54-Breakdown of Homeostasis Flashcards by Adam Rasmussen

What is homeostasis

normal steady state

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What happens when cells encounter physiologic stress

They must adapt, get injured, or die

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What is the most crucial event in evolution of disease

Cell death

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What happens after prolonged or severe injury

Cell death-necrosis or apoptosis

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What are the cellular adaptations to stress

Atrophy
Hypertrophy-physiologic or pathologic
Hyperplasia-physiologic or pathologic
metaplasia

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What is atrophy

Shrinking of cell to preserve function and survive

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What is hypertrophy

Cell enlarges, limited capacity to divide

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What is hyperplasia

More cells are produced if they are capable of replication

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What is metaplasia

Differentiation from one adult cell type to another

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What happens to skeletal muscle when it loses its innervation

denervation-atrophy, become small and angular

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What causes atrophy

Decreased workload
loss of innervation
Diminished blood supply
Inadequate nutrition
Loss of endocrine
aging

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what is an example of pathologic hypertrophy

Hypertension and enlargement of heart

Muscular Dystrophy

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What is an example of physiologic hypertrophy

Pregnancy from estrogen

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What is an example of physiologic hyperplasia

Pregnancy and proliferation of breast tissue

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What is the difference between hyperplasia and cancer

Hyperplasia is tightly controlled

Cancer has uncontrolled growth

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What is an example of metaplasia

Chronic smokers
Change of epithelium in branches from columnar to squamous

Gain survival, but loss of protection like mucous secretion and cilia

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Why does metaplasia occur

One cell type is sensitive to stress and is replaced by a type that can withstand the stress to try to survive

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What causes cell injury

EVERYTHING
Intrinsic-genetic
Acquired-everything else

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What does cell response to injurious stimuli depend on

Type, duration, severity

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What are the consequences of injurious stimulus

Cell type, status, adaptability, genetic make up

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Where are the sites of vulnerability for cell injury

Mitochondria, calcium, membrane, protein and DNA integrity

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What are the morphologic changes from injury

Biochemical changes

They are time dependent

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What does mitochondrial damage lead to

ATP depletion and increase ROS, necrosis and apoptosis

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ATP depletion is due to what

Decreased oxygen, reduced nutrients, mitochondrial damage, toxins

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If you have ATP depletion what can you test for

Lactic acidosis in serum blood test

Increase ROS leads to what

Damaged lipids, proteins, DNA

How does reduced ATP affect cells

Reduced ATP dependent sodium and calcium pumps, anaerobic glycolysis (lactic acid production and decreased pH), disruption of protein synthesis

How are ROS formed

Produced normally during redox reactions | Produced by phagocytic leukocytes (neutrophils and Macs) for destroying microbes

How does ROS contribute to disease

``` Cancer-mutation from free radicals atherosclerosis-plaque formation Aging-accumulative damage Toxicology-acetaminophen toxicology hypoxia ```

What are the sources of calcium

mitochondria, ER, extracellular space

What does increased calcium do

``` activate enzymes which leads to: Membrane damage Nuclear damage Decreased ATP trigger apoptosis ```

Most important sites of membrane damage are

Mitochondrial, lysosomal, plasma

What does damage to lysosomal membranes do

leak enzymes and digest cell components

What does damage to DNA and proteins lead to

Accumulation of damaged DNA, misfolded proteins.

What happens when damage exceeds repair mechanisms

apoptosis

What is ischemia

Decreased blood flow leading to loss of oxygen and nutrients

Does ischemic or hypoxic lead to faster injuries

ischemia

What is hypoxia

Decreased oxygen delivery, use anaerobic glycolysis as result

What happens to oxygen deprived cells

Decreased ATP, mitochondrial damage, accumulation of ROS, Ca influx

What happens during the sequence of changes in cell injury

``` Quickly lose cell function, but still reversible injury Death and irreversible, biochemical alterations ultrastructural changes (EM) Light microscope changes (AP) Gross morphological changes ```

How can you reverse cell injury

During early stages if damaging stimulus is removed

What are the 2 morphological correlates in reversible injury

Cell swelling | Fatty change

What causes cell swelling in reversible injuries

Failure of energy ion pumps, inability to maintain ionic and fluid homeostasis

What happens in reversible cell swelling

Loss of microvilli, swollen mitochondria, membrane blebbing

What happens in fatty change

Clear lipid vacuoles in cells participating in fat metabolism, caused from chronic alcohol use

What 2 characteristics cause irreversibility

Cannot correct mitochondria dysfunction | Profound disruption of membranes

What are the common early changes in necrosis

hypereosinophilia-really pink vacuolization Nuclear changes (pkynosis, karyorrhexis, karyolysis, disappearance)

What are the later changes in necrosis

Coagulation and liquefaction

What is coagulative necrosis

autolysis-intrinsic source | Preservation of cell outlines

What is a type of coagulative necrosis

Myocardial infarction, ischemic injury

What is liquefactive neccrosis

heterolysis-extrinsic source | Loss of cell outline

What is a type of liquefactive necrosis

Bacterial abscess

What is caseous necrosis

TB infection!! Cheese like appearance Aggregate of granular pink material tissue architecture obliterated

What is fat necrosis

Fat destruction from release of pancreatic lipases, liquefy membranes of fat cells Microscopically-shadowy outline with basophilic calcium deposits

What is fibrinoid necrosis

Immune reaction with antigens and antibodies in walls of arteries Bright pink appearance

What is dystrophic calcification

Calcification in dead or dying tissues, seen in plaques

What causes intracellular accumulation

Abnormal metabolism Abnormal protein folding and transport enzyme defect Incomplete lysosomal degradation

What are some intracellular accumulations

Lipids, proteins, glycogen, pigments

What accumulates in Alzheimer's

tau proteins

Is necrosis physiologic or non physiologic

ALWAYS PATHOLOGIC

What are the 2 ways to initiate apoptosis

Mitochondrial/intrinsic | Death receptor/extrinsic

nonmorphologic characteristics of necrosis

Pathologic, no gene transcription, unregulated, no energy, lysosome disruption, cell membrane leakage

Non morphologic characteristics of apoptosis

``` Physiologic and non physiologic Gene transcription Highly regulated Needs energy Cleave chromatic Lysosome intact cell membrane intact ```

Morphologic characteristics of necrosis

``` Death of groups karyolysis and karyorrhexis organelles destroyed Swelling Inflammatory response ```

Morphologic characteristics of apoptosis

``` Death in individual cells Chromatic clumping Organelles preserved Cell shrinkage No inflammation ```

Biochemical pathway that can be manipulated by pharmacology

Apoptosis-cancer