Anatomy and Pathophysiology of Bilateral Lower Lobe Pneumonia - Report

This report provides a detailed overview of bilateral lower lobe pneumonia, a serious lung infection affecting both lungs. It explores the anatomy and physiology, focusing on lobar pneumonia and the inflammatory processes within the lungs. The report explains the pathophysiology, including the stages of congestion, red hepatization, grey hepatization, and resolution. It highlights how the invading organisms release toxins, leading to inflammation, edema, and consolidation. The report also references the role of different organisms like Streptococcus pneumoniae. This assignment is a valuable resource for healthcare students seeking to understand the complexities of pneumonia and its progression within the lungs.

Apply anatomy and physiology
knowledge and an
understanding of relative
pathophysiology

INTRODUCTION
Bilateral lower lobe pneumonia or Bilateral interstitial pneumonia is a serious infection
that can inflame and scar your lungs. It's one of the interstitial lung diseases that affects the
tissues around the tiny air sacs get irritated and may fill with pus and other fluids in lungs.
Bilateral type of pneumonia affects both the lungs. One can get this type of pneumonia as a type
of Covid-19. As pneumonia gets worse, your lungs can develop permanent scars. When
interstitial tissue gets scarred, it may stiffen and make it hard to breathe (Kaufman and et.
al.,2020).
MAIN BODY
Anatomy and physiology of Bilateral Lower Lobe Pneumonia:
Lobar pneumonia is a form of pneumonia which is characterized by inflammatory
exudate within the intra-alveolar space resulting in consolidation that affects a large and
continuous area of the lobe of a lung. The invading organism starts multiplying, thereby
releasing toxins that cause inflammation and edema of the lung parenchyma. This leads to the
accumulation of cellular debris within the lungs. This leads to consolidation or solidification,
which is a term that is used for macroscopic or radiologic appearance of the lungs affected by
pneumonia. Bacterial pneumonia is mainly classified into lobar and diffuse depending on the
degree of lung irritation or damage.
The common organism that because lobar pneumonia is the Streptococcus pneumonia,
also known as pneumococcus, Haemophilus influenza and Moraxella catarrhally.
Mycobacterium tuberculosis, the tubercle bacillus, may also cause lobar pneumonia if pulmonary
tuberculosis is not treated promptly. The development of pneumonia requires that a pathogen
reach the alveoli and that the host defences are overwhelmed by microorganism virulence or by
the inoculum size. The endogenous sources of microorganisms are nasal carriers, sinusitis,
oropharynx, gastric, or tracheal colonization, and haematogenous spread (Wolff and et. al.,2021).
Pathophysiology of Bilateral Lower Lobe Pneumonia:
Lobar pneumonia is diffuse consolidation involving the entire lobe of the lung. Its
evolvement can be broken down into 4 stages as follows:

Congestion: This stage is characterized by grossly heavy and boggy appearing lung
tissue, diffuse congestion, vascular engorgement, and the accumulation of alveolar fluid rich in
infective organisms. There are few red blood cells (RBC) and neutrophils at this stage.
Capillaries in surrounding alveolar walls become congested and infection spread to the hilum
and pleura rapidly. Patient experiences coughing and deep breathing.
Red hepatization: It occurs in 2 or 3 days after congestion. Marked infiltration of red
blood cells, neutrophils, and fibrin into the alveolar fluid is seen. Grossly, the lungs appear red
and firm akin to a liver, hence the term hepatization. In this phase, lungs become hyperaemic and
alveolar capillaries are distended with the blood. Fibrinous fill the alveoli and by the presence of
many erythrocytes and fibrin within the alveoli.
Grey hepatization: This is an avascular stage, in this phase lungs become grey brown to
yellow because of the RBC breakdown and is associated with fibrinopurulent secretion and
hemosiderin, and the pressure exert in alveoli causes more compression on blood capillaries
which may resulting leukocytes transfer into congested alveoli due to the pressure.
Resolution: This is final stage of recovery, in this stage inflammatory fluid are resorbed
breakdown Characterized by clearing of the exudates by resident macrophages with or without
residual scar tissue formation, shortness of breath may be improved.

REFERENCES
Books and Journals
Kaufman, A.E., Naidu, S., Ramachandran, S., Kaufman, D.S., Fayad, Z.A. and Mani, V., 2020.
Review of radiographic findings in COVID-19. World Journal of Radiology, 12(8),
p.142.
Milla, S. and Lala, S., 2022. Problem Solving in Pediatric Imaging E-Book. Elsevier Health
Sciences.
Wolff, D., Radojcic, V., Lafyatis, R., Cinar, R., Rosenstein, R.K., Cowen, E.W., Cheng, G.S.,
Sheshadri, A., Bergeron, A., Williams, K.M. and Todd, J.L., 2021. National Institutes of
Health consensus development project on criteria for clinical trials in chronic graft-
versus-host disease: IV. the 2020 highly morbid forms report. Transplantation and
cellular therapy, 27(10), pp.817-835.