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Vet Path. > Block 1 Chart From Big (from Part 4 To End) > Flashcards

Block 1 Chart From Big (from Part 4 To End) Flashcards

1
Q

Early plasma membrane injury sign

A
  • increased membrane permeability -> increased amts of Na, Ca, and water
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2
Q

Late plasma membrane damage signs

A
  • blebs
  • vesicles
  • distorted microvilli
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3
Q

Last sign/stage of plasma membrane damage

A

Breaks in plasma membrane

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4
Q

Signs of mitochondrial damage

A
  • swelling
  • translucent matrix
  • condensation of mitochondrial matrical proteins (flocculation; EARLIEST SIGN)
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5
Q

Signs of ER damage

A
  • swelling
  • ribosomal detachment
  • disaggregation of polysomes
  • fragmentation
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6
Q

2 types of reversible cellular injury

A
  • cellular swelling
  • fatty change
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7
Q

Cellular swelling

A
  • early sign of cellular illness
  • cell unable to maintain ionic and fluid homeostasis
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8
Q

Fatty change

A
  • abnormal fat accumulation in parenchymal cells
  • late stage cell illness
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9
Q

Best Carmine stains

A

Glycogen

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10
Q

Oil red and sudan red stain

A

Fat/lipids

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11
Q

Necrosis/onchosis

A

Physical changes caused by degradation via lysosomal enzymes on lethally injured cell

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12
Q

Coagulative necrosis definition

A
  • gross and microscopic structure of tissue and some cells preserved
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13
Q

Physiology of coagulative necrosis

A
  • Structural and enzymatic proteins denatured; insoluble after cell death
  • state of coagulation
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14
Q

Microscopic and gross structure of coagulative necrosis

A
  • microscopically: tissue structure and cellular outlines recognizable; nuclei absent or pyknotic; cytoplasm: acidophilic and opaque
  • gross: tissue white/pale and dense
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15
Q

Coagulative necrosis causes…

A
  • sudden, severe ischemia
  • certain acute acting toxins
  • certain bacteria prod. toxins
  • mild burns
  • Zenker’s necrosis (coagulation of protein in sarcoplasm of only striated muscle)
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16
Q

Definition of liquefactive necrosis

A
  • necrosis that disintegrates into liquid mass causing loss of cellular and architectural outlines
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17
Q

Physiology of liquefactive necrosis

A
  • dead cells digested, creating defect filled by invading neutrophils
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18
Q

Microscopic and gross structure of liquefactive necrosis

A
  • microscopically: empty spaces w/ frayed and irregular edges or dehydrated neutrophil residue, tissue debris and fibrin
  • gross: cavity w/ clear fluid or abscess
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19
Q

Extras for liquefactive necrosis

A
  • occurs in nervous tissue (hi fat, low protein)
  • all necrotic tissue usually disappears by this slow process
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20
Q

Definition of caseous necrosis

A
  • combination of coagulative and liquefaction necrosis
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21
Q

Physiology of caseous necrosis

A
  • assc. w/ diseases with granulomatous lesions
  • caseous material stays in place for long pds. of time & calcify
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22
Q

Mircoscopic and gross structure of caseous necrosis

A
  • microscopic: cells not liquefied; outline not preserved; amorphous granular debris
  • gross: soft-firm, grayish white-yellow tissue similar to cottage cheese
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23
Q

T or F: liquefaction and disappearance seldomly occur in caseous necrosis

A

True

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24
Q

Enzymatic fat necrosis is in what tissue and assc. w/ what types of trauma

A
  • primarily in SQ adipose tissue
  • assc. w/ mechanical trauma and pressure
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25
Q

Pathology of enzymatic fat necrosis

A
  • unknown exactly
  • idea: damage to fat cells causes release of fatty acids
26
Q

Microscopic and gross structure of gangrenous necrosis

A
  • microscopic: combo of liquefactive and coagulative necrosis w/ bacteria
  • gross: in dry gangrene tissue, cool, dry, pale, shriveled like leather; wet gangrene swollen, soft, pulpy, stinks, and dark
27
Q

In gangrenous necrosis, if coagulative necrosis dominant, then which type of gangrene is present? What organs are assc?

A
  • dry gangrene
  • extremities
28
Q

In gangrenous necrosis, if liquefactive necrosis dominant, then which type of gangrene is present? What organs are assc?

A
  • wet gangrene
  • visceral organse
29
Q

Microscopic and gross structure of enzymatic fat necrosis

A
  • microscopic: macrophages in tissue
  • gross: soapy deposits in tissue
30
Q

Gangrenous necrosis definition

A
  • coagulative necrosis that has been invaded by saprophytic or putrefactive bacteria
31
Q

Physiology of gangrenous necrosis

A
  • tissues go through coagulative necrosis
  • saprophytic or putrefactive bacteria invade coagulated tissue; neutrophils attracted
  • liquefactive bacterial action and lysosomal enzymes released by neutrophils mod. coagulated tissue
32
Q

T or F: Gas gangrene invading bacteria produce large amts of gas

A

True

33
Q

Dystrophic calcification

A
  • Ca2+ salts deposited in dead/dying tissues
  • normal serum levels of Ca2+ IN ABSENCE OF DERANGEMENT IN Ca2+ metabolism)
34
Q

Metastatic calcification

A
  • occurs following some derangement in Ca2+ metabolism that results in hypercalcemia
35
Q

Pyknosis

A

Condensation of chromatin

36
Q

Karyorrhexis

A

Fragmentation of chromatin

37
Q

Karyolysis

A

Dissolution of chromatin by DNAses

38
Q

Adapted cell

A
  • altered, but steady state
  • functions performed at different level than a normal cell
39
Q

Sick cell

A
  • reversibly injured
  • damaged, not killed by injurious agent
40
Q

Dead cell

A
  • irreversibly injured cell
  • can be completely degraded by necrosis or apoptosis assc. mechanisms
41
Q

Liquefaction by autolysis & heterolysis w/ formation of cyst-like accumulations of fluid

A
  • when fluid accumulates faster than its drained away by blood and lymph
42
Q

Liquefaction by autolysis & heterolysis w/ formation of abscesses

A
  • when pyogenic bacteria present in necrotic tissue (pus)
43
Q

Encapsulation w/o liquefaction

A
  • little moisture
  • inflammatory rxn not intense enough to help w/ liquefaction of necrotic mass
  • proliferation of fibrous CT around the necrotic mass
44
Q

Desquamation or sloughing of necrotic tissue

A
  • separation of necrotic tissue from viable tissue on external/internal body surfaces
  • desquamation-> sloughing of thin layers -> larger masses
45
Q

Regeneration or replacement by CT of cells lost

A
  • terminal stage
  • after necrotic tissue removed, damaged organ/part restored as best as possible
46
Q

Post mortem putrefaction

A

Decomp. of tissues by bacteria enzymes (soft and stinky tissue)

47
Q

Rigor mortis

A
  • begins 1 to 6 hrs postmortem
  • disappears 24-48 hrs
  • enhanced by hi metabolic activity and temp.
  • delayed by cold temps and starvation
  • cardiac m. -> anterior skeletal m. -> posterior skeletal m.
48
Q

Algor mortis

A

Loss of body heat

49
Q

Hypostatic congestion

A

Accumulation of blood in ventral portions of body due to gravity

50
Q

Imbibition w/ bile

A

Leakage of bile thru autolyzed walls of gallbladder

51
Q

Pseudomeloanosis

A

Gray, black, or green pigment in tissues post mortem

52
Q

Postmortem emphysema

A

Accumulation of gas in tissues due to bacterial fermentation

(Not bloat)

53
Q

Postmortem rupture

A

Gases prod. by bacterial fermentation causes progressive distention of body structures until rupture

54
Q

Postmortem displacement of organs

A

Dead animal is rolled over and organs move from original position

(Usually intestines)

55
Q

Postmortem blood clotting

A
  • can be dark red or yellow
  • smooth, shiny
  • uniform texture
  • unattached to vessel or heart wall
56
Q

Antemortem clot

A
  • friable
  • rough surface
  • attached to vessel wall
57
Q

Left ventricle post mortem

A

Rigor mortis contracts strongly and empties its blood content

58
Q

Before rigor mortis (left ventricle)

A

Left ventricle has unclotted and non-hemolyzed blood

59
Q

After rigor mortis (left ventricle)

A
  • contains dark, hemolyzed, unclotted blood
60
Q

No rigor mortis (left ventricle)

A

Clotted blood

Vet Path. (10 decks)

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