Exam 1 Flashcards
(123 cards)
1
Q
What is a “lesion”
A
anything that is wrong
2
Q
What are the components to describing a lesion?
A
- Size
- Color
- Consistency
- Shape
- Surface
- Margins
- Distribution
- Location
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
4
Q
Define “pathgnomonic”
A
a lesion so characteristic of a disease, you can diagnose based on the lesion
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
6
Q
Give some examples of terms you could use to describe the shape of a lesion
A
Irregular, pedunculated, sessile, exophitic, dome shaped
7
Q
Define “etiology”
A
causes of lesions
8
Q
What are the 12 categories of etiology?
A
metabolic Inflammatory Neoplastic Infectious Vascular Anomalies Nutritional Degenerative Idiopathic Traumatic Toxic Iatrogenic
9
Q
What are two common causes of cell injury?
A
Hypoxia and free radical injury
10
Q
What are four sources of free radicals?
A
Radiation, Toxicity, Inflammation, normal mitochondrial function
11
Q
What are the three effects of free radicals?
A
Membrane lipid perioxidation
Protein cross linking
DNA fragmentation
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
13
Q
What do heat shock proteins do?
A
They recognize, bind, refold and chaperone a damaged cell to a lysosome to be degraded.
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
15
Q
What are three types if intracellular inclusions
A
Fatty change
Glycogen accumulation
Hydropic degeneration
16
Q
What are the mechanisms of fatty change?
A
Excessive fatty acid entry
Defective fatty acid oxidation
Decreased apoproteins
Defective secretion
17
Q
Which types of equids are pre-disposed to fatty liver?
A
Ponies, mini-horses and morgans
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
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
20
Q
What can cause Glycogen accumulation?
A
Canine steroid hepatopathy
Diabetes mellitus
Storage diseases
Neonates
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.
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
23
Q
Describe Canine steroid hepatopathy
A
liver becomes enlarged and friable, glycogen synthetase results in liver dysfunction
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
25
Define "malacia"
softening of cells in the CNS associated with cell death
26
What are the gross changes involved in cell death?
Softening
Discoloration
Ulceration
27
What are the microscopic changes associated with cell deat?
Pyknosis
Karyorrhexis
Karyolysis
Cytoplasmic increase in eosinophilia
28
Define "pyknosis"
shrunken, intensely basophilic nuclei- associated with cell death
29
Define Karyhrrhexis
nuclei that have broken into tiny pieces
30
Define Karyolysis
fading of the nucleus
31
Define "necrosis"
death of cells before the animal dies
32
What are the types of necrosis
```
Coagulative necrosis
Liquefactive necrosis
Caseous necrosis
Fat necrosis
Gangrene
```
33
Define "infarct"
focal areas of necrosis caused by ischemia
34
Histologically, what differentiates coagulative necrosis from liquefactive necrosis?
in coagulative necrosis, tissue architecture is preserved. In liquefactive necrosis, tissue architecture can no longer be observed.
35
What is coagulative necrosis caused by?
infarct or toxins
36
What is liquefactive necrosis caused by?
usually bacteria
| - not necessarily bacteria if it is found in the CNS
37
What causes caseous necrosis?
Mycobacterium tuberculosis and related organisms
38
What are the two types of fat necrosis?
Enzymatic and Nutritional/toxic
39
What is enzymatic fat necrosis?
pancreatic enzymes designed to digest fat get released into the abdomen and cause saponification
40
What is nutritional/toxic fat necosis?
ingestion of too much rancid fish causes all of the antioxidants to be used up and free radical injury to adipose tissue
41
What makes the fat look yellow in toxic fat necrosis?
serroid pigment
42
In non-carnivores, what can cause toxic fat necrosis?
| Which breeds are pre-disposed?
grazing fescue
Geurnseys and Jerseys are predisposed
Most common in older animals
43
What causes dry gangrene?
| Give some examples
ischemia
| - fescue foot, frostbite
44
What are the three types of gangrene?
Dry gangrene
wet gangrene
gas gangrene (black leg)
45
What causes wet gangrene?
Bacterial infection
46
What are the two types of apoptosis?
Physiologic and pathologic
47
When does physiologic apoptosis occur?
embryogenesis
Regression of temporary tissue
developing immune tolerance
tissue homeostasis
48
When does pathologic apoptosis happen?
Virus induced- canine distemper
Viral inhibition- pox virus
Autoimmunity
Neoplasia
49
What are the steps of apoptosis?
1. signaling
2. Control
3. Execution
4. Removal
50
What type of molecule is the execution step of apoptosis mediated by?
Caspases
51
What is "autolysis"
rotting of the body after death
52
What are two ways you may be able to tell autolysis from necrosis?
Autolysis won't show a host immune response
| Autolysis is diffuse, necrosis is generally localized
53
What factors contribute to autolysis?
```
Tissue type
Temperature
Bacteria
Insulation
Time
```
54
What is "post mortem interval?"
time between death and necropsy
55
What are some common postmortem lesions?
```
Gas accumulation
Gastric rupture
Post mortem discoloration
Algor mortis
Livor mortis
Rigor mortis
Euthanasia precipitate
```
56
What is algor mortis?
cooling of the body after death
57
What is livor mortis?
pooling of blood in gravity dependent areas after death
58
What are the types of post mortem discoloration?
Bile imbibition
Hemoglobin imbibition
Pseudomelanosis
59
What two things are required for pseudomelanosis?
blood and bacteria
60
How does formalin fix tissue?
it kills bacteria and stops enzymes, also hardens tissue by cross linking enzymes
61
What three factors affect formalin fixation?
pH- needs to be neutral, will turn acidic
Volume ratio
Time
62
Besides freezing, what other factors damage tissue for histopatholgy
Friction
compression
Electrocautery
Surgical margins
63
Define "edema"
accumulation of excess watery fluid in the interstitial space or body cavities
64
Define "anasarca"
generalized massive edema
65
Define "effusion"
giving something off such as liquid, light or smell
66
What type of edema is bottle jaw an example of?
localized subcutaneous edema
67
What does pitting edema suggest?
Chronicity- fibroblasts in SQ proliferate over time and form a meshwork
68
What is a seroma?
a localized fluid pocket, often seen in trauma
69
What are the three causes of edma?
Increased hydrostaic force
Decreased oncotic force
Lymphatic obstruction
70
Pair "oncotic" and "hydrostatic" with "arterial" or "venous"
on the venous side, pressure is mostly oncotic, arterial pressure is mostly hydrostatic
71
What is a reason you might see decreased oncotic force?
loss of protein or failure to produce enough protein
| -causes may be parasites, kidney disease, etc
72
What causes increased hydrostatic pressure?
Inefficient heart pumping
| -blood backs up and moves out of the vessels and into the interstitium
73
Define "hyperemia"
active filling of arterioles, with a goal to increase bloodflow
74
How would you tell hyperemia from congestion microscopically?
YOU CAN'T! trick question.
75
Give an example of pathologic hyperemia
Inflammation
76
How might you be able to distinguish hyperemia from congestion based on color of the tissue?
Hyperemia will be bright red
| Congestion will be cyanotic
77
Define congestion
passive filling of capillaries and veins due to lack of forward flow
78
What are the two most common causes of congestion?
decreased cardiac output, venous obstruction (both also causes of edema)
79
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?
"hemosiderin-laden macrophages"
| -called "heart failure cells"
80
True or false, any time you see an enhanced reticular pattern on a liver, you can safely call it a nutmeg liver.
False- nutmeg liver is only caused by chronic hepatic congestion. Lots of other things can also cause an enhanced reticular pattern
81
What might you see on the liver in a case of acute hepatic congetstion?
a layer of fibrin
82
Name three causes of congestion
Hypostatic congestion
Torsion/strangulation
Barbituate effect on spleen
83
Define hemorrhage
escape of blood from the cardiovascular system in a living organism
84
What are the three destinations for hemorrhage?
Outside the body
Inside the body
Into tissue
85
Define "hematoma"
a solid, tumor like swelling of clotted blood within a tissue
86
Define Epistaxis
bleeding from the nose
87
Define Hemoptysis
coughing blood
88
Define Hematemesis
vomiting blood
89
define hematuria
urinating blood
90
Define hematochezia
fresh blood in feces
91
Define hyphema
blood in the anterior chamber of the eye
92
What might a splenic hematoma be confused with? If it is very large, which on do you think it will be?
Splenic hematomas can be confused for a hemangiosarcoma
| - if it is very large, it is more likely a hematoma
93
What causes spenic hematomas?
nodular lymphoid hyperplasia
| - disrupts the normal architecture of the spleen and allows blood to pool there
94
What word would you use to describe a hemorrhage 3mm-3cm in diameter?
Ecchymotic
95
What word would you use to describe linear streaks of hemorrhage?
"paintbrush"
| - often seen on stomag and epicardial surface
96
How much blood do you have to lose to go into hypovolemic shock?
30%
97
What are the five major mechanisms of shock?
```
Cardiogenic
Hypovolemic
Anaphylactic
Neurogenic
Septic
```
98
List the steps in the mechanism of septic shock
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
How would you treat septic shock?
with fluids
100
Give an example of an infectious disease that may lead to septic shock
Canine parvovirus
101
Define "thrombosis"
pathologic coagulation of blood within the intact cardiovascular system
102
What are the four steps of coagulation
1. Transient vasconstriction
2. platelet reaction (primary hemostatis)
3. Fibrin clot (secondary hemostasis)
4. Anticoagulant controls
103
List some anticoagulant controls
antithrombin III
Thrombomodulin
Protein C
Plasminogen activators
104
which step of coagulation is also known as primary hemostatis?
platelet reaction
| -adherence and activation to form hemostatic plug
105
Which step of coagulation is also known as secondary hemostasis?
Fibrin clot
- coagulation cascade causes thrombin to be formed, which cleaves fibrinogen into fibrin and fibrin stabilizes the hemostatic plug
106
What are the three components of Virchow's triad?
Endothelial injury
Alterations in normal blood flow
Increased coagulability
107
List some causes of endothelial injury that would fall under Virchow's triad
```
Trauma
Parasites
Atherosclerosis
Arteriosclerosis
Inflammation- TNF and IL-1
```
108
What is the difference between atherosclerosis and arteriosclerosis?
atherosclerosis is fatty plaques
| arteriosclerosis is hard and not fatty plaques
109
What are some causes of alterations of normal blood flow that would fall under Virchow's triad?
chronic IV catheter
Aneurysm
Stasis
cardiac disfunction- causes turbulence
110
what are some causes of increased blood coagulability that would fall under Virchow's triad?
```
corticosteriods
protein loss (esp. antithrombin III)
Pancreatitis
Dehydration
Hormones
Neoplasia
```
111
Describe how lack of laminar flow leads to problems
loss of laminar flow allows platelets to come into contact with the epithelium, clotting factors separate from inhibitors and endothelial cells are activated
112
Describe "embolus"
intravascular material carried by the bloodstream to a site distant to its origin
113
Describe what a thrombus would look like
Pale tan colored
dry, rough and grainy
adhered to the vessel wall
contains lines of Zahn
114
What are lines of Zahn made of?
alternating bands of wite platelets and fibrin and red blood cells
115
Describe what a clot would look like
Dark, shiny and wet
| not adhered to vessel wall
116
What are the possible fates of thrombi?
Dissolution
Propagation
Embolization
Organization and Recanalization
117
List three important thrombotic conditions
Pulmonary thrombi
Distal aortic/iliac thromboembolism
DIC
118
Compare what an arterial infarct would look like compared to a venous infarct
arterial infarts appear pale due to lack of blood flow
| Venous infarcts appear dark red/purple due to associated congestion and hemorrhage
119
What are the two vessels that supply dual blood supply to the lungs?
bronchial and pulmonary arteries
120
What are the two vessels that supply blood to the liver?
Hepatic artery and portal vein
121
What is DIC characterized by?
Widespred microthrombi
| Consumption of platelets and coagulation factors resulting in spontaneous hemorrhage
122
What is DIC caused by?
excessive activation of coagulation which leads to abnormal clotting profile and formation of microthrombi
123
True or false DIC is a primary condition.
False, DIC is the result/complication of many conditions. For example: widespread endothelial injury, heat stroke, pancreatitis, massive tissue injury, sepsis, allergic toxic reaction
