Transcript Vascular and Lymphatic System Pathology

Vascular and Lymphatic
System Pathology
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Blood Flow
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Systemic blood flow is a circuit :
Heart →Arteries→ Arterioles→
Capillaries→ Venules→ Veins→ Heart
Artery – any vessels that carries
blood away from the heart.
Vein – any vessels that carries blood
toward the heart
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Structure of blood vessels
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Tunica intima
– Endothelium and connective tissue
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Tunica media
– Smooth muscle and elastic tissue
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Tunica externa or tunica adventitia
– Connective and elastic tissue
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Arteries
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Large arteries are elastic (conducting)
arteries – pressure reservoirs
Medium arteries are muscular
(distributing) arteries – more smooth
muscle
Contraction or relaxation of muscle
changes the size of the lumen, and so
controls the blood pressure in the
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vessel.
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Capillaries
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Only a single layer of endothelium and
a basement membrane
Connect arterioles and venules
Functional part of system
True capillaries begin at a precapillary
sphincter which controls blood flow
through the capillary
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Veins
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Relatively thin; less elastic
Larger in diameter than arteries
Have valves to prevent backflow of
blood
Flow to heart is assisted by contraction
of skeletal muscles
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Control of systemic
circulation
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Nervous control – innervated by
sympathetic nervous system ONLY
Cardiac control center (primarily in
medulla oblongata)
Heart has both Sympathetic and
Parasympathetic innervations.
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Baroreceptors and chemoreceptors:
– Monitor pressure
– Monitor blood levels of O2, CO2 and H+
– Send information to cardiovascular center,
which responds
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Compliance
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The increase in volume a vessel can
accommodate for a given increase in pressure.
– Depends on the ratio of elastic fibers to muscle fibers
in the vessel wall.
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Elastic arteries more compliant than muscular arteries
Veins more compliant than either artery (blood reservoirs)
Decreased compliance suggests an increased
stiffness of vessel wall.
Determines the vessel’s response to changes in
pressure.
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Blood pressure
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Mean arterial pressure is the average
in pressure in the arteries throughout
the cardiac cycle.
Depends on the compliance of the
arteries and the amount of blood in
the arterial system.
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Blood pressure
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BP = Cardiac Output * Total Peripheral
Resistance
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Lymphatic System
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A vascular system that runs “parallel” to
the blood vascular system
Flow does not circulate – begins in tissue
Returns to venous system at subclavian
veins
Fluid in vessels is lymph – mostly water
and proteins
Interstitial fluid→ lymphatic capillaries→
lymphatic vessels→ lymphatic trunks→
lymphatic ducts
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Lymph nodes
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Lie along lymphatic vessels
Contain lymphocytes that filter lymph
and eliminate microbes/damaged cells/
toxins
Biological filtration
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Diseases of Arteries and
Veins
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Thrombus- “clotting” in an unbroken
vessel
– Maintains a point of attachment
– Organized differently than a clot
– usually due to damage to endothelium
and exposure of collagen in the
basement membrane
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Arterial thrombus
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Forms where blood is moving rapidly
– see alternating lines of platelets and
red cells trapped in fibrin
Lines of Zahn
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Venous thrombus
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Forms differently due to decreased
blood flow
Mixed region at site of attachment
More blood clotting forms a
downstream red cap
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Factors that predispose to
thrombosis
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Endothelial damage
– Bacterial damage
– Damage to the myocardium
– Wear and tear – hemodynamic stress
 Hypertension increases this
 Arteriosclerosis
– Inflammation
– Tumors and irritation by their products
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Factors that predispose to
thrombosis
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Flow abnormalities
– Increases platelet contact with endothelium
– Reduction in flow:
 Arterial:
– Cardiac damage and decreased pumping
action
– Increased blood viscosity
 Venous:
– Physical inactivity
– Varicose veins
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– Turbulence:
 Damaged heart valves
 Congenital heart defects
 Compression of the vessel
 Weakened arterial wall - aneurysm
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Other Causes
Aging
 Immobilization
 Injury to vessel endothelium
 Increased clotting response
Effects:
 Decreased venous emptying
 Increased venous pressures
 Edema
 Pain
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Sequelae of Thrombosis
1 Resolution –
Anticoagulation system
Fibrolytic system
Moderate exercise increases thrombus
resolution
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2 Organization
The thrombus is digested by
phagocytes and replaced by connective
tissue – incorporating the thrombus into
the vessel wall.
May recanalize – small channels open
up and restore blood flow
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Recanalization
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3 Propagation –
Thrombus extends further down the
vessel, usually a vein.
Initial thrombus acts as a site for
further platelet adherence.
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Propagation
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4 Infarction –
an infarct is an area of necrosis caused
by ischemia and hypoxia.
More common in arteries than veins due
to blood flow patterns
Collateral circulation and anastomosis
prevent infarction
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Embolism – obstruction of vessel by matter
circulating in blood stream
– Matter could be fat, air, infant’s cells, in
addition to pieces of clot –
thromboemboli
– Thromboemoboli from the venous system
tend to end up in the:
lungs and liver
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Treatment
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Anticoagulants
Fibrinolytics – t-Pas
Prophylactic aspirin therapy
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Arterial Occlusions
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Arteriosclerosis – abnormal thickening
and hardening of the arterial walls
– Smooth muscle cells and collagen fibers
migrate into the tunica intima, causing
stiffening and thickening, narrowing the
lumen
– Can exacerbate high blood pressure, and
cause weakening and outpouching of
vessel walls
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Atherosclerosis
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A form of arteriosclerosis where soft
deposits of intra-arterial fat and fibrin
harden over time – atheroma
May see build up in skin – Xanthoma
or arcus in cornea.
In general, patients suffer few
symptoms unless > 60 % of blood
supply is blocked
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Progressive over years
– Starts with some injury to endothelium
 Smoking, hypertension, hyperlipidemia,
diabetes, autoimmune disease, and infection
– Inflammation, release of enzymes by macrophages
causes oxidation of LDL, which is then consumed by
macrophages – foam cells – accumulate to form
fatty streaks
– Fatty streaks of lipid material appear first as yellow
streaks and spots
– Smooth muscle cells proliferate, and migrate over
the streak forming a fibrous plaque
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Fibrous plaque results in necrosis of
underlying tissue and narrowing of
lumen
Inflammation can result in ulceration
and rupture of the plaque, resulting
in platelet adherence to the lesion =
complicated lesion
Can result in rapid thrombus
formation with complete vessel
occlusion → tissue ischemia and
infarction
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Clinical manifestations
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Signs and symptoms of inadequate
perfusion – TIAs, often associated with
exercise or stress
When lesion becomes complicated,
can result in tissue infarction
– Coronary artery disease –
myocardial ischemia
– In brain – major cause of stroke
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Treatment
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Exercise
Smoking cessation
Control of hypertension and/ or
diabetes
Reduce LDL cholesterol by diet or
medication or both
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Other arterial problems
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Aneurism – dilation in the arterial wall
Most arise in aorta or major branches
as a result of atherosclerotic wall
damage
Males over 50 at greatest risk for
aortic aneurysms
Disturbs blood flow, predisposing to
thrombus formation - can release
thromoemboli
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Asymptomatic until rupture
– Embolism
– Death
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Treatment by surgical repair
Aortic Dissection –bleeding into vessel
wall, separating vessel layers
– Men in 40-60 y.o. age group with
hypertension
– Younger persons with connective tissue
disease or congenital defects
– Presents with pain – life threatening
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Systemic Hypertension
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A consistent increase in arterial blood
pressure caused by increased Cardiac
output or increased peripheral resistance or
both
Leads to damage of vessel walls
If arteries constrict over a long time with
increased pressure in vessel, the wall
becomes thicker to withstand the stress.
Results in narrowing of arterial lumen
Leads to inflammatory response
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Causes one in eight deaths worldwide
Third leading cause of death in the
world
Affects 50 million Americans
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Primary hypertension
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Also called essential or idiopathic
hypertension
92- 95 % of all cases
No specific cause identified
Can happen with retention of sodium and
water → increased blood volume.
Also low dietary potassium, calcium and
magnesium intakes
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Other risk factors
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Smoking
– Nicotine is a vasoconstrictor
Greater than 3 alcoholic drinks/ day
– 2-4 drinks / week lowers blood pressure
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Suspected causes
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Interaction of genetics and
environment
Overactivity of sympathetic nervous
system
Overactivity of renin / angiotensin/
aldosterone system
Salt and water retention by kidneys
And others
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Secondary hypertension
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Caused by a systemic disease process
that raises peripheral resistance or
cardiac output = 5 - 10 % of cases.
Renal vascular disease
Adrenocortical tumors
Adrenomedullary tumors
Drugs ( oral contraceptives,
corticosteroids, antihistamines)
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Complicated hypertension
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Sustained primary hypertension that
damages the structure and function of
the vessels themselves.
Commonly affects heart, aorta,
kidneys, eyes, brain, and lower
extremities (target-organ damage).
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Clinical manifestations
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None in early stages other than elevated
BP
Some individuals never have symptoms;
others become very ill and die
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Treatment
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Modification of life style
Drugs
– Diuretics, beta-blockers, angiotensin
converting enzyme inhibitor
Compliance is often difficult – patients
stop taking medication when they feel
better – can get rebound effects
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Venous Disorders
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Varicose veins – dilations, can lead to
valvular insufficiency
Can occur in superficial veins
(saphenous) or deep veins
Causes of secondary varicose veins:
– Deep vein thrombosis
– Congenital defects and pressure on
abdominal veins
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Treatment
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Prevention – little can be done after valves
become incompetent
Avoid stressors, such as standing for long
periods
Elastic support stockings
Sclerotherapy – injections of drugs to
induce fibrosis of vessel
Surgical removal - but only when deep
vein are open.
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