Exam 2 Flashcards
Adaptive Response of a cell to_____ ________leads to an altered steady state
stimuli (stress)
If a cell is under stress for a short amount of time_____ injury happens and the cell _____
Reversible, adapts
If a cell is under stress for a long amount of time_____ injury happens and the cell _____
Irreversible, dies
In reversible injury, low ATP causes
- decreased oxi phos which leads to low ATP
- low ATP can be offset by glycolysis but it leads to low pH and low glycogen stores. this causes clumping of chromatin
- low ATP causes down regulation of Na+ which leads to an influx of water and sodium and a loss of potassium, this causes blebs and cellular swelling
- the other effects of low ATP are low protein synthesis, detachment of ribosomes and lipid deposition
In irreversible injury, low ATP causes
- membrane injury; loss of phospholipids, cytoskeletal alternation and lipid breakdown leads to enzymes leaving the cell and an influx of Ca+ which leads to increased Ca2+ in mitochondria
- low pH from glycolysis leads to the release of lysosomal enzyme which digests proteins and changed the nucleus
Leads to NECROSIS
Attributes of necrosis
- group of cells affected
- caused by injurious agents/events
-reversible events happen before it becomes irreversible - no ATP needed
- cells swell from H20 influx
-organelles and nuclear material is degraded by lysosomal enzymes (no longer organized)
-debris stimulates inflammatory cell response
Attributes of apoptosis
- programmed death
- affects single or a few cell
- irreversible
- Requires ATP
- Cells shrink as cytoskeleton is disassembled (like a building crumbling in on itself)
- organelles are membrane bound and organized
- molecules on vesicles membrane stimulare phagocytosis
- no inflammatory response
4 components in the inflammatory process
- vascularized connective tissue ( plasma, blood vessels)
- blood cells (neutrophils, monocytes, leukocytes as a whole )
- connective tissue cells (mast cells, fibroblasts, macrophages and lymphocytes)
- chemical mediators
whats the first step in leukocyte migration
- Margination
(Due to gaps in vascular wall from vasodilation, protein filled exudate flows out of the vessel, making the blood more viscous and pushing the RBC toward the center. the WBCs are pushed toward the edge of the blood vessel toward the gaps)
Irreversible cell injury is when the membrane is _____ and leads to ______
no longer intact, necrosis
What is the second step in leukocyte migration
Rolling
-cytokines cause the expression of adhesion molecules on the surface of both the endothelium (selectins) and the leukocyte (lewis); this slows down the leukocyte and prepares it for integrin activation and endothelial adhesion
What is the third step in leukocyte migration
Integrin activation and stable adhesion
Once the leukocyte is slow enough, the integrins on the leukocyte will bind with the Integrin ligand on the endothelial walls. these ligands are induced by proinflammatory cytokines. the integrins are now active and adhered to the endothelium wall of the blood vessel.
What is the fourth step in leukocyte migration
Transmigration (diapedesis)
PECAM-1 allows adhered leukocytes to through endothelial gaps in the tissue in a controlled manner.
What is the fifth and sixth steps in leukocyte migration
chemotaxis allows leukocytes to migrate (5th) to the infection site to begin phagocytosis (6th)
chemokines from bacteria, mast cells, and compliment proteins attract the leukocyte to the infection site. leukocytes recognize and kill pathogens via phagocytosis
What are the 3 major steps in phagocytosis
- recognition and attachment (opsonization)
- engulfment
- killing in an O2 dependent/independent manner
What is O2-dependent killing?
When something is phagocytosed, oxygen is engulfed with it. O2 is rapidly converted into O2* (reactive O2) via NADPH to NADP oxidation. O2* is made into H2O2. H2O2 can be converted into HOCl via myeloperoxidase (MPO) which degrades bacteria.
neutrophils have myeloperoxidase (MPO) granules in them
What is O2 independent killing
- bactericidal enzymes that degrade bacterial walls
- lysosomal enzymes that hydrolyze glycopeptide coats on bacteria
- lactoferrin
-cationic granular proteins
-defensins
The first step of inflammation in Lobar Pneumonia
Congestion- fluid in alveolar space
fibrin rich fluid spreads from alveoli to alveoli. this causes less gas exchange and a cough
The second step of inflammation in Lobar Pneumonia
Red Hepasitsation (airless lung and cough)
-neutrophils attack organisms and phagocytose them
The third step of inflammation in Lobar Pneumonia
Grey hepatisation (cough)
- macrophages come in and phagocytose dead neutrophils, bacteria, and fibrin (clotting factors)
The fourth step of inflammation in Lobar Pneumonia
Many routes from here;
-resolution, no scarring
-scar if immunocomp (fibrosis)
- abscess if it cant be cleared up
-spread to other parts of the body if it can be cleared up
-death if it can’t be cleared up
Histologically, what do the purple dots mean?
types of leukocytes/WBC present.
WBCs are not normally in the tissue, in inflammation they are
