Cell Injury and Adaptation 1 Flashcards
etiology
cause
disease etiology- causes
VINDICATES vascular infectious neoplastic drugs inflammatory/idiopathic congenital autoimmune disorders trauma endocrine/metabolic something else
pathogenesis
sequence of events in the response of cells or tissues to the etiologic agent
from initial stimulus to ultimate expression of disease
idiopathic
pathogenesis or etiology is unknown
pathognomonic
morphologic changes in cell and tissue structure are diagnostic of the disease
central dogma of anatomic pathology
molecular damage–> cellular dysfunction with morphologic abnormalities–> organ dysfunction–> clinical symptoms (disease)
hypertrophy
increase in size of individual cells in response to stimulus or injury
results in increased size and weight of an organ no new cells, just larger)
can be physiologic (due to increased workload in bodybuilders) or pathologic (systemic hypertension) or hormone induced (pregnancy- uterine hypertrophy)
increased production of cellular proteins
cardiac hypertrophy
signals in cell membrane activate complex web of signal transduction pathways increasing mechanical performance
however, eventually reaches a limit beyond which enlargement of muscle mass is no longer able to compensate–> lysis and loss of myofibrillar contractile elements, myocyte death, ventricular arrhythmias,
cardiac typertrophy treatment
diuretics- water pills
ACE inhibitors
Angiotension receptor blockers (ARBs)
natriuretic factor
expressed in atrium and ventricle in embryonic heart but is down regulated after birth; during hypertrophy, increased atrial natriuretic factor gene expression occurs which causes salt secretion by the kidney, decreases, blood volume and pressure and serves to reduce hemodynamic load
diuretics
elevates rate of bodily urine excretion; kidneys release sodium from blood and then water follows concentration gradient
ace inhibitors
Angiotensin-converting enzyme (ACE) inhibitors help relax blood vessels. ACE inhibitors prevent an enzyme in your body from producing angiotensin II, a substance in your body that narrows your blood vessels and releases hormones that can raise your blood pressure. This narrowing can cause high blood pressure and force your heart to work harder.
ARBs
antiotensin receptor blockers
Blockade of AT1 receptors directly causes vasodilation, reduces secretion of vasopressin, reduces production and secretion of aldosterone, amongst other actions – the combined effect of which is reduction of blood pressure.
hyperplasia
increase in absolute number of cells in respones to stimulus or persistent cell injury
ex. enlargement of breast during pregnancy due to influence of estrogen;
can only occur if tissue contains cells capable of dividing
physiologic hyperplasia
due to action of hormones or growth factors occurs in several circumstances: need to increase functional capacity of hormone sensitive organs; need for compensatory increase after damage or resection
pathologic hyperplasia
caused by excessive or inappropriate actions of hormones or growth factors acting on target cells;
endometrial hyperplasia- abnormal hormone-induced and benign prostatic hyperplasia- hormonal stimulation by androgens: these processes remains controlled and hyperplasia regresses if hormonal stimulation eliminated; can be precursors to cancer
can also be response to viral infections
mechanism of hyperplasia
result of growth factor driven proliferation of mature cells and, in some cases, by increased output of new cells from tissue stem cells;
ex. partial hepatectomy- growth factors in liver engage receptors on surviving cells and activate signaling pathways that stimulate cell proliferation
atrophy
reduction in the size of an organ or tissue due to decrease cell size and number ;
results from decreased protein synthesis or increased protein degradation in cells
pathologic atrophy
caused by decreased workload (fractured b one), loss of innervation (damage to nerves leads to atrophy of muscle fibers), diminished blood supply (ischemia due arterial occlusive disease; reduced blood supply in brain due to atherosclerosis-plaque build up in arteries), inadequate nutrition (cachexia- muscle wasting), loss of endocrine stimulation (loss of estrogen stimulation post menopause results in physiologic atrophy of endometrium, vaginal epithelium and breast), pressure (enlarging benign tumor can cause atrophy of surrounding uninvolved tissues)
physiologic atrophy
physiologic atrophy is common during normal development- embryonic structures, decrease in size of uterus post-partum;
why does protein synthesis decrease in atrophy?
reduced metabolic activity
degradation of cellular proteins
ubiquitin-proteasome pathway
cachexia
muscle wasting; catabolic conditions
metaplasia
reversible, induced change in the type of mucosal epithelium brought about by various forms of chronic injury (columnar to squamous)
ex. bronchi due to cigarette smoke, or in uterine cervix due to chronic inflammation from pathogenic viruses or bacteria;
one differentiated cell type replaced by other because that cell type is able to better withstand environment
mechanism of metaplasia
result of reprogramming of stem cells that are known to exist in normal tissues or of undifferentiated mesenchymal cells present in connective tissues ; brought about by signals generated by cytokines, GF, and extracellular matrix components in cells’ environment–> expression of genes that drive cells toward specific differentiation pw
dysplasia
disordered growth most commonly seen in squamous epithelial cells following chronic injury;
variations in size and shape, disorderly arrangement, and nuclear changes, consisting of enlargement, irregular borders, and hyperchromasia of individual cell nuclei;
usually cells divide at basal layer and mature up but in this case cells are dividing throughout- no order;
pre-malignant condition
cell response to injury
cells either return to normal, following removal of stimulus
adapt if injury is non-lethal and chronic
undergo cell death
hypoxemia
low concentration of oxygen in blood
ischemia
inadequate blood supply to organ
infarction
the obstruction of the blood supply to an organ or region of tissue, typically by a thrombus or embolus, causing local death of the tissue.
