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Cell AID - Coggle Diagram
Cell AID
Cell adaptation
Hypertrophy
Physiologic
Inc. workload skeletal muscles
Pathologic
Cardiac enlargement
HTN
Aortic valve
Mechanism
Mechanical trigger
Cell growth mediators
Conversion to fetal protein
Limit
degenerative changes
Hyperplasia
Physiologic
Compensatory hyperplasia
Hormonal hyperplasia
breast at puberty
Pathologic
Endometrial hyperplasia
BPH
HPV infection
May lead to cancer
Atrophy
Causes
Dec. workload
immobilisation
allow healing
loss of innervation
Dec. blood supply
dec. nutrition
aging
Mechanism
Dec. protein synthesis
Inc. proteolysis
Autophagy
Metaplasia
Transdifferentiation
Types
Epithelial
Vit. A
C to S
Smoker
S to C
GERD
Mesenchymal
Bone inside CT
May lead to malignancy
Cell injury
State
Reversible
Cellular swelling
Pallor
Turgor
Fatty change
TAG
Lipid vacuoles
Membrane blebbing
microvilli distortion
Myelin figures
Mitochondrial changes
ER dilatation
polysome dissociation
Nuclear alteration
Chromatin clumping
Irreversible
Inability to restore mitochondrial function
loss of plasma membrane structure
loss of DNA and cell integrity
Causes
Hypoxia & Ischemia
Arterial obstruction
dec. oxygenation
Loss of ATP
membrane transport
protein synthesis
lipogenesis
HIF-1
VEGF
VHL
Some tissues better suited
Liver & Muscle
Warburg effect
Effects
Dec. Na+ pump
Lactic acid accumulation
Structural protein defects
Reperfusion injury
Reversal of blood flow causes injury
Mechanism
Inc ROS
Mitochondria damaged
Enzyme leakage
no compensation
Influx of leukocytes, plasma proteins and complement
Membrane damage
Oxidative stress
Generation
Redox
Mitochondrial respiration
SOD
Fenton reaction
Oxidative burst
Defensive
Enzymes
NO
Peroxynitrite
Factors
Radiant energy
Inflammation
Reperfusion
Enzyme metabolism
Removal
SOD
GSH peroxidase
Catalase
Antioxidants
Injury
Lipid peroxidation
Protein cross-linking
DNA damage
Cellular signalling
Toxins
Direct
Mercurous chloride
Antineoplastic
Microorganism toxins
Latent
CCl4
CytP450
Infectious agents
Immunologic reactions
Hypersensitivity
Autoimmune
Chronic immune
ER stress
Accumulation of misfolded protein
Chaperone
Ubiquitination
Unfolded protein resposne
Causes
Aging
ID
Neurodegeneration
pH
Redox state
Diseases
Receptor deficiency
CFTR
Tay Sachs
Protein misfolded
Cruetzfeldt Jakob
Alzheimer
Retinitis Pigmentosa
Both
Antitrypsin def.
DNA damage
various causes
ROS
Mutations
p53 accumulation
BH3 sensor
Inflammation
Aging
Nutrition imbalance
Events
Mitochondrial dysfunction
Oxidative phosphorylation
Failure
Dec. ATP
Abnormal
ROS
High conductance channel
Cyt. c release
Defects in memb. permeability
Mit. membrane
Plasma membrane
Lysosomal membrane
Cell death
Necrosis
Cytoplasmic changes
Eosinophilia
Glassy appearance
glycogen particles lost
Moth eaten
Myelin figures
Nuclear changes
Pyknosis
Karyorhexis
Karyolysis
Fates of necrotic cells
Persist
Digest
Disappear
Degraded
Short FA
Calcified
Types
Coagulative
Architecture preserved
Infarcts
except CNS
Liquefactive
focal bacteria
CNS infarcts
Pus if inflammed
Gangrenous
Coagulative necrosis
superimposed liquefactive
Caseous
TB foci
Cheese-like
Granuloma
Fat
Pancreatic lipases
Fat saponification
Fibrinoid
Misc
Cardiac
CK and Troponin release
Bile duct
ALP release
Apoptosis
Causes
Physiologic
Embryogenesis
Turnover of proliferative tissues
Involution of hormone dependent tissues
Dec. Leukocyte count
Elimination of self reactive lymphocytes
Pathologic
DNA damage
Misfolded protein
Infection
Mechanism
Mitochondrial
Cyt C
Caspase 9
Bcl-2
Bcl-xL
BAX, BAK
BH3
Death receptor
Type I TNF
Fas
CD95
FasL
T-cell CD8
Caspase 8
Clearance
Phosphatidylserine
flipping
Proapoptotic factors
Macrophage receptors
Others
Necroptosis
TNF
RIP
Pyroptosis
Inflammosome
IL-1
IL-18
Autophagy
Lysosomal autodigestion
nutrient deprivation
Autophagolysosome
ER
Atrophy as adaptation
Myopathy + ischemic injury
IBD
polymorphisms
regulator of autophagy
Misc
Intracellular accumulations
Cholesterol and esters
Protein
Neurofibrillary tangles
Russel bodies
Albumin
Nephrotic syndrome
Glycogen
Pigments
Carbon
Anthracosis
Black
Coal worker
Lymph node and lung parenchyma
Lipofuscin
Brownish yellow
Wear and tear
Aging
Melanin
Brown black
Protect from UV
3 sources
Hemosidern
Golden-yellow
Hb- derived
excess iron
Prussian blue
Fatty changes
Dystrophic Calcification
CaPO4 crystals
Indicate necrosis or injury
Cause injury
valves
Metastatic
Aging
Mechanisms
Accumulation of DNA mutations
Dec. Cell replication
Werner synrome
Telomeres
Telomerase
Telomeropathies
Persistent inflammation
Inflammasome pathway
Defective protein homeostasis
IGF-1
Calorie restricting