chapter 2: cell response Flashcards
4 aspects of disease process
etiology: cause
pathogenesis:biochem process
morphologic changes: struct alterations in cells/organs
clinical manifestations: conseq of changes
etiology
genetic: multifact
acquired
all forms of disease start with what
molecular or structural alterations in cells
reversible functional and structural responses to changes in physiologic states, some pathologic that allows cell to survive and continue to function
adaption
examples of adaptions
hypertrophy hyperplasia metaplasia pregnancy atrophy pathologic stimuli
cell death happens when and from what
adaption is not achieved
ischemia
ifection
toxins
nutrient deprivation triggers what
autophagy
calcium deposited at sites of cell death is called
pathologic calcification
what is the most common stimulus for hypertrophy
increased workload
uterine hypertrophy process
estrogenic hormones act on SM on estrogen receptors
-increased synthesis of SM cells
3 basic steps in molecular pathogenesis of cardiac hypertrophy
integrated actions of mechanical sensors
-GFs, IGF1, FGF, a adrenergic agonists
signal transduction
- pi3 kinase/AKT pathway (exercised induced hypertrophy)
- GPCR: pathologic hypertrophy
Activation of txn factors
-mef2, nfat, gata4
when does physiologic hyperplasia occur
when need to increase fnct capacity of hormone sensitive organs
need compensatory increase after damage or resection
examples of physiologic hyperplasia
erythropoietin in blood cells
liver regen
glandular epithelium prolif of female breast at puberty
pathologic hyperplasia from
excessive or inappropriate actions of hormones or GF acting on target cells
separate from cancer but can increase chance of cancer
can be from viral infections
pathologic hyperplasia example
endometrial hyperplasia
-abnormal menstrual bleeding
BPH
papillomaviruses
2 mechanisms of hyperplasia
GF driven proliferation of mature cells
increased output of new cells from tissue stem cells
atrpohy: physiologic
embryonic structures going away
atrophy: pathological causes
WINE Blood Pressure
decreased workload
loss innervation
inadequate nutrition
loss endocrine stim
decreased blood
increased pressure
atrophy of the brain
narrows gyri
widens sulci
cellular changes in atrophy
less mitochondria
reduced RER
decreased metabolic demand
mechanisms of atrophy
decreased protein syn
increased protein degradation
some cell debris within autophagic vacuoles resist digestion and persist in cytoplasm called
residual bodies
lipofuscin granules
-brown discoloration of tissue
types of caner in barrett esophagus
adenocarcinomas: glandular
myositis ossificans
bone formation in muscle
after intramuscular hemorrhage