Lung Cancer: Pathophysiology, Treatment with Cisplatin, and Adverse Effects

Lung Cancer
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Lungs are the chief respiratory system’s organs.
They are responsible for performing gaseous
exchange.
A network of bronchi and bronchioles help in
transportation of inhaled air and substances to
the alveoli.
In the bronchi, there are putative stem cells,
which are the basal cells, and produce the
differentiated neuroendocrine, ciliated, and
mucous cells.
Upon reaching the alveoli oxygen is absorbed
from the air and it is passed into the blood for
circulation throughout the body.
On the other hand, carbon (iv) oxide is passed
from the blood into the alveoli and is expelled
through breathing out.
The lungs are also involved in defending the
body against harmful materials such as smoke,
microorganisms, and smoke.
These materials are trapped into mucus, a thick,
slippery fluid, and cilia helps to push the mucus
up the bronchi to be removed through
swallowing or coughing.
Introduction
Normal Physiology of Lungs

 The pathophysiology of lung cancer is
intricate.
 Constant exposure to carcinogens results to
dysplasia of lung epithelium (Siddiqui &
Siddiqui, 2019).
 Genetic mutation and subsequent alteration of
protein syntheis can occur.
 Cell cycle is then disrupted and carcinogenesis
is promoted .
 Types of lung cancer
◦ small cell lung cancer and
◦ non-small cell lung cancer
 Often, genetic mutations in proto-oncogenes
such as MYC, p53, and BCL2 lead to small cell
lung cancer
 Mutations in KRAS, EGFR and p16 lead to non-
small cell lung cancer
 Often, mutations on EGFR halts
◦ regulate apoptosis,
◦ normal proliferation of cells, and
◦ other cellular functions (Lemjabbar-Alaoui, Hassan,
Yang, & Buchanan, 2015)
 Lung cancer can also occur from
◦ structural reorganization of ALK (Anaplastic
Lymphoma Kinase) and ROS1
◦ amplification of proto-oncogenes
◦ oncogenic overexpression of gene by microRNAs
◦ inactivation of tumor suppressor genes
Pathophysiology of Lung Cancer