Upload
bharathi-priya
View
1.168
Download
0
Embed Size (px)
Citation preview
GOOD MORNING
PROF.S.P.GAYATHRE.M.S
ASSISTANT PROFESSORS: Dr.G.KARTHIKEYAN,M.S Dr.R.SYED RAJ,M.S
S4 UNIT
PATHOPHYSIOLOGY OF
VENOUS DISEASES
1.What are the two major veins of hand?
2.Have you ever seen varicose veins of hands?
Ulnar and radial vein
3.Do you know why?
GRAVITY
To overcome the effect of GRAVITY LOWER LIMB has some special mechanism
PRESSURE GRADIENT
HIGH PRESSURE
LOW PRESSURE
PERIPHERAL PUMP Calf , Thigh & Foot pump UNIDIRECTIONAL
NONREFLUXINGVALVES
NEGATIVEINTRATHORACIC PRESSURE
VIS-A-TERGOVENA COMITANTES
SYMPATHETIC ACTIVITY
FACTORS RESPONSIBLE FOR NORMAL
VENOUS RETURN
MOTOR PIPE TANKSOLEUS MUSCLE VEINS HEART
1.MUSCLE PUMP
STRUCTURE
DURING MUSCLE RELAXATION, PRESSURE WITHIN CALF COMPARTMENT FALLS
BLOOD FROM SUPERFICIAL VEINS ENTER DEEP VEINS
SUPERFICIAL VENOUS pressure cont. To fall TILL THRESHOLD IS REACHED
THRESHOLD IS APPROX. 30mmHg
VENOUS INFLOW NOW KEEPS PACE WITH EJECTION FROM DEEP VEINS
Patency of veinsCompetent valves
RELAXATION PHASE
RELAXATION CONTRACTION
DURING MUSCLE CONTRACTION, PRESSURE WITHIN CALF COMPARTMENT RISES TO 200-
300mmHg
BLOOD FROM DEEP VEINS ENTER IVC
VALVES OF PERFORATOR VEINS CLOSED
TO PREVENT REFLUX
CONTRACTION PHASE
AMBULATORY VENOUS HYPERTENSION
REFLUX OBSTRUCTIVE
2. NON REFLUXING VALVES
3.NEGATIVE INTRATHORACICPRESSURE
4.VIS-A-TERGO
12mmHg 32 mmHg
5.VENAE COMITANTES
PATHOGENESIS
Changes in Vein
Wall
Smooth Muscle Proliferation
Increased MMP
Collagen deposition
Decreased elastin content
Changes in vein wall
over stretching of veins
increase in size of veins but valve leaflets don’t expand
Secondary valvular Incompetence Backflow( reflux)
Pooling and further dilation of veins
Varicosity – Dilated Tortuous Veins
COMPETENT VALVE
INCOMPETENT VALVE
PRIMARY: Congenital weakness in vessel wall
Congenital absence of valves
Congenital Valvular incompetence
Familial (FOX C2 gene)
Lysosomal enzyme activity(Haardt)
Chronic inflammatory process(Class II MHC & Macrophages)
ETIOLOGY
SECONDARY :
OBSTRUCTION TO FLOW:
DESTRUCTION OF VALVES:
1.Pregnancy 2.Pelvic tumor: Ovarian ca Fibroid uterus3.Ascites4.Retroperitoneal fibrosis5.Iliac vein thrombosis
1.Deep vein thrombosis
HIGH PRESSURE FLOW:1.AV fistula
KLIPPEL TRENAUNAY SYNDROME
Gender
Age Ethnicity
Body mass index&height
Family history Pregnancy
occupation and lifestyle factor;
smokers, constipation occupations which involve
prolonged standing.
Traffic police Bus conductors Sports man Nurses Surgeons hair stylists Factory workers
OTHER RISK FACTORS
• C = CLINICAL CLASSIFICATION
• E = ETIOLOGICAL CLASSIFICATION
• A = ANATOMICAL CLASSIFICATION
• P =PATHO-PHYSIOLOGICAL
CEAP CLASSIFICATION
TELANGECTASIA :<1 mm
Spider veins, thread veins, hyphen webs
RETICULAR VEINS:Dilated, subdermal veins
1-3mm in diameter
CLASS 1
VARICOSE VEINS:Varicose veins are defined as dilated, usually tortuous, subcutaneous veins 3 mm in diameter measured in the upright position with demonstrable reflux.
CLASS 2
CLASS 3
DEPENDENT PITTING EDEMA:Result of increase in volume of fluid
Elevation/compression bandaging
CLASS 4A
PIGMENTATION:Brownish Discolouration
Hemosiderin depositionECZEMA :Erythematous dermatitis
Progress to blistering, weeping or scaling eruption of the skin
CLASS 4B
LIPODERMATOSCLEROSIS:Localised chronic inflammation and fibrosis of skin and subcutaneous tissueSevere stage of chronic venous diseaseATROPHIE BLANCHE:Localized white atrophic skin - dilated capillaries and hyperpigmentation
site
CLASS 5
HEALED ULCER:
CLASS 6
ACTIVE ULCER:epidermal defect
gaiter area
IDENTIFIED
IDENTIFIED
SAPHENA VARIX:Large groin varicosity
Painless lump
standing
recumbent
Cough impulse
CORONA PHLEBECTASIA:Fan shaped patterns of small intradermal veins
Site
Malleolar or Ankle Flares