ARTERY AND VEIN DISEASE

1. Presented by-
Pankaj Kumar Patel
M-5718
Presented to-
Dr. V.K. GUPTA

2. Arteriosclerosis
• Arteriosclerosis is the thickening, hardening and
loss of elasticity of the walls of arteries.
• This process gradually restricts the blood flow to
one's organs and tissues
• severe health risks brought on by atherosclerosis,
(specific form of arteriosclerosis)
build up of fatty plaques, cholesterol, and some other
substances in and on the artery walls

3. -
Arteriolosclerosis, unlike atherosclerosis
Only affects small arteries and arterioles,
Atherosclerosis 
This affects large and medium-sized arteries
Monckeberg's arteriosclerosis/ medial calcific sclerosis
commonly in arteries of the extremities
Hyperplastic arteriosclerosis 
Large and medium-sized arteries.
Hyaline arteriosclerosis
Deposition of homogenous hyaline in the small arteries and
arterioles

4. Normal Blood Vessel Wall
Blood vessel walls
1. The three tunics:
a) Tunica intima
(1) Endothelium
(2) Subendothelial layer
b) Tunica media
(1) Smooth muscle
(2) Elastin
c) Tunica adventitia (externa)
(1) CT(Connective tissue) surrounding TM(Tunica Media)
(2) Arterioles in larger vessels

5. Atherosclerosis
Atherosclerosis is a disease of large and medium-
sized muscular arteries and is characterized by –
1- endothelial dysfunction,
2-vascular inflammation, and
3-the buildup of lipids, cholesterol, calcium, and
cellular debris within the intima of the vessel wall.

6. .characterized by intimal lesions 
Atheromas ( Atheromatous plaques), that protrude
into vascular Lumina.

7. .
Atherosclerosis acutely or chronically diminished arterial perfusion,
mesenteric occlusion, sudden cardiac death, chronic lHD, and ischemic encephalopathy.

8. Risk Factors for Atherosclerosis
Major risk factors
 Increasing Age
 Male gender
Genetic abnormalities

9. 
Lesser, Uncertain Risks-
Obesity
Physical Inactivity
High carbohydrate intake
Lipoprotein
Hardened (trans)unsaturated fat intake

10. 
Potentially Controllable-
 Hyperlipidemia
Hypertension
Diabetes
C-reactive protein

11. Hyperlipidemia
Hypercholesterolemia- major risk factor
 Increased risk is low-density lipoprotein (LDL) cholesterol
("bad cholesterol").
higher levels of HDL correlate with reduced risk.

12. Hypertension
 If Left untreated,
roughly half of hypertensive patients will die or
congestive heart failure,

13. Diabetes Mellitus
Diabetes mellitus induces hypercholesterolemia as
well as a markedly increased predisposition to
atherosclerosis.
Myocardial infarction is twice as high in diabetic
patients

14. Pathogenesis of Atherosclerosis
expressed by the response-to-injury hypothesis.
atherosclerosis as a chronic inflammatory response
of the arterial wall to endothelial injury.
 Lesion progression 
interactions of modified lipoproteins, monocyte-
derived macrophages, T lymphocytes, and the
normal cellular constituents of the arterial wall.

15. Pathogenesis of Atherosclerosis
1. Endothelial Injury
 Initial triggering event for development
 Causes ascribed to endothelial injury in include
mechanical trauma, hemodynamic forces,
immunological and chemical mechanisms, circulating
toxins from systemic infections, viruses

16. Pathogenesis of Atherosclerosis
2. Intimal Smooth Muscle Cell Proliferation
 Endothelial injury  adherence aggregation and platelet
at the site of exposed sub endothelial connective tissue.
 Platelets released 
mitogens (PDGF, fibroblast growth factor, TNF-ά)
Proliferation of intimal smooth muscle cells

17. Pathogenesis of Atherosclerosis
3) Role of Blood Monocytes
Though blood monocytes do not possess receptors for
normal LDL, LDL does appear in the monocyte cytoplasm
to form foam cell.
Plasma LDL on entry into the intima undergoes
oxidation.
Oxidized LDL formed in the intima is readily taken up by
scavenger receptor on the monocyte to transform it to a
lipid laden foam cell.

18. Pathogenesis of Atherosclerosis
Oxidized LDL stimulates 
endothelial cells (EC)and macrophages 
the release of growth factors, cytokines, and
chemokines
Oxidized LDL = cytotoxic
ECs and smooth muscle cells (SMCs )
induce Endothelial dysfunction

19. Pathogenesis of Atherosclerosis
4) Role of Hyperlipidemia
Chronic hyperlipidemia 
increased permeability 
may initiate endothelial injury and dysfunction
 Increased serum conc of LDL and VLDL 
formation of foam cells

20. Progression of Atherosclerosis
Atherosclerotic Plaque-
The key processes intimal thickening and lipid
accumulation
 Three principal components:
1- Cells, macrophages, and T cells
2- ECM, including collagen, elastic fibers, and proteoglycans
3-Intracellular and extracellular lipid

22. Atherosclerosis- Symptoms
most often involves the arteries supplying the
heart, brain, kidneys, and lower extremities.
The major consequences of atherosclerosis.
1-Myocardial infarction (heart attack),
2-Cerebral infarction (stroke),
3-Aortic aneurysms,
4-Peripheral vascular disease (gangrene of the legs)

23. Tests and diagnosis
• Blood tests.
• Doppler ultrasound
• Other imaging tests.
• Angiogram.
• ECG

24. TREATMENT
• Anti-platelet medications.  aspirin,
- to reduce platelets clumping in narrowed arteries,
form a blood clot and cause further blockage.
• Anticoagulants.  heparin or warfarin (Coumadin),
• Blood pressure medications.
- angiotensin-converting enzyme (ACE) inhibitors
- calcium channel blockers

25. Angioplasty
• a balloon catheter is passed through the guiding catheter to the area
near the narrowing. A guide wire inside the balloon catheter is then
advanced through the artery until the tip is beyond the narrowing.
• the angioplasty catheter is moved over the guide wire until the
balloon is within the narrowed segment.
• balloon is inflated, compressing the plaque against the artery wall
• once plaque has been compressed and the artery has been
sufficiently opened, the balloon catheter will be deflated and
removed.

27. Stenting
• a stent is introduced into a blood vessel on a balloon catheter and
advanced into the blocked area of the artery
• the balloon is then inflated and causes the stent to expand until it fits
the inner wall of the vessel,
• the balloon is then deflated and drawn back
• The stent stays in place permanently, holding the vessel open and
improving the flow of blood.

28. Bypass surgery
• May create a graft bypass using a vessel from
another part of body or a tube made of synthetic
fabric. This allows blood to flow around the blocked
or narrowed artery.

29. Prevention of Atherosclerotic Vascular
Disease
Primary prevention aims at either delaying atheroma
formation
Secondary prevention is intended to prevent
recurrence of events such as myocardial infarction
or stroke in symptomatic patients
Prevention of Atherosclerotic Vascular
Disease
Primary prevention of atherosclerosis
 Control of hypertension
 Weight loss
 Exercise,
 lowering total and LDL blood cholesterol levels while increasing HDL (
by diet , statin).

30. Prevention of Atherosclerotic Vascular
Disease
Secondary prevention involves use of –
Aspirin (anti-platelet agent),
beta blockers (to limit cardiac demand),
Surgical interventions (e.g., coronary artery bypass
surgery, carotid endarterectomy).

31. Venous Disease
.

32. Venous System
• The peripheral venous system functions 
1- As a Reservoir to hold extra blood and
2- As a Conduit to return blood from the periphery to
the heart and lungs.

33. Histology
• Tunica intima –
endothelial layer on basement membrane.
• Tunica media –
smooth muscle and connective tissue.
• Tunica adventitia –
contains adrenergic fibres

35. Valves
• Allow the blood to flow only upwards (towards the
heart),

37. The Venous Pumping mechanism
• Large muscle groups contract compress the deep
veins pressure within the vein closes upstream valves
and opens downstream valves

38. .
• During muscle relaxation 
the vessel once again fills with blood 
the cycle is repeated during the next contraction

39. Venous System
• The deep system  the main way blood leaves the
leg and returns to the heart.
• The superficial system is just under the skin and
can be seen

40. Venous Insufficiency
• Superficial venous incompetence is the most common form of venous disease.

41. CEAP Classification
• “C” – Clinical findings
• “E” – Etiologic
• “A” – Anatomic
• “P” – Path physiologic

42. Clinical findings
• C0 = no visible venous disease
• C1 = telangiectatic or reticular veins
• C2 = varicose veins
• C3 = oedema
• C4 = skin changes without ulceration
• C5 = skin changes with healed ulceration
• C6 = skin changes with active ulcers

43. Etiologic
• Ec - congenital disease
- present since birth
• Ep – primary disease
- unknown cause
• Es – secondary disease
- known cause (post post- phlebitic trauma)

44. Anatomic
• Anatomical alteration of particular vein

45. Path physiologic
• Reflux – PR
• Obstruction – PO
• Reflux and obstruction - PRO

46. Venous Insufficiency
• The long saphenous vein and its tributaries are the
ones that most often form varicose veins.
• venous valve no longer perform their usual
function Retrograde flow through venous system
• Direct injury or superficial phlebitis may cause
primary valve failure

48. .
• Congenitally cause -
 weak vein walls may dilate under normal
pressures to cause secondary valve failure,
abnormal valves may be incompetent at normal
superficial venous pressures.
• Normal veins and normal valves may become
excessively distensible under the influence of
hormones (as in pregnancy).

50. Symptoms
• Aching and heaviness of the legs are common complaints,
particularly after standing up for a long time.
• Itching, a feeling of heat and tenderness over their veins

53. Varicose veins

54. Ulcers
• Decreased capillary flow WBC activation  chronic
inflammation
• Focal micro vascular ischemia

55. Evaluation
• Doppler and/or Duplex ultrasound examinations
 to determine which anatomic sites are involved

56. Photo plethysmography
• Easiest method to determine what effect these
abnormalities have on the function of the venous
system.
Strip chart recordings of photoplethysmographic
measurement venous refill time (VRT)

57. Treatment
Conservative measures designed to decrease
venous distension and reduce ambulatory venous
hypertension.

58. .
• Reduces the diameter of the veins
• Activates the fibrinolytic activity
• Reduces filtration of fluid out of the intravascular
space and improves lymphatic flow
• Reduces reflux and improves venous outflow
• Anti inflammatory

60. Compression
• Elastic compression stockings or bandages
• Inelastic compression garments or bandages
• Pneumatic compression pumps

61. Elastic Compression
• Fitting must include measurements
• The elastic in the stocking recoils and creates inward
pressure on the leg.
• This pressure may prevent the movement of blood from
the superficial to deep system

63. Inelastic compression
• Inelastic compression augments the emptying of
the veins by providing a rigid envelope around the
leg.

65. Pneumatic compression
• Pneumatic compression pumps are an effective
adjunct when patients have lymphedema , venous
ulceration, or severe edema.
• Pneumatic pumps should not be considered a
primary therapy

66. Sclerosing
• The key goal  to deliver minimum volume and
concentration of sclerosant that will cause
irreversible damage to the endothelium of the
abnormal vessel to be sclerosed, while leaving
adjacent normal , vessels untouched.
• Sclerosants 
1- Detergents
2-Hypertonic and Ionic Solutions
3-Cellular Toxins

67. Surgery
The primary goal  improve venous circulation by correcting venous insufficiency

68. Thank you