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General Pathology > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Characteristics of reversible cell injury

A

i. Light Microscopic Changes: Cell swelling, Chromatin clumping, Lipidosis
ii. Dilation of endoplasmic reticulum
iii. Ribosomal detachment from RER
iv. Loss of microvilli and cilia
v. Mitochondral swelling
vi. Chromatin clumping
vii. Membrane blebs
viii. Lipid accumulation
ix. Organ will be discolored, enlarged, or discolored

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2
Q

Characteristics of irreversible cell swelling

A

Nuclear changes!

a. Pyknosis
c. Chromatolysis
2. Increased eosinophilia of cytoplasm (can have vacuolization and/or calcification)
ii. High amplitude mitochondrial swelling
iii. Membrane defects of ER
iv. Lysomal membrane rupture

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3
Q

Occurs due to general mechanisms of cell injury. Dead cells have active proteases, phospholipidases, and endonucleases that will break down cell components

A

coagulation necrosis

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4
Q

Occurs in tissue with high neutrophil recruitment and enzymatic release with digestion of tissue. Also, occurs in tissues with high lipid content such as the brain.Loss of cell borders occurs.

A

Liquefactive necrosis

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5
Q

Occurs commonly with mycobacterial infections. Macrophages are recruited and cells become necrotic as the organism persists

A

caseous necrosis

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6
Q

ischemic necrosis of distal extremeties

A

gangrenous necrosis

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7
Q

Necrosis of adipocytes and white lesions in fat due to cleavage of neutral fat by lipase to triglycerides and FAs with precipitation of FA by calcium to form FA soaps

A

Fat necrosis

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8
Q

Triggered by specific cell-mediated stimulus or loss of signals
Can be pathogenic
Will see chromatin condensation and fragmentation, formation of membrane blebs and cell fragments being phagocytize

A

apoptosis

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9
Q

Commonly induced by ATP depletion (ischemia), free radicals, membrane damgae, or CA influx. Will see large amplitude of mitochondrial swelling, membrane defects, lysosomal membrane rupture, nuclear condensation, fragmentation, and dissolution

A

Necrosis (irreversible cell injury)

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10
Q

What are the 2 primary mechanisms in the induction of apoptosis

A

Extrinsic (death receptor initiated pathway)

Intrinsic (mitochondrial pathway)

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11
Q

TNF receptor or Fas receptors binding to ligands to activate initiator caspases or injury

A

extrinsic pathway of apoptosis

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12
Q

Increase in mitochondrial permeability releases pro-apoptotic molecules, like cytochrome c

A

intrinsic pathway of apoptosis

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13
Q

What role does Bcl-2 play in the development of apoptosis?

A

inhibitor at the intrinsic level

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14
Q

What factor released from mitochondria in response to injury induces capase cascade activation

A

cytochrome C

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15
Q

What cell components and/or cell functions are most susceptible to injury that induce necrosis?

A

cell membranes
aerobic respiration
synthetic apparatus (proteins, enzymes)
genetic apparatus

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16
Q

What terminal biochemical and structural processes are nduced by influx of large concentrations of calcium (from ER and cell exterior) into cytosole that occur in necrosis

A

phospholipase- leads to membrane phospholipis and membrane lysis

ATPase- leading to decreased ATP

Protease- leading to disruption of membrane and cytoskeletal proteins

Endonuclease- leading to damage in the nucleus

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17
Q

What are the main sources of free radicals in tissue that contribute to tissue injury?

A

absorption of radiation energy (UV light)
Redox reactions (e.g. FENTON REACITON)
Exposure to toxins such as oxygen, CCl4, drugs

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18
Q

How do free radicals contribute to cell injury and cell death?

A 
Lipid peroxidation of membranes (loss of membrane function, increased permeability)
DNA damage (leads to mutations and death)
Cross linking of proteins
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19
Q

Name 2 important free radical scavengers

A

Vitamin E and Glutathione

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20
Q

Terminates lipid peroxidation and membrane damage

A

Vitamin E

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21
Q

Decrease in cell size due to decrease in demand or lack of nutrients, oxygen, endocrine, or nerve stimulation

A

atrophy

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22
Q

Increase in cell size (substance)

A

hypertrophy

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23
Q

Increase in cell number

A

hyperplasia

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24
Q

Replacement of one adult cell type with another

A

metaplasia

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25
Q

Abnormal calcium deposit in normal tissue secondary to hypercalcemia

A

metastatic calcification

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26
Q

Elevated serum Ca and abnormal Ca metabolism that leads to calcification

A

Metastatic calcification

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27
Q

Hypervitaminosis D and Primary (or secondary) hyperparathyroidism

A

Metastatic calcificaiton

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28
Q

Abnormal calcium deposition in dead or degenerating tissue

A

Dystrophic calcification

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29
Q

Normal serum Ca levels and Ca metabolism that leads to calcification

A

Dystrophic calcification

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30
Q

Vitamin E or selenium deficiency (ex: white muscle disease) and renal infarction calcification

A

Dystrophic calcification

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31
Q

Accumulation of abnormal proteinaceous substances from several protein sources, eosinophilic, and accumulates between cells and has beta pleated sheet conformation

A

amyloidosis

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32
Q

Amyloid composed of immunoglobulin light chains- AL associated with beta cell proliferative diseases

A

Primary amyloidosis

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33
Q

amyloid composed of unique, non-immunogenic protein- SAA (serum amyloid A)

A

Secondary amyloidosis (most common in animals)

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34
Q

Islet amyloid in cats- islet amyloid polypeptide (IAPP)

A

Endocrine amyloidosis

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35
Q

Formation of senile plaques-APP (amyloid precursor protein)

A

Beta-amyloid amyloidosis

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36
Q

Brief mechanism that is responsible for chronic inflammatory reactions leading to the deposition of amyloid in tissues

A

chronic inflammation–>macrophage activation, interleukins 1 and 6 and TNF–>liver cells produce SAA–>SAA undergoes limited proteolysis–>AA protein

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37
Q

How does amyloid contribute to tissue dysfunction in renal amyloidosis

A

results in protein-losing nephropathy

marked increase in permeability of serum protein

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38
Q

How could you distinguish necrosis of skeletal muscle from autolysis in a cow during the gross examination of a necropsy

A

Both would cause tissue to be bale and diffuse changes..

Autolysis- there would be no tissue response (i.e. inflammation) and in necrosis there would be an inflammatory response

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39
Q 
Which of the following changes are seen in reversible cell injury?
A. Mitochondrial swelling
B. Swelling of ER
C. Pyknosis and karyorrhexis
D. A and B
E. A,B, C
A

D

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40
Q

Condensation of nucleus

A

Pyknosis

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41
Q

Nuclear condensation and fragmentation

A

Karyorrhexis

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42
Q

Chromatin disappearing

A

chromatolysis

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43
Q

Which are defining characteristics of necrotic cells?
A. Lipid accumulation in cyto B. Swelling of ER
C. Pyknosis and karyorrhexis
D. Nuclear chromatolysis
E. C and D

A

E

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44
Q

Which of the following mechanisms contributes most to cell death in hypoxic tissue injury?
A. ATP depletion
B. Free radical injury
C. DNA damage
D. Protein misfolding, E. Membrane damage.

A

A

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45
Q

Ischemia reperfusion injury is characterized by which of the following mechanisms of injury?
A. ATP depletion
B free radical injury
C. protein misfolding and apoptosis

A

A and B

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46
Q

Causes brown discoloration in tissue and brown, granular pigment in H and E stain

A

lipofuscin

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47
Q

What causes lipofusin reaction?

A

Lipid peroxidation reactions (free radical damage), increased with vitamin E deficiency

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48
Q

What stain is ideal for lipofuscin?

A

acid fast

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49
Q

Pigment that is derived from hemoglobin when RBC’s are phagocytized an degraded intraceullarly

A

Hemosiderin

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50
Q

Grossly looks reddened, but microscopically is a golden-brown pigment that is intracytoplasmic

A

hemosiderin

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51
Q

What stain is best for hemosiderin?

A

Prussian blue

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52
Q

Can form in increased heme breakdown, decreased hepatic uptake, impaired conjugation, impaired intra-hepatic excretion, bile duct obstruction

A

bilirubin

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53
Q

Seen grossly as very yellow tinged

A

bilirubin

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54
Q

Calcification in a renal infarct is most likely do for?

a. Dystrophic
b. Metastatic

A

dystrophic

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55
Q

Which of the following are mechanisms of metatstatic calcification?

a. CCL4 toxicity
b. Primary parathyroid tumor
c. Hypervitaminosis D
d. A, B, and C
e. B and C

A

E

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56
Q

Vitamin E deficiency and lipid peroxidation contributes to formation of which pigment?

a. Hemosiderin
b. Lipofuscin
c. Bilirubin
d. Melanin
e. Hematoidin

A

B

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57
Q

Which of the following pigments can result in brown pigmentation of organs and cytoplasm

a. Melanin
b. Hemosiderin
c. Lipofuscin
d. Bilirubin
e. A,B,C

A

E

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58
Q

The most common form of amyloidosis in animals is derived from?

a) Immunoglobulin- Primary
b) Serum amyloid A protein- secondary
c) Islet amyloid polypeptide
d) Apolipoprotein
e) Amyloid precursor protein

A

B

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59
Q

The form of amyloid associated with diabetes mellitus in cats:

a) Immunoglobulin- Primary
b) Serum amyloid A protein
c) Endocrine amyloid-islet amyloid polypeptide
d) Apolipoprotein
e) B amyloid

A

C

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60
Q

Which of the following mechanism most likely explains edema fluid with high protein content

a) increased hydrostatic pressure
b) Increased vascular permeability
c) Decreased oncotic pressure
d) Lymphatic obstruction
e) Sodium retention in renal disease

A

B

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61
Q

Accumulation of abnormal amounts of fluid in the intercellular and extracellular tissue spaces or body cavities

A

Edema

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62
Q

What has occurred with tissue that is swollen, and oozes clear or blood-tinged fluid when cut?

A

Edema

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63
Q

Seen microscopically as interstitial spaces enlarged, often with eosinophilic granular residue of protein in the edema fluid

A

edema

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64
Q

WHAT ARE THE MAJOR PATHOGENIC MECHANISMS THAT CONTRIBUTE TO EDEMA FORMATION

A

a. Increased hydrostatic pressure (increased BP in a capillary bed)
b. Increased vascular permeability (e.g. inflammation)
c. Decreased oncotic pressure (hypoalbuminemia)
d. Lymphatic obstruction
e. Sodium retention in renal disease

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65
Q

What are the basic pathogenetic mechanisms responsible for hemorrhage?

A
  1. Trauma and other injury
  2. Diapedesis (blood passing between endothelial cells at cell junctions)
  3. Hemorrhagic diathesis (diseases of bleeding)
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66
Q

What factors determine the path. significance of hemorrhage?

A

location
rate
volume

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67
Q

How does edema contribute to diminished tissue function?

A

causes fluid compression of adjacent structures
Creates diffusion/transportation barrier
Alters mechanical properties of tissue
Alter cell function in in interstitium

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68
Q

How does hemorrhage contribute to diminished tissue function?

A

i. Due to hypovolemia and anemia, you can get hypoxemia, can cause poor tissue perfusion locally, can become space occupying and compressive

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69
Q

Formation of fibrin clot

A

coagulation

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70
Q

process of resulting in the termination of hemorrhage

A

hemostasis

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71
Q

process of intravascular (or intracardiac) formation of a clot of fibrin and platelets during life

A

thrombosis

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72
Q

What role doe coagulation play in hemostasis and thrombosis?

A

helps stop hemorrhage (hemostasis)

Coagulation in non-hemorrhagic vessels will lead to a formation of thrombus

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73
Q

Which of the following mechanism most likely explains edema fluid with high protein content?

a) increased hydrostatic pressure
b) Increased vascular permeability
c) Decreased oncotic pressure
d) Lymphatic obstruction
e) Sodium retention in renal disease

A

B. Increased vascular permeability

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74
Q

What processes lead to activation of the intrinsic pathway for coagulation?

A

Activation of Hageman Factor (XII)

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75
Q

What processes lead to activation of the extrinsic pathway for coagulation?

A

release of thromboplastin (factor III) it is a membrane associated protein of lipoprotein

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76
Q

Are the two pathways (intrinsic and extrinsic) for coagulation ever activated simultaneously?

A

YES

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77
Q

What is Virchow’s triad? 


A

Alteration in vessel wall
Changes in blood flow
Changes in the blood that promotes thrombosis (HYPERcoagulation)

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78
Q

What is the role of platelets in coagulation and hemostasis?

A

Forms a platelet plug at the site of vessel injury, enhancing coagulation

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79
Q

What are the three main platelet functions involved in hemostasis?

A

adhesion
Platelet release action
Platelet aggregation

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80
Q

How do endothelial cells promote coagulation and thrombosis? 


A

release of thromboplastin and expose collagen when injured

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81
Q

How do endothelial cells inhibit coagulation and thrombosis? 


A

Synthesis and release of: Prostacyclin (PGl2), plasminogen activator, and NO
Binds to thrombin and thrombomodulin which activates protein C (has anticoag properties)

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82
Q

Thrombosis centrally involves coagulation, platelet aggregation and….

a) High blood flow
b) Increased vascular permeability
c) Increased hydrostatic pressure
d) Vessel wall
e) Lymphatic obstruction

A

D. Vessel wall

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83
Q

A thrombus carried from its site of vascular origin to a more distant vessel is a:

a) Thrombus
b) Embolus
c) Blood clot
d) Hematoma
e) Thromboembolus

A

B and E

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84
Q

Vessel wall damage can initiate coagulation via:

a) Collagen exposure and Hageman factor activation
b) Endothelial cell release of tissue factor (III)
c) Release of plasminogen activator
d) A and B
e) A,B,C

A

D

SN: plasminogen breaks down fibrin clot

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85
Q

Endothelial cells inhibit thrombosis by:

a) Thromboxane A2 production
b) Prostacyclin production
c) Bind inhibitors of thrombin
d) A, B, C
e) B, C

A

E

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86
Q

Damaged endothelial cells release the following to promote thrombosis

a) Tissue factor (III)
b) Antithrombin III
c) Von Willebran’s factor
d) A, B, C
e) A, C

A

E

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87
Q

What types of abnormalities might lead to a hypercoagulable state?

A
  1. decrease in anti-coag factors: protein C and S, or antithrombin
  2. Elevation in clotting factors like fibrogen, prothrombin, factors VII, VIII, and X
  3. in dieeminated neoplasia, extensive release of factor III
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88
Q

Protein C, S, and antithrombin III are

A

anti-coag factors

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89
Q

Fibrogen, prothrombin, and factors VII, VIII, and X promote?

A

clotting

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90
Q

Breaking down of a thrombus

A

fibrinolysis

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91
Q

What steps are needed for fibrinolysis to initiate?

A 
Factor XII (Hageman) activated plokallikrein-->kallikrein which helps plasminogen form plasmin 
Also, tissue plasminogen activator activates plasminogen-->plasmin

Plasmin then goes on to form fibrin split products

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92
Q

Which 3 major events are important in the pathogenesis of thrombosis?

A

Virchow’s triad

i. Alterations in vessel wall
ii. Changes in blood flow (stasis and turbulence)
iii. Changes in blood promoting thrombosis (hypercoagulability)

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93
Q

Firm, friable

Occlude vessel and often red, attached to wall

Often completely occlude vessel

Large thrombi can be laminated (Lines of Zahn)

A

Venous thrombus

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94
Q

iFirm, friable, and partially occlusive

Often attached to wall, grey to red

May be grossly laminated (Lines of Zahn)

A

arterial thrombus

95
Q

Seen microscopically as Laminated bands of eosinophilic fibrin and RBCs, interspersed necrotic leukocytes

A

thrombus (arterial)

96
Q

Rubbery consistency

Not attached to vessel wall

Red or yellow

A

postmortem blood clots

97
Q

Seen microscopically as fibrin and RBCs are NOT laminated due to lack of flow
and Do NOT contain necrotic leukocytes

A

postmortem blood clot

98
Q

What are the potential sequelae to thrombosis in a vein versus an artery? 


A

a. In vein: build up of hydrostatic pressure to the capillaries (proximally) will lead to edema, leads to a red (hemorrhagic) infarction
b. In artery, ischemia/infarction, leads to a white or

99
Q

What factors influence the development of an infarct? 


A

-Organ collateral blood supply (lung vs. kidney, lung has dual blood supply so usually does not become infarcted)
-Rate and severity of occlusion
-Vulnerability of tissue to hypoxia
-Oxygen carrying capacity
(Anemia- more likely to infarction formation)

100
Q

Localized area of ischemic necrosis resulting from occlusion of the arterial or venous supply

A

infarction

101
Q

What are the likely sequelae of thrombosis of a branch of a coronary artery versus thrombosis of a branch of the hepatic artery? 


A

a. Coronary artery infarction likely to occur because of single blood supply and extreme sensitivity to hypoxemia, resulting in death
b. Hepatic artery: likely t occur, but not as severe because of dul blood supply. Some necrosis may occur due to decreased oxygen to the liver

102
Q

Clinopathetic entity characterized by widespread thrombosis of microvascular beds with concurrent fibrinolysis and consumptive coagulation factors. It can terminate with widespread hemorrhage due to consumptive coagulopathy.

A

DIC (Disseminated Intravacular Coagulation)

103
Q

2 mechanism of how DIC can develop

A

i. Massive release of factor III (tissue thromboplastin or thromboplastic substances) in circulation (e.g. burns, sepsis, trauma, neoplasia)
ii. Widespread microvacular damage (gram negative septicemia, other fisseminated infection)
iii. Other cause could be this: Abnormal Clotting/platelets (e.g. liver disease, kidney disease)

104
Q

Features that characterize a large venous thrombus and allow differentiation from a postmortem blood clot include:

a) Dark red color
b) Contains cross-linked fibrin
c) Attach to vessel wall
d) Firm and friable
e) Soft and elastic
f) A,B,C,D
g) C,D
h) B,E

A

G, attach to vessel wall and firm and friable

105
Q

Thrombosis of which vessel is most likely to lead to severe edema in the tissue of the supplied or drained microvascular bed?

106
Q

Which of the following activate plasminogen to plasmin

a) Tissue plasminogen activator
b) Streptokinase
c) Kallikrein
d) A, B
e) A,B, C

A

All of them

107
Q

Which of the following tissues are resistant to infarction because they have dual blood supply

a) Cerebral cortex
b) Liver
c) Lung
d) A,B, C
e) B,C

A

E. liver and lung

108
Q 
Plasmin is activated by all the following except:
Tissue plasminogen activator 
Streptokinase 
Cytochrome c
Kallikrein
A

Cytochrome c

109
Q 
Which of the following is a potent inhibitor of apoptosis?
p53
BCL-2 
Cytochrome c 
Granzyme B
Ferrous iron
110
Q 
Hageman factor (XII) activation leads directly to the activation of which of the following:
Instrinsic coag cascade or extrinsic coag cascase
111
Q 
The most common protein precursor of amyloid in animals is:
interleukin-1
serum amyloid A
Beta2-microglobulin 
Immunoglobulin light chains 
calcitonin gene related peptide
112
Q 
Damage to endothelial cells releases which of the following to initiate the extrinsic coagulation system?
Prothrombin (II)
Platelet factor 3 
Thromboplastin (III)
Hageman factor (XII)
Stuart-Prower factor (X)
A

thromboplastin (III)

113
Q 
All of the following are components of Virchow's triad except:
Changes in vessel wall 
Changes in platelets
Changes in blood flow
Changes in blood (hypercoagulability)
A

Changes in platelets

114
Q 
Which of the following interacts with hydrogen peroxide to produce hydroxyl radical (OH)?
oxygen 
vitamin E
Hemosiderin 
Cytochrom c
Ferrous iron (Fe++)
A

Ferrous iron

115
Q 
The tissue pigment derived from the breakdown of red blood cells by macrophages: 
Hemosiderin 
Lipofuscin
Melanin
Hematin 
Calcification
A

Hemosiderin

116
Q 
The finding of any one of the following cellular changes indicates cell necrosis EXCEPT:
karyorrhexia 
chromatolysis 
nuclear pyknosis 
defects in plasma membranes 
swelling of the golgi apparatus
A

swelling of the golgi apparatus

117
Q 
Thrombosis in large arteries supplying distal extremeties (feet, ear, pinna) commonly lead to which of the following patterns in necrosis?
Gangrenous 
liquifactive 
coagulation
caseous 
fat
A

gangrenous

118
Q 
Which of the following inducers of cell death resulting in apoptosis mediates the process via intrinsic mitochondrial pathway?
TNF alpha 
cytotoxic T cells 
FAS ligand 
Growth factor withdrawal
A

Growth factor withdrawal

119
Q 
All of the following tissues are resistant to infarction because they have a dual blood supply except:
liver 
myocardium 
lung 
lung and liver
A

myocardium

120
Q 
Vitamin E deficiency leads to accumulation of which of the following in lysosomes?
Hemosiderin
Lipofuscim 
Bilirubin
Amyloid
Melanin
121
Q

Which of the following events or diseases leads to dystrophic calcification in tissues?
A.Chronic renal disease and uremia
B. Adenocarcinoma of the apocrine glands of the anal sac
C.Repeated injection in the jugular vein and chronic inflammation
D. A and C
E. A and B

A

C. Repeated injections

122
Q 
All of the following changes indicate cell necrosis EXCEPT: 
karyorrhexis 
chromatolysis 
nuclear pyknosis 
defects in plasma membranes 
swelling of the ER
A

Swelling of the ER

123
Q 
Which of the following are sources of free radicals in cells and tissues?
Respiratory chain enzymes and oxygen 
Cytochrome P450 monoxygenase 
NADPH oxidase 
High oxygen exposure 
All of the above
A

all of the above

124
Q

Endothelial cells inhibit thrombosis by:
A. Producing prostacyclin (PGl2)
B.Covering subendothelial collagen
C. Bind factors such as antithrombin III and thrombomodulin which contribute to anticoagulant activity
D. A and B
E. A, B, and C

A

all of the them

125
Q

Endothelial cells inhibit/reverse thrombosis at least in part by:

  1. inhibition of platelet aggregation via prostacyclin production
  2. inhibition of platelet aggregation via thromboxane A2 production
  3. Binds thrombin and thrombomodulin
  4. Release of thrombolastin
  5. Release of plasminogen activator

Choose the correct statements

A

1, 3, 5

  1. inhibition of platelet aggregation via prostacyclin production
  2. Binds thrombin and thrombomodulin
  3. Release of plasminogen activator
126
Q 
Sequelae to thrombosis include:
Propagation
Infarction
Recanalization 
Fibrinolysis 
Or all of the above
A

all of the above

127
Q 
The most common protein precursor of amyloid in animals seen in vet med is:
Interleukin-1 
Serum amyloid A (SAA or amyloid AA)
Beta 2 microglobulin 
Immunoglobulin light chains 
Calcitonin gene related peptide
A

Serum amyloid A

128
Q 
Release of which of the following molecules from mitochondria into cytosol is associated with activation of apoptosis?
p53 
ATP
Bcl-2 
Perforin 
cytochrome c
A

cytochrome c

129
Q 
Thrombosis in lage arteries supplying distal extremities (feet, ear, pinna) commonly leads to which of the following patterns of necrosis?
gangrenous 
Liquefactive 
coagulation 
caseous 
fat
A

gangrenous

130
Q 
Which tissues are highly susceptible to infarction because they lack a dual blood supply?
A. liver 
B.lung 
C.kidney 
D. A and B
E. B and C
131
Q 
A localized area of ischemic necrosis in tissue resulting from occlusion of the arterial or venous supply defines which of the following definitions?
Blood clot 
thrombus 
embolus 
infarct 
apoptosis
132
Q 
Damage to endothelial cells releases which of the following to initiate the extrinsic coagulation system?
Prothrombin (II)
Platelet factor 3
Thromboplastin (III)
Hageman factor (XII)
Stuart-power factor (X)
A

Thromboplastin (III)

Remember hageman is intrinsic

133
Q 
All of the following are components of Virchow's triad except:
Changes in vessel wall
Changes in platelets 
Changes in blood flow 
Changes in blood (hypercoagulability)
A

changes in platelets

134
Q

Amyloid has all of the following characteristics except:
Stains with Lugol’s iodine solution in gross specimens
Has alpha-helix structure
Stains with Congo red in histo tissue sections
Deposits in tissue are homogeneously eosinophilic
Can be derived from multiple precursor molecules

A

Does not have a alpha helix structure, it is beta

135
Q 
The mechanism of generalized body edema that occurs in dogs with long standing renal amyloidosis is:
Increased hydrostatic pressure 
Increased vascular permeability 
Decreased oncotic pressure 
lymphatic obstruction
Sodium retention
A

Decreased oncotic pressure

136
Q 
Which of the following interacts with hydrogen peroxide to produce hydroxyl radical (OH)?
Oxygen 
Vitamin E
Hemosiderin
Cytochrome C
Ferrous iron (Fe++)
A

Ferrous iron

137
Q 
The tissue pigment derived from breakdown of red blood cells by macrophages:
hemosiderin 
lipofuscin 
melanin
hematin
calcification
A

hemsiderin

138
Q 
Features that characterize a large venous thrombus and that are not found in a postmortem blood clots include: 
A. dark red color
B. attached to the vessel wall 
C. firm and friable 
D. soft and elastic 
E. B and C
139
Q 
Which of the following activate plasminogen to plasmin?
A. Tissue plasminogen activator
B. Streptokinase 
C. Kallikrein
D. A, B 
E. A, B, C
140
Q 
Inflammatory responses rarely, if ever, occur in response to:
A. Apoptosis 
B. Bacterial infection
C. Necrosis 
D. A and B
E. A and C
141
Q 
Ischemia reperfusion injury is characterized by which of the following?
A. ATP depletion 
B. Free radical injury 
C. Protein misfolding and apoptosis 
D. A and B
E. A, B, C
A

A and B (ATP and free radical)

142
Q 
Which of the following are mechanisms of metastatic calcification?
A. Carbon tetrachloride liver damage
B. Primary parathyroid adenoma 
C. Hypervitaminosis E
D. A, B, and C
E. B, C
A

Primary parathyroid tumor

note it is hypervitaminosis D not E

143
Q

The lines of Zahn refer to:

A

lines formed in large thrombi by interlaced bands of fibrin and platelets and blood while blood is flowing

144
Q

All of the following events commonly occur in the pathogenesis of secondary amyloidosis EXCEPT:
A.chronic inflammation
B. IL-1 and TNF alpha cytokine production by epithelial cells
C. SAA production by hepatocyte
D. Partial proteolytic cleavage of SAA to form amyloid in tissue
E. cytokine simulation of hepatocytic production of serum amyloid-associated (SAA) protein

A

B (not that it is IL 1, IL 6, and TNF but it is released by macrophages)

145
Q

Amyloid has all of the following characteristics EXCEPT:
Stains with Lugol’s iodine solution in gross specimens
Has beta pleated sheet structure
Stains with Prussian blue in histologic tissue sections
Deposits in tissue are homogeneously eosinophilic
Is derived from multiple precursor molecules

A

Stains with Prussian blue in histologic tissue sections

stains with congo red

146
Q 
Replacement of one cell type by another cell type as an adaptive response is?
atrophy 
hypertrophy
hyperplasnia
hypoplasia
metaplasia
A

metaplasia

147
Q 
All of the following types of cell injuries are likely to lead to cell necrosis EXCEPT those leading to:
ATP depletion
Membrane damage
Lipid accumulation
Free radical formation
Ca influx into cells
A

lipid accumulation

148
Q 
Which of the following pathogenetic mechanisms is most important in the edema that occurs in acute fibrinous pneumonia in cattle?
Increased hydrostatic pressure 
increased vascular permeability 
decreased oncotic pressure 
lymphatic obstruction
sodium retention
A

increased vasc. perm.

149
Q 
Calcium deposition that occurs in jugular vein walls after repeated venapuncture is an example of:
Ischemic necrosis 
liquefactive necrosis 
metastatic calcification 
dystrophic calcification
venous fibroelastosis and necrosis
A

dystrophic calcification

150
Q

All of the following pathologic response are more likely to occur following thrombosis of a vein as compared to a thrombosis in an artery EXCEPT:

  • hemorrhagic infarction
  • increased capillary hydrostatic pressure in the proximal vascular bed
  • Pale (white) infarct
A

pale (white) infarct

151
Q 
Lipofuscin is characterized by all of the following except: 
Brown pigment in cells 
Product of lipid peroxidation
Stains with prussian blue stain 
stains with acid fast stain
A

Stains with prussian blue stain

152
Q 
The mechanism of generalized body edema that occurs in dogs with long standing renal amyloidosis is: 
Increased hydrostatic pressure 
Increased vascular perm
Decreased oncotic pressure 
lymphatic obstruction
Sodium retention
A

decreased oncotic pressure (amyloidosis causes protein losing nephropathy)

153
Q

Endothelial cells inhibit or counter act thrombosis by all of the following mechanisms except:
Synthesize prostacyclin (PGl2)
Synthesize tissue plasminogen activator
Inhibit nitric oxide
Cover subsendothelial collagen
Bind antithrombin III to inhibit thrombin

A

Inhibit nitric oxide (it releases it)

154
Q 
Which of the following is found in histologic sections of thrombi, but not post mortem clots? 
A. Lamination
B. Necrotic leukocytes
C. Fibrin 
D. Erythrocytes 
E. A and B
A

E. lamination and necrotic leuks

155
Q 
All of the following are mechanisms of icterus EXCEPT: 
Decreased heme breakdown
decreased hepatic uptake of bili
Impaired bili conjugation
impaired bili excretion from hepatocytes
bile duct obstruction
A

decreased heme breakdown

156
Q

All of the following are causes of metastatic calcification EXCEPT:
Hypervitaminosis D
Hypovitaminosis E
Primary hyperparathyroidsim
Secondary nutritional hyperparathyroidism
Secondary renal hyperparathroidism

A

hypovitaminosis E (does not have anything with vitamin E)

157
Q 
Which tissue(s) is/are highly susceptible to infarction because it/they lack(s) a dual blood supply?
A.liver 
B.Cerebral cortex 
C. myocardium 
D. A,B
E. B,C
A

E. B and C

158
Q 
Which of the following is a physical mass carried from its site of origin in the vessel wall to a more distant site?
Thrombus 
Metastasis 
Infarct 
Embolus 
Blood clot
159
Q 
Injury to vascular endothelium with exposure of subendothelial cartilage leads to activation of the intrinsic coagulation cascade through activation of?
A. Hageman factor (XII)
B. Antithrombin III
C. Tissue factor (Thromboplastin, III)
D. A, B 
E. A, B, C
A

Hageman factor (XII)

160
Q 
Thrombosis in large arteries supplying distal extremities (feet, ear, pinna) commonly leads to which of the following patterns of necrosis?
Gangrenous 
coagulation
caseous 
fat
A

gangrenous

161
Q

All of the following are components of Virchow’s triad except?
Alterations in leukocyte migration through the vessel wall
Alterations in the vessel wall (endothelial damage)
Change in blood that promote hypercoagulability
Changes in blood flow

A

Alterations in leukocyte migration through the vessel wall

162
Q

Epithelial neoplasmas of the limb frequently lead to edema of the affected limb via the mechanism of?
Increased hydrostatic pressure
Increased vascular permeability
Decreased oncotic pressure
Lymphatic obstruction
Increased sodium retention in renal disease

A

increased hydro pressure

163
Q 
Which of the following changes is/are indicative of irreversible cell injury?
A. Pyknosis
B. Karyorrhexis
C. Apoptotic bodies 
D. A, B
E. A,B,C
A

A, B, and C

164
Q 
Which of the following contribute to formation of free radicals that initiate cell injury?
A. UV radiation
B. Carbon tetrachloride
C. Fenton reaction 
D. A, B
E. A, B, C
165
Q 
The most important mechanism contributing to cell death in infarction is?
Membrane damage
Protein misfolding 
Free radical injury
ATP depletion
DNA damage
A

ATP depletion

166
Q 
The most common form of amyloidosis in animals seen in veterinary practice is derived from?
Immununoglobulin
Amyloid precursor protein
Islet amyloid polypeptide
Apolipoprotein
Serum amyloid A protein
A

Serum amyloid A protein

167
Q 
Which of the following events commonly lead(s) to metastatic calcification?
A. hypovitaminosis D
B. Primary thyroid tumor 
C. Chronic renal disease
D. A, B
E. A, C
A

C. Chronic renal disease (note it is hypervitaminosis D and it is parathyroid tumor)

168
Q 
Endothelial cells inhibit thrombosis by?
A. Releasing thromboplastin 
B. Producing thromboxane A2
C. Producing prostacyclin
D. A, B
E. A, B, C
A

C. prostacyclin (others are plasminogen activator, NO, and thrombomodulin)

169
Q 
Postmortem venous blood cells are all of the following except?
A. Red
B. Firm and friable 
C. Attached to cell wall
D. A,B,C
E. B,C
170
Q 
All of the following are features of disseminated intravascular coagulation EXCEPT?
Multiorgan thrombosis 
Consumption of coag factors 
Terminal bleeding tendency
Decreased D diners 
Hypofibrinogenemia
A

decreased d dimers

171
Q 
Thrombosis of which of the following large caliber vessels is most likely to lead to ascites (hypoperitoneum)
Hepatic artery 
Portal vein
Renal artery
Renal vein
Colic artery
A

portal vein

172
Q 
Which causative agents often induce caseous necrosis as part of their pathogenesis?
A. Mycobacterium bovis
B. Fuscobacterium necrophorum
C. Salmonella typhimurium 
D. A and B
E. A, B, C
A

D. (Mycobacterium
bovis, M. avium, M. tuberculosis, as well as Corynebacterium ovis, Fusobacterium necrophorum and other chronic bacterial diseases. )

173
Q

What stain is used for lipofuscin?

174
Q

What stain is used for hemosiderin?

A

Prussian blue

175
Q

What stain is used for amyloid?

176
Q

What stain is used for melanin?

A

Fontana mason

177
Q

What stain is used for calcium?

178
Q 
An increase in cell size in tissue in response to injury is:
Atrophy
Hypertrophy
Hyperplasia 
Metaplasia 
Apoptosis
A

Hypertrophy

179
Q 
Which of the following are sources of or result in free radicals in cells and tissues?
A. Respiratory chain enzymes and oxygen 
B. Cytochrome P450 monoxygenase 
C. Carbon tetrachloride toxicity
D. A and B 
E. A, B, C
180
Q 
Replacement of one adult cell type with another cell type in tissue in response to injury is:
Atrophy 
Hypertrophy 
Hyperplasia 
Metaplasia
Apoptosis
A

Metaplasia

181
Q 
An increase in cell number in tissue response to injury is: 
Atrophy 
hypertrophy 
hyperplasia 
metaplasia
Apoptosis
A

Hyperplasia

182
Q

Which of the following are common sequelae of chronic thrombosis of the jugular vein?

  1. Macrophage and endothelial infiltration with recanalization
  2. partial fibrolysis
  3. pulmonary thromboembolism
  4. Metastatic calcification of the vein
  5. Dystrohphic calcification of the vein
A

1, 2, 3, 5

183
Q 
Free radicals contribute to cell injury and cell death by inducing:
A. Lipid peroxidation of membranes 
B. DNA damage
C. Cross linked proteins 
D. A and B
E. A, B, C
A

e. all of them

184
Q

Wndothelial cells inhibit/reverse thrombosis at least in part by:

  1. inhibition of platelet aggregation via prostacyclin production
  2. inhibition of platelet aggregation via thromboxane A2 production
  3. Binds thrombin and thrombodulin
  4. Release of thromboplastin
  5. Release of plasminogen factor
185
Q

An arterial thrombus usually has the following features that differentiate it from a postmortem clot:

  1. attach to vessel wall
  2. firm and friable
  3. rubber consistency
  4. laminated
  5. may be associated with pale (white) infarct
186
Q

Which of the following pathologic responses is more likely to occur following a thrombosis in a vein compared to a thrombosis in the artery?
A. hemorrhagic infarction
B. Increased capillary hydrostatic pressure in the proximal vascular bed
C. Septic infarction
D. A and B
E. A, B, C

A

D. A and B

187
Q 
Which of the following morphological changes in cells is most consistent with necrosis?
Nuclear pyknosis 
Mito swelling 
Cyctoplasmic eosinophilia
Cytoplasmic vascuolization
Apoptotic body phagocytosis
A

Nuclear pyknosis

188
Q 
Which of the following is responsible for directly mediating fibrin breakdown in fibrinolysis?
Hageman factor
Kallikrein
Complement factor 5 
Plasmin 
Thrombin
189
Q 
Which of the following morphological changes in cells is most consistent with necrosis?
Nuclear pyknosis 
Mito swelling 
Loss of microvilli 
Cytoplasmic vascuolization
ER swelling
A

nuclear pyknosis

190
Q 
Nuclear fragmentation occurs without cytoplasmic swelling in:
Apopotosis 
necrosis 
Lipidosis 
Cell generation 
None of the above
191
Q 
Pigment forming in lysosomes as a breakdown product of lipid membranes and lipid peroxidation:
Hemosiderin 
Lipofuscin 
Bilirubin 
Anthracosis
Melanosis
A

Lipofuscin

192
Q 
Pigment formed in lysosomes from red blood cell breakdown and iron complexes:
Hemosiderin 
Lipofuscin 
Bilirubin 
Anthracosis
Melanosis
A

hemosiderin

193
Q

The most common form of amyloidosis in animals is derived from?

a) Immunoglobulin- Primary
b) Serum amyloid A protein- secondary
c) Islet amyloid polypeptide
d) Apolipoprotein
e) Amyloid precursor protein

194
Q 
Free radicals contribute to cell injury and cell death by inducing:
A. Lipid peroxidation of membranes 
B. DNA damage
C. Cross linked proteins 
D. A and B
E. A, B, C
A

all of them

195
Q

The most common outcome of renal glomerular amyloidosis is:
A. Ischemic injury and infarction
B. Ischemic injury and tubular epithelial necrosis
C. Proteinuria and hypoalbuminemia
D. A and C
E. None of them

196
Q

Endothelial cells inhibit/reverse thrombosis at least in part by:

  1. inhibition of platelet aggregation via prostacyclin production
  2. inhibition of platelet aggregation via thromboxane A2 production
  3. Binds thrombin and thrombomodulin
  4. Release of thrombolastin
  5. Release of plasminogen activator
197
Q

Venous thrombus has the following features that differentiate it from a postmortem clot:

  1. attach to vessel wall
  2. firm and friable
  3. Rubbery consistency
  4. red
  5. Occude the lumen
A

1, 2,

Both are red, both occlude lumen

198
Q 
1. An increase in cell number associated with an increase in organ size is? 
A. Hypertrophy
B. Atrophy
C. Hypoplasia
D. Metaplasia 
E. Hyperplasia
A

E (CELL NUMBER), size is hypertrophy

199
Q

In the first lab, we saw vacuolated areas in the cytoplasm of hepatocytes in a case of coagulative necrosis. What is in this vacuolated area?

200
Q

How does lipid form in coagulative necrosis?

A

Damage to the ER decreases protein synthesis

201
Q

What evidence of hepatocellular necrosis could have been detected prior to death in the mouse with liver coagulative necrosis?

A

Elevated serum alanine aminotransferase that leaked from the necrotic hepatocytes into serum

202
Q

How might evidence of renal tubular necrosis have been obtained antemortem in the dog with a renal infarct in lab?

A

urinary sediment contains cellular casts

203
Q

How can you differentiate between karyorrhectic neuclei and apoptoic bodies?

A

They both have small fragments. However, karyo nuclei fragment in full-sized cells with swollen or hyper-eosinophilic cytoplasm. Apoptotic bodies bud off cells with a thin rim of non swollen cytoplasm and are smaller than the orginal lymphocytes

204
Q

What is a tool you can use to differentiate betwen necrotic and apoptotic cells?

A

Electron microscopy could show that there was no cell swelling (mito and ED) in cytoplasm of apoptotic bodies

205
Q

What mechanisms can account for apoptosis of splenic lymphocytes in this animal? (it was in lab)

A

endotoxin from bacteria, corticosteroid from stress, TNF alpha from endotoxin response all induce lymphocytic apoptosis

206
Q

What does caseous necrosis look grossly?

A

soft, off-white to light tan

207
Q

How does caseous necrosis develop?

A

chronic inflammation attracting macrophages over time leads to coagulation necrosis of cells without removal and continued degradation of cell components until cell boundaries and identifiable structure are lost

208
Q

What causative agents typically produce caseation necrosis?

A

mycobacteria sp., Fusobacterium necrophorum incite inflammatory reactions that induce recruitment of large macrophages and induced necrosis

209
Q

What two general pathogenetic mechanisms account for calcification of tissue?

A

dystrophic (cell injury/death) and metastatic calcification (hypercalcemia)

210
Q

Fat necrosis associated with necrotizing pancreatitis in a dog. Is likely due to dystrophic or metastatic calcification

A

dystrophic

211
Q

What would have been the gross appearance of calcified tissue?

A

white, chalky consistence

212
Q

What pathogenetic mechanisms can lead to hepatic lipidosis?

A 
increased lipid synthesis 
mobilization of peripheral fat with FFA presentation to liver 
Decreased hepatic FA oxidation
Decreased apoprotein synthesis 
Decreased lipoprotein export
213
Q

Which mechanism of hepatic lipodosis is likely the cause in a dairy cow?

A

mobilization of peripheral fat with FFA presentation to liver

214
Q

Why isn’t the lipid stained with either hematoxylin or eosin?

A

extraction of lipid by organic solvents during tissue processing

215
Q

What cell features separate changes in these hepatocytes (lipidosis) from necrosis seen in slide 4 (carbon tetrachloride toxicosis)?

A

no nuclear changes in lipidosis

216
Q

What would a liver with lipidosis have looked like grossly?

A

yellow brown, greasy on cut surface, sections float in acqueous solution

217
Q

Are hepatocellular lesions due to lipidosis reversible?

218
Q

What other pigments in cytoplasm might be confused with hemosiderin, and how could you differentiate between them?

A

lipofuscin (stains with acid fast, autofluoresces)
Bilirubin (stains with bile stains)
Hemosiderin stains with iron stains (prussian blue, Perl’s)

219
Q

What would be the fate of this hemosiderin if the lung had not been removed and the dog had survived?

A

Macrophage are removed from the lung via lymphatics and muscociliary escalator. Some hemo would be retained for moth and years.

220
Q

This is a section of stomach from a 14-year-old dog presented with a history of chronic renal disease for 2 years. It had elevated blood urea nitrogen (BUN) and creatinine in addition to other serum biochemical abnormalities that accompany and characterize chronic uremia. The dog also had ulcers in the oral cavity.
What is likely the mechanism of calcification?

A

metastatic

221
Q

what stain is used on calcium salts

222
Q

What is amyloid protein, and what different types are there?

A

bnormal protein substance of varying sequence deposited in extracellular space in beta-pleated sheet conformation. Types: primary, secondary, endocrine associated, aging and others.

223
Q

Renal amyloidosis in a dog

What type of amyloid is likely to be present in this dog, and what steps might have been important in its development?

A

Secondary from serum amyloid-associated (SAA) protein produced by liver. Chronic inflammation results in chronic or repeated production of IL-1 / IL-6 by macrophages which stimulates hepatocytes to produce SAA. SAA is subjected to partial proteolysis and various tissue sites to form amyloid deposits.

224
Q

What mechanisms associated with glomerular amyloidosis account for protein in renal tubules, and of what significance is this to the long-term health of the dog?

A

Glomerular permeability to serum protein including albumin is increased. Long term protein loss can lead to hypoalbuminemia and generalized edema due to decreased oncotic pressure.

225
Q

What pathogenetic mechanisms can lead to edema?

A

increased hydrostatic pressure, increased permeability, decreased oncotic pressure, lymphatic obstruction, increased sodium retention

226
Q

This cow had an acute fibrinous pneumonia due to a bacterial infection (e.g. - Mannheimia
hemolytica).
You can see some eosinophilic material in the interstitium

Which edematogenic mechanism is likely to be most important in this lung? Why?

A

Increased vascular permeability (protein in edema fluid stains with eosin)

Other edemas would not have this pink staining in the interstitium

227
Q

How would this thrombus have appeared grossly, and how would you differentiate it from a postmortem clot?

A

Thrombi are firm, friable, predominantly red due to trapped red cells and attached to wall of vessel. Postmortem clots are generally diffusely red and gelatinous (Jello-like) as well as not being attached to the vessel wall.

228
Q

What three processes are central to thrombosis?

A

change in vessel wall
change in blood flow
hypercoagulability

229
Q

This foal had severe bacterial enteritis for several days and was receiving repeated intravenous
injections and infusion with fluids.

What two major pathogenetic factors may have contributed to the formation of this thrombus? (Hint: 2 of 3 in Virchow’s triad)

A

Vessel injury, hypercoagulability

230
Q

What are possible sequelae to thrombosis?

A

propagation, fibrinolysis, organization/recanalization, infarction, thromboembolism

231
Q

How might bacterial infection in the intestine induce coagulation and platelet aggregation leading to thrombosis?

A

bacterial endotoxin can damage endothelium and stimulate platelet aggregation. Exotoxins can damage to endothelium releases thromboplastin and exposes collagen stimulating extrinsic and intrinsic coagulation pathways, respectively as well as stimulating platelet aggregation.

232
Q

What processes are likely to be contributing to mucosal necrosis in a case with enteritis and thrombus formation?

A

There may be direct bacterial injury, and the widespread thrombosis may also induce ischemia and infarction

233
Q

This 3-week-old foal had severe bacterial enteritis characterized by diarrhea, dehydration, leukopenia, and fever. It developed bilateral thrombosis of jugular veins and then started bleeding at other injection sites. It also developed melena (passage of black, digested blood in feces).

What pathologic process might be occurring to explain the multiorgan thrombosis and terminal bleeding tendency?

A

disseminated intravascular coagulation (DIC)

234
Q

What lab tests/results might be needed to confirm DIC?

A

Hemogram (thrombocytopenia, hypofibrinogenemia), elevated clotting times, elevated d-dimers

General Pathology (2 decks)

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