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Pathology - Congenital Heart Disease
Ventricular septal defect
• The predominant form of congenital heart disease (CHD). • An atypical perforation in the interventricular septum. • May manifest anywhere inside the septum, albeit the majority are located in the superior region. A minor ventricular septal defect (VSD) may possess minimal functional significance and may close spontaneously as the infant matures. Nonetheless, there persists a risk of infective endocarditis. A significant VSD results in a left-to-right shunt, leading to augmented volume overload on the right ventricle, accompanied with manifestations of heart failure.
Patent ductus arteriosus
• Continuation of the ductus arteriosus beyond 10 days of life. • Systemic blood flows from the aorta to the pulmonary artery, resulting in a left-to-right shunt. Blood flow to the lungs is augmented twofold, as is the amount returning to the left side of the heart, resulting in left ventricular hypertrophy. • Infective endocarditis is a common complication.
Atrial septal defect
• An atypical orifice in the atrial septum. The most prevalent location is the central region of the septum, distant from the atrioventricular valves. • Blood circulates from the left atrium to the right atrium, resulting in enhanced pulmonary circulation. • May be asymptomatic or lead to increased fatigue during childhood. • Many individuals appear in maturity due to atrial arrhythmias.
Atrioventricular septal defect
• A defect at the intersection of the atrial and ventricular septa. • In a complete atrioventricular septal defect (AVSD), there exists a combination of a low atrial septal defect (ASD) and a high ventricular septal defect (VSD), effectively creating a central orifice in the heart. • Most function similarly to a VSD, resulting in volume overload to the right ventricle. • The most prevalent form of congenital heart disease (CHD) observed in children with Down syndrome.
Tetralogy of Fallot
• Includes pulmonary stenosis, ventricular septal defect (VSD), overriding aorta, and right ventricular hypertrophy. • Pulmonary stenosis induces a right-to-left shunt and diminishes pulmonary blood flow, leading to cyanosis. Transposition of the major arteries • Misplacement of the aorta to the right ventricle and the pulmonary artery to the left ventricle. • Typically accompanied with a defect that facilitates the mixing of blood from both circulations (e.g., ventricular septal defect [VSD] or patent ductus arteriosus [PDA]), otherwise the anomaly is incompatible with survival.
Coarctation of the aorta
• A localized constriction of the aortic arch lumen distal to the left subclavian artery's origin. • In the infantile variant, a patent ductus arteriosus distal to the coarctation facilitates cardiac output to the lower body; however, this predominantly consists of deoxygenated blood from the right heart, resulting in cyanosis of the lower body.
• In the adult variant, a patent ductus arteriosus is absent.
Enhanced blood flow to the upper body results in the majority of individuals experiencing upper extremity hypertension. This kind is frequently unacknowledged until adulthood. Bicuspid aortic valves typically function adequately at birth and sometimes remain undiagnosed. Most bicuspid valves ultimately progress to calcific aortic stenosis, occurring at an earlier age than the usual senile aortic stenosis, or aortic regurgitation. • Elevated risk of aortic dissection in adulthood
Ventricular septal defect
• The predominant form of congenital heart disease (CHD). • An atypical perforation in the interventricular septum. • May manifest anywhere inside the septum, albeit the majority are located in the superior region. A minor ventricular septal defect (VSD) may possess minimal functional significance and may close spontaneously as the infant matures. Nonetheless, there persists a risk of infective endocarditis. A significant VSD results in a left-to-right shunt, leading to augmented volume overload on the right ventricle, accompanied with manifestations of heart failure.
Patent ductus arteriosus
• Continuation of the ductus arteriosus beyond 10 days of life. • Systemic blood flows from the aorta to the pulmonary artery, resulting in a left-to-right shunt. Blood flow to the lungs is augmented twofold, as is the amount returning to the left side of the heart, resulting in left ventricular hypertrophy. • Infective endocarditis is a common complication.
Atrial septal defect
• An atypical orifice in the atrial septum. The most prevalent location is the central region of the septum, distant from the atrioventricular valves. • Blood circulates from the left atrium to the right atrium, resulting in enhanced pulmonary circulation. • May be asymptomatic or lead to increased fatigue during childhood. • Many individuals appear in maturity due to atrial arrhythmias.
Atrioventricular septal defect
• A defect at the intersection of the atrial and ventricular septa. • In a complete atrioventricular septal defect (AVSD), there exists a combination of a low atrial septal defect (ASD) and a high ventricular septal defect (VSD), effectively creating a central orifice in the heart. • Most function similarly to a VSD, resulting in volume overload to the right ventricle. • The most prevalent form of congenital heart disease (CHD) observed in children with Down syndrome.
Tetralogy of Fallot
• Includes pulmonary stenosis, ventricular septal defect (VSD), overriding aorta, and right ventricular hypertrophy. • Pulmonary stenosis induces a right-to-left shunt and diminishes pulmonary blood flow, leading to cyanosis. Transposition of the major arteries • Misplacement of the aorta to the right ventricle and the pulmonary artery to the left ventricle. • Typically accompanied with a defect that facilitates the mixing of blood from both circulations (e.g., ventricular septal defect [VSD] or patent ductus arteriosus [PDA]), otherwise the anomaly is incompatible with survival.
Coarctation of the aorta
• A localized constriction of the aortic arch lumen distal to the left subclavian artery's origin. • In the infantile variant, a patent ductus arteriosus distal to the coarctation facilitates cardiac output to the lower body; however, this predominantly consists of deoxygenated blood from the right heart, resulting in cyanosis of the lower body.
• In the adult variant, a patent ductus arteriosus is absent.
Enhanced blood flow to the upper body results in the majority of individuals experiencing upper extremity hypertension. This kind is frequently unacknowledged until adulthood. Bicuspid aortic valves typically function adequately at birth and sometimes remain undiagnosed. Most bicuspid valves ultimately progress to calcific aortic stenosis, occurring at an earlier age than the usual senile aortic stenosis, or aortic regurgitation. • Elevated risk of aortic dissection in adulthood
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Pathology - Acute lower limb ischemia
Definition
A quick and abrupt interruption of the artery flow to the lower leg.
Epidemiology
• Incidence documented at 14 per 100,000 individuals annually.
Aetiology
• 60% attributable to acute thrombosis in a vessel with pre-existing atherosclerosis. • 30% resulting from a thromboembolus originating from a distant region, typically the heart. Common cardiac connections include atrial fibrillation, acute myocardial infarction, and ventricular aneurysm. Typical locations of impaction include the popliteal artery, common femoral artery, and aortic bifurcation. Less frequent causes encompass aortic dissection, trauma, and iatrogenic injury. The incidence of iatrogenic injury is increasing due to the rising use of endovascular operations.
Pathogenesis
• Abrupt obstruction of the arterial supply to the leg results in ischaemia.
• In the absence of intervention, irreparable tissue damage transpires within 6 hours. Extensive muscular necrosis results in hyperkalemia, acidosis, abrupt renal failure, and cardiac arrest.
Presentation • Abrupt emergence of pain and sensory loss in the extremity. • Upon examination, the limb exhibits pallor and coolness, accompanied by diminished or absent pulses. Prognosis: Limb loss occurs in 40% of cases. • Mortality in 20% of cases
Definition
A quick and abrupt interruption of the artery flow to the lower leg.
Epidemiology
• Incidence documented at 14 per 100,000 individuals annually.
Aetiology
• 60% attributable to acute thrombosis in a vessel with pre-existing atherosclerosis. • 30% resulting from a thromboembolus originating from a distant region, typically the heart. Common cardiac connections include atrial fibrillation, acute myocardial infarction, and ventricular aneurysm. Typical locations of impaction include the popliteal artery, common femoral artery, and aortic bifurcation. Less frequent causes encompass aortic dissection, trauma, and iatrogenic injury. The incidence of iatrogenic injury is increasing due to the rising use of endovascular operations.
Pathogenesis
• Abrupt obstruction of the arterial supply to the leg results in ischaemia.
• In the absence of intervention, irreparable tissue damage transpires within 6 hours. Extensive muscular necrosis results in hyperkalemia, acidosis, abrupt renal failure, and cardiac arrest.
Presentation • Abrupt emergence of pain and sensory loss in the extremity. • Upon examination, the limb exhibits pallor and coolness, accompanied by diminished or absent pulses. Prognosis: Limb loss occurs in 40% of cases. • Mortality in 20% of cases
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Pathology - Chronic lower limb ischemia
Definition: Persistent impairment of arterial circulation to the lower extremities.
Epidemiology:
Prevalent
. • Impacts 7% of men over the age of 50. The 4:5 ratio equates to 2:1.
Aetiology
• The majority of cases are attributable to atherosclerosis impacting the aorto-iliac, femoral, or popliteal and calf arteries, either individually or collectively.
Pathogenesis
• Unifocal illness typically leads to intermittent claudication. • A two-level illness typically leads to critical limb ischemia.
Presentation
• Intermittent claudication is defined by pain in the calf or thigh induced by physical activity and alleviated by rest. Critical limb ischaemia is defined by rest pain, tissue necrosis (gangrene or ulceration), or a Doppler ankle pressure of less than 50 mmHg.
Prognosis: One-third experiences improvement, one-third maintains stability, and one-third experiences deterioration. • 4% necessitate intervention, and 1% culminate in amputation
Definition: Persistent impairment of arterial circulation to the lower extremities.
Epidemiology:
Prevalent
. • Impacts 7% of men over the age of 50. The 4:5 ratio equates to 2:1.
Aetiology
• The majority of cases are attributable to atherosclerosis impacting the aorto-iliac, femoral, or popliteal and calf arteries, either individually or collectively.
Pathogenesis
• Unifocal illness typically leads to intermittent claudication. • A two-level illness typically leads to critical limb ischemia.
Presentation
• Intermittent claudication is defined by pain in the calf or thigh induced by physical activity and alleviated by rest. Critical limb ischaemia is defined by rest pain, tissue necrosis (gangrene or ulceration), or a Doppler ankle pressure of less than 50 mmHg.
Prognosis: One-third experiences improvement, one-third maintains stability, and one-third experiences deterioration. • 4% necessitate intervention, and 1% culminate in amputation
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Pathology - Aortic dissection
Definition: A rupture in the aortic wall allowing blood to flow through.
Epidemiology
• The majority of instances arise in persons aged 50 to 70 years. The 4:5 ratio equates to 2:1.
Aetiology
• The majority of instances are associated with hypertension. • Additional correlations include Marfan syndrome and congenital bicuspid aortic valve. The pathogenesis of aortic dissection in relation to hypertension remains contentious. • Suggested that the initial event is hemorrhage from a vasa vasorum into the media of the aorta. The intima experiences stress and ruptures, permitting blood to infiltrate the media and dissect along it. • Dissections may advance in the direction of the normal aortic blood flow (anterograde) or against it towards the aortic root (retrograde). • Dissections may re-enter the aortic lumen at a remote location, resulting in a 'double-barrelled' aorta, or may burst externally into the pericardial, pleural, or peritoneal cavities. Approximately 75% pertain to the ascending aorta or aortic arch (type A). Approximately 25% pertain to the descending aorta, without involvement of the ascending aorta or aortic arch (type B).
Presentation
• Intense, acute 'tearing' chest pain that may closely resemble acute myocardial infarction. • External rupture results in significant internal hemorrhage and shock.
Macroscopy
A rip is typically observable in the intima of the aorta at both the initiation and termination points of the dissection. • Should the dissection rupture externally, substantial volumes of blood clot will be present around the rupture site.
Histopathology
Microscopy offers limited insight into the reasons for dissection.
• The existence of significant degenerative alterations in the aorta wall of people under 60 years old suggests the potential for an inherited aortopathy, such as Marfan syndrome. Prognosis: Untreated cases have a significant death rate, with 50% succumbing within the first week.
• Treated cases exhibit favorable initial survival; but, they continue to be susceptible to mortality from rupture of the dissection or the emergence of a new dissection.
Definition: A rupture in the aortic wall allowing blood to flow through.
Epidemiology
• The majority of instances arise in persons aged 50 to 70 years. The 4:5 ratio equates to 2:1.
Aetiology
• The majority of instances are associated with hypertension. • Additional correlations include Marfan syndrome and congenital bicuspid aortic valve. The pathogenesis of aortic dissection in relation to hypertension remains contentious. • Suggested that the initial event is hemorrhage from a vasa vasorum into the media of the aorta. The intima experiences stress and ruptures, permitting blood to infiltrate the media and dissect along it. • Dissections may advance in the direction of the normal aortic blood flow (anterograde) or against it towards the aortic root (retrograde). • Dissections may re-enter the aortic lumen at a remote location, resulting in a 'double-barrelled' aorta, or may burst externally into the pericardial, pleural, or peritoneal cavities. Approximately 75% pertain to the ascending aorta or aortic arch (type A). Approximately 25% pertain to the descending aorta, without involvement of the ascending aorta or aortic arch (type B).
Presentation
• Intense, acute 'tearing' chest pain that may closely resemble acute myocardial infarction. • External rupture results in significant internal hemorrhage and shock.
Macroscopy
A rip is typically observable in the intima of the aorta at both the initiation and termination points of the dissection. • Should the dissection rupture externally, substantial volumes of blood clot will be present around the rupture site.
Histopathology
Microscopy offers limited insight into the reasons for dissection.
• The existence of significant degenerative alterations in the aorta wall of people under 60 years old suggests the potential for an inherited aortopathy, such as Marfan syndrome. Prognosis: Untreated cases have a significant death rate, with 50% succumbing within the first week.
• Treated cases exhibit favorable initial survival; but, they continue to be susceptible to mortality from rupture of the dissection or the emergence of a new dissection.
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Pathology – Varicose Veins
Definition: Tortuous and dilated superficial leg veins resulting from valvular incompetence.
Epidemiology
• Impact as much as 20% of the population. • Significant female predominance (5:4 ratio 9:1). Aetiology • The majority of cases are primary and idiopathic. • Secondary causes including pregnancy, substantial fibroids, and ovarian masses.
Mechanism of Disease Development
• Believed that valve cusps undergo degeneration and form perforations. • Valve incompetence elevates stress on the downstream valve. • Ultimately, a column of valves becomes inadequate, resulting in venous dilation.
Presentation
• The majority of patients present because of the unattractive appearance of the veins. • Discomfort, hurting, itching, and swelling may be present. • Symptoms may intensify towards the day's conclusion.
Complications
• Stasis dermatitis (varicose). • Varicose ulceration. • Lipodermatosclerosis. • Hemorrhaging. • Thrombosis (superficial thrombophlebitis)
Definition: Tortuous and dilated superficial leg veins resulting from valvular incompetence.
Epidemiology
• Impact as much as 20% of the population. • Significant female predominance (5:4 ratio 9:1). Aetiology • The majority of cases are primary and idiopathic. • Secondary causes including pregnancy, substantial fibroids, and ovarian masses.
Mechanism of Disease Development
• Believed that valve cusps undergo degeneration and form perforations. • Valve incompetence elevates stress on the downstream valve. • Ultimately, a column of valves becomes inadequate, resulting in venous dilation.
Presentation
• The majority of patients present because of the unattractive appearance of the veins. • Discomfort, hurting, itching, and swelling may be present. • Symptoms may intensify towards the day's conclusion.
Complications
• Stasis dermatitis (varicose). • Varicose ulceration. • Lipodermatosclerosis. • Hemorrhaging. • Thrombosis (superficial thrombophlebitis)
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Pathology - Abdominal aortic aneurysm
Definition
A permanent dilatation of the abdominal aorta exceeding 3 cm in diameter.
Epidemiology
The incidence is stated to be 5–10%.
Aetiology
Nearly all are attributable to aortic atherosclerosis.
Mechanism of disease development
Proteolytic enzymes compromise the aortic medium, resulting in aneurysmal alterations. Elevated concentrations of matrix metalloproteinases have been identified in aneurysmal aortas. These enzymes are recognized for their ability to breakdown elastin.
Pathology
Unruptured aneurysms are frequently asymptomatic; nonetheless, they may induce abdomen or back pain. Most are identified inadvertently during abdominal examination or imaging. Ruptured abdominal aortic aneurysms manifest as a surgical emergency characterized by abdominal discomfort and shock.
Macroscopy
The aorta exhibits dilation, typically occurring behind the renal arteries. Extensive atherosclerosis is consistently observed, frequently accompanied by secondary thrombosis and calcification.
Prognosis: The natural progression is characterized by gradual expansion. The risk of rupture is exponentially correlated with diameter. • Mortality following rupture surpasses 80%. Elective surgical intervention is recommended for aneurysms with a maximal diameter of 5.5 cm or greater.
Definition
A permanent dilatation of the abdominal aorta exceeding 3 cm in diameter.
Epidemiology
The incidence is stated to be 5–10%.
Aetiology
Nearly all are attributable to aortic atherosclerosis.
Mechanism of disease development
Proteolytic enzymes compromise the aortic medium, resulting in aneurysmal alterations. Elevated concentrations of matrix metalloproteinases have been identified in aneurysmal aortas. These enzymes are recognized for their ability to breakdown elastin.
Pathology
Unruptured aneurysms are frequently asymptomatic; nonetheless, they may induce abdomen or back pain. Most are identified inadvertently during abdominal examination or imaging. Ruptured abdominal aortic aneurysms manifest as a surgical emergency characterized by abdominal discomfort and shock.
Macroscopy
The aorta exhibits dilation, typically occurring behind the renal arteries. Extensive atherosclerosis is consistently observed, frequently accompanied by secondary thrombosis and calcification.
Prognosis: The natural progression is characterized by gradual expansion. The risk of rupture is exponentially correlated with diameter. • Mortality following rupture surpasses 80%. Elective surgical intervention is recommended for aneurysms with a maximal diameter of 5.5 cm or greater.
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Pathology - Deep vein thrombosis
Definition
• Thrombosis occurring in the deep veins of the leg. Epidemiology: Approximately 1 in 1000 individuals annually.
Aetiology • Pertaining to blood stasis and/or heightened blood coagulability. • Risk factors encompass immobilization, pregnancy, recent surgery (especially to the lower limb or pelvic), cancer, long-haul flights, smoking, oral contraceptive use, hormone replacement therapy, and thrombophilia. 2 Various contributing components frequently function within an individual.
Pathogenesis
• Impaired blood flow and/or heightened blood coagulability surpasses the efficacy of natural anticoagulants, resulting in thrombus formation within the deep veins of the leg. • The thrombus may develop in size as it extends along the vein's lumen.
Presentation: • Inflamed, painful, and swollen lower limb with a warm red hue. • Certain cases may be asymptomatic.
Complications
Three Pulmonary thromboembolism
Definition
• Thrombosis occurring in the deep veins of the leg. Epidemiology: Approximately 1 in 1000 individuals annually.
Aetiology • Pertaining to blood stasis and/or heightened blood coagulability. • Risk factors encompass immobilization, pregnancy, recent surgery (especially to the lower limb or pelvic), cancer, long-haul flights, smoking, oral contraceptive use, hormone replacement therapy, and thrombophilia. 2 Various contributing components frequently function within an individual.
Pathogenesis
• Impaired blood flow and/or heightened blood coagulability surpasses the efficacy of natural anticoagulants, resulting in thrombus formation within the deep veins of the leg. • The thrombus may develop in size as it extends along the vein's lumen.
Presentation: • Inflamed, painful, and swollen lower limb with a warm red hue. • Certain cases may be asymptomatic.
Complications
Three Pulmonary thromboembolism
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Pathology - Hypertension
Definition • Consistently raised blood pressure at a threshold where the advantages of therapy are unequivocal for the individual.
All patients with blood pressure equal to or over 160/100 mmHg should receive treatment. The decision to manage blood pressure at 140/90 mmHg is contingent upon additional risk factors.
Epidemiology:
Highly prevalent.
• Significant geographical and racial heterogeneity. • The incidence is estimated to be as high as 25–30% in Western nations.
Aetiology
• Ninety-five percent are of indeterminate origin ('important'). Five percent of instances are attributed to chronic kidney illness, phaeochromocytoma, adrenal cortical adenoma,coarctation of the aorta, pregnancy, and the oral contraceptive pill.
Pathogenesis
• Highly intricate, involving numerous factors such as sodium consumption and genetic predisposition, which seem to interact to induce hypertension.
• Chronic hypertension facilitates atherosclerosis in medium and large systemic arteries and induces thickening of minor arteries (arteriosclerosis) and arterioles (arteriolosclerosis). Hypertension elevates the workload of the left ventricle, resulting in left ventricular hypertrophy and ultimately left ventricular failure.
Presentation
• The majority of patients are asymptomatic and are diagnosed during blood pressure assessment. • Individuals exhibit symptoms indicative of end-organ damage resulting from hypertension, such as intracerebral hemorrhage, left ventricular failure, and chronic renal disease.
Prognosis
• Inadequate treatment of the disease elevates the risk of left ventricular failure, intracerebral hemorrhage, chronic renal disease, and aortic dissection.
Definition • Consistently raised blood pressure at a threshold where the advantages of therapy are unequivocal for the individual.
All patients with blood pressure equal to or over 160/100 mmHg should receive treatment. The decision to manage blood pressure at 140/90 mmHg is contingent upon additional risk factors.
Epidemiology:
Highly prevalent.
• Significant geographical and racial heterogeneity. • The incidence is estimated to be as high as 25–30% in Western nations.
Aetiology
• Ninety-five percent are of indeterminate origin ('important'). Five percent of instances are attributed to chronic kidney illness, phaeochromocytoma, adrenal cortical adenoma,coarctation of the aorta, pregnancy, and the oral contraceptive pill.
Pathogenesis
• Highly intricate, involving numerous factors such as sodium consumption and genetic predisposition, which seem to interact to induce hypertension.
• Chronic hypertension facilitates atherosclerosis in medium and large systemic arteries and induces thickening of minor arteries (arteriosclerosis) and arterioles (arteriolosclerosis). Hypertension elevates the workload of the left ventricle, resulting in left ventricular hypertrophy and ultimately left ventricular failure.
Presentation
• The majority of patients are asymptomatic and are diagnosed during blood pressure assessment. • Individuals exhibit symptoms indicative of end-organ damage resulting from hypertension, such as intracerebral hemorrhage, left ventricular failure, and chronic renal disease.
Prognosis
• Inadequate treatment of the disease elevates the risk of left ventricular failure, intracerebral hemorrhage, chronic renal disease, and aortic dissection.
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Pathology – Atherosclerosis
Definition
• An inflammatory condition affecting large and medium-sized systemic arteries, marked by the development of lipid-laden plaques within the arterial wall.
Epidemiology: Nearly universally observed to varying extents in all persons as they age.
Aetiology
Risk factors encompass age, male sex, diabetes mellitus, hypertension, tobacco use, and hyperlipidemia. Men who smoke exhibit a 70% elevated mortality rate from ischemic heart disease vs to non-smokers.
Pathogenesis
Endothelial injury induces an inflammatory and fibroproliferative response in the artery, resulting in atherosclerosis, as posited by the 'response to injury' hypothesis. • The endothelium can be compromised by various causes, including as smoking, hyperglycemia, and oxidized LDL. • Oxidized LDL is especially effective in promoting atherosclerosis due to its pro-inflammatory and pro-coagulant properties. Stable plaques characterized by a minimal presence of inflammatory cells and a robust fibrous cap constrict the arterial lumen, yet are less prone to precipitating acute problems. • Unstable plaques characterized by a higher concentration of inflammatory cells possess a thin fibrous cap susceptible to erosion, fissuring, or rupture. The exposure of the highly thrombogenic lipid core to the bloodstream induces an abrupt ischemic event in the organ supplied by the affected artery
Presentation
• Stable plaques induce signs of reversible ischemia in the affected organ, such as angina pectoris and chronic lower limb ischemia. • Unstable plaques precipitate acute ischemic events, including acute coronary syndromes, stroke, and acute lower limb ischemia.
Macroscopy
Atherosclerotic plaques are yellow, lipid-rich lesions located within the walls of big and medium-sized arteries. • Superimposed thrombus has a dark brown coloration. • Predilection sites include the coronary arteries, abdominal aorta, iliac arteries, and bifurcations of the carotid artery. Histopathology • The intima is enlarged by a plaque consisting of a lipid-dense core with an overlay of fibrous tissue. • In cases of superimposed thrombosis, a fibrin-rich clot may also be present, obstructing the artery.
Definition
• An inflammatory condition affecting large and medium-sized systemic arteries, marked by the development of lipid-laden plaques within the arterial wall.
Epidemiology: Nearly universally observed to varying extents in all persons as they age.
Aetiology
Risk factors encompass age, male sex, diabetes mellitus, hypertension, tobacco use, and hyperlipidemia. Men who smoke exhibit a 70% elevated mortality rate from ischemic heart disease vs to non-smokers.
Pathogenesis
Endothelial injury induces an inflammatory and fibroproliferative response in the artery, resulting in atherosclerosis, as posited by the 'response to injury' hypothesis. • The endothelium can be compromised by various causes, including as smoking, hyperglycemia, and oxidized LDL. • Oxidized LDL is especially effective in promoting atherosclerosis due to its pro-inflammatory and pro-coagulant properties. Stable plaques characterized by a minimal presence of inflammatory cells and a robust fibrous cap constrict the arterial lumen, yet are less prone to precipitating acute problems. • Unstable plaques characterized by a higher concentration of inflammatory cells possess a thin fibrous cap susceptible to erosion, fissuring, or rupture. The exposure of the highly thrombogenic lipid core to the bloodstream induces an abrupt ischemic event in the organ supplied by the affected artery
Presentation
• Stable plaques induce signs of reversible ischemia in the affected organ, such as angina pectoris and chronic lower limb ischemia. • Unstable plaques precipitate acute ischemic events, including acute coronary syndromes, stroke, and acute lower limb ischemia.
Macroscopy
Atherosclerotic plaques are yellow, lipid-rich lesions located within the walls of big and medium-sized arteries. • Superimposed thrombus has a dark brown coloration. • Predilection sites include the coronary arteries, abdominal aorta, iliac arteries, and bifurcations of the carotid artery. Histopathology • The intima is enlarged by a plaque consisting of a lipid-dense core with an overlay of fibrous tissue. • In cases of superimposed thrombosis, a fibrin-rich clot may also be present, obstructing the artery.
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Shock
Defi nition
• A generalized failure of tissue perfusion.
Aetiology
• Pump failure, e.g. acute myocardial infarction.
• Peripheral circulation failure, e.g. hypovolaemia, sepsis, anaphylaxis
, tension pneumothorax,large pulmonary embolus
Pathogenesis
• Pump or peripheral circulation failure leads to cardiovascular collapse.
• Prolonged inadequate tissue perfusion risks the development of
multiple organ failure.
Presentation
• Tachycardia due to increased sympathetic drive.
• Urine output declines (only apparent if the patient is catheterized).
• Hypotension.
2 Note up to 15 % of circulating volume may be lost before any clinical signs
become apparent.
Prognosis
1 Shock is a serious condition which leads to the development of multiple
organ failure if not rapidly addressed
Defi nition
• A generalized failure of tissue perfusion.
Aetiology
• Pump failure, e.g. acute myocardial infarction.
• Peripheral circulation failure, e.g. hypovolaemia, sepsis, anaphylaxis
, tension pneumothorax,large pulmonary embolus
Pathogenesis
• Pump or peripheral circulation failure leads to cardiovascular collapse.
• Prolonged inadequate tissue perfusion risks the development of
multiple organ failure.
Presentation
• Tachycardia due to increased sympathetic drive.
• Urine output declines (only apparent if the patient is catheterized).
• Hypotension.
2 Note up to 15 % of circulating volume may be lost before any clinical signs
become apparent.
Prognosis
1 Shock is a serious condition which leads to the development of multiple
organ failure if not rapidly addressed
