PA Unit 2

Esophagus reflux, where stomach acids are released into the esophagus.

Type 2 diabetes mellitus and atherosclerosis.

Sustained damage that reaches a non-returning point.

Increased oxidative stress and damage to cellular components.

It can kill the etiological agent but may further damage the cell, combining apoptosis and necrosis.

Death receptor pathway.

A process that is a midway between necrosis and apoptosis.

They exhibit progressive morphological and biochemical manifestations.

The cell can return to normal if the adaptation processes are successful.

White pearl areas formed by fatty acids combined with calcium.

'Programmed death of a cell' involving degradation of nuclear DNA and proteins.

A mitochondrial pathway involving cytochrome c and caspase activation.

Glandular epithelium.

Specific ligands on their membranes.

Estrogen stimulated smooth muscle hypertrophy and hyperplasia.

It diminishes their ability to respond to stress, leading to cell death.

Tuberculous infection.

Release of activated pancreatic enzymes into the pancreas and peritoneal cavity.

A clinical term used to describe a type of necrosis that is not purely a necrosis pattern.

The tendency of a tissue to occupy a place it is not supposed to, leading to serious consequences.

Hypoxia and ischemia.

A chain of self-reactions through caspases leads to cell death.

Activation of a cytosolic protein complex called inflammasome.

The cell will try to adapt in a limited number of ways.

The cell becomes permanently injured but may still be reversible if damage is not deep enough.

Immune reactions and deposition of antigen-antibody complexes in blood vessel walls.

The identification of a specific pathological process in a disease.

Mucus.

Cigarette smoke, poor food quality, and bacteria.

The cell digests its own components due to lack of external nutrients.

Hormonal causes during pregnancy.

Shrinkage in the size of cells due to loss of cell substance and metabolic processes.

Replacement of pseudo-stratified ciliary epithelium in the respiratory airways.

It can lead to neoplasia and potentially cancer.

Phosphatidylserine.

Massive pathologic enlargement of the cardiac muscle due to hypertension.

An increase in the number of cells in an organ, enlarging it.

Increased eosinophilia, discontinuities in membranes, marked dilation of mitochondria, and disruption of lysosomes.

A type of necrosis often seen in infarcts caused by ischemia, characterized by preserved tissue structures for several days.

Hypoxia and ischemia.

Squamous epithelium, with no cilia nor goblet cells.

Cell injury develops.

Ischemia is the most common cause of hypoxia.

Hypertrophy to generate higher contractile force, potentially leading to ischemia and hypoxia.

Hyper immune response and hypo immune response.

Accumulation of misfolded proteins, signaling for apoptosis.

Loss of defined edges of the plasma membrane and nucleus, and eosinophilia.

Aging and normal development.

The specific mechanism a disease needs to happen.

It can provoke neoplasia.

The breakdown of proteins maintaining the cytoskeleton structure.

Increased permeability of the plasma membrane and nucleus, leading to pallor, increased turgor, and swelling.

Glucose can saturate hemoglobin, preventing it from transporting oxygen, leading to hypoxia.

Cellular membranes fall apart, releasing cytoplasmic contents and triggering an inflammatory response.

1. Pyknotic nucleus, 2. Karyorrhexic nucleus, 3. Karyolytic nucleus.

Replacement of sensitive cells with more resilient cells for increased protection.

The expected progress of a specific disease.

The text does not specify the names of the reversible patterns.

Deficits in proteins, calories, and vitamins, as well as excessive dietary intake leading to obesity.

The appearance of triglyceride-containing lipid vacuoles in the cytoplasm, especially in organs involved in lipid metabolism.

Physiological and pathological hyperplasia.

Prostatic hyperplasia due to hormonal imbalance.

Necrosis occurring in the brain due to hypoxic cell death, often associated with bacterial infections and pus formation.

It undergoes fragmentation, known as karyorrhexis.

Reduced blood supply resulting in a deficiency of essential nutrients.

Various kinds, including burns.

Decrease in ATP levels.

A 'cheeselike' appearance due to calcification.

Decreased workload, loss of innervation, diminished blood supply, inadequate nutrition, loss of endocrine stimulation, and aging.

They maintain mitochondrial membrane integrity and prevent apoptosis.

They can undergo adaptation, reaching a new steady state that preserves functions as long as noxious stimuli are removed.

Oxygen deficiency.

Small, clear vacuoles in the cytoplasm, known as vacuolar degeneration.

Infections can damage cells by feeding on body-produced substances and altering normal cell physiology.

They can result in a lack of certain enzymes, changing cell physiology and leading to disease.

A form of irreversible cellular death triggered by deep and sustained damage.

Increased functional demand or hormonal stimulation.

An increase in the size of cells due to increased amounts of structural proteins and organelles.

Severe DNA damage or accumulation of misfolded proteins.