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VASCULAR TISSUE HISTOLOGY
DR ANTONY JOSEPH MBBS MD
INTRODUCTION TO THE
VASCULAR SYSTEM
HISTOLOGY OF ARTERIAL
SYSTEM
HISTOLOGY OF VENOUS
SYSTEM
CLINICAL ASPECT
CHAMBERS OF
HEART
GREAT VESSELS RELATED TO HEART ANTERIOR
ASPECT
POSTERIOR
ASPECT
TYPE OF
CIRCULATIONS
SYSTEMIC AND
PULMONARY
CIRCULATION
LEFT ATRIUM RECIEVES OXYGENATED
BLOOD FROM LUNGS VIA 4
PULMONARY VEINS. FROM LEFT
ATRIUM, BLOOD PASSES TO LEFT
VENTRICLE
FROM LEFT VENTRICLES, BLOOD IS PUMPED TO AORTA/ LARGE/
ELASTIC ARTERY THEN TO MEDIUM SIZE ARTERY/ MUSCULAR ARTERY
THEN TO SMALL ARTERIES THEN TO ARTERIOLES AND THEN
CAPILLARIES IN THE TISSUE WHERE THE GASOUS EXCHANGE TAKES
PLACE.
AFTER THE GASOUS EXCHANGE, THE DEOXYGENATED BLOOD PASSES
THROUGH THE POSTCAPILLARY VENULES THEN TO MUSCULAR
VENULE, THEN TO SMALL VEINS, MEDIUM VEINS & FINALLY LARGE
VEINS LIKE SUPERIOR & INFERIOR VENA CAVA.
SUPERIOR & INFERIOR VENA CAVA
DAINS BLOOD INTO RIGHT ATRIUM
FROM THERE, INTO RIGHT VENTRICLE,
WHICH PUMPS BLOOD INTO THE
PULMONARY TRUNK.
SYSTEMIC
CIRCULATION
MAJOR SYSTEMIC
ARTERIES
ARCH OF AORTA
& BRANCHES
COMMON CAROTID
ARTERIES &
BRANCHES
EXTERNAL
CAROTID ARTERY
BRANCHES
INTERNAL CAROTID ARTERY
& BRANCHES
CIRCLE OF
WILLIS
THORACIC-
UPPER LIMB
ARTERIES
LEFT
VENTRICLE
UPPER LIMB
ARTERIES
THORACIC-
ABDOMINAL
ARTERIES
THORACIC-
ABDOMINAL
ARTERIES.
ILLIAC ARTERY
BRANCHES
LOWER LIMB
ARTERIES
GASEOUS EXCHANGE IN
THE CAPILLARY BED
VEINS OF
UPPER LIMB
VEINS OF HEAD
AND NECK
THORACIC &
ABDOMINAL VEINS
VEINS OF
LOWER LIMB
RIGHT
ATRIUM
VEINS DRAINING INTO
SUPERIOR VENA CAVA
RIGHT
ATRIUM
VEINS DRAINING INTO
INFERIOR VENA CAVA
DRAINS STRUCTURES
BELOW THE DIAPHRAM
PULMONARY TRUNK / MAIN PULMONARY ARTERY CARRIES DEOXYGENATED BLOOD FROM RIGHT VENTRICLE TO RIGHT
AND LEFT LUNGS. IN LUNGS, IT DIVIDES INTO SUBBRANCHES AND IN END, IN ALVEOLI OF LUNGS IT FORMS CAPILLARY
NETWORK FOR GASOUS EXCHANGE.
CARBON DIOXIDE IS REMOVED AND OXYGEN IS DIFFUSED INTO THE BLOOD. THE PULMONARY VEINS CARRY
OXYGENATED BLOOD FROM THE LUNGS AND DRAINS INTO THE LEFT ATRIUM.
PULMONARY
CIRCULATION
GASEOUS EXCHANGE
IN ALVEOLI
4 PULMONARY VEINS CARRIES OXYGENATED BLOOD FROM LUNGS TO LEFT ATRIUM.
(1) RIGHT SUPERIOR – DRAINS UPPER & MIDDLE LOBES OF RIGHT LUNG.
(2) RIGHT INFERIOR – DRAINS INFERIOR LOBE OF RIGHT LUNG.
(3) LEFT SUPERIOR – DRAINS UPPER LOBE OF LEFT LUNG.
(4) LEFT INFERIOR – DRAINS LOWER LOBE OF LEFT LUNG
1
2
3
4
1
1
2
3
4
WHY PULMONARY VEINS ARE NOT CALLED ARTERIES EVEN IF THEY
CARRY OXYGENATED BLOOD ?
THAT’S BECAUSE BY DEFINITION, ANY VESSELS THAT CARRY BLOOD
TOWARDS HEART IS CALLED VEIN. AND ANY VESSEL THAT CARRY
BLOOD AWAY FROM HEART IS CALLED ARTERY.
NOW YOU KNOW WHY PULMONARY ARTERIES ARE NOT CALLED
VEINS EVEN IF THEY CARRY DEOXYGENATED BLOOD.
HISTOLOGY OF
ARTERIAL SYSTEM
HISTOLOGY OF
VENOUS SYSTEM
THREE LAYERS OF VASCULAR WALL
TUNICA
INTIMA
INNER MOST LAYER OF A VESSEL.
3 COMPONENTS
ENDOTHELIUM
SINGLE LAYER OF SQUAMOUS
EPITHELIAL CELLS.
BASAL LAMINA OF
ENDOTHELIUM
- THIN EXTRACELLULAR LAYER
COMPOSED OF COLLAGEN,
PROTEOGLYCANS,
GLYCOPROTEINS.
SUBENDOTHELIAL
CONNECTIVE TISSUE
- CONSIST OF LOOSE AREOLAR
CONNECTIVE TISSUE. IN ARTERIES
ND ARTERIOLES, SHEET LIKE
LAMELLA OF FENESTRATED
ELASTIC MATERIAL CALLED
INTERNAL ELASTIC MEMBRANE
ARE PRESENT..
1 2 3
FUNCTIONS OF
ENDOTHELIUM MAINTENANCE OF SELECTIVE PERMEABILITY
SIMPLE DIFFUSION, ACTIVE TRANSPORT, PINOCYTOSIS… ETC
MAINTENANCE OF NONTHROMBOGENIC BARRIER
SECRETION OF ANTICOAGULANT, SECRETION OF ANTITHROMBOGENIC AGENTS, SECRETION OF
PROTHROMBOGENIC AGENTS.
MODULATION OF BLOOD FLOW & VASCULAR RESISTANCE
SECRETION OF VASOCONSTRICTORS & VASODIALATORS.
1
2
3
FUNCTIONS OF
ENDOTHELIUM REGULATION OF CELL GROWTH
SECRETION OF GROWTH-STIMULATING AND GROWTH-INHIBITING FACTORS.
REGULATION OF IMMUNE RESPONSES
REGULATION OF LEUKOCYTE MIGRATION.
MAINTENANCE OF EXTRACELLULAR MATRIX, INVOLVEMENT IN
LIPOPROTEIN & CHOLESTROL METABOLISM.
4
5
6
TUNICA
MEDIA
MIDDLE LAYER, CONSISTS PRIMARILY OF
CIRCUMFERENTIALLY ARRANGED LAYER OF VASCULAR
SMOOTH MUSCLES.
IN ARTERIES, THIS LAYER IS THICK & EXTENDS
FROM INTERNAL ELASTIC MEMBRANE TO
EXTERNAL ELASTIC MEMBRANE. EXTERNAL
ELASTIC MEMBRANE IS A LAYER OF ELASTIN.
VARIABLE AMOUNTS OF ELASTIN, RETICULAR FIBERS &
PROTEOGLYCANS ARE PRESENT BETWEEN THE SMOOTH
MUSCLE CELLS OF THE TUNICA MEDIA.
TUNICA
ADVENTITIA
OUTERMOST CONNECTIVE TISSUE LAYER, COMPOSED
PRIMARILY OF LONGITUDINALLY ARRANGED COLLAGENOUS
TISSUE & FEW ELASTIC FIBERS. THESE CONNECTIVE TISSUE
ELEMENTS GRADUALLY MERGE WITH LOOSE CONNECTIVE
TISSUE SURROUNDING THE VESSELS.
TUNICA ADVENTITIA IS THIN IN ARTERIAL SYSTEM BUT QUIET
THICK IN VENULES & VEINS.
TUNICA ADVENTITIA ALSO HAS VASA VASORUM – SUPPLY BLOOD TO VASCULAR WALL.
ALSO NERVI VASORUM – NETWORK OF AUTONOMIC NERVES THAT CONTROL THE
CONTRACTION OF SMOOTH MUSCLES IN VESSEL WALLS.
ARTERIAL SYSTEM
CONDUCTING
VESSELS / ELASTIC
ARTERIES
AORTA
PULMONARY TRUNK
BRACHIOCEPHALIC TRUNK
COMMON CAROTID
SUBCLAVIAN ARTERY
DISTRIBUTION
VESSELS /
MUSCULAR
ARTERIES
BRACHIAL ARTERY
RADIAL ARTERY
ULNAR ARTERY
FEMORAL ARTERY
TIBIAL ARTERY
ARTERIOLES /
RESISTANCE
VESSELS
SMALLEST DIVISION OF
THE MUSCULAR
ARTERY. OFFER
PERIPHERAL
RESISTANCE THUS
REGULATING SYSTOLIC
ARTERIAL PRESSURE.
CAPILLARIES /
EXCHANGE
VESSELS.
VESSELS DIAMETERS TUNICA INTIMA TUNICA MEDIA TUNICA ADVENTITIA
LARGE ARTERY
(ELASTIC ARTERY) >10 mm
ENDOTHELIUM.
CONNECTIVE TISSUE.
SMOOTH MUSCLE.
SMOOTH MUSCLE.
ELASTIC LAMELLAE.
THINNER THAN TUNICA
MEDIA.
CONNECTIVE TISSUE.
ELASTIC FIBERS.
MEDIUM ARTERY
(MUSCULAR ARTERY) 2-10 mm
ENDOTHELIUM.
CONNECTIVE TISSUE.
PREDOMINENT INTERNAL ELASTIC
MEMBRANE.
SMOOTH MUSCLES.
COLLAGEN FIBERS.
LITTLE ELASTIC TISSUE.
THINNER THAN TUNICA
MEDIA.
CONNECTIVE TISSUE.
SOME ELASTIC FIBERS.
SMALL ARTERY
0.1-2 mm
ENDOTHELIUM.
CONNECTIVE TISSUE.
SMOOTH MUSCLE.
INTERNAL ELASTIC MEMBRANE.
SMOOTH MUSCLE (8-10 CELL
LAYERS).
COLLAGEN FIBERS.
THINNER THAN TUNICA
MEDIA.
CONNECTIVE TISSUE.
SOME ELASTIC FIBERS.
ARTERIOLES 10-100 ÎĽm ENDOTHELIUM.
CONNECTIVE TISSUE.
SMOOTH MUSCLE.
SMOOTH MUSCLE (1-2) CELL
LAYERS.
THIN ILL-DEFINED SHEATH OF
CONNECTIVE TISSUE.
CAPILLARIES 4-10 ÎĽm ENDOTHELIUM NONE NONE
ARTERY
MEDIUM SIZE/MUSCULAR ARTERY VS LARGE/ELASTIC ARTERY
CAPILLARIES
CAPILLARIES CAPILLARIES ARE THE SMALLEST DIAMETER
BLOOD VESSELS, OFTEN SMALLER THAN THE
DIAMETER OF AN RBC.
CAPILLARIES HAS SINGLE LAYER OF
ENDOTHELIAL CELLS AND ITS
BASAL LAMINA.
THE ENDOTHELIAL CELLS FORM A TUBE
JUST LARGE ENUF FOR THE PASSAGE OF
RBC – ONE AT A TIME.
CAPILLARIES ALLOW FLUID CONTAINING GASES,
METABOLITES AND WASTE PRODUCTS TO MORE
FREELY THROUGH THEIR THIN WALL.
RBC IN
CAPILLARY
3 TYPES: CONTINOUS, FENESTRATED & DISCONTINOUS.
PERICYTES
THESE ARE UNDIFFENTIATED
MESENCHYMAL STEM CELLS.
PERICYTES ARE CLOSELY
ASSOCIATED WITH
CAPILLARIES.
HISTOLOGY OF VEINS THE LAYERS OF VEINS ARE NOT DISTINCT OR
WELL DEFINED AS OF ARTERY.
VENULES ARE SUBCLASSIFIED
AS POSTCAPILLARY &
MUSCULAR VENULES.
POSTCAPILLARY VENULES
COLLECT BLOOD FROM
CAPILLARY NETWORK AND IS
CHARACTERIZED BY THE
PRESENCE OF PERICYTES.
PERICYTES ARE UNDIFFENTIATED MESENCHYMAL
STEM CELLS. THEY SYNTHESIS GROWTH FACTORS.
PERICYTES ARE MORE EXTENSIVE IN POSTCAPILLARY
VENULES THAN IN THE CAPILLARIES.
HISTOLOGY OF VEINS MUSCULAR VENULES ARE DISTINGUISHED FROM
POSTCAPILLARY VENULES BY A PRESENCE OF A
TUNICA MEDIA. PERICYTES ARE ABSENT IN
MUSCULAR VENULES.
SMALL VEINS ARE THE
CONTINUATION OF THE
MUSCULAR VENULES.
MEDIUM SIZE VEINS HAS ALL THE
THREE LAYERS, TUNICA MEDIA
OF THE MEDIUM SIZE VEINS ARE
MUCH THINNER THAN THE
MEDIUM SIZE ARTERY. JUST LIKE
LARGE VEIN.
TUNICA ADVENTISIA OF MEDIUM
SIZE VEIN IS MUCH THICKER THAN
THE MEDIUM SIZE ARTERY. JUST LIKE
LARGE VEIN.
1
2
3
4
LARGE VEIN
MEDIUM SIZE
VEIN
MEDIUM SIZE
ARTERY
VESSEL DIAMETER TUNICA INTIMA TUNICA MEDIA TUNICA ADVENTITIA
POSTCAPILLARY
VENULE
10-50 ÎĽm ENDOTHELIUM.
PERICYTES.
NONE. NONE.
MUSCULAR VENULES 50-100 ÎĽm ENDOTHELIUM SMOOTH MUSCLES (1-2 CELL
LAYERS)
THICKER THAN TUNICA MEDIA.
CONNECTIVE TISSUE.
SOME ELASTIC FIBERS.
SMALL VEINS 0.1-1 mm ENDOTHELIUM.
CONNECTIVE TISSUE.
SMOOTH MUSCLES (2-3 LAYERS)
SMOOTH MUSCLES (2-3 LAYERS
CONTINOUS WITH TUNICA
INTIMA)
THICKER THAN TUNICA MEDIA.
CONNECTIVE TISSUE.
SOME ELASTIC FIBERS.
MEDIUM VEINS 1-10 mm ENDOTHELIUM
CONNECTIVE TISSUE.
SMOOTH MUSCLES.
INTERNAL ELASTIC MEMBRANE
IN SOME CASES.
SMOOTH MUSCLE.
COLLAGEN FIBERS.
THICKER THAN TUNICA MEDIA.
CONNECTIVE TISSUE.
SOME ELASTIC FIBERS.
LARGE VEIN > 10 mm ENDOTHELIUM.
CONNECTIVE TISSUE.
SMOOTH MUSCLE.
SMOOTH MUSCLE (2-15 LAYERS)
COLLAGEN FIBER.
MUCH THICKER THAN TUNICA
MEDIA.
CONNECTIVE TISSUE.
SOME ELASTIC FIBERS.
LONGITUDINAL SMOOTH
MUSCLES.
GRADIENT OF BLOOD PRESSURE AT
DIFFERENT LEVELS OF VESSELS
ARTERIES – 120 mm HG
ARTERIOLES – 60 mm HG
ARTERIAL END OF CAPILLARY – 30 mm HG
VENOUS END OF CAPILLARY – 12 mm HG
LARGE VEIN – 5 mm HG
CLOSE TO RIGHT ATRIUM – ALMOST ZERO.
FACTORS INFLUENCING VENOUS BLOOD RETURN.
Factor # 1. Pressure Gradient
Factor # 2. Vis-a-Tergo (force acting from behind)
Factor # 3. Vis-a-Fronte (force acting from front)
Factor # 4. Skeletal Muscle Pump
Factor # 5. Thoracic Pump
Factor # 6. Abdominal Pump
Factor # 7. Venomotor Tone
Factor # 8. Posture and Gravity
Factor # 1. Pressure
Gradient
The pressure in the right atria
(central venous pressure) into
which the superior and inferior
vena cavae open is around 0
mm Hg. In the peripheral
veins, the pressure is around
5 mm Hg and the pressure in
the veins nearer to the heart
goes on decreasing. So the
blood flows from higher
pressure to lower pressure.
Factor # 2. Vis-a-Tergo
(force acting from
behind)
The contraction of the left
ventricle creates a pressure
that pushes blood from behind
all along the vascular tree
throughout the body.
Factor # 3. Vis-a-Fronte
(force acting from
front)
The pressure in the right
atrium is normally around 0
mm Hg. During ventricular
contraction, the atrio
ventricular ring is pulled down.
As a result of this, the atria get
expanded. This creates a
negative pressure in right
atrium and the negative
pressure is also created during
sudden rush of blood from
atria to ventricle.
Factor # 4. Skeletal
Muscle Pump
The veins are arranged in
between the skeletal muscle
fibers and are arranged parallel
to skeletal muscle fibers. So
when the muscle contracts the
veins get squeezed. Due to the
compressor effect of the
muscle fibers on the vein,
blood is made to flow through
them. However, blood is made
to flow in the direction of
heart due to the presence of
valves in veins, which prevent
back flow.
Factor # 5. Thoracic
Pump
During inspiration, the
intrapleural pressure becomes
more negative. A simultaneous
increase of pressure in the
abdomen and a more negative
pressure in thorax, increase
the pressure gradient for flow
of blood towards the heart
from the abdomen.
Factor # 6. Abdominal
Pump
When the abdominal muscles
contract, there will be increase
of intra-abdominal pressure
and hence compression of
veins occurs in the abdominal
region. This increases venous
return by increasing the
gradient towards the thoracic
cavity (heart).
Factor # 7. Venomotor
Tone
The constant excitatory
influence by sympathetic
nerves on the smooth muscle
of veins is called venomotor
tone. Because of this, the walls
of the veins remain in a
partially contracted state even
under resting condition. When
the venomotor tone is
increased, the capacity of veins
decreases. This increases the
venous return.
Factor # 8. Posture and
Gravity
As such the pressure in the
veins is very less. When
gravitational force acts on the
lower parts of body especially
in the erect posture, it will
decrease the venous return
from the lower limbs. The
gravitational force tries to pull
down blood from the
dependent parts of the body.
FACTORS - VENOUS DRAINAGE
ANSTOMOSIS
IT IS THE COMMUNICATION BETWEEN THE BLOOD
VESSELS – 3 TYPES – INTER-ARTERIAL, ARTERIO-
VENOUS, END-ARTERIES.
INTER-ARTERIAL
ANASTOMOSIS
TAKE PLACE BETWEEN ADJACENT ARTERIES BY
THEIR TRUNKS, BRANCHES AND SUB-BRANCHES.
EXAMPLE: B/W RIGHT & LEFT
GASTRIC ARTERY
ARTERIOVENOUS
SHUNTS
ARTERIOVENOUS SHUNT –
ALLOW BLOOD TO BYPASS
CAPILLARIES BY PROVIDING DIRECT
ROUTES BETWEEN ARTERIES &
VEINS.
AV SHUNTS ARE FOUND IN SKIN, THE
FINGERTIPS, NOSE, LIPS & ERECTILE
TISSUE OF PENIS & CLITORIS.
A-V SHUNT SERVES AS
THERMOREGULATION – CLOSING OF
THE AV SHUNT ALLOWS BLOOD TO
FLOW THROUGH CAPILLARY BED,
ENHANCING HEAT LOSS. OPENING AV
SHUNT IN SKIN REDUCE THE BLOOD
FLOW TO SKIN CAPILLARIES, THUS
CONSERVING BODY HEAT.
END-ARTERIES
MOST ARTERIES ANASTOMOSE WITH ONE ANOTHER AT
CAPILLARY AND PRE-CAPILLARY LEVEL. END-ARTERY
ARE THOSE WHICH DONOT FORM ANY PRE-CAPILLARY
ANASTOMOSIS.
EXAMPLES:
CENTRAL ARTERY OF
RETINA
CEREBRAL, SPLENIC,
RENAL ND VASA
RECTA OF SMALL GUT
CORONARY ARTERIES
ANATOMICALLY,
CORONARY ARTERIES
ARE NOT END
ARTERIES. BUT
FUNCTIONALLY THEY
BEHAVE AS END-
ARTERIES. AN
OBSTRUCTION IN
END-ARTERIES CAN
CAUSE LOCAL TISSUE
DEATH.
CLINICAL ASPECT OF VASCULAR TISSUE
ATHEROSCLEROSIS: MOST COMMON ACQUIRED
ABNORMALITY OF THE BLOOD VESSEL.
COMPLICATIONS OF ATHEROSCLEROSIS ARE
CORONARY HEART DISEASE, HEART ATTACK-MI,
STROKE & PERIPHERAL ARTERY DISEASE.
ATHEROSCLEROSIS AFFECTS TUNICA INTIMA OF
LARGE ELASTIC ARTERY WHICH LEAD TO
ENDOTHELIAL DYSFUNCTION.
THE ENDOTHELIAL INJURY IN ATHEROSCLEROSIS CAN OCCUR DUE TO HIGH LDL CHOLESTROL,
HYPERLIPIDEMIA, HYPERGLYCEMIA, HYPERTENSION, TOXINS – SMOKING ETC. THE DAMAGED
ENDOTHELIUM, INCREASES PERMEABILITY TO LDL CHOLESTROL ND INCREASED ADHERENCE OF
WBS (MONOCYTES) TO ENDOTHELIUM.
AS THE RESULT TO INJURY, MONOCYTES FROM BLOOD STEAM ENTER TUNICA INTIMA, AND GET
DIFFERENTIATED INTO MACROPHAGES. THESE MACROPHAGES PHAGOCYTIZE OXIDIZED LDL ND
TRANSFORM INTO FOAM CELL.
ATHEROMATOUS PLAQUE IS A THICK LAYER OF FIBROUS CONNECTIVE TISSUE CONTAINING
SMOOTH MUSCLE CELLS, MACROPHAGES, FOAM CELL, T LYMPHOCYTES, CELL DEBRIS ETC
AS THE SIZE OF ATHEROMATOUS PLAQUE INCREASES, BLOOD STASIS ND CLOTTING MAY LEAD TO
OCCLUSION OF VESSEL.
LUMEN
NARROWED/BLOCKED
CORONARY
ARTERY DISEASE /
MYOCARDIAL
INFACTION
CORONARY
ARTERY
DISEASE
TREATMENT
- Angioplasty
and stent
placement
Coronary artery bypass graft (CABG) or heart bypass or bypass surgery,
is a surgical procedure to restore normal blood flow to an obstructed coronary artery.
CABG
THROMBOEMBOLISM ACUTE RUPTURE OF AN
UNSTABLE ATHEROMATOUS
PLAQUE CAN LEAD TO EITHER
ACUTE OCCULATION OF ARTERY
(THROMBOSIS) OR DISTAL
SHOWERING OF PLAQUE
MATERIAL (EMBOLISM).
ACUTE OCCLUSION DOESNOT
ALLOW FOR THE
DEVELOPMENT OF
COLLATERALS AND THEREFORE
LEADS TO SYMPTOMS OF
ACUTE ISCHEMIA.
ACUTE MYOCARDIAL
INFARCTION, STROKE, ACUTE
LIMB ISCHEMIA ETC
TRANSIENT ISCHAEMIC
ATTACK (TIA)
TRANSIENT/TEMPORARY
EPISODE OF
NEUROLOGICAL
DYSFUNCTION CAUSED BY
FOCAL BRAIN, SPINAL
CORD OR RETINAL
ISCHEMIA WITHOUT
ACUTE INFARCTION.
USUALLY TIA WILL
RESOLVE WITHIN 24
HOURS.
CVA
MESENTRIC OCCLUSIVE
DISEASE.
LIFE THREATENING
CONDITION CAUSED BY
DECREASED BLOOD FLOW
TO THE BOWEL. IT IS
DIFFICULT TO DIAGNOSE.
4 TYPES
1. EMBOLIC OCCLUSION OF
MESENTRIC CIRCULATION.
2. ACUTE THROMBOSIS OF
MESENTRIC CIRCULATION.
3. NON-OCCULSIVE
MESENTRIC ISCHEMIA
4. MESENTRIC VENOUS
THROMBOSIS
NECROTIC BOWEL
NORMAL
MESENTRIC
OCCLUSIVE DISEASE
PERIPHERAL OCCLUSIVE
DISEASE
IN PERSONS ABOVE AGE 60.
MOST COMMON CAUSE IS
ATHEROSCLEROSIS OF
VESSELS.
RISK FACTORS:
HYPERTENSION, DIABETES,
OBESITY, SMOKING ETC
AORTO-ILLIAC
OCCULSION
PALE DUE TO
ABSENCE OF
BLOOD SUPPLY
FOR EVALUATING
PERIPHERAL ARTERIAL
OCCULSION, YOU
SHOULD FEEL THE
PERIPHERAL PULSE.
CLAUDICATION PAIN
COMMON IN
OCCULSIVE DISEASE
OF LOWER LIMBS.
THE PAIN OCCURS
DURING MUSCLE
ACTIVITY SUCH AS
WALKING. AND
DISAPPEARS AFTER
TAKING 2-3 MIN REST.
PERIPHERAL
OCCULSIVE DISEASE
CAN RESULT IN TISSUE
LOSS/ DEATH . DUE TO
LACK/INSUFFICENT
BLOOD PERFUSION.
CUTANEOUS PRESSURE NECROSIS / BED SORE IN BED RIDDEN PATIENTS. It is injuries
to skin and underlying tissue resulting from prolonged pressure on the skin.
SMALL VESSEL DISEASE –
RAYNAUD’S SYNDROME
Raynaud's disease causes some areas of your body
— such as your fingers and toes — to feel numb
and cold in response to cold temperatures or
stress. In Raynaud's disease, smaller arteries that
supply blood to your skin become narrow, limiting
blood flow to affected areas (vasospasm).
Women are more likely than men to have
Raynaud's disease, also known as Raynaud's or
Raynaud's phenomenon or syndrome. It appears to
be more common in people who live in colder
climates.
1
2
3
Raynaud's
disease
Limited scleroderma, also known as CREST syndrome
Buerger's disease is a rare disease of
the arteries and veins in the arms and
legs. In Buerger's disease — also called
thromboangiitis obliterans — your
blood vessels become inflamed, swell
and can become blocked with blood
clots (thrombi).
This eventually damages or destroys
skin tissues and may lead to infection
and gangrene. Buerger's disease usually
first shows in your hands and feet and
may eventually affect larger areas of
your arms and legs.
Virtually everyone diagnosed with
Buerger's disease smokes cigarettes or
uses other forms of tobacco, such as
chewing tobacco. Quitting all forms of
tobacco is the only way to stop
Buerger's disease. For those who don't
quit, amputation of all or part of a limb
is sometimes necessary.
Buerger's disease
Buerger's
disease
DIABETIC
NEUROPATHY –
OCCULTATION
OF VASA
NERVORUM –
THE BLOOD
VESSEL THAT
SUPPLY THE
NERVE.
FROST BITE
Frostbite is an injury
caused by freezing of the
skin and underlying tissues.
First your skin becomes very
cold and red, then numb,
hard and pale. Frostbite is
most common on the
fingers, toes, nose, ears,
cheeks and chin. Exposed
skin in cold, windy weather is
most vulnerable to frostbite.
FASCIOTOMY IS
PERFORMED IN
COMPARTMENT SYNDROME
TO RELIEVE THE PRESSURE
& RESORE THE
CIRCULATION
VARICOSE VEINS
Varicose veins are twisted, enlarged
veins. Any superficial vein may become
varicosed, but the veins most commonly
affected are those in your legs. That's
because standing and walking upright
increases the pressure in the veins of your
lower body.
• An achy or heavy feeling in your legs
• Burning, throbbing, muscle cramping
and swelling in your lower legs
• Worsened pain after sitting or standing
for a long time
• Itching around one or more of your veins
• Skin discoloration around a varicose vein
• Skin ulcers
Varicose
vein &
ulcer
Deep vein thrombosis
(DVT) occurs when a blood clot
(thrombus) forms in one or more of the
deep veins in your body, usually in your
legs. Deep vein thrombosis can cause
leg pain or swelling but also can occur
with no symptoms.
You can get DVT if you have certain
medical conditions that affect how your
blood clots. A blood clot in your legs
can also happen if you don't move for a
long time, such as after you have
surgery or an accident, when you're
traveling a long distance, or when
you're on bed rest.
Deep vein thrombosis can be very
serious because blood clots in your
veins can break loose, travel through
your bloodstream and get stuck in your
lungs, blocking blood flow (pulmonary
embolism). However, pulmonary
embolism can occur with no evidence
of DVT.
END
ARTERIES
DAMAGED
RETINA
An aneurysm is an abnormal bulge or ballooning in the wall of
a blood vessel. An aneurysm can burst (rupture), causing
internal bleeding and often leading to death. Aneurysms
usually don't cause symptoms, so you might not know you
have an aneurysm even if it's large.
BERRY ANEURYSM IN
THE CIRCLE OF WILLIS
RUPTURE OF
ANEURYSM IS A
LIFE THREATING
CONDITION
BERRY ANEURYSM
RUPTURE – YOU
CAN SEE THE
BLOOD CLOTS
CLIPPING OF ANEURYSM
CLIPPING
Smoking is the strongest risk
factor for aneurysm. It can
weaken the aortic walls,
increasing the risk not only of
developing an aortic aneurysm,
but also rupture. The longer and
more you smoke or chew
tobacco, the greater the chances
of developing an aortic
aneurysm.
Einstein died of leaking
abdominal aortic aneurysm at
the age 76.
Thank you

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HISTOLOGY OF VASCULAR TISSUE

  • 1. VASCULAR TISSUE HISTOLOGY DR ANTONY JOSEPH MBBS MD
  • 2. INTRODUCTION TO THE VASCULAR SYSTEM HISTOLOGY OF ARTERIAL SYSTEM HISTOLOGY OF VENOUS SYSTEM CLINICAL ASPECT
  • 4.
  • 5. GREAT VESSELS RELATED TO HEART ANTERIOR ASPECT
  • 8. LEFT ATRIUM RECIEVES OXYGENATED BLOOD FROM LUNGS VIA 4 PULMONARY VEINS. FROM LEFT ATRIUM, BLOOD PASSES TO LEFT VENTRICLE FROM LEFT VENTRICLES, BLOOD IS PUMPED TO AORTA/ LARGE/ ELASTIC ARTERY THEN TO MEDIUM SIZE ARTERY/ MUSCULAR ARTERY THEN TO SMALL ARTERIES THEN TO ARTERIOLES AND THEN CAPILLARIES IN THE TISSUE WHERE THE GASOUS EXCHANGE TAKES PLACE. AFTER THE GASOUS EXCHANGE, THE DEOXYGENATED BLOOD PASSES THROUGH THE POSTCAPILLARY VENULES THEN TO MUSCULAR VENULE, THEN TO SMALL VEINS, MEDIUM VEINS & FINALLY LARGE VEINS LIKE SUPERIOR & INFERIOR VENA CAVA. SUPERIOR & INFERIOR VENA CAVA DAINS BLOOD INTO RIGHT ATRIUM FROM THERE, INTO RIGHT VENTRICLE, WHICH PUMPS BLOOD INTO THE PULMONARY TRUNK. SYSTEMIC CIRCULATION
  • 10. ARCH OF AORTA & BRANCHES
  • 14.
  • 16.
  • 17.
  • 24.
  • 25.
  • 26. GASEOUS EXCHANGE IN THE CAPILLARY BED
  • 32. RIGHT ATRIUM VEINS DRAINING INTO INFERIOR VENA CAVA DRAINS STRUCTURES BELOW THE DIAPHRAM
  • 33. PULMONARY TRUNK / MAIN PULMONARY ARTERY CARRIES DEOXYGENATED BLOOD FROM RIGHT VENTRICLE TO RIGHT AND LEFT LUNGS. IN LUNGS, IT DIVIDES INTO SUBBRANCHES AND IN END, IN ALVEOLI OF LUNGS IT FORMS CAPILLARY NETWORK FOR GASOUS EXCHANGE. CARBON DIOXIDE IS REMOVED AND OXYGEN IS DIFFUSED INTO THE BLOOD. THE PULMONARY VEINS CARRY OXYGENATED BLOOD FROM THE LUNGS AND DRAINS INTO THE LEFT ATRIUM. PULMONARY CIRCULATION
  • 34.
  • 35.
  • 36.
  • 37.
  • 39. 4 PULMONARY VEINS CARRIES OXYGENATED BLOOD FROM LUNGS TO LEFT ATRIUM. (1) RIGHT SUPERIOR – DRAINS UPPER & MIDDLE LOBES OF RIGHT LUNG. (2) RIGHT INFERIOR – DRAINS INFERIOR LOBE OF RIGHT LUNG. (3) LEFT SUPERIOR – DRAINS UPPER LOBE OF LEFT LUNG. (4) LEFT INFERIOR – DRAINS LOWER LOBE OF LEFT LUNG 1 2 3 4 1 1 2 3 4
  • 40. WHY PULMONARY VEINS ARE NOT CALLED ARTERIES EVEN IF THEY CARRY OXYGENATED BLOOD ? THAT’S BECAUSE BY DEFINITION, ANY VESSELS THAT CARRY BLOOD TOWARDS HEART IS CALLED VEIN. AND ANY VESSEL THAT CARRY BLOOD AWAY FROM HEART IS CALLED ARTERY. NOW YOU KNOW WHY PULMONARY ARTERIES ARE NOT CALLED VEINS EVEN IF THEY CARRY DEOXYGENATED BLOOD.
  • 42. THREE LAYERS OF VASCULAR WALL
  • 43.
  • 44. TUNICA INTIMA INNER MOST LAYER OF A VESSEL. 3 COMPONENTS ENDOTHELIUM SINGLE LAYER OF SQUAMOUS EPITHELIAL CELLS. BASAL LAMINA OF ENDOTHELIUM - THIN EXTRACELLULAR LAYER COMPOSED OF COLLAGEN, PROTEOGLYCANS, GLYCOPROTEINS. SUBENDOTHELIAL CONNECTIVE TISSUE - CONSIST OF LOOSE AREOLAR CONNECTIVE TISSUE. IN ARTERIES ND ARTERIOLES, SHEET LIKE LAMELLA OF FENESTRATED ELASTIC MATERIAL CALLED INTERNAL ELASTIC MEMBRANE ARE PRESENT.. 1 2 3
  • 45.
  • 46. FUNCTIONS OF ENDOTHELIUM MAINTENANCE OF SELECTIVE PERMEABILITY SIMPLE DIFFUSION, ACTIVE TRANSPORT, PINOCYTOSIS… ETC MAINTENANCE OF NONTHROMBOGENIC BARRIER SECRETION OF ANTICOAGULANT, SECRETION OF ANTITHROMBOGENIC AGENTS, SECRETION OF PROTHROMBOGENIC AGENTS. MODULATION OF BLOOD FLOW & VASCULAR RESISTANCE SECRETION OF VASOCONSTRICTORS & VASODIALATORS. 1 2 3
  • 47. FUNCTIONS OF ENDOTHELIUM REGULATION OF CELL GROWTH SECRETION OF GROWTH-STIMULATING AND GROWTH-INHIBITING FACTORS. REGULATION OF IMMUNE RESPONSES REGULATION OF LEUKOCYTE MIGRATION. MAINTENANCE OF EXTRACELLULAR MATRIX, INVOLVEMENT IN LIPOPROTEIN & CHOLESTROL METABOLISM. 4 5 6
  • 48. TUNICA MEDIA MIDDLE LAYER, CONSISTS PRIMARILY OF CIRCUMFERENTIALLY ARRANGED LAYER OF VASCULAR SMOOTH MUSCLES. IN ARTERIES, THIS LAYER IS THICK & EXTENDS FROM INTERNAL ELASTIC MEMBRANE TO EXTERNAL ELASTIC MEMBRANE. EXTERNAL ELASTIC MEMBRANE IS A LAYER OF ELASTIN. VARIABLE AMOUNTS OF ELASTIN, RETICULAR FIBERS & PROTEOGLYCANS ARE PRESENT BETWEEN THE SMOOTH MUSCLE CELLS OF THE TUNICA MEDIA.
  • 49.
  • 50. TUNICA ADVENTITIA OUTERMOST CONNECTIVE TISSUE LAYER, COMPOSED PRIMARILY OF LONGITUDINALLY ARRANGED COLLAGENOUS TISSUE & FEW ELASTIC FIBERS. THESE CONNECTIVE TISSUE ELEMENTS GRADUALLY MERGE WITH LOOSE CONNECTIVE TISSUE SURROUNDING THE VESSELS. TUNICA ADVENTITIA IS THIN IN ARTERIAL SYSTEM BUT QUIET THICK IN VENULES & VEINS. TUNICA ADVENTITIA ALSO HAS VASA VASORUM – SUPPLY BLOOD TO VASCULAR WALL. ALSO NERVI VASORUM – NETWORK OF AUTONOMIC NERVES THAT CONTROL THE CONTRACTION OF SMOOTH MUSCLES IN VESSEL WALLS.
  • 51.
  • 52.
  • 53. ARTERIAL SYSTEM CONDUCTING VESSELS / ELASTIC ARTERIES AORTA PULMONARY TRUNK BRACHIOCEPHALIC TRUNK COMMON CAROTID SUBCLAVIAN ARTERY DISTRIBUTION VESSELS / MUSCULAR ARTERIES BRACHIAL ARTERY RADIAL ARTERY ULNAR ARTERY FEMORAL ARTERY TIBIAL ARTERY ARTERIOLES / RESISTANCE VESSELS SMALLEST DIVISION OF THE MUSCULAR ARTERY. OFFER PERIPHERAL RESISTANCE THUS REGULATING SYSTOLIC ARTERIAL PRESSURE. CAPILLARIES / EXCHANGE VESSELS.
  • 54. VESSELS DIAMETERS TUNICA INTIMA TUNICA MEDIA TUNICA ADVENTITIA LARGE ARTERY (ELASTIC ARTERY) >10 mm ENDOTHELIUM. CONNECTIVE TISSUE. SMOOTH MUSCLE. SMOOTH MUSCLE. ELASTIC LAMELLAE. THINNER THAN TUNICA MEDIA. CONNECTIVE TISSUE. ELASTIC FIBERS. MEDIUM ARTERY (MUSCULAR ARTERY) 2-10 mm ENDOTHELIUM. CONNECTIVE TISSUE. PREDOMINENT INTERNAL ELASTIC MEMBRANE. SMOOTH MUSCLES. COLLAGEN FIBERS. LITTLE ELASTIC TISSUE. THINNER THAN TUNICA MEDIA. CONNECTIVE TISSUE. SOME ELASTIC FIBERS. SMALL ARTERY 0.1-2 mm ENDOTHELIUM. CONNECTIVE TISSUE. SMOOTH MUSCLE. INTERNAL ELASTIC MEMBRANE. SMOOTH MUSCLE (8-10 CELL LAYERS). COLLAGEN FIBERS. THINNER THAN TUNICA MEDIA. CONNECTIVE TISSUE. SOME ELASTIC FIBERS. ARTERIOLES 10-100 ÎĽm ENDOTHELIUM. CONNECTIVE TISSUE. SMOOTH MUSCLE. SMOOTH MUSCLE (1-2) CELL LAYERS. THIN ILL-DEFINED SHEATH OF CONNECTIVE TISSUE. CAPILLARIES 4-10 ÎĽm ENDOTHELIUM NONE NONE
  • 56. MEDIUM SIZE/MUSCULAR ARTERY VS LARGE/ELASTIC ARTERY
  • 57.
  • 59. CAPILLARIES CAPILLARIES ARE THE SMALLEST DIAMETER BLOOD VESSELS, OFTEN SMALLER THAN THE DIAMETER OF AN RBC. CAPILLARIES HAS SINGLE LAYER OF ENDOTHELIAL CELLS AND ITS BASAL LAMINA. THE ENDOTHELIAL CELLS FORM A TUBE JUST LARGE ENUF FOR THE PASSAGE OF RBC – ONE AT A TIME. CAPILLARIES ALLOW FLUID CONTAINING GASES, METABOLITES AND WASTE PRODUCTS TO MORE FREELY THROUGH THEIR THIN WALL.
  • 61.
  • 62. 3 TYPES: CONTINOUS, FENESTRATED & DISCONTINOUS.
  • 63.
  • 64. PERICYTES THESE ARE UNDIFFENTIATED MESENCHYMAL STEM CELLS. PERICYTES ARE CLOSELY ASSOCIATED WITH CAPILLARIES.
  • 65. HISTOLOGY OF VEINS THE LAYERS OF VEINS ARE NOT DISTINCT OR WELL DEFINED AS OF ARTERY. VENULES ARE SUBCLASSIFIED AS POSTCAPILLARY & MUSCULAR VENULES. POSTCAPILLARY VENULES COLLECT BLOOD FROM CAPILLARY NETWORK AND IS CHARACTERIZED BY THE PRESENCE OF PERICYTES. PERICYTES ARE UNDIFFENTIATED MESENCHYMAL STEM CELLS. THEY SYNTHESIS GROWTH FACTORS. PERICYTES ARE MORE EXTENSIVE IN POSTCAPILLARY VENULES THAN IN THE CAPILLARIES.
  • 66. HISTOLOGY OF VEINS MUSCULAR VENULES ARE DISTINGUISHED FROM POSTCAPILLARY VENULES BY A PRESENCE OF A TUNICA MEDIA. PERICYTES ARE ABSENT IN MUSCULAR VENULES. SMALL VEINS ARE THE CONTINUATION OF THE MUSCULAR VENULES. MEDIUM SIZE VEINS HAS ALL THE THREE LAYERS, TUNICA MEDIA OF THE MEDIUM SIZE VEINS ARE MUCH THINNER THAN THE MEDIUM SIZE ARTERY. JUST LIKE LARGE VEIN. TUNICA ADVENTISIA OF MEDIUM SIZE VEIN IS MUCH THICKER THAN THE MEDIUM SIZE ARTERY. JUST LIKE LARGE VEIN. 1 2 3 4
  • 69. VESSEL DIAMETER TUNICA INTIMA TUNICA MEDIA TUNICA ADVENTITIA POSTCAPILLARY VENULE 10-50 ÎĽm ENDOTHELIUM. PERICYTES. NONE. NONE. MUSCULAR VENULES 50-100 ÎĽm ENDOTHELIUM SMOOTH MUSCLES (1-2 CELL LAYERS) THICKER THAN TUNICA MEDIA. CONNECTIVE TISSUE. SOME ELASTIC FIBERS. SMALL VEINS 0.1-1 mm ENDOTHELIUM. CONNECTIVE TISSUE. SMOOTH MUSCLES (2-3 LAYERS) SMOOTH MUSCLES (2-3 LAYERS CONTINOUS WITH TUNICA INTIMA) THICKER THAN TUNICA MEDIA. CONNECTIVE TISSUE. SOME ELASTIC FIBERS. MEDIUM VEINS 1-10 mm ENDOTHELIUM CONNECTIVE TISSUE. SMOOTH MUSCLES. INTERNAL ELASTIC MEMBRANE IN SOME CASES. SMOOTH MUSCLE. COLLAGEN FIBERS. THICKER THAN TUNICA MEDIA. CONNECTIVE TISSUE. SOME ELASTIC FIBERS. LARGE VEIN > 10 mm ENDOTHELIUM. CONNECTIVE TISSUE. SMOOTH MUSCLE. SMOOTH MUSCLE (2-15 LAYERS) COLLAGEN FIBER. MUCH THICKER THAN TUNICA MEDIA. CONNECTIVE TISSUE. SOME ELASTIC FIBERS. LONGITUDINAL SMOOTH MUSCLES.
  • 70. GRADIENT OF BLOOD PRESSURE AT DIFFERENT LEVELS OF VESSELS ARTERIES – 120 mm HG ARTERIOLES – 60 mm HG ARTERIAL END OF CAPILLARY – 30 mm HG VENOUS END OF CAPILLARY – 12 mm HG LARGE VEIN – 5 mm HG CLOSE TO RIGHT ATRIUM – ALMOST ZERO.
  • 71. FACTORS INFLUENCING VENOUS BLOOD RETURN. Factor # 1. Pressure Gradient Factor # 2. Vis-a-Tergo (force acting from behind) Factor # 3. Vis-a-Fronte (force acting from front) Factor # 4. Skeletal Muscle Pump Factor # 5. Thoracic Pump Factor # 6. Abdominal Pump Factor # 7. Venomotor Tone Factor # 8. Posture and Gravity
  • 72. Factor # 1. Pressure Gradient The pressure in the right atria (central venous pressure) into which the superior and inferior vena cavae open is around 0 mm Hg. In the peripheral veins, the pressure is around 5 mm Hg and the pressure in the veins nearer to the heart goes on decreasing. So the blood flows from higher pressure to lower pressure. Factor # 2. Vis-a-Tergo (force acting from behind) The contraction of the left ventricle creates a pressure that pushes blood from behind all along the vascular tree throughout the body. Factor # 3. Vis-a-Fronte (force acting from front) The pressure in the right atrium is normally around 0 mm Hg. During ventricular contraction, the atrio ventricular ring is pulled down. As a result of this, the atria get expanded. This creates a negative pressure in right atrium and the negative pressure is also created during sudden rush of blood from atria to ventricle.
  • 73. Factor # 4. Skeletal Muscle Pump The veins are arranged in between the skeletal muscle fibers and are arranged parallel to skeletal muscle fibers. So when the muscle contracts the veins get squeezed. Due to the compressor effect of the muscle fibers on the vein, blood is made to flow through them. However, blood is made to flow in the direction of heart due to the presence of valves in veins, which prevent back flow. Factor # 5. Thoracic Pump During inspiration, the intrapleural pressure becomes more negative. A simultaneous increase of pressure in the abdomen and a more negative pressure in thorax, increase the pressure gradient for flow of blood towards the heart from the abdomen. Factor # 6. Abdominal Pump When the abdominal muscles contract, there will be increase of intra-abdominal pressure and hence compression of veins occurs in the abdominal region. This increases venous return by increasing the gradient towards the thoracic cavity (heart).
  • 74. Factor # 7. Venomotor Tone The constant excitatory influence by sympathetic nerves on the smooth muscle of veins is called venomotor tone. Because of this, the walls of the veins remain in a partially contracted state even under resting condition. When the venomotor tone is increased, the capacity of veins decreases. This increases the venous return. Factor # 8. Posture and Gravity As such the pressure in the veins is very less. When gravitational force acts on the lower parts of body especially in the erect posture, it will decrease the venous return from the lower limbs. The gravitational force tries to pull down blood from the dependent parts of the body.
  • 75. FACTORS - VENOUS DRAINAGE
  • 76. ANSTOMOSIS IT IS THE COMMUNICATION BETWEEN THE BLOOD VESSELS – 3 TYPES – INTER-ARTERIAL, ARTERIO- VENOUS, END-ARTERIES.
  • 77. INTER-ARTERIAL ANASTOMOSIS TAKE PLACE BETWEEN ADJACENT ARTERIES BY THEIR TRUNKS, BRANCHES AND SUB-BRANCHES. EXAMPLE: B/W RIGHT & LEFT GASTRIC ARTERY
  • 78. ARTERIOVENOUS SHUNTS ARTERIOVENOUS SHUNT – ALLOW BLOOD TO BYPASS CAPILLARIES BY PROVIDING DIRECT ROUTES BETWEEN ARTERIES & VEINS. AV SHUNTS ARE FOUND IN SKIN, THE FINGERTIPS, NOSE, LIPS & ERECTILE TISSUE OF PENIS & CLITORIS. A-V SHUNT SERVES AS THERMOREGULATION – CLOSING OF THE AV SHUNT ALLOWS BLOOD TO FLOW THROUGH CAPILLARY BED, ENHANCING HEAT LOSS. OPENING AV SHUNT IN SKIN REDUCE THE BLOOD FLOW TO SKIN CAPILLARIES, THUS CONSERVING BODY HEAT.
  • 79. END-ARTERIES MOST ARTERIES ANASTOMOSE WITH ONE ANOTHER AT CAPILLARY AND PRE-CAPILLARY LEVEL. END-ARTERY ARE THOSE WHICH DONOT FORM ANY PRE-CAPILLARY ANASTOMOSIS. EXAMPLES: CENTRAL ARTERY OF RETINA CEREBRAL, SPLENIC, RENAL ND VASA RECTA OF SMALL GUT CORONARY ARTERIES
  • 80. ANATOMICALLY, CORONARY ARTERIES ARE NOT END ARTERIES. BUT FUNCTIONALLY THEY BEHAVE AS END- ARTERIES. AN OBSTRUCTION IN END-ARTERIES CAN CAUSE LOCAL TISSUE DEATH.
  • 81. CLINICAL ASPECT OF VASCULAR TISSUE
  • 82. ATHEROSCLEROSIS: MOST COMMON ACQUIRED ABNORMALITY OF THE BLOOD VESSEL. COMPLICATIONS OF ATHEROSCLEROSIS ARE CORONARY HEART DISEASE, HEART ATTACK-MI, STROKE & PERIPHERAL ARTERY DISEASE. ATHEROSCLEROSIS AFFECTS TUNICA INTIMA OF LARGE ELASTIC ARTERY WHICH LEAD TO ENDOTHELIAL DYSFUNCTION.
  • 83.
  • 84.
  • 85. THE ENDOTHELIAL INJURY IN ATHEROSCLEROSIS CAN OCCUR DUE TO HIGH LDL CHOLESTROL, HYPERLIPIDEMIA, HYPERGLYCEMIA, HYPERTENSION, TOXINS – SMOKING ETC. THE DAMAGED ENDOTHELIUM, INCREASES PERMEABILITY TO LDL CHOLESTROL ND INCREASED ADHERENCE OF WBS (MONOCYTES) TO ENDOTHELIUM. AS THE RESULT TO INJURY, MONOCYTES FROM BLOOD STEAM ENTER TUNICA INTIMA, AND GET DIFFERENTIATED INTO MACROPHAGES. THESE MACROPHAGES PHAGOCYTIZE OXIDIZED LDL ND TRANSFORM INTO FOAM CELL. ATHEROMATOUS PLAQUE IS A THICK LAYER OF FIBROUS CONNECTIVE TISSUE CONTAINING SMOOTH MUSCLE CELLS, MACROPHAGES, FOAM CELL, T LYMPHOCYTES, CELL DEBRIS ETC AS THE SIZE OF ATHEROMATOUS PLAQUE INCREASES, BLOOD STASIS ND CLOTTING MAY LEAD TO OCCLUSION OF VESSEL.
  • 88.
  • 90. Coronary artery bypass graft (CABG) or heart bypass or bypass surgery, is a surgical procedure to restore normal blood flow to an obstructed coronary artery.
  • 91. CABG
  • 92. THROMBOEMBOLISM ACUTE RUPTURE OF AN UNSTABLE ATHEROMATOUS PLAQUE CAN LEAD TO EITHER ACUTE OCCULATION OF ARTERY (THROMBOSIS) OR DISTAL SHOWERING OF PLAQUE MATERIAL (EMBOLISM). ACUTE OCCLUSION DOESNOT ALLOW FOR THE DEVELOPMENT OF COLLATERALS AND THEREFORE LEADS TO SYMPTOMS OF ACUTE ISCHEMIA. ACUTE MYOCARDIAL INFARCTION, STROKE, ACUTE LIMB ISCHEMIA ETC
  • 93. TRANSIENT ISCHAEMIC ATTACK (TIA) TRANSIENT/TEMPORARY EPISODE OF NEUROLOGICAL DYSFUNCTION CAUSED BY FOCAL BRAIN, SPINAL CORD OR RETINAL ISCHEMIA WITHOUT ACUTE INFARCTION. USUALLY TIA WILL RESOLVE WITHIN 24 HOURS.
  • 94.
  • 95. CVA
  • 96.
  • 97.
  • 98. MESENTRIC OCCLUSIVE DISEASE. LIFE THREATENING CONDITION CAUSED BY DECREASED BLOOD FLOW TO THE BOWEL. IT IS DIFFICULT TO DIAGNOSE. 4 TYPES 1. EMBOLIC OCCLUSION OF MESENTRIC CIRCULATION. 2. ACUTE THROMBOSIS OF MESENTRIC CIRCULATION. 3. NON-OCCULSIVE MESENTRIC ISCHEMIA 4. MESENTRIC VENOUS THROMBOSIS
  • 100. PERIPHERAL OCCLUSIVE DISEASE IN PERSONS ABOVE AGE 60. MOST COMMON CAUSE IS ATHEROSCLEROSIS OF VESSELS. RISK FACTORS: HYPERTENSION, DIABETES, OBESITY, SMOKING ETC AORTO-ILLIAC OCCULSION PALE DUE TO ABSENCE OF BLOOD SUPPLY
  • 101. FOR EVALUATING PERIPHERAL ARTERIAL OCCULSION, YOU SHOULD FEEL THE PERIPHERAL PULSE.
  • 102.
  • 103. CLAUDICATION PAIN COMMON IN OCCULSIVE DISEASE OF LOWER LIMBS. THE PAIN OCCURS DURING MUSCLE ACTIVITY SUCH AS WALKING. AND DISAPPEARS AFTER TAKING 2-3 MIN REST.
  • 104. PERIPHERAL OCCULSIVE DISEASE CAN RESULT IN TISSUE LOSS/ DEATH . DUE TO LACK/INSUFFICENT BLOOD PERFUSION.
  • 105. CUTANEOUS PRESSURE NECROSIS / BED SORE IN BED RIDDEN PATIENTS. It is injuries to skin and underlying tissue resulting from prolonged pressure on the skin.
  • 106. SMALL VESSEL DISEASE – RAYNAUD’S SYNDROME Raynaud's disease causes some areas of your body — such as your fingers and toes — to feel numb and cold in response to cold temperatures or stress. In Raynaud's disease, smaller arteries that supply blood to your skin become narrow, limiting blood flow to affected areas (vasospasm). Women are more likely than men to have Raynaud's disease, also known as Raynaud's or Raynaud's phenomenon or syndrome. It appears to be more common in people who live in colder climates.
  • 107. 1 2 3
  • 109. Limited scleroderma, also known as CREST syndrome
  • 110. Buerger's disease is a rare disease of the arteries and veins in the arms and legs. In Buerger's disease — also called thromboangiitis obliterans — your blood vessels become inflamed, swell and can become blocked with blood clots (thrombi). This eventually damages or destroys skin tissues and may lead to infection and gangrene. Buerger's disease usually first shows in your hands and feet and may eventually affect larger areas of your arms and legs. Virtually everyone diagnosed with Buerger's disease smokes cigarettes or uses other forms of tobacco, such as chewing tobacco. Quitting all forms of tobacco is the only way to stop Buerger's disease. For those who don't quit, amputation of all or part of a limb is sometimes necessary. Buerger's disease
  • 112. DIABETIC NEUROPATHY – OCCULTATION OF VASA NERVORUM – THE BLOOD VESSEL THAT SUPPLY THE NERVE.
  • 114. Frostbite is an injury caused by freezing of the skin and underlying tissues. First your skin becomes very cold and red, then numb, hard and pale. Frostbite is most common on the fingers, toes, nose, ears, cheeks and chin. Exposed skin in cold, windy weather is most vulnerable to frostbite.
  • 115.
  • 116.
  • 117. FASCIOTOMY IS PERFORMED IN COMPARTMENT SYNDROME TO RELIEVE THE PRESSURE & RESORE THE CIRCULATION
  • 118.
  • 119. VARICOSE VEINS Varicose veins are twisted, enlarged veins. Any superficial vein may become varicosed, but the veins most commonly affected are those in your legs. That's because standing and walking upright increases the pressure in the veins of your lower body. • An achy or heavy feeling in your legs • Burning, throbbing, muscle cramping and swelling in your lower legs • Worsened pain after sitting or standing for a long time • Itching around one or more of your veins • Skin discoloration around a varicose vein • Skin ulcers
  • 120.
  • 122. Deep vein thrombosis (DVT) occurs when a blood clot (thrombus) forms in one or more of the deep veins in your body, usually in your legs. Deep vein thrombosis can cause leg pain or swelling but also can occur with no symptoms. You can get DVT if you have certain medical conditions that affect how your blood clots. A blood clot in your legs can also happen if you don't move for a long time, such as after you have surgery or an accident, when you're traveling a long distance, or when you're on bed rest. Deep vein thrombosis can be very serious because blood clots in your veins can break loose, travel through your bloodstream and get stuck in your lungs, blocking blood flow (pulmonary embolism). However, pulmonary embolism can occur with no evidence of DVT.
  • 123.
  • 125.
  • 127. An aneurysm is an abnormal bulge or ballooning in the wall of a blood vessel. An aneurysm can burst (rupture), causing internal bleeding and often leading to death. Aneurysms usually don't cause symptoms, so you might not know you have an aneurysm even if it's large.
  • 128. BERRY ANEURYSM IN THE CIRCLE OF WILLIS
  • 129. RUPTURE OF ANEURYSM IS A LIFE THREATING CONDITION
  • 130. BERRY ANEURYSM RUPTURE – YOU CAN SEE THE BLOOD CLOTS
  • 133.
  • 134. Smoking is the strongest risk factor for aneurysm. It can weaken the aortic walls, increasing the risk not only of developing an aortic aneurysm, but also rupture. The longer and more you smoke or chew tobacco, the greater the chances of developing an aortic aneurysm. Einstein died of leaking abdominal aortic aneurysm at the age 76.