Lecture 57 - Gen Path Cell Injury Flashcards

1
Q

What is reversible cell injury defined as

A

altered state which will revert to normal upon the removal of the stimulus

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2
Q

What are two categories of Hallmark changes in reversible cell injury

A
  1. cell swelling
  2. clumped chromatin
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3
Q

cell swelling is caused by

A

altered sodium-potassium ion concentration which cause water influx

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4
Q

clumped chromatin is caused by

A

low oxygen environments that decrease cellular pH

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5
Q

What is another term for cell swelling

A

hydropic degeneration

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6
Q

On histology, how is cell swelling illustrated?

A

pallor without inflammation

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7
Q

T/F: fatty change is a reversible cell injury

A

TRUE

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8
Q

what is fatty change

A

accumulation of triglycerides in organs

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9
Q

what is the gross anatomy of fatty change

A

enlarged, pale, greasy

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10
Q

what are microscopic changes of fatty change

A

discrete, clear cytoplasmic vacuoles

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11
Q

What is considered irreversible cell injury? what are examples?

A

anything resulting in cell death

  1. necrosis
  2. apoptosis
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12
Q

what are the hallmark changes of irreversible cell death

A
  1. pyknosis (condensed chromatin)
  2. karyorrhexis (nuclear fragmentation)
  3. karyolysis (nuclear dissolution)
  4. hypereosinophilia
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13
Q

T/F: inflammation is a feature of reversible cell injury

A

FALSE

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14
Q

what two changes are specific to necrosis

A
  1. mineralization (calcium influx)
  2. inflammation
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15
Q

what are the types of necrosis

A
  1. Coagulative
  2. Lytic/Liquefactive
  3. Caseous
  4. Fat
  5. Gangrenous
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16
Q

Describe coagulative necrosis

A
  • pallor +/- hemorrhagic ring
  • hypereosinophilia
  • cellular outlines
17
Q

Describe Zenker’s necrosis (include common causes)

A
  • coagulative specific to skeletal mm.
  • Vitamin E/Se deficiency (white mm. disease)
  • capture myopathy
  • compartment syndrome
18
Q

Describe Lytic/Liquefactive necrosis

A
  • neutrophilic breakdown of tissue
  • cellular debris
  • pale, softened tissue
19
Q

Describe liquefactive necrosis in the CNS (-malacia)

A
  • macrophages play role
  • cavitation
  • ischemia or vascular event
20
Q

Describe caseous necrosis

A
  • white, soft, friable
  • granulomas present
  • common in heterophils and mycobacterium
21
Q

Describe fat necrosis

A
  • acute inflammation near/within adipose
  • white, chalky calcium soaps
  • basophilia
22
Q

Describe gangrenous necrosis

A
  • necrosis of extremities
  • black skin (dry)
  • w/ putrefaction (wet)
  • vascular disruption
23
Q

what are the physiologic causes of apoptosis

A
  1. immune surveillance (self-reactive T cells die in the thymus)
  2. Hormonal involution
  3. Embryologic reduction in cells
24
Q

what are the pathologic causes of apoptosis

A
  1. atrophy
  2. cell death in tumors/virus-mediated
  3. DNA damage
  4. accumulation of misfolded proteins
25
what are the two pathways of apoptosis are there
1. intrinsic (mitochondrial) 2. extrinsic (death receptor-initiated)
26
what changes are seen with apoptosis
- cell shrinkage - hypereosinophilia - chromatin clumping - no inflammation - reduction in organ/tissue size
27
what adaptations are reversible
1. hypertrophy 2. hyperplasia 3. metaplasia
28
Hypertrophy
increased cell size in striated/smooth mm.
29
Hyperplasia
increased cell number readily dividable tissues normal or excessive hormone stimulation
30
Metaplasia
one cell type converts to another chronic irritation or hormonal factors
31
atrophy
decrease in cell size or number
32
hypoplasia
failure of tissue/organ to reach mature/adult size distinguish by age and microscopic changes