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blood vessles

Dr. FERRARIS

PATHOLOGY REVIEWER

Classification of dissections. Type A (proximal) involves the ascending aorta,


either as part of a more extensive dissection (DeBakey I) or in isolation
(DeBakey II). Type B (distal or DeBakey III) dissections arise beyond the
takeoff of the great vessels. The serious complications predominantly occur
in type A dissections

classic clinical symptoms of aortic dissection


most common cause of death in aortic dissection is

sudden onset of excruciating pain, usually beginning in the anterior chest,


radiating to the back between the scapulae, and moving downward as the
dissection progresses
rupture of the dissection outward into the pericardial, pleural, or peritoneal
cavities
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The author of this document wishes you a successful examination. Dont forget to check your notes and books if anything seems confusing. This is
not intended to replace your review materials; instead this is primarily designed to assist you in your study regimen.
******* NOTHING FOLLOWS********

11

blood vessles
Dr. FERRARIS

PATHOLOGY REVIEWER

Thoracic Aortic Aneurysms give rise to signs and sx such as;

This occurs when blood splays apart the laminar planes of the media to
form a blood-filled channel within the aortic wall

Aortic dissection occurs principally in two groups;

Considered as the major risk of aortic dissection


Morphology of Aortic Dissection

aortic dissections are generally classified into two types

Obstruction of a branch vessel resulting in ischemic injury of


downstream tissues, for example, iliac (leg), renal (kidney),
mesenteric (gastrointestinal tract), or vertebral (spinal cord) arteries
Embolism from atheroma or mural thrombus
Impingement on an adjacent structure, e.g., compression of a ureter
or erosion of vertebrae
Presentation as an abdominal mass (often palpably pulsating) that
simulates a tumor
1. encroachment on mediastinal structures
2. respiratory difficulties due to encroachment on the lungs and airways,
3. difficulty in swallowing due to compression of the esophagus
4. persistent cough due to irritation of or pressure on the recurrent
laryngeal nerves
5. pain caused by erosion of bone (i.e., ribs and vertebral bodies),
6. cardiac disease as the aortic aneurysm leads to aortic valve dilation
with valvular insufficiency or narrowing of the coronary ostia causing
myocardial ischemia, and
7. rupture
Aortic dissection
- tears often occurs in the tunica media blood leaking out
cardiac tamponade (fatal)
Aortic dissection. A, An opened aorta with proximal dissection originating
from a small, oblique intimal tear (identified by the probe), allowing blood to
enter the media and creating an intramural hematoma (narrow arrows). Note
that the intimal tear has occurred in a region largely free of atherosclerotic
plaque and that propagation of the intramural hematoma is arrested at a site
more distally where atherosclerosis begins (broad arrow). B, Histologic view
of the dissection demonstrating an aortic intramural hematoma (asterisk).
Aortic elastic layers are black and blood is red in this section, stained with
the Movat stain.
(1) men aged 40 to 60, with antecedent hypertension (more than 90% of
cases of dissection); and (2) younger patients with systemic or localized
abnormalities of connective tissue affecting the aorta (e.g., Marfan
syndrome)
HPN
most frequent preexisting histologically detectable lesion is cystic
medial degeneration
inflammation is characteristically absent
usually initiates with an intimal tear, majority found in the ascending
aorta, usually within 10 cm of the aortic valve, such tears are typically
transverse or oblique and 1 to 5 cm in length, with sharp, jagged edges
dissection can extend along the aorta retrograde toward the heart as
well as distally, sometimes into the iliac and femoral arteries
dissecting hematoma spreads characteristically along the laminar
planes of the aorta, usually between the middle and outer thirds
often ruptures out through the adventitia causing massive hemorrhage
(e.g., in the thoracic or abdominal cavities) or cardiac tamponade
(hemorrhage into the pericardial sac)
some (lucky) instances, the dissecting hematoma reenters the lumen of
the aorta through a second distal intimal tear, creating a new vascular
channel and forming a double-barreled aorta with a false channel
a. More common (and dangerous) proximal lesions (called type A
dissections), involving either both the ascending and descending aorta
or just the ascending aorta (types I and II of the DeBakey classification)
b. Distal lesions not involving the ascending part and usually beginning
distal to the subclavian artery (called type B dissections or DeBakey
type III)

10

blood vessles
Dr. FERRARIS

PATHOLOGY REVIEWER


Pathogenesis of aneurysm

a.

The two most important disorders that predispose to aortic aneurysms


are
An aneurysm that can arise due to infection is termed as

atherosclerosis and hypertension

Mechanism of AAA

Morphology of the AAA


2 variants of AAA that are clinically important

Clinical Features of AAA

The intrinsic quality of the vascular wall connective tissue is poor e.g.
marfan syndrome (defective synthesis of the scaffolding protein fibrillin
leads to aberrant TGF- activity) and Loeys-Dietz syndrome (
mutations in TGF- receptors lead to abnormalities in elastin and
collagen I and III)
b. The balance of collagen degradation and synthesis is altered by local
inflammatory infiltrates and the destructive proteolytic enzymes they
produce
c. The vascular wall is weakened through loss of smooth muscle cells or
the inappropriate synthesis of noncollagenous or nonelastic ECM
Cystic medial degeneration. A, Cross-section of aortic media from a patient
with Marfan syndrome, showing marked elastin fragmentation and formation
of areas devoid of elastin that resemble cystic spaces (asterisks). B, Normal
media for comparison, showing the regular layered pattern of elastic tissue.
In both A and B, elastin is stained black.

Mycotic aneurysm
- can originate (1) from embolization of a septic embolus, usually
as a complication of infective endocarditis; (2) as an extension of
an adjacent suppurative process; or (3) by circulating organisms
directly infecting the arterial wall
Abdominal aorta has the highest preponderance of aneurysms caused by
atherosclerosis and this plaque in the intima causes compression of the
media resulting to decreased diffusion of nutrients and media therefore
undergoes necrosis and degeneration. Necrosis can result to thinning and
arterial weakness
Usually positioned below the renal arteries and above the bifurcation of the
iliac arteries. It can be saccular or fusiform
Inflammatory AAAs are characterized by dense periaortic fibrosis
containing abundant lymphoplasmacytic inflammation with many
macrophages and often giant cells
Mycotic AAAs are lesions that have become infected by the lodging of
circulating microorganisms in the wall, particularly in bacteremia from a
primary Salmonella gastroenteritis
Abdominal aortic aneurysm. A, External view, gross photograph of a large
aortic aneurysm that ruptured; the rupture site is indicated by the arrow. B,
Opened view, with the location of the rupture tract indicated by a probe. The
wall of the aneurysm is exceedingly thin, and the lumen is filled by a large
quantity of layered but largely unorganized thrombus.

Rupture into the peritoneal cavity or retroperitoneal tissues with


massive, potentially fatal hemorrhage

blood vessles
Dr. FERRARIS

PATHOLOGY REVIEWER


Distribution of atherosclerotic plaques (in descending order)

3 principal components of atherosclerotic plaques

Atherosclerotic plaques are susceptible to clinically important changes


such as ;

Vasoconstriction at the site of atheroma is stimulated by;

What are the classifications of aneurysm accdg to shape and size?

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
1. cells, including smooth muscle cells, macrophages, and T cells
2. ECM, including collagen, elastic fibers, and proteoglycans; and
3. intracellular and extracellular lipid
a. Rupture, ulceration or erosion of the intimal surface of the
atheromatous plaques exposes the blood to highly thrombogenic
substances and induces thrombosis, if px survives with the initial
thrombotic occlusion, the clot may incorporate into a growing
plaque.
b. Hemorrhage into a plaque. Rupture of the overlying fibrous cap,
or of the thin-walled vessels in the areas of neovascularization,
can cause intra-plaque hemorrhage; a contained hematoma may
expand the plaque or induce plaque rupture.
c. Hemorrhage into a plaque. Rupture of the overlying fibrous cap,
or of the thin-walled vessels in the areas of neovascularization,
can cause intra-plaque hemorrhage; a contained hematoma may
expand the plaque or induce plaque rupture
d. Aneurysm formation. Atherosclerosis-induced pressure or
ischemic atrophy of the underlying media, with loss of elastic
tissue, causes weakness resulting in aneurysmal dilation and
potential rupture
Schematic comparing vulnerable and stable atherosclerotic plaque. Whereas
stable plaques have densely collagenous and thickened fibrous caps with
minimal inflammation and negligible underlying atheromatous core,
vulnerable plaques (prone to rupture) are characterized by thin fibrous
caps, large lipid cores, and increased inflammation.

circulating adrenergic agonists


locally released platelet contents
impaired secretion of endothelial cell relaxing factors (nitric oxide)
relative to contracting factors (endothelin) as a result of endothelial cell
dysfunction, and possibly
mediators released from perivascular inflammatory cells.
A, Normal vessel.
B, True aneurysm, saccular type. The wall focally bulges outward and may be
attenuated but is otherwise intact.
C, True aneurysm, fusiform type. There is circumferential dilation of the
vessel, without rupture.
D, False aneurysm. The wall is ruptured, and there is a collection of blood
(hematoma) that is bounded externally by adherent extravascular tissues.
E, Dissection. Blood has entered (dissected) the wall of the vessel and
separated the layers. Although this is shown as occurring through a tear in
the lumen, dissections can also occur by rupture of the vessels of the vaso
vasorum within the media.
1. Saccular aneurysms are spherical outpouchings (involving only a
portion of the vessel wall); they vary from 5 to 20 cm in diameter and
often contain thrombus.
2. Fusiform aneurysms involve diffuse, circumferential dilation of a long
vascular segment; they vary in diameter (up to 20 cm) and in length,
and can involve extensive portions of the aortic arch, abdominal aorta,
or even the iliac arteries

PATHOLOGY REVIEWER


Fatty streaks

blood vessles
Dr. FERRARIS
Cigarette smoking
Fatty streaks are the earliest lesions in atherosclerosis. They are composed
of lipid-filled foamy macrophages. They begin as minute flat of yellow spots
that eventually coalesce into elongated streaks.
Fatty streak, a collection of foamy macrophages in the intima. A, Aorta with
fatty streaks (arrows), associated largely with the ostia of branch vessels. B,
Photomicrograph of fatty streak in an experimental hypercholesterolemic
rabbit, demonstrating intimal, macrophage-derived foam cells (arrows).
Gross views of atherosclerosis in the aorta. A, Mild atherosclerosis composed
of fibrous plaques, one of which is denoted by the arrow. B, Severe disease
with diffuse and complicated lesions (with plaque rupture and superimposed
thrombosis), some of which have coalesced.
Histologic features of atheromatous plaque in the coronary artery. A, Overall
architecture demonstrating fibrous cap (F) and a central necrotic (largely
lipid) core (C). The lumen (L) has been moderately compromised. Note that
a segment of the wall is free of plaque (arrow); the lesion is therefore
eccentric. In this section, collagen has been stained blue (Masson's
trichrome stain). B, Higher power photograph of a section of the plaque
shown in A, stained for elastin (black), demonstrating that the internal and
external elastic membranes are attenuated and the media of the artery is
thinned under the most advanced plaque (arrow). C, Higher magnification
photomicrograph at the junction of the fibrous cap and core, showing
scattered inflammatory cells, calcification (arrowhead) and
neovascularization (small arrows).
Atherosclerotic plaque rupture. A, Plaque rupture without superimposed
thrombus, in a patient who died suddenly. B, Acute coronary thrombosis
superimposed on an atherosclerotic plaque with focal disruption of the
fibrous cap, triggering fatal myocardial infarction. In both A and B, an arrow
points to the site of plaque rupture.

Major targets of atherosclerosis


Major consequences of atherosclerosis

The principal outcomes of atherosclerosis depend on the

The key processes of atherosclerosis are ___


Atherosclerotic plaques grossly appear (color) ___ and those
superimposed thrombus over ulcerated plaques is ____
Atherosclerotic plaques appears _____ and arranged ___

Large and medium- sized arteries


Since symptomatic atherosclerotic disease most often involves the arteries
supplying the heart, brain, kidneys, and lower extremities. Myocardial
infarction (heart attack), cerebral infarction (stroke), aortic aneurysms, and
peripheral vascular disease (gangrene of the legs) are the major
consequences of atherosclerosis.
size of the involved vessels, the relative stability of the plaque itself, and the
degree of degeneration of the underlying arterial wall
The natural history, morphologic features, main pathogenic events, and
clinical complications of atherosclerosis.

Intimal thickening and lipid accumulation


White to yellow; red to brown (and they vary from 0.3- 1.5 cm in diameter)
As patchy involving only a portion of any given arterial wall and arranged
eccentrically

blood vessles
Dr. FERRARIS

PATHOLOGY REVIEWER

Evolution of arterial wall changes in the response to injury hypothesis.


1, Normal.
2, Endothelial injury with adhesion of monocytes and platelets (the latter to
sites where endothelium has been lost).
3, Migration of monocytes and smooth muscle cells into the intima.
4, Smooth muscle cell proliferation in the intima with ECM production.
5, Well-developed plaque

Mechanism of endothelial injury

Two most important causes of endothelial dysfunction


Cascade of events in renal artery stenosis

HPN medications
HPN begets more vascular disorders such as

Mechanisms by w/h hyperlipidemia contributes to atherogenesis


Mechanism by which smooth muscle cells proliferation can also
potentiate the atherogenesis.

Predisposing factors of athereosclerosis accdg to Framingham Risk


Scale

Endothelial injury dysfunctional endothelial cells show increased


endothelial permeability, enhanced leukocyte adhesion, and altered gene
expression
hemodynamic disturbances and hypercholesterolemia
Stenosis of the renal artery dec. glomerular flow renin secretion
plasma angiotensin (liver) converted to angiotensin 1 vasopressor
activation by angiotensin 2 (lungs) aldosterone secretion by zona
glomerulosa (adrenal cortex) incr. in renal Na reabsorption incr.
water reabsorption increase blood volume incr. BP
Beta blockers, diuretics, Ca- channel blockers, angiotensin- converting
enzymes
Atherosclerosis, cerebral hemorrhages, hypertrophy of the heart cardiac
failure and eventually ischemia
Hyperlipidemia specifically hypercholesterolemia increases the production of
local oxygen free radicals and these ROS impair the endothelial cell function
and promotes decay of NO resulting to decreased vasodilation activity
Smooth muscle cells proliferation to compensate for the endothelial injury in
the intima also secrete ECM notable the collagen; this collagen provides
more support to stabilize the atheroma.
Hypothetical sequence of cellular interactions in atherosclerosis

Hypercholesterolemia
HPN
DM

blood vessles
Dr. FERRARIS

PATHOLOGY REVIEWER

The generic term reflecting arterial wall thickening and loss of elasticity
three general patterns, with differing clinical and pathologic
consequences:

An intimal lesion that protrudes into the vessel lumen causing thickening
is called
Components of atheroma

According to the response-to-injury hypothesis, atherosclerosis is


produced by the several events, these are ____

arrow: onion- skin lesions


Atherosclerosis
Arteriolosclerosis affects small arteries and arterioles, and may cause
downstream ischemic injury.
Mnckeberg medial sclerosis is characterized by calcific deposits in
muscular arteries in persons typically older than age 50. The deposits
may undergo metaplastic change into bone. Nevertheless, the lesions
do not encroach on the vessel lumen and are usually not clinically
significant
Atherosclerosis is the most frequent and clinically important pattern
Atheromas or atheromatous plaques
1.

Core- raised lesion with a soft, yellow, grumous core of lipid


(mainly cholesterol and cholesterol esters)
2. Fibrous cap- consists of smooth muscle cells, macrophages, foam
cells, lymphocytes, collagen, elastin, proteoglycans,
neovascularization
The major components of a well-developed intimal atheromatous plaque
overlying an intact media

Endothelial injury increased vascular permeability, leukocyte


adhesion, and thrombosis
Accumulation of lipoproteins mainly LDL
Monocyte adhesion to the endothelium, followed by migration into the
intima and transformation into macrophages and foam cells
Platelet adhesion
Factor release from activated platelets, macrophages, and vascular wall
cells smooth muscle cell recruitment, either from the media or from
circulating precursors
Smooth muscle cell proliferation and ECM production
Lipid accumulation both extracellularly and within cells

PATHOLOGY REVIEWER


Vascular tone is determined by ___
Role of kidneys in the regulation of the BP

Single-gene disorders cause severe but rare forms of hypertension

Effects of reduced renal sodium excretion in the BP.


Hypertension is associated with two forms of small blood vessel disease;

Morphology seen in hyaline arteriosclerosis

Hyaline formation is due to ___

Hyaline Arteriolosclerosis is to ____


Morphology seen in hyperplastic arteriosclerosis

blood vessles
Dr. FERRARIS
The balance between vasoconstricting and vasodilating influenecs
Through the renin-angiotensin system, the kidney influences both
peripheral resistance and sodium homeostasis. Renin is secreted by the
juxtaglomerular cells of the kidney in response to fall in blood pressure.
It converts plasma angiotensinogen to angiotensin I, which is then
converted to angiotensin II by angiotensinconverting enzyme.
Angiotensin II raises blood pressure by increasing both peripheral
resistance (direct action on vascular smooth muscle cells) and blood
volume (stimulation of aldosterone secretion, and increase in distal
tubular reabsorption of sodium).
the kidney also produces a variety of vascular relaxing, or
antihypertensive, substances (including prostaglandins and NO), which
presumably counterbalance the vasopressor effects of angiotensin
When blood volume is reduced, the glomerular filtration rate falls,
leading to increased reabsorption of sodium by proximal tubules,
thereby conserving sodium and expanding blood volume.
Natriuretic factors, including the natriuretic peptides secreted by atrial
and ventricular myocardium in response to volume expansion, inhibit
sodium reabsorption in distal tubules and thereby cause sodium
excretion and diuresis. Natriuretic peptides also induce vasodilation and
may be considered to represent endogenous inhibitors of the reninangiotensin system
o Gene defects affecting enzymes involved in aldosterone metabolism
(e.g., aldosterone synthase, 11-hydroxylase, 17-hydroxylase)
increase in secretion of aldosterone, increased salt and water
resorption, plasma volume expansion and, ultimately, hypertension
o Mutations affecting proteins that influence sodium reabsorption e.g.
salt- sensitive HPN called Liddle syndrome, is caused by mutations in
an epithelial Na+ channel protein that lead to increased distal tubular
reabsorption of sodium induced by aldosterone.
Decreased sodium excretion may lead sequentially to an increase in fluid
volume, increased cardiac output, and peripheral vasoconstriction, thereby
elevating blood pressure
o Hyaline Arteriolosclerosis
o Hyperplastic Arteriolosclerosis
homogeneous, pink hyaline thickening with associated luminal narrowing

red arrow: pink hyaline thickening; green arrow: narrowing


plasma protein leakage across injured endothelial cells, and increased
smooth muscle cell matrix synthesis in response to chronic hemodynamic
stress
Elderly, DM and nephroslcerosis
this lesion occurs in severe (malignant) hypertension; vessels exhibit onionskin lesions, characterized by concentric, laminated thickening of the walls
and luminal narrowing
laminations consist of smooth muscle cells with thickened, reduplicated
basement membranes; in malignant hypertension they are accompanied by
fibrinoid deposits and vessel wall necrosis (necrotizing arteriolitis),
particularly in the kidney.

PATHOLOGY REVIEWER


It is defined as an altered phenotype that impairs vasoreactivity or
induces a surface that is thrombogenic or abnormally adhesive to
inflammatory cells

Important roles of vascular smooth muscle cells

Growth promoters of the vascular smooth muscle cells

Growth inhibitors of the vascular smooth muscle cells

Describe the neointimal response occurs with any form of vascular


damage or dysfunction

The difference of neointimal smooth muscle cells and medial smooth


muscle cells
Diastolic and systolic threshold of blood pressure for HPN
95% of the HPN is caused by
BP is a fxn of ____
Major factors that determine blood pressure variation within and
between populations

blood vessles
Dr. FERRARIS
Endothelial dysfunction
- responsible for the for the initiation of thrombus formation,
atherosclerosis, and the vascular lesions of hypertension and
other disorders
- rapid in onset, reversible and independent of new protein
synthesis
normal vascular repair and pathologic processes such as
atherosclerosis
have the capacity to proliferate when appropriately stimulated
they can also synthesize ECM collagen, elastin, and proteoglycans and
elaborate growth factors and cytokines
also responsible for the vasoconstriction or dilation that occurs in
response to physiologic or pharmacologic stimuli.
PDGF
endothelin-1
thrombin
fibroblast growth factor (FGF),
interferon- (IFN-), and
interleukin-1(IL-1)
heparan sulfates
nitric oxide, and
TGF-
Vascular injury adjacent endothelial and medial smooth muscle cells
migrate into the intima proliferate and synthesize ECM neointima is
formed this neointima is covered by endothelial cells
Schematic of intimal thickening, emphasizing smooth muscle cell migration
and proliferation within the intima, with associated ECM synthesis. Intimal
smooth muscle cells may derive from the underlying media or may be
recruited from circulating precursors; they are shown in a different color from
the medial cells to emphasize that they have a proliferative, synthetic, and
noncontractile phenotype distinct from medial smooth muscle cells.

Neointimal cells are not capable of contraction


Diastolic pressure of >89 mmHg and systolic pressure >139 mmHg
Unknown etiology (idiopathic) called as essential HPN
CO and PVR
age, gender, body mass index, and diet, particularly sodium intake
Blood pressure regulation. A, The critical roles played by cardiac output and
peripheral resistance in modulating blood pressure. B, Interplay of reninangiotensin-aldosterone and atrial natriuretic peptide in maintaining blood
pressure homeostasis.

CO is highly dependent on ___ an is greatly influenced by __


PVR is determined by ___ and is influenced by___

Blood volume; sodium homeostasis


At the level of arterioles and is influenced by neural and hormonal factors

blood vessles
Dr. FERRARIS

PATHOLOGY REVIEWER

Arteriovenous fistulas are abnormal, typically small, direct connections


between arteries and veins that bypass the intervening capillaries. They
occur most commonly as developmental defects but can also result
from rupture of an arterial aneurysm into an adjacent vein, from
penetrating injuries that pierce arteries and veins, or from inflammatory
necrosis of adjacent vessels; intentionally created arteriovenous fistulas
are used to provide vascular access for chronic hemodialysis.
3. Fibromuscular dysplasia is a focal irregular thickening of the walls of
medium and large muscular arteries, including renal, carotid,
splanchnic, and vertebral vessels.
Heart
Berry aneurysm
2.

In AV fistula, the only communication between the artery and the vein is
This results to out pouching of the vessel in about 2 mm- 3 cm in
diameter
Most common site of berry aneurysm

In AV fistula, the the volume of the blood that goes back to the heart is
______ (increased or decreased)
Fibromuscular dysplasia is associated mostly in
Components of endothelial cells

a protein localized to interendothelial junctions


Constitutive activities of endothelial cells critical for normal vessel
homeostasis

Inducers of endothelial activation includes;

Activated endothelial cells express ___

The circle of willis


a. Jxn between the ACA and ACOM
b. The bifurcation of the MCA
c. Jxn between the PCA and PCOM
Increased over load (forward failure) of the heart
Younger women, and not linked to oral contraceptives or abnormalities in sex
hormones
Weibel-Palade bodies
intracellular membrane-bound storage organelles for von Willebrand's
factor
platelet-endothelial cell adhesion molecule-1 (PECAM-1 or CD31)
a. endothelial cells maintain a nonthrombogenic blood-tissue
interface
modulate vascular resistance
metabolize hormones
regulate inflammation
affect the growth of other cell types, particularly smooth muscle cells
cytokines and bacterial products, which cause inflammation and
septic shock
hemodynamic stresses and lipid products, critical to the pathogenesis
of atherosclerosis
advanced glycosylation end products (important in diabetes)
as well as viruses, complement components, and hypoxia
adhesion molecules
and produce cytokines and chemokines
growth factors
vasoactive molecules that result either in vasoconstriction or in
vasodilation
major histocompatibility complex molecules,
procoagulant and anticoagulant moieties
variety of other biologically active products
study this figure

blood vessles
Dr. FERRARIS

PATHOLOGY REVIEWER


QUESTIONS
Most clinically significant lesions in vascular system involves ____
(arteries or veins)

2 principal mechanism of vascular pathology


Compare to veins, arteries have _____ wall
The thickness of arterial wall ______ as it becomes smaller
Basic constituents of the walls of the vessels

Three concentric layers of the vessel


Intima is consists of ____
The intima is separated from the media by __
The muscular layer of the vessel near the lumen received oxygen and
nutrients via
Areas on the outer portions of the media receive insufficient oxygen and
nutrients, what structures serve to deliver enough oxygen and nutrients
esp. in large vessels?
The outer limit of the media of most arteries is termed as
External to the media w/c is made up of CT w/ nerve fibers and vasa
vasorum
3 types of arteries based on their size and structural features
principal points of physiologic resistance to blood flow
approximately the diameter of a red blood cell (7 to 8 m), have an
endothelial cell lining but no media
Blood flow from the capillaries
In many types of inflammation, vascular leakage and leukocyte
exudation occur preferentially in
Relative to arteries, veins have

Prevents the backflow of the venous blood to the to the heart


thin-walled, endothelium-lined channels that serve as a drainage system
for returning interstitial tissue fluid and inflammatory cells to the blood
3 major processes characterize blood vessel formation and remodeling

It is the de novo formation of blood vessels during embryogenesis


Describe the process of vasculogenesis

The primary growth factors involved in the process of vasculogenesis


This constitutes the process of new vessel formation in the mature
organism.
This refers to the remodeling of existing arteries in response to chronic
changes in pressure or flow, and results from an interplay of endothelial
celland smooth muscle cellderived factors
3 particularly significant vascular anomalies

ANSWERS

Arteries
1. Narrowing (stenosis) or complete obstruction of the vessel
2. Weakening of the vessel walls
Thicker
The thickness diminishes but the ratio of the wall thickness to the lumen
becomes greater
Endothelial cells, smooth muscle cells and ECM w/ includes elastin, collagen
and glycosaminoglycan
Intima, media and adventitia
Consists of a single layer of endothelial cells with minimal subendothelial
connective tissue
Internal elastic lamina
Direct diffusion from the vessel lumen facilitated by holes in the internal
elastic membrane
Vasa vasorum
External elastic lamina
Adventitia
1. Large arteries e.g. aorta and its branches
2. Medium- sized or muscular arteries e.g coronary and renal arteries
3. Small arteries and arterioles
Arterioles
Capillaries
Blood from capillary beds flows initially into the postcapillary venules and
then sequentially through collecting venules and small, medium, and large
veins.
Post capillary venules

Larger diameters, larger lumens, and thinner and less organized walls
Because of their support, veins are predisposed to irregular dilation,
compression, and easy penetration by tumors and inflammatory
processes
has a large capacity; approximately two thirds of all the blood is in veins
Valves (esp. in the extremity)
Lymphatics
1. vasculogenesis
2. angiogenesis
3. arteriogenesis
Vasculogenesis
Hemangioblast angiogenic precursors develop and migrate to the sites of
vascularization. These differentiate into endothelial cells that associate to
form a primitive vascular plexus; with time and the influence of local genetic,
metabolic, and hemodynamic factors, this network of cells remodels (through
pruning and/or vessel enlargement) into the definitive vascular system
VEGF
Angiogenesis
Arteriogenesis
1.

Developmental or berry aneurysms occur in cerebral vessels; when


ruptured these can be causes of fatal intracerebral hemorrhage