Pathophysiology Quiz: Peripheral Artery Disease Pad
20 questions · exam conditions
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Peripheral Artery Disease PadQuestion 1 of 20

While atherosclerosis affects the tunica intima, its progression also significantly impacts the tunica media. What is a primary pathological change that occurs in the tunica media underlying a large atherosclerotic plaque?

Hyperplasia and hypertrophy of smooth muscle cells, strengthening the vessel wall.
Deposition of amyloid protein, leading to increased vessel wall compliance.
Infiltration by B-lymphocytes and formation of ectopic lymphoid follicles.
Pressure atrophy and apoptosis of smooth muscle cells due to impaired nutrient diffusion.
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Pathophysiology Quiz: Peripheral Artery Disease Pad

Practice Peripheral Artery Disease Pad in Pathophysiology with focused quiz questions that help you check what you know, review explanations, and build confidence with test-style prompts.

What this quiz covers

This quiz focuses on Peripheral Artery Disease Pad, giving you a quick way to practice the rules, question types, and explanations that matter most for Pathophysiology.

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Try each quiz question before looking at the correct answer. Use the explanations to review missed ideas, then come back to similar questions until the pattern feels familiar.

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Question 1

While atherosclerosis affects the tunica intima, its progression also significantly impacts the tunica media. What is a primary pathological change that occurs in the tunica media underlying a large atherosclerotic plaque?

  1. Hyperplasia and hypertrophy of smooth muscle cells, strengthening the vessel wall.
  2. Deposition of amyloid protein, leading to increased vessel wall compliance.
  3. Infiltration by B-lymphocytes and formation of ectopic lymphoid follicles.
  4. Pressure atrophy and apoptosis of smooth muscle cells due to impaired nutrient diffusion. (correct answer)
Explanation: When approaching questions about atherosclerosis progression, remember that this disease process affects multiple layers of the arterial wall, not just the intima where plaques form. Understanding the secondary effects on deeper layers is crucial for grasping the complete pathophysiology. Large atherosclerotic plaques create a mechanical barrier that impairs nutrient and oxygen diffusion from the vessel lumen to the deeper layers of the arterial wall. The tunica media, which contains smooth muscle cells that normally maintain vessel structure and function, becomes compromised when these essential nutrients can't reach the cells effectively. This leads to pressure atrophy - a gradual weakening and shrinkage of smooth muscle cells due to mechanical compression and metabolic stress. Eventually, these cells undergo apoptosis (programmed cell death), significantly weakening the vessel wall. This makes option D correct. Option A is incorrect because the tunica media actually weakens rather than strengthens - hyperplasia and hypertrophy would suggest the opposite of what actually occurs. Option B misidentifies the pathological process; amyloid deposition is characteristic of different diseases like Alzheimer's or certain vasculopathies, not typical atherosclerosis. Option C describes an inflammatory process more characteristic of autoimmune conditions; while atherosclerosis involves inflammation, B-lymphocyte infiltration and ectopic lymphoid follicles in the media aren't primary features of atherosclerotic progression. For pathophysiology exams, remember that atherosclerosis questions often test your understanding of both primary lesion formation and secondary effects on surrounding tissues. Focus on how mechanical and metabolic consequences of plaque formation affect the entire vessel wall structure.

Question 2

Cigarette smoking is a potent risk factor for PAD. It accelerates atherosclerosis through multiple mechanisms. Which of the following describes a direct toxic effect of nicotine and other components of tobacco smoke on the vascular endothelium?

  1. They increase the production and bioavailability of the vasodilator nitric oxide.
  2. They promote an anti-inflammatory phenotype in resident macrophages within the intima.
  3. They cause endothelial activation, increase oxidative stress, and promote a prothrombotic state. (correct answer)
  4. They decrease circulating levels of LDL cholesterol and prevent its oxidation.
Explanation: Components of cigarette smoke, including nicotine and reactive oxygen species, are directly toxic to the vascular endothelium. They cause endothelial activation, which involves increased expression of adhesion molecules, enhanced permeability, and a shift towards a pro-inflammatory and prothrombotic state. Smoking also increases oxidative stress, which reduces nitric oxide bioavailability (impairing vasodilation) and promotes the oxidation of LDL, a key step in atherogenesis.

Question 3

A study investigates the role of inflammatory cytokines in PAD. Patients with severe claudication are found to have significantly elevated plasma levels of Tumor Necrosis Factor-alpha (TNF-α) compared to healthy controls.

Based on the passage, what is the most likely mechanism by which elevated TNF-α contributes to the pathophysiology of PAD?

  1. It promotes systemic vasodilation, causing a steal phenomenon that shunts blood away from ischemic limbs.
  2. It induces an anti-inflammatory state in the endothelium, promoting plaque regression and stability.
  3. It enhances endothelial expression of adhesion molecules and promotes a procoagulant surface. (correct answer)
  4. It stimulates the renal clearance of LDL cholesterol, reducing the lipid burden in the vessel wall.
Explanation: TNF-α is a potent pro-inflammatory cytokine that plays a central role in atherosclerosis. It acts on endothelial cells to increase their expression of adhesion molecules (like VCAM-1 and ICAM-1), which facilitates the recruitment of leukocytes into the vessel wall. It also shifts the endothelial phenotype towards a procoagulant state by increasing the expression of tissue factor and decreasing the expression of anticoagulant molecules, thereby promoting both plaque progression and thrombotic complications.

Question 4

In the context of PAD, oxidized low-density lipoprotein (oxLDL) is a key pathogenic molecule. Beyond being engulfed by macrophages to form foam cells, what is another crucial pro-atherogenic role of oxLDL within the vessel wall?

  1. It directly stimulates the proliferation of endothelial cells, leading to intimal hyperplasia.
  2. It inhibits the expression of adhesion molecules, preventing further leukocyte recruitment.
  3. It is chemotactic for smooth muscle cells and stimulates their migration from the media to the intima. (correct answer)
  4. It enhances the bioavailability of nitric oxide, promoting vasodilation and plaque stabilization.
Explanation: oxLDL has multiple pro-atherogenic effects. In addition to being taken up by macrophages, it acts as a chemoattractant, drawing smooth muscle cells from the tunica media into the tunica intima. Once in the intima, oxLDL and other factors stimulate these SMCs to proliferate and synthesize extracellular matrix (e.g., collagen), which contributes to the growth of the plaque and formation of the fibrous cap.

Question 5

A patient with PAD undergoes successful revascularization for a severe femoral artery stenosis. Immediately following the procedure, he develops increased pain, swelling, and muscle weakness in the limb. This ischemia-reperfusion injury is mediated primarily by:

  1. The sudden washout of accumulated lactic acid, causing a systemic metabolic alkalosis.
  2. The rapid influx of neutrophils and the generation of reactive oxygen species (ROS) in the newly perfused tissue. (correct answer)
  3. A parasympathetic nerve reflex triggered by restored blood flow, leading to profound vasodilation and edema.
  4. The dislodgement of the atherosclerotic plaque, which embolizes to the microvasculature.
Explanation: Ischemia-reperfusion injury is a paradoxical phenomenon where tissue damage is exacerbated upon restoration of blood flow. During the ischemic period, ATP is degraded to hypoxanthine. Upon reoxygenation, the enzyme xanthine oxidase converts hypoxanthine into uric acid, generating a burst of damaging reactive oxygen species (ROS). The restored flow also brings neutrophils to the area, which become activated and release more ROS and proteolytic enzymes, leading to microvascular damage, increased permeability, edema, and further tissue injury.

Question 6

A 72-year-old patient with critical limb ischemia (CLI) complains of burning pain in his foot that is worse at night when he is lying flat and is partially relieved by dangling the foot over the side of the bed. What is the pathophysiological explanation for the nocturnal exacerbation and postural relief of this rest pain?

  1. Gravity assists arterial inflow to the distal extremity when the leg is in a dependent position. (correct answer)
  2. Lying supine increases venous return, which paradoxically reduces arterial perfusion pressure.
  3. Nocturnal drops in heart rate and blood pressure reduce perfusion below a critical ischemic threshold.
  4. Metabolic demand of the peripheral nerves decreases when the leg is elevated.
Explanation: In CLI, arterial perfusion is so severely compromised that it is insufficient to meet even the basal metabolic demands of the tissues, especially nerves, causing rest pain. When the patient is supine, the heart must pump blood against gravity is minimal, but there's no gravitational assist. When the patient dangles the leg, gravity provides a small but significant hydrostatic pressure that assists the flow of blood down the arterial system to the foot, slightly improving perfusion and temporarily relieving the ischemic pain.

Question 7

A patient with established PAD is noted to have an ankle-brachial index (ABI) of 0.6. According to Poiseuille's law, which states that flow is proportional to the radius to the fourth power (r⁴), what is the primary hemodynamic consequence of the atherosclerotic lesion responsible for this ABI value?

  1. A substantial increase in blood viscosity due to systemic inflammation.
  2. A modest reduction in vessel radius causing a disproportionately large decrease in blood flow. (correct answer)
  3. An elongation of the stenotic segment, which linearly increases resistance to flow.
  4. A compensatory increase in perfusion pressure proximal to the stenosis.
Explanation: Poiseuille's law highlights the critical relationship between vessel radius and blood flow. Because flow is proportional to the radius to the fourth power, even a seemingly small reduction in the internal radius of an artery due to an atherosclerotic plaque causes a very significant, exponential decrease in the potential blood flow through that segment. This dramatic reduction in flow, and consequently pressure distal to the lesion, is the main reason for the decreased ABI and the resulting tissue ischemia.

Question 8

Leriche syndrome is a specific form of PAD involving occlusion of the aortoiliac segment. The classic triad of symptoms is claudication of the buttocks and thighs, absent femoral pulses, and erectile dysfunction. The erectile dysfunction is a direct result of:

  1. Ischemia of the sacral spinal cord nerves controlling erectile function.
  2. Compression of the pudendal nerve by the enlarged, atherosclerotic aorta.
  3. Psychogenic factors related to the stress of having a severe vascular disease.
  4. Reduced perfusion pressure in the internal pudendal arteries, which supply the corpora cavernosa. (correct answer)
Explanation: When you encounter questions about Leriche syndrome, focus on the underlying vascular anatomy and how aortoiliac occlusion affects downstream blood flow to understand the pathophysiology of each symptom. Leriche syndrome results from occlusion of the aortoiliac segment, which compromises blood flow to all structures supplied by the internal iliac arteries and their branches. Erectile function depends on adequate blood flow to the corpora cavernosa of the penis, which are supplied by the internal pudendal arteries—branches of the internal iliac arteries. When the aortoiliac segment is occluded, perfusion pressure drops significantly in these arteries, making it impossible to achieve the increased blood flow and engorgement necessary for erection. This explains why option D is correct. Option A incorrectly suggests a neurological cause. The sacral nerves controlling erectile function remain intact in Leriche syndrome—the problem is purely vascular, not neurogenic. Option B proposes mechanical compression of the pudendal nerve, but atherosclerotic plaques cause luminal narrowing and occlusion rather than external compression of nearby structures. Option C attributes the erectile dysfunction to psychological factors, but this misses the direct physiological mechanism. While chronic illness can have psychological effects, the erectile dysfunction in Leriche syndrome has a clear organic vascular cause. Remember that in peripheral arterial disease, symptoms directly correlate with which vascular territories are affected. Aortoiliac disease impacts the buttocks, thighs, and erectile function because these structures all depend on branches of the internal iliac arteries for their blood supply.

Question 9

Diabetes mellitus is a major risk factor for PAD and is associated with a more aggressive and diffuse pattern of disease. A key pathophysiological mechanism unique to hyperglycemia that accelerates atherosclerosis in these patients is:

  1. The formation of advanced glycation end-products (AGEs) that cross-link collagen and trap LDL. (correct answer)
  2. A profound decrease in circulating triglycerides, which reduces substrate for foam cell formation.
  3. Enhanced insulin signaling within vascular smooth muscle cells, promoting an anti-proliferative state.
  4. Hypo-osmolar cellular stress leading to endothelial cell apoptosis and desquamation.
Explanation: Hyperglycemia promotes the non-enzymatic glycation of proteins and lipids, forming advanced glycation end-products (AGEs). In the vessel wall, AGEs cross-link collagen, increasing arterial stiffness. They also bind to their receptor (RAGE) on endothelial cells and macrophages, promoting oxidative stress and inflammation. Furthermore, glycated matrix proteins can trap LDL particles in the intima, increasing their susceptibility to oxidation and uptake by macrophages, thereby accelerating plaque formation.

Question 10

In patients with PAD, chronic ischemia induces adaptive changes in the skeletal muscle of the affected limb. Which of the following represents a key metabolic adaptation within the muscle fibers aimed at coping with chronic hypoperfusion?

  1. A shift from oxidative (Type I) to glycolytic (Type II) fiber predominance. (correct answer)
  2. Increased mitochondrial density and enhanced capacity for aerobic respiration.
  3. Upregulation of myoglobin content to improve intracellular oxygen storage.
  4. Decreased activity of enzymes involved in fatty acid oxidation.
Explanation: Paradoxically, chronic ischemia in PAD leads to maladaptive changes in skeletal muscle. Instead of enhancing oxidative capacity, the muscle undergoes a fiber-type shift from fatigue-resistant, oxidative Type I fibers to fatigue-prone, glycolytic Type II fibers. This is accompanied by mitochondrial dysfunction, decreased capillary density, and muscle atrophy, which collectively worsen the muscle's ability to utilize the limited oxygen available, contributing to the symptoms of claudication.

Question 11

A patient with severe PAD develops a painful, non-healing ulcer on the tip of their third toe. Histological examination of a biopsy from the ulcer edge would most likely reveal tissue necrosis and a sparse inflammatory infiltrate. This condition, known as an arterial ulcer, is pathologically distinguished from a venous ulcer by which feature?

  1. Significant hemosiderin deposition in the surrounding dermis from red blood cell extravasation.
  2. A primary defect in arterial inflow leading to profound tissue ischemia and cellular death. (correct answer)
  3. Evidence of incompetent venous valves leading to retrograde blood flow and tissue edema.
  4. A robust granulation tissue response stimulated by high oxygen tension at the wound base.
Explanation: Arterial ulcers are caused by insufficient arterial blood supply (inflow), leading to severe tissue ischemia, hypoxia, and ultimately necrosis. This is the fundamental pathophysiological difference from venous ulcers, which are caused by sustained venous hypertension (impaired outflow) leading to edema, inflammation, and hemosiderin deposition. The ischemia in arterial ulcers also impairs the inflammatory and healing responses, resulting in sparse granulation tissue.

Question 12

In long-standing PAD, physical examination often reveals trophic changes such as thickened toenails, hair loss, and shiny, atrophic skin on the affected limb. These changes are a direct consequence of:

  1. Peripheral sensory neuropathy leading to unnoticed repetitive trauma.
  2. Chronic ischemia causing diminished metabolic activity and atrophy of dermal appendages. (correct answer)
  3. Impaired lymphatic drainage secondary to arterial inflammation.
  4. Hemosiderin deposition from chronic venous hypertension.
Explanation: The skin and its appendages (hair follicles, nail beds, sweat glands) are metabolically active tissues. Chronic hypoperfusion due to PAD reduces the delivery of oxygen and nutrients necessary to sustain their normal function and cell turnover. This leads to atrophy of these structures, resulting in the characteristic clinical findings of hair loss (alopecia), slow-growing and thickened nails, and thin, shiny, fragile skin.

Question 13

Diabetes mellitus is a major risk factor for PAD and is associated with a more aggressive and diffuse pattern of disease. A key pathophysiological mechanism unique to hyperglycemia that accelerates atherosclerosis in these patients is:

  1. The formation of advanced glycation end-products (AGEs) that cross-link collagen and trap LDL. (correct answer)
  2. A profound decrease in circulating triglycerides, which reduces substrate for foam cell formation.
  3. Enhanced insulin signaling within vascular smooth muscle cells, promoting an anti-proliferative state.
  4. Hypo-osmolar cellular stress leading to endothelial cell apoptosis and desquamation.
Explanation: Hyperglycemia promotes the non-enzymatic glycation of proteins and lipids, forming advanced glycation end-products (AGEs). In the vessel wall, AGEs cross-link collagen, increasing arterial stiffness. They also bind to their receptor (RAGE) on endothelial cells and macrophages, promoting oxidative stress and inflammation. Furthermore, glycated matrix proteins can trap LDL particles in the intima, increasing their susceptibility to oxidation and uptake by macrophages, thereby accelerating plaque formation.

Question 14

The initial step in the formation of an atherosclerotic plaque in peripheral artery disease (PAD) is endothelial dysfunction. In a patient with hyperlipidemia, which of the following molecular events is a primary consequence of this initial dysfunction, directly facilitating the progression to a fatty streak?

  1. Increased production of nitric oxide (NO), leading to excessive vasodilation and lipid trapping.
  2. Migration and proliferation of vascular smooth muscle cells (VSMCs) into the tunica intima.
  3. Upregulation of vascular cell adhesion molecule-1 (VCAM-1) on endothelial cells, promoting monocyte binding. (correct answer)
  4. Formation of a fibrous cap by activated platelets and fibrin deposition over the endothelium.
Explanation: Endothelial dysfunction, often caused by risk factors like hyperlipidemia, leads to a pro-inflammatory state. A key event is the upregulation of adhesion molecules like VCAM-1 on the endothelial surface. This allows circulating monocytes to adhere to the endothelium, which is the prerequisite step for their subsequent migration into the tunica intima, differentiation into macrophages, and uptake of oxidized LDL to become foam cells, forming the fatty streak.

Question 15

In the context of PAD, oxidized low-density lipoprotein (oxLDL) is a key pathogenic molecule. Beyond being engulfed by macrophages to form foam cells, what is another crucial pro-atherogenic role of oxLDL within the vessel wall?

  1. It directly stimulates the proliferation of endothelial cells, leading to intimal hyperplasia.
  2. It inhibits the expression of adhesion molecules, preventing further leukocyte recruitment.
  3. It is chemotactic for smooth muscle cells and stimulates their migration from the media to the intima. (correct answer)
  4. It enhances the bioavailability of nitric oxide, promoting vasodilation and plaque stabilization.
Explanation: oxLDL has multiple pro-atherogenic effects. In addition to being taken up by macrophages, it acts as a chemoattractant, drawing smooth muscle cells from the tunica media into the tunica intima. Once in the intima, oxLDL and other factors stimulate these SMCs to proliferate and synthesize extracellular matrix (e.g., collagen), which contributes to the growth of the plaque and formation of the fibrous cap.

Question 16

A 72-year-old patient with critical limb ischemia (CLI) complains of burning pain in his foot that is worse at night when he is lying flat and is partially relieved by dangling the foot over the side of the bed. What is the pathophysiological explanation for the nocturnal exacerbation and postural relief of this rest pain?

  1. Gravity assists arterial inflow to the distal extremity when the leg is in a dependent position. (correct answer)
  2. Lying supine increases venous return, which paradoxically reduces arterial perfusion pressure.
  3. Nocturnal drops in heart rate and blood pressure reduce perfusion below a critical ischemic threshold.
  4. Metabolic demand of the peripheral nerves decreases when the leg is elevated.
Explanation: In CLI, arterial perfusion is so severely compromised that it is insufficient to meet even the basal metabolic demands of the tissues, especially nerves, causing rest pain. When the patient is supine, the heart must pump blood against gravity is minimal, but there's no gravitational assist. When the patient dangles the leg, gravity provides a small but significant hydrostatic pressure that assists the flow of blood down the arterial system to the foot, slightly improving perfusion and temporarily relieving the ischemic pain.

Question 17

A patient with established PAD is noted to have an ankle-brachial index (ABI) of 0.6. According to Poiseuille's law, which states that flow is proportional to the radius to the fourth power (r⁴), what is the primary hemodynamic consequence of the atherosclerotic lesion responsible for this ABI value?

  1. A substantial increase in blood viscosity due to systemic inflammation.
  2. A modest reduction in vessel radius causing a disproportionately large decrease in blood flow. (correct answer)
  3. An elongation of the stenotic segment, which linearly increases resistance to flow.
  4. A compensatory increase in perfusion pressure proximal to the stenosis.
Explanation: Poiseuille's law highlights the critical relationship between vessel radius and blood flow. Because flow is proportional to the radius to the fourth power, even a seemingly small reduction in the internal radius of an artery due to an atherosclerotic plaque causes a very significant, exponential decrease in the potential blood flow through that segment. This dramatic reduction in flow, and consequently pressure distal to the lesion, is the main reason for the decreased ABI and the resulting tissue ischemia.

Question 18

A patient with PAD undergoes successful revascularization for a severe femoral artery stenosis. Immediately following the procedure, he develops increased pain, swelling, and muscle weakness in the limb. This ischemia-reperfusion injury is mediated primarily by:

  1. The sudden washout of accumulated lactic acid, causing a systemic metabolic alkalosis.
  2. The rapid influx of neutrophils and the generation of reactive oxygen species (ROS) in the newly perfused tissue. (correct answer)
  3. A parasympathetic nerve reflex triggered by restored blood flow, leading to profound vasodilation and edema.
  4. The dislodgement of the atherosclerotic plaque, which embolizes to the microvasculature.
Explanation: Ischemia-reperfusion injury is a paradoxical phenomenon where tissue damage is exacerbated upon restoration of blood flow. During the ischemic period, ATP is degraded to hypoxanthine. Upon reoxygenation, the enzyme xanthine oxidase converts hypoxanthine into uric acid, generating a burst of damaging reactive oxygen species (ROS). The restored flow also brings neutrophils to the area, which become activated and release more ROS and proteolytic enzymes, leading to microvascular damage, increased permeability, edema, and further tissue injury.

Question 19

Cigarette smoking is a potent risk factor for PAD. It accelerates atherosclerosis through multiple mechanisms. Which of the following describes a direct toxic effect of nicotine and other components of tobacco smoke on the vascular endothelium?

  1. They increase the production and bioavailability of the vasodilator nitric oxide.
  2. They promote an anti-inflammatory phenotype in resident macrophages within the intima.
  3. They cause endothelial activation, increase oxidative stress, and promote a prothrombotic state. (correct answer)
  4. They decrease circulating levels of LDL cholesterol and prevent its oxidation.
Explanation: Components of cigarette smoke, including nicotine and reactive oxygen species, are directly toxic to the vascular endothelium. They cause endothelial activation, which involves increased expression of adhesion molecules, enhanced permeability, and a shift towards a pro-inflammatory and prothrombotic state. Smoking also increases oxidative stress, which reduces nitric oxide bioavailability (impairing vasodilation) and promotes the oxidation of LDL, a key step in atherogenesis.

Question 20

While atherosclerosis affects the tunica intima, its progression also significantly impacts the tunica media. What is a primary pathological change that occurs in the tunica media underlying a large atherosclerotic plaque?

  1. Hyperplasia and hypertrophy of smooth muscle cells, strengthening the vessel wall.
  2. Deposition of amyloid protein, leading to increased vessel wall compliance.
  3. Infiltration by B-lymphocytes and formation of ectopic lymphoid follicles.
  4. Pressure atrophy and apoptosis of smooth muscle cells due to impaired nutrient diffusion. (correct answer)
Explanation: When approaching questions about atherosclerosis progression, remember that this disease process affects multiple layers of the arterial wall, not just the intima where plaques form. Understanding the secondary effects on deeper layers is crucial for grasping the complete pathophysiology. Large atherosclerotic plaques create a mechanical barrier that impairs nutrient and oxygen diffusion from the vessel lumen to the deeper layers of the arterial wall. The tunica media, which contains smooth muscle cells that normally maintain vessel structure and function, becomes compromised when these essential nutrients can't reach the cells effectively. This leads to pressure atrophy - a gradual weakening and shrinkage of smooth muscle cells due to mechanical compression and metabolic stress. Eventually, these cells undergo apoptosis (programmed cell death), significantly weakening the vessel wall. This makes option D correct. Option A is incorrect because the tunica media actually weakens rather than strengthens - hyperplasia and hypertrophy would suggest the opposite of what actually occurs. Option B misidentifies the pathological process; amyloid deposition is characteristic of different diseases like Alzheimer's or certain vasculopathies, not typical atherosclerosis. Option C describes an inflammatory process more characteristic of autoimmune conditions; while atherosclerosis involves inflammation, B-lymphocyte infiltration and ectopic lymphoid follicles in the media aren't primary features of atherosclerotic progression. For pathophysiology exams, remember that atherosclerosis questions often test your understanding of both primary lesion formation and secondary effects on surrounding tissues. Focus on how mechanical and metabolic consequences of plaque formation affect the entire vessel wall structure.