Hoofdstuk 1
Etiology is the origin of a disease, including the underlying causes and modifying
factors. Pathogenesis refers to the steps in the development of disease.
Traditionally, pathology is divided into general pathology and systemic pathology;
the former focuses on the cellular and tissue alterations caused by pathologic
stimuli in most tissues, while the latter examines the reactions and abnormalities of
different specialized organs.
The principal adaptive responses of cells are hypertrophy, hyperplasia, atrophy, and
metaplasia. Adaptive capability exceeds injury. Cell death can be harmful or
biologically relevant. Myocardium subjected to persistent increased load, as in
hypertension or with a narrowed (stenotic) valve, adapts by undergoing
hypertrophy—an increase in the size of the individual cells and ultimately the
entire heart—to generate the required higher contractile force. Not relieved or
ischemia muscle cells injury. It may undergo irreversible injury and cell death
(infarction) after complete or prolonged occlusion. Physiologic adaptations usually
represent responses of cells to normal stimulation by hormones or endogenous
chemical mediators. Pathologic adaptations are responses to stress that allow cells
to modulate their structure and function and thus escape injury. Such adaptations
can take several distinct forms.
Hypertrophy is an increase in the size of cells resulting in increase in the size of
the organ. Hypertrophy can be physiologic or pathologic and is caused either by
increased functional demand or by growth factor or hormonal stimulation. The
mechanisms driving cardiac hypertrophy involve at least two types of signals:
mechanical triggers, such as stretch, and trophic triggers, which typically are
soluble mediators that stimulate cell growth, such as growth factors and adrenergic
hormones. Muscle mass can no longer compensate for the increased burden in
, the heart several “degenerative” changes occur in the myocardial fibers, of which
the most important are fragmentation and loss of myofibrillar contractile elements.
The net result of these changes is ventricular dilation and ultimately cardiac failure.
Hyperplasia takes place if the tissue contains cell populations capable of
replication; it may occur concurrently with hypertrophy and often in response to the
same stimuli. Hyperplasia can be physiologic or pathologic. Physiologic hyperplasia:
Hormonal and compensatory hyperplasia. An important point is that in all of these
situations, the hyperplastic process remains controlled; if the signals that initiate it
abate, the hyperplasia disappears. Atrophy is the shrinkage in the size of the cell
by the loss of cell substance by decreased protein synthesis and increased protein
degradation in cells. The degradation of cellular proteins occurs mainly by the
ubiquitin-proteasome pathway. Nutrient deficiency and disuse may activate
ubiquitin ligases, which attach multiple copies of the small peptide ubiquitin to
cellular proteins and target them for degradation in proteasomes. In many
situations, atrophy is also accompanied by increased autophagy, with resulting
increases in the number of autophagic vacuoles. Autophagy (“self-eating”) is the
process in which the starved cell eats its own components in an attempt to survive.
Metaplasia is a reversible change in which one adult cell type (epithelial or
mesenchymal) is replaced by another adult cell type. In this type of cellular
adaptation, a cell type sensitive to a particular stress is replaced by another cell
type better able to withstand the adverse environment. Metaplasia is thought to
arise by reprogramming of stem cells to differentiate along a new pathway rather
than a phenotypic change (transdifferentiation) of already differentiated cells. In
smokers: ciliated epithelium stratified squamous epithelium some mechanisms
are lost such as mucus secretion and ciliary clearance of particulate matter.
Moreover, the influences that induce metaplastic change, if persistent, may
predispose to malignant transformation of the epithelium.
Etiology is the origin of a disease, including the underlying causes and modifying
factors. Pathogenesis refers to the steps in the development of disease.
Traditionally, pathology is divided into general pathology and systemic pathology;
the former focuses on the cellular and tissue alterations caused by pathologic
stimuli in most tissues, while the latter examines the reactions and abnormalities of
different specialized organs.
The principal adaptive responses of cells are hypertrophy, hyperplasia, atrophy, and
metaplasia. Adaptive capability exceeds injury. Cell death can be harmful or
biologically relevant. Myocardium subjected to persistent increased load, as in
hypertension or with a narrowed (stenotic) valve, adapts by undergoing
hypertrophy—an increase in the size of the individual cells and ultimately the
entire heart—to generate the required higher contractile force. Not relieved or
ischemia muscle cells injury. It may undergo irreversible injury and cell death
(infarction) after complete or prolonged occlusion. Physiologic adaptations usually
represent responses of cells to normal stimulation by hormones or endogenous
chemical mediators. Pathologic adaptations are responses to stress that allow cells
to modulate their structure and function and thus escape injury. Such adaptations
can take several distinct forms.
Hypertrophy is an increase in the size of cells resulting in increase in the size of
the organ. Hypertrophy can be physiologic or pathologic and is caused either by
increased functional demand or by growth factor or hormonal stimulation. The
mechanisms driving cardiac hypertrophy involve at least two types of signals:
mechanical triggers, such as stretch, and trophic triggers, which typically are
soluble mediators that stimulate cell growth, such as growth factors and adrenergic
hormones. Muscle mass can no longer compensate for the increased burden in
, the heart several “degenerative” changes occur in the myocardial fibers, of which
the most important are fragmentation and loss of myofibrillar contractile elements.
The net result of these changes is ventricular dilation and ultimately cardiac failure.
Hyperplasia takes place if the tissue contains cell populations capable of
replication; it may occur concurrently with hypertrophy and often in response to the
same stimuli. Hyperplasia can be physiologic or pathologic. Physiologic hyperplasia:
Hormonal and compensatory hyperplasia. An important point is that in all of these
situations, the hyperplastic process remains controlled; if the signals that initiate it
abate, the hyperplasia disappears. Atrophy is the shrinkage in the size of the cell
by the loss of cell substance by decreased protein synthesis and increased protein
degradation in cells. The degradation of cellular proteins occurs mainly by the
ubiquitin-proteasome pathway. Nutrient deficiency and disuse may activate
ubiquitin ligases, which attach multiple copies of the small peptide ubiquitin to
cellular proteins and target them for degradation in proteasomes. In many
situations, atrophy is also accompanied by increased autophagy, with resulting
increases in the number of autophagic vacuoles. Autophagy (“self-eating”) is the
process in which the starved cell eats its own components in an attempt to survive.
Metaplasia is a reversible change in which one adult cell type (epithelial or
mesenchymal) is replaced by another adult cell type. In this type of cellular
adaptation, a cell type sensitive to a particular stress is replaced by another cell
type better able to withstand the adverse environment. Metaplasia is thought to
arise by reprogramming of stem cells to differentiate along a new pathway rather
than a phenotypic change (transdifferentiation) of already differentiated cells. In
smokers: ciliated epithelium stratified squamous epithelium some mechanisms
are lost such as mucus secretion and ciliary clearance of particulate matter.
Moreover, the influences that induce metaplastic change, if persistent, may
predispose to malignant transformation of the epithelium.
