Cellular Adaptation, Injury, And Death Flashcards

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
Q

Reversible; one mature cell type is replaced by another mature cell type

A

Metaplasia

M=mature

26
Q

What can metaplasia transform into

A

Malignancy

27
Q

Abnormal cell growth of a specific tissue that results in cells that vary in size, shape, and organization

A

Cellular dysplasia

28
Q

Strongly implicated as a precursor of cancer

A

Cellular dysplasia

29
Q

Dysplasia, is it reversible

A

Potentially, but closer to cancer

30
Q

Most immediate precursor to cancer

A

Dysplasia

31
Q

Another name for dysplasia

A

Atypical cells

32
Q

Signs and symptoms of hepatitis

A

Liver inflammation

  • bilirubin concentration increases
  • jaundice/icterus in all body tissues
  • protein production ceases
  • can be induced by acetaminophen
33
Q

Most toxic vitamin

A

A, can kill you, others make you sick, don’t eat polar bear liver

E and D is next

34
Q

If you sample what was in a xanthoma (tumors around eyes)

A

Cholesterol

35
Q

Yellow sclera

A

Liver failure

36
Q

Kayser-Fleischer Rings

A

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
Q

Cosmetic condition causes by prolonged ingestion of silver salts

A

Argyria

Permanent

38
Q

Liver failure and protein production

A

Won’t produce proteins and will bleed out of every orifice

39
Q

Messy lysis of dead cells within living tissues. Huge inflammatory response, cytoplasmic membrane smooths

A

Necrosis (lots of inflammataion, tumor/calor/rumor/dolor)

40
Q

Programmed cell death, without inflammatory response, cell shrinks, chromatic becomes pyknotic and fragments, cytoplasmic membrane blebs

A

Apoptosis

41
Q

Cell shrinking

A

Apoptosis

42
Q

Cell swelling

A

Necrosis

43
Q

Necrosis and healing

A

Inhibits healing

44
Q

Sequence of necrosis

A
  • membrane damage
  • lysosomal enzymes leak into cytoplasm
  • cell and organelles swell
  • cellular contents leak out of cell
  • initiation of inflammatory response
45
Q

Exudates

A
  • necrosis produces inflammation

- inflamed vessels leak fluid and cells, makes pus

46
Q

Predict the protein concentration of an exudate

A

Very high, looks cloudy

47
Q

Exudate is indicative of what

A

Inflamed

48
Q

How to tell between exudates and transudate

A

Check protein concentration. If it is a high protein count and looks cloudy, it is exudates

49
Q

Adding acetic acid to an unknown fluid and it causes a lot of precipitate

A

Exudates

50
Q

Fluid is pushed through capillary due to high pressure

A

Transudate

51
Q

Protein level of transudate

A

Low

52
Q

Acute inflammatory cells

A
  • neutrophils (!!!)
  • mast cells
  • platelets
  • basophils
53
Q

Chronic inflammatory cells

A
  • B and T lymphocytes
  • macrophages (!!! Epithelioid cells in granuloma)
  • plasma cells
  • antibodies
54
Q

Granuloma

A
  • 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
Q

Mitochondrial changes in apoptosis

A

None

56
Q

Mitochondrial changes in necrosis

A

Swelling

57
Q

First apparent cellular changes of apoptosis

A

Shrinking

58
Q

First apparent cellular changes in necrosis

A

Swelling

59
Q

Telomeres and aging

A

Shortening telomeres causes aging

60
Q

Changes in senescence

A
  • 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
Q

Pangeria

A

Warners syndrome

  • premature puberty
  • short stature