04a: Pathology 1 Flashcards
List the cell/tissue adaptations to stress.
- Hyperplasia
- Metaplasia
- Hypertrophy
- Atrophy
Cell adaptation: Increase in number of cells, resulting in increased volume of tissue/organ.
Hyperplasia
T/F: Hyperplasia is indicative of pathology.
False - can be physiologic (ex: lactating breast) or pathologic (ex: BPH)
T/F: In both physiologic and pathologic hyperplasia, when the stimulus that induces it is removed, proliferation ceases.
True
Responses of uterus and breasts in pregnancy/lactation are examples of (hyperplasia/metaplasia/hypertrophy).
Both hyperplasia and hypertrophy (often occur in association)
T/F: Hypertrophy does not require a cell population
capable of cell division, but can occur in fully mature non-dividing cells.
True
Cell adaptation: Increase in size of cells, resulting in increased volume of tissue/organ.
Hypertrophy
Example(s) of physiologic hypertrophy.
- Hepatocyte hypertrophy (demand for drug metabolism)
2. Muscle hypertrophy
(X) appear to be the major triggers for physiologic hypertrophy. In pathologic states, (Y) signals may be more important.
X = mechanical stretch/sensors Y = alpha-adrenergic hormones, angiotensin, and growth factors
Cell adaptation: Shrinkage of a tissue due to loss of cell (substance/number).
Atrophy;
Either
(X) is a pathway responsible for
accelerated proteolysis in atrophy.
X = ubiquitin-proteasome
Sequestration of cell organelles into (X) that fuse with (Y) and digest enclosed material.
X = autophagic Y = lysosomes
Autophagy
Atrophic cells ultimately accumulate numerous shrunken
X) that contain only lipofuschin, the residue of (Y). These structures are called (Z
X = lysosomes Y = hydrolytic enzyme digestion Z = residual bodies
Metaplasia is (reversible/irreversible) change in which (epithelial/mesenchymal) cell is replaced by (X).
Reversible;
Either;
X = another adult cell type
Metaplasia is induced by (X) and results from the reprogramming of (Y) cells.
X = cytokines and growth factors Y = tissue stem
List the general causes of cell injury.
- Hypoxia
- Physical, chemical, infectious agents
- Immunologic reactions
- Genetics and nutrition
Reversible cell injury has which two characteristic features/changes in cell?
- Cell swelling
2. Fatty change/accumulation
Necrosis: Disruption/fragmentation of cell membranes, forming spiral aggregates called (X).
X = myelin bodies
A reliable morphologic characteristic of necrosis is (X) of which organelle?
X = absence or fragmentation
Nucleus
(Cell death/ultrastructural changes) occurs first on timeframe of changes in necrosis.
Cell death
(X) necrosis is typical of ischemic injury.
X = coagulative
Gangrenous necrosis is example of (fibrinoid/caseous/coagulative) necrosis.
coagulative
(X) necrosis shows no ghost outlines because dead cells undergo (Y). What is the gross appearance of this necrosis?
X = liquefactive Y = hydrolysis by enzymes from ruptured lysosomes
Viscous liquid then cavity
(X) necrosis is seen following bacterial infection.
X = liquefactive
(X) necrosis seen as result of lung abscess or CNS infarct.
X = liquefactive
(X) necrosis describes gross appearance of that seen in (Y) tissue in TB.
X = caseous (cheesy) Y = lung
(X) necrosis produced by action of free pancreatic enzyme on adjacent, mainly (Y), tissues.
X = Y = fat
In (X) necrosis, the release of FA from the tissue promotes early formation of (Y) deposits.
X = fat Y = Ca
(X) necrosis seen in immune reactions, involving (Y) structures.
X = fibrinoid Y = blood vessels
(X) necrosis: appearance of bright pink amorphous material called (Y). What forms this?
X = Y = fibrinoid
Ag and Ab and fibrin complexes
ATP depletion to (X)% levels is a potential deathblow to cell. This depletion is most frequently caused by (Y).
X = 5-10 Y = anoxia
Influx of (X) to cytosol has damaging effects to cell due to which 2 effects/mechanisms?
X = Ca
- Increase mito permeability
- Activates multiple cell enzymes (ATPases, proteases, endonucleases)
Re-perfusion of tissue following period of ischemia can be damaging to cells for what reason?
Major buildup of ROS
T/F: Apoptosis is more often a pathologic process than a physiologic one.
False - vise versa
T/F: Apoptotic process preserves targeted cell membrane intact.
True
Execution of (apoptosis/necrosis) is accomplished by activation of (X) enzymes cascade.
Apoptosis;
X = caspase
T/F: Both necrosis and apoptosis involve inflammatory response.
False - only necrosis
List some adaptive/physiologic causes of apoptosis.
- Organogenesis
- Hormone-dependent involution (ex: menstrual cycle)
- Cell deletion/replacement in proliferating cell populations
- Immune stuff (neutrophils, self-reactive lymphocytes)
(Apoptosis/necrosis) in response to (X) is the mechanism important in neurodegenerative diseases, such as AD and Parkinson’s.
Apoptosis;
X = misfolded protein accumulation in ER
Necroptosis resembles (apoptosis/necrosis) morphologically and (apoptosis/necrosis) mechanistically.
Necrosis; apoptosis
(Necrosis/apoptosis/necroptosis) is driven by signaling by RIP1 and RIP3 protein complexes.
Necroptosis
T/F: Cell swelling and membrane damage is seen in necroptosis.
True
T/F: Inflammatory reaction is seen in necroptosis.
True
T/F: Necroptosis is unique to pathological conditions.
False - also seen in some normal processes
The (extrinsic/intrinsic) (X) apoptotic pathway involves cell injury such as (Y).
Intrinsic;
X = mitochondrial
Y = DNA damage, protein misfolding
The (extrinsic/intrinsic) (X) apoptotic pathway occurs when ligands, often present on (Y) engage (Z) membrane receptors.
Extrinsic;
X = death receptor
Y = T lymphocytes
Z = TNF
The (extrinsic/intrinsic) (X) apoptotic pathway: bcl2 and bclx replaced by bak and bax on (Y) membrane. What does this do?
Intrinsic;
X = Y = mitochondrial
Increase membrane permeability and cytochrome c released into cytoplasm (activates caspase cascade)
