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Cardiovascular > Vascular Pathology 1 > Flashcards

Vascular Pathology 1 Flashcards

1
Q

Vascular Anomalies

A

1) BERRY ANEURYSMS:
- Typically found in the CIRCLE OF WILLIS

  • Associated with ADPKD
  • RUPTURE can cause FATAL SUBARACHNOID Hemorrhage

2) ARTERIOVENOUS FISTULAS:
- Artery —> Vein

  • Most commonly a DEVELOPMENTAL DEFECT, but may arise SECONDARY to Inflammation, Trauma, Rupture
  • May lead to RUPTURE and HEMORRHAGE, or to HIGH-OUTPUT Cardiac Failure

3) FIBROMUSCULAR DYSPLASIA:
- Focal THICKENING of INTIMA and MEDIA of Medium to Large Muscular Arteries, resulting in STENOSIS

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2
Q

Vascular Response to Injury

Normal vs Activated

A

1) Endothelial cells normally maintain a NONTHROMBOGENIC SURFACE under Normal Conditions
- Normotension, Laminar Blood Flow

2) Certain stimuli can INDUCE CHANGE in Endothelial Cell function leading to an ACTIVATED STATE:
- Turbulent Blood Flow
- Hypertension
- Complement, Bacterial Products, Lipid Products, Glycation End Products
- Viruses
- Hypoxia, Acidosis
- Components of Tobacco Smoke

3) The ACTIVATED STATE is characterized by expression of:
- ADHESION Molecules
- PROCOAGULATS and ANTICOAGULANTS
- VASOACTIVE Factors, GRWOTH Factors

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3
Q

Vascular Injury

Endothelial Dysfunction

A

1) Under Normal circumstances, Endothelial cells can cycle between BASAL and ACTIVATED STATES, to respond to various stimuli

2) When certain Stimuli are consistently present, however, the prolonged ACTIVATED STATE of the Endothelium may lead to ENDOTHELIAL DYSFUNCTION, often characterized by:
- Procoagulaiton
- Proinflamamtion
- Smooth Muscle Stimulation

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4
Q

Vascular Injury

Intimal Thickening

A

1) Loss of Endothelial cells secondary to tissue damage, or prolonged Endothelial Dysfunction leads to Vascular Injury

2) The stereotypical response to Vascular Injury is INTIMAL THICKENING!!!!!!!
- Smooth Muscle cells from the MEDIA MIGRATE to the INTIMA, where they PROLIFERATE and ELABORATE EXTRACELLULAR MATRIX

  • The INTIMA is thus thickened, potentially affecting BLODD FLOW in that Vessel
    3) Vascular Intimal Thickening is seen in response to any injury to the vessel, regardless of cause
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5
Q

Hypertensive Vascular Disease

General

A

1) Hypertension is ABNORMALLY High Blood Pressure (Systolic and/or Diastolic), which if untreated, may lead to END ORGAN DAMAGE
2) Almost 30% of the General Population is Hypertensive by guideline Criteria
3) INCREASED Prevalence is seen with ADVANCING AGE, and among African-Americans

4) HTN is a risk factor for:
- Atherosclerosis, Aortic Dissection
- Hypertensive Heart Disease
- Stroke
- Hypertensive Renal Disease

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6
Q

Hypertensive Vascular Disease

Risk Factors

A

1) In most people with HTN it is IDIOPATHIC, or ESSENTIAL HYPERTENSION (90 - 95%)
2) The remainder have SECONDARY HYPERTENSION, which is usually caused by a RENAL or ENDOCRINE DISORDER

3) Risk Factors for Essential HTN Include:
- High Sodium Intake
- Obesity
- Stress
- Smoking
- Physical Inactivity

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7
Q

Blood Pressure Components

A

BP = CO x TPR

CO:

1) Blood Volume
- Sodium
- Mineralcortoids
- Atrial Natriuteric Peptide

2) Cardiac Factors:
- Heart Rate
- Contractility

Peripheral Resistance
1) Humoral Constrictors and Dilators

2) Neural Constrictor and Dilators

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8
Q

Blood Pressure Regulation

A
  • BLOOD VOLUME and VASCULAR TONE is modified and maintained by the RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
  • In states of Low Volume or Low Peripheral Resistance, or a Decreased Glomerular Filtration Rate, RENIN is released by JUXTAGLOMERULAR CELLS in the AFFERENT ARTERIOLES in the Kidneys
  • Renin cleaves circulation ANGIOTENSINOGEN to form ANGIOTENSIN I
  • Angiotensin I is cleaved to form ANGIOTENSIN II by ACE
  • ANG II is a potent but short lived VASOCONSTRICTOR!!!!!
  • ANG II also stimulates Adrenal Cortex to release ALDOSTERONE, causing RENAL REABSORPTION of SODIUM and WATER
  • Resistance and Volume are INCREASED, Raising Blood Pressure
  • The volume expansion induces Myocardial Release of ATRIAL NATRIURETIC PEPTIDE, leading to Na+ Excretion and Diuresis, as well as Vasodilation, thus LOWERING Blood Pressure
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9
Q

Vascular Morphologic Changes in HTN

HYALINE ARTERIOSCLEROSIS

A
  • Increased Smooth Muscle Matrix Synthesis
  • Plasma PROTEIN LEAKAGE ACROSS DAMAGED ENDOTHELIUM!!!!!
  • Homogenous PINK (HYALINE) Thickening of the Vessel Wall, with associated LUMINAL NARROWING
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10
Q

Vascular Morphologic Changes in HTN

HYPERPLASTIC ARTERIOLOSCLEROSIS

A
  • Occurs in SEVERE HYPERTENSION

- SMOOTH MUSCLE CELLS form CONCETRIC LAMELLATION (“ONION SKINNING”) with resultant LUMINA NARROWING!!!!!

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11
Q

Atherosclerosis

A

1) Fibrous Cap:
- Smooth Muscle Cells, Macrophages, Foam Cells, Lymphocytes, Collagen

2) Necrotic Center:
- Cell Debris, Cholesterol Crystals, Foam Cells, Calcium

3) Media

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12
Q

Epidemiology and Risk Factors of Atherosclerosis

A

1) EXTREMELY COMMON, especially in the developed world
- “Causes more morbidity and Mortality (roughly half of all deaths) in the Western World than any other disorder

2) Prevalence and extent of disease is related to Multiple Risk Factors, which have SYNERGISTIC EFFECT!!!!
3) Constitutional and Modifiable Risk Factors

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13
Q

Constitutional Risk Factors of Atherosclerosis

A

1) Family History
2) Age
3) Gender

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14
Q

Modifiable Risk Factors (Major) of Atherosclerosis

A

1) HYPERLIPIDEMAI (Especially LDL)
2) HYPERTENSION
3) SMOKING
4) DIABETES MELLITUS

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15
Q

Other Modifiable Risk Factors for Atherosclerosis

A

1) Inflammation
2) Hyperhomocystinemia
3) Metabolic Syndrome

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16
Q

Pathogenesis of Atherosclerosis

Response to Injury Model

A
  • Chronic injury and/ or Dysfunction of Endothelium, leading to Chronic Inflammation and attempts to REPAIR THE TISSUE
    1) Chronic Endothelial “Injury”
    2) Endothelial Dysfunction
    3) Macrophage Activation, Smooth Muscle Activation
    4) Macrophage and Smooth Muscle Cells ENGULF LIPID (Fatty Streak)
    5) Smooth Muscle Proliferation, Collagen and other Extracellular Matrix Deposition, Extracellular Lipid
17
Q

Pathogenesis of Atherosclerosis

Endothelial Injury and Dysfunction

A

1) HEMODYNAMIC TURBULENCE:
- Atherosclerosis does NOT occur randomly in Vessels, nor does it occur everywhere uniformly

  • most lesion tend to occur at opening of EXITING VESSELS, Branch Points, Posterior Abdominal Aorta, due to flow disturbances normally seen in these locations

2) CIRCULATING LIPIDS:
- Lipids in Atheromatous plaques are predominantly CHOLESTEROL and CHOLESTEROL ESTERS

  • Accumulate in the INITMA, are taken up by MACROPHAGES and partially Oxidized
  • This modified LDL further accumulates within Macrophages and Smooth Muscle cells, forming FOAM CELLS and a lesion known as “FATTY STREAK”
  • This stimulates an Inflammatory response to accumulation of this toxic form of LDL
18
Q

Pathogenesis of Atherosclerosis

Inflammation

A
  • Accumulation of CHOLESTEROL CRYSTALS WITHIN MACROPHAGES is recognized by the Inflammasome, which leads to IL-1 SECRETION
  • More Macrophages and T-Lymphocytes are RECRUITED and ACTIVATED
  • Inflammatory CYTOKINES further activate ENDOTHELIAL CELLS, and Growth Factors stimulate Smooth Muscle Cells to MIGRATE to the INTIMA and PROLIFERATE
19
Q

Pathogenesis of Atherosclerosis

Smooth Muscle Proliferation and Matrix Deposition

A
  • Proliferating Smooth Muscle cells Synthesize Extracellular matrix including COLLAGEN
  • Due to the INTIMAL EXPANSION from FOAM CELLS and Extracellular Lipid, recruited inflammatory and Smooth Muscle Cells and INCREASED ECM, as ATHEROMATOUS PLAQUE is Formed!!!!!!!!
  • Over time, a SOFT Fibrofatty plaque becomes covered with a FIBROUS CAP (Dense Collagen Fibers). The Center of the Plaque is NECROTIC**, containing Lipid, Debris, FOAM CELLS and Thrombus, surrounded by a zone of Inflammatory and Smooth Muscle Cells
20
Q

Common Sites of Atherosclerosis Involvement

A

Descending order of Frequency:

  • Abdominal Aorta
  • Coronary Arteries
  • Popliteal Arteries
  • Internal Carotid Arteries
  • Circle of Willis
21
Q

Complications of Atherosclerotic Plaques

A

1) Rupture and Ulceration
- May lead to Thrombosis

2) Hemorrhage
- May follow Plaque Rupture

3) Embolism
- May follow Plaque Rupture

4) Aneurysm Formation

22
Q

Consequences of Atherosclerosis

1) STENOSIS of the ARTERIAL LUMEN

A
  • Plaques tend to continually grow because of repeated cycling through the Injury-Healing Process
  • The lumen of the affected Vessel gradually SHRINKS, eventually leading to ISCHEMIA DOWNSTREAM (A point known as CRITICAL STENOSIS- approximately 70% OCCLUDED!!!)
  • This may lead to Chronic Ischemia of Myocardium, Bowel, Brain, the Extremities
23
Q

Consequences of Atherosclerosis

2) ACUTE PLAQUE CHANGE

A
  • AN Acute THROMBUS may form over the Plaque, occluding the Artery. This may occur secondary to:
    a) RUPTURE of the Plaque
    b) EROSION or ULCERATION of the Plaque Surface
  • Hemorrhage into the plaque may acutely expand its volume
24
Q

Consequences of Atherosclerosis

3) SOME PLAQUES are MORE PRONE to RUPTURE THAN OTHERS

A
  • The FIBROUS CAP is continually being degraded and Resynthesizes (Remodeled)
  • INCREASED Inflammation in the plaque can ACCELERATE FIBROUS CAP DEGREDATION and INHIBIT ITS RESYNTHESIS, thus reducing the amount of Collagen in the Cap and Weakening it
  • Physical STRESSES can cause Plaque Disruption:
    a) Changes in Blood Pressure
    b) Vasoconstriction
25
Q

Aneurysms

A
  • A localized ABNORMAL DILATION of a BLOOD VESSEL or the Hear that may be CONGENITAL OR ACQUIRED
  • A “TRUE” Aneurysm is characterized by an INTACT (but thinned) MUSCULAR WALL at the SITE of the DILATION
  • A “FALSE” Aneurysm is a defect through the wall of the vessel or heart communication with an EXTRAVASCULAR HEMATOMA!!!!!
26
Q

Aneurysm Pathogenesis

A

1) An Aneurysm may occur whenever the Connective Tissue of the Vascular Wall is weakened, whether by acquired or Congenital Conditions
a) Defective Vascular Wall Connective Tissue (MARFAN SYNDROME: Defective FIBRILLAR Synthesis)

b) Net Degradation of Vascular Wall Connective Tissue (Inflammatory conditions such as Atherosclerosis —> Incr Matrix Metalloprotease

c) Weakening of the Vascular Wall by Ischemia
- ATHEROSCLEROSIS —> Ischemia of INNER Media

  • HYPERTENSION: Ischemia of OUTER Media
  • TERTIARY SYPHILIS: Ischemia of OUTER MEDIA (Thoracic Aorta)
27
Q

Aneurysm Pathogenesis

* Cystic Medial Degeneration*

A
  • Loss of Vascular Wall elastic tissue, or Ineffective ELASTIN SYNTHESSIS< leads to CYSTIC MEDIAL DEGENERATION, with disrupted and disorganized ELASTIN FILAMENTS and INCREASED Ground Substance (PROTEOGLYCANS!!!!!)
  • Cystic Medial Degeneration is a final common result of different conditions, including Ischemic Medial Damage and AMRFAN SYNDROME
  • The two most important causes of AORTIC ANEURYSMS are 1) ATHEROSCLEROSIS and 2) HYPERTENSION!!!!!
28
Q

Abdominal Aortic Aneurysm

A

1) Typically due to ATHEROSCLEROSIS!!!
2) Occur in the ABDOMINAL Aorta, usually BELOW the renal arteries, and often involve the common iliac arteries

3) More frequent in:
◦ Men
◦ Smokers
◦ 6th decade of life

4) Characterized by SEVERE ATHEROSCLEROSIS of the AORTA, of the aorta, covered with MURAL THROMBUS
5) May be detected as a PULSATING MASS in the abdomen!!!!!!!!

6) Complications include:
◦ RUPTURE and HEMORRHAGE
◦ OCCLUSION of branching arteries and downstream ischemia 
◦ EMBOLISM
◦ Impingement on another structure
29
Q

Abdominal Aortic Aneurysm Rupture risk is related to Aneurysm size

A

Less than 4 cm:
- Negligible

4 to 5 cm:
- 1%

5 to 6 cm:
- 11% Rupture!!!!!

Greater than 6cm:
- 25% RUPTURE!!!!

30
Q

Thoracic Aortic Aneurysm

A

1) Often due to HYPERTENSION, or less commonly congenital defect in connective tissue synthesis (MARFAN)

2) Clinical presentation often due to:
◦ Impingement
a) Lower respiratory tree
b) Esophagus
c) Recurrent Laryngeal Nerves

◦ Aortic valvular insufficiency
◦ Rupture

31
Q

Aortic Dissection

A

1) Occurs when BLOOD ENTERS DEFECT in the INTIMA and travels through a tissue plane within layers of the aortic media.

2) Aortic dissection OCCURS IN:
◦ Hypertensive males, 40-60
◦ Patients with disorders of vessel connective tissue (Marfan)

3) The primary risk factor is HYPERTENSION!!!!!!
4) Classic Presentation: SEVERE CHEST PAIN, RADIATING OT THE BACK BETWEEN THE SCAPULAE

32
Q

Aortic Dissection Pathogenesis

A

1) BLOOD ENTERS AORTIC WALL VIA AN INTIMAL TEAR (cause generally unknown), forming an intramural hematoma
2) Usually, in HYPERTENSIVE PATIENTS, there is some degree of CYSTIC MEDIAL DEGENERATION (but in many cases there is little or none)
3) Most dissections arise in the ASCENDING AORTA

33
Q

Type A and B Aortic Dissections

A

1) TYPE A DISSECTIONS: Involving the ASCENDING AORTA, are MORE COMMON and associated with HIGHER MORBIDITY and MORTALITY
2) The MOST COMMON CAUSE of Feath (for Both Types) is RUPTURE. Dissection may also extend along Aterieal Branches of the Aorta, causing potential OCCLUSION of those vessels
3) TYPE A Dissections are treated by ANTIHYPERTENSIVE therapy and an attempt to surgically repair the INTIMAL TEAR!!!

Cardiovascular (4 decks)

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