Cellular Adaptation, Injury, And Death Flashcards

(61 cards)

1
Q

What are the 4 mechanisms of cell injury

A
  1. Free radical formation
  2. Hypoxia and ATP depletion
  3. Disruption of intracellular Ca[++ homeostasis
  4. Membrane damage
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2
Q

Role of free radical injury in diabetes related complications

A

When the sugar is in high amounts, it gets oxidized and produces a lot of free radicals

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3
Q

Five mechanisms that can cause membrane damage

A
  • increased cytosolic Ca++
  • loss of membrane phospholipids
  • cytoskeleton damage
  • reactive oxygen species
  • lipid breakdown products
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4
Q

Liquid peroxifation, oxidative modification to proteins, DNA effects

A

Free radical formation

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5
Q

Deprives cell of O2 and interrupts aerobic respiration

A

Hypoxia and ATP depletion

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6
Q

Free radicals and diabetes

A
  • high blood sugar
  • glucose oxidizes
  • free radical induced oxidative damage
  • proteins are oxidatively modified
  • immunologic component (trigger systemic inflammation)
  • structural component (impact normal function)
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7
Q

What does hypoxia affect

A

Na/K pumps

Protein synthesis

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8
Q

Hypoxia and lactic acid

A

If high levels of lactic acid are present, it is a sign of stress in the body during hypoxia, not good prognosis

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9
Q

Membrane damage

A

Increased Ca++
Cytoskeletal damage
Reactive oxygen species

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10
Q

Reversible responses in cellular damage

A
Atrophy
Hypertrophy
Hyperplasia
Metaplasia
Dysplasia 

In order of worsening condition

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11
Q

Shrinkage in the size of the cell

A

Cellular atrophy

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12
Q

What is cellular atrophy due to

A
Lack of use 
Loss of inner action
Diminished blood supply 
Inadequate nutrition
Loss of endocrine stimulation 
Aging 
Pressure
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13
Q

Change in cell number

A

Hyperplasia

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14
Q

Change in cell types

A

Metaplasia

M=mature
Replace one normal mature cell type with another normal mature cell type

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15
Q

Abnormal cells

A

Dysplasia

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16
Q

Change in cell size

A

Atrophy and hypertrophy

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17
Q

Cells increase in size, not numbers

A

Cellular hypertrophy

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18
Q

What is cellular hypertrophy cause by

A

Increases functional demand or specific hormonal stimulation

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19
Q

Increase in the number of cells in an organ or tissue

A

Cellular hyperplasia

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20
Q

Usually results in an increased tissue volume

A

Hyperplasia

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21
Q

Physiologic examples of cellular hyperplasia

A

Uterine and breast growth during pregnancy

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22
Q

Pathological examples of cellular hyperplasia

A

Benign prostatic hyperplasia

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23
Q

Physiological examples of cellular hypertrophy

A

Body builders muscles

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24
Q

Pathological examples of cellular hypertrophy

A

Heart in HTN

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25
Reversible; one mature cell type is replaced by another mature cell type
Metaplasia | M=mature
26
What can metaplasia transform into
Malignancy
27
Abnormal cell growth of a specific tissue that results in cells that vary in size, shape, and organization
Cellular dysplasia
28
Strongly implicated as a precursor of cancer
Cellular dysplasia
29
Dysplasia, is it reversible
Potentially, but closer to cancer
30
Most immediate precursor to cancer
Dysplasia
31
Another name for dysplasia
Atypical cells
32
Signs and symptoms of hepatitis
Liver inflammation - bilirubin concentration increases - jaundice/icterus in all body tissues - protein production ceases - can be induced by acetaminophen
33
Most toxic vitamin
A, can kill you, others make you sick, don't eat polar bear liver E and D is next
34
If you sample what was in a xanthoma (tumors around eyes)
Cholesterol
35
Yellow sclera
Liver failure
36
Kayser-Fleischer Rings
Copper rings in the descemet's membrane (Free copper) Wilsons diseases - earliest sign is the rings - copper not bound by the carrier protein - copper is being deposited in other areas and having a toxic effect - presents with psychiatric symptoms - treatable
37
Cosmetic condition causes by prolonged ingestion of silver salts
Argyria Permanent
38
Liver failure and protein production
Won't produce proteins and will bleed out of every orifice
39
Messy lysis of dead cells within living tissues. Huge inflammatory response, cytoplasmic membrane smooths
Necrosis (lots of inflammataion, tumor/calor/rumor/dolor)
40
Programmed cell death, without inflammatory response, cell shrinks, chromatic becomes pyknotic and fragments, cytoplasmic membrane blebs
Apoptosis
41
Cell shrinking
Apoptosis
42
Cell swelling
Necrosis
43
Necrosis and healing
Inhibits healing
44
Sequence of necrosis
- membrane damage - lysosomal enzymes leak into cytoplasm - cell and organelles swell - cellular contents leak out of cell - initiation of inflammatory response
45
Exudates
- necrosis produces inflammation | - inflamed vessels leak fluid and cells, makes pus
46
Predict the protein concentration of an exudate
Very high, looks cloudy
47
Exudate is indicative of what
Inflamed
48
How to tell between exudates and transudate
Check protein concentration. If it is a high protein count and looks cloudy, it is exudates
49
Adding acetic acid to an unknown fluid and it causes a lot of precipitate
Exudates
50
Fluid is pushed through capillary due to high pressure
Transudate
51
Protein level of transudate
Low
52
Acute inflammatory cells
- neutrophils (!!!) - mast cells - platelets - basophils
53
Chronic inflammatory cells
- B and T lymphocytes - macrophages (!!! Epithelioid cells in granuloma) - plasma cells - antibodies
54
Granuloma
- dead material and macrophages at its center (epithelioid cells) - body attempted to heal the necrotic tissue - surrounded by a rim of lymphocytes - associated with chronic inflammation
55
Mitochondrial changes in apoptosis
None
56
Mitochondrial changes in necrosis
Swelling
57
First apparent cellular changes of apoptosis
Shrinking
58
First apparent cellular changes in necrosis
Swelling
59
Telomeres and aging
Shortening telomeres causes aging
60
Changes in senescence
- gradual atrophy of tissues and organs - dementia - loss of skin elasticity - grating and loss of hair - CV damage-atherosclerosis/bruising - loss of lens elasticity-opacity-vision
61
Pangeria
Warners syndrome - premature puberty - short stature