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Veterinary General Pathology > Cellular Pathology (Lec. 03) > Flashcards

Cellular Pathology (Lec. 03) Flashcards

1
Q

cells are able to maintain normal structure and function (e.g. ion balance, pH, energy metabolism) in response to normal physiologic demands

A

homeostasis

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2
Q

any stimulus or succession of stimuli of such magnitude that tends to disrupt the homeostasis of the organism

A

stress

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3
Q

as cells encounter some stresses they may make functional or structural adaptations to maintain viability/ homeostasis

A

cellular adaptation

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4
Q

What is cell injury?

A

Cell injury occurs if the limits of adaptive response are exceeded, or in certain instances when adaptation is not possible.

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5
Q

What is reversible cell injury?

A

Reversible cell injury is the removal of stress or injurious stimulus that results in complete restoration of structural and functional integrity.

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6
Q

If severe stimulus persists in a cell, what will happen?

A

Irreversible cell injury

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7
Q

It is a type of cell death characterized by severe membrane injury and enzymatic degradation; always a pathologic process

A

Necrosis

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8
Q

What is apoptosis?

A

A regulated form of cell death. Can be physiologic or pathologic process.

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9
Q

one of the most important and common causes of cell injury and cell death

A

hypoxia

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10
Q
  1. oxygen deficiency
  2. blood supply deficiency
A
  1. hypoxia
  2. ischemia
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11
Q

Hypoxia occurs with? (3)

A
  1. Deficient blood supply (Ischemia)
  2. Reduced oxygen-carrying capacity of the blood
  3. Interference with respiratory chain / oxidative phosphorylation
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12
Q

What are some infectious agents that can cause cell injury?

A

a. Viruses
b. Bacteria / rickettsiae / chlamydia
c. Fungi
d. Protozoa
e. Metazoan parasite

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13
Q

cell injury occurs if stimulus prolonged and/or exceeds ability to adapt

A

overworked cells

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14
Q

prolonged lack of stimulation (e.g. disuse, denervation, lack of trophic hormones) can lead to atrophy and eventually the loss of cells

A

underworked cells

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15
Q

the cumulative effects of a lifetime of cell damage (chemical, infectious, nutrition, etc) lead to a diminished capacity of aged cells / tissues to maintain homeostasis and adapt to harmful stimuli

A

cell aging

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16
Q

What are the 2 types of nutritional imbalance?

A

deficiency and overnutrition

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17
Q

combined effects of environmental factors and 2 or more mutated genes (eg neoplasia, hypertension, coronary artery disease)

A

multifactorial inheritance

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18
Q

What are the different chemical, drugs and toxins that can cause cell injury?

A
  1. Inorganic poisons
  2. Organic poisons
  3. Manufactured chemicals
  4. Physiologic compounds
  5. Plant toxins
  6. Animal toxins
  7. Bacterial toxins / Mycotoxins
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19
Q

What are the three types of immunologic reactions that can cause cell injury?

A
  1. Immune response
  2. Hypersensitivity reactions
  3. Autoimmune diseases
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20
Q

What are the four intracellular system that are particularly vulnerable to injury?

A
  1. cell membranes
  2. mitochondria
  3. protein synthesis, folding and packaging
  4. genetic apparatus
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21
Q

chemical species with a single unpaired electron in outer orbit (donate or steal electrons, extremely unstable)

A

free radicals

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22
Q

Generation of free radicals (4)

A
  1. Cellular metabolism
  2. Enzymatic metabolism of exogenous chemicals
  3. Ionizing radiation
  4. Divalent metals
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23
Q

Where are the main sites of damage of Free radicals? (3)

A
  1. Damage of membranes
  2. Damage of proteins
  3. Damage to DNA
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24
Q

What are the protective mechanism of the cell against free radicals?

A
  1. Storage and transport proteins
  2. Antioxidants
  3. Enzymes involved in neutralizing free radicals
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25
Q

What are some pathologic causes of atrophy?

A
  1. decreased workload (disuse atrophy)
  2. loss of innervation
  3. loss of hormonal (trophic) stimulation,
  4. reduced blood supply / hypoxia, inadequate nutrition, compression
    (by tumors, etc.)
  5. persistent cell injury
  6. aging (senile atrophy).
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26
Q

not dead or necessarily badly injured but they have a reduced functional capacity

A

atrophic cells

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27
Q

What are the two main types of reversible cell injury recognized?

A

Cellular swelling and fatty change

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28
Q

the most common and most important response to cellular injuries of all types, including mechanical, anoxic, toxic, lipid peroxidation, viral, bacterial and immune mechanisms

A

cellular swelling

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29
Q

Etiology of cellular swelling

A

a. injury, then

b. results to loss of ion and fluid homeostasis

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30
Q

As water continues to accumulate inside the cell, many vacuoles of variable sizes appear in the cytoplasm. It is called as?

A

hydropic or vacuolar degeneration

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31
Q

Other term for hydropic degeneration when severity increased especially in viral infected cells

A

Ballooning degeneration

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32
Q
  • literally may imply a “sick cell”
  • a reversible form of injury
  • an adaptive change that may progress to cell death (necrosis)
A

degeneration

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33
Q

What are the ultrastructural changes of cellular swelling especially ischemia?

A
  1. Plasma membrane - blunting, loss of microvilli, blebbing, myelin figures appear
  2. ER - swelling of cisternae, detachment of ribosomes in Rough Endoplasmic Reticulum
  3. Mitochondria - swelling, appearance of small densities
  4. Nucleus - clumping of chromatin
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34
Q

It is the abnormal accumulation of lipids within the cell.

A

Fatty change

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35
Q

Fatty change occurs mainly in cells dependent on fat metabolism, give 1 organ.

A

liver

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36
Q

refers to the rapid death of a limited portion of an organism and is
considered to be the final stage in irreversible degeneration

A

necrosis

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37
Q

the term used for the entire process of degeneration and death of cells

A

necrobiosis

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38
Q

Gross indicators or Characteristics of Necrosis

A
  1. Loss of color or paleness of the tissue
  2. Loss of strength of the tissue as it softens
  3. A definite zone of demarcation between necrotic and viable tissue
  4. Location or pattern of the lesion
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39
Q

term used to describe the range of morphologic changes that occur
following cell death in living tissue

A

necrosis

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40
Q

What are the 7 types of Necrosis?

A
  1. Coagulation necrosis
  2. Liquefactive necrosis
  3. Caseous necrosis
  4. Gangrenous necrosis
  5. Fat necrosis
  6. Infarction
  7. Zenker’s Necrosis
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41
Q

a shallow area of necrosis confined to epidermis that heals without
scarring

A

erosion

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42
Q

an excavation of a surface produced by necrosis and sloughing of the
necrotic debris and implies involvement of the tissue below the surface layer

A

ulcer

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43
Q

a piece of necrotic tissue in the process of separation from viable tissue and implies a process of shedding when used with reference to a surface

A

slough

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44
Q

an area of liquefactive necrosis of the nervous tissue. Literally means
“softening”

A

malacia

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45
Q

an isolated necrotic mass

A

sequestrum

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46
Q

Gross appearance
* affected tissue is liquefied; becomes a soft to viscous fluid

  • if process was initiated by inflammation, the liquid is often mostly dead
    neutrophils (ie called pus)
A

Liquefactive necrosis

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47
Q

removal of organs (esp eyes, tongue, rectum) of carcass by carrion eating animals (e.g., dogs, coyotes, ravens, vultures)

A

postmortem scavenging

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48
Q

rigidity or stiffening of muscles after death due to contraction of muscle fibers as ATPs are depleted or exhausted

A

rigor mortis

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49
Q

gradual cooling of the body after death

A

algor mortis

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50
Q

gravitational pooling/settling of blood to the dependant regions (“down side”)
of the body. In this instance, you will know the position of the individual when it
was dead.

A

livor mortis

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51
Q

▪ occurs in heart and vessels

▪ rbc’s may separate from plasma (esp in animals with high fibrinogen levels, eg
horses) = “chicken fat clot”

A

postmortem clotting

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52
Q

▪ HgB released by rbc breakdown (after death) → staining tissues.

▪ especially lining of heart and blood vessels; also common in tissues of aborted
fetuses and frozen tissues.

A

hemoglobin imbibition

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53
Q

leakage of bile from gall bladder and major bile ducts which stains adjacent
tissues green to yellow

A

bile imbibition

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54
Q

term used to describe an artifactual black discoloration of tissues (similar in an
appearance to melanosis)

A

pseudomelanosis

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55
Q

refers to the enzymatic decomposition of organic material (tissue) with production of foul-smelling compounds (eg H2S, NH3,
mercaptans), especially by saprophytic / putrefactive bacteria

A

putrefaction (rotting)

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56
Q

occurs when saprophytic bacteria produce gas,
causing gaseous distention of G-I tract, organs and body cavities

A

postmortem emphysema

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57
Q

with swelling of viscera (due to postmortem emphysema) rectal prolapse, visceral dislocation, gastric rupture (horses), diaphragmatic hernia

A

postmortem ruptures and organ displacements

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58
Q

Give the other enzymes used to evaluate tissue damage. (3)

A
  1. Lactic dehydrogenase (LHD)
  2. Creatine phosphokinase (CPK)
  3. Alkaline phosphatase (AP
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59
Q

released from the cytoplasm of injured liver
cells (in moderate injury)

A

Alanine transaminase

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60
Q

located in mitochondria and is released in more
extensive injury. This occurs in liver, muscles

A

Aspartate transaminase

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61
Q

brown to black pigment in the airways of monkeys with lung mites

A

Pneumonyssus simicola

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62
Q

malarial pigment from excretion of catabolized hemoglobin
(large deposits in macrophages of spleen and liver)

A

plasmodia

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63
Q

liver fluke of ruminants; see black discoloration of
tissue around bile ducts due to regurgitated iron-porphyrin pigment
(“fluke puke”)

A

fascioloides magna

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64
Q

deposition of asbestos into lung, associated with mesotheliomas, and
chronic lung injury

A

asbestosis

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65
Q

deposition of silica dust in the lungs, is a special problem for miners;
causes granulomatous pneumonia

A

silicosis

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66
Q

deposition of carbon particles (esp from air pollution), into lungs /
lymph nodes

A

anthracosis

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67
Q

Give examples of exogenous pigments.

A

carbon, soot, dusts, silica, asbestos, tattoo pigment

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68
Q

microscopically elongate, needle-like crystals, often in picket fence type arrangement

A

cholesterol cleft

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69
Q

end product of nitrogen metabolism, so, any significant renal dysfunction (including dehydration) can lead to abnormal accumulations/deposits of urates

A

uric acid (birds and reptiles)

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70
Q

Give two examples of crystals.

A
  1. Calcium oxalate
  2. Urates and uric acid
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71
Q

a term that describes widespread of deposition of
calcium in tissues of individual treated with a calcium sensitizer

A

calciphylaxis

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72
Q

Deposition of calcium salts in vital tissues and is always associated with
hypercalcemia

A

metastatic calcification

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73
Q

Term sometimes used for extensive metastatic calcification

A

calcinosis

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74
Q

calcification of injured cells (no hypercalcemia or other disturbances of
calcium homeostasis).

A

dystrophic calcification

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75
Q

What are the characteristics of dystrophic calcification?

A

Grossly appearance is white, irregular areas, sometimes dry and gritty

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76
Q

True or False.

Occurrence of dystrophic calcification is most prominent when there is a good supply in the injured tissue.

A

True.

77
Q

Gross characteristics of metastatic calcification.

A

often as white plaques or streaks

78
Q

Occurrence of urates and uric acid (3)

A

birds, reptiles, humans

79
Q

Gross and microscopic characteristics of urates and uric acid.

A

Gross - chalky white masses in tissues or frosting of crystals on serosal membranes

Microscope - variably sized clear crystals, frequently associated with macrophages

80
Q

death of single cells as a result of activation of a genetically programmed
“suicide” pathway

A

apoptosis

81
Q

Give three examples of physiologic causes of apoptosis.

A
  1. Embryonic development (sculpting of digits)
  2. Cells undergoing normal turnover
  3. Immune System such as depletion of autoreactive T cells in thymus
82
Q

What are some pathologic causes of apoptosis? (5)

A
  1. DNA damage
  2. Misfolded proteins
  3. Specific infectious agents
  4. Specific immune response
  5. Pathologic atrophy of organs after duct obstruction (eg pancreas,
    kidney, salivary gland)
83
Q

Give the morphologic features of Apoptosis.

A
  1. Cell shrinkage
  2. Chromatin condensation
  3. Blebs formation
  4. Phagocytosis of cell bodies
84
Q

What are the lipids that can accumulate in the intracellular space? (3)

A
  1. Triglycerides
  2. Inherited storage diseases
  3. Cholesterol accumulation
85
Q

accumulation of lipids in smooth muscle cells
and macrophages in walls of arteries / arterioles

A

atherosclerosis

86
Q

tumor like masses in skin formed by clusters of foamy macrophages; seen with inherited or acquired
hyperlipidemic states

A

xanthomas

87
Q

name given to any substance, intracellular or extracellular, which has a homogeneous, glassy, eosinophilic appearance

A

hyaline

88
Q

a nonspecific term for hyaline material within an arterial wall.
- the presence of plasma proteins / Ag-Ab / complement within
a damaged vascular wall causes intense eosinophilic staining

A

fibrinoid

89
Q

a pathologic proteinaceous substance (95% amyloid fibrils) which is
resistant to proteolysis

A

amyloid

90
Q

insoluble aggregates that result from the self-assembly of abnormally folded proteins

A

amyloid fibrils

91
Q

a disorder of protein folding in which normally soluble proteins are deposited as abnormal, insoluble fibrils that disrupt tissue structure and function

A

amyloidosis

92
Q

Refers to the deposition of calcium salts in soft tissues. Usually occurs following tissue necrosis.

A

Pathologic calcification / calcification

93
Q

bright yellow-brown homogenous pigment occasionally seen at sites
of previous hemorrhage

A

hematoidin

94
Q

end product of heme degradation (no iron); mostly from
senescent rbc’s via macrophages

A

bilirubin

95
Q

blood and tissues produces a yellow discoloration, called jaundice or icterus.

A

bilirubin

96
Q

when a massive accumulation of hemosiderin causes cell damage

A

hemochromatosis

97
Q

common in sheep because of the reduced biliary
excretion of copper in this species

A

copper toxicity

98
Q

What is the major organ involved in the regulation of copper levels?

A

Liver

99
Q

insoluble, intracellular, brown-black pigment derived from tyrosine.

A

melanin

100
Q

(colored substances) are those that originate in the
animal

A

endogenous substances

101
Q

semipermeable membrane with pumps for ionic / osmotic homeostasis

A

plasma membrane

102
Q

site for transcription of genes

A

nucleus

103
Q

site for oxidative phosphorylation

A

mitochondria

104
Q

Functions of Smooth ER.

A

a. lipid biosynthesis
b. detoxification of harmful compounds
c. sequestration of Ca 2+ ions

105
Q

assist proper folding of proteins and transport across organelle
membranes

A

chaperones

106
Q

degrade both excess proteins and incorrectly folded (misfolded)
proteins

A

proteasomes

107
Q

provide structure and movement of cells/organelles/ granules/ surface molecules/
phagocytosis

A

cytoskeleton

108
Q

It provides enzymatic digestion of materials in the cell

A

lysosomes

109
Q

Give examples of microtubules.

A

flagella, cilia, mitotic
spindle

110
Q

Function of peroxisomes

A

catalase and oxidase for metabolism of hydrogen peroxide (free radicals) and fatty acids

111
Q

Mechanisms and biochemistry of atrophy.

A

a. decreased amount of substance
b. organelles removed by phagocytosis
c. cell shrinks n volume and shut down its differentiated function

112
Q

organs are increased in size due to an increase in cell size without cellular proliferation

A

hypertrophy

113
Q

etiology of hypertrophy

A
  1. response to increased workload
  2. a response to trophic signals
  3. response to certain drugs or toxins
114
Q

mechanisms and biochemistry of hypertrophy

A
  1. anabolic processes exceed catabolic ones
  2. increase in organelles / total cellular proteins
115
Q

This type of cellular adaptation has cellular enlargement due to a proportional increase in the number and size of organelles.

A

hypertrophy

116
Q

True or false.

Cellular swelling is the same as hypertrophy.

A

False. Cell swelling is due to an increased intake of fluid by the cell.

117
Q

increase in organ size or tissue mass caused by an increase in the number
of constituent cells

A

hyperplasia

118
Q

Give the two features that consistently characterize irreversibility of cell injury.

A
  1. Inability to reverse mitochondrial dysfunction.
  2. Profound disturbances of membrane function
119
Q

have a cloudy appearance or cloudy swelling

A

cellular swelling

120
Q

may be an expression of cell injury or a stage of injury in cells that are
destined to die

A

fatty change

121
Q

disorder of purine metabolism with hyperuricemia and deposition of urates in tissues

A

gout (humans)

122
Q

Gross appearance of urates and uric acids (gout)

A

chalky white masses in tissues (called “tophi”) or “frosting” of crystals on serosal membranes.

123
Q

Its origin are plants with high levels of oxalic acid, eg halogeton, rhubarb,
greasewood.

Occurs in cats and dogs due to ingestion of antifreeze.

A

calcium oxalate

124
Q

Possible occurrence of calciphylaxis?

A
  1. primary hyperparathyroidism
  2. renal failure
  3. vitamin d toxicosis
  4. paraneoplastic syndrome
  5. may occur naturally by overfeeding mineral and vitamins
125
Q

most common manifestation of cell death

A

coagulation necrosis

126
Q

coagulative necrosis is characteristic of hypoxic / ischemic death of cells in all tissues, except for?

A

Brain

127
Q

In coagulative necrosis, it predominates over enzymatic digestion.

A

protein denaturation

128
Q

dissolution /fading of the nucleus

A

karyolysis

129
Q

shrunken and densely basophilic nuclei

A

pyknosis

130
Q

nuclear fragmentation

A

karyorrhexis

131
Q

occurs when enzymatic digestion of necrotic cells predominates over protein
denaturation

A

liquefactive necrosis

132
Q

seen in many bacterial infections, due to attraction of neutrophils which contain potent hydrolases which are capable of digesting dead cells

A

liquefactive necrosis

133
Q

typical lesion seen with specific bacterial diseases, eg tuberculosis, caseous
lymphadenitis

A

caseous necrosis

134
Q

What is the gross appearance of caseous necrosis?

A

grey-white and dry with friable (ie crumbly) to pasty texture; note,
caseous = cheese like

135
Q

True or False.

Caseous necrotic cells do not retain cellular outline as seen with coagulation
necrosis

A

true

136
Q

True or false.

Caseous necrotic cells do not undergo complete dissolution as seen in liquefactive necrosis.

A

true

137
Q

Occurs when saprophytic bacteria grow in necrotic tissue.

A

gangrene necrosis

138
Q

What is the requirement for gangrene?

A

necrosis (dead cells) and putrefaction (rotting)

139
Q

occurs in necrotized portion of the skin with moisture loss due to evaporation and drainage and presence of saprophytic bacteria

A

dry gangrene

140
Q

common cause of dry gangrene?

A

ischemia

141
Q

Where are the usual location of dry gangrene?

A

Extremities such as the tail, ears or limbs

142
Q

when the coagulative necrosis of dry gangrene is modified by the liquefactive action of invading saprophytic / putrefactive bacteria

A

wet gangrene

143
Q

color is usually black, with gas bubbles and may have much hemorrhage and edema in and around the lesion

A

wet/moist gangrene

144
Q

production of gas bubbles in the necrotic tissue by invading bacteria (esp. Clostridia)

A

gas gangrene

145
Q

type of necrosis distinguished by its location within body fat stores, esp. abdominal or subcutaneous fat

A

fat necrosis

146
Q

a form of coagulative necrosis resulting from a sudden deprivation of blood supply. Commonly occurring in areas or organs with end artery (i.e., kidney) blocked by thromboembolic lesions

A

infarction

147
Q

a type of coagulative necrosis in striated muscles characterized by loss of striations following necrosis

A

Zenker’s Necrosis (Zenker’s degeneration)

148
Q

Chemical composition of most common forms of amyloid?

A
  1. Protein AA
  2. Protein AL
  3. Familial Amyloid
  4. Endocrine amyloid
149
Q

Occurences are:

  1. prehepatic jaundice - primarily with increased breakdown of
    erythrocytes, eg hemolytic disease.
  2. hepatic jaundice - with failure of conjugation or excretion.
  3. post hepatic jaundice - obstruction of bile duct flow
A

Bilirubin

150
Q

the transition metals (copper and iron), accept or
donate free electrons during certain intracellular reactions, ie
catalyze free radical formation

A

divalent metals

151
Q

hydrolyzes water into hydroxyl (OH) and
hydrogen (H
) free radicals

A

ionizing radiation

152
Q

Generation of free radicals (4)

A
  1. Cellular metabolism
  2. Enzymatic metabolism of exogenous chemicals
  3. Ionizing radiation
  4. Divalent metals
153
Q

either block the formation of free radicals or inactivate
/ scavenge them (eg: Vitamin A, E, C

A

antioxidants

154
Q

Examples of enzymes which are involved in neutralizing free radicals?

A
  1. Glutathione peroxidase
  2. Superoxide dismutase
  3. Catalase
155
Q

General considerations of cell injury

A

a) the cellular response to injurious stimuli is dependant on the type of injury,
its duration and its severity

b) consequences of an injurious stimulus are dependent on the type of cell
injured and its current status, ie nutritional, hormonal, metabolic, oxygen
requirement, etc.

156
Q

steroid hepatopathy

A

hepatocytes of dogs with excess corticosteroids

157
Q

A result of immunoglobulin accumulating in the cisternae of RER

A

Russell bodies

158
Q

Seen lightly eosinophilic, amorphous, hyaline material deposited extracellularly

A

Amyloid

159
Q

melanin is derived from

A

tyrosine

160
Q

melanocytes are derived from

A

Neural crest cells

161
Q

blood and stomach HCI results to

A

melena

162
Q

dystrophic calcification does not bear much clinical significance other than

A

indicates previous parasitic larval migration

163
Q

He said, “Once you know the normal and the artifacts, all the rest is pathology.”

A

Dr. T Van Winkle

164
Q

Also called as Alanine Transaminase

A

Serum glutamic pyruvic transaminase

165
Q

Also called as Aspartate transaminase

A

Serum glutamic oxaloacetic transaminase

166
Q

hypostatic congestion

A

livor mortis

167
Q

due to improperly buffered (acidic) formalin reacting with blood from
tissues

A

acid hematin

168
Q

represents stored iron recovered from the hemoglobin of destroyed rbc’s

A

hemosiderin

169
Q

one of the most crucial events in pathology and can affect any type of cell

A

cell death

170
Q

double MINT

A

malformation
miscellaneous
infectious
immune
neoplastic
nutritional
trauma
toxicity

171
Q

protective mechanism of cell against free radicals that can catalyze formation of reactive oxygen forms

A

iron and copper

172
Q

chemical that damages mitochondrial cytochrome oxidase then blocks oxidative phosphorylation

A

cyanide

173
Q

prevents citrate from being used in the citric acid cycle

A

fluroacetate (converted to fluorocitrate)

174
Q

may be an expression of cell injury or a stage of injury in cells that are
destined to die

A

fatty change

175
Q

soluble dye used to confirm fatty change

A

oil red o (stains red if lipid)

176
Q

morphologic appearance of necrosis is due to

A
  1. denaturation of proteins
  2. enzymatic digestion of the cell
177
Q

often used to describe the changes that occur in all of the cells after an animal has died

A

autolysis
proper term = postmortem autolysis, postmortem decomposition

178
Q

dead neutrophils

A

pus

179
Q

common in birds since heterophils don’t have the potent hydrolytic enzymes
to liquefy cells

A

caseous necrosis

180
Q

hardening of intestine

A

lipomatosis

181
Q

this term is applied to necrosis of surface epithelia

A

slough

182
Q

a piece of necrotic tissue separating from viable tissue

A

slough

183
Q

indicates selective elimination of cells

A

apoptosis

184
Q

Adipose Tissue seen in skeletal muscles and myocardium sometimes called

A

muscle steatosis

185
Q

familial amyloid can occur in

A

humans, shar pei dogs, abyssinian cats

186
Q

as seen in “brown gut syndrome”

A

lipofuscinosis

187
Q

stains black with a Von Kossa special stain

A

dystrophic calcification

188
Q

stains positive with Perl’s Prussian blue

A

hemosiderin

189
Q

locally precipitated bilirubin

A

hematoidin

Veterinary General Pathology (4 decks)

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