Patho- Anatomy week 1 Lecture

PATHOLOGIES OF BLOOD VESSELS

• The size of the vessel is important when it comes to the type of pathology that develops there.
• There are smaller veins, large and medium sized arteries and small capillaries.
• Atherosclerosis is a disorder of large arteries because it needs specific structure of the vessels to be
developed.
• Hypertensive disorders affect medium sized arteries. Because they have more smooth muscles and
therefore more possibility of spams.
• Vasculitis mainly develops in capillaries. So also known as capillaritis.
• Veins mostly involve phlebitis.

ATHEROSCLEROSIS
• Aorta has lamina elastica (internal/external). These aren’t found in veins, capillaries or other small arteries.
• The main pathogenesis here is hyperlipidemia.
• So balance between the amount of lipid uptake n the type of lipid (LDL/HDL) uptake is also important.
• When lipid is eaten along with sweet and carbonated drinks, the insulin production will be considerably high,
so insulin will store lipids too.
• When there are excess lipids ingested, macrophages will be activated.
• Endothelial cells will also be activated. They further activate macrophages.
• Some of them will try to engulf/phagocyte lipids and produce foamy cells.
• Another portion will release growth factors.
• Platelets will recruit too. They will release PDGF (platelet derived growth factor).
• Myocytes from the media will emigrate into the intima via fenestrations.
• Myocytes will undergo de-differentiation and now will look like fibroblasts.
• Fibroblasts like myocytes will now relase collagen, covering the pool of engulfed lipids. Thus forms a plaque.

Fate of the plaque →

- Occlusion (partial/complete)
- Breakdown of the plaque and formation of thrombus. Thrombus can cause partial/complete occlusion.
*If complete occlusion takes place tissue will undergo infarction and die by ischemic necrosis.
*If partial occlusion occurs there will be gradual sclerosis due to continuous moderate hypoxia. Thus
develops fibrotic tissue.

• Organs mostly affected by atherosclerosis: brain, heart and less likely kidneys.
Timings
• 1st step can last for decades.
- Here lipid deposition happens but plaque not yet visibly formed.
- Yellowish discolorations will be seen.
• After about the 3rd decade plaques will be formed.
• With time the plaque could break down due to large size and may lead to complications in the organs.
• Rupture of the vessel due to plaque is commonly seen in the brain.
• Areas with the damage will undergo sclerosis and calcification. So aorta losses its elasticity.
HYPERTENSIVE DISEASE
• Hypertension is a symptom.
• Could be due to variable reasons:
- Hormonal factors
- Neural factors alter peripheral resistance of the vessel
- Local factors
- Blood volume
Alter cardiac output
- Cardiac factors

• Primary reason of hypertension comes from blood vessels.

• Essential hypertension → primary developing in blood vessels. Also known as muphus hypertonicus?!
• Vascular hypertensive disease is another type of hypertensive disorder.
• Hypertension is usually due to chronic unresponsive stress. Usually prolonged negative emotions.
• Hypertension occurs due to prolong spasms of medium sized blood vessels, therefore the stress should have
to applied for a long time.
• Hypertension could be genetically predisposed. Usually due to varied Na metabolisms.
• Because of high pressure the vessel wall may get damaged and albumin, globulin etc. may get in from blood
and sclerosis develops along the blood vessel.
• Genetically induced hypertension could occur when sodium retention takes place and water excretion
decreases and cardiac output increases.
• Functional way mainly relates to hormones and environmental factors.
• Left ventricle workload increases due to increased blood volume and may lead to left ventricular
hypertrophy.
• When hypertension develops in the renal artery, hypoxic conditions develop and renin-angiotensin system
increases. Thus further increasing blood pressure. (visual cycle?!)

Fig. 10.5 Hypertensive vascular disease. (A) Hyaline arteriolosclerosis. The

arteriolar wall is thickened with the deposition of amorphous proteinaceous
material (hyalinized), and the lumen is markedly narrowed. (B) Hyperplastic
arteriolosclerosis (“onion-skinning”) (arrow) causing luminal obliteration
(periodic acid–Schiff stain). (B, Courtesy of Helmut Rennke, MD, Brigham and
Women’s Hospital, Boston, Massachusetts.)

o Different type of disorders include ; Bening coarse →develops slowly step-wise with age
Hyalinized lumen with less diameter

Malignant coarse → follows vasculitis

Occurs in young men mainly
Develops faster along with fibrinoid necrosis
Onion skin layering takes place

• Monckeberg sclerosis occurs in large arteries mainly in males. Looks like atherosclerosis but here plaques
are not formed inside.
• So narrowing and thrombosis doesn’t happen. Only media will be affected.
ANEURYSMS

• Congenital or acquired dilation of blood vessels.

• Types could be ; True → when all layers of the wall will be involved in dilation
False → when only the outer most layer is involved
Easily ruptured
• Aneurysm is a complication of atherosclerosis and Marfan syndrome.
• Mostly develop in abdominal aorta.

AORTIC DISSECTION
• Also a complication of Marfan syndrome which has dificency in collagen due to lack of fibrillin.
• Occurs inside and the vessel splits due to abnormal structural contents of the aorta.
• Types of dissections ; Type A → could happen anywhere along the vessel and also in the proximal portions.
Type B → only distal parts will be involved
VASCULITIS
• There are different types :
- Temporal arteritis (giant cell)→
More localized and type IV hypersensitivity reaction with granuloma formation happens.
Effects large to small arteries of the head (temporal artery)
Leads to deafness and blindness
- Takayasu arteritis →
Granulomatous vasculitis in medium to large sized arteries
Usually develope in aortic arch
- Polyarteritis Nodosa →
systemic vasculitis of small to medium sized arteries, usually in visceral & renal vessels.
Develops in multiple sites
Could be the reason for an acute abdomen because intestines will be affected.
Begins with fibrinoid swelling and followed by fibrinoid necrosis of the vessel wall.
In the site of necrosis thrombus will be formed and also may undergo calcification
- Kawasaki disease → acute illness of infancy and childhood, related to medium sized vessels. This is coronary
arteries’ vasculitis.
- Good posture syndrome → type II hypersensitivity reaction. Affects blood vessels of the respiratory system
and kidneys.
- Microscopic polyangiitis→ necrotizing vasculitis affecting capillaries and small venules

**The main issue with capillary vasculitis is that renal glomerulus is formed by this type of vessels and also other
renal capillaries. so the pores between the cells decrease in size and therefore the blood cells may get damaged
causing hemolysis and thus renal failure. Also uremia will be observed.

**Morphological appearance of any vasculitis ; smudgy, fibrinoid necrosis

Fig. 10.24 Takayasu arteritis. (A) Aortic arch angiogram showing reduced
flow of contrast material into the great vessels and narrowing of the brachiocephalic,
carotid, and subclavian arteries (arrows) (C) Histologic appearance in active Takayasu aortitis illustrating
destruction and fibrosis of the arterial media associated with mononuclear
infiltrates and giant cells (arrows).

Fig. 10.25 Polyarteritis nodosa, associated with segmental

fibrinoid necrosis
and thrombotic occlusion of a small artery. Note that part
of the vessel
(upper-right, arrow) is uninvolved. (Courtesy of Sidney
Murphree, MD, Department
of Pathology, University of Texas Southwestern Medical
School, Dallas, Texas.)

TUMORS OF BLOOD VESSELS

• Could be ; Benign→ hemangiomas & lymphangiomas

Malignant→Angiosarcomas

• Hemangiomas; Slow growing

Mostly occur in the face & liver
After surgical removal of hemangiomas, keloids maybe formed
Capillary hemangiomas have strawberry like appearance
• In pregnant and elderly women pyogenic granulomas. Usually observed in the oral cavity.
• Telangiectasia are hemangiomas with limited growth.
• With HIV patients is observed Kaposi sarcoma. Here no external growth is observed, only patches and
hemorrhages occur.