GLORIOUS POLYTECHNIC COLLEGE
MPENDAE ZANZIBAR
DEPARTMENT OF CLINICAL MEDICINE
BASIC TECHNICIAN CERTIFICATE IN CLINICAL MEDICINE
SEMESTER TWO-SEPTEMBER INTAKE 2022/2023
…………………………………………………………………………………………………
ASSIGNMENT: ONE
…………………………………………………………………………………………………
MODULE CODE:
CMT04210
MODULE NAME:
PATHOLOGY
INSTRUCTOR’S NAME:.
DR.ROSEMERRY &DR.MARYAM KHAMIS
STUDENT’S NAME:.
REG.NUMBER:
ABDULKARIM MUSSA KHAMIS
NS0700/0282/2019
QUESTION
1.Describe the vascular changes and cellular event that take place in acute inflammation
2.Differentiate between necrosis and apoptosis
15/ 05/ 2023.
……….………………………
Date of Submission
Signature.
QN 1
Inflammation is part of the complex biological response of vascular tissues to harmful
stimuli, such as pathogens, injury or trauma, and irritants. Inflammation is a protective
attempt by the organism to remove injurious stimuli and initiate the healing process.
Inflammation is not a synonym for infection, even in cases where inflammation is caused by
infection. Rather, it refers to the response of the body to try and fight the infection. While
inflammation is an important mechanism of innate immunity, it can harm the body in cases of
allergy, autoimmunity, and infections in tissues with poor regenerative capacity such as the
heart.
Vascular change
Vasodilation : An inflammatory response can be caused by any of numerous
inflammatory mediators released from innate immune system cells. The most common short
term mediators are histamine and seratonin from mast cells, but bradykinin, complement
proteins, some interleukins, prostaglandins, and TNF-alpha may also trigger inflammation
from other types of cells. Circulating mast cells contain toll-like receptors, which can detect
pathogen-associated molecular patterns (PAMPS) on the surface of pathogens and release an
inflammatory mediator such as histamine in response. Alternatively, mast cells may release
inflammatory mediators due to signals from damaged cells (which will release clotting
factors) during trauma or injury. After an inflammatory mediator is released in the
bloodstream, a period of transient vasoconstriction, lasting only a few seconds, occurs. Then
blood vessels expand to undergo vasodilation from the stimulus of the vasoactive
inflammatory mediator, which increases blood flow to the area. This causes slowing and
stasis of red blood cells, which can be involved in the clotting response needed to stop
bleeding in the case of injury. Vasodilation is the reason for the redness, heat, and pain
associated with inflammation.
Increased Vascular Permeability :The next step of acute inflammation is an increase in
vascular permeability due to inflammatory mediator activity, which causes the blood vessels
to become more permeable. Normally only water and small compounds can exit the
bloodstream into the tissues, but during inflammation, large proteins in the bloodstream, such
as serum albumins, can leak out and into the tissues. Water follows these proteins due to the
force of oncotic pressure that the proteins exert. This is called exudate, a form of edema. As
exudate accumulates within the tissues, they become swollen. The exudate may carry
antimicrobial proteins and antibodies into the tissues, and stimulates lymphatic drainage.
Leukocyte Migration to the Tissues :The next step of the acute inflammatory
response is chemotaxis migration of neutrophils to the affected area. Neutrophils are recruited
to the site of inflammation by various cytokines. Other inflammatory mediators, such as
TNF-alpha and IL-1, increase the expression of adhesion molecules on vascular endothelial
cells. The neutrophils loosely attach to the endothelial cells through use of selectins, a process
called rolling. Then integrins firmly attach to the adhesion molecules on the endothelial cells,
which is called adhesion.Together, rolling and adhesion are referred to as margination, the
accumulation of leukocytes on the endothelium.
Cellular event
Margination :First, margination will happen, where the leukocytes accumulate at the
periphery of the vessels instead of in the centre due to stasis of the blood flow in the
capillaries.
Rolling :When the endothelial cells are already activated by local mediators and
cytokines, they express adhesion molecules, allowing the leukocytes attach loosely to the
surface and is able to “roll” on the vessel wall. This mechanism is called rolling, and the
adhesion molecules are usually P-selectin and E-selectin.
Adhesion :While the leukocyte is rolling on the vessel wall, it will search for
integrins to adhere more strongly to the endothelial cells. The endothelial cells will express
intercellular adhesion molecule-1 (ICAM1), that binds to Leukocyte function-associated
antigen-1 (LFA-1) on the leukocyte, or Vascular cell adhesion molecule-1 (VCAM-1) that
binds to integrin very late antigen-4 (VLA-4) on the leukocyte.
Transmigration :After being arrested on the vessel wall, the leukocyte starts to
migrate through the vessel wall by squeezing between intercellular junctions. Platelet
endothelial cell adhesion molecule-1 (PECAM-1) is expressed on both leukocytes and
endothelial cells to mediate the binding events of the leukocyte that are needed to cross the
endothelium.
Chemotaxis :After escaping the capillaries, the leukocyte moves along a chemical
gradient toward the site of infection or injury.When the leukocyte is at the inflammation site,
it will get activated by microbes, products of necrotic cells and mediators. The removal of
pathogens by phagocytosis follows these steps:
Phagocytosis (engulfment) : Phagocytosis is the process of engulfment and
internalization by specialized cells of particulate material, which includes invading
microorganisms, damaged cells, and tissue debris. These phagocytic cells include
polymorphonuclear leukocytes (particularly neutrophiles), monocytes and tissue
macrophages
QN 2
Apoptosis is a pre-programmed cell death process that occurs in multicellular organisms.
Many biochemical events occur which leads to characteristic cell changes and death. While
Necrosis is a type of cell injury that results due to the premature death of cells in
living tissue by autolysis. External factors such as infection, or trauma which result in the
unregulated digestion of cell components are its causes.
Parameter
Apoptosis
Necrosis
Meaning
Cell death is
Premature and
preprogrammed generally
unprogrammed cell death
and starts by normal, healthy process.
processes in the body.
Cause
Natural
Caused due to external
factors on the cell or tissue,
such as infection, toxins, or
trauma.
Effects
Usually beneficial.
Always detrimental.
Symptoms
No noticeable symptoms.
Decreasing blood flow at the
affected site, inflammation,
tissue death, etc.
Medical Treatment
Very rarely needs treatment.
Always requires medical
treatment.
Conclusion
Apoptosis is a highly regulated and controlled process that confers advantages during an
organism’s life cycle. It begins when the nucleus of the cell begins to shrink. After the
shrinking, the plasma membrane blebs and folds around different organelles. Necrosis is the
death of body tissue. It occurs when very less blood flows to the tissue. This can be from
injury, radiation, or chemicals. Necrosis cannot be reversed. Necrosis may follow a wide
variety of injuries, both physical and biological in nature
Inflammation is part of the innate defense mechanism of the body against infectious or noninfectious etiologies. This mechanism is non-specific and immediate. There are five
fundamental signs of inflammation that include: heat (calor), redness (rubor), swelling
(tumor), pain (dolor), and loss of function (functio laesa)
References
1. Ferrero-Miliani L, Nielsen OH, Andersen PS, Girardin SE. Chronic inflammation:
importance of NOD2 and NALP3 in interleukin-1beta generation. Clin Exp Immunol.
2007 Feb;147(2):227-35. - PMC - PubMed
2. Understanding Pathology .Sue E. Huether ,Kathryn L .McCnce .SIXTH EDITION
,Elsevier 2017