Mason Exam 1 Flashcards
(91 cards)
1
Q
Morphological diagnosis
A
Description of the lesion,
uses accurate, anatomical nomenclature
2
Q
Elements to include in morphological diagnosis (7)
A
color size shape number location margins consistency
3
Q
3D ATP
A
tissue type process +/- adjective degree duration distribution
4
Q
-itis
A
inflammatory process
5
Q
- osis
- opathy
A
degenerative process
6
Q
- trophy
- plasia
- oma
A
disorder of growth process
7
Q
-oma
A
tumor
8
Q
-plasia
A
formation, development
9
Q
-trophy
A
nutrition, growth
10
Q
degree
A
minimal mild moderate marked severe
11
Q
duration
A
peracute
acute
subacute
chronic
12
Q
distribution
A
focal multifocal locally extensive regionally extensive disseminated diffuse
13
Q
disseminated
A
affecting more than 1 tissue/organ
14
Q
diffuse
A
throughout whole organ,
severity may range but no compeltely healthy tissue is seen.
15
Q
Pathogenesis
A
sequence of abnormalities that leads to disease
16
Q
Etiology
A
cause of disease
17
Q
Etiological diagnosis
A
diagnosis denoting cause of lesion,
Includes cause and tissue process
18
Q
What does cell response to injury depend on?
A
- cell type & it’s physiologic state
2. type, duration, and severity of injury
19
Q
Types of cell injury that can occur with oxygen deprivation
A
- hypoxia
- ischemia
- infarction
20
Q
Hypoxia
A
low oxygen, causes cell swelling
21
Q
Ischemia
A
absence of blood flow
22
Q
infarction
A
tissue death due to absence of bloodflow
23
Q
Terms for cell swelling
A
- hydropic change/degeneration
- cloudy swelling
- vacuolar change/degeneration
24
Q
Hydropic change
A
- cell swelling due to water accumulation
- reversible
- most common type of cell injury
25
Hydropic degeneration
1. cell swelling due to water accumulation
2. worse than change
3. not reversible
26
pyknosis
small, shrunken nucleus (sign of transition into irreversible cell injury, cell death)
27
karyorrhexis
torn/fragmented nucleus (sign of cell death)
28
karyolysis
destruction of nucleus (only see faded outline, sign of cell death)
29
Ischemia/reperfusion
injury that occurs once blood flow returns
30
What things can be involved in cell injury?
1. ATP
2. Calcium
3. Membrane damage
4. Mitochondria
5. ROS
31
Major players in ischemia reperfusion injury
calcium, ROS
32
Fatty change/degeneration
1. Occurs in liver, sometimes kidney
2. deposition injury (cell damage = excess intracellular lipid accumulation
3. 2nd most common type of cell injury
33
Name 5 ROS's
1. superoxide
2. singlet oxygen
3. hydroxyl radical
4. nitric oxide
5. hydrogen peroxide
34
Xanthine oxidase
pro-oxidant
| formed during ischemia, with reperfusion, forms ROS's
35
Fenton & Haber Weiss reactions
generate ROS (pro-oxidant)
36
Superoxide dismutase
antioxidant, inactivates superoxide
37
catalase
antioxidant, inactivates hydrogen peroxide
38
Gulathione peroxidase/reductase
antioxidant
39
Vitamins A, C, E
| Transferrin, Lactoferrin, Caeruloplasmin
antioxidants
40
Lipid peroxidation
1. free radicals steal electrons from lipids in cell membrane, cause damage
2. lipid radicals react with O2
41
2 potential mechanisms of cell injury secondary to redox biotransformation reactions
CCL4 or Acetominophen in cats
| generation of pneumotoxicants in acute interstitial pneumonia
42
Materials that can enlarge cells
1. Glycogen
2. Hypertrophy of organelles
3. Storage diseases (congenital or acquired)
43
Hyaline
pink, eosinophilic, homogenous glassy material (can be intra or extracellular)
44
Things often described as hyaline
1. intracellular protein deposits
2. edema fluid
3. fibrin
4. amyloid
45
Amyloid
1. permanent deposit of protein in the tissue
2. location/tissue determines whether or not amyloidosis is caused
3. stains with congo-red
46
Common places to see amyloidosis
1. lymphoid follicles
2. pancreatic islets & renal medulla in cats
3. glomeruli in dogs
4. hepatic sinusoids in birds
5. nasal submucosa in horses
47
Lipofuscin pigment
1. lipid breakdown product in lysosomes
2. often incidental except lipofuscinosis
3. Ceroid subtype in brain
48
Lipofuscinosis
"brown dog gut"
| sub clinical, linked to a vitamin E deficiency
49
Anthracosis
carbon pigmentation
common in lungs, urban environments
incidental
50
Melanosis
1. incidental pigmentation of tissues in pigmented animals
2. often seen in pleura and meninges
3. reactive melanosis of damaged skin (e.g. itchy dogs)
51
Pseudomelanosis
post mortem finding, reaction with iron in hemoglobin
52
Hemosiderin
1. lighter brown granular pigment
2. large accumulations of ferritin
3. occurs at sites of hemorrhage
53
Hematoidin
1. green/yellow variant of hemosiderin
| 2. occurs during wound resolution when macrophages are removing iron
54
Biliruben
1. in bile
| 2. causes greenish/brown non-granular pigment, can be very yellow
55
Dystrophic calcification
1. mineralization of damaged or dead tissue
| 2. often seen in granulomas or muscle necrosis
56
Metastatic calicification
1. mineralization of living tissue
2. due to excess calcium and phosphorus in blood, precipitates out into tissue
3. gastric mucosa, blood vessels, basement membranes in lungs & kidney
57
Causes of metastatic calcification
1. hypervitaminosis D
2. renal disease
3. primary hyperparathyroidism
4. hyperadrenocorticism
5. paraneoplastic syndrome
58
2 concurrent processes of necrosis
protein denaturation, enzymatic digestion
59
Necrosis vs. apoptosis
1. necrosis is passive, degradative, inflammatory, karyolysis
2. apoptosis is active, coordinated, non-inflammatory, pyknosis & karyorrhexis but no karyolysis, see cytoplasmic eosinophilia
60
coagulative necrosis
tissue architecture is maintained, but cytologic detail is lost
61
liquefactive necrosis
tissue is liquified
62
caseous necrosis
chunky cheese, can look laminated
63
Fat necrosis
tissue is saponified, white/chalky
64
Autolysis
rotting/decomp
| all tissues infected, non inflammatory
65
tissues that undergo rapid autolytic change
1. adrenal
2. CNS
3. liver
4. gut
66
Gangrene
ischemia-induced necrosis
67
dry gangrene
coagulative necrosis followed by drying of the tissue (e.g. frostbite, some intoxications)
68
wet gangrene
liquefactive necrosis, involves opportunistic bacteria
69
List things that can cause disturbances of circulation
1. Hemorrhage
2. Congestion
3. Edema
4. Homeostasis
5. Thrombosis, embolism & infarction
70
Hemorrhage
loss of blood from within vasculature
| only occurs during life
71
Petechia
pinpoint hemorrhage (up to 1 mm diameter)
72
Ecchymosis
larger points of hemorrhage (up to few cm diameter)
73
Purpura
petechiae and ecchymoses on mucus membranes
74
Hemo-
| Hema-
hemorrhage
75
Causes of hemorrhage
1. local factors affecting blood vessels
| 2. systemic factors affecting vessels or blood
76
What determines the severity of hemorrhage?
rate, amount, location
77
effects of hemorrhage
1. external (loss of blood fluids, protein, iron)
2. internal (blood components mostly recovered)
3. Secondary
78
secondary effects of hemorrhage
1. resorption of fluid
2. erythrocytes lysed and phagocytosed
3. fibrinolysis
4. potential scarring
79
Apoptosis
genetically programed cell death
| non-inflammatory, little to no tissue remodeling/scarring
80
Apoptosis occurs in...
1. tissues undergoing physiologic or post-pathologic atrophy
2. embryonic tissues
3. damaged/killed cells
4. injured cells
5. hematopoietic cell lines
81
Pyroptosis
1. appropriate inflammatory response with cell death (e.g. intracellular pathogens)
2. see swelling, lysis of cell, cytokines
3. caspace-1 dependent cell death
82
pyronecrosis
inflammatory programmed cell death
83
autophagy
1. non-inflammatory programmed cell death
2. survival mech - produces orderly atrophy
3. see vacuolization, degradation of cell components, no chromatin condensation
84
Apoptotic bodies
1. key part of apoptosis
2. phagocytes consume and recycle cell parts
3. as if cell never existed
85
extrinsic pathway of apoptosis triggered by
membrane receptors
adapter proteins regulate (TNF, Fas receptors)
86
intrinsic pathway of apoptosis triggered by
injury (ROS, radiation, hypoxia) or loss of apoptotic suppression triggering mitochondrial change
Bcl-2 family regulates
87
perforin/granzyme pathway of apoptosis triggered by
cytotoxic T cell
88
execution phase pathway of apoptosis
1. where initiation pathways converge
2. caspase 3 activated
3. triggers activation of endonucleases and proteases
89
DNA damage-mediated apoptosis
1. DNA damage triggers p53
| 2. p53 stops cell cycle to allow DNA repair, unless damage too extensive, then triggers apoptosis
90
Disorders of decreased apoptosis
neoplasia
| autoimmune disease
91
Disorders of increased apoptosis
1. neurodegenerative disorders
2. exacerbated damage in ischemic injury
3. virus-induced lymphocyte depletion in acquired immune deficiency syndromes
