1: Cell Response And Adaptations Flashcards
Etiology
Initiating cause of a disease
Pathogenesis
Sequence of molecular, biochemical, and cellular events that lead to disease development
Four steps of disease leading to S/S
- Etiology
- Pathogenesis
- Morphological changes
- Clinical manifestation (S/S)
Disease
Any deviation from normal structure/function of a part/organ/system as manifested by characteristic symptoms and signs
Disorder
A derangement or abnormality of function; a morbid physical or mental state
Neoplasm
A new + abnormal growth, specifically when uncontrolled and progressive
Syndrome
A set of sx that occur together - the sum of signs of any morbid state
When can cardiac-specific enzymes be detected in the blood after MI?
As early as two hours, but sometimes not until 4-12 hours later
Myelin figures
Phospholipids derived from damaged cell membranes that appear in reversible cell injury
Major mechanism of apoptosis
Mitochondrial pathway
Three anti-apoptotic and three pro-apoptotic proteins
Anti: BCL2, BCL-XL, MCL1
Pro: cytochrome C, BAX, BAK
Function of anti-apoptotic proteins
Keep mito outer membrane impermeable to prevent leakage of cytochrome C into cytosol
How does BAX-BAK complex function?
Oligomerize within outer mito membrane and promote mito permeability
Regulated apoptosis initiators: two other names
Sensors, BH3-only proteins
BH3 only protein functions
Sensors of cell stress and damage to regulate balance between pro- and anti-apoptotic proteins
Examples of regulated apoptosis initiators/BH3-only proteins
BAD, BIM, BID, Puma, Noxa
How is extrinsic pathway of apoptosis initiated?
FasL binds Fas receptor (a TNFR)
What cell types express FasL?
CD4 T cells and some CD8 T cells
What protein can inhibit extrinsic mechanism of apoptosis? How?
FLIP: binds pro-caspase-8 but cannot cleave and activate it
Pyroptosis
Programmed cell death + IL-1 and fever
Necroptosis
Necrosis through a controlled molecular pathway
Characteristics of necroptosis
Loss of ATP, swelling of cell, ROS generation, lysosomal enzyme release, rupture of plasma membrane
Does necroptosis utilize caspases?
Nope
Some clinical settings where necroptosis occurs
Steatohepatitis, acute pancreatitis, ischemia-reperfusion injury, neurodegenerative diseases
Mechanism of pyroptosis
Microbe enters cell -> activate inflammasome -> activates caspase 1 -> forms IL-1
Ferroptosis
Cell death triggered by excess intracellular Fe or ROS that overwhelms the antioxidant defenses -> lipid peroxidation -> cell death resembling necrosis
Autophagy
Survival mechanism to maintain the integrity of cells by recycling essential metabolites and clearing debris
What condition is autophagy usually associated with?
Atrophy
Disease states where dysregulation of autophagy occurs
CA, IBD, neurodegenerative disorders
Principle cell targets of injury
Mito, cell membrane, machinery for protein synthesis, DNA
Where is most intracellular Ca sequestered?
Mito and ER
Some initiators of cell adaptations
Physiologic changes (H’s, GFs), metabolic alterations, physical injury, infection, chronic irritation
Two checkpoints in mitosis and what they do
G2-M: check for damaged or Unduplicated DNA
G1-S: check for damaged DNA
When things accumulate in a cell, where can they accumulate?
Cytoplasm, in organelles, in nucleus
How does caloric restriction increase longevity (two ways)
- Reduces signal intensity of IGF-1 pathway
- Increases sirtuins-> contributes to metabolic adaption of caloric restriction + promote genomic integrity by activating DNA repair enzymes
