Chapter 2: Cell Responses to Stress and Toxic Insults: Adaptation, Injury, Death Flashcards
Pathology
study of structural, biochemical, functional changes in cells, tissues, organs that underlie disease
Disease
any deviation/interruption of the normal structure of a part, organ, system of the body as manifested by characteristic symptoms and signs
Disorder
a derangement or abnormality of function; a morbid physical or mental state
Neoplasm
any new and abnormal growth, specifically new growth of tissue in which the growth is uncontrolled and progressive
4 aspects of the disease process
- etiology- cause; genetic or acquired
- pathogenesis- biochemical and molecular mechanisms of disease
- morphologic changes: structural alterations induced in cells and organs; used to follow disease progression
- clinical manifestations: functional consequences of the changes
Adaptations
reversible functional and structural responses to change in physiologic states/pathologic stimuli, during which new but altered steady states are achieved, allowing the cell to survive and continue to function
Hypertrophy
adaptation involving increase in cell size
Hyperplasia
adaptation involving increase in cell number
Atrophy
adaptation involving decrease in cell size, number, and metabolic activity
Decreased nutrients, decreased stimulation
Metaplasia
adaptation involving change in phenotype of cells
due to chronic irritation
Syndrome
A set of symptoms that occur together; a symptom complex; the sum of signs of any morbid state
Cell injury
due to reduced O2 supply, chemical injury, microbial infection
Cellular aging
cumulative sublethal injury over long life span
Transitioning myocardial cells show what?
adaptation–>cell injury–>cell death
Triphenyltetrazolium colors myocardium magenta to see this
adapted: hypertrophy due to increased BP because of the mechanical effort needed
reversibly injured: no gross/microscopic changes, but cellular swelling and fat accumulation
What is the most common stimulus for skeletal muscle hypertrophy?
increased work load
What is the most common stimulus for hypertrophy in cardiac muscle?
increased hemodynamic load from HTN or faulty valves
Cardiac hypertrophy causes release of what?
TGF-beta, IGF1, FGF, vasoactive factors (alpha-adrenergic agonists, endothelin 1, and angiotensin II)
What pathways are activated when cardiac hypertrophy occurs?
PI3K/AKT (important in exercise hypertrophy) and G proteins (important in pathologic hypertrophy)
Next step after the activation of the 2 pathways
TF’s are activated (GATA4, NFAT, and MEF2) which work to increase the synthesis of more proteins–>hypertrophy
What happens when the genes for the heart are switched back to the fetal form?
myosin heavy chain reverts to the B form instead of the A isoform–>slower contraction, conserves energy
Cardiac hypertrophy also causes increased ANP release…why?
usually only seen in embryological heart
ANP is increased because it causes Na+ secretion from the kidney–>decreases blood volume and pressure–>reduces hemodynamic load
Eventual conclusion of heart hypertrophy
myocardial fibers undergo lysis and loss of contractile elements–>myocyte death can occur
To prevent this, inhibitors of NFAT, GATA4, and MEF2 are given
Hormonal hyperplasia
female breast (glandular epithelial cells) during puberty or pregnancy
Compensatory hyperplasia
occurs when a lobe of a liver is donated and the remaineder of the liver grows back to compensate for the loss
intrahepatic stem cells regenerate during hepatitis
Bone marrow after blood loss/hemolysis