1. Vascular and Lymphatic System Pathology

2. Blood Flow Systemic blood flow is a circuit :
Heart →Arteries→ Arterioles→ Capillaries→ Venules→ Veins→ Heart
Artery – any vessels that carries blood away from the heart.
Vein – any vessels that carries blood toward the heart

4. Structure of blood vessels
Tunica intima
Endothelium and connective tissue
Tunica media
Smooth muscle and elastic tissue
Tunica externa or tunica adventitia
Connective and elastic tissue

7. Arteries
Large arteries are elastic (conducting) arteries – pressure reservoirs
Medium arteries are muscular (distributing) arteries – more smooth muscle
Contraction or relaxation of muscle changes the size of the lumen, and so controls the blood pressure in the vessel.

9. Capillaries Only a single layer of endothelium and a basement membrane
Connect arterioles and venules
Functional part of system
True capillaries begin at a precapillary sphincter which controls blood flow through the capillary

11. Veins Relatively thin; less elastic Larger in diameter than arteries
Have valves to prevent backflow of blood
Flow to heart is assisted by contraction of skeletal muscles

15. Control of systemic circulation
Nervous control – innervated by sympathetic nervous system ONLY
Cardiac control center (primarily in medulla oblongata)
Heart has both Sympathetic and Parasympathetic innervations.

16. Baroreceptors and chemoreceptors:
Monitor pressure
Monitor blood levels of O2, CO2 and H+
Send information to cardiovascular center, which responds

17. Compliance
The increase in volume a vessel can accommodate for a given increase in pressure.
Depends on the ratio of elastic fibers to muscle fibers in the vessel wall.
Elastic arteries more compliant than muscular arteries
Veins more compliant than either artery (blood reservoirs)
Decreased compliance suggests an increased stiffness of vessel wall.
Determines the vessel’s response to changes in pressure.

18. Blood pressure
Mean arterial pressure is the average in pressure in the arteries throughout the cardiac cycle.
Depends on the compliance of the arteries and the amount of blood in the arterial system.

19. Lymphatic System
A vascular system that runs “parallel” to the blood vascular system
Flow does not circulate – begins in tissue
Returns to venous system at subclavian veins
Fluid in vessels is lymph – mostly water and proteins
Interstitial fluid→ lymphatic capillaries→ lymphatic vessels→ lymphatic trunks→ lymphatic ducts

22. Lymph nodes Lie along lymphatic vessels
Contain lymphocytes that filter lymph and eliminate microbes/damaged cells/ toxins
Biological filtration

24. Diseases of Arteries and Veins
Thrombus- “clotting” in an unbroken vessel
Maintains a point of attachment
Organized differently than a clot
usually due to damage to endothelium and exposure of collagen in the basement membrane

25. Arterial thrombus
Forms where blood is moving rapidly – see alternating lines of platelets and red cells trapped in fibrin
Lines of Zahn

26. Venous thrombus Forms differently due to decreased blood flow
Mixed region at site of attachment
More blood clotting forms a downstream red cap

27. Factors that predispose to thrombosis
Endothelial damage
Bacterial damage
Damage to the myocardium
Wear and tear – hemodynamic stress
Hypertension increases this
Arteriosclerosis
Inflammation
Tumors and irritation by their products

28. Factors that predispose to thrombosis
Flow abnormalities
Increases platelet contact with endothelium
Reduction in flow:
Arterial:
Cardiac damage and decreased pumping action
Increased blood viscosity
Venous:
Physical inactivity
Varicose veins

29. Turbulence:
Damaged heart valves
Congenital heart defects
Compression of the vessel
Weakened arterial wall - aneurysm

30. Other Causes Aging Immobilization Injury to vessel endothelium
Increased clotting response
Effects:
Decreased venous emptying
Increased venous pressures
Edema
Pain

31. Sequelae of Thrombosis
1 Resolution –
Anticoagulation system
Fibrolytic system
Moderate exercise increases thrombus resolution

32. 2 Organization
The thrombus is digested by phagocytes and replaced by connective tissue – incorporating the thrombus into the vessel wall.
May recanalize – small channels open up and restore blood flow

33. Recanalization

34. 3 Propagation –
Thrombus extends further down the vessel, usually a vein.
Initial thrombus acts as a site for further platelet adherence.

35. Propagation

36. 4 Infarction –
an infarct is an area of necrosis caused by ischemia and hypoxia.
More common in arteries than veins due to blood flow patterns
Collateral circulation and anastomosis prevent infarction

38. Embolism – obstruction of vessel by matter circulating in blood stream
Matter could be fat, air, infant’s cells, in addition to pieces of clot – thromboemboli
Thromboemoboli from the venous system tend to end up in the:
lungs and liver

40. Treatment Anticoagulants Fibrinolytics – t-Pas
Prophylactic aspirin therapy

42. Arterial Occlusions
Arteriosclerosis – abnormal thickening and hardening of the arterial walls
Smooth muscle cells and collagen fibers migrate into the tunica intima, causing stiffening and thickening, narrowing the lumen
Can exacerbate high blood pressure, and cause weakening and outpouching of vessel walls

44. Atherosclerosis
A form of arteriosclerosis where soft deposits of intra-arterial fat and fibrin harden over time – atheroma
May see build up in skin – Xanthoma or arcus in cornea.
In general, patients suffer few symptoms unless > 60 % of blood supply is blocked

45. Progressive over years
Starts with some injury to endothelium
Smoking, hypertension, hyperlipidemia, diabetes, autoimmune disease, and infection
Inflammation, release of enzymes by macrophages causes oxidation of LDL, which is then consumed by macrophages – foam cells – accumulate to form fatty streaks
Fatty streaks of lipid material appear first as yellow streaks and spots
Smooth muscle cells proliferate, and migrate over the streak forming a fibrous plaque

46. Fibrous plaque results in necrosis of underlying tissue and narrowing of lumen
Inflammation can result in ulceration and rupture of the plaque, resulting in platelet adherence to the lesion = complicated lesion
Can result in rapid thrombus formation with complete vessel occlusion → tissue ischemia and infarction

49. Clinical manifestations
Signs and symptoms of inadequate perfusion – TIAs, often associated with exercise or stress
When lesion becomes complicated, can result in tissue infarction
Coronary artery disease – myocardial ischemia
In brain – major cause of stroke

50. Treatment Exercise Smoking cessation
Control of hypertension and/ or diabetes
Reduce LDL cholesterol by diet or medication or both

51. Other arterial problems
Aneurism – dilation in the arterial wall
Most arise in aorta or major branches as a result of atherosclerotic wall damage
Males over 50 at greatest risk for aortic aneurysms
Disturbs blood flow, predisposing to thrombus formation - can release thromoemboli

52. Asymptomatic until rupture
Embolism
Death
Treatment by surgical repair
Aortic Dissection –bleeding into vessel wall, separating vessel layers
Men in y.o. age group with hypertension
Younger persons with connective tissue disease or congenital defects
Presents with pain – life threatening

53. Systemic Hypertension
A consistent increase in arterial blood pressure caused by increased Cardiac output or increased peripheral resistance or both
Leads to damage of vessel walls
If arteries constrict over a long time with increased pressure in vessel, the wall becomes thicker to withstand the stress.
Results in narrowing of arterial lumen
Leads to inflammatory response

54. Causes one in eight deaths worldwide
Third leading cause of death in the world
Affects 50 million Americans

55. Primary hypertension Also called essential or idiopathic hypertension
% of all cases
No specific cause identified
Can happen with retention of sodium and water → increased blood volume.
Also low dietary potassium, calcium and magnesium intakes

56. Other risk factors Smoking Nicotine is a vasoconstrictor
Greater than 3 alcoholic drinks/ day
2-4 drinks / week lowers blood pressure

57. Suspected causes Interaction of genetics and environment
Overactivity of sympathetic nervous system
Overactivity of renin / angiotensin/ aldosterone system
Salt and water retention by kidneys
And others

58. Secondary hypertension
Caused by a systemic disease process that raises peripheral resistance or cardiac output = % of cases.
Renal vascular disease
Adrenocortical tumors
Adrenomedullary tumors
Drugs ( oral contraceptives, corticosteroids, antihistamines)

59. Complicated hypertension
Sustained primary hypertension that damages the structure and function of the vessels themselves.
Commonly affects heart, aorta, kidneys, eyes, brain, and lower extremities (target-organ damage).

60. Clinical manifestations
None in early stages other than elevated BP
Some individuals never have symptoms; others become very ill and die

61. Treatment Modification of life style Drugs
Diuretics, beta-blockers, angiotensin converting enzyme inhibitor
Compliance is often difficult – patients stop taking medication when they feel better – can get rebound effects

62. Venous Disorders
Varicose veins – dilations, can lead to valvular insufficiency
Can occur in superficial veins (saphenous) or deep veins
Causes of secondary varicose veins:
Deep vein thrombosis
Congenital defects and pressure on abdominal veins

63. Treatment
Prevention – little can be done after valves become incompetent
Avoid stressors, such as standing for long periods
Elastic support stockings
Sclerotherapy – injections of drugs to induce fibrosis of vessel
Surgical removal - but only when deep vein are open.