Cellular Adaption Lecture Flashcards

1
Q

What causes cellular adaptions?

A

Increased demand, reduced nutrients supply or other forms of “stress”

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2
Q

What causes cellular injury?

A

Limits of the adaptive response are reached or if adaptation is not possible

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3
Q

What is ischemia/hypoxia?

A

Oxygen deprivation

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4
Q

What are physical agents that cause injury?

A

Mechanical trauma, extremes of temperature

Changes in atmospheric pressure, radiation, shock (electricity)

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5
Q

What is cellular adaptation?

A

Cells response to excessive physiological stresses or pathological stimuli –> cell reaches steady state where it maintains viability and function

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6
Q

What is autocrine signaling?

A

Cell responds to signaling substances that they themselves secrete

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7
Q

What is paracrine signaling?

A

Cell produces substances that affect only a target cell in close proximity

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8
Q

What is endocrine signaling?

A

Hormones are synthesized by cells of the endocrine organs and act on target cells distant from their site of synthesis

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9
Q

What are subcellular adaptations?

A

Mitochondria increase in number to better meet the metabolic needs of organisms
but under different stresses these can take on abnormal sizes and shapes

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10
Q

What are lysosomes?

A

Membrane-bound intracellular organelles that contain a variety of hydrolytic enzymes
Take unwanted materials from the outside and move tehm within the cytosol

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11
Q

What are primary lysosomes?

A

Synthesized in the rER and packaged in the golgi
They fuse with membrane bound vacuoles containing material to be digested forming a secondary lysosomes or phagolysosomes

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12
Q

What is the cytoskeleton consist of and what is it critical for?

A

Microtubules, actin filaments, myosin filaments, and other intermediate filaments
Critical for cell locomotion, transport, and movement of intracellular organelles

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13
Q

What disease are caused via the disruption of the cytoskeleton?

A

Alzheimer’s where neurofibrillary tangles become common in neurons via microtubule-associated proteins and neurofilaents –> loses ability to communicate

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14
Q

What is hyperplasia?

A

increase in number

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15
Q

What is hypertrophy?

A

Increase in size

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16
Q

What are the three ways cellular adaptions occur?

A

Cell growth and differentiation
Atrophy (skrinkage)
Metaplasia (reversible replacement)

17
Q

What are the three types of cells?

A

Continuously dividing (skin, oral cavity)
Quiescent (stable) cell (liver, kidney)
Nondividing (permanent) cells (neurons, cardiac)

18
Q

What stimulates cell growth?

A

Injury, mechanical forces acting on a tissue, or cell death

19
Q

What is cellular hyperplasia?

A

Physiologically: hormonal (increase in function) and compensatory (increase tissue mass)
Pathologically: Hormonal (abnormal menstrual bleeding), growth factors and viral infections

20
Q

Define atrophy

A

Reduction in cell size and number

21
Q

Physiological Atrophy during fetal development?

A

Notochord –> vertebral column
Tonsils –> after puberty
Thymus –> during puberty

22
Q

Pathological atrophy is caused by?

A

Decrease workload, loss of innervation, diminished blood supply, inadequate nutrition, aging, pressure

23
Q

What is metaplasia?

A

Change in cell type –> reprogramming tissue cells via growth factors, cytokines and

24
Q

What does the cell membrane help maintain?

A

Ionic gradients and osmotic homeostatsis

25
Q

What does aerobic respiration help maintain?

A

oxidative metabolism and ATP

26
Q

What are the six common biochemical mechanisms important to the mediation of cell injury and death?

A
  1. Decrease ATP synthesis and ATP depletion
  2. Defects in membrane permeability
  3. Loss of calcium homeostasis and increased intracellular calcium
  4. Oxygen and oxygen derived free radicals
  5. Irreversible mitochondrial damage
  6. Protein misfolding and DNA damage
27
Q

What are the consequences of decreasing intracellular ATP?

A

Increase anaerobic glycolysis which decreases glycogen and pH and increase lactic acid
Decrease in protein synthesis, ER swelling, cellular swelling, etc

28
Q

What are the consequences of loss of calcium homeostatsis?

A

Intracellular calcium when increased can activate a number of ezymes (ATPase, endonucleases, phopholipiases, etc)

29
Q

What are the pathologic effects of ROS?

A

Cell injury and death
ROS reacts with FA to induce oxidation which genrates lipid peroxidases that disrupt the plasma membrane
ROS reacts with proteins to cause abnormal folding and DNA causing mutations and breaks

30
Q

What are the ROS removal techniques?

A

Antioxidants
SOD converts O2- to H2O2
Glutathione peroxidase converts OH to H20
Catalase converst H2O2 to H20

31
Q

Define reperfusion injury

A

Detrimental changes that occur upon reistatement of blood flow to the tissue
Cells die after blood flow resumes

32
Q

What are some examples of reperfusion injury?

A

Increase ROS

Release of cytokines and cell adhesion molecules