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Veterinary Pathology > Unit 2 - 2.1-2.4, 2.7 > Flashcards

Unit 2 - 2.1-2.4, 2.7 Flashcards

1
Q

A retrogressive process in which cells deteriorate and show a corresponding and variable degree of functional inhibition, chemical alteration, and morphologic change

A

cellular injury

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2
Q

What is the sequence of events for cellular injury?

A
  1. biochemical alteration
  2. functional abnormality
  3. morphological change
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3
Q

What occurs within the cell to a point where the cell with either recuperate or die?

A

degeneration

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4
Q

What is it called when an injury occurs that the cells can recover from?

A

subnecrotic or sublethal damage

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5
Q

What happens if necrosis occurs within a small enough area?

A

the viable neighboring cells will replace the dead ones via proliferation

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6
Q

What happens if the area of necrosis is too large for the cells surrounding it to adapt?

A

the gap will be replaced with fibrous CT

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7
Q

negative response of the cell to injury

A

degeneration

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8
Q

Cells have a very limited:

A

number of responses to injury

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9
Q

4 injury classifications:

A
  1. deficiency of a critical material
  2. lack of cellular energy production
  3. accumulation of abnormal substances
  4. physical injury
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10
Q

visible changes

A

morphologic changes

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11
Q

Why might it be difficult to see morphologic changes?

A

the cell has to live long enough after the injury for the morphologic change to develop

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12
Q

What system kicks in when the Krebs cycle isn’t working?

A

anaerobic glycolysis

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13
Q

What is the end product of glycolysis?

A

lactic acid

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14
Q

Why is a build up of lactic acid bad?

A

lowers cellular pH and eventually blood pH

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15
Q

How much ATP is yielded from the Kreb’s cycle?

A

36

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16
Q

How much ATP is yielded from glycolysis?

A

2

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17
Q

normal blood pH:

A

7.4

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18
Q

What can occur when the blood pH goes down to 7.0 (acidosis)?

A

cardiac arrhythmias, CNS dysfunction

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19
Q

What can occur when the blood pH goes up (alkalosis)?

A

neuromuscular excitability, decreased myocardial contractility, arrhythmias

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20
Q

Why do cells that do a lot of synthesizing have blue staining cytoplasm?

A

because they have a lot of endoplasmic reticulum

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21
Q

What enzyme is necessary to transport glucose across the cell membrane of hepatocytes, muscle cells, and adipose cells?

A

insulin

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22
Q

When is insulin not required for glucose transport?

A

into the brain

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23
Q

characterized by accumulation of lipid within non-adipose cells

A

fatty change

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24
Q

Where is fatty change most commonly seen? Less commonly?

A
  • liver

- heart and kidney

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25
Q

Gross appearance of fatty change?

A

tissue is lighter in color (yellow to white); may have a prominent lobular pattern; swollen and friable

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26
Q

List the three reasons fatty acids enter hepatocytes:

A
  1. beta-oxidation to produce energy (ATP)
  2. synthesis of lipoproteins and cholesterol
  3. synthesis and export of triglycerides (requires phospholipids and proteins)
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27
Q

List the three factors that will lead to the appearance of fat in a cell:

A
  1. more fat arrives in the hepatocytes than the hepatocyte can process
  2. decreased beta-oxidation of fatty acids
  3. impaired synthesis or release of lipoproteins
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28
Q

What are three ways that can increase the amount of fat entering the hepatocyte past the point that the hepatocyte can process?

A
  1. high fat diets
  2. fat mobilization (anorexia, pregnancy, lactation)
  3. endocrine issues (esp. diabetes)
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29
Q

What three methods can lead to decreased beta-oxidation of fatty acids?

A
  1. hypoxia from anemia or passive congestion
  2. vitamin deficiencies (niacin, riboflavin)
  3. toxins that impair mitochrondrial function
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30
Q

What two ways can synthesis or release of lipoproteins be impaired?

A
  1. toxins (damage membranes, inhibit protein synthesis)

2. viral infection

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31
Q

generally without physiologic effect unless more severe changes also accompany it

A

fatty change

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32
Q

List four diseases in which fatty liver is prominent and can be fatal:

A
  1. ketosis
  2. pregnancy toxemia
  3. hepatic lipidosis and hypoglycemia (toy breed puppies)
  4. hepatic lipidosis syndrome (cats, ponies, donkeys, and miniature horses)
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33
Q

What is the major source of fat for the liver?

A

GI tract

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34
Q

What three main tissues use lipids for energy?

A

heart, skeletal muscle, liver

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35
Q

the process by which fatty acids are broken down in mitochondria to generate Acetyl-CoA:

A

beta-oxidation

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36
Q

fatty acids cannot be converted into _____________ in animals

A

glucose

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37
Q

What activates the adipocytes to activate hormone sensitive lipase when blood sugar is low?

A

glucagon

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38
Q

What happens once hormone sensitive lipase is activated and what does this accomplish?

A

converts triglycerides into free fatty acids;
the low solubility of free fatty acids allows them to bind to serum albumin and can be transported to muscle and liver for oxidation

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39
Q

What inhibits hormone sensitive lipase?

A

insulin

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40
Q

What, other than glucagon, can activate hormone sensitive lipase?

A

stress

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41
Q

metabolic pathway that results in the generation of glucose from non-carbohydrate carbon substrates

A

gluconeogensis

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42
Q

What do triglycerides get broken down into once they enter the hepatocytes from the blood?

A

glycerol and fatty acids

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43
Q

What does beta-oxidation depend on?

A

oxygen

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44
Q

What is the main source of energy for hepatocytes?

A

oxidation of fatty acids

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45
Q

What are most fatty acids metabolized to?

A

phospholipids

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46
Q

Which tissue type synthesizes more triglyceride than the liver?

A

adipose

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47
Q

What are the two most common causes of hypoxia and thus, decreased beta oxidation of fatty acids?

A

anemia and central passive congestion

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48
Q

When doing a cross-section of a liver, what is a common way to tell if its morpholigic changed is indicative of fatty liver?

A

grease/fats left on the knife

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49
Q

What happens if a liver is extremely fatty?

A

it will float in formalin or water

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50
Q

How would the consistency of a fatty liver feel?

A

friable; break easily between fingers

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51
Q

What are the bright red areas you can see in yellow livers with very distinct lobular patterns?

A

blood in the central veins of the hepatic lobules

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52
Q

Where does blood flow to in the liver?

A

from the portal triad to the central vein

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53
Q

Why are the centrilobular regions of the liver the most vulnerable to hypoxia?

A

it’s the lowest of any part of the lobule; last in line to receive oxygen

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54
Q

What is the major significance of fatty change

A

it tells us that we must look for the cause

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55
Q

a condition in which there are excessive ketones (acetoacetic acid and beta-hydroxybutyric acid) in the blood

A

ketosis

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56
Q

When can ketosis occur in cows?

A

at peak lactation

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57
Q

When can ketosis occur in sheep and goats?

A

in late gestation

58
Q

Why can ketosis occur in pregnant or nursing animals?

A

high energy expenditure (inadequate quality/intake of food)

59
Q

How does acetyl-CoA have to enter the Krebs Cycle?

A

bound to oxaloacetate

60
Q

What does the liver do to oxaloacetate when carbohydrates are inadequate?

A

converts it to glucose (via gluconeogenesis)

61
Q

If all of the oxaloacetate is being converted to glucose, what happens to the acetyl-CoA?

A

converts it to ketones (which build up in the blood)

62
Q

Why can’t fat be visualized on a normal histological slide?

A

tissue gets soaked in xylene which dissolves the fat

63
Q

How can you visualize fat on a slide?

A

freeze tissue, then stain with Oil-red-O

64
Q

What type of dog breed commonly gets hepatic lipidosis?

A

toy breed dog puppies

65
Q

Puppies with hepatic lipidosis typically present with what 2 major clinical signs?

A

neurological signs (due to brain swelling) and cerebral neuronal necrosis (secondary to hypoglycemia)

66
Q

microvesicular type hepatic lipidosis looks like:

A

vacuolation consisting of many small vacuoles (as opposed to a few large ones)

67
Q

a fairly common idiopathic disease that occurs mostly in obese cats following a period of anorexia

A

hepatic lipidosis

68
Q

Why is hepatic lipidosis a major problem in cats compared to other animals?

A

their hepatocytes become dysfunctional when filled with fat

69
Q

a condition in which the liver fails to remove certain chemicals (especially ammonia and mercaptans) from the portal blood

A

hepatic encephalopathy

70
Q

Can cross the blood-brain barrier and is toxic to astrocytes, causing them to swell:

A

ammonia

71
Q

thought to act as false neurotransmitters

A

mercaptans

72
Q

a purely descriptive term referring to a waxy, homogenous, amorphous, solid, translucent appearance

A

hyaline degeneration

73
Q

seen as a hyalinization of collagen - grossly it has a smooth, white, glossy appearance

A

connective tissue hyaline

74
Q

describe the microscopic appearance of extracellular hyaline

A

hyalinized area containing no or relatively few nuclei and stains intensely pink with H&E

75
Q

What is the effect of connective tissue hyaline in scars?

A

no effect

76
Q

What is the effect of connective tissue hyaline in vessel walls?

A

inelasticity - high blood pressure

77
Q

What is the effect of depositional hyaline?

A

interferes with fluid exchange

78
Q

hyaline materials deposited around cells:

A

depositional hyaline

79
Q

What is the significance of tubular casts?

A

an indication of severe damage to the renal glomerulus, usually due to glomerular amyloidosis or glomerulonephritis

80
Q

The deposition of a protein especially in the spleen, kidney, and liver. Lymph node and adrenal may be involved:

A

amyloid extracellular hyaline

81
Q

What stain placed on the cut surface of an organ with amyloidosis will generally impart a red-brown color?

A

Lugol’s iodine

82
Q

Seen especially in kidney tubular epithelium and adrenal cortical cells as small cytoplasmic hyaline droplets

A

hyaline droplet degeneration

83
Q

Seen as bright-pink staining globules in the cytoplasm of plasma cells. Seen in chronic diseases or those associated with a hyperammaglobulinemiaL

A

Russell bodies

84
Q

may be intranuclear or intracytoplasmic, single or multiple and basophilic or eosinophilic

A

viral inclusion bodies

85
Q

seen as a rhomboid, red staining crystal in the nucleus of liver and kidney epithelium of the dog and cat (cause and significance unknown)

A

crystalline inclusion bodies

86
Q

Purplish staining, homogenous or concentrically laminated bodies which may occur in the alveoli of the prostate, mammary gland or lung

A

corpora amylacea

87
Q

What is the significance of corpora amylacea intracellular hyaline?

A

may indicate a past inflammatory process

88
Q

keratin of squamous epithelium that may accumulate excessively in conditions of chronic irritation or altered metabolism

A

keratohyaline

89
Q

Where are cytoplasmic inclusions more common?

A

epithelial cells of the respiratory tract, urinary bladder mucosa, and stomach

90
Q

What is the name of the inclusion body that is a hallmark for rabies?

A

Negri bodies

91
Q

refers to the location of the tumor outside of the bone marrow

A

extramedullary

92
Q

Occurs when your bone marrow produces abnormal antibodies that can’t be broken down; deposited in your tissues as amyloid and cannot be broken down

A

primary amyloidosis (AL)

93
Q

protein deposits accumulate in one or more organ systems in the body; caused by chronic infection or inflammatory disease

A

secondary amyloidosis (AA)

94
Q

Primary protein of AL amyloid is:

A

serum amyloid A (SAA)

95
Q

List the common sites for amyloid to occur (5):

A

kidney, liver, spleen, lymph nodes, and adrenal

96
Q

What color should normal kidneys be?

A

mahogany brown

97
Q

Why is albumin the protein that most often leaks into the nephron?

A

low molecular weight

98
Q

What is a consequence of urinating gram quantities of protein at micturition?

A

weight loss and muscle wasting

99
Q

combination of generalized edema, ascites, and pleural effusion and hypercholersterolemia secondary to protein losing nephropathy:

A

nephrotic syndrome

100
Q

What is the primary way that amyloid causes damage?

A

compression of normal tissue resulting in ischemia (and often organ failure)

101
Q

Why is calcium build up a sequelae of necrosis (known as dystrophic calcification)?

A

regulation of influx of Ca++ into cytoplasm can no longer be controlled; accumulates in the mitochondria

102
Q

deposition of calcium salts in otherwise normal tissues because of elevated levels of serum calcium

A

metastatic calcification

103
Q

Occurs in multiple tissues including liver, pancreas and kidney as an accumulation of glycogen in cytoplasmic vacuoles.

A

Glycogen infiltration

104
Q

Describe the gross appearance of organs with glycogen infiltration:

A

organs may be lighter in color

105
Q

How does glycogen infiltration appear microscopically?

A

fuzzy lined vacuoles, single or multiple, in cytoplasm

106
Q

Where can you see glycogen infiltration in well fed animals?

A

liver

107
Q

What does glycogen infiltration affect in poorly controlled DM?

A

B cells of islets of Langerhands, duct epithelium of the pancreas, renal tubular epithelium

108
Q

Which two types of tumors often have heavy glycogen infiltration?

A

seminoma and renal carcinoma

109
Q

Treating dogs with what drug will increase liver glycogen? What is this called?

A

corticosteroids; steroid hepatopathy

110
Q

What disease of horses can cause glycogen infiltration?

A

polysaccharide storage myopathy

111
Q

What is the effect of glycogen infiltration?

A

not harmful but indicates a fault in the metabolism of the cell

112
Q

What is the form in which glucose is normally stored within hepatocytes in the liver?

A

glycogen

113
Q

What is a major metabolic disease affecting glucose metabolism that all of you are familiar with?

A

DM

114
Q

What color does PAS stain glycogen?

A

magenta

115
Q

Glucocorticoids are often induced by:

A

stress

116
Q

reduction in mass of a tissue or organ

A

atrophy

117
Q

increase in the size of cells, resulting in enlargement or rogans

A

hypertrophy

118
Q

increased number of cells in an organ or tissue

A

hyperplasia

119
Q

transformation or replacement of one adult cell type with another

A

metaplasia

120
Q

any change that results in loss of the ability to maintain the normal or adapted homeostatic state

A

cell injury

121
Q

Hallmarks of Cell Degeneration:

A

cell swelling, fatty change, glycogen accumulation, lipofuscin, hyaline changes, amyloid, calcification, gout

122
Q

A complex protein that accumulates within cells; homogeneous pink materal

A

amyloid

123
Q

more common in birds and reptiles, but can occur in other species (assoc. with renal dz due to decreased excretion of urates)

A

gout

124
Q

accumulation of lipid (TG) within vacuoles within cells

A

fatty change

125
Q

the oxidized products from membrane lipids (yellow to brown)

A

lipofuscin

126
Q

dense, homogenous, glossy, translucent; many causes (protein leak most common)

A

hyaline changes

127
Q

no nuclear displacement with:

A

glycogen accumulation

128
Q

What are the three pathogeneses for fatty change?

A

overload, injury to cells, deficiencies

129
Q

What are the three pathogenic mechanisms for glycogen accumulation?

A
  1. severe hyperglycemia
  2. high glucocorticoids
  3. lysosomal storage disease
130
Q

cytoplasm contains rounded, eosinophilic droplets, vacuoles, or aggregates

A

hyaline droplets

131
Q

protein casts within renal tubules

A

hyaline casts

132
Q

compacted collagen, scar tissue

A

CT hyaline

133
Q

Describe the gross appearance of calcification:

A

chalky, white tissue; hard, gritty on cut surface

134
Q

Describe the gross appearance of amyloid:

A

enlarged, pale, waxy, translucent

135
Q

Has dark blue staining material, along BM, stippled throughout cell, large clumps. What is this the microscopic appearance of?

A

calcification

136
Q

Widespread excessive calcification:

A

calcinosis

137
Q

What is the term used for calcification in the cavities or lumina?

A

calculi/calculus

138
Q

Accumulation or urate crystals

A

gout

139
Q

White, firm, crystal depsoits on gross appearance:

A

gout

140
Q

Granulomas with radiating crystalline material on microscopic appearance:

A

gout

141
Q

What is the most common action for toxins?

A

free radicals

Veterinary Pathology (14 decks)

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