1. Atherosclerosis. Types. Risk factors for atherosclerosis.

In atherosclerosis, inflammatory and immune cells, smooth muscle cells, lipid and connective tissue
progressively accumulate in the intima of large and medium-sized elastic and muscular arteries. The
classic atherosclerotic lesion is best described as a fibroinflammatory lipid plaque (atheroma).
An atheromatous plaque consist of a raised lesion with a soft, yellow, grumous core of lipid (mainly
cholesterol and cholesterol esters) covered by a firm, white fibrous cap. Besides obstruction blood flow,
atherosclerotic plaques weaken the underlying media and can themselves rupture, causing acute
catastrophic vessel thrombosis.
Risk factors
• A family history of early heart disease.
• An unhealthy diet.
• Diabetes.
• High blood pressure.
• High cholesterol.
• High levels of C-reactive protein (CRP), a marker of inflammation.
• Lack of exercise.
• Obesity.

2.Morphology of atherosclerosis. Complication of

atherosclerosis.
Grossly recognizable atherosclerosis begins as a fatty streak and progresses to an atherosclerotic plaque.
➢Fatty streak are cd-filled foam cells but are not significantly raised and thus do not cause any disturbance in
blood flow. They begin as multiple minute yellow, flat spots that can coalesce into elongated streaks, 1 cm long
on longer.
➢Atherosclerotic plaque – also called fibrous or fibrofatty plaques impinge on the lumen of the artery and
grossly appear white to yellow; thrombosis superimposed over the surface of ulcerated plaques is red-brown in
color. Plaque

Complication:
Complications of atherosclerosis include: stroke or TIA in the brain, angina (chest pain), heart
attack, sudden death, heart failure kidney failure, erectile dysfunction and PAD (peripheral artery
disease).

3. Benign hypertension. Definition. Morphology.

Benign – has a slow clinical course. Patients can survive with the diseases for 10-20byears or more.
Note, that despite the designation of “benign’’, all forms of hypertension are associated with
increased morbidity and mortality

Morphology:
Hyaline arteriolosclerosis: associated with benign hypertension. This vascular lesion consists of a
homogeneous pink hyaline thickening of the walls of arterioles with loss of underlying structural
detail and with narrowing of the lumen.
4. Malignant hypertension. Definition. Morphology.
Malignant – has a rapid clinical course. Death occur within 1 to 3 years. Patients have retinal
hemorrhage, papilledema and renal failure. Malignant hypertension can arise in the
background of “benign” hypertension, or it can arise de novo.

Morphology :
•Hyperplastic arteriolosclerosis: associated with malignant hypertension. Hyperplastic
arteriolosclerosis is associated with “onion-scin”, concentric, laminated thickening of the
walls of
arterioles with luminal narrowing.

5. Aneurysm. Definition. Types.

An aneurysm (“true” aneurysm) is a localized abnormal dilation of the wall of a blood vessel
involving all layers.
A “false” aneurysm (pseudoaneurysm) is a defect in the wall allows blood to escape the vessel or
organ and accumulate outside the wall. False aneurysms can result from trauma
Types of aneurysm
➢ Saccular aneurysm: saccular outpouching from one side of
the affected vessel
➢Fusiform aneurysm: generalized dilation of the entire
circumference of the affected vessel

6. Morphology of aneurysms
➢Abdominal aortic aneurysm (AAA) – usually positioned below the renal arteries and above
the bifurcation of the aorta, AAA can be saccular or fusiform, as large as 15 cm in diameter and
as long as 25 cm. The aneurysm frequently contains a bland, laminated, poorly organized mural
thrombus that may fill some of or all of the dilated segment.

7. Complications of aneurysm.
•Emboli from atherosclerotic plagues that form within the aneurysm.
•Thrombosis: aneurysm allows for stagnation of blood and formation of thrombi, with or
without resultant emboli.
•Rupture of aneurysm with resultant hemorrhage. Triad: abdominal pain, hypotension and
pulsatile abdominal mass.
•Obstruction od branch vessels. •Impingement on neighboring structures

8. Aortic dissection. Definition. Types

Aortic dissection is separation of the aortic media by blood entering the wall through an intimal
tear. In contracts to atherosclerotic and syphilitic aneurysms, aortic dissection may or may not be
associated with aortic dilation. Consequently, the older term “dissecting aneurysm” is discouraged.
Types:

Type I involves the ascending aorta, arch, and descending thoracic aorta and may progress to involve the
abdominal aorta. Type II is confined to the ascending aorta. Type IIIa involves the descending thoracic
aorta distal to the left subclavian artery and proximal to the celiac artery.
9. Classification of Aortic dissection.

(1)Stanford classification

1-Type A ascending aorta

2- Type B descending aorta

(2) DeBakey Classification

1- Type 1 ascending aorta, arch and descending aorta

2- type 2 ascending only
3- Type 3 descending only

10.Complications of aortic dissection

if the second tear is in the intima in another location: results in a “double-barrel” aorta, the most
benign complication of an aortic dissection.
•if the second tear is in the pericardial sac: results in hemopericardium and possible cardiac
tamponade.
•with involvement of the aortic valve ring: disrupts stability of the valve, leading to aortic
insufficiency.
•if the second tear is into the pleural cavity: results in hemothorax.
•if the second tear is into the retroperitoneum: results in retroperitoneal hemorrhage.

11. Vasculitis. Definition. Types.

Vasculitis is inflammation of the vessels, which most commonly has an infectious or immune-
mediated cause. In most forms of vasculitis.
In the most forms of vasculitis the pathological changes in the vessels are broadly similar.
There are many types of vasculitis, and most of them are rare. Vasculitis might affect just one
organ, or several. The condition can be short term or long lasting.
12. Giant cells arteritis. Clinical manifestations. Morphology

includes visual disturbances (diplopia and visual loss) and unilateral temporal headache and jaw
claudication. Patients can have an elevated erythrocyte sedimentation rate.
•Microscopic morphology: granulomatous inflammation of vessel wall with disruption of elastic
lamellae.

13. Kawasaki arteritis. Clinical manifestations. Morphology.

Kawasaki disease classically presents in children younger than 5 years of age who present with a
high fever (up to 400 C, or 104 F) for more than 5 days; with conjunctivitis, strawberry tongue,
cervical lymphadenopathy; and with peeling erythematous rash of lips, palms and soles of feet
Morphology: similar to polyarteritis nodosa but with less prominent fibrinoid necrosis.

14. Varicose Veins. Morphology

A varix is a localized bulge in a vein analogous to a saccul
varicose veins show wall thinning at the points of maximal dilatation with smooth muscle
hypertrophy and intimal fibrosis in adjacent segments; elastic tissue degeneration and spotty
medial calcifications (phlebosclerosis) also occur. Focal intraluminal thrombosis (due to
stasis) and venous valve deformities (rolling and shortening) are common.

15. Vascular tumors. Benign tumors.

Hemangiomas – are common benign tumors of small capillaries.
Microscopic morphology:
-Capillary (small, back to back, capillary-like vessels) -Cavernous (large, blood-filled spaces).

16. Vascular tumors. Malignant tumors.

•Angiosarcoma - lesions most commonly develop in the soft tissues of the
lower limbs, the head and neck of elderly individuals. •Kaposi’s sarcoma – develop in patients with
acquired immune
deficiency following HIV infection.
Morphology gross- patches progress to raisedplaques, which progress to nodules. Microscopic –
spindled cells, extravasated
red blood cells.