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General Pathology > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

What is a “lesion”

A

anything that is wrong

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2
Q

What are the components to describing a lesion?

A
  1. Size
  2. Color
  3. Consistency
  4. Shape
  5. Surface
  6. Margins
  7. Distribution
  8. Location
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3
Q

What are the components of anatomical pathology? What does an anatomical pathologist “do?”

A 
Necropsy/Autopsy
Biopsy
Antemortem examination
Post mortem examination
Gross pathology
Histopathology
Ultrastructure
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4
Q

Define “pathgnomonic”

A

a lesion so characteristic of a disease, you can diagnose based on the lesion

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5
Q

What is the difference between “dome shaped” and “exophitic”?

A

both are raised, but if something is dome shaped, you can go over it with clippers, if it’s exophitic, you’ll cut it off if you use clippers

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6
Q

Give some examples of terms you could use to describe the shape of a lesion

A

Irregular, pedunculated, sessile, exophitic, dome shaped

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7
Q

Define “etiology”

A

causes of lesions

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8
Q

What are the 12 categories of etiology?

A 
metabolic
Inflammatory
Neoplastic
Infectious
Vascular
Anomalies
Nutritional
Degenerative
Idiopathic
Traumatic
Toxic
Iatrogenic
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9
Q

What are two common causes of cell injury?

A

Hypoxia and free radical injury

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10
Q

What are four sources of free radicals?

A

Radiation, Toxicity, Inflammation, normal mitochondrial function

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11
Q

What are the three effects of free radicals?

A

Membrane lipid perioxidation
Protein cross linking
DNA fragmentation

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12
Q

What does the severity of cell injury depend on?

A

Cell type (neurons are very sensitive to hypoxia)
Nutrition (antioxidants are good)
Previous injury (heat shock proteins)
Reperfusion injury

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13
Q

What do heat shock proteins do?

A

They recognize, bind, refold and chaperone a damaged cell to a lysosome to be degraded.

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14
Q

What caused reperfusion injury?

A

Blood supply getting off cut off is a common cause of hypoxia, when blood flow is restored, there are more free radicals

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15
Q

What are three types if intracellular inclusions

A

Fatty change
Glycogen accumulation
Hydropic degeneration

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16
Q

What are the mechanisms of fatty change?

A

Excessive fatty acid entry
Defective fatty acid oxidation
Decreased apoproteins
Defective secretion

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17
Q

Which types of equids are pre-disposed to fatty liver?

A

Ponies, mini-horses and morgans

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18
Q

What does fatty liver look like? What is its morphology?

grossly and histologically

A

Enlarged, yellow and friable

  • if lesion is very severe, liver may float
  • Histologically you will see lipid droplets in the cytoplasm
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19
Q

When would you expect to see hepatic lipidosis in ruminants?

A

A fat cow has high energy demand- generally early lactation or if fetus is very large- body mobilizes fat and overwhelms the liver

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20
Q

What can cause Glycogen accumulation?

A

Canine steroid hepatopathy
Diabetes mellitus
Storage diseases
Neonates

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21
Q

What is hydropic degeneration

A

a reverisble and transient condition- identical in appearance to glycogen accumulation, but very rarely seen. Often progresses to death.

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22
Q

What are storage diseases?

What do they lead to?

A

A defect in an enzyme that should be processing glycogen

  • affects the whole body, but liver is most affected because it processes so much glycogen
  • leads to glycogen accumulation
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23
Q

Describe Canine steroid hepatopathy

A

liver becomes enlarged and friable, glycogen synthetase results in liver dysfunction

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24
Q

Histogolicly, how can you tell glycogen accumulation from fatty liver?

A

In fatty liver, the droplets are round. They are not as regularly shaped in glycogen accumulation

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25
Q

Define “malacia”

A

softening of cells in the CNS associated with cell death

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26
Q

What are the gross changes involved in cell death?

A

Softening
Discoloration
Ulceration

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27
Q

What are the microscopic changes associated with cell deat?

A

Pyknosis
Karyorrhexis
Karyolysis
Cytoplasmic increase in eosinophilia

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28
Q

Define “pyknosis”

A

shrunken, intensely basophilic nuclei- associated with cell death

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29
Q

Define Karyhrrhexis

A

nuclei that have broken into tiny pieces

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30
Q

Define Karyolysis

A

fading of the nucleus

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31
Q

Define “necrosis”

A

death of cells before the animal dies

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32
Q

What are the types of necrosis

A 
Coagulative necrosis
Liquefactive necrosis
Caseous necrosis
Fat necrosis
Gangrene
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33
Q

Define “infarct”

A

focal areas of necrosis caused by ischemia

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34
Q

Histologically, what differentiates coagulative necrosis from liquefactive necrosis?

A

in coagulative necrosis, tissue architecture is preserved. In liquefactive necrosis, tissue architecture can no longer be observed.

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35
Q

What is coagulative necrosis caused by?

A

infarct or toxins

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36
Q

What is liquefactive necrosis caused by?

A

usually bacteria

- not necessarily bacteria if it is found in the CNS

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37
Q

What causes caseous necrosis?

A

Mycobacterium tuberculosis and related organisms

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38
Q

What are the two types of fat necrosis?

A

Enzymatic and Nutritional/toxic

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39
Q

What is enzymatic fat necrosis?

A

pancreatic enzymes designed to digest fat get released into the abdomen and cause saponification

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40
Q

What is nutritional/toxic fat necosis?

A

ingestion of too much rancid fish causes all of the antioxidants to be used up and free radical injury to adipose tissue

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41
Q

What makes the fat look yellow in toxic fat necrosis?

A

serroid pigment

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42
Q

In non-carnivores, what can cause toxic fat necrosis?

Which breeds are pre-disposed?

A

grazing fescue
Geurnseys and Jerseys are predisposed
Most common in older animals

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43
Q

What causes dry gangrene?

Give some examples

A

ischemia

- fescue foot, frostbite

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44
Q

What are the three types of gangrene?

A

Dry gangrene
wet gangrene
gas gangrene (black leg)

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45
Q

What causes wet gangrene?

A

Bacterial infection

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46
Q

What are the two types of apoptosis?

A

Physiologic and pathologic

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47
Q

When does physiologic apoptosis occur?

A

embryogenesis
Regression of temporary tissue
developing immune tolerance
tissue homeostasis

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48
Q

When does pathologic apoptosis happen?

A

Virus induced- canine distemper
Viral inhibition- pox virus
Autoimmunity
Neoplasia

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49
Q

What are the steps of apoptosis?

A
  1. signaling
  2. Control
  3. Execution
  4. Removal
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50
Q

What type of molecule is the execution step of apoptosis mediated by?

A

Caspases

51
Q

What is “autolysis”

A

rotting of the body after death

52
Q

What are two ways you may be able to tell autolysis from necrosis?

A

Autolysis won’t show a host immune response

Autolysis is diffuse, necrosis is generally localized

53
Q

What factors contribute to autolysis?

A 
Tissue type
Temperature
Bacteria
Insulation
Time
54
Q

What is “post mortem interval?”

A

time between death and necropsy

55
Q

What are some common postmortem lesions?

A 
Gas accumulation
Gastric rupture
Post mortem discoloration
Algor mortis
Livor mortis
Rigor mortis
Euthanasia precipitate
56
Q

What is algor mortis?

A

cooling of the body after death

57
Q

What is livor mortis?

A

pooling of blood in gravity dependent areas after death

58
Q

What are the types of post mortem discoloration?

A

Bile imbibition
Hemoglobin imbibition
Pseudomelanosis

59
Q

What two things are required for pseudomelanosis?

A

blood and bacteria

60
Q

How does formalin fix tissue?

A

it kills bacteria and stops enzymes, also hardens tissue by cross linking enzymes

61
Q

What three factors affect formalin fixation?

A

pH- needs to be neutral, will turn acidic
Volume ratio
Time

62
Q

Besides freezing, what other factors damage tissue for histopatholgy

A

Friction
compression
Electrocautery
Surgical margins

63
Q

Define “edema”

A

accumulation of excess watery fluid in the interstitial space or body cavities

64
Q

Define “anasarca”

A

generalized massive edema

65
Q

Define “effusion”

A

giving something off such as liquid, light or smell

66
Q

What type of edema is bottle jaw an example of?

A

localized subcutaneous edema

67
Q

What does pitting edema suggest?

A

Chronicity- fibroblasts in SQ proliferate over time and form a meshwork

68
Q

What is a seroma?

A

a localized fluid pocket, often seen in trauma

69
Q

What are the three causes of edma?

A

Increased hydrostaic force
Decreased oncotic force
Lymphatic obstruction

70
Q

Pair “oncotic” and “hydrostatic” with “arterial” or “venous”

A

on the venous side, pressure is mostly oncotic, arterial pressure is mostly hydrostatic

71
Q

What is a reason you might see decreased oncotic force?

A

loss of protein or failure to produce enough protein

-causes may be parasites, kidney disease, etc

72
Q

What causes increased hydrostatic pressure?

A

Inefficient heart pumping

-blood backs up and moves out of the vessels and into the interstitium

73
Q

Define “hyperemia”

A

active filling of arterioles, with a goal to increase bloodflow

74
Q

How would you tell hyperemia from congestion microscopically?

A

YOU CAN’T! trick question.

75
Q

Give an example of pathologic hyperemia

A

Inflammation

76
Q

How might you be able to distinguish hyperemia from congestion based on color of the tissue?

A

Hyperemia will be bright red

Congestion will be cyanotic

77
Q

Define congestion

A

passive filling of capillaries and veins due to lack of forward flow

78
Q

What are the two most common causes of congestion?

A

decreased cardiac output, venous obstruction (both also causes of edema)

79
Q

What special type of cells might you see in the lungs in a case of pulmonary congestion?
What is the special name for this type of cell?

A

“hemosiderin-laden macrophages”

-called “heart failure cells”

80
Q

True or false, any time you see an enhanced reticular pattern on a liver, you can safely call it a nutmeg liver.

A

False- nutmeg liver is only caused by chronic hepatic congestion. Lots of other things can also cause an enhanced reticular pattern

81
Q

What might you see on the liver in a case of acute hepatic congetstion?

A

a layer of fibrin

82
Q

Name three causes of congestion

A

Hypostatic congestion
Torsion/strangulation
Barbituate effect on spleen

83
Q

Define hemorrhage

A

escape of blood from the cardiovascular system in a living organism

84
Q

What are the three destinations for hemorrhage?

A

Outside the body
Inside the body
Into tissue

85
Q

Define “hematoma”

A

a solid, tumor like swelling of clotted blood within a tissue

86
Q

Define Epistaxis

A

bleeding from the nose

87
Q

Define Hemoptysis

A

coughing blood

88
Q

Define Hematemesis

A

vomiting blood

89
Q

define hematuria

A

urinating blood

90
Q

Define hematochezia

A

fresh blood in feces

91
Q

Define hyphema

A

blood in the anterior chamber of the eye

92
Q

What might a splenic hematoma be confused with? If it is very large, which on do you think it will be?

A

Splenic hematomas can be confused for a hemangiosarcoma

- if it is very large, it is more likely a hematoma

93
Q

What causes spenic hematomas?

A

nodular lymphoid hyperplasia

- disrupts the normal architecture of the spleen and allows blood to pool there

94
Q

What word would you use to describe a hemorrhage 3mm-3cm in diameter?

A

Ecchymotic

95
Q

What word would you use to describe linear streaks of hemorrhage?

A

“paintbrush”

- often seen on stomag and epicardial surface

96
Q

How much blood do you have to lose to go into hypovolemic shock?

A

30%

97
Q

What are the five major mechanisms of shock?

A 
Cardiogenic
Hypovolemic
Anaphylactic
Neurogenic
Septic
98
Q

List the steps in the mechanism of septic shock

A
  1. infectious organism gets into blood stream ( into blood is the important part)
  2. bacteria releases toxin
  3. toxin activates a system wide inflammatory response
  4. Activated endothelium and inflammatory cells release cytokines
99
Q

How would you treat septic shock?

A

with fluids

100
Q

Give an example of an infectious disease that may lead to septic shock

A

Canine parvovirus

101
Q

Define “thrombosis”

A

pathologic coagulation of blood within the intact cardiovascular system

102
Q

What are the four steps of coagulation

A
  1. Transient vasconstriction
  2. platelet reaction (primary hemostatis)
  3. Fibrin clot (secondary hemostasis)
  4. Anticoagulant controls
103
Q

List some anticoagulant controls

A

antithrombin III
Thrombomodulin
Protein C
Plasminogen activators

104
Q

which step of coagulation is also known as primary hemostatis?

A

platelet reaction

-adherence and activation to form hemostatic plug

105
Q

Which step of coagulation is also known as secondary hemostasis?

A

Fibrin clot
- coagulation cascade causes thrombin to be formed, which cleaves fibrinogen into fibrin and fibrin stabilizes the hemostatic plug

106
Q

What are the three components of Virchow’s triad?

A

Endothelial injury
Alterations in normal blood flow
Increased coagulability

107
Q

List some causes of endothelial injury that would fall under Virchow’s triad

A 
Trauma
Parasites
Atherosclerosis
Arteriosclerosis
Inflammation- TNF and IL-1
108
Q

What is the difference between atherosclerosis and arteriosclerosis?

A

atherosclerosis is fatty plaques

arteriosclerosis is hard and not fatty plaques

109
Q

What are some causes of alterations of normal blood flow that would fall under Virchow’s triad?

A

chronic IV catheter
Aneurysm
Stasis
cardiac disfunction- causes turbulence

110
Q

what are some causes of increased blood coagulability that would fall under Virchow’s triad?

A 
corticosteriods
protein loss (esp. antithrombin III)
Pancreatitis
Dehydration
Hormones
Neoplasia
111
Q

Describe how lack of laminar flow leads to problems

A

loss of laminar flow allows platelets to come into contact with the epithelium, clotting factors separate from inhibitors and endothelial cells are activated

112
Q

Describe “embolus”

A

intravascular material carried by the bloodstream to a site distant to its origin

113
Q

Describe what a thrombus would look like

A

Pale tan colored
dry, rough and grainy
adhered to the vessel wall
contains lines of Zahn

114
Q

What are lines of Zahn made of?

A

alternating bands of wite platelets and fibrin and red blood cells

115
Q

Describe what a clot would look like

A

Dark, shiny and wet

not adhered to vessel wall

116
Q

What are the possible fates of thrombi?

A

Dissolution
Propagation
Embolization
Organization and Recanalization

117
Q

List three important thrombotic conditions

A

Pulmonary thrombi
Distal aortic/iliac thromboembolism
DIC

118
Q

Compare what an arterial infarct would look like compared to a venous infarct

A

arterial infarts appear pale due to lack of blood flow

Venous infarcts appear dark red/purple due to associated congestion and hemorrhage

119
Q

What are the two vessels that supply dual blood supply to the lungs?

A

bronchial and pulmonary arteries

120
Q

What are the two vessels that supply blood to the liver?

A

Hepatic artery and portal vein

121
Q

What is DIC characterized by?

A

Widespred microthrombi

Consumption of platelets and coagulation factors resulting in spontaneous hemorrhage

122
Q

What is DIC caused by?

A

excessive activation of coagulation which leads to abnormal clotting profile and formation of microthrombi

123
Q

True or false DIC is a primary condition.

A

False, DIC is the result/complication of many conditions. For example: widespread endothelial injury, heat stroke, pancreatitis, massive tissue injury, sepsis, allergic toxic reaction

General Pathology (1 decks)

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