Download S07 Patho Dr Manar Blood Vessel

THE BLOOD VESSELS
Manar hajeer, MD, FRCPath
University of Jordan
Faculty of medicine, pathology department.
Vascular pathology:
1- Narrowing or complete obstruction of vessel
lumina, either progressively (e.g., by
atherosclerosis) or precipitously (e.g., by
thrombosis or embolism).
2- Weakening of vessel walls, causing dilation
and/or rupture.

AIMS:
Atherosclerosis.
 Hypertensive vascular disease.
 Aneurysms.
 Aortic dissection.

ATHEROSCLEROSIS
Characterized by intimal lesions called atheromas
(atherosclerotic plaques) that protrude into vascular
lumina.
Atherosclerotic plaque consists of raised lesion with soft
yellow core of cholesterol covered by a firm, white
fibrous cap.
COMPLICATIONS OF ATHEROMAS:
1. Obstructs blood flow.
2. weakens the underlying media.
3. Rupture, causing acute catastrophic vessel thrombosis.
EPIDEMIOLOGY :
I. Major constitutional risk factors
A-Age :
Has a dominant influence.
Accumulation of atherosclerotic plaque is a progressive
process, but it does not usually become clinically
manifest until lesions reach a critical threshold.
Between ages 40 and 60, the incidence of myocardial
infarction in men increases fivefold.
B- Gender
- Premenopausal women are relatively protected against
atherosclerosis.
- After menopause, the incidence of atherosclerosis-related
diseases increases and with greater age eventually
exceeds that of men.
C- Genetics
- In some instances it relates to familial clustering of other
risk factors , such as hypertension or diabetes.
- Also familial hyperlipidemia , specifically
hypercholesteremia.
II. Major modifiable risk factors
1- Hyperlipidemia
The low-density lipoprotein (LDL) cholesterol ("bad
cholesterol"); has an essential physiologic role delivering
cholesterol to peripheral tissues. In contrast, high-density
lipoprotein (HDL, "good cholesterol") mobilizes
cholesterol from atheromas and transports it to the liver
for excretion in the bile.
Consequently, higher levels of HDL correlate with
reduced risk of atherosclerosis.

High dietary intake of cholesterol and saturated fats
(present in egg yolks, animal fats, and butter, for
example) raises plasma cholesterol levels.

Diets low in cholesterol and/or with higher ratios of
polyunsaturated fats lower plasma cholesterol levels.
Omega-3 fatty acids (abundant in fish oils) are
beneficial.
 (trans)unsaturated fats produced by artificial
hydrogenation of polyunsaturated oils (used in baked
goods and margarine) adversely affect cholesterol
profiles.
 Exercise raises HDL levels, whereas obesity and
smoking lower it.

2. Hypertension:
Both systolic and diastolic levels are important.
o On its own, hypertension can increase the risk of IHD by
approximately 60% in comparison with normotensive
populations.
o Left untreated, roughly half of hypertensive patients will
die of IHD or congestive heart failure, and another third
will die of stroke.
3- Cigarette Smoking:
 A well-established risk factor in men, and an increase in
the number of women who smoke probably accounts for
the increasing incidence and severity of atherosclerosis
in women.
 Prolonged smoking of one pack daily increases the death
from IHD by 200%. Smoking cessation reduces that risk
substantially.
4- Diabetes Mellitus:
- The incidence of myocardial infarction is twice as in nondiabetic individuals.
- There is also an increased risk of strokes.
- There is 100 fold increased risk of gangrene of the lower
extremities.
PATHOGENESIS
Atherosclerosis as a chronic inflammatory response of
the arterial wall to endothelial injury.
 Endothelial Injury and dysfunction:
Endothelial loss by mechanical denudation, hemodynamic
forces and other factors results in intimal thickening; and
in the presence of high-lipid diets, typical atheromas
ensue.
 Inflammation :
Inflammatory cells and mediators are involved in the
initiation, progression, and the complications of
atherosclerotic lesions.

CAUSES OF ENDOTHELIAL INJURY AND
DYSFUNCTION

(hypertension, hyperlipidemia, hyperglycemia, smoking,
hemodynamic factors).

Lipids: Impair endothelial cell function by increasing
local production of reactive oxygen species. Lipoproteins
when oxidized accumulate within the intima, and the
oxidized LDL is ingested by macrophages.
ATHEROSCLEROTIC PLAQUES
The key processes in atherosclerosis are intimal
thickening and lipid accumulation.
Plaques cause intimal thickening and impinge on the lumen
of the artery and grossly appear white to yellow .
Atherosclerotic lesions are patchy, involve only a portion
of the arterial wall ; in early lesions.
DISTRIBUTION OF PLAQUES

In humans, the abdominal aorta is typically much more
frequently involved than the thoracic aorta.

In descending order, the most extensively involved
vessels are the lower abdominal aorta, the coronary
arteries, the popliteal arteries, the internal carotid
arteries, and the vessels of the circle of Willis.

Vessels of the upper extremities are usually spared, as are
the mesenteric and renal arteries except at their ostia.
COMPLICATIONS OF ATHEROSCLEROSIS
1.Rupture, ulceration or erosion of atheromatous plaques
induce thrombus formation and such thrombi can
partially or completely occlude the lumen and lead to
ischemia .
2.Atheroembolism.
3.Aneurysm formation.
SYMPTOMATIC ATHEROSCLEROTIC DISEASE
a. Coronary arteries causing , Myocardial infarction
(heart attack),
b. Cerebral vessels causing cerebral infarction (stroke),
c. Lower extremities: peripheral vascular disease
(gangrene of the legs)
d. Aortic aneurysms,
PRIMARY PREVENTION PROGRAMS
Aims:
a. Delaying atheroma formation.
b. Encouraging regression of established lesions in persons
who have not yet suffered a serious complication of
atherosclerosis.

PRIMARY PROGRAMS
INCLUDE:
a. Cessation of cigarette smoking.
b. Control of hypertension.
c. Weight loss, exercise.
d. Lowering LDL blood cholesterol levels while increasing
HDL ( by diet or statins).
SECONDARY PREVENTION PROGRAMS
Are to prevent recurrence of events such as myocardial
infarction or stroke in symptomatic patients and
involves:
a. The use of aspirin (anti-platelet agent),
b. Statins,
c. Beta blockers (to limit cardiac demand),
d. Surgical interventions (e.g., coronary artery bypass
surgery, carotid endarterectomy).

- These can successfully reduce recurrent myocardial or
cerebral events.
HYPERTENSION
Elevated blood pressure is called hypertension, it is one of
the major risk factors for atherosclerosis.
Pathogenesis of Hypertension
1- 90% to 95% of hypertension is idiopathic (essential)
which is compatible with long life, unless a
myocardial infarction, or stroke supervenes.
2. Secondary hypertension (5%):
a. Renal diseases.
b. Narrowing of the renal artery by atheroma (renovascular
hypertension).
c. Endocrine causes: diseases of the adrenal glands, such
as primary aldosteronism, Cushing syndrome or,
pheochromocytoma.
MALIGNANT HYPERTENSION
A rapidly rising blood pressure (>200\120 mmHg)
that if untreated leads to death within 1 or 2 years.
 Complicates 5% of hypertension cases.
 The clinical syndrome is characterized by:
1. Severe hypertension (diastolic pressure over
120mmHg),
2. Renal failure.
3. Retinal hemorrhages with or without papilledema

1. ESSENTIAL HYPERTENSION
- Alterations in renal sodium homeostasis and/or vessel
wall tone underlie essential hypertension.
- Both increased blood volume and increased peripheral
resistance contribute to the increased pressure.
- Results from an interplay of genetic and environmental
factors (stress, obesity, smoking, physical inactivity, and
heavy consumption of salt) affecting cardiac output and/or
peripheral resistance.
VASCULAR PATHOLOGY IN HYPERTENSION
a- It accelerates atherogenesis.
b- It induces degenerative changes in the walls of arteries
that potentiate aortic dissection and hemorrhagic
stroke .
c. It is associated with small vessel disease: Hyaline
arteriolosclerosis and hyperplastic arteriolosclerosis.
1. HYALINE ARTERIOLOSCLEROSIS
Consists of pink hyaline thickening of the walls of arterioles
with narrowing of the lumen.
 Is seen frequently in elderly patients, whether normotensive
or hypertensive, but more generalized and severe in patients
with hypertension.
 Also common in diabetics.

2. HYPERPLASTIC ARTERIOLOSCLEROSIS.
- Related to more acute or severe elevations of blood
pressure
- It is characteristic of (but not limited to) malignant
hypertension.
- Associated with acute cerebral and/or renal injury.
- It is associated with onion-skin thickening of arterioles
with luminal narrowing.
ANEURYSM
Is a localized abnormal dilation of a blood vessel or the heart,
and its types:
1.True aneurysm:
- It involves all three layers of the arterial wall (intima, media,
and adventitia) (Examples: :Atherosclerotic, syphilitic or
the attenuated wall of the heart “ventricular aneurysms”)
2. False aneurysm ( pseudoaneurysm)
- Is a breach in the vascular wall leading to an extravascular
hematoma that communicates with the intravascular space
("pulsating hematoma").
- Example: Ventricular ruptures after myocardial infarctions that
are contained by a pericardial adhesion .
Both true and false aneurysms can rupture, often with
catastrophic consequences.
Causes of aneurysms:
1. The main cause of aortic aneurysms is atherosclerosis.
2. Vasculitis .
3. Mycotic aneurysm: Infection of a major artery that
weakens its wall, can originate from:
a. Embolization of a septic thrombus, as a complication of
infective endocarditis.
b. Extension of an adjacent suppurative process.
ABDOMINAL AORTIC ANEURYSM (AAA)
- Atherosclerosis, is the most common cause of
aneurysms.
- Atherosclerotic plaques compress the underlying media
and also compromise nutrient and waste diffusion from
the vascular lumen into the arterial wall.
- The media consequently undergoes degeneration and
necrosis, thus allowing the dilation of the vessel.

Atherosclerotic aneurysms occur most frequently in
the abdominal aorta (often abbreviated AAA), but the
common iliac arteries, the aortic arch, and descending
parts of the thoracic aorta can also be involved.
THE CLINICAL CONSEQUENCES OF AAA :
1. Rupture into the peritoneal cavity with massive fatal
hemorrhage.
2. Obstruction of a vessel resulting in ischemic injuryrenal (kidney infarction), mesenteric (GI tract
infarction).
3. Embolism from atheroma or thrombus.
4. Compression of a ureter .
5. An abdominal mass (often palpably pulsating) that
simulates a tumor .
The risk of rupture is related to the size of the
aneurysm, varying from nil for AAAs of 4cm or less
to 25% per year for aneurysms larger than 6 cm.
- Aneurysms of 5 cm or more are managed aggressively,
usually by surgery.
AORTIC DISSECTION
- Is a catastrophic event ,whereby blood split apart the
laminar planes of the tunica media to form a bloodfilled channel within the aortic wall.
- This channel often ruptures through the adventitia and
into various spaces where it causes either:
1. Massive hemorrhage.
2. Cardiac tamponade (haemorrhage into the pericardial
sac).
CAUSES:
1. Men aged 40 to 60 years with hypertension (more than
90% of cases)
2. Younger patients with systemic or localized
abnormalities of connective tissue affecting the aorta
(e.g., Marfan syndrome)
3. Iatrogenic, complicating arterial diagnostic
catheterization.
4. Rarely, dissection of the aorta or other branches,
including the coronary arteries, occurs during or after
pregnancy.

Dissection is unusual in the presence of
atherosclerosis or other causes of medial scarring,
such as syphilis, because the medial fibrosis inhibits
propagation of the dissecting hematoma.
Regardless of the underlying etiology that causes medial
weakness, the trigger for the intimal tear and initial
intramural aortic hemorrhage is not known in most
cases.
 Nevertheless, once the tear has occurred, blood flow
under systemic pressure dissects through the media,
augmenting progression of the medial hematoma.
 Accordingly, aggressive pressure-reducing therapy
may be effective in limiting an evolving dissection.
