Cell death

graph TD
    X[Nprmal Cell] ==> X1[Stress];
    X1 ==> X1a[Reversible Cell injury] 
    X1a ==>|stress not Removed| X1b[Irreversible Cell Injury];
    X1b ==> X1b1[Necrosis]
    X ==> X2[other factors
    like CD8+ killing  ];
    X2 ==> X2a[Apotosis];

Necrosis

• Cell swelling
• Loss of Nucleus by

  pyknosis Karyorrhexis Karyolysis

graph TD
    X{Typess of Cell Death} -.|External Cause|.-> X1[Necrosis];
    X1 ==> X1a[+ Inflammatory Reaction]
    X1a ==>|based on Type and Location of Injury| Z[Types of Necrosis];
    Z ==>|loss of Blood Supply| Z1[Coagulative Necrosis];
    Z1 ==>|resupply of Blood| Z1a[Red infarction]
    Z ==>|Infection| Z2[Liqufative Necrosis];
    Z2 ==>|DIgestion of Tissue my
    Enzymes| Z2a[Eg; Microglial Destruction of Brain tissue,Abscess by neutrophils , Pancreas Digestion my It's enzymes]
    Z ==>|Coagulative Necrosis of :octicons-arrow-down-24:er Limbs| Z3[Gangrenous Necrosis]
    Z3 ==>|if infected by Mirobes| Z3a[Wet Gangrene]
    Z ==> Z4[Casesous Necrosis];
    Z4 ==>|combination of Coagulative and Liqufative Necrosis on infected region| Z4a[Liquid- Neutrophils , COagulative -Mycobacterium , Fungus cells]
    Z ==>|digestion of Fat| Z5[Fatty necrosis];
    Z5 ==> Z5a(injury to fat and Calcium binding to injured fat cells  digested by lipase enzyme); 
    Z ==>|damage to BLood vessel| z6[Fibrinoid Necrosis];
    X -.|programmed.-> X2[Apotosis];
    X2 ==> X2a[No Inflammatory Reaction];
    XXX[Calcium deposition ]==> xz1[Dystropic CAlcification] & xz2[Metastatic Calification];
    xz1 ==> xz1a[Depostion of Calcium on dead cells]
    xz1a ==> xz1ab[Cancerous overgrow , improper blood supply death of cells calcium deposostion aka <mark> Somma bodies</mark>]; 
    xz2 ==> xz2a[Metasatic Calcification - Pathologically elevated Calcium deposition on cells]
    xz2a ==> xz2ab[Eg;Bone cancer]

Charateristics	Necrosis	Apotosis
Cell Size	Increase	Decrease
Nucleus	Pyknosis
	Karyohexis
	Karyolysis	Fragmented by endonucleases
Membreane	DAmaged	intact altered structure
Cytoplasmic Contents	Digestion by enzymes	released as apopotic bodies
Inflammation	Present	Not Present
Cause	Pathology

Apoptosis

Falling of leaves in greek

1. Shrinkage of Cell
2. Fragmentation of Cell into small pieces Apoptotic Bodies
3. ENgulfed by macrophage without inflammation

Apoptosis Initiators

1. Intrinsic
2. Extrinsic

graph TD
    X[Initiatores of Apotosis] ==> X1[Intrinsic] & X2 [Extrensic];
    X1 ==>X1a[mitochondria]
    X1a ==> X1ab[relases of Cytochrome C into Cytoplasm]
    X2 ==> X2a[Fas-FasL ligand Activation]  & X2b[TNF receptor Activation] & X2c[Granzyme and Porins]
    Z[Activation of Capases];
    X1a ==> Z;
    X2a ==> Z;
    X2b ==> Z;
    X2c ==> Z;

Capsases Activation

graph TD
    X[Extrinsic Pathway] ==> x1[Activation of TNF receptor ,FAs ligand ,Granulozyme by CD8+];
    x1 ==> x1a[Activation of Capsases- 8,10];
    X1a ==> X1b[Activation of Capsases 3,6];
    Z[Intrensic PAthway] ==> Z1[Activation of Capsases 9];
    x1b ==> x1bq[Activation of DNAse enzyme and othes]
    X1b ==> Zeeee[Apotosis];

Intrinsic Pathway

graph LR
    X[Proteins Regulating Intrinsic Pathway] ==> X1[Anti-Apotitic] & X2[Pro-Apototic];
    X1 ==>|proteins overexpressed inB-Cell lymphoma  | X1a[BCL2 proteins]
    X1a ==> x1ab[Makes Mitochondrial membrane impermiable];
    X2 ==> X2a[BAK,BAX]
    X2a -.withdrawl of growth factors,DNA damage 
    from radiation,protein misfolding.-> X2a1[Activation of BAK,BAX];
    X2a1 ==> X2a1a[INcrease the Permiablity of Mitochandrail membreane 
    Cytochrome C into Cytoplasm];
    Z[Activation of Capsase 9];