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Definition of Aging:
I. Cellular Aging
Aged mitochondria have a decreased ability to survive
hypoxic insult.
Oxidative phosphorylation decreased progressively. DNA and RNA synthesis of structural and enzymatic proteins decreased progressively. Senescent cells have a decreased capacity for uptake of nutrients and for repair of chromosomal or genetic damage. Cells disclose morphologic features with increasing age.
Error-catastrophe theory
Genome-Based Theories
Finite doubling potential of cells somatic mutations programmed aging
Aging and the Lungs Less elastic and compliant with aging Tend to become expanded secondary to
elderly men.
Magnitude of bone loss is dependent on physical activity, nutrition, and hormonal changes.
Diseases of aging
Age dependent disease: direct consequence of physiologic
senescence
Age related disease: occurs with increasing frequency with
age.
The three leading causes of death in people 75 to 84 years of
THROMBOSIS
Three primary factors predispose to thrombus formation, the so-called Virchow triad: (1) Endothelial injury (2) Slowing of blood flow
Virchow triad in thrombosis. Endothelial integrity is the single most important factor. Note that injury to endothelial cells can affect local blood flow and/or coagulability; abnormal blood flow (stasis or turbulence) can, in turn, cause endothelial injury. The elements of the triad may act independently or may
Thrombi may develop anywhere in the cardiovascular system, but they are commonly seen in veins. The propagating tail may not be well attached and, particularly in veins, is prone to fragmentation, creating an embolus.
Mural thrombi. (A) Thrombus in the left and right ventricular apices, overlying a white fibrous scar. (B) Laminated thrombus in a dilated abdominal aortic aneurysm.
Thrombosis
Propagation.
Fragmentation and embolus formation.
Dissolution.
Organization and recanalization.
fibrin.
Embolism
Types of embolism
1- PULMONARY THROMBOEMBOLISM
95% of instances,
venous emboli originate from deep
2- SYSTEMIC THROMBOEMBOLISM
emboli traveling within the arterial circulation.
Most (80%) arise from intra-cardiac mural thrombi. two thirds of which are associated with left ventricular wall infarcts
3- FAT EMBOLISM
Microscopic fat globules may be
found in the circulation after
4- AIR EMBOLISM
Gas bubbles within the circulation can obstruct
vascular flow. enter the circulation during obstetric procedures or as a consequence of chest wall injury.
Infarction
An infarct is an area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage in a particular tissue. Nearly 99% of all infarcts result from thrombotic or
Red
(hemorrhagic)
infarcts
(1) with venous occlusions (such as in ovarian torsion);
and
kidney)
Examples of infarcts. (A) Hemorrhagic, roughly wedge-shaped pulmonary infarct. (B) Sharply demarcated white infarct in the spleen.
Septic
infarctions
may
develop
when
embolization occurs by fragmentation of a bacterial vegetation from a heart valve or when microbes seed an area of necrotic tissue.
Shock
Shock, or cardiovascular collapse, is the final common pathway for a number of potentially lethal clinical events, including severe hemorrhage, extensive
reduction in:
1.cardiac output
Clinical Examples
Ventricular rupture Arrhythmia Myocardial infarction
Principal Mechanism
Failure of myocardial pump owing to intrinsic myocardial damage, extrinsic pressure, or obstruction to outflow
Hypovolemic
or
Septic
Peripheral vasodilation and pooling of blood; endothelial activation/injury; leukocyte-induced damage; disseminated intravascular coagulation; activation of cytokine cascades
Less commonly:
1.Neurogenic shock
2.Anaphylactic shock
Clinical Course
The clinical manifestations depend on the precipitating insult.
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