BASIC PATHOLOGY (KPT20101P)

LAB REPORT NO: 6

TITLE: BLOOD VESSEL ABNORMALITIES

SESSION: SEPT 2021

No. STUDENT’S NAME: MATRIC NO:

1. RASHVINI A/P RAJAN 012020092162
2. CHOONG KAI XUAN 012020092018

LECTURER’S NAME: NOOR AZIMAH AHMAD

PROGRAMME: BFS RUBRIC
T/ O/I: 5
DEPT/FACULTY: FHLS M/M: 4
R/D: 8
DUE DATE: 3rd DECEMBER 2021 C/Q: 2
F: 1
T: 20
INTRODUCTION

The circulatory system consists of blood arteries that transport blood away from and towards
the heart. Arteries transport blood away from the heart, whereas veins transport blood back to the
heart. The circulatory system carries oxygen, nutrients, and hormones to cells while also removing
waste products such as carbon dioxide. The normal anatomic structures, healthy physiologic
regulation, and normal biochemical composition of blood are the most fundamental requirements
for normal circulatory function. Blood vessel abnormalities, also known as vascular anomalies,
are birthmarks or growths made up of abnormally formed blood vessels. These growths, which
can be made up of arteries, veins, capillaries, lymph vessels, or any combination of these, might
create functional or aesthetic issues. While many vascular malformations are apparent at birth,
some do not manifest until later in a child's life, even into adolescence. Vascular abnormalities
are prevalent, with vascular tumours such as haemangiomas developing in one out of every ten
full-term infants. Vascular abnormalities are classified into two types such as vascular tumours
and vascular malformations. There are several forms of vascular tumours, the vast majority of
which are benign. Infantile haemangiomas are by far the most common kind of vascular tumour,
often growing for 6 to 12 months before beginning to decrease (regress). Vascular abnormalities,
on the other hand, are present from birth, albeit they may not be visible for several years.
Abnormalities in vascular development generate vascular anomalies. During development, these
illnesses cause an increase in the number of abnormally twisted and enlarged blood arteries to
congregate in a particular region. Most vascular abnormalities arise in the absence of a family
history and are not inherited. However, there are some uncommon hereditary types. Several of
these illnesses have been linked to genetic defects. blood vessel abnormalities are being
observed in the histopathology slides for this lab experiment. This focuses on the morphology of
thrombus, atherosclerosis and emboli.

OBJECTIVES

1. To study the blood vessel abnormalities

2. To observe the atherosclerosis of aorta, coronary atherosclerosis, fat embolism after leg
fracture, hyaline thrombus, and mixed thrombus microscopically
3. To learn the correct techniques on handling the microscope
MATERIALS

● Microscope
● Atherosclerosis of aorta slide
● Coronary slide
● Fat embolism after leg fracture slide
● Hyaline thrombus slide
● Mixed thrombus slide
● Immersion oil
● Lens paper

PROCEDURES

1. The atherosclerosis of aorta slide prepared in the laboratory was taken from the
microscopic slide box while the microscope was set up.
2. The atherosclerosis of aorta slide was observed using the microscope under 40X, 100X,
400X and 1000X magnification respectively. A few drops of immersion oil were applied on
the slide when observing it under 1000X magnification. Lens paper was used to wipe the
excess immersion oil on the slide.
3. The observation of the microscopic image of the atherosclerosis of aorta under the
magnification which provided its histologic characteristics clearly was taken in pictures.
4. Step 1 to step 3 were repeated by replacing atherosclerosis of aorta slide with coronary
slide, fat embolism after leg fracture slide, hyaline thrombus slide, and mixed thrombus
slides respectively.
5. After the observation of the slides, the microscope and the slides were placed at its origin
place.
Result

Slide Microscopic image

Fatty streak

Plaque

Calcium
accumulation

Figure 1.1: Atherosclerosis of aorta under 40X magnification.

Atherosclerosis
of aorta
Plaque

Calcium
accumulation

Fatty streak

Figure 1.2: Atherosclerosis of aorta under 100X magnification.

 Plaque

Calcium
accumulation

Fatty streak

Figure 1.3: Atherosclerosis of aorta under 400X magnification.

Calcium
accumulation
Coronary
atherosclerosis Lumen

Figure 2.1: Coronary atherosclerosis under 40X magnification.

 Fibrous cap

Red blood cells

Mononuclear
white blood cells

Calcium
accumulation

Plaque

Fatty streak

Lumen

Figure 2.2: Coronary atherosclerosis under 100X magnification.

Fibrous cap

Red blood cells

Fatty streak

Calcium
accumulation

Plaque

Figure 2.3: Coronary atherosclerosis under 400X magnification.

 Fat embolism

Fat embolism
after leg
Figure 3.1: Fat embolism after leg fracture under 40X magnification
fracture

Fat embolism

Haematopoietic
bone marrow cells

Figure 3.2: Fat embolism after leg fracture under 100X magnification
 Fat embolus
composed
of fat fills

Organized thrombus

Figure 3.3: Fat embolism after leg fracture under 400X magnification

Haematopoietic
bone marrow cells

Fat
droplets

Figure 3.4: Fat embolism after leg fracture under 1000X magnification
 Loss of cells in
arteriolar segment

Hyaline
thrombus

Figure 4.1: Hyaline thrombus under 40X magnification.

Leukocyte

Fibroblast

Figure 4.2: Hyaline thrombus under 100X magnification.

 Wall of vein

Mixed Figure 5.1: Mixed thrombus under 40X magnification.

thrombus

Vascular invasion

Endothelial cells
growing into
organizing thrombi

Figure 5.2: Mixed thrombus under 100X magnification.

 Fibrin threads

Leukocyte

Figure 5.3: Mixed thrombus under 400X magnification.

Cellular emboli

Neoplastic cell

Figure 5.4: Mixed thrombus under 1000X magnification.

DISCUSSION

Atherosclerosis of aorta is the accumulation of lipid, cells, and matrix components, including
minerals that have built up the fatty and waxy substance, plaque in the inside wall of aorta. The
plaque buildup will harden and weaken the wall of the aorta, making the wall stretch or tear and
causing a blood clot to form. The blood clot or the piece of plaque can travel to other parts of your
body blocking blood flow, leading to stroke, aortic aneurysm, aortic dissection, limb ischemia and
other diseases. Once the atherosclerosis of aorta is diagnosed, it must be treated immediately
before serious complications occur. The microscopic observation of plaque is a large colourless
foam which consists of macrophages. The formation of plaque is the earliest lesion of
atherosclerosis that indicates the process of taking up a lot of cholesterol. Plaque was discovered
in Figure 1.1, Figure 1.2 and Figure 1.3. Histologically, atherosclerosis of aorta has the mineral
especially calcium accumulation which appears as crackless and dark purple in colour. The
severity of the calcium accumulation can be observed from its colour. The darker the purple
colour, the severer the calcium accumulation. In Figure 1.1, Figure 1.2 and Figure 1.3, the calcium
accumulation found was mild as it was light purple colour and crackless. Fatty streak is the first
grossly visible lesion in the development of atherosclerosis. It appears as an irregular yellow-
white discoloration on the luminal surface of an artery. However, after staining the atherosclerosis
of aorta tissue, the fatty streak is shown as a granular whitish substance. If the fatty streak is large
enough, it will become plaque. Therefore, the fatty streak must be treated immediately when it is
found to prevent it from further forming plaque and developing atherosclerosis. The fatty streak
was found in Figure 1.1, Figure 1.2 and Figure 1.3.

Coronary atherosclerosis is a hardening of a coronary artery specifically due to an atheromatous

plaque and is one of the famous causes of death in Malaysia. The process may begin in childhood
and often progresses when people grow older if the person takes high cholesterol and fatty food
every day since young. High intake of alcohol and tobacco smoke also increase the risk of
damaging the arterial wall and causing coronary atherosclerosis. Plaques are the product of fats,
cholesterol, platelets, cellular waste products, calcium and other substances. The deposits of
plaque in the coronary artery not only damage endothelium, but also cause blockage of blood
flow and narrow lumen which will lead to insufficient oxygen supply and death. Thus, the lumen
in Figure 2.1, Figure 2.2 and Figure 2.3 was narrow. Besides, the deposits further stimulate the
cells in the artery walls to produce factors that promote the proliferation of smooth muscle cells
and the accumulation of lipids to deteriorate coronary atherosclerosis. The plaque was observed
as large white foam in Figure 2.2 and Figure 2.3. The granular whitish substance found in Figure
2.2 and Figure 2.3 was the fatty streak that will form the plaque when it is large enough. The dark
purple colour area discovered in Figure 2.1, Figure 2.2 and Figure 2.3 was the severe stage of
calcium accumulation or calcification as the affected area was large and dark in purple colour.
The calcium accumulation is one of the histological characteristics of coronary atherosclerosis.
Since the coronary atherosclerosis may block the blood flow, the red blood cell is common in
retaining in the coronary artery. The red blood cells were discovered in Figure 2.2 and Figure 2.3.
The slide of coronary atherosclerosis observed was chronic because only mononuclear white
blood cells (macrophages and lymphocytes) were found in Figure 2.2. The fibrous cap is a layer
of fibrous connective tissue which is thicker and less cellular than the normal intima and contains
macrophages and smooth muscle cells. Normally, it is found in atherosclerotic plaques. Because
of this, fibrous cap becomes the histological characteristics of atherosclerosis. Fibrous cap was
observed in Figure 2.2 and clearer in Figure 2.3.

The third slide that has been observed was fat embolism after leg fracture under the
magnification of 40X, 100X, 400X and 1000X. Fat embolism is an acute circulatory disturbance
produced by trauma, shown anatomically by the presence of fat globules inside circulation arteries
and the subsequent alterations that these create, and clinically by the presence of restlessness,
dyspnea, delirium, coma, and, in some cases, death. Fat embolism is usually caused by trauma.
In this situation, the trauma is induced by a fracture of bones, which is most likely to result in fat
embolism. It may also be caused by a blunt damage to adipose tissue or a rupture of specific
viscera rich in fat, such as the liver, however this sort of event is uncommon. It may occur in some
surgical procedures when significant trauma is used in the forced correction of bones and joints,
such as in the osteoclasis surgery. In Figure 3.1 and Figure 3.2, the fat embolism and
hematopoietic bone marrow cells were observed. Blood cells and their progenitors, barrier cells,
adipocytes, and macrophages are among the cell types found in hematopoietic tissue. The cells
of the hematopoietic tissue are not randomly placed, but rather have a specific arrangement within
the tissue. To occur, hematopoiesis must be maintained by a microenvironment capable of
recognizing and retaining hematopoietic stem cells as well as providing factors such as cytokines
essential to sustain stem cell proliferation, differentiation, and maturation along committed
lineages. The hematopoietic microenvironment is made up of adventitial reticular cells like barrier
cells, endothelial cells, macrophages, adipocytes, bone lining cells including osteoblasts, and
extracellular matrix components. In Figure 3.3, fat embolus composed of fat fills and organized
thrombus was discovered, whereas in Figure 3.4, hematopoietic bone marrow cells and fat
droplets were found. A thrombus is an intravascular accumulation of fibrin and platelets that is
often in laminated layers and is linked to the vessel wall or valve. The thrombus may also contain
leukocytes and erythrocytes. Thrombi are most usually encountered in big and medium-sized
arteries and, less frequently, in veins. Blood coagulation inside the circulatory system is aberrant,
and the hemostatic block formed from the constituents of moving blood is known as a thrombus.
When there is a breach in the vessel wall, a thrombus might develop as a repair process. A
pathological condition occurs when an overly strong response generates a thrombus big enough
to impede blood flow.

The next slide that has been observed was hyaline thrombus under the magnification of 40X
and 100X. A hyaline thrombus is a transparent white clog created by the agglutination of red blood
corpuscles that partially or completely fills a capillary, tiny artery, or vein. In Figure 4.1, the loss
of cells in arteriolar segment was discovered whereas in Figure 4.2, leukocyte and fibroblast were
found. This demonstrates that apoptotic cells form during apoptosis, which is a controlled form of
cell death that allows the removal of cells during physiological or pathological processes. The loss
of cells, particularly on the arterial segment, would cause activation of blood coagulation and
instability of atherosclerotic plaque, leading to increased thrombus formation. Apoptotic
inflammatory cells including macrophages and T-lymphocytes are common in atherosclerotic
plaque and may contribute to plaque instability. During the process of endothelial cell death, the
anticoagulant characteristic of the endothelial cell surface may be lost, while their adhesiveness
to leukocytes increases. These modifications might play a role in the fast advancement of the
atherosclerotic process.

The last slide that has been observed is mixed thrombus under the magnification of 40X, 100X,
400X and 1000X. Mixed thrombus is the combination of white and red or also known as layered
thrombus that consists of attached to the vessel wall head (white thrombus), body (mixed
thrombus) and tail (red thrombus) which is usually located in veins and aneurysms. Mixed
thrombus also can be defined as a laminated thrombus, where the layers of different ages being
of different colour or consistency (bsmu, n.d.). Figure 5.1 shows the wall of the vein and Figure
5.2 shows the vascular invasion and endothelial cells growing into organizing thrombi. Vascular
invasion (VI), also known as blood and/or lymph vessel invasion (LBVI), is the presence of tumor
cells within the lumen of a blood or lymph vessel, resulting in the production of circulating tumor
cells. In lymph node-negative patients with breast carcinoma, bladder cancer, non-small cell lung
cancer, and colorectal cancer, the presence of vascular invasion was revealed to be a major
predictive indicator for a poor clinical outcome (Li P, et al). Endothelium is the innermost single
layer of cells lining blood arteries, forming endothelial cells that offer a surface for thrombosis
development, as well as vitally regulating blood flow and homeostasis. Endothelium serves as a
barrier between blood coagulation factors and subendothelial prothrombotic extracellular matrix
components. Endothelial cells also release or express vasoactive substances, which influence
platelet reactivity, coagulation, fibrinolysis, and vascular contractility, all of which contribute to
thrombotic development (Wang et al., 2018, #). Furthermore, in Figure 5.3, leukocyte and fibrin
threads were discovered. When tissue injury causes bleeding, thrombin, a clotting enzyme,
converts fibrinogen near the site into fibrin. Fibrin molecules then bind together to create long
fibrin threads that entangle platelets, forming a spongy mass that hardens and contracts to form
the blood clot (Fibrin | Biochemistry, n.d.). Lastly, in Figure 5.4, cellular emboli and neoplastic cell
were discovered. Neoplastic cells pass through the endothelium and pericyte barrier that forms
the micro vessel walls. Neoplastic cells promote the development of tortuous new blood arteries
with higher permeability.

Question
1. Relate the consequences of pulmonary embolism based on its morphology.
Pulmonary embolism is a blockage in one of the pulmonary arteries in the lungs. Normally,
pulmonary is caused by the blood clots that travel to the lungs from deep veins in the legs or,
rarely, from veins in other parts of the body. As pulmonary embolism blocks the bloods flow to
lung, it is life-threatening. Thanks to science and technology nowadays, the risk of death of
pulmonary embolism is reduced by the anti-coagulation or blood thinners. Morphology of
pulmonary embolism is started by the large emboli which lodge in the main pulmonary artery or
major branches or at the bifurcation as a “saddle embolus”. This results in the blockage of blood
flow through the lungs, ensuing the failure of the right side of the heart and eventually leading to
death. In the early stages, the pulmonary infarct is hemorrhagic and appears as a raised, red-
blue area. Often, the apposed pleural surface is covered by a fibrinous exudate. Within 48 hours,
the red cells begin to lyse and the infarct becomes paler and eventually red-brown as hemosiderin
is produced. With the passage of time, fibrous replacement begins at the margins as a gray-white
peripheral zone and eventually converts the infarct into a contracted scar. Histologically, the
diagnostic feature of acute pulmonary embolism is the ischemic necrosis of the lung substance
within the area of hemorrhage, affecting the alveolar walls, bronchioles, and vessels. If the infarct
is caused by an infected embolus, it is modified by a more intense neutrophilic inflammatory
reaction. Such lesions are referred to as septic infarcts, and some convert to abscesses. When
the acute pulmonary embolism is present in the body for at least 6 months, it will progress to
chronic pulmonary embolism which is more harmful to the body.
CONCLUSION

In conclusion, the practical was conducted successfully as the atherosclerosis of aorta, coronary
atherosclerosis, fat embolism after leg fracture, hyaline thrombus and mixed thrombus were
observed microscopically to study blood vessel abnormalities. Through the practical, the correct
techniques on handling the microscope also were learnt.

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