Systemic Pathology Lecture 2

Front 1

Define Atherosclerosis - 7 major points.

Back 1

(1) Disease of LARGE and MEDIUM sized arteries
(2) Progressive Accumulation of lipids, smooth muscle cels, and connective tissue within the intima.
(3) Intimal thickening with atheroma (fibrofatty plaque) formation.
(4) Narrowing of vessel lumen can cause ischemia.
(5) Weakening of tunica media
(6) Major complications account for greater than 50% annual mortality in the US.
(7) Ischemic heart disease is the leading cause of death in the United States.

Front 2

Define the classic Atheroma.

Back 2

The classic atheroma is defined as having a raised focal intimal plaque with a necrotic lipid core, covered by a fibrous cap.

Front 3

What are the constituents of the classic Atheroma?

Back 3

(1) Cells - smooth muscle cells, macrophages, and leukocytes
(2) Connective Tissue extracellular matrix - collagen, elastic fibers, proteoglycans
(3) Lipids - cholesterol and cholesterol esters, intracellular and extracellular

Front 4

What might the center of larger plaques contain?

Back 4

yellow, grumous debris hence, atheroma

Front 5

What is a fatty streak?

Back 5

A fatt streak is
- an early lesion
- possible precursor to an atheroma
- not significantly raised
- no disturbances in blood flow
- Lipid-filled foam cells with T lymphocytes and extracellular lipids
-virtually seen in all children by age 10.

Front 6

What is a fibrofatty plaque?

Back 6

A fibrofatty plaque is
- an intermediate lesion
- focal raised lesions with disturbances in blood flow
- fibrous cap with smooth muscle, monocytes, lymphocytes, foam cells, and connective tissue
- lipid core - necroticc debris, cholesterol, foam cells

Front 7

What is a complicated lesion?

Back 7

- Advanced lesion
- patchy or massive calcification
- causes weakening of tunica media, los of elastic tissue with aneurismal dilation

Front 8

What may cause a complicated lesion to rupture and what happens?

Back 8

Hemorrhage may cause a complcated lesion to rupture or ulcerate which leads to exposure of thrombogenic components or an atheroembolization

Front 9

What is another name for superimposed thrombosis - which may occur in complicated lesions?

Back 9

Superimposed thrombosis is also called atherothrombosisand occurs in complicated lesions.

Front 10

What are some major complications associated with atherosclerosis?

Back 10

- Myocardial Infarction
- Sudden Cardiac death
- Chronic Ischemic Heart Disease
- Aortic Aneurysms
- Cerebral Infarction
- Ischemic Encephalopathy
Peripheral Vascular Disease
- Mesenteric occlusion

Front 11

What are the statistics of Ischemic heart disease?

Back 11

- most common type of heart disease in the USA
- Accounts for more than 80% of cardiac deaths

Front 12

Describe coronary atherosclerosis in relation to fibrofatty and complicated plaques.

Back 12

Fibrofatty and complicated plaques cause inimal and medial thickening with luminal stenosis. Acute plaque change is the critical factor in acute syndromes. Inadequate blood flow increases oxygen demands for the heart.

Front 13

Acute coronary syndroms such as acute MI, unstable angina, and sudden death share a common pathophysiology with

Back 13

Coronary atherosclerotic plaque disruption and intraluminal platelet-fibrin thrombus formation.

Front 14

What are possible causes of acute plaque change?

Back 14

(1) Hemorrhage into atheroma
(2) Rupture or fissuring of plaque, with exposure of thrombogenic constituents
(3) Erosion or ulceration, with exposure of thrombogenic basement membrane

Front 15

What are the three MI localizations? What is the most common of the three?

Back 15

(1) Left Antererior Descending (LAD)
(2) Left Circumflex Artery (LCx)
(3) Right Coronary Artery (RCA)
The most common is LAD.

Front 16

What are the primary manifestations of ischemic heart disease?

Back 16

(1) Angina Pectoris
(2) Myocardial Infarction
(3) Chronic Ischemic Heart Diseas
(4) Sudden Death

Front 17

What are the three types of angina pectoris?

Back 17

(1) Stable Angina - typical angina
(2) Prinzmetal angina - variant angina
(3) Unstable angina - crescendo angina

Front 18

What are some characterisitics of Angina Pectoris?

Back 18

- substernal chest pain of limited duration
- it is the most common symptom of cardiac ischemia, where the stenosed arteries cannot meet the oxygen demands

Front 19

How is stable angina relieved?

Back 19

Stable Angina is relieved by rest and nitroglycerin.

Front 20

Whicn angina can occur at rest? What are each associated with?

Back 20

Atypical and Unstable angina can occur at rest. Atypical angina is associated with coronary spasms while unstable angina is associated with acute plaque change, nonocclusive thrombosis, and vasoconstriction.

Front 21

Describe acute myocardial infarction.

Back 21

Acute myocardial infarction is associated with a discrete focus of ischemic necrosis in the heart. The development of acute MI is related to the duration of the ischemia and metablic rate of ischemic tissue. It is frequently the result of acute plaque change in coronary artery thrombosis. Infarcts involve LV more commony and extensively than RV.

Front 22

What is the duration of ischemia to cause an acute myocardial infartion?
How long does it take for dissolution of thrombus?

Back 22

ischemia to cause an acute myocardial infarction is only 20-30 minutes. It takes usually 12-23 hours for dissolution of thrombus.

Front 23

Describe Sudden Cardiac Death.

Back 23

Sudden cardiac death is unexpected death within 1 hour of onset of cardiac symptoms. It is often the initial presentation of Ischemic Heart Disease.Can occur with or without coronary thrombosis. Frequently, a regional ischemia cuases lethal arrhythmia. Most have severe coronary atherosclerosis with critical stenosis.

Front 24

What are three myocardial infarction complications?

Back 24

(1) myocardial free wall ruptures
(2) aneurysm
(3) Mural thrombosis

Front 25

What is the MI complication - myocardial free wall ruptures?

Back 25

MI free wall ruptures occurs early on - first three weeks. It occurs at junction of infarct and normal muscle. It results in hemopericardium and death from tamponade.

Front 26

What is the myocardial infarction complication - aneurysm?

Back 26

After transmural AMI, wall bulges outward during systole. As infarct matures, fibrous scar progressively stretches. This is increased risk for myocardial rupture Predisposes to mural thrombosis and increases the workload.

Front 27

What is the myocardial complication - mural thrombosis?

Back 27

Mural thrombosis is seen in almost 50% of AMI, especially after apical artifacts. It basically predisposes body to systemic embolization.

Front 28

Describe Myocardial Infarction therapy.

Back 28

Since the size of the infarct is a huge predictor in morbidity and mortality, the goal of therapy is to try to limit its size. It is also important to restore arterial blood flow through (1) thromobolytic enzymes (2) Percutaneous Transluminal Coronary angioplasty (PTCA) and (3) Coronary Artery Bypass Graft (CABG)

Front 29

What is the definition of vascular aneurysms? What is the most common occurence?

Back 29

Vascular aneurysms are localized, abnormal dilations of blood vessels caused by congenital or acquired weakness in the vessel medial - may also occur in the cardiac chamber. The most common occurence is in the aorta or heart.

Front 30

What are the classification of aneurysms?

Back 30

(1) Location
(2) Configuration
(3) Etiology

Front 31

What is the pathogenisis of triple A or Abdominal Aortic Aneurysm? What is it always associated with?

Back 31

AAA is due to abnormal aortic dilation with diameter increased by at least 50%. It is always associated with severe atherosclerosis is 50% associated with hypertension.

Front 32

What is the morphology of Abdominal Aortic Aneurysm?

Back 32

(1) Severe atherosclerosis
(2) Dilation which is distal to renal artery and proximal to iliac bifurcation. There is a frequency for mural thrombosis with potential for thromboembolism.

Front 33

What are the clinical signs of an Abdominal Aortic Aneurysm?

Back 33

The clinical signs include -
(1) Abdominal mass that is pulsatile
(2) Abdominal pain from aneurysm expansion
(3) Acute ischemia to lower limbs.
Rupture is feared.

Front 34

What are the key features of the clasic abdominal aortic aneurysm?

Back 34

(1) Severe atherosclerosis
(2) Infrarenal Location
(3) Fusiform Dilation
(4) Mural thrombosis
(5) Thromboembolism risk
(6) Atheroembolism risk
(7) Rupture

Front 35

What is the definition of aortic dissection?

Back 35

Aortic dissection is defined as a dissection of blood in between and along the laminar planes of the media, forming a blood-filled channel within the aortic wall. It is a dissecting intramural hematoma and frequently ruptures. It is NOT usually associated with an aneurysmal swelling.

Front 36

What are the two groups with aortic dissection predisposition?

Back 36

(1) Men, 40-60 years old, antecedent hypertension
(2) Younger patients with connective tissue disorders - such as Morphan's syndrome

Front 37

What are common predisposing factors to aortic dissection?

Back 37

(1) Weakened aortic media
(2) Most common - cystic medial degeneration
(3) Aging - results in focal elastin loss and medial fibrosis
(4) spontaneous intimal laceration of vasa vaorum hemorrhage

Front 38

What is the morhology for aortic dissection?

Back 38

(1) Intimal tear in ascending aorta
(2) dissection separates the aorta along media - extending proximally and distally
(3) may involve greater vessels
(4) extravascular rupture is the most frequent cause of death
(5) may reenter lumen - "double-barreled aorta"

Front 39

What are the clinical signs of an aortic dissection?

Back 39

- acute onset of severe "tearing" pain in anteror chest, radiating to the back
- loss of arterial pulse
- murmur or aortic regurgitation
- MI
- hypotension
- cardiac tamponade
- overal mortality less than 20%

Front 40

What is the pathogenesis of venous thrombosis?

Back 40

(1) Stasis - heart failure, chronic venous insufficency, postoperative immobilization, prolonged bed rest
(2) Endothelial injury - trauma, surgery, childbirth
(3) Hypercoagulable states - oral contraceptives, late pregnancy, carcinoma
(4) Advanced age
(5) Sickle Cell Anemia

Front 41

what is the natural history of venous thrombosis?

Back 41

(1) Lysis
(2) Propagation
(3) Organization
(4) Embolization

Front 42

Where are the most common venous thrombi?

Back 42

The most common venous thrombi are found in the deep leg veins. These usually remain small but may serve as a nidus for thrombus propagation to involve larter iliofemoral veins. They also may dislodge and be carried to the lungs.

Front 43

What are clinical signs for DVT and pulmonary embolim?

Back 43

DVT is frequently asymptomatic. Calf tendernss. Occlusion DVT associated with conjestion, edema, cyanosis. Large venous thrombi represent a potential hazard to life, may dislodge and be carried to the lungs as pulmonary emboli.

Front 44

What are clinical signs of pulmonary embolism?

Back 44

(1) Massive pulmonary embolism, Cardiac collapse, and sudden death.
(2) Pulmonary infarction with pleuratic chest pain, hemoptysis, and effusion
(3) Pulmonary embolism without infarction, transient dyspnea and tachypnea.

Front 45

What are some potentioal pulmonary emboli sources?

Back 45

(1) Thrombi - most frequent
(2) Air
(3) Tumor
(4) Fat
(5) Amniotic Fluid

Front 46

What is the most frequent source of pulmonary embolism?

Back 46

DVT

Front 47

What is massive thromboembolism associated with?

Back 47

Acute right heart failure.