Disorders of Arterial

Circulation
Cres P. Quinzon
Oman College of Health Sciences
1st Trimester 2019-2020
Disorders of Arterial Circulation

•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
Disorders of Arterial Circulation

•4.Differentiate berry and saccular

aneurysms
•5.Describe the etiology, pathogenesis of
aortic dissection and abdominal aortic
aneurysms
•6. Describe the etiology and pathogenesis
of aortic, abdominal and dissecting
aneurysms
Hyperlipidemia
Fat Transport in the Body
Lipoproteins cover the
fats and travel through
REVIEW ONLY the water-based
Digestion of fats in environment of the
intestines from the body
Fats in the liver by the bile and
mouth pancreatic lipase from
the pancreas

Lipoproteins
HDL’s take
transported in the
cholesterol back lymphatic system
to liver where it is and enter the
removed from the bloodstream
system

LDL’s remain in the blood,

deliver cholesterol to cells,
where it fills important jobs
Hyperlipidemia

•is an excess of lipids in the blood

•Lipids are classified as triglycerides or
neutral fat, phospholipids, and
cholesterol.
Hyperlipidemia

•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.
Hyperlipidemia

•3. Cholesterol, its chemical and physical

activity is similar to that of other lipid
substances.
Classification of Lipoproteins

•Cholesterol and triglyceride are

insoluble in plasma, they are
encapsulated by a stabilizing coat of
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
•Etiology :
•There are five types of lipoproteins based on
their densities:
•Chylomicrons (fat from intestines to liver, skeletal muscles
and adipose tissues)
•very–low-density lipoprotein (VLDL), carry (newly
synthesised) triglycerides from the liver to adipose tissue.
•intermediate-density lipoprotein (IDL), (same as LDL)
•low-density lipoprotein (LDL), deliver cholesterol to cells,
where it fills important jobs
•high-density lipoprotein (HDL) (from body to liver for
removal)
Hyperlipidemia

•Etiology : cont

•Serum cholesterol levels may be

elevated as a result of an increase in any
of the lipoproteins—the chylomicrons,
VLDL, IDL, LDL, or 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)
Hyperlipidemia

•Pathogenesis:
• Hypercholesterolemia (hyperlipoproteinemia) can be
classified as :

• Primary hypercholesterolemia describes elevated

cholesterol levels that develop independent of other
health problems or lifestyle behaviors
• Secondary hypercholesterolemia is associated with
other health problems and behaviors.
 Hyperlipidemia

Primary Secondary
hypercholesterolemia hypercholesterolemia
ETIOLOGY
genetic basis (defective obesity with high-calorie intake,
synthesis of apoproteins, lack of diabetes mellitus, hypothyroidism,
receptors, defective receptors, nephrotic syndrome and obstructive
liver disease;
or defects in the handling of
Medications such as beta-blockers,
cholesterol in the cell) estrogens, and protease inhibitors
(used in the treatment of human
immunodeficiency virus [HIV]
Primary Hyperlipidemia Pathogenesis

Gene mutation for the LDL

receptors (mostly found in the
liver)

LDL receptors in the

blood

blood cholesterol levels in the

blood are markedly elevated
Secondary Hyperlipidemia Pathogenesis

High calorie diets, Diabetes

Mellitus increase the
increase
production of VLDL
triglycerides
(hyperliporoteinemia)

VLDL conversion to
Increase LDL
Suppress LDL cholesterol
synthesis
receptor
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.
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
• Non-traditional Risk Factors:
• C-reactive protein (CRP)- serum marker for systemic
inflammation
• High-sensitivity CRP may be a better predictor of
cardiovascular risk than lipid measurement alone
• Homocysteine- an amino acid in animal protein
• inhibits elements of the anticoagulant cascade
Associated with endothelial damage, which is thought to be
an important first step in the development of
atherosclerosis
• Infectious Agents- (e.g., Chlamydia pneumoniae, herpesvirus,
cytomegalovirus)
• The organisms may play a role in atherosclerotic
development and initiating and enhancing the
inflammatory response
Atherosclerosis

•Pathogenesis
•The lesions associated with atherosclerosis
are of three types :
- fatty streak
- fibrous atheromatous plaque,
- complicated lesion
 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
Streaks foam cells.

• gray to pearly white appearance due to the macrophages

Fibrous that ingest and oxidize accumulated lipoproteins and
atheromatous
plaque
form a visible fatty steak

Complicate
• contain hemorrhage, ulceration, and scar tissue deposits.
d lesions
Atherosclerosis

• The development of atherosclerotic lesions is

a progressive process involving
• (1) endothelial cell injury,
•(2) migration of inflammatory cells,
• (3) SMC (smooth muscle cells ) proliferation and
lipid deposition, and
•(4) gradual development of the atheromatous
plaque with a lipid core.
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.
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

•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

•Etiology: weakness of the vessel wall caused

by:

•congenital defects,
•trauma,
•infections, and
•atherosclerosis
Aneurysm
True Aneurysm False Aneurysm
• aneurysm is • or pseudoaneurysm
bounded by a presence of a localized
complete vessel wall tear in the inner wall of
the artery with
formation of an
• blood remains hematoma that causes
within the vascular vessel enlargement
compartment
Aneurysm
 TRUE ANEURYSM

Berry aneurysm Saccular aneurysm Fusiform aneurysm

true aneurysm that true aneurysm that true aneurysm that

consists of a small, extends over part of involves the entire
spherical dilation of the circumference of circumference of the
the vessel at a the vessel and appears vessel; gradual and
bifurcation. (circle of saclike. progressive dilation of
Willis) the vessel.
Aortic Aneurysm

•may involve any part of the aorta—the

ascending aorta, descending aorta,
thoracoabdominal aorta, or abdominal aorta.

•Multiple aneurysms may be present.

Aortic Aneurysm Ascending aorta

Descending aorta

Thoracic aorta
Aneurysm
 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
• Congenital defects of aorta (structural)
• Potential complication of cardiac surgery and
catheterization
Aortic Dissection Aneurysm