Cell Adaptation and Injury Mindmap

Cell Adaptation and Injury Mindmap

1. ATROPHY

   • -Decrease in cell size -Number of cells doesn't change
   • Disuse atrophy
     • -Decreased energy requirement -Cell structure changes: Muscles have less ER, mitochondria, filament
   • Denervation atrophy
     • -Nerve stimulation to muscle lost -Ex: Stroke patient
   • Lack of hormone stimulation
   • Inadequate nutrition
   • Ischemia
     • -Decreased blood flow to organ -Leads to atrophy of cells and organ itself

2. HYPERTROPHY

   • -Increase in cell size --> tissue --> organ -Occurs in cells that can't increase in numbers (Ex: cardiac and striated -Increased protein, myofilaments, mito
   • Physiologic
     • -Ex: athletes -proportional increase in width and length of muscle cell -Changes stimulated by stretch of muscle fibers -Promoted by biochemical signals (growth hormone and other ligands --> protein production)
   • Pathophysiologic
     • -Ex: Heart failure -Cells not proportional, malformed, not functioning properly -Change due to different signal molecules 

3. HYPERPLASIA

   • -Increase in number of cells in tissue/organ -Occurs in cells that can undergo mitosis -Mechanism: activation of genes controlling cell proliferation -Increased rate of cell division
   • Physiologyic
     • -Compensatory response, leads to regeneration and healing -
     • Compensatory hyperplasia
     • Hormonal hyperplasia
   • Pathologic

4. METAPLASIA

   • -One cell type is replaced by another that is better able to survive -Mechanism: undifferentiated cells reprogrammed -Ex: In smokers, bronchial epithelial cells replaced by squamous cell 

5. DYSPLASIA

   • -Abnormal change in size, shape and organization of cells -Not a true adaptive change -Associated with irritation and inflammation

6. Stressors

   • Excessive use
   • Chemical exposure
   • Hypoxia
   • Physical Trauma
   • Infection and immune reactions
   • Genetic chagnes
   • Nutritional Imbalance

7. Cell Injury

   • -Cell membrane, unable to maintain homeostasis
   • Causes
     • IC Accumulation of substances
       • -Cell tries to dispose if they could -Accumulates in cytoplasm or organelles
       • Causes
         • Excessive
           • Too much normal body substance Ex: fat in liver (alcoholic cirrosis)
         • Abnormal endogenous substance
           • Abnormal lipids in brain (Tay Sachs disease)
         • Exogenous substance
           • From environment  Ex: Coal dust in miner lungs
     • Tissue calcification
       • Dystrophic
         • Ca salts deposited in injured tissues Ex: Atherosclerosis plaques (contains ca) Ex: Tuberculosis lesions, includes calcified granulomas
       • Metastatic
         • Hypercalcemia- deposits to normal tissues -Also leads to renal calculi (kidney stones)
     • Physical agents
       • Damage cell structure 
       • Mechanical trauma
         • Direct damage to cells
       • Temp extremes
         • Damage to cells, organelle and enzymes -Hypothermia and frostbite
       • Electrical injury
         • damages tissues, disrupts cardiac and nerve impulses
       • Radiation
         • -Interrupt cell replication, cause mutation, kill cells -Cause cancers like leukemia 
     • Chemical exposure
       • Mechanisms: injure cell membranes, chemicals block enzyme pathways, coagulate proteins, toxic to cells (ex: liver cells) 
       • Drugs
         • Ex: Acetominophen toxic to liver
       • Lead
         • Interferes with nerve and brain development  -May be toxic to children
       • Mercury
         • Toxic to nerves and kidneys
     • Infections
       • Biologic agents invade and destroy cells -Viruses change cell DNA -Bacteria produce toxins -Microorganisms cause inflammatory/immune response
   • Mechanisms
     • -Lead to anaerobic metabolism, cell swelling and direct injury to cells 
     • Free Radicals
       • Molecules with unpaired electrons -Unstable/reactive -Damage cell membranes, DNA, tissues 
       • ROS
         • Reactive oxygen species -Oxygen-containing molecules that include free radicals -Produced by normal process (Ex: metabolic burst accompanying phagocytosis)
         • Oxidative stress
           • -Occurs when body unable to eliminate ROS -Plays role in aging and development of disease (Ex: cancer)
     • Hypoxic Cell Injury
       • Lack of oxygen, interrupts oxidative metabolism, generation of ATP -Heart, brain and kidneys cells damaged quickly 
       • Hypoxia
         • Lack of sufficient O2 to body cells, tissues and organs
         • Causes
           • -Blocked blood vessels -Respiratory disease, blocks inhalation and diffusion of oxygen across alveolar membrane 
           • Blocked blood vessels
           • Respiratory disease
           • Loss of hemoglobin
             • Carries oxygen to cells Leads to anemia 
           • Tissue edema
             • Can block oxygen from getting to cells
           • Inability to use oxygen
             • Ex: lactic acidosis -Cells unable to use oxygen even though it's being delivered to them
         • Results
           • Decreased ATP production, cells swell -Na/K pump fails -Na and water move into clls -Vacuoles form -Cytoplasm swells -Cells degenerate and rupture
           • Call membrane damange
             • -Cell destruction releases markers  >Troponin from damaged heart cells >AST/ALT from damaged liver cells 
       • Hypoxemia
         • Lack of O2 in the blood specifically 
       • Ischemia
         • Lack of enough oxygen to cells or organ -Leads to anaerobic metabolism -Ex: Myocardial eschemia- coronary arteries blocked 
         • Reperfusion Injury
           • -Occurs when O2 restored to ischemic tissue -Ischemia causes increase in ATP consumption, production of xanthine dehydrogenase -O2 --> metabolizes xanthine to produce massive amounts of superoxide hperoxide -Radicals cause membrane damage, ca overload of mitochondria -Mito pores open, ATP escapes, cells die 
           • Free Radicals
             • -Product of xanthine dehydrogenase metabolism from influx of O2 during reperfusion injury
       • Anoxia
         • Lack of oxygen to cells Ex: brain - cerebral anoxia 
     • Impaired Ca homeostasis
       • -Ca/Mg pump uses ATP to move Ca out of cell (only precise small amount needed in cell) -Cell membrane damage allows Ca to enter cell -Activates enzymes (proteases, lipases, protein kinases) that damage cell membranes, cytoskeleton, proteins, chromatin *-ases are enzymes that breakdown
   • Outcomes
     • Recovery
     • Apoptosis
       • -Programmed cell death -Purpose: removed injured cells -Cell fragments engulfed by phagocytes
       • Execution Pathways
         • carried out by proteolytic enzymes called caspases
         • Extrinsic Pathway
           • Activated by FAS ligand
         • Intrinsic Pathway
           • Activated by signals like ROS
           • ROS
             • Activates intrinsic pathway, which signals apoptosis 
     • Cell Death
       • -Cell death to organ or tissue -Loss of cell membrane activity and enzyme breakdown of cell parts
       • Liquefaction necrosis
       • Coagulation necrosis
       • Gangrene
         • Large area of necrosis 
         • Dry
           • Area shrinks, wrinkles -Turns black
         • Wet
           • Swollen, bacteria 
   • Cell aging theories
     • -Molecular: Mutation or changes in gene expression -Cellular: senescence involving free radical injury, telomere shortening (happens with every cell division), apoptosis -Decline in integrative functions of organ systems  *Senescence- decline of functioning with age