pathology 1st quiz Flashcards

0
Q

What characterizes pyknosis?

A

Nuclear shrinkage, round shape, dark blue/black with H&E stain, nucleolus not visible

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1
Q

What cells are highly vulnerable to to acute cellular swelling?

A

Cardiac myocytes, proximal renal tubule cells, hepatocytes, endothelium,

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2
Q

What microscopic changes happen during karyorrhexis?

A

Chromatin breaks up, scattered. Happens in purulent exudate when neutrophils break up.

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3
Q

What is karyolysis?

A

Lysis of nuclear Chromatin and leaks out of nuclear membrane.

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4
Q

What 2 changes can happen during necrosis of cytoplasm?

A
  1. Increased eosinophilia of cytoplasm (basophilia are lost, eosin binds to denatured intacytoplasmic proteins)
  2. Depletion of glycogen - glassy homogenous appearance
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5
Q

Where is coagulative necrosis usually seen?

A

Infarcts from loss of blood supply
Toxic products of certain bacteria like nerobacillosis
Poison, burns, electricity, X-ray

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6
Q

What causes zenkers necrosis?

A
Certain infections
Animals fed coffee senna and coyotillo plant
White muscle dz
Gossypol alkaloid in pigs
Malignant hyperthermia
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7
Q

Where does liquefactive necrosis ( colliquative) occur?

A

Cns, and abscesses

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8
Q

What characterizes fat necrosis both grossly and microscopically?

A

Gross- white firm chalky

Micro-large shadowy outline of fat cells

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9
Q

Which animals get peritoneal fat necrosis and why?

A

Young cattle - tall fescue grazing with fungus

Cattle, sheep, horses - summer fescue toxicosis, severity increases with hot weather

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10
Q

Where can traumatic fat necrosis occur?

A

Fat under skin and pelvic canal

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11
Q

What are the mechanisms of disposal of necrotic tissue?

A

Liquefaction by Auto lysis and heterolysis, removal by blood and lymph
Liquefaction with abcess formation
Encapsulation by fibrous tissue
Desquamation and sloughing - surfaces, intestine, brochi, renal tubes
Calcification

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12
Q

How can dry gangrene occur?

A

Loss of blood supply
In ergot poisoning
Tight bandage
Excess cold

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13
Q

Where is dry gangrene mostly found?

A

Extremity of tail, ear or limb

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14
Q

Where can moist gangrene occur and why?

A

Lung - aspiration pneuomonia
Intestine - torsion, cuts blood supply
Mammary gland - mastitis caused by putrefaction bacteria

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15
Q

How does gas gangrene occur?

A

Anaerobic bacteria penetrating wounds or spread from intestine

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16
Q

What are the 4 morphological features of apoptosis?

A

Cell shrinkage
Chromatin condense, fragment into apoptosis bodies
Phagocytosis of cell by macrophages
No inflammation

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17
Q

Timeline for rigor mortis

A

1 to 6 hrs after death and persists for 1 to 2 days

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18
Q

What term is used for cooling of the cadaver after death?

A

Algor mortis

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19
Q

What is livor mortis?

A

Hypo static congestion - pooling of blood on one side of the animal

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20
Q

where does hemoglobin imbibition occur?

A

heart and arteries. - red staining of tissues by lysed rbcs

can occur in acute intra vascular hemolysis

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21
Q

when does bile imbibition occur?

A

1-6 hours after death adjacent to gsll bladder

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22
Q

term for blue green discoloration of tissues by iron-sulfide. takes 18-24 hours

A

pseudomelanosis

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23
Q

what are pale foci on the liver caused from?q

A

increasEd intra abdominal pressure

bacterial action from tthe gut into portal vein

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24
Q

what is the difference between bloating and ruminal tympany?

A

bloat line -
in ruminal tympany a sharp line demarcates between pale bloodless distal esophagus and congested proximal esophagus (bloating happens after death - no bloat line) CONFUSING

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25
Q

when and where does mucosal sloughing occur?

A

1-6 hours

rumen

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26
Q

what 5 conditions lead to fatty change?

A

excessive fatty acid release
defects iformation of lipoproteins
decreased oxidation of FA from mitochondrial injury
hepatic lipidoses. cats.
hyperlipidemic condition in horses and dogs

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27
Q

what are the gross appearances of fatty change in liver, heart, and kidney?

A

liver- pale, enlarged, rounded edges
heart. - tan streak in myocardium, flabby
kidney - radial tan streaking in cortex and medulla

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28
Q

what are microscopic appearance of fatty change in liver, heart, and kidney?

A

liver - small or large vacuoles in cells
heart - small vacuoles in sarcoplasm
kidney - variable sized droplets in cytoplasm of pct and ascending loop of henle, cats have normal amount in prox tube

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29
Q

how can fat tissue be stained?

A

must be frozen and use oil red, sudan 3 and 4, osmic red, nile blue

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30
Q

what are the 3 main causes of glycogen deposition?

A

diabetes
glycogen storage dz
drug induced metabolic dz - corticosteroids, transitory

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31
Q

which type of glycogenoses occurs in toy breeds and cause hypoglycemia?

A

type 1

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32
Q

what type of glycogenoses is a deficiency in lysosomal acid maltase and glycogen accumulates in brain, muscle and liver?

A

type. 2 , pompes dz

occurs in calves, corriedal sheep, lapland dogs, japanese quails

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33
Q

which glycogenoses is caused by a deficiency in glycogen brancher enzyme and occurs. in norweigian forest cats and quarter and american horses?

A

type 4

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34
Q

whee does glycogen deposit in type 4 glycogenosis?

A

cardiac muscle, purkinje fibers and liver

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35
Q

which typeof glycogenosis i s caused by deficiecny in phosphofructokinase?

A

type 7

english springer spaniels

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36
Q

which glycogenosis is a deficiecny in debranching enzyme and found in german shepherds?

A

type 3

coris dz

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37
Q

what are the 2 types of morphological lesions seen in lysosomal storage dz?

A

primary - increased size and number of secondary lysosomes

secondary- abnormal cellular and extracellular products

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38
Q

which cells is amyloid light protein chain derived from?

A

plasma cells, contains immunoglobulin light chains

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39
Q

where does amyloid associated protein come from

A

secreted from liver cells in response to cytokines from inflammation

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40
Q

what type of amyloidosis has to do with plasma cells?

A

primary amyloidosis

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41
Q

which amyloidosis is associated with chronic inflammation and is seen in horses used for antiserum?

A

secondary amyloidosis

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42
Q

which type of amyloidosis is heterogenous chemically?

A

localized amyloidosis

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43
Q

which type of fibril protein is associated with primary amyloidosis and which species are effected?

A

AL (light chain)

cats and dogs

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44
Q

which protein is associated with secondary amyloidosis and what species does it effect?

A

AA(amyloid associated protein)

mainly dog cat and horse

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45
Q

which breeds get familial amyloidosis?

A

siamese cats
abyssynian cats
sharpeis

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46
Q

what are the 3 most common organs affected by amyloidosis?

A

kidneys
liver
spleen

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47
Q

what are the 2 gross patterns of spleen amyloidosis?

A

deposits in splenic follicles - “sago spleen”

splenic sinuses - sheet like deposit, “bacon spleen”

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48
Q

where is amyloid found most commonly in the kidney in most species?

A

glomeruli

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49
Q

where can amyloidosis be found in the kidneys of cats?

A

peritubular tissue

walls of blood vessels

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50
Q

renal infarcts due to amyloidosis are common in what species?

A

dogs

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51
Q

amyloidosis of spleen can cause what problem?

A

clotting disturbances

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52
Q

what can liver amyloidosis lead to?

A

impaired metabolic activity

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53
Q

what are the 2 type of intracellular hyaline changes?

A

pct of kidney - reaborption of plasma because of excessive leakage from glomerular capillaries
chronic alcoholism in liver of humans

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54
Q

where are equine intimal bodies found?

A

subendothelial space arterioles in GI tract

less common is heart, lung, kidney, brain

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55
Q

where are hyaline changes found in edema dz of pigs?

A

subendothelial in arterioles in brain

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56
Q

where are hyaline changes found in chronic damage to glomeruli?

A

glomerular tuft

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57
Q

where is hyaline found in hyaline membrane dz?

A

alveoli in premature infants

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58
Q

where is extracellular hyaline found in diabetes patients and dogs sometimes?

A

walls of arterioles in kidney

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59
Q

which stain makes amyloid and hyaline appear the same?

A

H and E

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60
Q

which stain can differentiate between amyloid and hyaline?

A

congo red will stain amyloid red

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61
Q

what is dystrophic calcification?

A

deposition of calcium salts in dead or degenerating tissues not related to calcium level inblood

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62
Q

what are the 3 hypotheses for dystrophic calcification?

A

local alkalinity
fatty acids attract it
alkaline phosphotase in dead tissue

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63
Q

where is dystrophic calcification usually seen?

A
caseous lesions of tuberculosis
degenerating tumors
old thrombi
atheromatous lesions in bv
dead parasites
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64
Q

what is the gross appearance of dystrophic calcification?

A

white irregulary round particles, gritty when cut

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65
Q

what are the three dyes used for calcium salts?

A

purple. - H and E
black - van kossa
dull red - alizarin red s

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66
Q

what is metastatic calcification?

A

deposition of calcium salts as a result of high blood calcium into non damaged tissues
lesions similar to dystrophic

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67
Q

what are the 5 causes of hypercalcemia?

A
hyperparathyroidism
renal failure
excess of vit d 
granulomatous dz -  tb, fungal, 
malignancy
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68
Q

what are the 3 neoplasms that cause hypercalcemia in dogs and cats?

A

lymphoma
anal sac adenocarcinoma
multiple myeloma

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69
Q

wherre is calcium deposition normal in bovine?

A

allantois and amnion of placenta

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70
Q

where can metastatic calcification be found?

A

basement membrane of aorta and muscular arteries

lungs, kidney, muscle and skin

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71
Q

where is metastatic calcification never found in dogs and cats?

A

arteries

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72
Q

what is a serious consequence of long standing hypercalcemia?

A

renal failure. - ischemic tubular necrosis

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73
Q

what are the 2 forms of gout and what kinds of species are they seen?

A

articular form in joints
visceral form in pleura, peritoneum, pericardium, liver, kidneys
in birds and reptiles

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74
Q

what are the 2 forms of calcinosis?

A

calcinosis cutis - hyperadrenocorticism in dogs

calcinosis circumstripta - dystrophic

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75
Q

what are the 2 causes of gout?

A

incomplete metabolism of nucleic acid

damage to kidneys

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76
Q

what does gout look like grossly?

A

thin grayish layer over serous membranes

white chalk in joints and kidneys

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77
Q

what. does gout look like microscopically?

A

grayish crystalline material

many wbcs around inflammation

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78
Q

what is pnemoconiosis?

A

retention of organic or mineral dust particles in lungs

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79
Q

what is anthracosis and what is seen-in gross lesions?

A

black areas on ventral lungs and in lymph nodes

80
Q

what does anthracosis look like microscopically?

A

black granules inside macrophages

does not stain, resistant to solvents

81
Q

what can a large amount of anthracosis cause?

A

fibrosis of lung, predispose to pulmonary infection

82
Q

what is siderosis?

A

iron dust inhaled as iron oxide

83
Q

where are lesions of melanosis found?

A

lungs
pleura
meninges
heart

84
Q

which species can get melanomas?

A

horses and dogs

85
Q

what color is CO poisoning in blood?

A

bright red

86
Q

what can methmoglobin be caused by?

A

nitrates, chlorates,

other iv hemolysis

87
Q

what are the 3 main pigments derived from hemoglobin?

A

hemosiderin
hematin
bilirubin

88
Q

what does hemosiderin look like grossly and microscopically?

A

grossly - not detected
micro- golden pigment in cytoplasm of macrophages
stains blue with potassium ferrocyanide

89
Q

what are the 3 main causes of hemosiderin pigment?

A

hemolytic dz
chronic venous congestion of lungs
hemosiderosis. - local areas. of hemorrhage

90
Q

what are the macrophages that pick up rbcs during pulmonary congestion?

A

heart failure cells

91
Q

what is the stage during heart failure where the lungs become fibrosed and have hemosiderin pigmeent?

A

brown induration

92
Q

what cells are effected by hemochromatosis?

A

cytoplasm of hepatocytes

tubular epithelium of kidney

93
Q

what is formalin pigment?

A

hematin pigment caused by acid, dark brown

does not stain for iron

94
Q

what parasites cause parasite hematin?

A

malaria and trematodes

95
Q

where is icterus usually seen in the body?

A

eyes
omentum
mesentery

96
Q

what is unconjugated bilirubin called?

A

hemobilirubin

97
Q

what type of jaundice is associated with a large amount of uncojugated bilirubin?

A

prehepatic jaundice/hemolytic

98
Q

which jaundice is associated with degenerative changes in liver cells?

A

hepatic/toxic jaundice

99
Q

what are the 4 obstructions in the liver that can lead to post hepatic jaundice?

A

swollen hepatic cells
parasites in bile ducts
stones in bile ducts
tumors putting pressure on ducts

100
Q

which solution do you compare sample to to diagnose jaundice?

A

potassium dichromate

101
Q

What does direct van den berg indicate?

A

conjugated bilirubin (obstructive jaundice)

102
Q

What does indirect van den berg reaction indicate?

A

hemolytic jaundice

103
Q

What is Type 1 photosensitization?

A

photodynamic plant or drug ingested in absence of liver dz

104
Q

what are the two plant families causing type 1 photosensitization?

A

Helianthrones and furocoumarines

105
Q

Which drug has been associated with type 1 photosensitization?

A

phenothiazine

106
Q

What is the disease caused by an inherited metabolic defect in synthesis of normal heme pigment?

A

Congenital erythropoietic porphyria - pink tooth

107
Q

What is type 2 photosensitization?

A

hepatogenous, sometimes happens when chlorophyll cant be broken down by ruminants because of liver damage

108
Q

Where can lipofuscin be found?

A

brain, heart, skeletal muscle, and smooth muscle

109
Q

What does lipofuscin look like microscopically?

A

yellow brown granules in cytoplasm

110
Q

What conditions is lipofuscin found?

A

wasting dz, senility, emaciation

111
Q

What deficienc is ceroid pigment associated with?

A

choline deficiency

112
Q

Where can ceroid pigment be found?

A

yellow brown pigment in liver cells of horse, dog, cattle, pig, and rat

113
Q

What term is used to explain the gross appearance of ceroid pigment?

A

“yellow fat dz” or “brown dog gut”

114
Q

What 2 disorders of the circulation redistribute blood within a part of the vascular system?

A

Hyperemia - large amount of blood in organ or tissue

ischaemia - restriction in blood supply

115
Q

What 2 circulation disorders cause a loss of circulating blood volume?

A

hemorrhage

fluid loss

116
Q

What 2 circulation disorders cause accumulation of extra vascular fluid?

A

transudate - edema

exudate - inflammatory

117
Q

what 2 circulation disorders cause solid masses to develop in blood?

A

thrombosis

embolism

118
Q

What is active hyperemia?

A

abnormal accumulation of arterial blood in arterioles (physiological or pathological)

119
Q

What is passive hyperemia?

A

accumulation of blood in veins because of dilation

120
Q

What are 2 examples of acute local passive hyperemia?

A
organ misalignment (teloscoping)
venous thrombosis or embolism
121
Q

What is compression by tumors or fibrosis an example of?

A

chronic local passive hyperemia

122
Q

What are the 2 effects of local passive hyperemia?

A

increased venous pressure –> edema

anoxia, necrosis

123
Q

What is the consequence of hyperemia in highly vascular organs?

A

massive outpouring of fluid –> shock, gangrene

124
Q

What are three causes of general passive hyperemia?

A

cardiac failure
impeded venous return
increased pulmonary resistance

125
Q

What are the long term effects of general passive hyperemia?

A

edematous with hemorrhage in lungs then fibrosed and loss of function
liver - periacinar degeneration

126
Q

what are 2 causes of ischaemia?

A

heart failure

obstruction of an artery

127
Q

Term for passive movement of rbcs into EV spaces through small endothelial defects

A

diapedesis

128
Q

Term for large and blotch hemorrhages (2-3 cm)

A

ecchymoses

129
Q

Term for intermediate type hemorrhages up to 1 cm

A

purpura

130
Q

Term for extensive areas of hemorrhages especially in mucosal and serous surfaces

A

paint brush hemorrhage

131
Q

What can cause hemorrhage by anoxic necrosis of vessel wall?

A

passive hyperemia

132
Q

What amount of blood can be lost acutely and not show drastic clinical effects?

A

10-20%

133
Q

How can plasma decrease it’s osmotic pressure?

A

loss of protein

134
Q

What 2 causes increase the loss of protein from the body?

A
renal dz (renal edema)
parasitic infections
135
Q

What can cause increased hydrostatic pressure leading to edema?

A

passive congestion (cardiac edema)

136
Q

What 2 causes lead to local edema?

A

local passive hyperemia

lymphatic obstruction

137
Q

What 3 causes lead to generalized edema?

A

passive hyperemia, hypoproteinemia, increased sodium retention

138
Q

Where does the generalized edema go in each species?

A

Dog - peritoneal cavity
Cat - throacic cavity
Ruminants - submandibular and peritoneum
Horse - limbs

139
Q

Term for generalized edema under the skin

A

anasarca

140
Q

Term for edema in peritoneal cavity

A

ascitis

141
Q

Term for edema fluid in scrotal layers

A

hydrocele

142
Q

What are the three reasons for pulmonary edema?

A

heart failure
irritating gases
inflammatory process

143
Q

What are the two biggest differences between inflammatory and non-inflammatory edema?

A

non-inflammatory never clots

inflammatory has inflammatory cells

144
Q

What is another name for inflammatory edema? non-inflammatory edema?

A

inflammatory - exudate

non - transudate

145
Q

What happens to long standing edema?

A

organized by fibrous tissue

146
Q

What is Virchow’s triad (3 causes of thrombosis)?

A

alteration in vascular endothelium
alteration in blood flow
alteration in constituents of the blood

147
Q

How is thrombosis caused by damage in endothelium of blood vessels?

A

build up of clotting factors after platelets lost

148
Q

What are some causes of vascular endothelial damage?

A

arteritis, phlebitis, endocarditis, arteriosclerosis, atherosclerosis, IV injection of irritants

149
Q

How does stasis of blood flow cause thrombosis?

A

occurs in veins, reduces inflow of clotting inhibitors

150
Q

How does turbulence of blood flow cause thrombosis?

A

platelets come in contact with endothelium more frequently

151
Q

What cells make up the layered appearance of thrombi?

A

white layer - platelets and leukocytes

red layer - fibrin, rbc, leukocytes

152
Q

What is a clot made of?

A

uniform network of fibrin with platelets, leukocytes and rbcs

153
Q

What is the difference between a thrombi and a clot?

A

thrombus - attached to wall, layered

clot - uniform

154
Q

What type of thrombus is found in rapidly moving blood and composed mostly of platelets and fibrin?

A

white or pale thrombi

155
Q

What type of thrombus is found in veins and is largely made of RBCs?

A

red thrombi

156
Q

What type of thrombus does not occlude the lumen of the blood vessel?

A

mural thrombus

157
Q

What type of thrombus completely blocks the vessel?

A

occlusive thrombus

158
Q

What parasite can cause thrombosis in mesenteric artery of horses?

A

strongylus vulgaris

159
Q

What thrombus can cause lameness in horses?

A

iliac arteries

160
Q

In cattle, an abcess in the adjacent liver parenchyma can cause thrombi in what vessel?

A

posterior vena cava

162
Q

What are the four fates of thrombi?

A

resolution - fibrinolysis
organization - recanalization
abcess - bacteria, pyemia
emboli - breaks free

163
Q

What is the definition of DIC? (disseminated intravascular coagulation)

A

diffuse intravascular thrombosis occurs in microvasculature

164
Q

What causes is DIC secondary to?

A

disorder in platelet activation

release of thromboplastin into circulation from tissue damage

165
Q

The clinical effects of DIC are due to a balance between what 2 proteases?

A

Thrombin

Plasmin

166
Q

What protease is dominant in DIC if thrombosis is occurring?

A

thrombin

167
Q

What protease is dominant in DIC if bleeding is occurring?

A

plasmin

168
Q

How does death occur in acute DIC?

A

extensive microthrombosis and circulatory failure –> shock and organ failure

169
Q

How does the acute DIC become chronic DIC?

A

Liver and bone marrow increase production of coagulation factors and platelets

170
Q

What species is DIC principally reported in?

A

dogs

171
Q

How can DIC be diagnosed?

A
prolonged prothrombin time
hypofibrinogenemia (horses --> hyper)
FDPs
schistocytes
decreased coagulation factors and antithrombin 3
172
Q

Where does an emboli get lodged if it originates in the venous system or right side of heart?

A

lungs

173
Q

Where does an emboli get lodged if it originates in the left heart or arterial system?

A

systemic capillary bed

174
Q

Effects of embolism depend on what three things?

A

degree of occlusion
speed of onset
presence of collateral supply to affected organ

175
Q

What 2 places in the body have good collateral circulation?

A

limbs

lungs

176
Q

What parts of the body have bad collateral circulation?

A
spleen
kidney
brain
heart
skin
177
Q

What is an infarction?

A

loss of blood supply and necrosis

178
Q

What is the most common type of emboli?

A

thrombo-emboli

179
Q

What trauma can cause release of fat into circulation and cause emboli?

A

bone fracture

subcutaneous trauma

180
Q

Where do fat emboli usually get stuck?

A

lung capillaries

181
Q

What pathological effect happens after gas gets into circulation?

A

acute right side heart failure

182
Q

Where do bacterial emboli usually get lodged?

A

lungs
kidney
brain
liver

183
Q

What are 2 other causes other than thrombus and emboli that cause infarctions?

A

torsion of blood vessels

hypoperfusion in shock

184
Q

Where are dull infarcts usually seen?

A

solid organs like kidney and heart

185
Q

Where are red infarcts usually seen?

A

soft organs - lung, spleen, intestine

186
Q

What type of necrosis lesions are seen in infarcts?

A

coagulative necrosis

187
Q

What is the infarct like in the kidney?

A

conical

188
Q

What do infarcts look like in the brain?

A

anemic, liquefactive necrosis

189
Q

What is an infarct like in the intestine?

A

hemorrhagic
gangrene
fatal

190
Q

What do infarcts look like in the lungs?

A

hemorrhagic

alveoli contain blood

191
Q

When do infarcts happen in the mammary gland?

A

severe mastitis

involves large area

192
Q

What are infarcts in the liver less severe?

A

dual blood supply

193
Q

What clinical signs might be present if large areas are infarcted?

A

shock from histamine absorption

194
Q

What 3 most common causes of shock?

A
  1. heart failure - cardiogenic shock
  2. low blood volume - hypovalemic shock
  3. alteration in blood vessel size - vasculogenic shock
195
Q

What 2 things accumulate in blood that lead to acidosis in shock?

A

Pyruvic and lactic acid

196
Q

What are the 3 main changes in tissues from shock?

A

necrosis
hemorrhage
microthrombi in capillaries

197
Q

What is gout?

A

uric acid and urates are deposited in tissues

198
Q

What is calcinosis?

A

calcification in or under the skin