Lesson #10 - Exam 2 Flashcards
(104 cards)
Cell injury will ensure following what?
disruption of homeostatic cellular mechanisms.
How does Ca++ overload cause cell injury?
Increased calcium causes dysfunction of:
1. ATPase - Decreased ATP production.
2. Phospholipase - Decreased production of phospholipids.
3. Protease - Causes disruption of membrane and cytoskeletal proteins.
4. Endonuclease - Causes nuclear chromatin damage.
When there is a lot more calcium in the cytosol compared to the extracellular matrix, ____________________ will occur.
Dystrophic calcification.
Two ways to maintain the calcium concentration gradient:
- Passive impermeability to calcium ions.
- The ATP-dependant active extrusion of calcium ions out of the cell.
True or false: Microscopic deposition of calcium salts will cause reversible cell injury .
FALSE - MACROscopic deposition of calcium salts will cause lethal cell injury and calcification of structures.
___________ is seen in chronic renal failure, which has depositions in the eye, heart, and blood vessels.
Calcification.
__________ is a medical condition that results from a previous disease.
Sequale.
Reversible injury:
Goes back to normal.
Irreversible injury:
Severe. Causes necrosis, apoptosis, and pyroptosis.
Persistent but sub-lethal injury:
Causes functional cell adaptations.
____________________: injury to the cell caused by a persistent stress, that can be relieved by functional changes.
Cellular adaptations.
Hypertrophy:
- A cellular adaptation.
- Causes increased cell size.
Hyperplasia:
- A cellular adaptation.
- Causes increased cell number.
Atrophy:
- A cellular adaptation.
- Causes decreased cell size.
Metaplasia:
- Cellular adaptation.
- Changes one cell to a different type of cell.
Dysplasia
- Cellular adaptation.
- Disorderly cell growth.
True or false: All cellular adaptations are benefitting the cell.
FALSE - Some cellular adaptations can be harmful to the cell.
Examples of harmful cellular adaptations:
- Dysplasia can transform CIS cells into precancerous lesions.
- Hypertrophy of cardiac muscles due to increased workload.
Timescale to sequale injury:
- ATP depletion.
- Biochemical dysfunction.
- Early ultrastructural changes.
(All steps above this are reversible injury) - Late ultrastructural changes.
- Early light microscopic changes.
- Late light microscopic changes.
(Second half is when injury becomes irreversible
In _____________, pathological changes may be minimal or absent, due to a fast timescale not allowing full pathological mechanisms.
Acute injury.
Typical pathological findings 15 minutes after injury:
- Endoplasmic reticulum swelling and ribosome dislocation.
- Membrane rupture.
- Mitochondrial inclusions.
Typical pathological findings 4-8 hours after injury:
- Hypereosionphillia of the cytoplasm.
- Karolysis.
- Coagulative necrosis.
- Influx of neutrophils.
__________________ presents as leakage of pro-apoptotic proteins. Causing decreased ATP production, resulting in downstream effects.
Mitochondrial damage.
________ of ________, causes increased mitochondrial permeability, and activation of many cellular enzymes.
Entry of calcium.