Cell Adaptation and Injury Mindmap

Nota:

• -Decrease in cell size -Number of cells doesn't change

1. Disuse atrophy

   Nota:

   • -Decreased energy requirement -Cell structure changes: Muscles have less ER, mitochondria, filament
2. Denervation atrophy

   Nota:

   • -Nerve stimulation to muscle lost -Ex: Stroke patient
3. Lack of hormone stimulation
4. Inadequate nutrition
5. Ischemia

   Nota:

   • -Decreased blood flow to organ -Leads to atrophy of cells and organ itself

Nota:

• -Increase in cell size --> tissue --> organ -Occurs in cells that can't increase in numbers (Ex: cardiac and striated -Increased protein, myofilaments, mito

1. Physiologic

   Nota:

   • -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)
2. Pathophysiologic

   Nota:

   • -Ex: Heart failure -Cells not proportional, malformed, not functioning properly -Change due to different signal molecules 

Nota:

• -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

1. Physiologyic

   Nota:

   • -Compensatory response, leads to regeneration and healing -
   1. Compensatory hyperplasia
   2. Hormonal hyperplasia
2. Pathologic

Nota:

• -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 

Nota:

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

1. Excessive use
2. Chemical exposure
3. Hypoxia
4. Physical Trauma
5. Infection and immune reactions
6. Genetic chagnes
7. Nutritional Imbalance

Nota:

• -Cell membrane, unable to maintain homeostasis

1. Causes
   1. IC Accumulation of substances

      Nota:

      • -Cell tries to dispose if they could -Accumulates in cytoplasm or organelles
      1. Causes
         1. Excessive

            Nota:

            • Too much normal body substance Ex: fat in liver (alcoholic cirrosis)
         2. Abnormal endogenous substance

            Nota:

            • Abnormal lipids in brain (Tay Sachs disease)
         3. Exogenous substance

            Nota:

            • From environment  Ex: Coal dust in miner lungs
   2. Tissue calcification
      1. Dystrophic

         Nota:

         • Ca salts deposited in injured tissues Ex: Atherosclerosis plaques (contains ca) Ex: Tuberculosis lesions, includes calcified granulomas
      2. Metastatic

         Nota:

         • Hypercalcemia- deposits to normal tissues -Also leads to renal calculi (kidney stones)
   3. Physical agents

      Nota:

      • Damage cell structure 
      1. Mechanical trauma

         Nota:

         • Direct damage to cells
      2. Temp extremes

         Nota:

         • Damage to cells, organelle and enzymes -Hypothermia and frostbite
      3. Electrical injury

         Nota:

         • damages tissues, disrupts cardiac and nerve impulses
      4. Radiation

         Nota:

         • -Interrupt cell replication, cause mutation, kill cells -Cause cancers like leukemia 
   4. Chemical exposure

      Nota:

      • Mechanisms: injure cell membranes, chemicals block enzyme pathways, coagulate proteins, toxic to cells (ex: liver cells) 
      1. Drugs

         Nota:

         • Ex: Acetominophen toxic to liver
      2. Lead

         Nota:

         • Interferes with nerve and brain development  -May be toxic to children
      3. Mercury

         Nota:

         • Toxic to nerves and kidneys
   5. Infections

      Nota:

      • Biologic agents invade and destroy cells -Viruses change cell DNA -Bacteria produce toxins -Microorganisms cause inflammatory/immune response
2. Mechanisms

   Nota:

   • -Lead to anaerobic metabolism, cell swelling and direct injury to cells 
   1. Free Radicals

      Nota:

      • Molecules with unpaired electrons -Unstable/reactive -Damage cell membranes, DNA, tissues 
      1. ROS

         Nota:

         • Reactive oxygen species -Oxygen-containing molecules that include free radicals -Produced by normal process (Ex: metabolic burst accompanying phagocytosis)
         1. Oxidative stress

            Nota:

            • -Occurs when body unable to eliminate ROS -Plays role in aging and development of disease (Ex: cancer)
   2. Hypoxic Cell Injury

      Nota:

      • Lack of oxygen, interrupts oxidative metabolism, generation of ATP -Heart, brain and kidneys cells damaged quickly 
      1. Hypoxia

         Nota:

         • Lack of sufficient O2 to body cells, tissues and organs
         1. Causes

            Nota:

            • -Blocked blood vessels -Respiratory disease, blocks inhalation and diffusion of oxygen across alveolar membrane 
            1. Blocked blood vessels
            2. Respiratory disease
            3. Loss of hemoglobin

               Nota:

               • Carries oxygen to cells Leads to anemia 
            4. Tissue edema

               Nota:

               • Can block oxygen from getting to cells
            5. Inability to use oxygen

               Nota:

               • Ex: lactic acidosis -Cells unable to use oxygen even though it's being delivered to them
         2. Results

            Nota:

            • Decreased ATP production, cells swell -Na/K pump fails -Na and water move into clls -Vacuoles form -Cytoplasm swells -Cells degenerate and rupture
            1. Call membrane damange

               Nota:

               • -Cell destruction releases markers  >Troponin from damaged heart cells >AST/ALT from damaged liver cells 
      2. Hypoxemia

         Nota:

         • Lack of O2 in the blood specifically 
      3. Ischemia

         Nota:

         • Lack of enough oxygen to cells or organ -Leads to anaerobic metabolism -Ex: Myocardial eschemia- coronary arteries blocked 
         1. Reperfusion Injury

            Nota:

            • -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 
            1. Free Radicals

               Nota:

               • -Product of xanthine dehydrogenase metabolism from influx of O2 during reperfusion injury
      4. Anoxia

         Nota:

         • Lack of oxygen to cells Ex: brain - cerebral anoxia 
   3. Impaired Ca homeostasis

      Nota:

      • -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
3. Outcomes
   1. Recovery
   2. Apoptosis

      Nota:

      • -Programmed cell death -Purpose: removed injured cells -Cell fragments engulfed by phagocytes
      1. Execution Pathways

         Nota:

         • carried out by proteolytic enzymes called caspases
         1. Extrinsic Pathway

            Nota:

            • Activated by FAS ligand
         2. Intrinsic Pathway

            Nota:

            • Activated by signals like ROS
            1. ROS

               Nota:

               • Activates intrinsic pathway, which signals apoptosis 
   3. Cell Death

      Nota:

      • -Cell death to organ or tissue -Loss of cell membrane activity and enzyme breakdown of cell parts
      1. Liquefaction necrosis
      2. Coagulation necrosis
      3. Gangrene

         Nota:

         • Large area of necrosis 
         1. Dry

            Nota:

            • Area shrinks, wrinkles -Turns black
         2. Wet

            Nota:

            • Swollen, bacteria 
4. Cell aging theories

   Nota:

   • -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