2 - Cellular Response to Stress and Toxic Insults: Adaptation, Injury, and Death Flashcards Preview

Chapters 1-9 - Robbins Pathologic Basis of Disease, 9th Edition > 2 - Cellular Response to Stress and Toxic Insults: Adaptation, Injury, and Death > Flashcards

Flashcards in 2 - Cellular Response to Stress and Toxic Insults: Adaptation, Injury, and Death Deck (71)
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Is the ICF calcium level high or low relative to the ECF?

Very low (and this small amount is sequestered in the mitochondria and ER)


Why must intracellular calcium remain low?

Calcium activates phospholipases, proteases, ATPases, and endonucleases


How does the reperfusion of ischemic zones lead to ischemic-reperfusion injuries?

Oxygen- and calcium-rich ECF hits the ischemic zone and free radicals and calcium flood the damaged cells (thus leading to free radical damage and further calcium-induced damage)


Where do the toxic free radicals come from in reperfusion injury?

Polymorphonuclear leukocytes that infiltrate the ischemic site during reperfusion


What are the two main signs of reversible cell injury? What are some other signs?

Cellular swelling and fatty change;

decrease in ATP synthesis, decrease in pH, chromatin clumping, cellular swelling, ER dilation, loss of cytoskeletal structure


What leads to the swelling in damaged cells?

ATP deficiencies lead to a decrease in sodium-potassium ATPase activity


What is the main sign of irreversible cell damage?

Cell membrane damage


What are some of the causes of irreversible cell damage?

Decreased membrane phospholipids (excess phospholipase activity), lipid breakdown products;
cytoskeletal abnormalities (excess protease activity), loss of intracellular amino acids;
reactive oxygen species (reperfusion injury)


Why are free radicals so dangerous?

They can interact (and damage) all types of macronutrients; they can induce the formation of further free radicals


How can free radicals be formed within cells?

Radiation absorption, oxidative reactions, metabolism of exogenous chemicals / drugs


Normally, oxygen is reduced in the cell to form water. If a cell contains excess oxygen, what other products can be formed due to partial reductions?

Superoxide (O2 —> O2 -), hydrogen peroxide (O2 —> H2O2), and hydroxyl (O2 —> OH-) ions


How is superoxide produced naturally in the cell?

A variety of oxidative enzymes can turn O2 into O2-


How is hydrogen peroxide produced naturally in the cell?

Superoxide dismutase turns O2- into H2O2


How are hydroxyl ions produced naturally in the cell?

Ionizing radiation hydrolyzes water from H2O to OH-


Define pyknosis.

Clumping of nuclear chromatin, nuclear shrinkage, increased basophilia


Define karyolysis.

Fading basophilia of chromatin (increased DNAse activity destroys chromatin).


Define karyorrhexis.

Nuclear fragmentation.


What are the four main types of necrosis? What are two other types?

Coagulative, liquefactive, caseous, and fat necrosis; gangrenous, fibrinoid


What generally causes coagulative necrosis?

Hypoxia in all tissues except the CNS


What generally causes liquefactive necrosis?

Focal bacterial infections (due to WBC accumulation) or CNS hypoxia


What organism generally causes caseous necrosis (a type of coagulative necrosis)?

Mycobacterium tuberculosis


What generally causes fat necrosis?

Abnormal release of activated pancreatic lipases into pancreatic or peritoneal tissues


How are necrotic cells cleaned up?

Leukocytes and parenchymal cells phagocytose the remains


Do necrotic cells show eosinophilia or basophilia? Which is the natural state of the cell?

Eosinophilia; normally, the cell is basophilic due to RNA in the cytoplasm


What is the morphology of apoptosis?

Cell shrinkage, chromatin condensation, cytoplasmic surface blebs, apoptotic bodies


What is an apoptotic body?

Small fragments of the original cell containing tightly packed organelles (little phospholipid balls of cytoplasm and organelles)


Does apoptosis lead to inflammation like necrosis does?



Does apoptosis usually happen in groups of cells?

No, it usually happens in single cells.


What are the main causes of necrosis versus apoptosis?

Hypoxia, toxins;

physiology (i.e. cell density regulation), pathology (i.e. a method of deleting abnormal and damaged cells)


Why would an inhibition in gene expression lead to apoptosis?

The apoptosis-suppressing proteins have a much shorter half-life than the apoptosis-inducing proteins.

So, if gene expression stops, the suppressing proteins are degraded before the inducing proteins and apoptosis occurs.