2. Running Head: DEEP VEIN THROMBOSIS
1
DEEP VEIN THROMBOSIS
6
PATHOPHYSIOLOGY CASE STUDY
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Leona was overweight and she was suffering from
atherosclerosis even before she travelled. Her trip to Australia
led to the developments of thrombosis. Atherosclerosis refers to
the condition where cholesterol, calcium and fats (also referred
to as plaque) build inside the arteries (Badimon, et.al, 2012).
Arteries are the vessels in the body that transport oxygenated
blood from the heart to the other parts of the body. Therefore
constriction of the blood vessels that arises from plaque deposit
limits the transportation and flow of oxygenated blood in the
body. Hyper-coagulation is an acquired or inherited condition
and in most cases arises due to cancer, pregnancy, trauma,
obesity, prolonged rest or immobility. Given that Leona was
overweight, the prolonged immobility over the course of her
flight played a role in the development of deep vein thrombosis.
3. Leona had acquired hyper-coagulation because she was
overweight, and coupled with the long flight, clots developed in
her leg (Rissanen, 2014). These two conditions resulted in the
formation of blood clots in the vein (venous thrombosis) that
occur in the deep vein which runs from the thigh muscles to the
calf of the leg. Leona was a cigarette smoker and this exposed
her to a high risk of thrombus development as it initiates the
exacerbation of the process of atherosclerosis (Diana, 2013).
Being overweight, a smoker and immobile increased the
possibility of development of deep vein thrombosis. Other
factors that exposed Leona to the development of DVT include
inactivity and previous venous thromboembolism.
Platelets are cells that are found in the blood and their
origination is the megakaryocytic cytoplasm which is located in
the bone marrow. The cells circulate in the body as the blood
moves playing a homeostatic role and also assisting in the
formation of the thrombus layer following an endothelial injury
(Badimon, et.al, 2012). Arterial diseases and coronary diseases
are often as a result of atherosclerosis. Lymphocytes and lipids
accumulate in the large arteries leading to inflammation. This
lymphocyte and lipids deposition leads to the thickening of the
arterial walls and the constrictions of the arteries. This limits
the movement of platelets (in the blood) whose main role is to
aid n clotting of blood when one is injured. The deposition of
plaque and disruption of the flow of platelets causes the
platelets to “stick” to each other through membranous union
upon injury. This activation of the clotting cascade causes
atherothrombosis, Atherosclerosis therefore limits the platelet
functionality with regards to blood clotting after injury or after
an endothelial lining (Davis, 2015). The platelets are not only
involved in homeostatic functions and formation of thrombus
but they are also involved in transporting regulatory molecules
when an inflammation occurs in mediation of the progress of
atherosclerosis.
When an individual is travelling on a plane for long periods,
they are relatively immobile. Stasis causes platelets and
4. activated clotting factors to accumulate. Immobility also leads
to a decrease in the chemical interactions with the inhibitors of
coagulation. Ultimately this increases the risk of formation of
thrombus, In Leona’s case, her weight and habit of smoking
were increased risk factors for thrombus formation.
Atherosclerosis disrupts blood flow and it also damages the
endothelium thereby increasing the adherence of the platelets
(Rissanen, 2014). The platelets are also increasingly sensitive to
factors that lead to aggregation and adhesiveness. The adhering
platelets lodge growth factors that enhance the proliferation of
the smooth muscles in the wall of the arteries. As a result, the
aggregation of the platelets contribute to the formation and
progression of atherosclerosis. These two conditions increase
the possibility of cogulability. Atherosclerosis causes an
increase in the functions of the platelets through adherence and
aggregation. In contrast, immobility causes hypercoagulability
as it causes a spike in the procoagulation factors. Blood clots
form after the crack of the fibrous cap in the atherosclerotic
plaque thereby reducing the amount of blood that is flowing
through that specific blood vessel.
Clots can dislodge and travel from their point of formation. This
may lead to a reduction of blood flow in organs such as the
lungs, heart and brain. A blood clot that has dislodged is
referred to as an embolus. Approximately 80% of heart attacks
occur as a result of the formation of an undesirable clot that
blocks the flow of blood in arteries that supply the heart with
blood. Immobility of the limbs also raises the possibility of clot
occurrence because it slows down the process of blood
circulation thereby increasing the likelihood of pooling
(Badimon, et.al, 2012). When a pool of blood is static, this is
an ideal environment for the formation of a clot. According to
reports obtained from the World Health Organization, the risks
of developing deep vein thrombosis double when one travels in
a plane. However, the risk of DVT formation is still very
minimal considering that only one 1 in 6,000 people can
develop DVT from remaining completely immobile during a
5. flight.
Heparin is an anti-coagulant drug that prevents formation of
blood clots. It is also referred to as a blood thinner as it serves
the purpose of thinning blood to ensure that it flows more easily
through constricted vessels. It is used to prevent formation and
treat blood clots that have lodged in the lungs, veins or in the
arteries. Heparin also prevents the formation of new clots and
it also limits the already formed clots from enlarging. It is able
to do this by inhibiting the production of proteins that have to
be formed in order for the clot to be formed (Ziegelstein, 2016).
In the absence of these proteins, blood clots cannot be formed.
Heparin injections or therapy that are administered by a health
institution are the right way to contain Leona’s condition. The
injection delivers an intravenous solution deep into the veins.
The intravenous injection gets straight to the veins and
therefore it will aid Leona in felling batter much faster. Tablets
would have also delayed the anticoagulation process in Leona’s
case. However, if the therapist chose to use Heparin tablets,
which would have been administered orally, it would have taken
a longer time for the drug to be absorbed into the blood system.
Since the Heparin injection is administered in liquid form, it is
easy for it to get absorbed into the blood and it is also easier for
it to flow through the entire body. The effects of the Heparin
would therefore be felt all over the body thereby reducing the
size of the already formed clots and preventing the formation of
other clots. The tablets would not be the best option to contain
Leona’s situation as it would only derail the recovery process.
Leona’s condition had escalated from bad to worse and it
therefore needed to be contain as fast as possible.
6. References
Badimon, L., Padró, T., & Vilahur, G. (2012). Atherosclerosis,
platelets and thrombosis in acute ischaemic heart disease.
European Heart Journal , 60-74.
Diana, J. N. (2013). Tobacco Smoking and Atherosclerosis:
Pathogenesis and Cellular Mechanisms.
Rissanen, P., et al,(2014). Weight change and blood
coagulability and fibrinolysis in healthy obese women. Int J
Obes Relat Metab Disord, 25(2):212-218,
Davis, J.W., et al,(2015) Effects of tobacco and non-tobacco
cigarette smoking on endothelium and platelets. Clinical
Pharmacological Therapy, 37(5):529-533
Ziegelstein, R.C., et al, (2016). Platelet function in patients
with major depression. Intern Med J, 39(1):38-43