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Cellular Pathology - Coggle Diagram

- - - - eosinophile appearance (🚫DNA)
        
        E.g. acute hepatitis = viral cytolysis (red appearance)
      - vitrous + homogenous (🚫glycogen)
      - vacuolized: enz. digestion + intra.c. organites
    - - Caryolysis (dissolved DNA (no basophile DNA = eosin appearance enz. = DNAses)
        
        M.E.:
      - pyknosis (irrev. chrom. condensation/retract) (Black dot stuff)
        
        M.O.:
        
        M.E.:
      - karyorrhexis (frag. nucleus)
        
        M.E.:
      - 🚫nucleus
  - - - Coagulation necrosis:
        
        Protein denat
        
        Hypoxia ++
        
        Macro appearance:
        firm tissues, white-gray
        
        Micro:
        cell shape preserved
        
        Eosin
        
        Coagulated
        
        🚫nucleus
        
        Heart: acute infarctus
        
        "Ischemic" necrosis
        
        Kidney
      - Gangrenic necrosis:
        Ischemia + anaerobic germes
      - Fibrinoid necrosis: homogenous + eosin + same coloration as fibrin
    - - Liquefaction necrosis: no abcess
        
        Proteolytic digestion dead c.
        
        Macro:
        Liquid soft mass
        Yellow if polynucleic
        
        Micro:
        .complete disappearance of c.
        tissue can't be recon'd
        C. debris
        Macrophages + altered polynucs
      - Steato-necrosis:
        adipose tissue, usually observed at acute pancreatitis
        pancr. enz. liberated (+++)
        
        Macro:
        chalk-like, white
      - Casseous necrosis: carac tuberculosis
  - - - Physio:
        
        Embryo dev
        
        Remodeling bone/cartilage (participates)
        
        Immuno system maturing
        
        NS maturing
        
        Homeostasis epith c.
        
        intestinal crypts
        
        endometrium
      - Patho:
        
        abnormal (cancerous) c.
        
        c. infected by virus
        
        hepatitis
        
        HIV
    - - ++apoptosis:
        
        prolif symptoms
        
        CANCER
        
        autoimmunity
        
        viral infections
      - ++prolif:
        
        tissue loss
        
        Degen diseases
        
        AIDS
        
        ischemia
    - - initiation
        
        Lesions DNA
        
        irradiation
        
        UV radiations
        
        gamma radiation
        
        genotoxins
        
        Activation of receptors death site
        
        anti-tumor agents
        
        interrupt cell cycle
        
        growth factors inhibited
      - decision
        
        Bcl-2 agents family attacks death site
        
        Cyt-2 goes to site
      - degradation
        
        caspase activation (cascade)
        
        cell proteins get cleaved
        
        modif membranes
        
        reorg cytoskeleton
        
        chromatin condensation
        
        fragmentation DNA
        
        forming apoptotic bodies
        
        clearance + degrad apoptotic bodies
    - - Memorize slides 83-84
        
        Depleting growth factors
        
        interactions with proteins TNFR-TNF, Fas-FasL
        
        Activate initiator caspases
        
        Activate executor caspases
        
        Fragmenting DNA via endonucleases activated by p53
        
        Degrading cytoskeleton
        
        Cytotoxic lymphocytes degrade c. via toxin radiation
        
        e.g. Granzyme B
    - - M.E.:
        
        Nucleus (+++):
        
        nucleolus anomalies (fibrillary)
        
        Chromatin condensation
        
        Disparage of nucl. envelope + Frag. nucleus
        
        Reduced to apoptotic bodies
        
        Cytoplasm
        
        mito swelling + loss of double membranes
      - M.O.
        
        Cell retration
        
        Chromatin condensation
        
        Cytoplasm bubbles formation
        
        Cell fragmentation into several bits -> apoptotic bodies
        
        Phagocytosis of apop bodies via macrophages
        
        NO starting inflamm rx
      - Basic steps:
        
        Condensation
        
        Fragmentation
        
        Phagocytosis
- - - - Ionizing radiation
        
        Kills cells via water radiolysis: H2O ⇒ H + OH
        
        Attacks membs via perox + DNA
        
        Stops replication OR apoptosis
        
        non-proliferative c. are killed via radio ++doses
      - Exogenous chemical products (CCl4)
        
        Can provoke c. lesions
        
        directly: combination intra.c. organelles/molecules like CCl4
        
        indirectly: via transformation into toxic metabolites
      - Redox rx (normal breathing)
      - Metal donors of electrons (Fe, Cu)
    - - Peroxidation of lipid membranes
      - Oxydation of membrane AGs (?)
      - Peroxide production (reactive, unstable)
      - Auto-cat chain rx
      - Alterative oxydations proteins
        
        Leads to fragmentation proteins
      - DNA lesions
        
        F.R.@Thymine = break DNA (++@aging/cancer c.)
    - - Antioxydants
      - Transition metal
        transport proteins
      - Enz. systems
        
        Catalase
        
        Glutation peroxydase
- - - - If irrev. still = apoptosis
        
        Apoptosis = 🚫inflamm process BUT influx of histiocytes ⇒ macrophages (@cell debris)
    - - Necrosis = exogenous stim + inflamm process started (e.g. coagulation)
- - - - Hydroponic:
        swollen mito = water enters the cell
- - - - Anatomopathology: morpho manifs
        
        Clinical manifestations
- - - - Hyperplasia
        
        ++mass tissue/organ/part of organ via ++c.
        NO MODIF FX SHAPE (Architecture)
        
        = ++ fxal hyperactivity
        
        stays controled by reg mechs c. prolif
        
        ++assoc hypertrophy c.
        
        ++@rapid renew tissues
        
        Epidermis
        
        Intestinal epith
        
        Hepatic parenchyma
        
        Physio vs. Patho:
        
        Physio:
        
        compensate organ post-surgery (e.g. partial hepatectomy)
        
        hormonal organ (e.g. mammary during preg)
        
        Patho:
        
        e.g. endometrium: hyperestrogenias
        
        limited region of organ = nodular hyperplasia
        
        liver
        
        prostate
      - Hypoplasia + Aplasia: ↓#c. via ↓/🚫c.✖️(multiplication)
        
        Conditions to apparate:
        
        Medullar: post-ionizing radio
        
        Senescence (++age): endometrial/testicular HYPOpl
    - - Hypertrophy:
      - Atrophy: bigger ↓# of c.
        Hypotrophy: ↓size of c.
        
        C. Atrophy: ↓fx. activity = ↓size of c.
        
        Atrophy organ = aplasia + atrophy = via. c. atrophy OR ↓# c.
        
        Physio Atrophy: hormonal involution; thymus (@puberty), ovaries (@menopause)
        
        Patho Atrophy: muscular via innervation suppression
        adipocyte atrophy via denutrition state
    - - Metaplasia
        
        transform. tissue from structure fx 1 to structure fx 2 = reversible adaptation via regression; ++ epith. c.
        
        pathogenia: metap = reprog. stem c. epith/mesenchyma (different paths of differentiaition)
        
        physio: cytogen chorion metap endometrium
        
        patho: via toxic/chem/hormonal/inflamm
        
        slides 37/8/9/40 ANKI examples