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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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What is the definition of cellular adaptations?
Cells adapt to environmental stress through reversible changes in size, number, phenotype, metabolic activity, or function.
What is a key point regarding cellular adaptation?
Remove the stimulus → adaptation reverses (except dysplasia/neoplasia).
What is atrophy?
A decrease in cell size or number, also known as 'shrinkage'.
What are the mechanisms of atrophy?
Decreased protein synthesis, increased protein degradation, and autophagy.
What does the acronym DANISH represent in the context of atrophy causes?
Disuse, Aging, Neuropathic, Ischemia, Starvation, Hormonal.
What is hypertrophy?
An increase in cell size (not number), also referred to as 'getting bigger'.
In what type of tissues does hypertrophy occur?
In cells that cannot divide (permanent tissues).
What are examples of physiologic hypertrophy?
Skeletal muscle from exercise, uterine smooth muscle during pregnancy, cardiac muscle in athletes.
What is pathologic hypertrophy?
Hypertrophy that occurs as a result of stress, such as left ventricular hypertrophy from hypertension.
What is hyperplasia?
An increase in cell number.
What requirements exist for hyperplasia to occur?
Hyperplasia only occurs in labile or stable tissues, never in permanent tissues like neurons.
What are examples of physiologic hyperplasia?
Hormonal: breast development during puberty, endometrial proliferation; Compensatory: liver regeneration.
What is metaplasia?
The replacement of one differentiated cell type with another.
What causes metaplasia?
Response to chronic stress or irritation.
What is an example of metaplasia in the esophagus?
Barrett's esophagus: normal stratified squamous epithelium replaced with columnar epithelium.
What is dysplasia?
Disordered growth and differentiation, considered a pre-cancer warning sign.
What features characterize dysplasia?
Loss of uniformity of cells, loss of architectural orientation, increased mitotic activity, and pleomorphism.
What is reversible injury in cell pathology?
An early stage of cell injury where the cell can recover upon removal of the stressor.
What is irreversible injury, or 'point of no return'?
Severe cell damage where loss of membrane integrity and cell death occurs.
What are the generalized features of necrosis?
Uncontrolled cell death, pathologic, membrane rupture, and inflammatory response.
What is coagulative necrosis?
The most common type of necrosis where architecture is preserved for several days following ischemic injury.
Where does coagulative necrosis most frequently occur?
Heart and kidney, typically due to ischemia.
What is liquefactive necrosis characterized by?
Complete digestion of dead cells leading to a viscous liquid mass.
What causes liquefactive necrosis in brain tissue?
Brain ischemia, since it has a high lipid content.
What condition is commonly associated with caseous necrosis?
Tuberculosis (TB), resulting in granuloma formation.
What defines fat necrosis?
A specialized form of necrosis affecting adipose tissue.
What is the primary cause of enzymatic fat necrosis?
Acute pancreatitis.
What does fibrinoid necrosis appear like?
Fibrin-like appearance due to immune complexes deposited in blood vessel walls.
What is gangrenous necrosis?
A clinical term that describes necrosis of extremities, which can be dry or wet.
What distinguishes dry gangrene?
Coagulative necrosis due to ischemia without infection.
What is wet gangrene characterized by?
Liquefactive necrosis caused by ischemia with a bacterial infection.
Which type of necrosis always results in inflammation?
Necrosis.
What type of death is apoptosis?
Programmed cell death that is ATP-dependent and orderly.
What are the two pathways of apoptosis?
Intrinsic (mitochondrial) pathway and extrinsic (death receptor) pathway.
Which proteins are involved in the intrinsic pathway of apoptosis?
Bcl-2 family proteins (BAX, BAK) that regulate mitochondrial pore formation.
What is the significance of caspases in apoptosis?
They are essential for executing the cell death program.
What triggers the extrinsic pathway of apoptosis?
External signals like Fas ligand and TNF-α.
What role do pattern recognition receptors (PRRs) play in inflammation?
They recognize pathogen-associated molecular patterns (PAMPs) to initiate immune responses.
What are the five cardinal signs of inflammation?
Rubor (redness), tumor (swelling), calor (heat), dolor (pain), and functio laesa (loss of function).
What is the sequence of vascular events in acute inflammation?
Transient vasoconstriction, vasodilation, increased vascular permeability, and stasis.
What does margination refer to in inflammation?
The process where leukocytes line up along the endothelium.
What triggers the rolling of leukocytes?
Interactions between selectins on endothelium and sialyl-Lewis X on leukocytes.
What is chemotaxis?
The directed migration of leukocytes towards the site of injury.
What causes the cells of the adaptive immune response to be recruited during inflammation?
Persistent inflammatory signals that lead to the recruitment of lymphocytes.
What mediates pain during acute inflammation?
Bradykinin and prostaglandins.
What is the function of reactive oxygen species (ROS) in immune responses?
They play a key role in microbial killing during respiratory bursts.
How do cytokines like TNF-α contribute to inflammation?
They activate endothelium, cause fever, and promote coagulation.
What are acute-phase reactants?
Proteins synthesized by the liver in response to inflammation.
Which acute-phase reactant significantly increases during inflammation?
C-Reactive Protein (CRP).
What does increased ESR in inflammation signify?
Erythrocyte Sedimentation Rate increases due to fibrinogen causing RBC aggregation.
What is the role of prostaglandins in inflammation?
They mediate vasodilation, increased permeability, pain, and fever.
What are lipoxins?
Anti-inflammatory mediators that promote resolution of inflammation.
What changes occur in myocardial infarction over the first 24 hours?
Coagulative necrosis begins, and neutrophil infiltration occurs by 12-24 hours.
What causes gangrenous appendicitis?
Obstruction (fecalith) leading to ischemia and bacterial invasion.
What is the relationship between HPV and cervical dysplasia?
HPV infection can cause cervical dysplasia, which is a precursor to cancer.
What are the common clinical correlations associated with chronic inflammation?
Conditions like tuberculosis, autoimmune diseases, and ongoing tissue damage.
What element of acute inflammation signals the transition from neutrophils to macrophages?
Monocytes begin to arrive at 24-48 hours.
What type of tissue typically undergoes scarring or fibrous tissue formation?
Permanent tissue that cannot regenerate, such as neurons and cardiac myocytes.
What clinical implication does Bcl-2 overexpression have?
It is associated with follicular lymphoma, as the cells do not undergo apoptosis.