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Gen Path > EXAM 1 > Flashcards

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
Q

pedunculated

A

having a stalk or peduncle

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26
Q

exophytic

A

growth outward (protruding from the surface)

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27
Q

endophytic

A

growth inward

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28
Q

papillary

A

having fronds or villous projections

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29
Q

cystic

A

forming one or more cavities - generally containing fluid or other matierial

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30
Q

expansile

A

causing compression of surrounding tissue
-important in neoplasia, most expansile tumors tend to be benign

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31
Q

infiltrative

A

spread into surrounding tissue
-important for neoplasia, more likely to be malignant

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32
Q

encapsulated

A

lesion surrounded by an outer rim of different tissue

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33
Q

ulcerated

A

complete loss of the epithelial surface

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34
Q

eroded

A

partial loss of epithelium

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35
Q

morphologic diagnosis

A

concise summary of the important aspects of a lesion

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36
Q

etiologic diagnosis

A

a concise summary of the cause and main lesion

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37
Q

histopathology

A

microscopic examination of tissues to study the manifestations of dz

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38
Q

What organ can be placed in formalin WHOLE?

A

Brain

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39
Q

PCR

A

identify pathogen genetic material

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40
Q

Limitations of histopathology

A
  • access to tissues (invasive)
  • turnaround time
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41
Q

FNA benefits

A

low invasiveness, quick turnaround time

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42
Q

FNA drawbacks

A

no tissue architecture, very small samples

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43
Q

cell injury

A

any alteration that impairs the ability of the cell to fxn normally

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44
Q

hypoxia

A

reduced oxygen in tissues

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45
Q

susceptibilty of cell types to hypoxia

A

neurons - sensitive
cardiac muscle, hepatocytes - intermediate
skeletal muscle fibroblasts, skin - resistant

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46
Q

antioxidants and effect on free radicals

A

they catalyze enzymatic reaction that reduces free radicals to water

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47
Q

common antioxidants in the body

A

superoxide dismutase, catalayse, Vit C, Vit E

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48
Q

Direct Toxicity (chemical cell injury)

A

the chemical in its orignal state is capable of causing injury

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49
Q

Indirect Toxicity (chemical cell injury)

A

the chemical is only (or particularly) injurious after metabolization within the body

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50
Q

atrophy, hypertrophy, hyperplasia and metaplasia are examples of what type of response?

A

Cell Adaptation Response

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51
Q

atrophy

A

a decrease in size or amount of cell, tissue, or organ

52
Q

hypertrophy

A

cell enlargement

53
Q

hyperplasia

A

number of cells increases

54
Q

metaplasia

A

change of one adult cell type to another (potentially reversible)

55
Q

fatty change

A

lipid accumulation within cells primarily seen in liver
(AKA hepatic steatosis, hepatic lipidosis, fatty liver)

56
Q

fatty change- tension lipidosis

A

a focal change, incidental lesion- due to tension on an organ

57
Q

icterus

A

yellow mucus membranes
aka jaundice

58
Q

cyanosis

A

purple mucus membranes

59
Q

what is an elevated ALT a marker of

A

hepatocellular injury

60
Q

what is an elevated ALP indicitive of

A

marker of cholestasis (stoppage of bile flow)

61
Q

necrosis

A

cell death by injury

62
Q

apoptosis

A

programmed cell death

63
Q

coagulative necrosis

A

see retention of cellular outline and architecture, but hypereosinophilic cytoplasm and karyolysis

64
Q

what causes coagulative necrosis

A

acute hypoxic injury

65
Q

liquefactive necrosis

A

reduction of tissue to liquid or to forming a cavity
(abscesses!)

66
Q

what is the most commin necrosis in CNS? (brain)

A

liquefactive

67
Q

Caesous necrosis

A

loss of arcitecture, exudate is solid and friable, often layered

68
Q

Gangrenous necrosis types

A

Dry, wet/moist, or gas

69
Q

fat necrosis usually leads to

A

saponification

70
Q

fibrinoid necrosis

A

necrosis resulting from immune-complex deposition in the walls of arteries along with fibrin
(used exclusively for microscopic lesions)

71
Q

mineralization

A

deposition of mineral in SOFT tissues

72
Q

typical gross appearance of mineralization

A

white, chalky/gritty, firm to hard

73
Q

where does dystrophic mineralization occur

A

dead or degenerate cells

74
Q

serum calcium levels w/ dystrophic mineralization

A

normal levels

75
Q

in what kinds of tissue does metastatic mineralization occur

A

normal, otherwise healthy tissue

76
Q

serum caclium levels with metastatic mineralization

A

high levels

77
Q

What type of stain is used to confirm mineralization

A

Von Kossa Stain

78
Q

Where can you see dystrophic mineralization?

A

fat necrosis, necrotic muscle, granulomas, dead parasites…

79
Q

What are the 4 causes of metastatic mineralization?

A
  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
Q

Common sites of metastatic mineralization?

A

gastric mucosa, renal tubular basement membranes, lung- alveolar walls, blood vessel walls

81
Q

calcinosis

A

mineralization in or under the skin (dystrophic)

82
Q

calculi

A

mineralized stones in hollow of tubular organs (urinary tract, gallbladder and bile ducts, intestines)

83
Q

ossification

A

formation of bone within soft tissues

84
Q

calcinosis cutis

A

mineraliztion of dermal collagen
(common in dogs with excess glucocorticoids - ie. Cushings Syndrome)

85
Q

uroliths

A

calculi in urinary tract

86
Q

nephroliths

A

calculi in kidneys

87
Q

bezoars

A

balls of material (plant/hair) generally in the intestinal tract

88
Q

common sites of ossification

A

lung, dura of spinal cord, cartilage and tendon of aging joints…

89
Q

Glycogen hepatopathy

A

abnormal glucose or glycogen metabolism (diabetes mellitus, canine steroid hepatopathy)

90
Q

microscopic appearance of glycogen accumulation

A

cytoplasmic vacuolation

91
Q

Hyaline substance accumulation

A

accumulation of hyaline proteins- intra or extracellular

92
Q

Amyloid

A

starch-like proteins- extracellular aggregates of misfolded proteins

93
Q

How does amyloid cause damage?

A

no inflammation, damage via pressure atrophy of adjacent tissues

94
Q

Primary Amyloidosis (AL)

A

abnormal plasma cells -> secrete Igs and light chains accumulate
(may be localized or systemic)

95
Q

Secondary/Reactive Amyloidosis (AA)

A

Serum amyloid A secreted from the liver. produced during inflammation, generally a systemic distribution

96
Q

Which type of amyloidosis is most common in animals?

A

AA (Secondary)

97
Q

Gross appearance of Amyloidosis

A

depends on amount and location. Organs may appear enlarged and waxy

98
Q

Where does amyloidosis occur in the liver?

A

Space of Disse

99
Q

Where does amyloidosis occur in the spleen?

A

in the white pulp

100
Q

Where does amyloidosis occur in the kidney?

A

glomeruli

101
Q

What is the special stain for Amyloidosis and how does it appear?

A

Stain = congo red
Apple green fluorescence

102
Q

Gout

A

deposition of urates or uric acid in tissues (white chalky material, often in reptiles or birds)

103
Q

Visceral gout

A

Gout on serosal surfaces

104
Q

Articular Gout

A

Gout around joints

105
Q

pneumoconiosus

A

exogenous pigment due to inhated dust particles

106
Q

anthracosis

A

exogenous pigment due to carbon (inhalation)

107
Q

pigment effect of tetracycline

A

deposited in developing teeth and bone causing yellow discoloration

108
Q

carotenoid pigments

A

exogenous pigments. fat soluble, of plant origin

109
Q

what cells produce melanin

A

melanocytes

110
Q

where is melanin found

A

hair, skin, iris, retina, etc

111
Q

piebaldism

A

patchy absence of pigment

112
Q

hyperpigmentation

A

increased melanin due to chronic UV exposure, chronic irritation

113
Q

melanosis

A

pigment in aberrant locations such as lungs, liver, meninges, serosa (incidental!)

114
Q

lipofuscin

A

age pigment - undegradable remnants of cell products and organelles. Accumulates in lysosomes

115
Q

What color is hemoglobin when it is well oxygenated

A

bright red

116
Q

what color is hemoglobin when it is poorly oxygenated

A

dark red

117
Q

Stages/colors of hemoglobin breakdown

A

hemoglobin (Red) –> unoxygenated hemoglobin (purple) –> biliverdin (green) –> bilirubin (yellow)

118
Q

hyperbilirubinemia

A

increase in circulating bilirubin. grossly visible as icterus/jaundice

119
Q

pre-hepatic (hemolytic) hyperbilirubinemia

A

excess of RBC breakdown (causes: autoimmune dz, toxins, erythrocyte parasites..)

120
Q

hepatic (toxic) hyperbilirubinemia

A

any liver dz that interferes with conjugation of bilirubin in liver (causes: hepatotoxins, inflammation, lipidosis…)

121
Q

post-hepatic (obstructive) hyperbilirubinemia

A

obstruction of bile flow from the liver (causes: cholelithiasis, neoplasia, inflammation…)

122
Q

hemosiderin

A

brown pigment - storage form of iron usually foundin macrophages

123
Q

hematoidin

A

yellow pigment - crystalline breakdown product of hemoglobin sometimes found in areas of previous hemorrhage

124
Q

parasite hematin

A

black pigment - produced by parasite digestion of hemoglobin

125
Q

porphyrins

A

photodynamic pigments, which produce free radicals when exposed to UV light. can cause damage to unpigmented skin

Gen Path (3 decks)

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