CELLULAR DAMAGE AND INJURY

Inflammation
Pneumonia Etiology:
Infectious agents: bacteria, fungi, viruses; and
non-infectious agents: toxins, chemicals

Pathophysiology:
Black deposits Any infectious organisms that reach the alveoli
are likely to be highly virulent. They may
Puss cells overwhelm the macrophages, resulting in the
production of a fibrin-rich exudate that fills the
infected and neighboring alveolar spaces,
causing them to stick together, rendering them
airless. The inflammatory response also results
in a proliferation of neutrophils which can
damage lung tissues, leading to fibrosis and
pulmonary edema, which impairs lung
expansion. It can also lead to developmental
pleural effusion resulting to reduced gaseous
exchange. Respiratory and heart rate increases
as a response to decreased oxygen and rising
carbon dioxide levels. The air sacs will be filled
with fluid or pus (purulent material), causing
cough with phlegm or pus, fever, chills and
difficulty in breathing.

Morphology:
Presence of black deposits and puss cells
Miliary Tuberculosis of Lung Etiology:
Infectious agent: Bacteria (Mycobacterium
tuberculosis)

Pathophysiology:
Tuberculosis infection in the lungs results in
Pink exudate erosion of the epithelial layer of alveolar cells
Emphysema and the spread of infection into a pulmonary
vein. Bacteria reach the left of the heart and
enter the systematic circulation, they may
RBCs
multiply and infect extra pulmonary organs.
Once infected, the cell mediated immune
response is activated. The infected sites
become surrounded by macrophages which
form granuloma, giving typical appearance of
military tuberculosis.

Morphology:
Granuloma formation, massive group of WBCs

Foreign Body Granuloma Etiology:

A foreign body granuloma is a manifestation of
the skin’s immune system, which defends
against “non-self” materials such as carbon
pigments, cosmetic fillers, medications, and
mineral and metallic particles, and other biotic
and abiotic materials such as splinters.

Fibrosis Pathophysiology:
Multinucleated Giant The development of foreign body granuloma is
cell under the control both the humoral and cell-
mediated system pathways and most likely
represents hypersensitivity reaction to a foreign
antigen. The initial response to most foreign
materials is the recruitment of neutrophil to the
site. The neutrophils are unable to adequately
eradicate the foreign materials and so the
monocytes and macrophages are attracted to
the area to engulf the foreign materials.
Activated macrophages produce a wide range
of cytokines that attract more chronic
inflammatory cells including lymphocytes. The
granulomatous response is an attempt by the
body to “wall off” the foreign materials.

Morphology:
Microscopically: Presence of giant cells and
lymphocytes and plasma cells, bottle-shaped
histiocytes
 Etiology:
Pustule of Variola Infectious agent: Virus (Variola)

Pathophysiology:
The virus is acquired from inhalation. The virus
starts in the lungs whereby the virus invades
the bloodstream and spread to the skin,
intestines, lungs, kidneys, and brain. The virus
activity in the skin cells creates a rash that
starts as macules then vesicles form. Then
pustules appear after a person becomes
infected.

REFERENCES:
Bhardwaj, A. & Jain, V. (2019). Pneumonia Pathology. Retrieved on February 9, 2020 from
https://www.ncbi.nlm.nih.gov/books/NBK526116/
Murrell, D. (2018). Miliary Tuberculosis. Retrieved on February 9, 2020 from
https://www.healthline.com/health/miliary-tuberculosis#picture
Chaudhary, M. (2014). Retrieved on February 9, 2020 from
https://www.slideshare.net/mobile/chaudharymahesh/miliary-tuberculosis-dr-mahes
Burkemper, N. (n.d). Foreign Body Granuloma. Retrieved on February 9, 2020 from
https://www.dermatologyadvisor.com/home/decision-support-in-medicine/dermatology/foreign-body-
granuloma-foreign-body-reaction/
Tesini, B.( 2019). Smallpox. Retrieved on February 9, 2020 from
https://www.merckmanuals.com/professional/infectious-diseases/pox-viruses/smallpox