Volume 03 Issue 03-2023
39
American Journal Of Applied Science And Technology
(ISSN
–
2771-2745)
VOLUME
03
I
SSUE
03
Pages:
39-43
SJIF
I
MPACT
FACTOR
(2021:
5.
705
)
(2022:
5.
705
)
(2023:
7.063
)
OCLC
–
1121105677
Publisher:
Oscar Publishing Services
Servi
ABSTRACT
This paper analyzes modern methods and technologies for diagnosing and treating patients with coronavirus. And so,
when the coronavirus settles in the endothelial cells (the inner wall of the blood and lymphatic vessels), a thrombus
(thrombosis) is created. Thrombosis - intravital formation of blood clots (thrombi) inside the blood vessels, preventing
the free flow of blood through the circulatory system.
KEYWORDS
Coronovirus, thrombus, thrombosis, hemocoagulation , viscosity, hemostasis, coagulation, vasospasm, adhesion,
fibrinogen.
INTRODUCTION
When a blood vessel is damaged, the div uses
platelets and fibrin to form a blood clot to prevent
blood loss. Under certain conditions, blood clots can
form in the bloodstream even without vascular
Research Article
WHEN THE WHOLE WORLD, STARTING FROM DECEMBER 2019, IS
CONCERNED ABOUT THE "CORONAVIRUS" -COVID-2019, HOW CAN
BIOPHYSICS HELP?
Submission Date:
March 17, 2023,
Accepted Date:
March 22, 2023,
Published Date:
March 27, 2023
Crossref doi:
https://doi.org/10.37547/ajast/Volume03Issue03-07
Sodikov N. O.
Samarkand State Medical University, Uzbekistan
Muminova Z. A.
Tashkent Chemist - Technological Institute, Uzbekistan
Khasanova D.
Samarkand State Medical University, Uzbekistan
Journal
Website:
https://theusajournals.
com/index.php/ajast
Copyright:
Original
content from this work
may be used under the
terms of the creative
commons
attributes
4.0 licence.
Volume 03 Issue 03-2023
40
American Journal Of Applied Science And Technology
(ISSN
–
2771-2745)
VOLUME
03
I
SSUE
03
Pages:
39-43
SJIF
I
MPACT
FACTOR
(2021:
5.
705
)
(2022:
5.
705
)
(2023:
7.063
)
OCLC
–
1121105677
Publisher:
Oscar Publishing Services
Servi
damage. The cell is held together by membranes. 10-6
cm2 membrane plane has from 10 to 500 channels.
Coronavirus clogs these channels, creates a blood clot
and the cells begin to die. The div at this moment
does everything to restore these damages as quickly as
possible. This is due to the process of blood clotting,
when a lot of viruses enter the div at the same time
and they infect a large number of blood vessels. Blood
coagulation ( hemocoagulation ) is the most important
stage of the hemostasis system, responsible for
stopping blood loss in case of damage to the vascular
system of the div. Clotting leads to imbalance and
starts to create a lot of blood clots and this is the main
cause of death. By determining the viscosity and
coagulability of blood in humans, it is possible to
determine in what form a person will have an infection
- in a mild or severe form.
At such moments, so that the disease does not
proceed in a severe form, it is necessary to regulate the
activity of the blood coagulation system, preventing
the coagulation system from being strongly activated,
i.e. suppress it for a while, thereby providing the lungs
with a few days of respite until the immune system
defeats the virus.
To
prevent
negative
consequences, it is required to fully decipher the
mechanism of blood coagulation. Blood coagulation is
preceded by the stage of primary vascular-platelet
hemostasis. This primary hemostasis is almost entirely
due to vasoconstriction and mechanical blockage of
platelet aggregates at the site of damage to the
vascular
wall.
Actually,
blood
coagulation
(hemocoagulation, coagulation, plasma hemostasis,
secondary hemostasis) is a complex biological process
of formation of fibrin protein strands in the blood,
which polymerizes and forms blood clots, as a result of
which the blood loses its fluidity, acquiring a curdled
consistency.
METHODS
The process of hemostasis is reduced to the formation
of a platelet -fibrin clot. Conventionally, it is divided
into three stages: 1. temporary (primary) vasospasm 2.
platelet plug formation due to platelet adhesion and
aggregation;
3.
retraction
(contraction
and
compaction) of the platelet plug.
Vascular injury
is accompanied by immediate activation of platelets.
Adhesion (sticking) of platelets to connective tissue
fibers along the edges of the wound is due to
Glycoprotein von Willebrand factor. Simultaneously
with adhesion, platelet aggregation occurs: activated
platelets attach to damaged tissues and to each other,
forming aggregates that block the path of blood loss.
A platelet plug appears. From platelets that have
undergone adhesion and aggregation, various
biologically active substances (ADP, adrenaline,
norepinephrine, and others) are intensively secreted,
which lead to secondary, irreversible aggregation.
Simultaneously with the release of platelet factors,
thrombin is formed, which acts on fibrinogen to form a
fibrin network in which individual erythrocytes and
leukocytes get stuck - a so-called platelet -fibrin clot
(platelet plug) is formed.
RESULTS
Thanks to the contractile protein thrombosthenin,
platelets are pulled towards each other, the platelet
plug contracts and thickens, and its retraction occurs.
In its simplest form, the process of blood coagulation
can be divided into three phases: 1-phase activation
includes a complex of successive reactions leading to
the formation of prothrombinase and the transition of
prothrombin to thrombin; 2- phase of coagulation - the
formation of fibrin from fibrinogen; 3-phase retraction
- the formation of a dense fibrin clot. The lungs may be
the epicenter of Covid-19, but scientists believe it can
also enter the circulatory system by infiltrating our
Volume 03 Issue 03-2023
41
American Journal Of Applied Science And Technology
(ISSN
–
2771-2745)
VOLUME
03
I
SSUE
03
Pages:
39-43
SJIF
I
MPACT
FACTOR
(2021:
5.
705
)
(2022:
5.
705
)
(2023:
7.063
)
OCLC
–
1121105677
Publisher:
Oscar Publishing Services
Servi
arteries. How exactly the virus attacks the heart and
blood vessels remains a mystery, but experts believe
the infection can cause blood clots and heart attacks
because the virus binds to ACE2 receptors on the cells
that line our blood vessels and heart. Patients with
Covid in the hospital show signs of serious heart and
vascular problems. And We see that in a significant
proportion of patients, blood clots form in the arteries
entering the heart. One study published in the scientific
journal JAMA Cardiology found that 20 percent of 416
patients hospitalized in Wuhan with the coronavirus
had heart damage.
An increased likelihood of
blood clots appears to be one of the features of severe
Covid disease. This may explain why patients with
diabetes and cardiovascular disease are at risk for
severe illness with Covid-19, as their vascular system is
already under additional stress.
Biologically,
the process of thrombosis is the norm - this mechanism
is designed to protect a person from heavy bleeding,
and natural thrombolysis is sufficient to destroy small
blood clots, platelets and proteins. But with
coronavirus, the process of thrombolysis will be
difficult, the vessels (and the heart) experience a very
high load, including toxic viral, cytokinin , and the risk
of thrombosis increases by 3-6 times! If a patient
suffers from severe viral pneumonia, has a history of
atherosclerosis, aneurysms, chronic cardiovascular
pathologies, then coronavirus can turn into a disaster.
The vascular walls become thinner, and at the same
time, blood clots are formed, which dissolve with great
difficulty, especially at high temperatures. In some
patients with coronavirus,
a
cytokinin
storm
occurs - an excessive, pathological immune response
to the virus with the release of a huge amount of
protective cytokine molecules. However, they kill not
only the virus, but also destroy healthy cells of the
human div, including the same endothelial ones. Any
infection, viral and especially bacterial, affects blood
clotting. The severity of the consequences, including
thrombotic, depends on the characteristics of the
pathogen and the patient's div. Moreover, for
example, the owners of the first blood group have a
lower risk of thrombosis, while in people with the
second and third this risk is almost 30% higher. There
are patients who naturally have thinner vascular
endothelium. There are patients with genetically
determined
thrombophilia
(a
mutation
that
significantly increases the risk of severe thrombosis).
And thus we come to three conclusions: 1) the cause of
death is not always pneumonia or respiratory failure; 2)
the cause of death is often thrombosis (heart attack,
stroke, pulmonary embolism), as well as toxic damage
to the heart and blood vessels (myocarditis, heart
failure) - the presence of pneumonia is an aggravating
factor; 3) the cause of death can be indirect or direct
infection of other internal organs - the brain, kidneys,
gastrointestinal tract, and the presence of chronic
diseases and pneumonia is an aggravating factor. In
some of the dead, the virus was found even in the
cerebrospinal fluid.
Therefore, the primary task of
treatment for coronavirus is to destroy the infection,
while the high temperature must be brought down and
heparin preparations are prescribed to anticoagulate
the blood and detoxify the div. Late initiation of
anticoagulant therapy is an unfavorable factor that
increases the risk of death.
The most common and
severe complication after coronavirus is thrombosis,
especially with stenosis - vasoconstriction, and
aneurysm ruptures (protrusion of the vessel wall with
its thinning). It should be borne in mind that the
vascular endothelium damaged by the virus recovers
slowly, and the processes occurring in the div give an
increased load on the entire circulatory system.
Thrombi, jelly-like clots of blood, cellular components
and proteins, are formed due to damage to blood
vessels, and even against the background of thickening
(clotting disorders) of the blood. They grow over time
Volume 03 Issue 03-2023
42
American Journal Of Applied Science And Technology
(ISSN
–
2771-2745)
VOLUME
03
I
SSUE
03
Pages:
39-43
SJIF
I
MPACT
FACTOR
(2021:
5.
705
)
(2022:
5.
705
)
(2023:
7.063
)
OCLC
–
1121105677
Publisher:
Oscar Publishing Services
Servi
and circulate in the blood without the patient
suspecting or feeling that a blood clot is forming. These
blood clots can block the arteries of the heart and
brain. Therefore, a complication of coronavirus can be
a heart attack or stroke. Pulmonary embolism (PE) is
no less a threat to life. Moreover, often blood clots that
block the vessels of the lungs initially form in the deep
veins of the legs, after which they break off and move.
Therefore, if there are symptoms such as:
-
sudden unexplained shortness of breath
-
chest pain,
-
blood in cough discharge
-
chest wheezing
-
fainting, cold sweat, and dizziness,
-
a sharp increase in heart rate at rest.
CONCLUSION
The patient is urgently recommended to do a CT scan
of the pulmonary artery with contrast. Unfortunately,
in most cases, such diagnosis is post-symptomatic, as is
the diagnosis of stroke. CT angiography is performed
using contrast. It allows you to see blood clots,
neoplasms, aneurysms, pathologically narrowed
sections of blood vessels. Sometimes ultrasound copes
with this task, while the result of the examination is
perfectly complemented by CT data. Ultrasound allows
you to assess the dynamics of blood flow, to recognize
its violation, while CT is the most reliable method of
visual assessment of blood vessels. As soon as a large
blood clot is detected in the bloodstream, the patient
is prescribed special drugs (thrombolytics, statins) to
reduce it or an invasive thrombolysis procedure.
Therapy and prevention of diseases of the
cardiovascular system after coronavirus should be
comprehensive. Only a doctor can individually select
the necessary diagnostic and therapeutic measures.
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Volume 03 Issue 03-2023
43
American Journal Of Applied Science And Technology
(ISSN
–
2771-2745)
VOLUME
03
I
SSUE
03
Pages:
39-43
SJIF
I
MPACT
FACTOR
(2021:
5.
705
)
(2022:
5.
705
)
(2023:
7.063
)
OCLC
–
1121105677
Publisher:
Oscar Publishing Services
Servi
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