CARDIOVASCULAR DISEASES

LECTURE 2

Dr. SAMAHIR ELKHIDIR

Assistant professor of
pathology MBBS. MD
 Lecture
outlines
 Aneurysms and Dissection
 Vasculitis.
 Disorders of the venous
system.
 Disorders of the lymphatic
system.
 Vascular tumors.
 {1}Aneurysms and
Dissection
► Aneurysms & dissections are abnormal
vascular dilations.
► Aneurysms are outpouchings that
involve all three vessel wall layers
(intima, media & adventitia.
► Dissection occurs when blood enters
the arterial wall itself & dissecting
between the layers through surface
defect.
► The most common & important
vascular aneurysms &
dissections involves the aorta.
 Causes of Aortic aneurysms
 Atherosclerosis (in the abdominal aorta), most
common .
 Hypertension (in the ascending thoracic aorta), most

common.
 Syphilis

 Trauma

 Vasculitis

 Congenital defects (Berry aneurysm)

 Infections(mycotic aneurysms )

Accelerates wall destruction & dilation. Caused by:

 septic embolization From bacterial endocarditis,

 adjacent suppurative process,

 Pathogenesis of
Aneurysms
Aneurysms results from poor vessel structure, it occurs due to:
Loss of medial SMCs or
Defects in extracellular
change in SMC synthesis by
matrix: Ischemia
• Inflammation which
produces matrix Atherosclerotic thickening of
metalloproteinase. the intima cause ischemia of
• Defective elastic tissue in the inner media by increasing
Marfan syndrome. the diffusion distance from the
• Defective collagen III lumen, systemic hypertension
synthesis in Ehlers- cause luminal narrowing of the
Danlos syndrome. aortic vasa vasorum, leading
• Histologically, thosecross-
Defective collagen changes are collectively
to ischemia called
of the outer
cystic
linkingmedial degeneration
in vitamin C media..
 Abdominal Aortic
Aneurysm

 Occur in male smokers over age 50

 Usually located below the
renal arteries & above the
iliac bifurcation.
 Can be saccular or Fusiform
 Pathogenesis involves medial
SMC loss & increased matrix
degradation.
 Histology reveals severe
complex atherosclerosis with
markedly attenuated media.
 Complications

 Vascular occlusion & thrombus

formation: due to aneurysmal dilation
& abnormal vascular flow
 Atheroembolism
 Compression of adjacent structures
 Rupture: risk of rupture increases with the
maximal diameter of the AAA. The
operative mortality rate is high. Because
aortic atherosclerosis is usually
accompanied by severe coronary
atherosclerosis, patients with AAA also have
a high incidence of ischemic heart disease.
 Thoracic Aortic
Aneurysm

Etiology:
 Hypertension (most common cause)
 Marfan syndrome & (Syphilis rare cause).
Signs & symptoms
are due to:
 Aortic root dilation (aortic valve insufficiency)
 Rupture.
 Encroachment on mediastinal structures:
including airways (dyspnea), esophagus
(dysphagia), recurrent laryngeal nerves
(cough), or vertebral bodies (bony pain).
 Aortic
Dissection
 Dissection of blood within the aortic media to form a
blood-filled channel within the aortic wall
 Often leads to rupture, causing sudden death through
massive hemorrhage or cardiac tamponade.
 Aortic dissection is not usually associated with
marked pre- existing aortic dilation.
 Dissection is uncommon in atherosclerosis or in other
conditions with medial scarring because the fibrosis
limits dissection propagation.
 Etiology of aortic dissection
Occurs in the following two groups mainly:
1. >90% Hypertensive males 40-60 years
old; the aortas typically exhibit variable
degrees of cystic medial degeneration,
2. Younger individuals with connective
tissue defects that affect the aorta
(e.g., Marfan syndrome).
3. Other causes include: trauma,
complications from therapeutic or
diagnostic arterial cannulation &
hormonal & physiologic changes
associated with pregnancy.
Pathogenesis:
 Medial degeneration triggers intimal tear that begins the

dissection.
 Once the tear is initiated, blood flow under systemic
pressures advances the dissection plane.
Morphology:
 Most of the dissections begin as a tear within the first 10

cm above the aortic valve. The dissection plane can

extend retrograde to the heart &/or anterograde, to the
great arteries & major branches.
 Rupture through the wall of the aorta will
cause massive hemorrhage.
 Histology: cystic medial degeneration, most
 Clinical Features
► Dissections are classified into the following:
▪Type A: commonest & dangerous, proximal
lesions involving the ascending aorta.
▪Type B: distal lesions usually begin distal
to the subclavian artery.
► The complications of dissection depend on
the portion of the aorta affected
► Presentation: sudden onset of sever pain,
begin in the anterior chest, radiate to the
back & move downward.
► Death from rupture into the pericardium,
thorax, or abdomen.
Vasculiti
s
 Vasculit
is
 Vasculitis is a general term for vessel wall
inflammation.
 The two most common pathogenic mechanisms of

vasculitis
 Immune-mediated inflammation.
 Infectious vasculitis.
 Patients presented with:

 Ischemia to downstream tissues (vessel injury &

thrombosis)
Fever :elevatedbody temperature.
Systemic manifestations (fever, malaise &
Malaise: general feeling of discomfort, illness, or lack of well-been.
arthralgias).
Arthralgia: joint pain.
 Organ dysfunction.
Disorders of the venous
system
 Veins
disorders
 Vein disorders are extremely common
 90% of venous diseases

are:
1. Varicose veins.
2. Deep venous thrombosis
Thrombophlebitis
and/or
Thrombophlebitis: inflammation of the wall of the vein with associated
thrombosis
Phlebothrombosis.
phlebothrombosis, formation of a blood clot in a vein that is not inflamed.
 Varicose Veins

 These are typically superficial lower

extremity veins that are dilated &
tortuous due to chronically elevated
intraluminal pressure.
 Although thrombosis is common,
superficial varicosities are rarely
sources of clinically significant emboli.
 Two other important sites for
varicosities are esophageal varesis &
rectal haemorrhoids.
Causes includes:
1.Obesity
2.Pregnancy
3.Hereditary venous defects
4.Prolonged dependent leg
position.
Pathogenesis
Vein dilation leads to:
 Incompetent valves.
 Vascular stasis.
 Persistent edema.
 Stasis dermatitis
(trophic skin
changes).
 Impaired circulation
 Poor healing
 Varicose ulcers.
Dermatitis :inflammation of the skin
Esophageal varices
 Esophageal varices are typically due to portal
vein hypertension (secondary to cirrhosis or
hepatic or portal vein thrombosis)
 Portal hypertension opens portosystemic shunts
with increased flow into veins at the
gastroesophageal junction (esophageal varices).
 Esophageal varices are important because their
rupture can lead to exsanguination.
 Haemorrhoids
 Rectum (haemorrhoids) result from primary
dilation of the anorectal venous plexus as a result
of increase pressure (secondary to pregnancy or
chronic constipation).
 Complications:
 Ulceration & bleeding
 Thrombosis
 Painful inflammation.
 Caput medusa a form of varicosities in
periumbilical veins, occur in liver cirrhosis & portal
hypertension.
 Thrombophlebitis &
Phlebothrombosis

 These terms denotes venous thrombosis &

inflammation.
 Sites:
 90% of thromboses occur in deep leg veins
 The periprostatic plexus in men
 Ovarian and pelvic veins in women
 Migratory thrombophlebitis: malignancy
associated hypercoagulability due to pro-
coagulant elaboration characterized by
sporadic thrombosis at various sites.
 Superior Vena Cava
Syndromes

 SVC syndrome is caused by

neoplasms compressing or invading
the SVC (primary bronchogenic
carcinoma).
 The resulting vascular obstruction
produces cyanosis & marked dilation
of head, neck & arm veins.
 Inferior Vena Cava
Syndromes
 Inferior vena cava (IVC) syndrome is caused
by extrinsic IVC compression.
 Certain neoplasms (hepatocellular & renal cell
carcinomas), tend to grow & obstruct the IVC.
 IVC obstruction cause leg edema, distention of
the lower abdominal superficial collateral
veins & when renal veins are involved massive
proteinuria.
 Disorders of the
Lymphatic system
 Lymphangiti
s
 Lymphangitis denotes the inflammation
occurring when infections spread into
lymphatics.
 β-hemolytic streptococci are a common
cause.
 Lymphangitis presents as painful subcutaneous
red streaks, often with tender regional
lymphadenopathy (lymphadenitis).
 Dilated lymphatics are filled with neutrophils &
macrophages.
 Lymphedema
It is a lymphatic obstruction & dilation, with increases in
interstitial fluid.
 Causes:

▪Primary hereditary lymphatic agenesis (Milroy

disease).
▪Secondary causes: Malignancy, resection of regional
lymph nodes, Filariasis, lymphatic scarring (post
inflammation or radiation).
 Prolonged lymphedema causes

 Interstitial fibrosis
 Peau d’orange (orange peel) appearance in
cutaneous tissues
 Ulcers
Vascular tumors
 Tumors
 Tumors of blood vessels & lymphatics include:
 Benign: hemangiomas (extremely common)
 Locally aggressive neoplasms that metastasize
infrequently: Kaposi sarcoma
 Highly malignant: angiosarcomas.
 Vascular neoplasms arise either from endothelium
(hemangioma, lymphangioma, angiosarcoma) or
cells that support or surround blood vessels.
 Hemangiomas

 Very common lesions (7% of all benign paediatric

tumors).
 Capillary hemangiomas: are the most common
type of vascular tumor, occurring in skin or
mucous membranes.
 They range from 1 mm to several centimetres in
size, composed of packed aggregates of
capillary-sized, thin-walled vessels.
 The juvenile (strawberry) hemangioma variant is
present at birth in 1 of 200 children, grows
Tongue hemangioma
Juvenile (strawberry) hemangioma
Juvenile (strawberry) hemangioma