Chronic venous insufficiency pathophysiology CVD of the lower limb, Hemorrhoidal disease, and DUB in women

1. Chronic venous
insufficiency
Pathophysiology and
treatment

2. Introduction to the Human
Cardiovascular System

3. INTRODUCTION
The cardiovascular
system is transport
system of body
It comprises blood,
heart and blood
vessels.
The system supplies
nutrients to and remove
waste products from
various tissue of body.

4. The cardiovascular system
includes 2 circuits
• The cardiovascular system
includes 2 circuits:
1. Pulmonary circuit which
circulates blood through the
lungs
• The pulmonary artery carries
Deoxygenated blood from the
right ventricle to the lungs
where blood becomes oxygenated
• The pulmonary veins returned
oxygenated blood to the left
side of the heart

5. Introduction to Cardio Vascular
System
• Components of Cardiovascular system
1.Blood
2.Blood Vessels and Types of Blood
Vessels
3.Heart

6. BLOOD VESSELS
• Blood Vessels ,a
closed network of
tubes
•These includes:
 Arteries
 Capillaries
 Veins

7. Heart
• Hollow, cone shaped
muscle
• Heart composed of 4
heart chambers
1.2 Atria (atrium)
 Upper chambers that
receive blood
 Separated by interatrial
septum
2.2 Ventricles
 Lower chambers that

8. Structure of Heart Wall
1.PERICARDIUM Outer layer
which is a protective
serous membrane made of
connective tissue
2.MYOCARDIUM Middle layer
oMade up of cardiac
muscle
oPump blood
3. ENDOCARDIUM Inner
layer made up of
epithelium and connective

9. Wall of Arteries and Veins
composed of 3 Layers
• Tunica Externa or
Adventitia Connective
tissue-collagen
• Tunica Media Muscular
tissue and elastic
fibers
• Tunica Intima Simple
squamous epithelium
(endothelium) and
elastin

10. Arteries
• Thick-walled vessels that
transport blood via the aorta
from the heart to the tissues
• Types of Arteries
1. Large size arteries (Aorta)
2. Middle size Arteries
3. Small size arteries
(Arterioles)

11. Veins
• Transport Blood from the
capillaries back to the right
side of the heart
• There is little Vascular smooth
muscle & connective tissue makes
the veins more distensible as
they accumulate large volumes of
blood
• Veins have one-way Valves
1. The venous valves are abundant
in the distal lower extremity
and decreases proximally with
no valves in superior and
inferior vena cava

12. Veins
Vein Carries
unoxygenated blood
towards the heart
• Types of Veins
1.Large size Veins (Vena
cava)
2.Middle size Veins
3.Small size Veins
(Venules)

13. Capillaries
• Capillaries
“Microcirculation”
1.blood flow between
arterioles, capillaries
and venules
2.Exchange of
Gases, Nutrients, and
Waste Between Blood and
Tissue Occurs in
the Capillaries
3.Exchange is controlled by
2 forces Hydrostatic and
Colloidal Osmotic
pressures

14. Capillary Exchange
• At the arterial end of a
capillary, the blood
pressure is higher than
the osmotic pressure;
therefore, water tends to
leave the bloodstream.
• In the midsection, oxygen
and carbon dioxide follow
their concentration
gradients.
• At the venous end of a
capillary, the osmotic

15. Lymphatic system
• The lymphatic system works
with the circulatory system
, The two systems are
closely linked to each other
• Functions of Lymphatic
system
1. Return of plasma
I. Extra plasma that has been
filtered out of the blood and
is in the interstitial fluid
may need to be returned to
the blood and this can be
done through the lymphatic
system (lymph vessels)

16. Lymphatic system
• Lymph capillaries
• Lymphatic vessels
• Lymph nodes
1. Filtration sites along the
lymphatic system
2. Produce white blood cells
to fight viruses and other
infections (immune
defense)
• Lymphatic trunks
• Collecting ducts

17. Chronic Venous
Diseases (CVD)
Lower limb

18. Lower Extremity Venous System
1. Superficial venous system run
between the dermis and the muscle
fascia
• Greater saphenous vein medially
• lesser saphenous vein laterally
2. Deep venous system intramuscular
or Intermuscular ,named after the
artery they accompany
• Posterior Tibial vein
• Anterior Tibial vein
• Join to form the popliteal vein
• Become the superficial femoral vein
• Joined by the deep femoral vein to
form the common femoral vein
• Renamed the common Iliac vein

19. Perforator veins
1. Connect superficial to deep
veins at various levels.
2. The direction of blood flow
:from superficial to deep
veins.
3. Guarded by valves so that the
flow is unidirectional, i.e.
Towards deep veins.
4. Reversal of flow occurs due
to incompetence of
perforators which will lead
to varicose veins

20. Factors Affecting Venous
Return
• Blood is drained from superficial to deep veins
of legs through perforating veins and through
deep veins it is carried to heart. Back flow of
blood is impossible.
• Intrinsic Factors
1. Venous wall contraction (Venous tone)
2. Valve Integrity
3. Musculovenous Pump
4. Abdomino -thoracic Pump and Cardiac Pump
• Extrinsic Factors
1. Gravity
2. External Compression
3. Temperature

21. MUSCULO-VENOUS PUMP
• Muscular contraction
expel blood from the
deep venous system
• As the muscles relax
Blood is drawn from the
superficial to the deep
system, thereby lowering
the superficial venous
pressure.
• Competent valves are
required to prevent

22. Venous valves
• Delicate structures
• The venous valves are
abundant in the distal
lower extremity and number
of valves decreases
proximally, with no valves
in superior and inferior
vena cava
• Prevent reverse flow in
the veins Ensure that the
blood is pumped from the
superficial to the deep

23. Abdomino - thoracic Pump and
Cardiac Pump
• Abdomino - thoracic Pump
1.Inspiration decreases intra
thoracic pressure promoting venous
return
2.Expiration reverses the process
• Cardiac Pump
Normal cardiac pulsations cause
negative pressure in RA and RV that
have aspiration effect on the venous

24. Varicose Vein pathophysiology
• Venous Distensibility The venous wall differs
from the arterial wall in that it is highly
distensible
• The accumulation of blood in the veins of the
lower limbs upon standing is limited by
I. Venous tone (Contraction of venous wall)
II.presence of valves
III.Effective contraction of the calf muscles
• Causes of Varicose veins Venous stasis
(Venous hypertension) is the main cause ,either
1. Primary varicose veins , without known cause
(develop for no obvious reason)

25. Varicose Vein pathophysiology
• In varicose veins, the primary defect is
an exaggerated distensibility of the
veins:
1. Genetics Abnormal connective tissue
composition of the venous wall.
2. Age
3. Obesity
4. Hormones, Female sex Hormones
(estrogens and progesterone) The media
of human saphenous veins expresses
progesterone receptors, suggesting that
the hormone can act directly on the
venous wall and cause relaxation of the
vein wall
5. Sedentary life/ occupation (sitting or
standing position at work) leads to

26. Varicose Vein pathophysiology
- Venous hypertension
• Laminar Blood flow keeps
leukocytes in Central
layer of blood stream
away from endothelium
and prevents endothelium
from expression of
cellular adhesion
molecules
• Venous hypertension
induces Turbulence in
blood flow which will
result in
1. leukocytes become in
contact with
endothelium.
2. Endothelium expression

27. Varicose Vein pathophysiology
- Remodeling of Venous wall
• Inflammation and damage
of venous wall due to
Leukocyte migration ,
activation and production
proteolytic enzymes and
Oxygen free radicals
• Vein wall show
Hypertrophic areas
alternated by Atrophic
areas
• Hypertrophic areas with
Accumulated
1. Extra cellular matrix

28. Varicose Vein pathophysiology
- Venous Valve destruction (a
partially mobile leaflet or a completely
“frozen valve.”)
• Valve dysfunction can
occur due to inflammation
as result of Leukocyte
infiltration , activation
and migration into the
endothelium of proximal
surfaces of the vein
valves and promote
destruction and
remodeling of the valves
which results in valvular
insufficiency and Venous
Reflux (Varicose

29. Varicose Vein pathophysiology
- Microcirculation
(Capillaries)
• Sustained hypertension at
the capillary level is
associated with elongation
and dilation of the
capillary bed
• Expression of ICAM 1 and
VCAM 1 results in leukocyte
adhesion and migration
through the vessel wall
into the extravascular
tissues , neutrophils
become activated and

30. Varicose Vein pathophysiology
- Skin changes (Ulceration/
Venous ulcer)
• White cell trapping theory:
1. Venous hypertension
expression of leukocyte
adhesion molecules adherence
of leukocytes to the
capillary endothelial cells.
2. The trapped cells become
activated releasing
proteolytic enzymes and
oxygen free radicals which
produce tissue destruction.
• Fibrin cuff theory :
1. Capillary hyper permeability
will allow Fibrin leakage and
deposition around capillary

31. Varicose Vein pathophysiology
- Skin changes (Ulceration/
Venous ulcer)
• Cutaneous iron overload:
1. extravasations of red
blood cells.
2. The iron is released
from the hemoglobin and
deposited within the
tissue which promote the
production of oxygen
free radicals and lipid
peroxides which in turn
can lead to tissue
destruction

32. Varicose Vein pathophysiology
- Lymphatic system (Lymphatic
overload )
1. The increased permeability
of capillaries causes
leakage of excess fluid
and interstitial edema.
2. Lymphatic vessels
transport capacity is
limited, After they are
overloaded, they become
insufficient and gradually
they become damaged.
3. Lymph vessels are
hypertrophic and

33. Varicose Vein pathophysiology
1.HIGH TEMPERATURE
2.PROLONGED
Standing or
sitting
3.HORMONAL FACTORS
4.GENETIC FACTORS
Increased
Venous wall
distensibil
ity
Valvular
incompetence
Increased
venous
pressure
Increased
Capillary
pressure
Inflamm
ation
Venous wall
remolding
Valvular
destruction
Fluid
leakage
and edema
Inflamm
ation
Ulcer
ation
Venous Reflux
(perforating and
Superficial veins
vein)

34. Symptoms of CVD
• Venous disease is
symptomatic as soon as
wall damage occurs
Accompanied early by
feelings of
1.Pain
2.Itching
3.Heaviness
4.Swelling
5.Cramps

35. Progression of chronic venous
disease (Venous hypertension
is key)
MACRO
circulatio
n
Valve
damage
Vein wall
remodeling
Reflux
Capillary
damage
Skin Changes
(C4)
Edema
(C3)
Capillary
leakage
Varicose
Veins (C2)
MICRO
circulatio
n
Venous Ulcer
(C5,6)
Venous Hypertension

36. Classification and severity scoring
of chronic venous disease
• The CEAP
classification was
proposed and
subsequently adopted
worldwide as a basis
for improved patient
description
1. Clinical
2. Etiology
• Ec: congenital.
• Ep: primary.
• Es: secondary (post
thrombotic).
3. Anatomy
• S: superficial veins.
• P: perforator veins.
• D: deep veins
4. Pathology
• Pr: reflux.
• Po: obstruction.
• Pr,o: reflux and
obstruction.
• Pn: no venous
pathophysiology

39. Symptoms of Varicose veins
• Telangiectasia(spider veins) : A
confluence of dilated intradermal
venules of less than 1 mm in
caliber..
• Reticular veins (blue veins) :
Dilated bluish sub dermal veins
usually from I mm to less than 3
mm in diameter. They usually are
tortuous.
• Varicose veins : Subcutaneous
dilated , tortuous veins equal to
or more than 3 mm in diameter

40. Symptoms of Varicose veins
• Edema : An increase in volume of
fluid in the skin and
subcutaneous tissue
characteristically indenting
with pressure. Venous edema
usually occurs in the ankle
region, but it may extend to the
leg and foot.
• Pigmentation : A brownish
darkening of the skin resulting
from extravasated blood, which
usually occurs in the ankle

41. Symptoms of Varicose veins
• Lipodermatosclerosis (LDS):
Localized proliferation of
the dermal capillaries and
fibrosis on subcutaneous
tissue It is a combination of
induration , pigmentation and
inflammation
• Atrophic blanche or white
atrophy : Localized, often
circular whitish and atrophic
skin area surrounded by

42. Symptoms of Varicose veins
• venous ulcer : Full thickness
defect of the skin most
frequently in the ankle region
that fails to heal spontaneously
and is sustained by CVD.
• Most common site medial aspect of
ankle & lower 1/3rd of leg
• characteristic features:
• Vertically oval
• Painless
• Irregular, Ragged ,Sloping
edges

43. Treatment
• OBJECTIVE OF TREATMENT OF CVD
1. 1st to rapidly and powerfully relieve patients
from symptoms and pain in order to help them
recover a better quality of life.
2. 2nd to protect VV patients from further
complications.
• Leg elevation and regular exercise
• Use of elastic compression stockings.
• Injection sclerotherapy.
• Endovenous laser treatment and radiofrequency
ablation
• Saphenous vein ligation and stripping

44. Use of elastic compression stockings.
Injection sclerotherapy.
Endovenous laser treatment and radiofre
Saphenous vein ligation and stripping
surgical excision using the "stab avuls

45. Haemorrhoidal diseases
/ piles

46. Anatomy of the Anal Canal
• Anatomical anal canal,
extending from dentate line
to anal verge to is only 2
cm in length
• The anal canal is lined
with squamous epithelium
below the dentate line, and
columnar epithelium above
• Internal Anal Sphincter
1. Involuntary
2. Circular muscle layer
• External Anal Sphincter
1. Voluntary
2. Striated muscle layer

47. Hemorrhoids
• The term “hemorrhoids”
refers 2 different vascular
structures:
1. Internal haemorrhoidal
plexus, which is sub
mucosal (Typically, there
are 3 major cushions
located in right anterior,
right posterior, and left
lateral aspect of the anal
canal)
2. External haemorrhoidal
plexus, which is
subcutaneous.
• Internal Hemorrhoidal

48. Hemorrhoids (Arteriovenous
Shunt)
• Within each Internal
Hemorrhoid Plexus ,
there is an
Arteriovenous plexus
formed by direct
communication between
the terminal branches of
rectal arteries and
their corresponding
veins
• Arteriovenous shunt
contains smooth muscle

49. Internal Hemorrhoids function
• The function of the internal sphincter itself
is not sufficient to ensure complete closure of
the anal canal.
• Internal hemorrhoids play an important role to
keep intestinal contents in the rectum.
1. At rest, vascular are filled with blood and
are in contact with each other causing the
anal canal to close and the pressure in the
sphincter to increase.
2. During defecation Internal hemorrhoids are
squeezed and emptied out of blood which allow
passage of rectal content

50. Causes of Haemorrhoidal
diseases
• Acute intrarectal or
abdominal pressure are
predisposing factors
(Straining , Chronic
constipation /diarrhea
, Prolonged sting on
Toilet , Pregnancy )
• The origin of
haemorrhoidal disease
can be either
1. Mechanical theory,
the supportive
structure of the
haemorrhoidal plexus
undergoes excessive

51. Degeneration
of Connective
tissue which
fix the
internal
hemorrhoid to
rectal wall
Favors
stagnation
and stasis of
blood in
vascular
plexus of
internal
hemorrhoid
Leukocytes
marginated
and become in
contact with
endothelial
cells
Leukocytes
adhesion ,
migration and
activation
releasing
proteolytic
enzymes and
Capillary
hyper
permeability
, Fragility
and necrosis
of capillary
wall
internal
hemorrhoid
easily
traumatized
by passage of
stool and
bleed
Internal Hemorrhoids
pathogenesis
Chronic
Constipation /
Diarrhea
Pregnancy
Prolonged
sitting on
toilets
Straining
Vascular
abnormalities
Increased
flow in AV
plexus

52. Types and complications
• Types
1. Internal
2. External
3. Mixed
• Complications
1. Strangulation of internal Hemorrhoids
2. Anemia
3. Perianal dermatitis
4. Thrombosis of external Hemorrhoids

53. Classified according to origin
of hemorrhoid.
External
hemorrhoid
Internal
hemorrhoid
Below dentate
line
Above dentate
line
Lined by
squamous
epithelium
Lined by
columnar
epithelium
Painful Not painful
Prone to
thrombosis if
vein ruptures
(Thrombosed
May prolapse
outside anal
canal
(prolapsed

54. Symptoms of Internal
Hemorrhoids
1. Bleeding most common
and earliest symptom
Bright red painless
bleeding especially at
the end of defecation
2. Prolapse
3. Tenesmus
4. Pruritus
5. Pain and discomfort
Hemorrhoids are
usually painless.
6. Discharge (Soiling) A
constant mucous

55. Internal Hemorrhoids :
• Internal Hemorrhoids Disease Manifested by two
main symptoms
1. Painless Bleeding
2. Protrusion
3. Pain is rare as they originate above dentate
line
Gr I
Gr

56. Treatment of hemorrhoids has
to achieve 3 objectives:
• Eliminate mechanical and local triggering
factors (lifestyle modification)
I. Dietary measures, must include fiber-rich
food and abundant liquids
II.Mechanical laxatives, such as Vaseline or
liquid paraffin,
III.Avoiding consumption of stimulating drinks
(tea, coffee), alcohol and spices.
IV.avoiding smoking, a sedentary lifestyle, and
a sitting position for prolonged periods of
time.

57. Treatment
• Conservative:
 Medical
Invasive therapy
1. Injection
sclerotherapy
2. Rubber band ligation
3. Cryotherapy
4. Photocoagulation
• Surgical:
1. Open
haemorrhoidectomy
2. Closed
haemorrhoidectomy
3. White head
haemorrhoidectomy
4. Laser
haemorrhoidectomy
5. Diathermy
haemorrhoidectomy

58. Chronic venous disease during pregnancy
Haemorrhoidal disease during pregnancy
Dysfunctional Uterine Bleeding

59. Dysfunctional Uterine
Bleeding
DUB

60. Female reproductive system
• Ovaries
• Fallopian tubes
• Uterus
1. Perimetrium - external
serosa layer
2. Myometrium - middle
muscular layer ,smooth
muscle
3. Endometrium inner
layer simple columnar
epithelium
• Cervix
• Vagina

61. Menstrual cycle
• Averages 28 days
1. Follicular phase (2
weeks)
• Menstruation (Blood,
serous fluid and
endometrial tissue are
Discharged) occurs
during first 3 to 5
days of cycle
Uterus replaces lost
endometrium and
follicles grow
2. Luteal phase (2

62. Dysfunctional uterine bleeding
• DUB is defined as abnormal uterine
bleeding in the absence of organic
disease.
• Dysfunctional uterine bleeding is
the most common cause of abnormal
vaginal bleeding during a woman's
reproductive years.
• A normal menstrual cycle is
characterized by an approximate flow

63. Abnormal uterine bleeding
• DUB refers to abnormal bleeding from the uterus
and can be characterized clinically by amount,
duration, and periodicity:
1. Menorrhagia - Prolonged (>7 d) or excessive (>80
mL daily) uterine bleeding occurring at regular
intervals
2. Metrorrhagia - Uterine bleeding occurring at
irregular and more frequent than normal intervals
3. Menometrorrhagia - Prolonged or excessive uterine
bleeding occurring at irregular and more frequent
than normal intervals
4. Intermenstrual bleeding - Uterine bleeding of

64. CAUSES
Disruption of normal hormonal regulation of peri
ods e.g. excess Oestrogen
Intrauterine Devices (IUD’s)
Dysfunctional Uterine Bleeding
Damage of the
microcirculation
Leukocytes
migration
Venous stasis
Leukocytes
adhesion
Leukocytes
activation
Bleeding
Hormonal disturbances

65. Mechanical trauma
Inflammation
Capillary fragility
Menorrhagia
Dysmenorrhea
IUCD-INDUCED BLEEDING
• Abnormal uterine
bleeding is the most
common complication of
IUD use.
• Minor Metrorrhagia
during the insertion
and the initial 2 or 3
cycles is common and
has no pathological
significance.
• The true complications

66. Treatment of Menorrhagia
Medical therapy for menorrhagia may include:
• Nonsteroidal anti-inflammatory drugs (NSAIDs).
NSAIDs, such as ibuprofen or naproxen sodium ,
help reduce menstrual blood loss. NSAIDs have the
added benefit of relieving painful menstrual
cramps (dysmenorrhea).
• Oral contraceptives. Aside from providing birth
control, oral contraceptives can help regulate
menstrual cycles and reduce episodes of excessive
or prolonged menstrual bleeding.
• Oral progesterone. The hormone progesterone can
help correct hormone imbalance and reduce
menorrhagia.

67. Thanks