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BMI3707- SOLVED EXAM PAPERS AND ASSIGNMENT - PAST 6 YEARS - GET YOUR A+ NOW WITH SCIENCERATUTORS

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Are you a student enrolled in BMI3707 Clinical Pathology 3, seeking top-notch exam preparation materials and assignment solutions? Look no further! Sciencera Tutor is proud to present our comprehensive and expertly crafted BMI3707 Clinical Pathology 3 Exam Paper and Assignment Package. What You'll Get: Detailed Exam Paper: Our exam paper is designed to reflect the actual exam format and content. It includes a wide range of questions covering the essential topics from BMI3707 Clinical Pathology 3, ensuring you're thoroughly prepared for your assessment. Step-by-Step Assignment Solutions: We provide meticulously solved assignments that not only meet the course requirements but also serve as valuable learning resources. Use them as a reference to ace your assignments with ease.

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Subido en
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CLINICAL PATHOLOGY III
BMI3707




rubbia khalid
TEACH ME 2 https://www.teachme2.com/tutors/rubbia-29398

,Question 1

1.1 What are the functions of normal endothelial cells

The functions of normal endothelial cells involve regulated mediator secretion or altered surface
protein expression. This is vital for normal homeostasis. In a nutshell, functions of normal
endothelial cells are not limited to:

a) Anti-thrombotic

b) Maintains vascular tone through both vasoconstrictor and vasodilator actions

c) Metabolizes hormones and lipoproteins

d) Transfers gases and

e) Delivers salutes or hormones to and removes toxic metabolites from tissues.



1.2 Name the types and complications of aneurysms

Aneurysms is a bulge that occurs on the blood vessels walls. It occurs when there is erosion in
the media. It occurs in arteries and occasionally the left ventricle. Aneurysm occurs at points of
weakness usually due to atheroma and sometimes due to inflammation damage caused by
diseases like syphilis. It can be occasionally caused by connective tissues abnormalities and
sometimes following trauma (Finlayson & Newell, 2009, p77). There are four types of aneurysm
which are:

a) Fusiform aneurysm which is a spindle shaped aneurysm typical of atheroma. This is the most
common type of aneurysm.

b) Saccular aneurysm which occur after focal vessel damage example after trauma or infection.
Bacteria from the bloodstream may find its home on the atheromatous plaque which is often
seen after operating bacteria rich sites such as bowel. A transient bacteraemia is usually present.
The roughened wall over an atheromatous plaque, often with underlying thrombus, provides a
nidus for infection.

,c) Berry aneurysm is a congenital weakness in the media at the branching point of cerebral
vessels. It is not related to atheroma.

d) Aortic aneurysm is of partial thickness. Dissection is typical of Marfan Syndrome but it can
also occur in elderly patients. A tear of the intima precipitates blood to flow along the congenitally
weak media. This may rapture back into the aorta or rapture through the adventia thereby
causing death by cardiac tamponade or exsanguinations

Complications of aneurysms include:

a) Rapture which manifests with pain depending on location of rapture, low blood pressure,

a rapid heart rate and light-headedness.

b) Thrombosis- depending on where the clot has traveled to, thromboembolism can cause pain
in the extremities or the abdomen. Stroke can ensue if the clot travels to the brain.

c) Thromboembolism (Finlayson & Newell, 2009, p77).

d) Re-bleeding - an aneurysm that has ruptured or leaked has a high chance of bleeding again.

e) Vasospasm – after brain aneurysm ruptures, blood vessels in the brain may narrow erratically

f) Hydrocephalus - a condition in which fluids accumulate in the brain usually in young children
thereby enlarging the head and sometimes causing brain damage

g) Hyponatremia – is a condition that occurs when sodium levels in the blood are abnormally
low



1.3 List four common acyanotic congenital heart defects

Acyanotic condition is when the systemic blood is adequately oxygenated. There are four
common acyanotic congenital heart defects which are Ventricular septal defect, Atrial Septal
defect, Patent ductus arteriosus and coarctation of the aorta.

a) Ventricular septal defects (VSDs) being the most frequent congenital malformations that affect
the heart. The defect is located on the membranous part of the interventricular septum. It permits
left to right shunt of a proportion of oxygenated blood in the left ventricle into the right ventricle

, b) Atrial septal defect in which we have defects arising from the ostium secondum and is located
in the region of the fossa ovalis. Ostium primum defects are situated near aterioventricular valves
and are associated with Down Syndrome.

c) Patent ductus arteriosus which is a duct that connects the pulmonary artery to the aortic arch
which functions to shunt blood away from the lungs to maintain systemic circulation.

d) Coarctationof the aorta which is the narrowing of the aorta that occurs near the ductus
arteriosus distal to the left subclavian artery (Mhkombo, 2018).



Question 2

2.1 Distinguish between arteriosclerosis and atherosclerosis

Arteriosclerosis Atherosclerosis
Hardening of arterioles Hardening of arteries due to atheroma
Damage of vessels is by pressure which Is caused by build-up of fatty plaque,
permits build up of proteins into vessels walls cholesterol and other substances in the artery
walls. Also caused by high blood pressure,
smoking or high cholesterol
Leads to ischemia Leads to creation of a bump which can
become bigger potentially creating a blockage
The usual cause is hypertension which affects Fibrosis and calcification of the plaque
the arterioles, the vessels mainly responsible reduces distensibility of the artery and cause
for peripheral vascular resistance hardening
High blood pressure leads to duplication of This does not cause hypertension as the
elastic laminae and an increase in the smooth vessels which determine peripheral vascular
muscle component of the wall, which narrow resistance are not affected
the lumen and thicken the wall
Plasma proteins are forced into the wall of the
artery, where they form an amorphous
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