Karteikarten: Cell Injury and Death Mechanisms — 24 Karten

Homeostasis — definition?

Steady functional state of a cell.

Adaptation — role?

Reversible cellular changes to survive stress.

Cell injury — triggers?

Exceeds adaptive limits, nutrient deficiency, or function impairment.

Reversible injury — hallmark?

Cell swelling and hydropic change.

Irreversible injury — key feature?

Severe membrane damage and mitochondrial failure.

Necrosis pattern — coagulative?

Architecture preserved, seen in infarcts.

Necrosis pattern — liquefactive?

Tissue digested into pus, common in brain.

Necrosis pattern — caseous?

Cheeselike, granuloma-like, in tuberculosis.

Necrosis pattern — fat?

Chalky deposits from pancreatic lipase activity.

Necrosis pattern — fibrinoid?

Bright pink immune complex deposits in vessel walls.

Apoptosis — morphology?

Cell shrinkage, chromatin condensation, apoptotic bodies.

Apoptosis — pathways?

Mitochondrial (BAX/BAK) and extrinsic (Fas/FADD).

Autophagy — process?

Sequestration of cytoplasm into autophagosomes for degradation.

Necroptosis — mechanism?

RIPK1/RIPK3/MLKL pathway causing membrane rupture.

Oxidative stress — cause?

Excess ROS damaging lipids, proteins, DNA.

Lipid peroxidation — effect?

Membrane damage via free radicals attacking fatty acids.

Hypoxia — definition?

Reduced oxygen supply to tissues.

Reperfusion injury — paradox?

Restored blood flow causes further cell damage.

Chemical injury — example?

Mercuric chloride binding to sulfhydryl groups.

Infectious injury — mechanism?

Pathogens damage cells directly or via immune response.

Immunologic injury — example?

Complement activation and immune complex deposition.

Cellular adaptation — types?

Hypertrophy, hyperplasia, atrophy, metaplasia.

Intracellular pigment — example?

Lipofuscin, hemosiderin, carbon (anthracosis).

Calcification — types?

Dystrophic (injury sites) and metastatic (hypercalcemia).