Chapter 11: Blood vessels

Question 1

Three types of arteries

Answer 1

• large elastic arteries (aorta)
• medium muscular arteries (renal)
• small arteries and arterioles

Question 2

How are veins different from arteries?

Answer 2

• larger diameters, larger lumens, thinner and less well organized walls
• more susceptible to compression and penetration by tumors

Question 3

Define vasculogenesis, angiogenesis and arteriogenesis

Answer 3

Vasculogenesis: the formation of new vessels during embryologic development
Angiogenesis: new vessel formation in the mature organism
Arteriogenesis: remodelling of existing vessels

Question 4

Response to vascular injury

Answer 4

• stimulation of smooth muscle and extracellular matrix growth, creating a neointima
• intimal thickening is the response to any vascular injury but also occurs in non-injured but aging vessels

Question 5

Major causes of hypertension

Answer 5

• idiopathic (>90% of cases)
• renal (GN, renal artery stenosis, etc)
• endocrine (Cusings, pheo, acromegaly, etc.)
• cardiovascular (coarct, polyarteritis nodosa)
• neurologic (increased ICP, sleep apnea)

Question 6

Malignant hypertension

Answer 6

• severe hypertension with associated retinal hemorrhage, renal failure, etc, can progressive to death in a 1-2 years
• may arise de novo but often superimposed on pre-existing hypertension

Question 7

Risk factors in hypertension

Answer 7

• nonmodifiable: age, genetic makeup, gender, family history

- modifiable: hypercholesterolemia, hypertension, smoking, diabetes

Question 8

Steps in atherosclerosis

Answer 8

• endothelial injury or dysfunction
• accumulation of LDL in the vessel wall
• monocyte adhesion with transformation of macrophages into foam cells in the plaque
• platelet adhesion
• smooth muscle cell recruitment via platelet derived factors
• smooth muscle proliferation and ECM production
• lipid accumulation

Question 9

What is the relationship of inflammation to the development of atherosclerosis?

Answer 9

• normal endothelial cells don’t bind inflammatory cells, but dysfunctional ones express adhesion molecules for inflammatory cells
• monocytes transform into macrophages that phagocytize lipid and recruit more inflammatory cells via cytokines and elaborate growth factors that promote smooth muscle proliferation

Question 10

What is the role of smooth muscle proliferation in atherosclerosis?

Answer 10

• smooth muscle converts the fatty streak into a mature atheroma
• smooth muscle cells synthesis ECM components that stabilize the plaque
• activated inflammatory cells cause smooth muscle cell apoptosis and thereby destabilize plaques

Question 11

What are the three main components of atherosclerotic plaques?

Answer 11

• cells: smooth muscle cells, macrophages, T cells
• extracellular matrix: collagen, elastic fibres, proteoglycans
• intra and extracellular lipid

Question 12

Complications of atherosclerotic plaques

Answer 12

• plaque rupture, with exposure of the blood to thrombogenic substances in the plaque, resulting in thrombosis
• hemorrhage into the plaque, which can result in rupture
• atheroembolism
• aneurysm resulting from weakening of the underlying elastic wall

Question 13

Define a critical stenosis of a vessel due to atherosclerosis

Answer 13

• the degree of stenosis at which blood flow is significantly impeded with demand exceeding supply
• approximately 70% occlusion
• patients usually become symptomatic at this level

Question 14

What are “vulnerable plaques”?

Answer 14

-those predisposed to rupture due to their composition, which may include thin fibrous caps, large components of foam cells and extracellular lipid or those with few smooth muscle cells

Question 15

Define pseudoaneurysm

Answer 15

-a defect in the vessel wall leading to an extravascular hematoma that communicates with the vessel

Question 16

Pathogenesis of aneurysms

Answer 16

• intrinsically weak vessel walls (e.g. Marfan syndrome)
• local inflammation or proteolytic enzymes make collagen degradation dominant over collagen synthesis (e.g. decreased levels of TIMP)
• vessel weakening through loss of smooth muscle cells or deposition of inappropriate ECM components: cystic medial degeneration

Question 17

Clinical consequences of abdominal aortic aneurysms

Answer 17

• rupture & hemorrhage
• occlusion of structure such as ureter
• embolism
• occlusion of ostia of a branch vessel
• presentation as an abdominal mass simulating a tumor

Question 18

Two groups of patients who develop aortic dissection

Answer 18

• hypertensive men age 40-60

- young patients with localized or systemic abnormalities of collagen or other components of vessels

Question 19

Most common preexisting lesion in aortic dissection?

Answer 19

-cystic medial degeneration

Question 20

Immune complex vasculitis

Answer 20

• SLE, polyarteritis nodosum
• drug-induced vasculitis
• viral infection-related vasculitis

Question 21

Possible mechanism for ANCA-associated vasculitis

Answer 21

• ANCAs form in a susceptible host or as a result of induction by drugs or microbes
• re-exposure or other stimulus cause surface expression of MPO or PR3 which react with ANCAs causing vascular injury
• neutrophils degranulate and generate ROS which cause endothelial injury

Question 22

Polyarteritis nodosa

Answer 22

• 30% of patients have chronic hep B, suggesting immune complex-mediated injury
• segmental transmural necrotizing vasculitis of medium and small arteries
• lungs less commonly affected
• lesions are of varying ages

Question 23

Microscopic polyangiitis

Answer 23

• lesions are all the same age at the same time

- necrotizing glomerulitis and pulmonary capillaritis are common

Question 24

Features of Churg-Strauss syndrome

Answer 24

• peripheral eosinophilia, asthma, allergic rhinitis, lung infiltrates, small vessel necrotizing vasculitis and extravascular necrotizing granulomas
• ANCAs present in <50%
• myocardial infiltrates of eosinophils cause cytotoxicity and is the cause of death in some cases

Question 25

Features of WG

Answer 25

• necrotizing granulomatous vasculitis of small to medium arteries
• necrotizing granulomas of the upper respiratory tract
• necrotizing crescentic glomerulonephritis
• probably related to a T cell mediated hypersensitivity reaction to an inhaled antigen

Question 26

Thrombangiitis obliterans (Buerger disease)

Answer 26

• segmental, thrombosing acute and chronic inflammation of medium and small arteries esp. tibial and radial arteries
• smokers <35 years old (therefore probably related to smoking-induced endothelial toxicity)
• thrombi typically contain microabscesses

Question 27

Primary vs. secondary Raynaud phenomenon

Answer 27

Primary: exaggeration of central and local vasomotor responses to cold and emotional stress; more often in young women; usually no significant vessel structural changes and usually benign course
Secondary: vascular insufficiency of the extremities due to other diseases such as SLE, scleroderma, etc

Question 28

Complications of angioplasty

Answer 28

• immediate: embolism and abrupt reclosure due to thrombosis
• later: proilferative restenosis: intimal thickening occurring in up to 50% of patients by 6 months; this can be seen with and without stents placed

Question 29

What is the long term patency of saphenous vein grafts?

Answer 29

• 50% at 10 years
• early occlusion due to thrombosis
• months to years: intimal thickening, atherosclerosis, aneurysm (usually after years)

Question 30

How does HHV8 induce development of KS?

Answer 30

-disrupts cellular proliferation controls and prevents apoptosis by producing p53 inhibitors and a viral homologue of Cyclin D