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
2
Q
Late plasma membrane damage signs
A
- blebs
- vesicles
- distorted microvilli
3
Q
Last sign/stage of plasma membrane damage
A
Breaks in plasma membrane
4
Q
Signs of mitochondrial damage
A
- swelling
- translucent matrix
- condensation of mitochondrial matrical proteins (flocculation; EARLIEST SIGN)
5
Q
Signs of ER damage
A
- swelling
- ribosomal detachment
- disaggregation of polysomes
- fragmentation
6
Q
2 types of reversible cellular injury
A
- cellular swelling
- fatty change
7
Q
Cellular swelling
A
- early sign of cellular illness
- cell unable to maintain ionic and fluid homeostasis
8
Q
Fatty change
A
- abnormal fat accumulation in parenchymal cells
- late stage cell illness
9
Q
Best Carmine stains
A
Glycogen
10
Q
Oil red and sudan red stain
A
Fat/lipids
11
Q
Necrosis/onchosis
A
Physical changes caused by degradation via lysosomal enzymes on lethally injured cell
12
Q
Coagulative necrosis definition
A
- gross and microscopic structure of tissue and some cells preserved
13
Q
Physiology of coagulative necrosis
A
- Structural and enzymatic proteins denatured; insoluble after cell death
- state of coagulation
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
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)
16
Q
Definition of liquefactive necrosis
A
- necrosis that disintegrates into liquid mass causing loss of cellular and architectural outlines
17
Q
Physiology of liquefactive necrosis
A
- dead cells digested, creating defect filled by invading neutrophils
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
19
Q
Extras for liquefactive necrosis
A
- occurs in nervous tissue (hi fat, low protein)
- all necrotic tissue usually disappears by this slow process
20
Q
Definition of caseous necrosis
A
- combination of coagulative and liquefaction necrosis
21
Q
Physiology of caseous necrosis
A
- assc. w/ diseases with granulomatous lesions
- caseous material stays in place for long pds. of time & calcify
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
23
Q
T or F: liquefaction and disappearance seldomly occur in caseous necrosis
A
True
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
25
Pathology of enzymatic fat necrosis
- unknown exactly
- idea: damage to fat cells causes release of fatty acids
26
Microscopic and gross structure of gangrenous necrosis
- 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
In gangrenous necrosis, if coagulative necrosis dominant, then which type of gangrene is present? What organs are assc?
- dry gangrene
- extremities
28
In gangrenous necrosis, if liquefactive necrosis dominant, then which type of gangrene is present? What organs are assc?
- wet gangrene
- visceral organse
29
Microscopic and gross structure of enzymatic fat necrosis
- microscopic: macrophages in tissue
- gross: soapy deposits in tissue
30
Gangrenous necrosis definition
- coagulative necrosis that has been invaded by saprophytic or putrefactive bacteria
31
Physiology of gangrenous necrosis
- 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
T or F: Gas gangrene invading bacteria produce large amts of gas
True
33
Dystrophic calcification
- Ca2+ salts deposited in dead/dying tissues
- normal serum levels of Ca2+ IN ABSENCE OF DERANGEMENT IN Ca2+ metabolism)
34
Metastatic calcification
- occurs following some derangement in Ca2+ metabolism that results in hypercalcemia
35
Pyknosis
Condensation of chromatin
36
Karyorrhexis
Fragmentation of chromatin
37
Karyolysis
Dissolution of chromatin by DNAses
38
Adapted cell
- altered, but steady state
- functions performed at different level than a normal cell
39
Sick cell
- reversibly injured
- damaged, not killed by injurious agent
40
Dead cell
- irreversibly injured cell
- can be completely degraded by necrosis or apoptosis assc. mechanisms
41
Liquefaction by autolysis & heterolysis w/ formation of cyst-like accumulations of fluid
- when fluid accumulates faster than its drained away by blood and lymph
42
Liquefaction by autolysis & heterolysis w/ formation of abscesses
- when pyogenic bacteria present in necrotic tissue (pus)
43
Encapsulation w/o liquefaction
- little moisture
- inflammatory rxn not intense enough to help w/ liquefaction of necrotic mass
- proliferation of fibrous CT around the necrotic mass
44
Desquamation or sloughing of necrotic tissue
- separation of necrotic tissue from viable tissue on external/internal body surfaces
- desquamation-> sloughing of thin layers -> larger masses
45
Regeneration or replacement by CT of cells lost
- terminal stage
- after necrotic tissue removed, damaged organ/part restored as best as possible
46
Post mortem putrefaction
Decomp. of tissues by bacteria enzymes (soft and stinky tissue)
47
Rigor mortis
- 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
Algor mortis
Loss of body heat
49
Hypostatic congestion
Accumulation of blood in ventral portions of body due to gravity
50
Imbibition w/ bile
Leakage of bile thru autolyzed walls of gallbladder
51
Pseudomeloanosis
Gray, black, or green pigment in tissues post mortem
52
Postmortem emphysema
Accumulation of gas in tissues due to bacterial fermentation
(Not bloat)
53
Postmortem rupture
Gases prod. by bacterial fermentation causes progressive distention of body structures until rupture
54
Postmortem displacement of organs
Dead animal is rolled over and organs move from original position
(Usually intestines)
55
Postmortem blood clotting
- can be dark red or yellow
- smooth, shiny
- uniform texture
- unattached to vessel or heart wall
56
Antemortem clot
- friable
- rough surface
- attached to vessel wall
57
Left ventricle post mortem
Rigor mortis contracts strongly and empties its blood content
58
Before rigor mortis (left ventricle)
Left ventricle has unclotted and non-hemolyzed blood
59
After rigor mortis (left ventricle)
- contains dark, hemolyzed, unclotted blood
60
No rigor mortis (left ventricle)
Clotted blood
