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HISTOLOGY

CARDIOVASCULAR SYSTEM II

Post-capillary venules

Infection/inflammation

Capillaries
High

-- postcapillary venules veins

endothelial venules (cuboidal cells)

Loosest

ZO

Inflammation:

leukocyte exudation

Post-Capillary Venule

PCV becomes small vein

Lymph node

Note the endothelial cells (arrow heads). They are high cuboidal in nature,
therefore these vessels are called HEV (high endothelial vessels). These
vessels possess the loosest junctional complexes, facilitating the entry of
immune cells (arrow) from the lumen into the connective tissue, during
inflammation or as a normal phenomenon in locations such as lymph nodes.

lymphocyte

EC

Post capillary venule

HEVs play an important role in homing effect in lymphoid organs like lymph node.
This is the site where lymphocytes enter a lymph node from circulation.

Small Vein

Small vein
Small Artery

Small artery and vein


T. intima: endothelium, subendothelial connective tissue
T. media: very few smooth muscle cells, arranged in circular fashion
T. adventitia: more developed than media

Medium-sized Veins

Muscular artery

Vein

T. intima: endothelium, sparse sub endothelial connective tissue


T. media: few smooth muscle cells, arranged in circular fashion
T. adventitia: well developed than media

Medium-sized veins (cont)

VALVES (ARROWHEAD) PREVENT BLOOD BACKFLOW

The veins are characterized by the presence of valves, which are folds of
t. intima, supported by fibroelastic connective tissue.
These prevent the backflow of blood, as they drain the blood toward the heart
against gravity, assisted in most cases by skeletal muscles, through which
they travel.

MUSCULAR VEIN (Ex: Vena cava)

t. intima

Tunica intima

Tunica media Circularly arranged smooth


muscle cells + connective
tissue

Tunica adventitia:
Longitudinal smooth muscle
bundles

t.media

t. adv

* Continuous milking of blood


toward the heart against
gravity.

Large vein / muscular vein example vena cava

Tunica media

Tunica media

Tunica adventitia

Large Vein (H&E)

T. intima
T. media

T. adventitia
IVC

?
Example : Vena cava

LYMPHATIC
SYSTEM

Returns excess tissue fluid to circulation

Starts off as blind-ended lymphatic capillaries and empty into the circulation;
unidirectional valves

Flow is sluggish and aided by contraction of skeletal muscles

Bundles of filament anchor vessels to surrounding CT

No clear cut separation into tunics

Lack tight junctions: proteins and large molecules return to vascular


compartment.

Not present in nervous tissue, bone marrow and cartilage

Impaired function - edema

Lymphatic
capillary

venule

arteriole

Lymphatic

Lymphatic

Afferents

Efferent

Lecture Recap

All vessels, except arterioles, capillaries and post capillary venules,


have 3 layers:
Tunica intima
Tunica media
Tunica adventitia

T. intima

T. media T. adventitia -

Endothelial cells - store factor VIII in Webel-Palade bodies.


Subendothelial connective tissue (S.E.C.T)-smooth
muscle cells, collagen & elastin provide support.
Involvement in formation of atheromas in atherosclerosis.
IEL -feature of all arteries (NOT prominent in elastic
vessels like aorta due to large number of elastic fibers in
tunica media
SMC, elastin, collagen embedded in ground substance
EEL-external elastic lamina feature of muscular artery
Dense connective tissue-collagen type I fibers, elastin
and cells. Vasa vasorum; Nervi vascularis.

T. intima
T.media

T.adventitia

Elastic artery
Muscular Artery

Arteriole

Continuous capillary

Fenestrated capillary

Continuous capillary

T. Adv

Sinusoidal capillary

Muscular vein

Clinical Considerations

Atherosclerosis
Marfans Syndrome
Aortic Aneurysm
Cerebral Aneurysm
Peripheral Vascular Disease
Varicose veins
Lymphedema

Cardiovascular Diseases

Affects heart and circulatory system


Predominant damage to blood vessel occurs due to atherosclerosis
and hypertension
Atherosclerosis- Formation of atheroma in the wall, which can
decrease blood flow the region/can rupture /or perforate and are
prone for clot formation (thrombus), which can travel as emboli.
INFLAMMATORY DISEASE
Hypertension- Can cause damage to smaller blood vessels by
scarring, hardening, narrowing of blood vessels and eventually
become less elastic. It can both predispose and accelerate
development of atherosclerosis.
Arterioles - Radius is equal to the thickness of the wall.
Resistance is inversely proportional to the diameter.

Major clinical manifestations of cardiovascular diseases


Coronary
Heart
Disease

Cerebrovascular
Disease

Peripheral
Vascular
Disease

Angina

Stroke

Gangrene

Heart attack Transient ischemic


attack
Sudden
death
Heart
failure

Dementia

Intermittent
Claudication

ATHEROSCLEROSIS

Characterized by lesions of the t. intima called atheromas or fibro-fatty plaques


that may protrude into and obstruct the vascular lumen - also weakening the
underlying t. media
Hardening of arteries = arteriosclerosis

Symptoms:

OOoohawwChest pains!!

Shortness of breath..
Back pain..
Pain radiating to the jaw..

Heart disease begins when cholesterol, fatty material, and calcium build up in
the arteries, a process known as atherosclerosis.

Risk factors:
Smoking
HTN
DM
Hypercholesterolemia

Lack of exercise
Unhealthy diet
Stress
Type A personality

Histopathogenesis
LDL in the blood contains
triglycerides and lipids. These are
insoluble in water medium of blood.
When there is excessive LDL, the
endothelial cells produce free
radicals which oxidize this LDL.
This oxidized product now initiates
migration of monocytes into the
tunica intima, which now become
macrophages.
Smooth muscle cells (SMC ) also
migrate from the t. media to the t.
intima (subendothelial CT).

SMC and macrophages engulf


oxidized LDL to form foam
cells
SMC proliferate and secrete
collagen and other ECM
thickens t. intima forming fatty
streaks
Cytokines from the SMC
converts these fatty streaks into
fibrofatty plaques - which bulges
into the lumen and also
compresses the t. media
Results in luminal obstruction &
weakened vascular walls
(aneurysm)

Electrocardiogram (ECG or EKG).

Echocardiography

Stress tests

Computerized tomography (CT) scans

Coronary angiography via cardiac catheterization is


considered the "gold standard" of heart disease tests

Progression of atherosclerosis

Luminal obstruction of the coronary artery will lead to ischemia of the


myocardium
Ischemic changes

Normal myocardium

Phagocytocytosis of the myocytes

SEQUELAE OF CORONARY VASCULAR OCCLUSION

PCI- Percutaneous Coronary Intervention

CABG-Coronary artery bypass graft

Marfans Syndrome

Autosomal dominant connective


tissue disorder with
characteristic skeletal,
cardiovascular and ocular
manifestations.

Defect in the Fibrillin-1 gene


-fibrillin is a glycoprotein that
forms a scaffold on which
elastin is deposited- elastic
fibers.

Abnormal production and


fragmentation of elastic fibers of
t. media = weakened wall >
aortic aneurysm and dissection
and death.

AORTIC ANEURYSM

Cerebral Aneurysm

Angiograms of Aneurysms Pre and Post Treatment

Endovascular coiling treatment with platinum coils.


Another treatment is surgical clipping of aneurysm.

Peripheral Artery Disease


6-7 times prone to stroke or heart
disease
Major cause is atherosclerosis
Another is diabetes

Predisposing condition

Dx: doppler ultrasound


Arteriogram can pinpoint the
location of block

S & S:
Pain and numbness
Claudication
Decreased wound healing
Tissue death-gangrene
Leading cause of amputations

Varicose veins
Intrinsic weakness of the t. media of veins
or defect in the valves that hamper flow of
blood to the heart.
Occurs anywhere but most common in the
legs (women), anorectally (hemorrhoids),
or in the spermatic cord (varicocele)

Esophageal Varices

Hemorrhoids

Varicocele

Causes:
Lymphedema

Penoscrotal lymphedema

Trauma
Post surgical
Post radiation
Inflammation
Parasitic obstruction
Obstruction due to
metastasis

filarial

Obstruction to lymphatics