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Form & Function 1 > Lecture 57 - Gen Path Cell Injury > Flashcards

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
Q

what are the two pathways of apoptosis are there

A
  1. intrinsic (mitochondrial)
  2. extrinsic (death receptor-initiated)
26
Q

what changes are seen with apoptosis

A
  • cell shrinkage
  • hypereosinophilia
  • chromatin clumping
  • no inflammation
  • reduction in organ/tissue size
27
Q

what adaptations are reversible

A
  1. hypertrophy
  2. hyperplasia
  3. metaplasia
28
Q

Hypertrophy

A

increased cell size
in striated/smooth mm.

29
Q

Hyperplasia

A

increased cell number
readily dividable tissues
normal or excessive hormone stimulation

30
Q

Metaplasia

A

one cell type converts to another
chronic irritation or hormonal factors

31
Q

atrophy

A

decrease in cell size or number

32
Q

hypoplasia

A

failure of tissue/organ to reach mature/adult size
distinguish by age and microscopic changes

Form & Function 1 (66 decks)

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