Impact of NSCLC on Nigel's Breathing Difficulty and Liver Metastasis

P a g e | 1
Q1 ... (answer)
Non-small cell lung cancer (NSCLC) is associated with the abnormal differentiation
of lung cancer cells that accumulate across the lungs and exhibit the tendency to spread to
other body parts (Zappa & Mousa 2016). Most of the lung cancer cases comprise of NSCLC
and subjected to chemotherapy for treatment. Various types of NSCLC include
adenocarcinoma, squamous cell carcinoma, and large cell carcinoma. Adenocarcinoma
impact outer pulmonary regions and develops at a slow pace. The early detection of this lung
cancer type makes it unique from other NSCLC types (Zappa & Mousa 2016). However,
squamous cell carcinoma impacts the inner pulmonary airways through the development of
flat-cells. Large cell carcinoma spontaneously invades any pulmonary region at a greater pace
and usually diagnosed at an advanced stage. Nigel in the presented case appears to be
affected with large cell carcinoma based on metastasis and rapid spread of the cancer cells
across the pulmonary regions (Zappa & Mousa 2016). Breathing difficulty proves to be the
preliminary clinical manifestation in NSCLC patients. Nigel’s breathing difficulty in the
presented case could have emanated from various NSCLC complications including flu, cold,
pneumonia, stress, anxiety, fatigue, medication, or anaemia (Mulvihill 2018). Dyspnoea is a
commonly reported finding in NSCLC and reportedly occurs under the sustained impact of
pulmonary airflow obstruction (Ban et al. 2016). Breathing difficulty in Nigel’s case is
indicative of pulmonary system deterioration and substantially elevates his risk for mortality
and other life-threatening pathophysiological complications (Zappa & Mousa 2016).
Dyspnoea substantially elevates the physiological stress of the patients affected with NSCLC
(non-small cell lung cancer) (Shin et al. 2014). The undifferentiated NSCLC cells
spontaneously metastasise to bronchi, pericardium, liver, diaphragm, and pleura of the
affected patient. Accordingly, NSCLC in the presented case impacted Nigel’s liver, thereby
leading to the development of secondary liver cancer. The NSCLC metastasis also facilitates
the transfer of cancer cells to the vertebral column, oesophagus, trachea, great vessels, and
mediastinum (Myers & Wallen 2019). Furthermore, the development of cancer cells across
contralateral lung drastically disrupts the total lung capacity, tidal volume, and overall
breathing potential. The NSCLC metastatic processes continue to deteriorate the normal
anatomical structures and physiological functioning of pericardium and pleura. The eventual
development of pericardial and pleural effusions leads to breathing difficulty or shortness of
breath in the affected patients (LCA 2019). Accordingly, Nigel’s incapacity to attain desired
air volume in the presented clinical scenario not only causes shortness of breath/breathing

P a g e | 2
difficulty but also elevates the risk of chest tightness, laboured breathing, suffocation,
smothering, and uncomfortable breathing.
The psychogenic and pulmonary factors related to Nigel’s shortness of breath
emanate from his chest wall, lungs, and airway receptors (Williams et al. 2012). Nigel’s
NSCLC manifestations substantiate his elevated burden of symptoms and comorbidities
(Philip et al. 2015). Secondary liver cancer in NSCLC patients develops under the impact of
metastatic processes and proves to be a significant prognostic factor for pulmonary
adenocarcinoma (Ren et al. 2016). Liver metastasis in Nigel’s case elevates his risk of
clinical symptoms including weight loss, weakness, and gastrointestinal complications
(Cancer-Council 2018). Liver proves to the commonest location that experiences metastatic
invasion in NSCLC patients that eventually elevates the risk for systemic disease and related
clinical complications (Keshamouni, Arenberg & Kalemkerian 2009, p. 357). 50% incidences
of liver metastases are recorded in a range of NSCLC scenarios (Carlo & Makuuchi 2015, p.
63).
Q2 ... (answer)
Chemotherapy medications in Nigel’s case have been administered in the context of
minimizing the risk of NSCLC relapse. Chemotherapy medication administration is based on
toxifying the lung cancer cells in a manner to control their abnormal invasion and metastasis.
Hepatic first-pass metabolism is based on a serious of metabolic processes that occur in the
liver in the context of optimising chemotherapy drug’s concentration before its assimilation
in the vascular flow or systemic circulation. Cytochrome P-450 significantly assists the
hepatic first-pass metabolism of chemotherapy drugs. Cisplatin-based chemotherapy in
Nigel’s case might deteriorate his hepatic first-pass metabolism in a manner to increase its
platinum absorption while elevating the risk of thrombocytopaenia, nephrotoxicity, severe
vomiting, and nausea (CCA 2018). Cisplatin administration to Nigel also elevates his risk of
hepatotoxicity (due to its elevated distribution above 12litre per metre square) under the
impact of secondary liver cancer. Secondary liver cancer in the presented case will
substantially elevate his oxidative stress and hepatic malonaldehyde while reducing the
concentration of antioxidant enzymes and glutathione. Cisplatin’s first pass metabolism’s
deterioration in the presented scenario will elevate Nigel’s serum hepatic enzymes under the
impact of secondary liver cancer. Nigel’s impaired hepatic functions in the presented context
will drastically increase the level of cisplatin hepatotoxicity. This will eventually deteriorate

P a g e | 3
the physiological functioning of Nigel’s liver to a considerable extent. The histopathological
alterations in Nigel’s liver will be based on sinusoidal dilatation, portal infiltration of
inflammatory cells, hepatocyte, degeneration, and necrosis (Dasari & Tchounwou 2014).
These outcomes will substantially elevate Cisplatin’s half-life and minimize the pace of its
excretion. Eventually, cisplatin’s elevated retention in Nigel’s body will elevate his risk of
serious or life-threatening comorbidities including cardiotoxicity, nephrotoxicity, allergic
reactions, myelosuppression, gastrotoxicity, and ototoxicity. Similarly, Nigel’s liver
metastasis-based hepatic dysfunction disrupts the hepatic first-pass metabolism in a manner
to decrease its clearance to 27%, thereby elevating the risk of adverse effects or toxicity to
many-fold (Kenmotsu & Tanigawara 2015).
Hepatic dysfunction in secondary liver cancer patients drastically reduces its unbound
clearance as compared to NSCLC patients who remain unaffected with liver metastasis.
Similarly, secondary liver cancer in the presented context will substantially elevate Nigel’s
level of baseline alkaline phosphatase and transaminases in a manner to reduce Docetaxel’s
elimination between the range of 22%-38% (Kenmotsu & Tanigawara 2015). Secondary
hepatic cancer in Nigel’s case will substantially impact his morphine’ metabolism, thereby
elevating the risk of neurotoxicity and other adverse mental health outcomes. Hepatic
metabolism’s disruption in Nigel’s case will substantially downgrade its hepatic excretion
process. The restricted metabolism of morphine to hydro-morphine, codeine, and neuro-
morphine will eventually decrease its hepatic clearance, thereby elevating its half-life
(Soleimanpour et al. 2016). Furthermore, a drastic decrease in serum albumin level under the
impact of secondary liver cancer will substantially impact the morphine
distribution/accumulation pattern in Nigel’s body. Morphine will induce an extended effect
because of hepatic impairment in Nigel’s case. Similarly, ondansetron in Nigel’s case will
experience a substantial decrease in first pass metabolism under the impact of secondary
hepatic cancer. Nigel’s hepatic complications will also reduce his ondansetron binding
percentage while minimizing the level of its clearance. Accordingly, Nigel will experience a
greater risk of Ondansetron-related complications including constipation, malaise, dry mouth,
fatigue, and headache (Griddine & Bush 2019). Nigel’s secondary liver cancer will impact
the functionality of cytochrome-P450 in a manner to reduce Dexamethasone’s first pass
metabolism and clearance percentage. Eventually, dexamethasone’s extended retention in
Nigel’s body will further deteriorate his liver function, thereby leading to cloudy swelling,
liver enzyme elevation, and fatty change (TGA 2016). Dexamethasone’s reduced first pass

P a g e | 4
metabolism based on secondary hepatic cancer will also elevate the risk of his systemic
toxicity.
Q3 ... (answer)
Cisplatin moderately enhances the survival advantage for NSCLC patients (Sarin et
al. 2017). Cisplatin therapy will moderately arrest the pathophysiological cycle of Nigel’s
lung cancer cells while effectively altering the p-53 pathway. Cisplatin will also induce
apoptosis of the tumour cell lines and formation of DNA-adduct. The obstruction of G2/M
will minimize the frequency of Nigel’s metastatic processes while increasingly damaging the
DNAs of the lung cancer cells. The cytotoxicity of cisplatin will be mediated by intrastrand
DNA crosslinking and in the context of hampering the growth of lung cancer cells. Docetaxel
in Nigel’s case will predominantly inhibit his microtubules’ depolymerization and enhance
the tubulin structures of lung cancer cells in the context of challenging their mitotic cycle
(He, Wang & Li 2015). Docetaxel will potentially arrest tumour cells’ metaphase and
downgrade their further multiplication and metastasis. Docetaxel will also interrupt Nigel’s
interphase cellular activities through microtubular network disruption (WBPL 2017).
Docetaxel monotherapy will effectively elevate Nigel’s therapeutic response rate and one-
year survival rate in the presented scenario (Comer & Goa 2000).
Morphine in the presented scenario will substantially help in reducing the frequency
and quality of his right upper quadrant and chest pain. Opioid receptors in Nigel’s central and
peripheral nervous systems will effectively mediate the effects of the administered IV
morphine. The glucuronidation of morphine in the presented scenario will result in the
production of metabolites including morphine-3-glucuronide and morphine-6-glucuronide
(Simmons, MacLeod & Laird 2012). The analgesic activities of these metabolites will
effectively reduce Nigel’s cancer-related pain sensation and related complications.
Morphine’s sedation capacity will effectively induce 24 hours analgesia in Nigel’s case
because of his hepatic cancer-related liver impairment (TGA 2019). However, this will help
in maintaining low dosages of morphine in the context of acquiring therapeutic outcomes.
Ondansetron IV administration on Nigel’s case will effectively assist in reducing the
frequency of his nausea and vomiting episodes that repeatedly occur under the consistent
impact of chemotherapy medications. Ondansetron will influence the functionality of 5-HT3
serotonin receptors (Aschenbrenner & Venable 2009, p. 1020). The concomitant
administration of ondansetron with chemotherapy drugs in Nigel’s case will effectively