasodilation in heart failure patients by the removal of the vasoconstrictor II, an increment in the circulating and kinins tissue level, and an increase in the synthesis of the prostaglandin. ACE inhibitors also attenuate actions of other hormones useful in vasoconstriction such as vasopressin. It is likely that ACE inhibitors cause down-regulation of the central and peripheral sympathetic nervous systems (Bullock & Manias 2013).
Why ACE inhibitors are a drug of choice
Ace inhibitors improve the prognosis and symptoms of heart failure, they improve blood flow to the skeletal muscle during exercise and they also reduce LV hypertrophy which is a risk factor for prognosis and cardiovascular diseases.
Pulmonary edema is caused by alterations in fluid distribution between pulmonary blood vessels and the lung tissue.  Using fluid dynamics and changes in fluid pressure, explain the link between heart failure and pulmonary edema.(3 marks)
Bullock & Manias (2013), states that pulmonary edema is caused by an imbalance between the forces that drive fluids into the alveoli and the mechanism of the removal of the fluids. Cardiogenic edema is caused by high pulmonary capillary hydrostatic pressures while the alveolar barrier remains intact. In some tissue, anatomical structures limit the enlargement of the tissue spaces due to edema genic stress (Bullock & Manias 2013). Consequently, the incapability of the of the tissues to expand their interstitial volume leads to slight increments in the filtration of the transcapillary fluid which induce huge pressure increase of the interstitial fluid. This, in turn, reduces the gradient of the vascular transmural and physically compresses capillaries, consequently reducing perfusion of the nutritive tissue (McDonagh, 2011).
Compare and contrast the actions of the loop and thiazide diuretics (4 marks)
Both the loop and the thiazide diuretics increase the delivery of sodium to the distal segment of the distal tubule.

The loop diuretics acts by inhibiting the sodium-potassium-chloride cotransporter in the distal tubule while the thiazide diuretics act by inhibiting the sodium-chloride transporter in the distal tubule (Bullock & Manias 2013).
The action of the loop diuretics leads to a significant increase in the concentration of the sodium ions in the distal tubule while the thiazide diuretics leads to a less increase in the concentration of the sodium ions in the distal tubule.
The loop diuretics leads to the reabsorption of about 25% of the sodium ions load while the thiazide diuretics leads to the reabsorption of about 5% of the filtered sodium load
The loop diuretics are more effective than the thiazide diuretics because their action leads to a significant increment in the concentration of sodium ions in the distal tubule.

At what stages do the diuretics and the peripheral vasodilators interrupt the pathophysiology of heart failure?(3 marks)

The diuretics and the peripheral vasodilators interrupt the pathophysiology of heart failure at stages B, C and D. (Bullock & Manias, 2013).
Compare and contrast the general characteristics of the following drug groups:

the TCAs and the SSRIs


Both TCA and SSRI are antidepressants.
Both TCAs and SSRIs work by boosting the level of serotonin and norepinephrine (Akbar, 2013).


TCAs act as strong inhibitors in the uptake of both norepinephrine and serotonin while SSRIs act as weak inhibitors in the norepinephrine reuptake but strong inhibitors in the serotonin reuptake (Bullock & Manias 2013).
TCAs lacks selectivity leading to more side effects such as dizziness, constipation, dry mouth, and drowsiness while SSRIs are highly selective hence fewer side effects (Akbar, 2013).
the non-selective MAOIs and the RIMAs


Both non-selective MAOIs and the RIMAs are antidepressants.
Both of the antidepressants act on the enzyme monoamine oxidase
Both lead to the increment of the quantity of serotonin and noradrenaline

In contrast, non-selective MAOIs work by blocking the activity of the enzyme monoamine oxidase while the RIMAs work by reducing the activity of the enzyme monoamine oxidase (Akbar, 2013).

the TCAs and the tetracyclic antidepressants

Both act as inhibitors in the reuptake of both serotonin and norepinephrine
Both lead to more side effects
Both are antidepressants
In contrast, TCAs have three rings in the chemical structure while tetracyclic antidepressants have four rings in the chemical structure (Bullock & Manias 2013).

the TCAs and the non-selective MAOIs

Both TCAs and non-selective MAOIs are antidepressants
Both boost the level of norepinephrine and serotonin
In contrast, TCAs work by inhibiting the reuptake of both serotonin and norepinephrine while non-selective MAOIs work by blocking the activity of monoamine oxidase (Akbar, 2013).

the SSRIs and the SNRIs

Both SSRIs and the SNRIs are depressants
Both affect the reabsorption of serotonin
In contrast, while both SSRIs and SNRIs affect the reabsorption of serotonin, SNRIs also affect the levels of norepinephrine in the brain (Akbar, 2013)
Akbar, S. (2013). Depression, Antidepressant Drugs and St. John’s Wort. Trafford on Demand Pub.
Baldo, B., & Pham, N. (2013). Drug Allergy. New York, civil-engineering: Springer.
Bryan, L. (2012). Antimicrobial Drug Resistance. Burlington: Elsevier Science.
Bullock, S., & Manias, E. (2013). Fundamentals of Pharmacology. Melbourne: P.Ed Australia.
Chandrasekar, P. (2016). Infections in the immunosuppressed patient. Oxford: Oxford University Press.
Elsevier Science. (2013). Cancer Drug Design and Discovery.
El-Sherif, N., & Ramana Reddy, C. (2013). The Pathophysiology and Pharmacotherapy of Myocardial Infarction. Burlington: Elsevier Science.
McDonagh, T. (2011). Oxford textbook of heart failure. Oxford: Oxford University Press.
Morgan, E. (2012). Allergic reactions to drugs. [Place of publication not identified]: Springer.
Nijkamp, F., & Parnham, M. (2011). Principles of immunopharmacology. Basel: Springer.
Piscitelli, S., Rodvold, K., & Pai, M. (2011). Drug Interactions in Infectious Diseases. Totowa, NJ: Humana Press.
Priestman, T. (2012). Cancer Chemotherapy in Clinical Practice. London: Springer London.
Vora, A. (2017). Childhood Acute Lymphoblastic Leukemia. Cham: Springer International Publishing.

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