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pathology > exam 1 > Flashcards

exam 1 Flashcards

1
Q

what is unselective injury?

A

necrosis

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2
Q

what is selective injury?

A

apoptosis

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3
Q

what is ischemia?

A

inadequate blood supply to an organ or part of the body

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4
Q

ischemic cell injury what is the point of irreversible injury?

A

-membrane injury
-unrepairable damage to cell infrastructure
-lysosome rupture

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5
Q

during ischemic cell injury what is considered reversible cell injury?

A

-mitochondrial damage
-decrease ATP
-decrease oxidative phosphorylation
-decrease protein synthesis
-lots of swelling in cell etc

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6
Q

when there is small number of cell death in tissue what occurs?

A

viable neighboring cells replace the dead ones by proliferation

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7
Q

if there is a large number of cell deaths in a tissue or organ what occurs?

A

little ability to regenerate and/or the gap will be filled with fibrous connective tissue

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8
Q

hydronic degeneration

A

water move into the cells
aka balloon degeneration

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9
Q

is hydropic degeneration reversible and what is it?

A

-reversible acute cellular swelling
-earliest morphological changes of mitochondria and ER

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10
Q

what happens to the cells in bovine papular stomatitis?

A

on tongue
-ballooning degeneration
-viral inclusion bodies

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11
Q

what can cause hepatic lipidosis?

A
  1. excessive delivery of FFAs from fat stores or diet
  2. decreased oxidation or use or use of FFAs
  3. impaired synthesis of apoprotein
  4. impaired combination of protein and trigylcerides to form lipoproteins
  5. impaired release if lipoproteins from hepatocytes
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12
Q

how do we know this is the liver?

A

lobules
portal area

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13
Q

what is the difference between these two slides of the liver

A

left is fat accumulation
right is glycogen accumulation

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14
Q

pyknosis

A

irreversible condensation of chromatin in the nucleus of a cell
condensed

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15
Q

karyorrhexis

A

fragmentation of the nucleus

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16
Q

karyolysis

A

the nucleus is extremely pale

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17
Q

two pathways of apoptosis

A
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18
Q

two pathways of apoptosis

A
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19
Q

what are the 4 morphological features of cellular necrosis

A

pykinosis
karyorrhexis
karyolysis
absence of nucleus

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20
Q

what is the initiator caspsase for the intrinsic pathway for apoptosis

A

caspase 9

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21
Q

what is the initiator caspase for the extrinsic pathway for apoptosis

A

caspase 8

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22
Q

what are the executioner caspases

A

3, 6, 7, 12

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23
Q

histologically what is the difference between hepatic lipidosis and a glycogen accumulation in the liver

A

in hepatic lipidosis the nuclei is often pushed to periphery and vacuoles have distinct borders
and while glycogen accumulation in the liver the nuclei stays central and vacuoles have irregular or indistinct borders

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24
Q

what organ is this and what is the problem

A

brain
lysosomal storage disease (contents cannot be released due to lack of enzymes)

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25
Q

necrosis vs apoptosis

A
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26
Q

what are the key morphological feature if apoptosis

A

-cell shrinkage
-chromatin condensation
-cytoplasmic blebs and apoptotic bodies
-phagocytosis of apoptotic bodies

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27
Q

how does hematoxylin stain and what does stain?

A

stains blue –> purple
*basophilic
-nuclei
-bacteria
-calicum

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28
Q

how does eosin stain and what gets stained?

A

stains pink –> red
*eosinophilic
-cytoplasm
-collagen
-fibrin
-RBC
*protein is pink

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29
Q

what is amphiphilic when staining

A

shows up both purple and pink

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30
Q

describe coagulative necrosis

A

denaturation with dense/rigid texture to dead cells
(ex myocardial necrosis)

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31
Q

describe liquefaction necrosis

A

process of complete enzymatic digestion of cells, usually in the brain

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32
Q

describe caseous necrosis

A

cheesy, coagulative granulomatous reaction
(ex lung tuberculosis)

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33
Q

describe fat necrosis

A

saponification, fatty acids mixed with calcium, chalky white
(ex acute pancreatitis)

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34
Q

describe gangrenous necrosis

A

necrosis due to ischemia of distal extremities (moist dry and gas)

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35
Q

what type of necrosis is this?

A

coagulative necrosis
-on the left it is showing dry necrosis, the myofibril cells are fragmented, nuclei lost, leukocytes are present to clear sarcoplasmic debris

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36
Q

what type of necrosis is this?

A

suppurative necrosis
-this is a form of liquefactive necrosis
-acute inflammatory cells release proteolytic enzymes that destroy the surrounding tissue

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37
Q

histologically when you are looking at a tissue that is necrosis what do you expect to see?

A

-increased eosinophilia (RNA degradation)
-glassy appearance (glycogen loss)
-cytoplasmic vacuolation
-karyolysis
-ghost cells

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38
Q

define infarction

A

obstruction of the blood supply to an organ or tissue causing local death of the tissue

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39
Q

what type of necrosis is this?

A

caseous necrosis
-cheesy appearance
-combo of coagulative and liquefactive necrosis
-granulomatous inflammation

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40
Q

what type of necrosis is this?

A

coagulative necrosis

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41
Q

what are labile cells? give some examples

A

continuously cycling
-epithelia of the mouth, skin, gut and bladder, and bone marrow cells

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42
Q

what are quiescent tissue (stable cells)? give some examples

A

-divide infrequently but can be stimulated to divide when cells are lost
- liver, renal tubular cells, fibroblasts, endothelial cells, smooth muscle cells, chondrocytes, and osteocytes of connective tissue

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43
Q

what are permanent cells? give some examples

A

-non dividing tissue
-cells cannot be replaced when lost and they have very limited capacity to divide
-neurons, cardiac muscle cells, and photoreceptors in retina

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44
Q

atrophy

A

reduction in the function mass or size of the cell, tissue, or organ

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45
Q

hypertrophy

A

increase in the functional mass or size of a cell, tissue, or organ

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46
Q

hyperplasia

A

increase in the number of cells

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47
Q

difference between ulceration and erosion

A

ulceration destroys the basement membrane and erosion doesn’t touch the basement membrane

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48
Q

concentric hypertrophy

A

develops in a concentric fashion, thickening from the outside toward the lumen

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49
Q

eccentric hypertrophy

A

caused by addition of sarcomeres in series leading to enlarge and dilate chamber with relative wall thinning

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50
Q

can the brain regenerate or undergo fibrosis?

A

no it cannot, significant damage results in cavitation

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51
Q

what are the key responses to bone injury and the healing process

A

-bone can alter its shape or mass
-bone can be replaced with woven bone (new bone) rather than lamellar (pre-existing)
-periostieum can form bone

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52
Q

what is exogenous pigmentation

A

a pigment taken on from an external source
-anthracosis (carbon) like smokers

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53
Q

what is endogenous pigmentation

A

a pigment produced by the cell
-melanin, lipofusion, ceroid

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54
Q

what are hematogenous pigments

A

hemoglobin, parasite hematin (fluke exhaust0, hemosiderin, bilirubin

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55
Q

what histological features distinguish them?

A

cellular atypia

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56
Q

why did the coat change?

A

-copper deficiency
tyrosinase needs copper in order to make melanin

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57
Q

what is lipofusion and what type of pigmentation is it?

A

-endogenous pigmentation
-yellow-brown
-no harm, wear and tear pigment due to aging

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58
Q

what is ceroid and why type of pigment is it?

A

-endogenous pigment
-yellow-green
-deleterious effect to cells
-vit e deficiency

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59
Q

what is an amyloid

A

pathogenic protein-based material

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60
Q

what is the most common form amyloid seen in non-human species

A

reactive (secondary to inflammation)

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61
Q

to identify lead poisoning what type of staining do you need

A

acid-fast stain

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62
Q

difference between dystrophic calcification and metastatic calcification (hypercalcemia)

A

-dystrophic is localized and blood Ca levels are normal
-metastatic calcification has high calcium blood levels, calcium deposits throughout the body

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63
Q

identify pynkinosis, karyorrhexis, karyolysis, and the normal nucleus

A
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64
Q

give pathogenesis

A

coagulative necrosis caused by ischemia following NSAID use (renal papillary necrosis)
-local prostaglandin synthesis protects glomeruli and tubules from ischemia. inhibition of prostaglandin synthesis by NSAIDs via inhibition of COX1 and 2 predisposes kidney to hypoperfusion and to ischemia > then papillary necrosis

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65
Q
A
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66
Q

what is edema

A

abnormal accumulation of fluid in the interstitial and body cavities

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67
Q

what are four causes of edema

A
  1. increased microvascular permeability (leaky vessels)
  2. increased vascular hydrostatic pressure
  3. decreased intravascular osmotic pressure
  4. decreased lymphatic drainage
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68
Q

what are the two major causes of non-inflammatory edema and transudate

A

-hepatic failure, reduce production of albumin (reduce oncotic pressure bc albumin draw in fluid)
-heart failure (increase hydrostatic pressure)

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69
Q

function of albumin

A

helps keep fluid from leaking out of blood vessels

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70
Q

where is albumin produced

A

liver

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71
Q

hyperemia blood flow and perfusion

A

active
arteriole dilation (erythema in skin)

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72
Q

congestion blood flow and perfusion

A

passive
impaired/decreased outflow of blood

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73
Q

hemostasis

A

physiological response to vascular damage and stop bleeding to prevent loss
-normal

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74
Q

thrombosis

A

inappropriate activation of the hemostatic process in a blood vessel
-clotting blood too much
-abnormal

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75
Q

what is the Virchow triad

A

-factors that contribute to hemostasis and thrombosis
1. endothelia injury
2. alterations in blood flow
3. blood hypercoaglability

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76
Q

what is the hemostatic process

A
  1. primary hemostasis
  2. secondary hemostasis
  3. fibrinolysis
  4. tissue/ vascular repair at damage site
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77
Q

what is primary hemostasis

A

transient vasoconstriction and platelet aggregation to form platelet plug at the site of damage

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78
Q

von willebrand factor

A

protein in the blood that helps blood clot, like glue

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79
Q

what is secondary hemostasis

A

coagulation to form a meshwork of fibrin
-tissue factor that initiates extrinsic pathway of coagulation cascade

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80
Q

fibrinolysis

A

removes platelet/fibrin plug
-cleavage of plasminogen to plasmin

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81
Q

what factors are vitamin K dependent?

A

II, VII, IX, X
1972

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82
Q

coagulation cascade

A
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83
Q

function of plasmin

A

digests fibrin clots and releases fibrin degradation products and inhibits additional fibrin formation

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84
Q

what is the most potent and clinically significant coagulation inhibitor and is produced by endothelium and hepatocytes

A

antithrombin III

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85
Q

three major anticoagulant-antothrombotic systems on endothelial cells

A
  1. protein C-protein S thrombomodulin system
  2. antithrombin III (prevents coagulation from happening)
  3. tissue factor pathway inhibitor
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86
Q

petechia hemorrhage

A

pinpoint
minor vascular damagee

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87
Q

ecchymosis hemorrhage

A

more extensive vascular damage

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88
Q

suffusive hemorrhage

A

larger
contiguous areas of tissue
paintbrush

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89
Q

how much loss of blood volume to be considered an exsanguination

A

40% loss of blood volume

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90
Q

major determinants of thrombosis?

A

-virchows triad
-specifcally alterations in the endothelium which results in increased production of pro-coagulant substances and decreased production of anti-coagulant substances

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91
Q

thrombus resolution

A
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92
Q

what is the function of von willebran factor vWF

A

protein in the blood that helps blood clot

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93
Q

what factors are consisted of in the intrinsic pathway of the coagulation cascade?

A

XII, XI, IX, VIII
$12 no $11.98

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94
Q

what factors is the extrinsic pathway of the coagulation cascade consisted of?

A

tissue factor (III)
VII

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95
Q

what factors does the common pathway consist of in the coagulation cascade?

A

X
prothrombin (II) thrombin
fibrinogen (I)
fibrin clot (XIII)

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96
Q

what factor is the last enzyme in the coagulation cascade

A

thrombin (factor II)

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97
Q

what helps activate fibrinogen (factor I) to turn into fibrin (XIII)?

A

thrombin (facrtor II)

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98
Q

what is the most potent inhibitor to inhibit coagulation

A

antithrombin III

99
Q

what type of infarct is this?

A

acute red infarct
-red and often swollen or slightly raised (hemorrhage)

100
Q

what type of infarct is this?

A

subacute pale infarction
-affect areas become pale and often still surrounded by zones of hyperemia
(necrosis–> swelling–> force blood out of infarcted region–> pale appearance)

101
Q

what type of infarct is this?

A

chronic infarct
-pale, shrunken, firm, fibrosis

102
Q

what is disseminated intravascular coagulation (DIC)

A

when the coagulation cascade is inappropriately set off, causing massive coagulation which leads to consumption of platelets, coagulation factors, and increase fibrinolysis
-since the coagulation factors are exhausted any small trauma can lead to uncontrolled bleeding

103
Q

endotoxemia causing vasculitis would incite which mechanism of edema?

A

increased vascular permeability

104
Q

what type of cell is dominated by acute inflammation

A

neutrophils

105
Q

what are the 5 cardinal signs of inflammation

A

redness
swelling
heat
pain
loss of function

106
Q

what cytokines play a role in acute inflammation

A

IL 1, IL 6, TNF

107
Q

what chemokine is big activator and chemotaxis for neutrophils

A

IL 8

108
Q

phases of acute inflammation

A

1.fluidic (exudative), dilte and localize
2. cellular, deliverinig white blood cells
3. reparative

109
Q

steps of leukocyte adhesion cascade

A

margination
rolling
adhesion
diapedesis (migration)
chemotaxis

110
Q

what inhibits phospholipases

A

steroids

111
Q

what blocks cyclooxygenase

A

NSAIDs

112
Q

what is the main outcome/goals of the activated complement cascade

A

-formation of C5a and C3a (inducing inflammation by attracting leukocytes)
-formation of C3b (opsonization)
-formation of the membrane attack complex (pore in microbial surface)

113
Q

what is a driver of fever

A

PGE2

114
Q

what are 2 examples of positive (increase inflammation) acute phase proteins

A

C-reactive proteins
serum amyloid a

115
Q

what is an example of a negative (decrease inflammation) acute phase protein

A

albumin

116
Q

morphaologial diagnosis

A

fibrinosuppurative epidcarditis/pericarditis

117
Q

what type of hypersensitivity is most common with atopic forms of allergens and what immunologic component is it associated with?

A

type I hypersensitivity and IgE

118
Q

what type of hypersensitivity is most common with auto immune disorders and what immunologic component is it associated with?

A

type II hypersensitivity
IgG and IgM

119
Q

what is primary immunodeficiency disease

A

congenital or genetic defect

120
Q

what is secondary immunodeficiency disease

A

acquired

121
Q

what is vascular leakage

A

when fluid leaks idiot body cavities rather than tissues
-effusion

122
Q

transudate or serous

A

clear watery fluid

123
Q

educate

A

-thick and cloudy fluid
hemorrahagic
serosanguious
purulent
chylous fibrinous

124
Q

describe this effusion

A

serosanguinous

125
Q

pyo pus has neutrophils

A

:)

126
Q

describe effusion

A

pyothorax

127
Q

describe effusion

A

chylothorax

128
Q

when an animal has gout due to the lack of what enzyme? and how does the enzyme work

A

-gout is an accumulation of gout crystals (uric acid) in the joint or viscera
-due to lack of the enzyme uricase (that converts blood uric acid into allantoin which is normally excreted out

129
Q

what are the major players of chronic fibrosis when looking histologically

A

-mononuclear inflammatory cells (macrophages, lymphocytes, plasma cells)
-fibroblasts

130
Q

types of chronic inflammation

A

-abscess
-granuloma/granulomatous inflammation (nodular, diffuse)
-eosinophilic inflammation/granuloma (parasites, no specific antigen)
-lymphocytic to lymphoplasmacytic inflammation

131
Q

what are the three distinct morphologic nodular (tuberculoid) granuloma areas

A

-inner most: macrophages, multinucleated giant cells caseating (central necrosis)
-middle: macrophages, epithelioid macrophages, multinucleate giant cells
-outermost: lymphocytes, plasma cells, fibroblasts with a fibrous capsule

132
Q

what is diffuse (lepromatous) granuloma

A

poorly demarcated
widespread distribution
-non-caseating aggregates of macrophages, variable degree of fibrosis

133
Q

what is an example of diffuse/lepromatous granuloma

A

Johne’s disease (cattle, sheep, and goats)
-lesion occurring in the ileum and colon

134
Q

what are some examples of nodular (tuberculoid) granuloma

A

-mycobacterium bovis of mycobacterium tuberculosis
-valley fever

135
Q

what are some examples of eosinophilic granulomas

A

-eosinophilic dermatitis (cutaneous habronemiasis)
-oral eosinophilic granulomas

136
Q

what is FIP and its pathogenesis

A

-chronic-active inflammation

ingestion of feline enteric corona virus (fecal-oral)-> replication in enerocytes and peyers patches of intestine-> mutation and replication in macrophages and blood monocytes->virus infected macrophages disseminate to multiple organs-> host immune response -> pyograulomatous vascutlitis

137
Q

phases of wound healing

A
  1. HEMOSTASIS (immediately after injury) accumulation of platelets exposed collagen
  2. INFLAMMATION (acute)
  3. PROLIFERATION (granulation tissue, angiogenesis, epithelialization)
  4. MATUREATION (remodeling of collagen, blood vessels regress and collagen synthesis eventually stops then scar)
138
Q

what is a critical growth factor in wound healing and what does it act on

A

-TGF-beta
-acts on keratinocytes, fibroblasts, endothelial cells, monocytes

139
Q

what is granulation tissue

A

exposed connective tissue that forms within a healing wound

140
Q

process of granulation tissue to healing by fibrosis

A

necrosis of tissue framework–>dead tissue and acute inflammatory exudate are removed–> space fills with fibrovascualr tissue (granulation tissue)–> eventually gets replaced by immature fibrous connective tissue –> scar

141
Q

give pathogenesis of hemoperricardium causing cardiac tamponade

A

ruptured right auricular hemanigosarcoma -> compression of heart from blood -> decreased diastolic filling time -> decreased cardiac output

142
Q

how much of the 60% of fluid body weight is made of intracellular fluid?

A

40% intracellular fluid

143
Q

how much of the 60% of fluid body weight is made up of extracellular fluid?

A

20% total
plasma 4%
interstitium 16%

144
Q

what is the extracellular matrix also called

A

intersitium

145
Q

what is the extracellular matrix made up of?

A

-structural (collagen type I, elastin)
-adhesive (fibronectin, laminin)
-absorptive components (glycosaminoglycans, proteoglycans)

146
Q

what is the difference between lymphatic and venule interendothelial junctions

A

venules or arterioles allow movement of fluid between blood and interstitum where as lymphatic vessel junctions allow things to pass but can also expand and shut/seal it off

147
Q

what controls fluid movement in the body?

A

-hormones
-receptors
-osmotic and hydrostatic forces
-integrity of the vascular system

148
Q

what hormones in the body control fluid movement

A

-RAAS (vasoconstriction and water retention)
-artial natriuretic peptide (ANP) by cardiomyocytes (promoting renal sodium and water excretion and stimulating vasodilation)

149
Q

what receptors in the body help regulate/control fluid movement and where are they located?

A

-osmoreceptors in hypothalamus
-baroreceptors in blood vessels

150
Q

what is shock

A

cardio vascular collapse
circulatory failure
-systemic hypoperfusion due to macro- and/or micro-circulatory failures

151
Q

what is the pathogenesis of shock

A

hypotension > impaired tissue perfusion > cellular hypoxia > anaerobic metabolism > cellular degeneration > cell death

152
Q

what are the two types of macrocirculatory failure shock

A

cardiogenic
hypovolemic

153
Q

what is cariogenic shock and what are some examples

A

-failure of the heart to adequately pump blood
- myocardial infarction, ventricular tachycardia, fibrillation, arrhythmias, hic cardiomyopathy (HCM), dilated cardiomyopathy (DCM), cardiac output obstruction (pulmonary embolism, aortic stenosis), pericardial tamponade

154
Q

what is hypovolemic shock

A

reduced circulation of blood volume by massive blood loss or fluid (vomiting, diarrhea or burns) leading to decreased vascular pressure and tissue hypoperfusion

155
Q

main difference between macro and micro circulatory failure

A

macro is decrease volume of the heart but micro total blood volume is the same it is just being maldistributed

156
Q

what type of shock is microcirculatory failure and explain what it is

A

blood maldistribution
-decrease peripheral vascular resistance and polling of blood in vascular peripheral tissue

157
Q

what are three types of blood maldistribution shock

A
  1. anaphylactic shock: generalized type I (Ig E) hypersensitivity
  2. septic shock: most common type- endotoxemia
  3. neurogenic shock: trauma, particular trauma to nervous system, electrocution, fear , emotional stress
158
Q

what does DIC result in pathologically

A
  1. small blood clot formation inside blood vessels throughout body
  2. consumption of coagulation proteins and platelets > disruption of normal coagulation causing abnormal bleeding
  3. clots plug normal blood flow to organs (kidneys, distal extremities) > ischemic injury
159
Q

what is acute respiratory distress syndrome ARDS

A

multifactorial source of injury to respiratory capillary endothelium (generally primary) and epithelium (diffuse alveolar damage, necrosis, often secondary)

160
Q

what does TLR-4 do to the endothelium and monocytes/macrophages in septic shock

A

-when LPS (of gram negative bacteria) bind to endothelium it down-regulates the anticoagulants (tissue factor pathway inhibitor and theombomodulin)
-when LPS binds to monocytes/macropahges it increases production of IL-1,IL-6, TNF

161
Q

what are some inciting causes of ARDS

A

endotoxemia, sepsis, disseminated pulmonary infections, extensive trauma, burns, transfusions, DIC, pancreatitis, aspiration of gastric contents

162
Q

what is happening during neurogenic shock

A

if there is trauma, spinal cord injury, fear, electricity > the body triggers generalized autonomic nervous system > sympathetic tone gets lost and the parasympathetic tone dominates, vasodilation > massive peripheral vasodilation w bradycardia > pooling of blood > hypoperfusion

163
Q

stages in development of shock

A

-compensation: heart rate increases, peripheral vasoconstriction, ADH and angiotensin II released > increased blood pressure and blood is diverted to vital tissue
-progression: anaerobic metabolism > acidosis , vasodilation
-irreversible: cell and tissue necrosis, leading to multi-organ failure and death

164
Q

what is metaplasia

A

-reversible exchange within a tissue of one mature cell type (differentiated adult cells) for another mature (adult) cell type (changing cell types)
-requires “reprogramming” of reserved cells (stem cells)

165
Q

what is dysplasia

A

-atypical differentiation, disorderly arrangement
-may be partially reversible
-it often develops at sites of chronic inflammation
*disorganized

166
Q

steps in neoplastic transformation

A
  1. initation: irreversible genetic change in replicating cell population
  2. promotion: reversible; do not affect DNA directly, create an environment that gives initiated cells a growth advantage over the rest of the population
  3. progression: irreversible/reversible, conversion of benign tumor to an increasingly malignant tumor and ultimaelty to metastatic tumor (promoting own blood supply, proliferating, detaching and moving to distant sites)
167
Q

what are the heritable alterations contributing yo carcinogenesis

A

DNA mutation
epigenetic changes
chromosomal alt

168
Q

what origin are -carinoma from

A

epithelial origin

169
Q

what origin are -sarcoma from

A

mesenchymal origin

170
Q

what is the bengin and malignant neoplasms for glandular epithelium

A

-benign: adenoma
-malignant: carcinoma

171
Q

what is the benign and malignant neoplamsmic terms for squamous epithelium

A

-bengin: papilloma
-malignant: squamous cell carcinoma

172
Q

what is the benign and malignant neoplasmic terms for liver

A

-benign: hepatoma
-malignant: heptatocellular carcinoma

173
Q

what is the benign and malignant neoplamic term for skeletal muscle

A

-bengin: rhabdomyoma
-malignant: rhadomyosarcoma

174
Q

what its benign and malignant neoplamic term for smooth muscle

A

-benign: leiomyoma
-malignant: leiomyosarcoma

175
Q

what is the bengin and malignant neoplasmic term for bone

A

-benign: osteoma
-malignant: osteosarcoma

176
Q

what tumor-like lesion is hamartoma

A

disorganized, mature tissue in normal location

177
Q

what tumor-like lesion is choristoma

A

disorganized, ,nature tissue in abnormal location (ectopic)

178
Q

what is the descriptor word for this tumor

A

pedunculate
polypoid

179
Q

descriptor word for this tumor

A

papillary

180
Q

decriptor word for this tumor

A

ulcerated

181
Q

descriptor word for this tumor

A

sessile
attached to base without stalk

182
Q

descriptor word for this tumor

A

annular
ring shaped

183
Q

descriptor word for this tumor

A

fungating
marked ulceration and necrosis, bad smell

184
Q

describe the pattern of this histological image of this tumor

A

sheets (common for round cell tumor)

185
Q

describe the pattern of this histological image of this tumor

A

packets
common in neuroendocrine tumors

186
Q

describe the pattern of this histological image of this tumor

A

nests
common in invasive carcinoma

187
Q

describe the pattern of this histological image of this tumor

A

cords
often seen in epithelial tumors

188
Q

describe the pattern of this histological image of this tumor

A

lobules
common in some epi tumors

189
Q

describe the pattern of this histological image of this tumor

A

acini
indicative of glandular epithelial origin

190
Q

describe the pattern of this histological image of this tumor

A

lobules
indicative of glandular epithelia origin

191
Q

describe the pattern of this histological image of this tumor

A

cystic
seen in some glandular tumors

192
Q

describe the pattern of this histological image of this tumor

A

whorls
seen in mesenchymal (connective tissue) tumors

193
Q

describe the pattern of this histological image of this tumor

A

papillary
glandular tumors

194
Q

describe the pattern of this histological image of this tumor

A

bundles
typically mesenchymal tumors

195
Q

what is the mechanism for invasion, stepping from benign to malignant

A

-impairment of cell adhesion
-basement membrane (basal lamina) degradation via proteases
-extension into permissive tissue, cleavage of basement membrane protein generates novel sites that bind to receptors on tumor cells and stimulate migration

196
Q

stages of invasion and metastasis

A
  1. transformed cells must detach from main mass, adhere to and penetrate the basement membrane and enter the cellular matrix
  2. intravastion- extension through endothelium, interaction with lymphoid cells and coating with platelets (formation of tumor emboli)
  3. extravasation- extension back through endothelium, formation of metastatic deposit, and angiogenesis
197
Q

what are the common metastatic routes to go other places in the body

A
  1. hematogenous (preferred routes for sarcomas)
  2. lymphatic (preferred by carcinomas)
  3. transcoelomic exfoliation and implantation (mesotheliomas)
198
Q

what is the paraneoplastic syndrome associated with apocrine adenocarcinoma of the anal sac

A

hypercalcemia

199
Q

what is your diagnosis?

A

-neoplastic round cells
-solid sheets
-basophilic cytoplasmic granules
-eosinophils present

200
Q

routes for hematogenous to get to places in the body

A
201
Q

diagnosis and route of metastasis

A

cholangiocellular carcinoma with transcolemic exfoliation and implantation

202
Q

diagnosis and route of metastasis

A

humeral osteosarcoma with metastasis to lung

203
Q

paraneoplastic syndrome

A

symptom complexes that cannot be directly attruvited to local or distant tumors
ex hypercalcemia

204
Q

what are the primary effects of tumors

A

-loss of function: metastatic or primary tumors in lungs leading to impaired respiration
-pain and discomfort: specific sites such as bone

205
Q

explain mechanism of septic shock

A

most common cause is endotoxins that produce gram - bacteria, the LPS from the gram - bacterial cell wall forms a complex with blood proteins and LPS binds to TLR-4

206
Q

what is morphological diagnosis and tissue change

A

endocardiosis
myxomatous metaplasia

207
Q

what is the diagnosis

A

oligodendrolioma

208
Q

what is your diagnosis

A

lymphoma (round cell tumor)

209
Q

classify this hemorrhage

A

petechial hemorrhage

210
Q

capillaries vs lymphatics

A

-capillaries: atertial-venous transition, tissue to blood nutrient and waste transition
-lymphatics: bind end capillaries that dump into venous system, low pressure valved that depend on forces like muscle contraction to maintain flow, large gaps that allow fluid and proteins to move in and out of interstitium

211
Q

when LPS induces a high production of TNF, IL1, IL6/IL8, NO, PAF what occurs

A

they promote high systemic vasodilation and increased vascular permeability > intravascular plasma protein loss decreased oncotic forces > additional intravascular fluid loss > toxins and cytokines induce loss of peripheral vascular tone > hypotension > hypoperfusion > septic shock

212
Q

what are some heritable alterations that contribute to carcinogenesis

A

DNA mutations
epigenetic changes
chromosomal alterations

213
Q

spindle cells are usually associated with what type of neoplastic cell

A

sarcoma

214
Q

brain tumors are usually named for the cell type in the brain, what are the names for astrocytes and oligodendorcytes

A

astrocytoma
oligodendroglioma

215
Q

what things are pro-apoptotic

A

BAX and BAK

216
Q

what things are anti-apoptotic

A

BCL2 and BCL-XL

217
Q

what is the significance of cells in G0?

A

quiestant cells that are able to regenerate with tissue damage

218
Q

what is eccentric hypertrophy

A

thickening of the cells in series (side by side) learning to an enlarged and dilated chamber with wall thinning

219
Q

what happens in reaCtive amyloidosis

A

amyloid A desposits accumulate as acute phase proteins are produced during inflammation

220
Q

what is the pathogenesis of hemoperricardium?

A

ruptured R auricular hemangiosarcoma leads to compression of heart causing decreased diastolic filling and decreased CO eventually death

221
Q

what is an organizing hematoma

A

trauma causing vessel to rupture

222
Q

what are saddle thrombi

A

cardiac emboli that lodge at the bifurcation of the iliac arteries

223
Q

where do venous emboli usually lodge

A

pulmonary circulation causing infarcts or right sided heart failure

224
Q

what is the function of C reactive protein

A

binds to bacteria and fungi and activates compliment

225
Q

what is type 3 hypersensitivity

A

IgM and IgG mediated
ex: systemic lupus erythematosus

226
Q

what is type 4 hypersensistivity

A

T lymphocyte mediated
ex: contact dermatitis Johnes disease

227
Q

what is an example of chronic inflammation and neoplasia

A

feline injection site sarcoma

228
Q

mechanism for FISS

A

persistent injection site inflammation and genetic predisposition leading to neoplastic transformation of fibroblasts

229
Q

what is the most common place for a hemangiosarcoma in dogs?

A

right auricle

230
Q

what determines the extent of LPS intoxication?

A

dose
low: local inflammation
moderate: systemic effects with clinical symptoms
high: septic shock

231
Q

what are the driving causes of each type of microcirculatory failure

A

anaphylactic and endotoxic: cytokines
neurogenic: autonomic discahrge

232
Q

what is the pathogenesis of hypopvolemic shock

A

initial compensation > with progression metabolism shifts to glycoysis > progressive morphologic deterioration of cells

233
Q

what structures are epithelial origin

A

oral
GI
skin

234
Q

what structures are mesenchymal origin

A

bone
fibroblasts
muscle

235
Q

what is plasmacytoma (plasma cell tumor)?

A

benign tumor composed of plasma cells

236
Q

what is multiple myeloma

A

malignant tumor composed of plasma cells

237
Q

what is histiocytoma

A

bengin tumor composed of macrophages

238
Q

what is histolytic sarcoma

A

malignant tumor composed of macrophages

239
Q

what tumor types typically use hematogenous metastasis

A

sarcomas

240
Q

what tumor types typically use lymphatic metastasis

A

carcinomas

241
Q

what is the preferrential site for prostatic carcinoma metastasis

A

bone

242
Q

what is the preferential site for osteosarcoma metastasis

A

lung

243
Q

what are the main neoplasia types associated with hypercalcemia as a paraneoplastic syndrome

A

lymphoma
apocrine adenocarcinoma of the anal sac in dogs

244
Q

what tumor types have grading systems

A

cutaneous mast cell tumors
mammary gland neoplasia
soft tissue sarcomas

pathology (10 decks)

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