Pathology Flashcards
Apoptosis
- Noninflammatory cell death. Nuclear fragmentatoin and blebs forming
- Lupus may occur because of self reaction to apoptoti blebs
Intrinsic Pathway
- Loss of a growth factor or cellular injury leads to death of cell
- Increase in bax and decrease in BCL-2 leads to an increase in cyt c leakage from mitochondria leading to activation of caspaces
Extrinsic Pathway
FAS-L from T cells interacts with FAS on cell activating BAD and caspaces
-Also can be from perforin and granzyme that cause activation of caspaces
Ca
Increase in intracellular Ca causes activation of caspaces and cellular death
Necrosis
-Inflammatory process from irreversible cell damage
Gangrene
-Ischemic death. If not infected is considered dry, and if is infected, is considered wet
Fibrinoid Necrosis
-Occurs in vasulitis and in RA
Soponification
-Lipase digestion post infarct leads to Ca binding within dead tissue and decrease in plasma calcium
Irreversible Cell Injury
- Plasma Membran Ruptire
- Influx of Ca
- Lysosomal or mitochondrial Rupture
- Nuclear fragmentation
Brain areas vulnerable to ischemic injury
-Pyramidal cells of hipocampus and purkinje cells of cerebellum
Kidney
- Straight portion of the proximal tubule (medulla)
- Thick ascending limb of the loop of henle (medulla)
- Both have limited blood supply and increased metabolic demand
Shock
- Cardiogenic/hypovolemic: Increased TPR, decreased CO, cool clammy patient
- Septic: Vasodialtion leads to warm, red patient with decreased TPR and normal CO
Acute Inflammation
-Neutrophil, eosinophils, complement, Ab
Chronic
-Monocytes and lymphocytes predominate
Leukocyte extravasation
- Margination becuse of dilation and turbulent flow
- Rolling: P selectin from WP and E selectin, release due to IL-1 and IL-6 interact with sialyl lewis acid X on leukocytes
- Tight adhesion: ICAMs on endothelium and Integrins on leukocytes
- Tranmigration: Pecam, homotypic
- Chemotactic by: Bacterial products (LPS), IL-8, C5a, LTB4, Kalikrein