Adaptations, Necrosis, Apoptosis & Inflammation

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A comprehensive set of flashcards covering high-yield concepts in adaptations, necrosis, apoptosis, and inflammation for medical students preparing for exams.

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59 Terms

1
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What is the definition of cellular adaptations?

Cells adapt to environmental stress through reversible changes in size, number, phenotype, metabolic activity, or function.

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What is a key point regarding cellular adaptation?

Remove the stimulus → adaptation reverses (except dysplasia/neoplasia).

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What is atrophy?

A decrease in cell size or number, also known as 'shrinkage'.

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What are the mechanisms of atrophy?

Decreased protein synthesis, increased protein degradation, and autophagy.

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What does the acronym DANISH represent in the context of atrophy causes?

Disuse, Aging, Neuropathic, Ischemia, Starvation, Hormonal.

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What is hypertrophy?

An increase in cell size (not number), also referred to as 'getting bigger'.

7
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In what type of tissues does hypertrophy occur?

In cells that cannot divide (permanent tissues).

8
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What are examples of physiologic hypertrophy?

Skeletal muscle from exercise, uterine smooth muscle during pregnancy, cardiac muscle in athletes.

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What is pathologic hypertrophy?

Hypertrophy that occurs as a result of stress, such as left ventricular hypertrophy from hypertension.

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What is hyperplasia?

An increase in cell number.

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What requirements exist for hyperplasia to occur?

Hyperplasia only occurs in labile or stable tissues, never in permanent tissues like neurons.

12
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What are examples of physiologic hyperplasia?

Hormonal: breast development during puberty, endometrial proliferation; Compensatory: liver regeneration.

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What is metaplasia?

The replacement of one differentiated cell type with another.

14
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What causes metaplasia?

Response to chronic stress or irritation.

15
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What is an example of metaplasia in the esophagus?

Barrett's esophagus: normal stratified squamous epithelium replaced with columnar epithelium.

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What is dysplasia?

Disordered growth and differentiation, considered a pre-cancer warning sign.

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What features characterize dysplasia?

Loss of uniformity of cells, loss of architectural orientation, increased mitotic activity, and pleomorphism.

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What is reversible injury in cell pathology?

An early stage of cell injury where the cell can recover upon removal of the stressor.

19
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What is irreversible injury, or 'point of no return'?

Severe cell damage where loss of membrane integrity and cell death occurs.

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What are the generalized features of necrosis?

Uncontrolled cell death, pathologic, membrane rupture, and inflammatory response.

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What is coagulative necrosis?

The most common type of necrosis where architecture is preserved for several days following ischemic injury.

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Where does coagulative necrosis most frequently occur?

Heart and kidney, typically due to ischemia.

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What is liquefactive necrosis characterized by?

Complete digestion of dead cells leading to a viscous liquid mass.

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What causes liquefactive necrosis in brain tissue?

Brain ischemia, since it has a high lipid content.

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What condition is commonly associated with caseous necrosis?

Tuberculosis (TB), resulting in granuloma formation.

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What defines fat necrosis?

A specialized form of necrosis affecting adipose tissue.

27
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What is the primary cause of enzymatic fat necrosis?

Acute pancreatitis.

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What does fibrinoid necrosis appear like?

Fibrin-like appearance due to immune complexes deposited in blood vessel walls.

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What is gangrenous necrosis?

A clinical term that describes necrosis of extremities, which can be dry or wet.

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What distinguishes dry gangrene?

Coagulative necrosis due to ischemia without infection.

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What is wet gangrene characterized by?

Liquefactive necrosis caused by ischemia with a bacterial infection.

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Which type of necrosis always results in inflammation?

Necrosis.

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What type of death is apoptosis?

Programmed cell death that is ATP-dependent and orderly.

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What are the two pathways of apoptosis?

Intrinsic (mitochondrial) pathway and extrinsic (death receptor) pathway.

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Which proteins are involved in the intrinsic pathway of apoptosis?

Bcl-2 family proteins (BAX, BAK) that regulate mitochondrial pore formation.

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What is the significance of caspases in apoptosis?

They are essential for executing the cell death program.

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What triggers the extrinsic pathway of apoptosis?

External signals like Fas ligand and TNF-α.

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What role do pattern recognition receptors (PRRs) play in inflammation?

They recognize pathogen-associated molecular patterns (PAMPs) to initiate immune responses.

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What are the five cardinal signs of inflammation?

Rubor (redness), tumor (swelling), calor (heat), dolor (pain), and functio laesa (loss of function).

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What is the sequence of vascular events in acute inflammation?

Transient vasoconstriction, vasodilation, increased vascular permeability, and stasis.

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What does margination refer to in inflammation?

The process where leukocytes line up along the endothelium.

42
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What triggers the rolling of leukocytes?

Interactions between selectins on endothelium and sialyl-Lewis X on leukocytes.

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What is chemotaxis?

The directed migration of leukocytes towards the site of injury.

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What causes the cells of the adaptive immune response to be recruited during inflammation?

Persistent inflammatory signals that lead to the recruitment of lymphocytes.

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What mediates pain during acute inflammation?

Bradykinin and prostaglandins.

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What is the function of reactive oxygen species (ROS) in immune responses?

They play a key role in microbial killing during respiratory bursts.

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How do cytokines like TNF-α contribute to inflammation?

They activate endothelium, cause fever, and promote coagulation.

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What are acute-phase reactants?

Proteins synthesized by the liver in response to inflammation.

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Which acute-phase reactant significantly increases during inflammation?

C-Reactive Protein (CRP).

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What does increased ESR in inflammation signify?

Erythrocyte Sedimentation Rate increases due to fibrinogen causing RBC aggregation.

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What is the role of prostaglandins in inflammation?

They mediate vasodilation, increased permeability, pain, and fever.

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What are lipoxins?

Anti-inflammatory mediators that promote resolution of inflammation.

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What changes occur in myocardial infarction over the first 24 hours?

Coagulative necrosis begins, and neutrophil infiltration occurs by 12-24 hours.

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What causes gangrenous appendicitis?

Obstruction (fecalith) leading to ischemia and bacterial invasion.

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What is the relationship between HPV and cervical dysplasia?

HPV infection can cause cervical dysplasia, which is a precursor to cancer.

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What are the common clinical correlations associated with chronic inflammation?

Conditions like tuberculosis, autoimmune diseases, and ongoing tissue damage.

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What element of acute inflammation signals the transition from neutrophils to macrophages?

Monocytes begin to arrive at 24-48 hours.

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What type of tissue typically undergoes scarring or fibrous tissue formation?

Permanent tissue that cannot regenerate, such as neurons and cardiac myocytes.

59
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What clinical implication does Bcl-2 overexpression have?

It is associated with follicular lymphoma, as the cells do not undergo apoptosis.