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Vet Path > Intro Vet Path (1-11) > Flashcards

Intro Vet Path (1-11) Flashcards

1
Q

this is the mechanism of disease development i.e. the sequence of events occurring following exposure to the inciting agent/event

A

pathogenesis

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2
Q

this diagnosis is based on the predominant lesions and refers to the structural changes that are seen in cells or tissues in association with the disease process

A

morphologic diagnosis

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3
Q

this diagnosis specifically identifies the etiology

A

etiological diagnosis

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4
Q

how much volume of buffered formalin should be used to fix tissues?

A

10x their volume

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5
Q

this is the stain routinely used in diagnostic pathology

A

Hematoxylin & Eosin (H&E)

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6
Q

this is a special histological stain that stains for fat

A

Oil Red-O (red)

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7
Q

this is a special histological stain that stains for glycogen

A

PAS (Periodic acid-Schiff) (pink)

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8
Q

this is a special histological stain that stains for Haemosiderin

A

Perl’s Prussian Blue Reaction (blue)

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9
Q

this is a special histological stain that stains for connective tissue

A

Massons Trichrome (green)

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10
Q

this is a special histological stain that stains for basement membranes

A

Jones’ stain (black)

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11
Q

this is the incomplete or underdevelopment of tissue or organ

A

hypoplasia

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12
Q

this is an increase in number of cells

A

hyperplasia

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13
Q

this is when one adult cell type is replaced by another adult cell type

A

metaplasia

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14
Q

this is when there is alteration in the size, shape or organization of a tissue

A

dysplasia

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15
Q

this is when an organ does not develop at all - rudimentary tissue only present

A

aplasia

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16
Q

this is failure to develop due to lack of embryonic primordial tissue

A

agenesis

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17
Q

this is an increase in the size of cells resulting in an increase in the size of the organ (no new cells, just bigger cells)

A

hypertrophy

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18
Q

cellular swelling appears as this in the cytoplasm which do not stain for fat or glycogen

A

clear vacuoles

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19
Q

this type of necrosis is when basic cell outlines are preserved due to delayed proteolysis - acute

A

coagulative necrosis

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20
Q

this type of necrosis has a friable ‘cheese’ like appearance, chronic lesion, may develop dystrophic calcification

A

caseous necrosis

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21
Q

this type of necrosis has cavity/cavities filled with liquefied debris

A

liquefactive necrosis

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22
Q

specific necrosis of fat

A

fat necrosis

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23
Q

destructive fragmentation of the nucleus; chromatin is distributed regularly throughout the cytoplasm

A

karyorrhexis

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24
Q

disintegration and dissolution of the nucleus of a necrotic cell

A

karyolysis

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25
Q

this is the shrinkage or condensation of a cell with increased nuclear compactness or density

A

pyknosis

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26
Q

what’s another term for fatty change

A

lipidosis

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27
Q

this is the accumulation of intracytoplasmic lipid

A

lipidosis

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28
Q

what does lipidosis look like with H&E stain?

A

punched out holes (fat doesnt stain. with H&E)

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29
Q

list 3 examples of situations where glycogen accumulation might occur

A
  1. Corticosteroid therapy
  2. diabetes mellitus
  3. glycogen storage disease
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30
Q

this is when serum calcium levels are normal but the calcium is deposited in tissue that is already dead or dying

A

dystrophic calcification

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31
Q

this is when the primary problem is hypercalcemia causing damage to intracellular organelles

A

metastatic calcification

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32
Q

these inflammatory cells have condensed, dark purple chromatin that is segmented into lobes connected by filaments

A

neutrophils

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33
Q

these inflammatory cells have a segmented nucleus and granules (orange/pink) in the cytoplasm

A

eosinophils

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34
Q

these inflammatory cells are small round cells with a round nucleus, dense chromatin, and scant rim of clear cytoplasm

A

lymphocytes

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35
Q

these inflammatory cells are a round cell with abundant deep blue cytoplasm with a pale area next to the nucleus (Golgi apparatus)

A

plasma cells

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36
Q

these inflammatory cells are oval/irregularly shaped cells with dense granular cytoplasm often obscuring the nucleus and other organelles

A

mast cells

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37
Q

these inflammatory cells have an ovoid/irregular nucleus and the cytoplasm contains vacuoles and granules

A

macrophages

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38
Q

clear or yellow watery fluid occurring early in most inflammatory lesions

A

serous exudate

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39
Q

thick and gelatinous consistency inflammatory response in respiratory and GI tract where mucus secreting cells are prominent

A

catarrhal exudate

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40
Q

this occurs where damage is more severe allowing larger molecular weight proteins to leak through endothelium; causes surfaces of organs to be red and covered by white/yellow exudate

A

fibrinous exudate

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41
Q

thick white/yellow material often bacterial in origin

A

suppurative/purulent exudate

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42
Q

this is when a lesion involves the whole organ or whole of a specified area

A

diffuse

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43
Q

this is when multifocal lesions ‘join up’ with each other

A

multifocal to coalescing

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44
Q

this is used for describing a portion of a tubular organ

A

segmental

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45
Q

this is used to describe multiple small lesions

A

miliary

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46
Q

what 3 things must you know in order to draw conclusions about a lesion?

A
  1. how the animal died
  2. when the animal died
  3. conditions post mortem
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47
Q

this is when a lesion is characteristic or indicative of a particular disease

A

pathognomic

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48
Q

multifocal lesions usually imply this type of spread

A

systemic/hematogenous spread

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49
Q

a raised lesion implies this

A

something has been added

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50
Q

a depressed lesion implies this

A

something has been lost

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51
Q

a flat lesion can imply this

A

acute process or incidental color change

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52
Q

a lesion of this color is due to an increase in amount of blood (hemorrhage, congestion)

A

red to red/black

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53
Q

a lesion of this color indicates melanin, exogenous carbon, putrefactive bacteria, or hemosiderin

A

black to brown/black

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54
Q

a lesion of this color is usually bile pigment (seen in PM areas of liver and intestine); some fungal pathogens

A

green

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55
Q

a lesion of this color may indicate fat, bile pigment (bilirubin), fibrin, cellular exudates, neoplasms

A

yellow

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56
Q

a lesion of this color may indicate exudates, neoplasia, connective tissue (cartilage, bone)

A

white

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57
Q

a hard lesion implies this

A

mineral density (cartilage, bone, mineral salt deposition)

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58
Q

list the 10 steps of the PM prosection

A
  1. external examination
  2. initial dissection
  3. neck region
  4. open abdomen and thorax
  5. removal of thoracic viscera
  6. removal of abdominal viscera
  7. musculoskeletal systems
  8. nervous system
  9. special senses
  10. individual organ dissections
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59
Q

name the organs incised/examined in the neck region during a PM prosection

A

tongue, soft palate, hyoid apparatus, tonsils, R/P lymph nodes, thyroids, oesophagus, trachea

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60
Q

name the thoracic viscera removed during a PM prosection

A

heart, lungs (leave oesophagus connected to stomach)

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61
Q

name the abdominal viscera removed during a PM prosection

A

(intestines, stomach, liver and spleen), adrenals, (kidneys, ureters, bladder)

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62
Q

how should tissue samples for histopathology be stored from a PM

A

fixed in 10x 10% buffered formalin

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63
Q

this is the cooling of body after death (can aid in estimating time of death)

A

algor mortis

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64
Q

this is an effect of gravity, often evident in lungs and kidneys - PM change

A

hypostatic congestion

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65
Q

Blood coagulation in vessels; careful not to mistake for thrombosis - PM change

A

postmortem clotting of blood

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66
Q

this is when pigment from bile is absorbed by liver/other organs in contact with gall bladder (ex. GI tract) - PM change

A

biliary imbibition

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67
Q

this is a green/black discoloration due to conversion of iron to iron sulphide by GI bacteria - PM change

A

pseudomelanosis

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68
Q

this is invasion by gas producing bacteria - PM change

A

emphysema

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69
Q

this PM change begins approximately 2-4 hours after death; rigidity of skeletal muscles due to lack of ATP (sustained contraction)

A

rigor mortis

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70
Q

this is the process whereby the release of intracellular lytic enzymes results in self digestion of tissues

A

autolysis

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71
Q

this PM change occurs when dead tissue is invaded by anaerobic organisms such as Clostridia; tissue turns green/brown

A

putrefaction

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72
Q

these changes occur around the time of death/time of irreversible circulatory failure and often leads to vascular congestion

A

agonal changes

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73
Q

this PM change may result in food material being present in the airways and possibly alveoli

A

agonal regurgitation of GI contents

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74
Q

name 3 PM changes that may be associated with administration of barbiturates

A
  1. local reaction
  2. barbiturate crystals
  3. splenomegaly
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75
Q

this incidental finding occurs when hyperplastic nodules of tissue develop in organs but can be mistaken for genuine neoplasms

A

nodular hyperplasia

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76
Q

this PM change occurs due to inhaled carbon particles being phagocytose by alveolar macrophages which can become visible as multiple small black foci in lung tissue

A

anthracosis

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77
Q

this is the degeneration and proliferation in the arterial wall resulting in loss of elasticity and hardening; common PM change but usually incidental

A

arteriosclerosis

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78
Q

long time steroid use can lead to this where glucocorticoids induce glycogen synthetase to increase storage of glycogen within hepatocytes, can be up to 20x the normal size

A

steroid-induced hepatopathy

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79
Q

Total Body Water (TBW) comprises this percent of body weight

A

60%

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80
Q

Intracellular Fluid (ICF) makes up this much of total body water

A

40%

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81
Q

Extracellular Fluid (ECF) makes up this much of total body water

A

20%

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82
Q

interstitial fluid (component of ECF) makes up this much of total body water

A

15%

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83
Q

plasma (component of ECF) makes up this much of total body water

A

5%

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84
Q

this is extracellular fluid around cells

A

interstitial fluid (ISF)

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85
Q

this is extracellular fluid within blood vessels

A

intravascular fluid (IVF)

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86
Q

this is extracellular fluid produced by specialized cells (ex: CSF, synovial fluid)

A

transcellular fluid (TSF)

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87
Q

this is a proteolytic enzyme that is produced by specialized juxtaglomerular cells in the glomerular afferent arteriole in response to decr. renal profusion

A

renin

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88
Q

this is a serum globulin produced by the liver which is converted by renin into angiotensin I

A

angiotensinogen

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89
Q

this is produced by RAAS and increases aldosterone production which enhances renal Na+ and water reabsorption

A

angiotensin II

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90
Q

this controls permeability of distal tubules and collecting ducts. when it’s present, water permeability is high, allowing water to follow Na into the blood stream so urine output is low

A

ADH (anti-diuretic hormone)

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91
Q

this is a group of diverse peptide hormones released by the heart in response to stretching of the heart & reduce cardiac output and blood pressure

A

ANF (atrial natriuretic factor) or ANP (peptide)

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92
Q

these are vital in most of life’s processes and affect the volume of fluid present in each body fluid compartment

A

electrolytes

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93
Q

this is when the ratio of total body Na to total body water is increased (may be caused by water deficiency or sodium excess)

A

hypernatremia

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94
Q

what is the overall effect of hypernatremia

A

cell dehydrates and eventually dies

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95
Q

this is when the ratio of total body Na to total body water is decreased (may be caused by sodium deficit or water excess)

A

hyponatremia

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96
Q

this is the overall effect of hyponatremia caused by a sodium deficit

A

hemoconcentration and circulatory failure

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97
Q

this is the overall effect of hyponatremia caused by water excess

A

CNS convulsions and death

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98
Q

water distribution between plasma and interstitium is mainly determined by these 2 forces acting against each other

A

hydrostatic pressure and oncotic pressure

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99
Q

this force tends to pull water out of the vessels into the interstitium

A

hydrostatic pressure

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100
Q

this force is the osmotic pressure created by the plasma proteins that pulls water from the interstitium into the vessels

A

oncotic pressure

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101
Q

this is an accumulation of excess interstitial fluid. it can be generalized or localized

A

oedema

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102
Q

this is a type of generalized oedema where the fluid tends to sink with gravity so that the ventral abdomen and limbs are mainly affected

A

dependent oedema

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103
Q

this is severe diffuse subcutaneous oedema, where a finger pushed into the expanded interstitium leaves an indentation

A

pitting oedema

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104
Q

this is severe, generalized oedema

A

anasarca

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105
Q

this is when excessive fluid leaks into a body cavity lined by mesothelial cells (peritoneum, pleural, pericardium)

A

effusion

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106
Q

name 4 causes of excessive fluid leakage from the vasculature (that may lead to oedema or effusion formation)

A
  1. incr hydrostatic pressure
  2. decr oncotic pressure
  3. incr microvascular permeability
  4. decr lymphatic drainage
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107
Q

right heart failure can lead to this type of oedema

A

peripheral oedema

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108
Q

left heart failure can lead to this type of oedema

A

pulmonary oedema

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109
Q

generalized heart failure can lead to this type of oedema

A

generalized oedema

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110
Q

oedema caused by lymphatic obstruction if often this type

A

localized

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111
Q

pulmonary oedema is mainly caused but these 2 mechanisms

A

increased hydrostatic pressure and increased vascular permeability

112
Q

this type of effusion is a clear/pale yellow fluid characterized by low protein and cellular content

A

transudate

113
Q

this effusion type has <25 g/l protein and <1 cell x10^9/l cellular content

A

transudate

114
Q

this effusion type has >30 g/l protein and >5 cell x10^9/l cellular content

A

exudate

115
Q

pleural transudate is called this

A

hydrothorax

116
Q

abdominal transudate is called this

A

hydroperitoneum or ascites

117
Q

pericardial transudate is called this

A

hydropericardium

118
Q

this type of effusion is a turbid, deep yellow/orange to brown fluid characterized by high protein and cellular content

A

exudate

119
Q

cytological analysis of exudates reveals high numbers of this type of cell

A

neutrophils (& other inflammatory cells)

120
Q

effusion due to neutrophilic inflammation in the pleura is called this

A

pyothorax

121
Q

this type of effusion can vary from clear to mild turbid with variable color (yellow to pink)

A

modified transudate

122
Q

name some cell types that might be seen in low lumbers in transudate effusion

A

macrophages, mesothelial cells, neutrophils, occasional lymphocytes

123
Q

this type of effusion is caused by leakage or rupture of lymphatic vessels and is usually turbid and white in color

A

chylous

124
Q

this type of effusion is caused by leakage of blood into a body cavity and has a bloody appearance

A

hemorrhagic

125
Q

this type of effusion is caused by urinary tract rupture and leakage of urine in the abdomen

A

uroperitoneum

126
Q

this is another word for cardiac collapse

A

shock

127
Q

name 3 life-threatening events that can lead to shock

A
  1. severe hemorrhage
  2. extensive trauma or burns
  3. sepsis
128
Q

name the 3 categories of shock

A
  1. cardiogenic
  2. hypovolemic
  3. blood maldistribution
129
Q

this type shock results from failure of the heart to adequately pump blood

A

cardiogenic shock

130
Q

this type of shock is due to reduced circulating volume resulting from blood or fluid loss (hemorrhage, vomiting, diarrhea, extensive burns)

A

hypovolemic shock

131
Q

if volume reduction is around this percent in hypovolemic shock, then return to normal can occur

A

10%

132
Q

if volume reduction is around this percent in hypovolemic shock, then BP and CO fall dramatically

A

35-45%

133
Q

this type of shock is characterized by decreased peripheral vascular resistance and pooling of blood peripheral tissues

A

blood maldistribution

134
Q

name the 3 main types of maldistribution shock

A
  1. neurogenic shock
  2. anaphylactic shock
  3. septic shock
135
Q

this is a life-threatening reaction to an infection which causes the immune system to overreact and damage the body’s own tissues and organs

A

sepsis

136
Q

this occurs when a bacterial infection enters the bloodstream

A

septicemia

137
Q

this is the most common cause of septic shock; it is a lipopolysaccharide (LPS) in the wall of gram negative bacteria

A

endotoxin

138
Q

name the 3 stages of shock

A
  1. non-progressive stage
  2. progressive stage
  3. irreversible stage
139
Q

during this stage of shock, mechanisms aimed at vasoconstriction are overcome leading to widespread vasodilation and multi organ failure/DIC

A

irreversible stage

140
Q

during this stage of shock, compensatory mechanisms are overcome and there is blood pooling, tissue hypoperfusion and cellular injury leading to necrosis

A

progressive stage

141
Q

during this stage of shock, the body compensates and blood flow is maintained to critical organs (heart, kidney, brain)

A

non-progressive stage

142
Q

name some clinical features of shock

A

hypotension, weak pulse and tachycardia, hyperventilation, decr. urine production, hypothermia

143
Q

name some morphologic features of shock

A

congestion and pooling of blood, oedema and hemorrhage, thrombosis, cellular necrosis

144
Q

this occurs when arteriolar dilation increases blood flow to the tissue (active process) which leads to tissue redness

A

hyperemia

145
Q

this is due to reduced outflow of blood from a tissue (passive process)

A

congestion

146
Q

hyperemia is an active or passive process?

A

active process

147
Q

congestion is an active or passive process?

A

passive process

148
Q

this is the escape of blood from vessels due to vascular rupture or damage which may lead to loss of blood from the body or blood accumulating within surrounding tissue/body cavity

A

hemorrhage

149
Q

this is a massive accumulation of blood within a tissue

A

hematoma

150
Q

this is an accumulation of blood within the thorax

A

hemothorax

151
Q

this is a 1-2mm hemorrhage in the skin, mucus membranes and serial surfaces

A

petechiae

152
Q

this is a 3mm+ hemorrhage in the skin, mucus membranes and serial surfaces

A

purpura

153
Q

this is a 1-3cm hemorrhage in the skin, mucus membranes and serial surfaces

A

ecchymoses

154
Q

this is a hemorrhage in the skin, mucus membranes and serial surfaces that affects large contiguous areas of tissue

A

suffusive hemorrhage

155
Q

the significance of hemorrhage depends on these 3 factors of blood loss

A

volume, rate, and location

156
Q

this is the physiological process which stops hemorrhage and is a highly regulated, complex interrelationship between blood vessels, platelets and coagulation factors

A

hemostasis

157
Q

name the 4 steps/processes of hemostasis

A
  1. vascular response (transient effect)
  2. platelet response (primary hemostasis)
  3. coagulation cascade (secondary hemostasis)
  4. fibrinolysis (tertiary hemostasis)
158
Q

this step of hemostasis is when vascular injury causes arteriolar vasoconstriction

A

vascular response

159
Q

this step of hemostasis includes platelet adherence, activation, and aggregation to form a hemostatic plug

A

platelet response (primary hemostasis)

160
Q

this step of hemostasis is when clotting factors are activated to form thrombin which converts fibrinogen to fibrin to stabilize primary hemostatic plug and stop further hemorrhage

A

coagulation cascade (secondary hemostasis)

161
Q

this step of hemostasis is to prevent over-production or persistence of fibrin and to control hemostatic plug formation

A

fibrinolysis (tertiary hemostasis)

162
Q

these act as weak anticoagulants and can be measured to diagnose pro-thrombin states

A

fibrin degradation products (FDPs)

163
Q

this is a cause of primary hemostasis disorders and is decreased platelet numbers in peripheral blood

A

thrombocytopenia

164
Q

this is the most common cause of thrombocytopenia

A

platelet clumping (pseudothrombocytopenia)

165
Q

name 4 causes of true thrombocytopenia

A
  1. decreased production
  2. increased destruction or utilization of platelets
  3. sequestration of platelets
  4. inherited causes
166
Q

this is an inherited disorder of a specific adhesion molecule between platelets and endothelial cells essential for primary homeostasis

A

von Willebrands disease (vWD)

167
Q

this type of hemostasis disorder is due to coagulation factor deficiencies

A

disorders of secondary hemostasis

168
Q

Hemophilia A is a deficiency of this coagulation factor

A

VIII (8)

169
Q

Hemophilia B is a deficiency of this coagulation factor

A

IX (9)

170
Q

these are sex-linked coagulation factor disorders with a recessive inheritance pattern where males are affected (disorders of secondary hemostasis)

A

hemophilia A and B

171
Q

this type of hemostasis disorder is mostly associated with disseminated intravascular coagulation/DIC which results in clot formation in the microvasculature

A

disorders of tertiary hemostasis

172
Q

primary hemostasis can be evaluated by these 3 tests

A
  1. platelet count
  2. platelet function
  3. buccal mucosal bleeding time (BMBT)
173
Q

secondary hemostasis can be evaluated by these 5 tests

A
  1. prothrombin time (PT)
  2. activated partial thromboplastin time (aPTT)
  3. activated clotting time (ACT)
  4. whole blood clotting time (WBCT)
  5. thrombin clot time (TCT)
174
Q

tertiary hemostasis can be evaluated by these 2 tests

A

evaluation of FDPs and D-dimers

175
Q

this is a mass of platelets, fibrin, red and white blood cells, which is attached to the wall of the cardiovascular system

A

thrombus

176
Q

what is the difference between an ante-mortem thrombus and a post-mortem clot surface

A

thrombus: granular, dry, dull
clot: smooth, moist, shiny

177
Q

what is the difference between an ante-mortem thrombus and a post-mortem clot texture

A

thrombus: firm or friable
clot: elastic or gelatinous

178
Q

what is the difference between an ante-mortem thrombus and a post-mortem clot structure

A

thrombus: variegated (maybe laminated)
clot: homogenous

179
Q

what is the difference between an ante-mortem thrombus and a post-mortem clot color

A

thrombus: white (arterial), OR red (veins), OR red/white laminate (arteries, large veins, heart)
clot: dark red OR “chicken fat”

180
Q

what is the difference between an ante-mortem thrombus and a post-mortem clot shape

A

thrombus: ovoid, flat, or pear-shape
clot: conforms to vessel shape

181
Q

which is easier to remove: an ante-mortem thrombus or a post-mortem clot?

A

post-mortem clot (thrombus is attached to vessel wall or chord tendinae)

182
Q

name the 3 main factors that predispose to thrombus formation (Virchow’s Triad)

A
  1. damage to epithelium
  2. altered blood flow
  3. hypercoagulability of blood
183
Q

venous thrombi tend to have this appearance

A

red, soft, loose vascular attachment

184
Q

thrombi in heart or arteries often have this appearance

A

pale (red-grey), firm, attached to wall, striated/laminar

185
Q

the clinical significance of thrombosis depends on these 3 factors

A

size, location, rate of formation

186
Q

name the 4 possible fates of a thrombus

A
  1. dissolution
  2. propagation
  3. organization and recanalization
  4. embolization
187
Q

this is when the thrombus is completely removed by fibrinolysis

A

dissolution

188
Q

this is when additional platelets and fibrin accumulate and extend/elongate the thrombus along the vessel wall toward the heart

A

propagation

189
Q

this is when the thrombus is invaded by endothelial cells and fibroblasts forming granulation tissue with subsequent fibrosis

A

organization

190
Q

this is when capillary channels in a large organizing thrombus anastomose and allow blood flow to be re-established

A

recanalization

191
Q

this is when fragments of the thrombus break off and travel to other sites in the body via the vasculature

A

embolization

192
Q

this is a solid or gaseous mass carried by the bloodstream from its point of origin to a distant site within the circulation

A

embolus

193
Q

this is the most common type of embolism, where fragments of thrombi detach and spread throughout circulation

A

thromboembolism

194
Q

this type of embolus occurs if a large enough volume of air is injected into the circulation - can accumulate in pulmonary trunk and form a fatal airlock

A

gas embolism

195
Q

adipocytes from bone marrow may be released into circulation following bone fractures leading to this type of embolus

A

fat embolism

196
Q

this is due to reduction or failure of blood flow to or from a tissue/organ and results in tissue hypoxia and reduced nutrient supply

A

ischemia

197
Q

name 3 possible causes of ischemia

A
  1. arterispasms
  2. compression of vessels
  3. thromboembolism
198
Q

extent and consequences of ischemia depend on these 4 factors

A
  1. degree of occlusion
  2. speed of occlusion
  3. presence of collateral circulation
  4. vulnerability of tissues/cells to ischemia
199
Q

this is a segmental or localized area of coagulative necrosis due to occlusion of the blood supply

A

infarction

200
Q

macroscopic appearance of an infarction

A

red or pale, wedge-shaped

201
Q

a venous occlusion will give this color infarction

A

red

202
Q

an arterial occlusion will give this color infarction

A

pale

203
Q

this is widespread pathologic activation of hemostasis within the vascular system resulting in generalized intravascular thrombosis

A

DIC (disseminated intravascular coagulation)

204
Q

the intrinsic pathway of the coagulation cascade involves these coagulation factors

A

12, 11, 9, 8

205
Q

the extrinsic pathway of the coagulation cascade involves this coagulation factor

A

7

206
Q

the common pathway of the coagulation cascade involves these coagulation factors

A

10, 5, 2 (13)

207
Q

what is hemoptysis?

A

coughing up blood

208
Q

what is epistaxis?

A

nose bleed

209
Q

what is hematochezia?

A

fresh blood in feces

210
Q

this is the increased tendency to hemorrhage after minor injury

A

hemorrhagic diathesis

211
Q

this is a prolonged/persistent inflammatory response that comprises varying combinations of inflammation, tissue injury and repair

A

chronic inflammation

212
Q

name 4 infectious causes of chronic inflammation

A
  1. Mycobacterium spp.
  2. fungi
  3. parasites
  4. viruses
213
Q

name the 3 main components of chronic inflammation

A
  1. inflammation
  2. tissue destruction
  3. tissue repair attempts
214
Q
A
215
Q

these inflammatory cells play a huge role in adaptive immunity against infectious agents and produce cytokines that influence other inflammatory cell types

A

lymphocytes (B & T)

216
Q

these inflammatory cells produce antibodies and often accompany lymphocytes in chronic inflammation

A

plasma cells

217
Q

name the 3 main functions of macrophages in chronic inflammation

A
  1. phagocytosis
  2. secrete cytokines
  3. initiation of repair
218
Q

inflammation mediated by IgE (hypersensitivity) or parasitic infections will be dominated by this type of cell

A

eosinophils

219
Q

persistence of infectious agents in chronic inflammation can lead to the continues presence of these cells

A

neutrophils

220
Q

this is a distinct form of inflammation which is always chronic with macrophages predominate

A

granulomatous inflammation

221
Q

this is discrete clusters/nodules of macrophages separated by host tissue

A

granulomas

222
Q

this is discrete clusters of macrophages AND neutrophils

A

pyogranulomas

223
Q

this is a type of chronic inflammation where macrophages are predominate but neutrophils are also present

A

pyogranulomatous

224
Q

these are macrophages that become activated to the extent that they develop abundant cytoplasm

A

epithelioid macrophages

225
Q

name 5 systemic effects of chronic inflammation

A
  1. leucocytosis (mediated by IL-1 and TNF-alpha)
  2. low grade pyrexia
  3. acute phase response
  4. cachexia (mediated by TNF-alpha)
  5. anemia
226
Q

these are the two types of reactions of repair

A

regeneration and scar formation

227
Q

this is when surviving cells have the capacity to proliferate and to replace damaged components

A

regeneration

228
Q

name the three groups of cells in regeneration based on proliferative capacity

A

labile, stable, permanent

229
Q

this group of regenerative cell is continually lost and replaced by maturation of stem cells and proliferation of mature cells

A

labile

230
Q

this group of regenerative cell are quiescent cells in G0 phase of cell cycle or will divide in response to injury to loss

A

stable

231
Q

this group of regenerative cell is terminally differentiated and non-proliferative in postnatal life

A

permanent

232
Q

this type of repair happens if tissue injury results in damage to parenchymal or epithelial cells, if it destroys the connective tissue framework or if non-dividing cells are damaged

A

scar formation

233
Q

name the 3 main steps in scar formation

A

angiogenesis, formation of granulation tissue, remodeling

234
Q

this step of scar formation is the formation of new blood vessels

A

angiogenesis

235
Q

this step of scar formation is migration and proliferation of fibroblasts and deposition of collagen, together with new blood vessels

A

formation of granulation tissue

236
Q

this step of scar formation is when the connective tissue matures and reorganizes to produce a stable fibrous scar

A

remodeling

237
Q

this type of scar is due to exuberant formation of granulation tissue; most common in distal limbs of horses

A

hypertrophic scars

238
Q

this is the abnormal growth of a tissue into a mass; usually recognized by the fact its cells have abnormal growth patterns, are no longer under the control of normal homeostatic growth controlling mechanisms and have no functional value

A

neoplasia

239
Q

this literally means “swelling” and is not necessarily neoplastic

A

tumor

240
Q

these tumors arise in any of the tissues of the body and grow locally; they can grow to a large size but are not invasive

A

benign tumors

241
Q

what is the clinical significance of benign tumors

A

can cause local pressure, cause obstruction, or form a space-occupying lesion

242
Q

these are often small tumors that arise in the epithelium; appears to contain cancer but tumor remains in epithelial layer

A

in-situ tumors

243
Q

this is any malignant growth or tumor caused by abnormal and uncontrolled cell division, able to invade tissues locally and able to spread to other parts of the body through the lymphatic system or blood stream

A

cancer

244
Q

a severe lack of differentiation in malignant tumors is referred to as this

A

anaplasia

245
Q

what is the growth rate of benign tumors

A

slow & periods of dormancy

246
Q

what is the mode of growth of benign tumors by?

A

expansion

247
Q

what is the mode of growth of malignant tumors by?

A

initially expansion then invasion

248
Q

name the tissue/cell of origin for the benign tumor

suffix -oma (fibroma, lipoma, chondroma)

A

mesenchymal or nervous tissue

249
Q

name the tissue/cell of origin for the benign tumor

referred to as adenoma

A

glandular epithelium

250
Q

name the tissue/cell of origin for the benign tumor

referred to as papilloma

A

protective epithelium

251
Q

name the tissue/cell of origin for the malignant tumor

addition of ‘sarcoma’ (fibrosarcoma, liposarcoma, chondrosarcoma)

A

mesenchymal

252
Q

name the tissue/cell of origin for the malignant tumor

referred to as adenocarcinoma

A

glandular epithelium

253
Q

name the 5 types of round cell tumors

A
  1. Lymphoma
  2. Transmissible Venereal Tumor (TVT)
  3. Mast Cell Tumor
  4. Plasmacytoma and multiple myeloma
  5. Histiocytoma
254
Q

round cell tumors tend to form this histiological pattern

A

solid sheets

255
Q

epithelial tumors form these histiological patterns

A

nests, cords, islands, acini, tubules, or trabeculae

256
Q

mesenchymal tumors form these histiological patterns

A

interlacing streams, bundles, fascicles

257
Q

this means variation in cell size

A

anisocytosis

258
Q

this means variation in nuclear size

A

anisokaryosis

259
Q

this means variation in cell shape

A

pleomorphism

260
Q

this means the distant spread of a neoplasm and is often the cause of death in most patients

A

metastasis

261
Q

name the 3 different routes od metastasis

A
  1. hematogenous
  2. lymphatic
  3. transcoelomic
262
Q

name the 5 steps/stages of metastasis

A
  1. subset of cells detaches from main mass and breaches the basement membrane
  2. cells pass thrugh ECM and enter a nearby vessel
  3. tumor cells form embolus that travels to distant site in blood or lymph
  4. adhesion of tumor cells to endothelial cells
  5. metastatic deposit forms and grows with help of angiogenesis
263
Q

this is a cellular oncogene that does not have transforming potential to form tumors in its native state but can be altered to lead to malignancy

A

proto-oncogene

264
Q

most proto-oncogenes are key genes involved in these two things

A
  1. cell growth
  2. proliferation
265
Q

name the 6 possible modes of action of proto-oncogenes in the normal cell (oncogene classes)

A
  1. growth factors
  2. growth factor receptors
  3. protein kinases
  4. signal transducers
  5. nuclear proteins
  6. transcription factors
266
Q

name the 4 possible mechanisms of oncogene activation

A
  1. chromosomal translocation
  2. gene amplification
  3. point mutations
  4. viral insertions
267
Q

mutations or translocations of these genes produce positive signals leading to uncontrolled growth

A

oncogenes

268
Q

mutations or translocations of these genes leads to a loss of inhibitory functions leading to tumor formation

A

tumor supressor genes

269
Q

this was the first gene to inform mechanisms of tumor suppressor genes

A

retinoblastoma gene (Rb)

270
Q

this is the most frequently inactivated gene in human neoplasia

A

p53

271
Q

name the 7 hallmark capabilities of cancer/alterations in cellular physiology that collectively dictate malignant growth

A
  1. self-sufficiency in growth
  2. insensitivity to anti-growth signals
  3. ability to evade programmed cell death (apoptosis)
  4. limitless replicative potential
  5. ability to sustain angiogenesis
  6. ability to invade and metastasize
  7. ability to evade host immunity
272
Q

name the 3 broad categories of cancer causing agents

A
  1. oncogenic viruses
  2. chemical carcinogens
  3. physical agents (radiation)
273
Q

what viruses are included as oncogenic viruses

A

DNA viruses and Retroviruses

274
Q

name the oncogenic virus group

important oncogenic virsuses of cats, cattle and chickens;
can promote carcinogenesis through activation of cellular oncogenes by integrating adjacent to them;
FeLV (lymphomas and leukemia

A

retroviruses

275
Q

name the oncogenic virus group

ex: papilloma virus (esp. Bovine PV), lifecycle of virus tightly coupled with differentiation process of epithelial cell & can transform benign wart to a squamous cell carcinoma;
also herpes viruses (known to cause Marek’s disease in chickens)

A

DNA viruses

276
Q

name 4 chemical carcinogens involved with veterinary cancers

A
  1. bracken fern (with papilloma viruses in cattle)
  2. herbicides (canine lymphoma)
  3. Aflatoxin
  4. cyclophosphamide (chronic inflammation and transitional carcinoma)
277
Q

what 2 ways can radiation cause cancer

A
  1. cause errors in DNA replication
  2. cause production of oxygen free radicals

Vet Path (12 decks)

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