Cell Injury and Adaptation 1

Question 1

etiology

Answer 1

cause

Question 2

disease etiology- causes

Answer 2

VINDICATES
vascular
infectious
neoplastic
drugs
inflammatory/idiopathic
congenital
autoimmune disorders
trauma
endocrine/metabolic
something else

Question 3

pathogenesis

Answer 3

sequence of events in the response of cells or tissues to the etiologic agent
from initial stimulus to ultimate expression of disease

Question 4

idiopathic

Answer 4

pathogenesis or etiology is unknown

Question 5

pathognomonic

Answer 5

morphologic changes in cell and tissue structure are diagnostic of the disease

Question 6

central dogma of anatomic pathology

Answer 6

molecular damage–> cellular dysfunction with morphologic abnormalities–> organ dysfunction–> clinical symptoms (disease)

Question 7

hypertrophy

Answer 7

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

Question 8

cardiac hypertrophy

Answer 8

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,

Question 9

cardiac typertrophy treatment

Answer 9

diuretics- water pills
ACE inhibitors
Angiotension receptor blockers (ARBs)

Question 10

natriuretic factor

Answer 10

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

Question 11

diuretics

Answer 11

elevates rate of bodily urine excretion; kidneys release sodium from blood and then water follows concentration gradient

Question 12

ace inhibitors

Answer 12

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.

Question 13

ARBs

Answer 13

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.

Question 14

hyperplasia

Answer 14

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

Question 15

physiologic hyperplasia

Answer 15

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

Question 16

pathologic hyperplasia

Answer 16

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

Question 17

mechanism of hyperplasia

Answer 17

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

Question 18

atrophy

Answer 18

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

Question 19

pathologic atrophy

Answer 19

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)

Question 20

physiologic atrophy

Answer 20

physiologic atrophy is common during normal development- embryonic structures, decrease in size of uterus post-partum;

Question 21

why does protein synthesis decrease in atrophy?

Answer 21

reduced metabolic activity

Question 22

degradation of cellular proteins

Answer 22

ubiquitin-proteasome pathway

Question 23

cachexia

Answer 23

muscle wasting; catabolic conditions

Question 24

metaplasia

Answer 24

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

Question 25

mechanism of metaplasia

Answer 25

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

Question 26

dysplasia

Answer 26

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

Question 27

cell response to injury

Answer 27

cells either return to normal, following removal of stimulus
adapt if injury is non-lethal and chronic
undergo cell death

Question 28

hypoxemia

Answer 28

low concentration of oxygen in blood

Question 29

ischemia

Answer 29

inadequate blood supply to organ

Question 30

infarction

Answer 30

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.