Page 1
COLLINS MWANANGOMBE SHANDU
MBChB-candidate
university of Lusaka
Applied Clinical Pathology Study notes
VASCULAR DISORDERS
Content;
1. Notes (Exam Preparation)
a. Atherosclerosis ……………………….………… Pg.2-4
b. Aneurysms …………………………………….……. Pg.5-8
c. Hypertension Vascular Disease …….…… Pg.9-10
d. Vasculitis
1) Giant-Cell (Temporal) Arteritis………………… Pg.11
2) Polyarteritis Nodosa ……………………………. Pg.12
3) Wegener's Granulomatosis ……………………. Pg.13
4) Vascular Tumors ……………………………… Pg.14-15
2. Questions Of The Chapter (Tutorial)…………... Pg.16
NOTES
1. ATHEROSCLEROSIS
Def: atherosclerosis is primarily a progressive disease of intima characterized by
lesions called atheroma or grossly characterized by arterial wall thickening due
to deposition of LDL, smooth muscle proliferation in the intima.
Pathophysiology
1. There is an Endothelial dysfunction or injury which cause;
Pathology self-study notes undergraduate Unilus (student)
, Page 2
2. Increased vascular permeability and Platelet adhesion and thrombosis
3. Monocyte and T lymphocytes adhesion to endothelium, monocytes
transformed into macrophages and produce of oxygen free radicals produced
locally together with dysfunctional endothelial cells to oxidize the LDLs and
phagocytose to form foam cells which may undergo apoptosis and release lipids
to form lipid-rich center (necrotic core in atheromatous plaques).
4. LDLs crosses the endothelium into the intima. Oxidized LDL causes
activated macrophages to produce Cytokine increases leukocyte adhesion and
Chemokines
Histology:
intimal smooth muscle cells, cellular debris& cholesterol, foamy macrophages,
macrophages, lymphocytes, adherence platelets, all in the intima.
Gross:
fatty streak, ulcerated plaque, fatty spots.
Complications of atherosclerosis:
1. Aneurysm formation: damage the elastic tissue causes weakening the wall
result in aneurysmal dilation which may rupture.
2. Rupture/ulceration: Plaque protruding can disturb the blood flow resulting in
turbulent flow of blood which can damage the endothelium cause rupture.
2. Hemorrhage into a plaque: It may occur due to rupture of the fibrous cap of
the plaque or of the thin-walled vessels formed due to neovascularization.
3. Thrombosis and embolism: Ulceration exposes blood to highly thrombogenic
subendothelial collagen, favors thrombus formation, occlusive lead to ischemia.
4. Atheroembolism: Plaque rupture, discharge atherosclerotic debris into the
bloodstream and results in atheroemboli.
6. Calcification: It may occur in the central necrotic area of the plaque
(dystrophic calcification).
RISK FACTORS
Modifiable Risk Factors
1. Hyperlipidemia: Increase in the serum lipids mainly cholesterol
(hypercholesterolemia) is a major modifiable risk factor.
Pathology self-study notes undergraduate Unilus (student)
, Page 3
2. Hypertension: Incidence of atherosclerosis increases as BP rises above the
normal, and this excess risk is related to both systolic and diastolic levels of
blood pressure.
3. Cigarette smoking: It is the most important avoidable cause of atherosclerosis,
is more severe and extensive among smokers than in nonsmokers.
4. Diabetes mellitus: It is a potent risk factor for atherosclerosis, associated with
hypercholesterolemia.
Nonmodifiable/Constitutional Risk Factors
1. Increasing age: Age is the most powerful independent risk factor. Clinical
manifestation of atherosclerosis is usually observed after middle age and the
lesions progressively rise with each decade.
2. Sex: Premenopausal women have lower incidence of atherosclerosis-related
diseases compared to males of the same age group.
3. Family history: Atherosclerotic disease often runs in families. Familial
predisposition is usually multifactorial, due to genetic, environmental and
lifestyle factors.
4. Genetic abnormalities: Most common inherited modifiable risk factors
(hypertension, hyperlipidemia, and diabetes mellitus) are polygenic.
Additional Risk Factors
1. Inflammation: It plays a role in atherogenesis and may be a risk factor.
2. C-reactive protein (CRP) level: It is a marker of systemic inflammation and
predicts the risk of atherosclerosis related diseases.
3. Hyperhomocysteinemia: rare autosomal recessive inborn error, results in
elevated circulating homocysteine → premature and severe atherosclerosis.
4. Metabolic syndrome: It is associated with central obesity, insulin resistance.
5. Increased Lipoprotein, LDL is associated with increased risk.
6. Raised procoagulant levels: thrombin, platelet activation and raised
fibrinogen.
7. Inadequate physical activity: Lack of exercise doubles the risk.
Pathology self-study notes undergraduate Unilus (student)
COLLINS MWANANGOMBE SHANDU
MBChB-candidate
university of Lusaka
Applied Clinical Pathology Study notes
VASCULAR DISORDERS
Content;
1. Notes (Exam Preparation)
a. Atherosclerosis ……………………….………… Pg.2-4
b. Aneurysms …………………………………….……. Pg.5-8
c. Hypertension Vascular Disease …….…… Pg.9-10
d. Vasculitis
1) Giant-Cell (Temporal) Arteritis………………… Pg.11
2) Polyarteritis Nodosa ……………………………. Pg.12
3) Wegener's Granulomatosis ……………………. Pg.13
4) Vascular Tumors ……………………………… Pg.14-15
2. Questions Of The Chapter (Tutorial)…………... Pg.16
NOTES
1. ATHEROSCLEROSIS
Def: atherosclerosis is primarily a progressive disease of intima characterized by
lesions called atheroma or grossly characterized by arterial wall thickening due
to deposition of LDL, smooth muscle proliferation in the intima.
Pathophysiology
1. There is an Endothelial dysfunction or injury which cause;
Pathology self-study notes undergraduate Unilus (student)
, Page 2
2. Increased vascular permeability and Platelet adhesion and thrombosis
3. Monocyte and T lymphocytes adhesion to endothelium, monocytes
transformed into macrophages and produce of oxygen free radicals produced
locally together with dysfunctional endothelial cells to oxidize the LDLs and
phagocytose to form foam cells which may undergo apoptosis and release lipids
to form lipid-rich center (necrotic core in atheromatous plaques).
4. LDLs crosses the endothelium into the intima. Oxidized LDL causes
activated macrophages to produce Cytokine increases leukocyte adhesion and
Chemokines
Histology:
intimal smooth muscle cells, cellular debris& cholesterol, foamy macrophages,
macrophages, lymphocytes, adherence platelets, all in the intima.
Gross:
fatty streak, ulcerated plaque, fatty spots.
Complications of atherosclerosis:
1. Aneurysm formation: damage the elastic tissue causes weakening the wall
result in aneurysmal dilation which may rupture.
2. Rupture/ulceration: Plaque protruding can disturb the blood flow resulting in
turbulent flow of blood which can damage the endothelium cause rupture.
2. Hemorrhage into a plaque: It may occur due to rupture of the fibrous cap of
the plaque or of the thin-walled vessels formed due to neovascularization.
3. Thrombosis and embolism: Ulceration exposes blood to highly thrombogenic
subendothelial collagen, favors thrombus formation, occlusive lead to ischemia.
4. Atheroembolism: Plaque rupture, discharge atherosclerotic debris into the
bloodstream and results in atheroemboli.
6. Calcification: It may occur in the central necrotic area of the plaque
(dystrophic calcification).
RISK FACTORS
Modifiable Risk Factors
1. Hyperlipidemia: Increase in the serum lipids mainly cholesterol
(hypercholesterolemia) is a major modifiable risk factor.
Pathology self-study notes undergraduate Unilus (student)
, Page 3
2. Hypertension: Incidence of atherosclerosis increases as BP rises above the
normal, and this excess risk is related to both systolic and diastolic levels of
blood pressure.
3. Cigarette smoking: It is the most important avoidable cause of atherosclerosis,
is more severe and extensive among smokers than in nonsmokers.
4. Diabetes mellitus: It is a potent risk factor for atherosclerosis, associated with
hypercholesterolemia.
Nonmodifiable/Constitutional Risk Factors
1. Increasing age: Age is the most powerful independent risk factor. Clinical
manifestation of atherosclerosis is usually observed after middle age and the
lesions progressively rise with each decade.
2. Sex: Premenopausal women have lower incidence of atherosclerosis-related
diseases compared to males of the same age group.
3. Family history: Atherosclerotic disease often runs in families. Familial
predisposition is usually multifactorial, due to genetic, environmental and
lifestyle factors.
4. Genetic abnormalities: Most common inherited modifiable risk factors
(hypertension, hyperlipidemia, and diabetes mellitus) are polygenic.
Additional Risk Factors
1. Inflammation: It plays a role in atherogenesis and may be a risk factor.
2. C-reactive protein (CRP) level: It is a marker of systemic inflammation and
predicts the risk of atherosclerosis related diseases.
3. Hyperhomocysteinemia: rare autosomal recessive inborn error, results in
elevated circulating homocysteine → premature and severe atherosclerosis.
4. Metabolic syndrome: It is associated with central obesity, insulin resistance.
5. Increased Lipoprotein, LDL is associated with increased risk.
6. Raised procoagulant levels: thrombin, platelet activation and raised
fibrinogen.
7. Inadequate physical activity: Lack of exercise doubles the risk.
Pathology self-study notes undergraduate Unilus (student)
