Lusaka Apex Medical
University
Faculty Of
Medicine
Pathology Assignment 1
Name : Pempula Simfukwe
Student ID: 1902000336
Course Code: PTH3610
Lecturer : Mr Kachinda
Due Date : 7/08/23
Group : E
Question 1
a) Inflammation is the bodys response to harmful stimuli, such
as pathogens, damaged cells, or irritants. It involves a series of
complex processes aimed at removing the cause of injury and
promoting tissue repair.
b) General features of inflammation include redness, heat,
swelling, pain, and loss of function. These signs are a result of
increased blood flow, accumulation of immune cells, and tissue
changes at the site of injury.
c) Inflammation can be triggered by various causes, including
infections, injuries, autoimmune reactions, and exposure to
harmful substances like toxins. The immune system activates in
response to these triggers to initiate the inflammatory
response.
d) The recognition of microbes and damaged cells involves the
immune system's ability to detect pathogen-associated
molecular patterns (PAMPs) and danger-associated molecular
patterns (DAMPs). Immune cells, like macrophages, have
receptors that identify these patterns, triggering an immune
response and inflammation when detected.
Question 2
Acute inflammation is a rapid and short-term response of the
body's immune system to harmful stimuli, such as infections,
injuries, or tissue damage. It is a protective mechanism that
aims to eliminate the cause of injury or infection and initiate
the healing process.
a) Vascular changes: During acute inflammation, the affected
blood vessels dilate, leading to increased blood flow to the
affected area. This is called vasodilation. As a result, the blood
vessel walls become more permeable, allowing fluid, immune
cells, and proteins to enter the tissue.
b) Cardinal signs: The cardinal signs of acute inflammation are
redness, heat, swelling (tumor), pain (dolor), and sometimes
loss of function. These signs are the body's natural responses to
the inflammatory process and are primarily caused by the
increased blood flow, fluid accumulation, and immune cell
activity in the affected area.
c) Morphological Features: Acute inflammation is characterized
by the presence of neutrophils, a type of white blood cell, at
the site of injury or infection. These neutrophils migrate to the
affected area and actively engage in combating pathogens or
foreign substances. Tissue damage might also lead to the
release of chemical signals, such as cytokines, which attract
immune cells and initiate the inflammatory response.
d) Possible outcomes: The outcome of acute inflammation can
vary. In some cases, the inflammation successfully eliminates
the harmful stimulus, and tissue healing and repair occur.
However, if the inflammation persists or is too intense, it can
lead to tissue damage and contribute to chronic inflammation.
In severe cases, the inflammation might not be adequately
controlled and can result in tissue destruction, abscess
formation, or even systemic effects if the inflammation spreads
throughout the body.
Question3
Mediators of inflammation are molecules that play a crucial role
in the body's immune response. They include cytokines,
chemokines, prostaglandins, leukotrienes, histamines, and
more. These molecules regulate various aspects of the
inflammatory process, such as vasodilation, increased vascular
permeability, recruitment of immune cells, and activation of
other immune responses. They work together to coordinate the
body's defense against harmful stimuli like pathogens or tissue
damage.
Question 4
Acute inflammation involves a series of morphological changes
that occur in response to tissue injury or infection. These
patterns are:
Vasodilation: Blood vessels in the affected area widen, leading
to increased blood flow. This causes redness and warmth in the
area.
Increased Vascular Permeability: The permeability of blood
vessels increases, allowing fluid, proteins, and white blood cells
to leak into the tissue. This leads to swelling (edema).
Emigration of Leukocytes: White blood cells (leukocytes),
particularly neutrophils, exit the blood vessels and move
towards the site of injury through a process called chemotaxis.
Phagocytosis: Neutrophils and macrophages engulf and digest
debris, pathogens, and dead cells. This process helps in clearing
the site of infection or injury.
Chemical Mediators: Various chemical mediators, such as
histamines, prostaglandins, and cytokines, are released. These
substances help amplify and regulate the inflammatory
response.
Fibrin Deposition: Fibrinogen is converted to fibrin, which
forms a mesh-like structure around the site of injury. This helps
to localize the infection and prevent its spread.
Tissue Repair: Acute inflammation sets the stage for tissue
repair. After the harmful agents are removed, tissue
regeneration can occur.
Question 5
inflammation is a prolonged immune response that persists
over an extended period. It can result from various factors, such
as infections, autoimmune disorders, or long-term exposure to
irritants. Unlike acute inflammation, which is a short-lived and
protective response, chronic inflammation can have detrimental
systemic effects. Chronic inflammation is a complex immune
response that extends beyond the normal healing process. It
involves the persistent activation of immune cells, such as
macrophages, lymphocytes, and fibroblasts. These cells release
various signaling molecules, including cytokines, chemokines,
and growth factors.
Over time, the continuous release of these inflammatory
mediators can lead to tissue damage and remodeling. In chronic
inflammatory conditions, the immune system may struggle to
fully resolve the issue, causing a cycle of tissue destruction and
attempted repair.
Systemic effects of chronic inflammation can occur due to the
circulation of these inflammatory molecules throughout the
body. Cytokines like interleukin-6 (IL-6) and tumor necrosis
factor-alpha (TNF-alpha) can enter the bloodstream and affect
distant tissues. For instance, they might influence the liver to
produce proteins like C-reactive protein (CRP), a marker of
inflammation, which is used in clinical assessments.
Pathologically, chronic inflammation can cause cellular stress,
DNA damage, and genetic mutations. This, in turn, can increase
the risk of cancer development. Additionally, the persistent
activation of immune cells can contribute to tissue fibrosis,
where excess connective tissue accumulates, impairing organ
function. An example of this is seen in the progression of liver
cirrhosis.
The immune system's inability to properly regulate
inflammation in chronic conditions can also lead to
autoimmune disorders, where the body's immune cells
mistakenly attack its own healthy tissues. Rheumatoid arthritis
and systemic lupus erythematosus are examples of such
conditions.
In summary, chronic inflammation's systemic effects are
characterized by a cascade of immune responses and the
release of inflammatory molecules, leading to tissue damage,
altered organ function, increased cancer risk, fibrosis, and
potential autoimmune reactions. Understanding these
pathways is crucial for developing effective treatments and
interventions for various chronic inflammatory diseases.
References
-Steven A. Franklin. (2002). Immunology and Evolution of
Infectious Disease. United Kingdom. Princeton University Press.
-Charles N. Serhan, Peter A. Ward, Derek W. Girloy. (2010).
Fundamentals Of Inflammation. New York, Melbourne, Madrid.
Cambridge University Press.
-Jon C. Aster, Vinay Kumar. (2014). Robbins and Cotran
Pathologic Basis of Disease, 9th ed. Philadelphia. Elsevier
Health Sciences.
-Richard L. Kradin. (2017). Diagnostic Pathology of Infectious
Disease, 2nd ed. Chicago. Elsevier Health Sciences.
