10.13 Injury/ Inflammation/ Healing / Cancer Flashcards
_ is an increased size of cells
Hypertrophy is an increased size of cells
* Ex: weight lifting
_ is a non-neoplastic increase in the number of cells in an organ/tissue
Hyperplasia is a non-neoplastic increase in the number of cells in an organ/tissue
* Physiologic not pathologic
* Ex: mammary tissue increasing during pregnancy
_ is a reduced size of cells or organs
Atrophy is a reduced size of cells or organs
* Ex: old people don’t use muscles so they lose them
_ is a conversion of one differentiated cell type to another
Metaplasia is a conversion of one differentiated cell type to another
Once changes occur to the _ of the cell, the damage is irreversible and cell death will proceed via _ or _
Once changes occur to the nucleus of the cell, the damage is irreversible and cell death will proceed via necrosis or apoptosis
A normal nucleus will appear round with chromatin still _ and nuclear membrane _
A normal nucleus will appear round with chromatin still dispersed and nuclear membrane still intact
_ is when the nucleus shrinks into a blue-black dot due to the chromatin clumping
Pyknosis is when the nucleus shrinks into a blue-black dot due to the chromatin clumping
_ is the fading or disappearance of the nucleus (less blue and distinct)
Karyolysis is the fading or disappearance of the nucleus (less blue and distinct)
_ is the fragmentation of the nucleus
Karyorrhexis is the fragmentation of the nucleus
One big difference between necrosis and apoptosis is that _ is always pathologic
One big difference between necrosis and apoptosis is that necrosis is always pathologic
(Necrosis/ apoptosis) usually involves mutliple cells within the tissue
Necrosis usually involves mutliple cells within the tissue
Another difference in necrosis and apoptosis is that _ can be initiated intrinsically
Another difference in necrosis and apoptosis is that apoptosis can be initiated intrinsically
* Apoptosis- intrinsic or extrinsic signal
* Necrosis- extrinsic signal (burn, hypoxia, toxin)
A series of steps involved in apoptosis ultimately release _ from the mitochondria which causes a _ cascade and disrupts the cytoskeleton
A series of steps involved in apoptosis ultimately release cytochrome c from the mitochondria which causes a caspase cascade and disrupts the cytoskeleton
The intrinsic apoptotic pathway begins with DNA damage activating _ and increasing _
The intrinsic apoptotic pathway begins with DNA damage activating P53 and increasing BAX/BAK
* Leads to cyt c release –> caspase cascade –> cytoskeleton disruption
Alternatively, apoptosis can be triggered extrinsically by _ ligand or by _ adaptive immune cells
Alternatively, apoptosis can be triggered extrinsically by Fas Ligand or by CD8+ adaptive immune cells
_ necrosis is the most common type of necrosis and is caused by loss of blood flow (ischemia)
Coagulative necrosis is the most common type of necrosis and is caused by loss of blood flow (ischemia)
_ necrosis is a type of necrosis associated with abscess formation with intense infiltration of neutrophils (pus-forming)
Liquifactive necrosis is a type of necrosis associated with abscess formation with intense infiltration of neutrophils (pus-forming); it is caused by enzymatic lysis of cells
* Ex: lung abscess with liquifactive necrosis and cavitation
* Neural tissue liquefaction
How would necrotic myocytes look different from normal?
Necrotic myocytes (following MI) are hyper-eosinophilic (pink) and have ghost cells (lack nuclei)
_ necrosis occurs when granuloma formation leads to the death of surrounding tissue
Caseous necrosis occurs when granuloma formation leads to the death of surrounding tissue
What are the common causes of caseous necrosis?
TB infection, histoplasmosis
* These are granuloma-forming
_ necrosis occurs from a breakdown of triglycerides and resulting fat saponification (due to pancreatitis)
Fat necrosis occurs from a breakdown of triglycerides and resulting fat saponification (due to pancreatitis)
_ necrosis is the deposition of fibrin and immune complexes in blood vessel walls
Fibrinoid necrosis is the deposition of fibrin and immune complexes in blood vessel walls
* Associated with vasculitis, autoimmune disease, hypertensive emergencies
4 cardinal signs of acute inflammation:
- Swelling (tumor)
- Redness (rubor)
- Heat (calor)
- Pain (dolor)
What is the goal of acute inflammation?
- We want to deliver effective molecules to the site of injury/inflammation –> vasodilation
- We want to cause blood clotting at the site –> clotting
- We want to promote repair of the tissue –> recruit inflammatory cells
How do we recruit and activate inflammatory cells to come to the site of infection?
Increase expression of leukocyte adhesion molecules on endothelial cells
During acute inflammation, the first innate immune cells to arrive are _
During acute inflammation, the first innate immune cells to arrive are neutrophils
* They will kill microorganisms via phagocytosis
Neutrophil response will peak about _ hours after injury/infection
Neutrophil response will peak after 24 hours after injury/infection
_ are the predominant cell type 48-72 hours after injury/infection
Macrophages are the predominant cell type 48-72 hours after injury/infection
What are the steps of neutrophil migration?
- Margination: increased vascular permeability leads to increased hemoconcentration which increases the probability of neutrophils contacting the endothelium; “marginate” meaning they move toward the periphery of blood flow
- Rolling: slows the neutrophil down; Sialyl-lewis glycoproteins interact with the “selectin speed bumps”
- Binding: tight adhesion with ICAM-1 on the endothelium stops the neutrophil in place
- Diapedesis: neutrophil crawls between endothelial cells (PECAM-1)
- Chemotaxis: IL-8
Neutrophil rolling involves _ glycoproteins on the neutrophil interacting with _ on the endothelium
Neutrophil rolling involves sialyl-lewis glycoproteins on the neutrophil interacting with E-selectin, P-selectin on the endothelium; selectin speed bumps slow down neutrophil
Neutrophil binding involves an integrin on the neutrophil interacting with _ on the endothelium
Neutrophil binding involves an integrin on the neutrophil interacting with ICAM-1 on the endothelium
Diapedesis/ migration of neutrophils through the endothelium involves _
Diapedesis/ migration of neutrophils through the endothelium involves PECAM-1