Blood Vessel Pathology - Jarzembowski Flashcards
What layers does the internal elastic lamina separate?
Which vessels do not feature external elastic laminae?
Internal elastic lamina separates the tunicas intima and media.
Small vessels (eg arterioles) will not contain an external elastic lamina. Obviously, neither will capillaries.
What is the primary histological difference between large and medium arteries?
Large (elastic) features elastic fibers between smooth muscle layers.
Medium (muscular) features a tunica media that is mostly just smooth muscle–elastic only in laminae and adventitia.
Describe the appearance of an arteriole on histology, with respect to its wall layers.
What is the physiological importance of arterioles (distinct from other vessel calibers)?
The media consists essentially of only smooth muscle cells. The internal elastic lamina is thin or missing, and the external is entirely missing.
Provides largest source of resistance to circulation; can affect blood pressure and flow to capillary beds.
How does the thickness of a capillary wall compare to its lumen?
What types of cells are present at the capillary level?
Thin; large cross-sectional area by comparison (7-8µm diameter).
Endothelium & pericytes.
Are each of the following vessels muscular, or elastic?
Pulmonary artery
Coronary artery
Renal artery
Common carotid artery
Pulmonary = Elastic
Coronary = Muscular
Renal = Muscular
(Common) Carotid = Elastic
Where in the vascular circuit can leukocytes extravasate/transmigrate?
At the post-capillary venule.
Where is most of the body’s blood located at any given time?
In venous circulation.
Recall the (general!) roles of the following mediators:
Endothelin
Von Willebrand Factor
E-selectin
Prostacyclin
Endothelin: Vasoconstriction following injury. (Also purkinje fiber differentiation)
Von Willebrand Factor: Prothrombotic. (abscence = bleeding disorder)
E-selectin: Pro-inflammatory. (interacts with Sialyl-Lewis X for rolling)
Prostacyclin: Anticoagulant. (PGI2)
What precedes endothelial cell activation?
What factors can contribute to endothelial cell activation?
What is the result of endothelial activation?
Stimulation (recall: rapid vs delayed/expressive responses)
Turbulent flow, hypertension, cytokines/complement, infectious agents, glycation, hypoxia/acidosis, etc etc etc.
Expression of procoagulant, inflammatory, adhesive factors. Stuff.
What trait of vascular smooth muscle cells is critical to their role in vascular disease?
How is “intimal” smooth muscle different than “medial” smooth muscle?
Vascular smooth muscle cells synthesize ECF elements such as collagen, elastin, and proteoglycans. They migrate to the Tunica Intima as part of vascular repair/pathology & proliferate there.
Intimal (in the Tunica Media) cannot contract.
Describe the two basic pathologies of vascular disease.
Give some examples of how different vessels are affected differently by these diseases.
Narrowing/obstruction of the lumen or weakening/rupture of the wall.
Weakening & rupture is a greater concern for larger vessels, where pressures are greater (and consequences worse). Atherosclerosis is a bigger problem in medium vessels, while hypertension mostly concerns the smaller vessels.
Distinguish between Arteriosclerosis, Atherosclerosis, and Arteriolosclerosis.
Arteriosclerosis is an umbrella term for many vessel conditions. Atherosclerosis concerns large/medium arteries. Arteriolosclerosis concerns smaller arteries & arterioles.
What is Mönckeberg arteriosclerosis?
A benign calcification off the media and IEL of muscular arteries. Seen in older patients, it is unrelated to atherosclerosis and is not clinically significant.
Describe some of the clinical syndromes seen when the following vessels are affected by atherosclerosis:
Renal artery
Iliac or popliteal
Mesenteric
Renal artery: Secondary hypertension
Iliac or popliteal: Lower limb/gangrenous necrosis.
Mesenteric: Bowel infarction & necrosis.
What is the pre-clinical sign of atherosclerosis?
Describe its composition & appearance.
The fatty streak.
A collection of lipids, macrophages, and and lymphocytes which accrues on the walls of larger vessels as flat dots or streaks.
Describe the process by which LDLs can contribute to plaque formation.
LDL at the vessel wall is oxidized by endothelial cells or macrophages, resulting in oxLDL.
oxLDL is taken up by Macrophages/foam cells via scavenger receptors, and are activated to release inflammatory cytokines.
Describe the appearance of a fibrofatty plaque.
The plaque consists of a fatty, necrotic yellow core with a thin white fibrous cap. They are initially eccentric, but may coalesce to impinge on the lumen (sometimes massively so).
Distinguish between an advanced/vulnerable plaque and a stable plaque.
Vulnerable/Advanced: Thinner cap and more inflammation; higher risk of complications eg aneurysm, rupture, erosion, hemorrhage, embolism.
Stable: Thicker fibrous cap and smaller lipid core, with less inflammation.
What are the consequences of thrombosing of a vessel plaque?
What can cause this?
Thromboses increase the size of the plaque, narrowing the lumen until it is completely occluded. It may also throw fragments as emboli to distal vascular sites.
Shear stress, high LDLs, smoking, turbulent flow…
Advanced plaques may calcify. How does this look different from the calcification seen in Mönckeberg arteriosclerosis?
The calcium deposits are located in the intima, rather than in the tunica media.
Describe how most aneurysms form.
High pressure or ischemia causes atrophy of the tunica media, thinning the wall and predisposing it to rupture.
Regarding the pathogenesis of atherosclerosis:
What are some initial causes of endothelial injury?
Lipid accumulation
Hemodynamic stressors
Inflammation/Infection
(Hypertension, Homocysteine, Cigarette smoke?)
Regarding the pathogenesis of atherosclerosis:
How does endothelial injury contribute to plaque formation?
Injured endothelium is more permeable and attracts the activity of inflammatory cells (eg macrophages, T-cells) which cause local transformations (eg produce fibrogenic mediators)
Regarding the pathogenesis of atherosclerosis:
What role do microbial infections play? Which ones?
Not clear yet, but the inflammatory response can clearly exacerbate atherosclerosis.
Herpes virus, CMV, Chlamydia are listed. Presumably more…
What is a telltale sign of chronic hyperlipidemia?
Accumulation of lipoproteins in the tunica intima.
