EXAM 1 Flashcards

1
Q

Pathology

A

the study of a dz

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2
Q

What are the types of Lesions?

A

DAMNIT,V
Degenerative, Anomalous , Metabolic, Neoplastic, Inflammatory, Traumatic, Vascular

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3
Q

Pathogenesis

A

How a dz is acquired to result in lesions

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4
Q

Pathophysiology

A

what the lesions do to the function of the body (symptoms, morbidity, mortality)

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5
Q

Cause of death vs mechanism of death

A

Cause: the agent or insult
Mechanism: pathogenesis/pathophysiology

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6
Q

Rigor mortis

A

postmortem change - contraction of muscles

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7
Q

Algor mortis

A

postmortem change - the body equilibrates with the ambient temperature

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8
Q

Livor mortis

A

postmortem change - red discoloration of the skin due to settling of blood by gravity

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9
Q

Autolysis

A

natural breakdown of cells

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10
Q

Examples of autolysis

A
  • loss of cellular detail
  • softening of tissues
  • bile imbibition
  • hemoglobin imbibition
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11
Q

Putrefaction

A

breakdown of cells by overgrowth of cadaver bacteria

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12
Q

examples of putrefaction

A
  • pseudomelanosis
  • gas distention/bubbles in tissue
  • bloat
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13
Q

examples of degenerative lesion

A
  • osteoarthritis
  • steroid-induced skin atrophy
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14
Q

example of anomalous lesions

A

congenital anomalies (extra digits, ears, etc)

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15
Q

Pathologic Lesion

A

causing morbidity/mortality

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16
Q

Pathognomonic

A

characteristic of only one known dz/condition

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17
Q

Incidental Lesion

A

insignificant lesion. abnormal, but not causing a significant problem

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18
Q

Acute Lesion

A

recent onset or of short duration

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19
Q

chronic lesion

A

been going on a while (anything beyond 3-4 days)

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20
Q

edema indication

A

wet/excess fluid

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21
Q

hemorrhage indication

A

too soft

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22
Q

indication of presence of fibrin

A

too hard

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23
Q

lesion distribution descriptions

A
  • focal (one lesion)
  • multifocal (multiple discretely identifiable lesions)
  • locally extensive (an entire region of an organ)
  • diffuse
  • segmental (important for tubular organs)
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24
Q

nodular

A

elevated, circumscribed mass of rounded or irregular shape

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25
pedunculated
having a stalk or peduncle
26
exophytic
growth outward (protruding from the surface)
27
endophytic
growth inward
28
papillary
having fronds or villous projections
29
cystic
forming one or more cavities - generally containing fluid or other matierial
30
expansile
causing compression of surrounding tissue -important in neoplasia, most expansile tumors tend to be benign
31
infiltrative
spread into surrounding tissue -important for neoplasia, more likely to be malignant
32
encapsulated
lesion surrounded by an outer rim of different tissue
33
ulcerated
complete loss of the epithelial surface
34
eroded
partial loss of epithelium
35
morphologic diagnosis
concise summary of the important aspects of a lesion
36
etiologic diagnosis
a concise summary of the cause and main lesion
37
histopathology
microscopic examination of tissues to study the manifestations of dz
38
What organ can be placed in formalin WHOLE?
Brain
39
PCR
identify pathogen genetic material
40
Limitations of histopathology
* access to tissues (invasive) * turnaround time
41
FNA benefits
low invasiveness, quick turnaround time
42
FNA drawbacks
no tissue architecture, very small samples
43
cell injury
any alteration that impairs the ability of the cell to fxn normally
44
hypoxia
reduced oxygen in tissues
45
susceptibilty of cell types to hypoxia
neurons - sensitive cardiac muscle, hepatocytes - intermediate skeletal muscle fibroblasts, skin - resistant
46
antioxidants and effect on free radicals
they catalyze enzymatic reaction that reduces free radicals to water
47
common antioxidants in the body
superoxide dismutase, catalayse, Vit C, Vit E
48
Direct Toxicity (chemical cell injury)
the chemical in its orignal state is capable of causing injury
49
Indirect Toxicity (chemical cell injury)
the chemical is only (or particularly) injurious after metabolization within the body
50
atrophy, hypertrophy, hyperplasia and metaplasia are examples of what type of response?
Cell Adaptation Response
51
atrophy
a decrease in size or amount of cell, tissue, or organ
52
hypertrophy
cell enlargement
53
hyperplasia
number of cells increases
54
metaplasia
change of one adult cell type to another (potentially reversible)
55
fatty change
lipid accumulation within cells primarily seen in liver (AKA hepatic steatosis, hepatic lipidosis, fatty liver)
56
fatty change- tension lipidosis
a focal change, incidental lesion- due to tension on an organ
57
icterus
yellow mucus membranes aka jaundice
58
cyanosis
purple mucus membranes
59
what is an elevated ALT a marker of
hepatocellular injury
60
what is an elevated ALP indicitive of
marker of cholestasis (stoppage of bile flow)
61
necrosis
cell death by injury
62
apoptosis
programmed cell death
63
coagulative necrosis
see retention of cellular outline and architecture, but hypereosinophilic cytoplasm and karyolysis
64
what causes coagulative necrosis
acute hypoxic injury
65
liquefactive necrosis
reduction of tissue to liquid or to forming a cavity (abscesses!)
66
what is the most commin necrosis in CNS? (brain)
liquefactive
67
Caesous necrosis
loss of arcitecture, exudate is solid and friable, often layered
68
Gangrenous necrosis types
Dry, wet/moist, or gas
69
fat necrosis usually leads to
saponification
70
fibrinoid necrosis
necrosis resulting from immune-complex deposition in the walls of arteries along with fibrin (used exclusively for microscopic lesions)
71
mineralization
deposition of mineral in SOFT tissues
72
typical gross appearance of mineralization
white, chalky/gritty, firm to hard
73
where does dystrophic mineralization occur
dead or degenerate cells
74
serum calcium levels w/ dystrophic mineralization
normal levels
75
in what kinds of tissue does metastatic mineralization occur
normal, otherwise healthy tissue
76
serum caclium levels with metastatic mineralization
high levels
77
What type of stain is used to confirm mineralization
Von Kossa Stain
78
Where can you see dystrophic mineralization?
fat necrosis, necrotic muscle, granulomas, dead parasites...
79
What are the 4 causes of metastatic mineralization?
1. renal failure (phosphate retention induces hypercalcemia) 2. vitamin D toxicity (rodenticides, calcinogenic plants, therapeutic overdose) 3. Parthormone and PTH related protein 4. Lysis of bone
80
Common sites of metastatic mineralization?
gastric mucosa, renal tubular basement membranes, lung- alveolar walls, blood vessel walls
81
calcinosis
mineralization in or under the skin (dystrophic)
82
calculi
mineralized stones in hollow of tubular organs (urinary tract, gallbladder and bile ducts, intestines)
83
ossification
formation of bone within soft tissues
84
calcinosis cutis
mineraliztion of dermal collagen (common in dogs with excess glucocorticoids - ie. Cushings Syndrome)
85
uroliths
calculi in urinary tract
86
nephroliths
calculi in kidneys
87
bezoars
balls of material (plant/hair) generally in the intestinal tract
88
common sites of ossification
lung, dura of spinal cord, cartilage and tendon of aging joints...
89
Glycogen hepatopathy
abnormal glucose or glycogen metabolism (diabetes mellitus, canine steroid hepatopathy)
90
microscopic appearance of glycogen accumulation
cytoplasmic vacuolation
91
Hyaline substance accumulation
accumulation of hyaline proteins- intra or extracellular
92
Amyloid
starch-like proteins- extracellular aggregates of misfolded proteins
93
How does amyloid cause damage?
no inflammation, damage via pressure atrophy of adjacent tissues
94
Primary Amyloidosis (AL)
abnormal plasma cells -> secrete Igs and light chains accumulate (may be localized or systemic)
95
Secondary/Reactive Amyloidosis (AA)
Serum amyloid A secreted from the liver. produced during inflammation, generally a systemic distribution
96
Which type of amyloidosis is most common in animals?
AA (Secondary)
97
Gross appearance of Amyloidosis
depends on amount and location. Organs may appear enlarged and waxy
98
Where does amyloidosis occur in the liver?
Space of Disse
99
Where does amyloidosis occur in the spleen?
in the white pulp
100
Where does amyloidosis occur in the kidney?
glomeruli
101
What is the special stain for Amyloidosis and how does it appear?
Stain = congo red Apple green fluorescence
102
Gout
deposition of urates or uric acid in tissues (white chalky material, often in reptiles or birds)
103
Visceral gout
Gout on serosal surfaces
104
Articular Gout
Gout around joints
105
pneumoconiosus
exogenous pigment due to inhated dust particles
106
anthracosis
exogenous pigment due to carbon (inhalation)
107
pigment effect of tetracycline
deposited in developing teeth and bone causing yellow discoloration
108
carotenoid pigments
exogenous pigments. fat soluble, of plant origin
109
what cells produce melanin
melanocytes
110
where is melanin found
hair, skin, iris, retina, etc
111
piebaldism
patchy absence of pigment
112
hyperpigmentation
increased melanin due to chronic UV exposure, chronic irritation
113
melanosis
pigment in aberrant locations such as lungs, liver, meninges, serosa (incidental!)
114
lipofuscin
age pigment - undegradable remnants of cell products and organelles. Accumulates in lysosomes
115
What color is hemoglobin when it is well oxygenated
bright red
116
what color is hemoglobin when it is poorly oxygenated
dark red
117
Stages/colors of hemoglobin breakdown
hemoglobin (Red) --> unoxygenated hemoglobin (purple) --> biliverdin (green) --> bilirubin (yellow)
118
hyperbilirubinemia
increase in circulating bilirubin. grossly visible as icterus/jaundice
119
pre-hepatic (hemolytic) hyperbilirubinemia
excess of RBC breakdown (causes: autoimmune dz, toxins, erythrocyte parasites..)
120
hepatic (toxic) hyperbilirubinemia
any liver dz that interferes with conjugation of bilirubin in liver (causes: hepatotoxins, inflammation, lipidosis...)
121
post-hepatic (obstructive) hyperbilirubinemia
obstruction of bile flow from the liver (causes: cholelithiasis, neoplasia, inflammation...)
122
hemosiderin
brown pigment - storage form of iron usually foundin macrophages
123
hematoidin
yellow pigment - crystalline breakdown product of hemoglobin sometimes found in areas of previous hemorrhage
124
parasite hematin
black pigment - produced by parasite digestion of hemoglobin
125
porphyrins
photodynamic pigments, which produce free radicals when exposed to UV light. can cause damage to unpigmented skin