week 2 lecture Flashcards

1
Q

define perfusion

A

-delivery of oxygen, nutrients
-removal of waste
-bathing cells in fluid

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2
Q

define ischemia

A

stoppage of blood flow

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3
Q

define hypoxia

A

low oxygen state

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4
Q

what is the most common cause of cellular injury? what does it lead to

A

-ischemia
-leads to cellular and tissue hypoxia (lack of oxygen & poor blood flow)

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5
Q

what is the key intervention for a hypoxic injury?

A

remove the source of injury and allow the cell to correct itself

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6
Q

what does “-megaly” mean?

A

swelling on the organ level

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7
Q

what is hepatomegaly?

A

swelling of the liver

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8
Q

what is splenomegaly?

A

swelling of the spleen

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9
Q

When our cells experience stressors it causes proteins to become misfolded but luckily our body respond well to an excess of misfolded proteins. What are two ways that our body responds?

A

-Increased synthesis of chaperones = ability to fix and REPAIR damaged proteins
-Activation of ubiquitin-proteasome pathway → leads to degranulation (break-down) of unfolded proteins to less harmful forms

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10
Q

cellular adaptation: hyperplasia & example & medication

A

-increases in cell number
-repeated friction or cell injury → ex: corns and calluses development
-Medication SE: dilantin → gingival hyperplasia

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11
Q

cellular adaptation: atrophy & example

A

-decrease in cell size
ex: disuse following a cast

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12
Q

cellular adaptation: hypertrophy & example

A

-increase in cell size
ex: workout → muscle growth

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13
Q

cellular adaptation: dysplasia

A

-disorderly change to cell shape, size, and arrangement
-precursor to cancer

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14
Q

cellular adaptation: metaplasia & example

A

-change of cell shape, response to repeated cell injury
-Ex: Barrett’s esophagus: change from squamous epithelial cells to columnar epithelial cells

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15
Q

Which type of irreversible cell injury is “messy”? Why might we describe it like this? How does it happen?

A

necrosis! it is accompanied by inflammation that continues to affect neighboring cells
Membrane rupture → cell will explode → cells contents leakage → inflammation

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16
Q

Which type of irreversible cell injury is “neat”? Why might we describe it like this?

A

apoptosis is “programmed cell death” → neat and tidy process, with NO inflammation

17
Q

Is apoptosis always pathological? Explain and give an example.

A

No, it is a normal part of the body processes
ex: shedding of uterine lining during menstruation

18
Q

what are two types of environmental signals a cell can receive that induce apoptosis?

A
  1. withdrawal of “survival” signals that normally suppress apoptotic pathways (AKA cells are no longer getting signals)
  2. extracellular signals such as the fas ligand will bind to cell and trigger death cascade = “death receptors” (AKA receive signals from outside that tell them to self destruct)
19
Q

what is the internal pathway that can also induce apoptosis?

A

severe cell damage can trigger p53 to trigger cell death
ex: protective against cancer development

20
Q

what are the two factors that cause cellular and molecular damage (relating to cellular aging)? give an example for each.

A
  1. progressive decline in the proliferation and reparative capacity of cells
    ex: not as good as repairing cells and making new cells
  2. exposure to damaging environmental and metabolic factors
    ex: accumulation of damage to cells
21
Q

describe two theories of cellular aging

A
  1. Free Radical Theory = accumulated cell damage over time
  2. Programmed Senescence Theory = cells have a limited number of divisions, limited by telmores (ends of chromosomes) once they reach a critical limit
22
Q

what is somatic death?

A

death of an entire organism

23
Q

what do we use as proof of somatic death?

A

cessation of respirations and heartbeat

24
Q

what is rigor mortis? when does it occur and end?

A

stiffened muscles following death due to influx of calcium from muscle cells
-body remains rigid for 0-6 hours
-then flaccid 24-48 hours