Apoptosis and Cell Adaptations Flashcards
why have apoptosis
Maintainer of homeostasis
Uses for Apoptosis
Normal Cell turnover
Embryogenesis
Immune function
why have a normal cell turnover
Cells with short half-life
Tissue involution due to loss of growth factor stimulation
importance of Apoptosis in immune function
Elimination of auto-reactive T cells
NK and CTL killing of foreign cells
what would cause excessive Apoptosis
AIDS Ischemia
Neurodegenerative diseases
Myelodysplasia
Toxin induced liver injury
what causes inhibition of Apoptosis
Cancer - Folllicular lymphoma, carcinomas of the boob, prostate and ovaries
Autoimmune disease - SLE
viral disease: HSV, poxvirus, adenovirus
what generally happens in apoptosis
Chromatin condensation Cell shrinkage Blebbing Apoptosic body phagocytosis with no inflammation
mechanisms of apoptosis
mitochondrial/intrinsic pathway death receptor (extrinsic) pathway
what causes mitochondrial pathways of apoptosis
CEll injury via:
GRowth factor withdrawal
DNA damage
Protein misfolding
what causes the death receptor (extrinsic pathway
Receptor-ligand Interactions
- fas
- TNF rector
pathway for mitochondrial (intrinsic pathway)
cell injury activates BCL-2 family sensors
this activates BCL-2 family effectors (bax, bak)
to mitochondria which activates Cytochrome C and other pro-apoptotic proteins
INitiator caspases
Execution caspases
breakdwon of cytoskelton and endonuclease activation
pathway of death recepto pathways
receptor binding leads to activation of adaptor protein initiator caspases Executioner caspases Breakdown of cytoskeleton Endonuclease activation
major difference in necrosis and Apoptosis
Necrosis involves swelling with leakage of contents
Apoptosis involves shrinkage with no spilling
stimuli in necrosis vs apoptosis
Necrosis is pathologic and Apoptosis is physiolgoic and pathologic
morphology of necrosis and apoptosis
Necrosis is multiple cells, with swelling and lysis
Apoptosis is single cell with shrinkage, chromatin condensation, and apoptosis bodies
Response by host to necrosis and apoptosis
Necrosis: inflammation
Apoptosis: no inflammation
what causes adaptive changes
Persistent (Chronic) stress/injury
are morhologic changes specific to type of chronic stress
No, seldom specific
similar responses at the cel level do what to the organ
may lead to different morphologic changes in the organ, despite similar respond in cell
are chronic cell injury insults very big
Might be minimal
length of chronic cell injury
is prolonged compared to acute cell injury
what are celular adaptations
Change in cell size
Change in cell number
Changes in cell differentiation
Abnormal intracellular accumulations
atrophy
shrinking cells
Hypertrophy
Growing cells
Hyperplasia
More cells
Metaplasia
Changes in cell differentiation with concurrent alterations of tissue organ function
when does cellular adaptations lead to greater output from tisssue
Hyperplasia
Hypertrophy
causes of etrophy
Decreases workload Loss of inervation Decreased blood Inadeqate nutration Decreased hormonal stimulation aging local pressure
what is squamous metaplasia of the bronchus
when the normal columnar epithlium becomes squamous
- no longer ciliary, so have to cuagh
what is intestinal metaplasia of the esophagus
where the esophagus starts to become like the intestines due to lots of vomiting
what is the normal constituents of cells
H2O, lipids, protein, carbs, maybe some calcium
what are the abnormal substances of cells
Endogenous or exogenous, pigments
mechanisms of intracellular accumulations
Abnormal metabolism
Defect in protein folding and transport
lack of enzyme
Ingestion of indigestible materials
what happens in the defect in protein folding and trasport
accumulation of abnormal proteins
technical name of fatty liver
TRiglyceride Accumulation steatosis
Xanthoma
CHolresterol Accumulation
what do cells look like in from cholesterol accumulation Xanthoma
Foamy macrophages filled with cholesterol
what does Cholesterol in vessels lead to
Atherosclerosis
Cholesterol thrombus
what diseases are caused by protein accumulation
Alpha1-anti-trypsin deficiency
Mallory bodies
Alzheimer’s
what does glycogen storage disease lead to
More glycogen
more lipid
big decerase in glucose 6-phosphatase activity
decreased phosphorylase activity
decreased fructose 1,6-diphosphatase activity
