Module 2 Heart & Vasculature Structure and Function) Flashcards
What are the three layers of the heart wall and their key cell types?
✅ Answer:
Endocardium: Endothelial cells lining the heart chambers.
Myocardium: Cardiomyocytes (main contractile force), fibroblasts, capillaries.
Epicardium: Outer connective tissue; contains vessels and nerves.
What is surprising about the composition of the myocardium based on modern cell mapping studies?
✅ Answer: Cardiomyocytes make up the majority of the heart’s mass but not the majority of its cell number. Non-myocyte cells (fibroblasts, endothelial cells, immune cells) dominate numerically.
How does fibroblast function differ in various heart regions?
✅ Answer: Fibroblasts are regionally specialized (e.g., FB1 in ventricles, FB2 in atria) and express different ECM genes — they tailor the extracellular matrix to regional mechanical and functional needs.
fb 1 : Secretes stronger ECM (e.g., more type I collagen) to handle high pressure/contraction force
fb 2: Secretes softer ECM (e.g., more type III collagen, more elastic) for more flexibility
Differentiate between endomysium and perimysium in the heart.
✅ Answer:
Endomysium: ECM surrounding individual cardiomyocytes; more type III collagen (elastic).
Perimysium: ECM surrounding bundles of fibers; more type I collagen (strength).
What are the roles of type I and type III collagen in the heart?
✅ Answer:
Type I: Provides tensile strength; prevents overstretching.
Type III: Provides elasticity; allows diastolic filling.
The Type I/III ratio affects heart stiffness and compliance.
What pathology arises from a mutation in collagen XV?
✅ Answer: Disrupted interstitial ECM, increased vascular permeability, misaligned cardiomyocytes → cardiomyopathy and heart failure.
Name and describe the three layers of heart valves.
Ventricularis: Elastic side; rich in fibrillin-1, fibulins → allows stretch and recoil.
Spongiosa: Cushioning layer; contains hyaluronic acid, proteoglycans → absorbs pressure, prevents delamination.
Fibrosa: Strength layer; rich in collagen I, III, V → provides stiffness and integrity.
What matrix changes occur in Marfan syndrome and how do they affect valve function?
✅ Answer:
Caused by fibrillin-1 mutations.
Leads to valve thickening, prolapse, and increased risk of aortic aneurysm due to poor elastin network.
Compare the structural differences between arteries and veins.
✅ Answer:
Arteries: Thicker media, more smooth muscle and elastic laminae, pressure reservoirs.
Veins: Thinner walls, larger lumens, volume reservoirs.
Where are collagen types I and III located in arterial walls and what do they do?
✅ Answer:
Type I: Adventitia; prevents overstretching.
Type III: Media; provides compliance and strength.
Why is elastin critical in large arteries like the aorta?
✅ Answer:
Allows elastic recoil during diastole.
Absence leads to hyperproliferation of smooth muscle cells, vessel narrowing, and postnatal lethality in mice.
Explain the stress-strain curve and Young’s modulus in relation to heart or vessel tissue.
✅ Answer:
Stress-strain curve shows how much a tissue deforms under force.
Young’s modulus is the slope of the linear region → measures tissue stiffness.
Elastin has low modulus (very stretchy), collagen has high modulus (strong, stiff).
Why do vessels require both elastin and collagen?
✅ Answer:
Elastin allows vessels to stretch with pulse pressure (systole).
Collagen limits overexpansion and provides strength (prevents rupture).
Their combined mechanical properties create the nonlinear elastic behavior essential for vascular function.
