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Disorders of Arterial Circulation

Disorders of Arterial
Circulation
Cres P. Quinzon
Oman College of Health Sciences
1st Trimester 2019-2020
•OBJECTIVES:
•1.Describe the etiology and
pathogenesis of hyperlipidemia
•2.Describe the etiology and
pathogenesis of artherosclerosis
•3.Differentiate between a true and false
aneurysm

Hyperlipidemia
Fat Transport in the Body
Disorders of Arterial Circulation Lipoproteins cover the
fats and travel through
REVIEW ONLY the water-based
Digestion of fats in environment of the
•4.Differentiate berry and saccular Fats in the
intestines from the
liver by the bile and
body
aneurysms mouth pancreatic lipase from
the pancreas
•5.Describe the etiology, pathogenesis of
Lipoproteins
aortic dissection and abdominal aortic HDL’s take
transported in the
cholesterol back
aneurysms to liver where it is
lymphatic system
and enter the
•6. Describe the etiology and pathogenesis removed from the
system
bloodstream

of aortic, abdominal and dissecting

aneurysms LDL’s remain in the blood,
deliver cholesterol to cells,
where it fills important jobs

Hyperlipidemia Hyperlipidemia

•is an excess of lipids in the blood
•Lipids are classified as triglycerides or
neutral fat, phospholipids, and
cholesterol.
•1. Triglycerides are fatty acids that are
used in energy metabolism.
•2. Phospholipids are important
structural constituents of lipoproteins,
blood clotting components, the myelin
sheath, and cell membranes.

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Hyperlipidemia Classification of Lipoproteins

•Cholesterol and triglyceride are

•3. Cholesterol, its chemical and physical insoluble in plasma, they are
activity is similar to that of other lipid encapsulated by a stabilizing coat of
substances. water-soluble phospholipids and
proteins (called apoproteins)
•These particles, which are called
lipoproteins, transport cholesterol and
triglyceride to various tissues for
energy utilization, steroid hormone
production, and bile acid formation

Hyperlipidemia Hyperlipidemia

•Etiology : •Etiology : cont

•There are five types of lipoproteins based on
their densities: •Serum cholesterol levels may be
•Chylomicrons elevated as a result of an increase in any
•very–low-density lipoprotein (VLDL), of the lipoproteins—the chylomicrons,
•intermediate-density lipoprotein (IDL), VLDL, IDL, LDL, or HDL
•low-density lipoprotein (LDL), and
•high-density lipoprotein (HDL)

Hyperlipidemia

•Etiology: cont
•Nutrition
•Genetics
•Medications (beta-blockers, estrogens and
protease inhibitors)
•Comorbid conditions (additional disorders
occurring with the primary disease)
•Metabolic diseases ( diabetes,
hyper/hypothyroidism)

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Hyperlipidemia Hyperlipidemia

Primary Secondary
•Pathogenesis:
hypercholesterolemia hypercholesterolemia
• Hypercholesterolemia (hyperlipoproteinemia) can be
classified as : ETIOLOGY
genetic basis (defective obesity with high-calorie intake,
synthesis of apoproteins, lack of diabetes mellitus, hypothyroidism,
• Primary hypercholesterolemia describes elevated nephrotic syndrome and obstructive
receptors, defective receptors,
cholesterol levels that develop independent of other liver disease;
or defects in the handling of
health problems or lifestyle behaviors Medications such as beta-blockers,
cholesterol in the cell) estrogens, and protease inhibitors
• Secondary hypercholesterolemia is associated with
(used in the treatment of human
other health problems and behaviors. immunodeficiency virus [HIV]

Primary Hyperlipidemia Pathogenesis Secondary Hyperlipidemia Pathogenesis

Gene mutation for the LDL

receptors (mostly found in the
liver) High calorie diets, Diabetes
Mellitus increase the
increase
production of VLDL
triglycerides
(hyperliporoteinemia)
LDL receptors in the
blood
VLDL conversion to
Increase LDL
Suppress LDL cholesterol
blood cholesterol levels in the receptor
synthesis

blood are markedly elevated. activity

Atherosclerosis

•Atherosclerosis is a type of arteriosclerosis

( hardening of the arteries )

•formation of fibrofatty lesions in the intimal

lining of the large- and medium-sized arteries
such as the aorta and its branches, the
coronary arteries, and the large vessels that
supply the brain, thereby, obstructing blood
flow.

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Atherosclerosis
•Etiology and Risk Factors:
Hypercholesterolemia, increasing age, family
history of premature CHD, male sex, cigarette
smoking, obesity and visceral fat,
hypertension, diabetes mellitus, cigarette
smoking, hypertension
•The role of inflammation in the etiology of
atherosclerosis has emerged over the last few
years.

Atherosclerosis
• Etiology and Risk Factors: cont Atherosclerosis
• Non-traditional Risk Factors:
• C-reactive protein (CRP)- serum marker for systemic
inflammation
• High-sensitivity CRP may be a better predictor of •Pathogenesis
cardiovascular risk than lipid measurement alone •The lesions associated with atherosclerosis
• Homocysteine- an amino acid in animal protein
are of three types :
• inhibits elements of the anticoagulant cascade
Associated with endothelial damage, which is thought to be - fatty streak
an important first step in the development of
atherosclerosis - fibrous atheromatous plaque,
• Infectious Agents- (e.g., Chlamydia pneumoniae, herpesvirus, - complicated lesion
cytomegalovirus)
• The organisms may play a role in atherosclerotic
development and initiating and enhancing the inflammatory
response

Atherosclerosis Atherosclerosis
Lesions Associated with Atherosclerosis
• thin, flat, yellow intimal discolorations that progressively enlarge by
becoming thicker and slightly elevated as they grow in length.
Fatty • consist of macrophages that have become distended with lipid to form foam
Streaks cells. • The development of atherosclerotic lesions is
a progressive process involving
• gray to pearly white appearance due to the macrophages
Fibrous that ingest and oxidize accumulated lipoproteins and • (1) endothelial cell injury,
atheromatous
plaque
form a visible fatty steak •(2) migration of inflammatory cells,
• (3) SMC (smooth muscle cells ) proliferation and
Complicate
• contain hemorrhage, ulceration, and scar tissue deposits. lipid deposition, and
d lesions •(4) gradual development of the atheromatous
plaque with a lipid core.

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1. Endothelial Cell Injury
• smoking, elevated LDL levels,
immune mechanisms, and
mechanical stress cause
endothelial injury with adhesion
of monocytes and platelets
4. Plaque Structure
• “foam cells” accumulate to
form atherosclerotic plaques
fibrous cap is formed, and may
rupture and lead to
hemorrhage or thrombotic
occlusion of the vessel lumen.
Aneurysm
•An aneurysm is an abnormal localized
dilation of a blood vessel.
•Aneurysms can occur in arteries and veins,
but they are most common in the aorta.
Aneurysm
True Aneurysm
• aneurysm is bounded by a
complete vessel wall
• blood remains within the
vascular compartment
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2. Migration of Inflammatory Cells
• monocytes transform into
macrophages, engulf lipoproteins,
largely LDL and migrate between the
endothelial cells to localize and adhere
in the intima.
3. Lipid Accumulation and
Smooth Muscle Cell
Proliferation
•Activated macrophages
release toxic oxygen
species that oxidize LDL,
ingest the oxidized LDL to
become “foam cells”
Aneurysm
•Etiology: weakness of the vessel wall caused
by:
•congenital defects,
•trauma,
•infections, and
•atherosclerosis
Aneurysm
False Aneurysm
• or pseudoaneurysm presence
of a localized tear in the
inner wall of the artery with
formation of an hematoma
that causes vessel
enlargement
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TRUE ANEURYSM

Berry aneurysm Saccular aneurysm Fusiform aneurysm Aortic Aneurysm

true aneurysm that true aneurysm that true aneurysm that
consists of a small, extends over part of the involves the entire •may involve any part of the aorta—the
spherical dilation of the circumference of the vessel circumference of the
vessel at a bifurcation. and appears saclike. vessel; gradual and ascending aorta, descending aorta,
(circle of Willis) progressive dilation of the thoracoabdominal aorta, or abdominal aorta.
vessel.

•Multiple aneurysms may be present.

Aortic Aneurysm Ascending aorta

Aneurysm

Descending aorta

Thoracic aorta

Etiology and Pathogenesis

Abdominal Aortic Aortic Dissection (dissecting aneurysm)
Aneurysm
• most common causes • hemorrhage into the vessel wall with
of aortic aneurysm- longitudinal tearing of the vessel wall to
Atherosclerosis, form a blood-filled channel
degeneration of the • is an acute, life threatening condition
vessel • caused by conditions that weaken or
• Degeneration of the cause degenerative changes in the
vessel media layers of the aorta.
• 40-60 years age group, men
• Hypertension, more
• Hypertension
in men, after 50 years
• degeneration of medial layer of blood vessel
• Smoking • Pregnancy Aortic Dissection Aneurysm
• Congenital defects of aorta (structural)
• Potential complication of cardiac surgery and
catheterization