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Veterinary General Pathology > Disturbances in circulation pt2 > Flashcards

Disturbances in circulation pt2 Flashcards

1
Q

Activation of the sympathetic nervous system produces (2) to redistribute blood to vital organs

A
  1. peripheral vasoconstriction
  2. tachycardia
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2
Q

Activation of the apneustic and pneumotaxic areas of the brain

A

Stimulation of the respiratory centers in the brain

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3
Q

Stimulation of adrenal gland releases these chemicals

A
  1. Adrenal medulla - catecholamines (epinephrine and norepinephrine)
  2. Adrenal cortex - glucocorticoids
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4
Q

result toconservation of sodium ions and water by increasing kidney tubular
reabsorption

A

Activation of the Renin-Angiotensin-Aldosterone Axis

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5
Q

Counter Regulatory Mechanisms operating at early stages of shock

A
  1. Activation of Sympathetic Nervous System
  2. Stimulation of the respiratory centers in the brain
  3. Stimulation of adrenal gland
  4. Activation of the Renin-Angiotensin-Aldosterone Axis
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6
Q

Hypovolemic Shock

A

includes hemorrhage and traumatic shock; inadequate blood or plasma volume

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7
Q

Cardiogenic Shock

A

shock resulting from myocardial infarction; failure of myocardial pump due to intrinsic myocardial damage

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8
Q

shock associated with toxemia and septicemia, including endotoxemia

A

septic or toxic shock

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9
Q

Neurogenic Shock

A

resulting from severe fright, pain and trauma without hemorrhage

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10
Q

as a result of massive degranulation of mast cells following antigen-antibody interaction

A

anaphylactic shock

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11
Q

Stages of shock

A
  1. Stage of ischemic hypoxia
  2. Stage of stagnant hypoxia
    3.. Stage of irreversibility
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12
Q

(non-progressive phase) where there occurs reflex vasoconstriction in an attempt to maintain blood pressure and
cardiac output

A

stage of ischemic hypoxia

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13
Q

associated with gradual fading of pre-capillary vasoconstriction with pooling of blood in the capillary, a decline in venous return, and diminishing blood pressure

A

stagnant hypoxia

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14
Q

shift of fluid from the intravascular space to the extravascular space and microembolization of capillaries

A

stage of irreversibility

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15
Q

phase that the counter regulatory mechanisms are activated

A

stage of ischemic hypoxia

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16
Q

state of peripheral circulatory failure caused by sudden and severe injury

A

shock

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17
Q

shock is a syndrome of?

A

diminishing blood pressure in the capillary bed

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18
Q

anaerobic glycolysis results in accumulation of this acid which cause acidosis

A

Lactic acid/lactate

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19
Q

True or false.

Decrease in pH (as caused by accumulation of lactate) perpetuates the state of shock.

A

True. As pH decrease, ATP production decrease and extend state of shock.

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19
Q

DIC phase associated with subsequent formation of
thrombin

A

hypercoagulable phase

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20
Q

leads to platelet aggregation and fibrin formation resulting to microthrombosis of vascular capillaries, and infarction in many organs

A

hypercoagulable phase

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21
Q

Clotting factors depleted during hypocoagulable phase

A
  1. fibrinogen
  2. Factor VIII (anti-hemophilic factor)
  3. Factor V (proaccelerin)
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22
Q

associated with the activation of
the fibrinolytic system with consequent release of fibrin and fibrinogen
degradation products that suppresses fibrin polymerization

A

hypocoagulable phase

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23
Q

area of coagulative necrosis caused by ischemia and is due to obstruction of the blood supply following thrombosis or embolism

A

infarct

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24
Q

process of infarct called

A

infarction

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25
Q

cells and tissues most susceptible to infarction

A

▪ brain,
▪ renal tubular epithelia,
▪ heart muscles, and
▪ most parenchymal tissues

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26
Q

resistant to infarction such that the
stromal support of infracted tissues survives while the parenchyma succumb to
infarction

A

fibroblasts

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27
Q

artery ramifies into smaller branches as it ends

A

Functional End-Artery

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28
Q

Functional end artery organs where infarction are commonly seen

A
  1. kidneys
  2. heart muscles
  3. brain
  4. spleen
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29
Q

there are separate blood supply that often has several functional anastomotic channels

A

Parallel system

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30
Q

pulmonary and hepatic infarctions rarely occur but may happen if dual blood supply is compromised, such as in?

A

chronic passive venous congestion

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31
Q

organs that have two separate blood
supply originating from different points (dual blood supply)

A
  1. lungs (pulmonary artery and bronchial artery)
  2. liver (hepatic artery and portal vein)
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32
Q

thrombo-embolic colic in the horse is cause by ___ obstructing the
cranial mesenteric artery

A

Strongylus vulgaris

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33
Q

Thrombotic or embolic occlusion
rarely leads to infarction in organs with parallel system, but happens so when?

A

occlusion occurs at the root of the blood vessel

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34
Q

localized anemia

A

ischemia

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35
Q

ischemia results to infarction if it lodges in organs with so called

A

end arteries

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36
Q

if ischemia is partial or gradual it results to

A

atrophy

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37
Q

oxygenation of blood is normal, but the tissues cannot utilize oxygen due to damage to certain critical cellular respiratory processes such as that seen in cyanide poisoning

A

histotoxic anoxia

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38
Q

caused by low hemoglobin or reduced capacity of blood to carry oxygen as in carbon monoxide poisoning

A

anemic anoxia

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39
Q

result from insufficient oxygenation of blood as may occur in severe pneumonia

A

anoxic anoxia

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40
Q

ischemia due to reduced flow of oxygenated blood as in hypovolemic shock

A

stagnant anoxia

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41
Q

reduction of blood supplies maybe partial called

A

hypoxia

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42
Q

anoxia

A

complete reduction in the oxygen supplied to tissues

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43
Q

reduction in the flow of arterial blood to an organ or tissue result to

A

ischemia

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44
Q

end result of ischemia depend on

A
  1. organ involved
  2. degree of occlusion/anoxia
  3. presence of collateral circulation
  4. size of blood vessels
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45
Q

Causes of ischemia

A
  1. Compression of blood vessels
  2. Obstruction
  3. Functional lesion
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46
Q

stagnant anoxia example

A

hypovolemic shock

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47
Q

anoxic anoxia may occur in

A

severe pneumonia

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48
Q

Anemic Anoxia example

A

carbon monoxide poisoning

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49
Q

histotoxic anoxia example

A

cyanide poisoning

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50
Q

solid mass transported from one part of the body to another through the circulatory system

A

emboli

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51
Q

process of a solid mass being transported from one part of the body to another
through the circulatory system

A

embolism

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52
Q

embolus can be:

A
  1. fragments of thrombi
  2. fat cells
  3. tumor cells
  4. aggregates of bacteria and parasites
  5. bone marrow cells
  6. amniotic cells
  7. foreign bodies
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53
Q

produces emboli of pieces of skin or hair

A

venipuncture

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54
Q

One of the notorious “seeders” of emboli that causes multiple embolisms in the
kidneys

A

bacterial valvular endocarditis

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55
Q

Valvular thrombosis of the left chamber of the heart usually produces emboli in the

A

systemic circulation

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56
Q

valvular thrombosis in the left chamber of the heart cause emboli at the?

A

Systemic circulation

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57
Q

organs with end artery

A

brain, kidneys, spleen and myocardium

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58
Q

detachment of thrombi in the vessel wall can cause

A

emboli

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59
Q

thrombi become larger and larger eventually obstructing the lumen of the blood vessel where they are formed

A

propagation

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60
Q

portions of the thrombi break and
are carried into the circulation

A

fragmentation to form thrombo-emboli

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61
Q

lysis of the thrombi by plasma-derived
fibrinolytic system or through slow phagocytosis by phagocytic cells

A

dissolution by fibrinolysis

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62
Q

invasion and growth of fibrous tissue could happen, along with recanalization and restoration of blood flow

A

fibrous tissue organization

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63
Q

Once thrombi are formed, there are four possible outcomes

A
  1. Propagation
  2. Fragmentation to form thrombo-emboli
  3. Dissolution by fibrinolysis
  4. Fibrous tissue organization
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64
Q

Thrombi are clinically important for two reasons

A

a) they cause obstruction of blood vessels
b) they can be a source of emboli

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65
Q

in cat species, thrombosis at this site cause hind limb paralysis

A

distal aorta

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66
Q

in horse species, thrombosis at this site is usually caused by strongyle infection

A

cranial mesenteric arteries

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67
Q

trailing thrombi with one end attached and
the other freely moving

A

obturating thrombi

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68
Q

straddles the bifurcation of blood vessels

A

saddle thrombi

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69
Q

Canalized thrombi

A

allows partial flow of blood

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70
Q

Occluding thrombi

A

blocks the entire lumen of the blood vessel

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71
Q

Valvular thrombi

A

attached to the valves of the heart

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72
Q

Mural thrombi

A

attached to the endocardial wall of heart

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73
Q

Based on location of thrombi:

A

a. Cardiac thrombi
b. Arterial thrombi
c. Venous thrombi
d. Lymphatic thrombi
e. Capillary thrombi or hyaline thrombi

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74
Q

septic thrombi

A

contains bacteria

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75
Q

aseptic thrombi

A

no pathogenic agent present

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76
Q

parasitic thrombi

A

contains parasites such as filarial worms

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77
Q

red thrombi

A

composed of all blood cell components

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78
Q

pale or white thrombi

A

composed entirely of platelets

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79
Q

layered red and white thrombi

A

laminated or mixed thrombi

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80
Q

pale gray-tan mass consisting of bands of fibrin and platelets mixed with coagulated red blood cells

A

arterial thrombi

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81
Q

when arterial thrombi builds up, head and tail are in what colors?

A

Head - pale
Tail - darker red

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82
Q

During propagation concentric laminations are formed

A

lines of Zahn

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83
Q

they are dark red, moist or gelatinous and are easier to dislodge

A

venous thrombi

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84
Q

resemble intravascular clots of whole blood due to slow blood flow and as influenced by gravity

A

venous thrombi

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85
Q

It is the carbohydrate-rich cell coat present in endothelial lining cells which prevents circulating cells from adhering to the surface

A

glycocalyx

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86
Q

negatively-charged surface of
endothelial lining lead to a mutual electrostatic repulsion between two sets
of negatively charged cells

A

surface negativity theory

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87
Q

prostaglandin that prevent platelet
aggregation by converting platelet aggregation factors into unstable substances

A

Prostacyclin (PG12)

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88
Q

Theories on Non-thrombogenic Vascular Endothelia

A
  1. Glycocalyx theory
  2. Surface negative theory
  3. Surveillance system theory
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89
Q

prostacyclin convert these platelet aggregation factors to unstable forms

A
  1. endoperoxidase
  2. thromboxane A2
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90
Q

hemostasis steps

A
  1. vascular contraction
  2. stasis of blood
  3. endothelial adhesion
  4. blood coagulation
  5. platelet aggregation
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91
Q

formation of ante mortem clot within the blood vessels

A

thrombosis

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92
Q

2 mechanisms of blood coagulation

A
  1. intrinsic clotting mechanism
  2. extrinsic clotting mechanism
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93
Q

intrinsic clotting mechanism

A

involves the components normally present in the plasma

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94
Q

extrinsic clotting mechanism

A

involves tissue component in addition to the components from the blood

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95
Q

two systems of coagulation both activate this factor which lead to fibrin formation

A

(Factor X) stuart-prower factor

96
Q

Diseases that result in marked bleeding tendencies

A

hemorrhagic diathesis

97
Q

indicates former hemorrhage

A
  1. hemosiderin-laden macrophages
  2. erythrophagocytosis
98
Q

clinical term applied to an animal that has extensive petechial and ecchymotic hemorrhages on serous and mucous surfaces

99
Q

usually occur on serosal or mucosal surfaces and are visible but cannot be palpated

A

Petechiae, ecchymosis, paint-brush hemorrhages

100
Q

Metrorrhagia

A

Passage of blood through the uterus

101
Q

Hemothorax

A

Hemorrhage into the thoracic cavity

102
Q

Hemoptysis

A

Coughing out of blood

103
Q

hemoperitoneum

A

Hemorrhage into the peritoneal cavity

104
Q

hemopericardium

A

Hemorrhage into the pericardial sac

105
Q

hematochezia

A

defecation of blood

106
Q

three-dimensional collection of blood coagula

A

hematocyst/hematoma

107
Q

hematocyst/hematoma

A

sufficient red cells come out in one area to form lump

108
Q

hematemesis

A

vomition of blood

109
Q

hemarthrosis

A

hemorrhage into joint spaces

110
Q

extravasation

A

Extensive hemorrhage within the substance of the tissue

111
Q

Nasal bleeding or bleeding from the nostrils

112
Q

entorrhagia

A

passage of blood to alimentary tract (digestive tract)

113
Q

paint brush hemorrhage

A

Linear or streaked appearance of hemorrhage

114
Q

Blotchy or irregular areas of hemorrhage up to 3 centimeters in diameter

A

ecchymosis

115
Q

Minute, pin-point foci of hemorrhage up to 2 millimeter in diameter

116
Q

critical sites of hemorrhage

A

brain and heart

117
Q

effect of hemorrhage depend on

A
  1. location of hemorrhage
  2. volume of blood lost
  3. rate of blood lost
118
Q

blood escapes from the vasculature

A

hemorrhage

119
Q

implies rupture of a blood vessel

120
Q

hemorrhage by diapedesis

A

passive process where blood
escapes from minute pores of the vascular endothelia as observed in events of hyperemia of inflammation

121
Q

causes of hemorrhagic diathesis

A
  1. Liver disease
  2. Deficiencies in blood coagulation factors
122
Q

deficiency of this vitamin cause deficiency of prothrombin

123
Q

condition in dogs where deficiency of platelets caused by infectious agents

A

canine ehrlichiosis

124
Q

thrombocytopenia

A

deficiency of platelets

125
Q

hemorrhagic diathesis can be seen in hereditary anomaly such as in?

A

congenital hemophilia

126
Q

classification of pathological hyperemia

A
  1. Duration of hyperemia (acute or chronic)
  2. Extent of hyperemia (general or local)
  3. The underlying mechanism (active or passive)
127
Q

occurs as a manifestation of some alterations in blood flow characteristics

A

pathological hyperemia

128
Q

True or false

Pathological hyperemia is a result of some underlying pathological process, not a cause of alteration.

129
Q

Hyperemia can be observed in?

A
  1. Inflammation
  2. Cardiac failure
  3. Obstructive venous disease
130
Q

due to engorgement of the vascular bed following an increase in arteriolar flow into the area

A

Acute local active hyperemia

131
Q

passive engorgement of the drainage area due to obstruction in the venous drainage

A

acute local passive hyperemia

132
Q

tissues involved are dark red in color grossly than bright red, as they are engorged with poorly oxygenated blood

A

acute local passive hyperemia

133
Q

organ or organ system develops chronic inflammatory lesions which progress to fibrosis and obstruction tissue’s venous drainage

A

chronic local passive hyperemia

134
Q

Examples of physiological hyperemia

A
  1. Exercise
  2. Stomach and intestine digestion
  3. stimulation of erectile tissues
  4. blushing
135
Q

refers to a local increase in the volume of blood in
tissues due to dilation of the small blood vessels

136
Q

refers to the damming of blood in an area due to diminished venous outflow, and is considered
a form of passive hyperemia

A

congestion

137
Q

Characteristics of exudate (active process)

A
  • high protein content
  • increased specific gravity
  • increased number of inflammatory cells
138
Q

Characteristics of transudate (passive process)

A
  • Low protein content
  • Low specific gravity
  • Low or absence on inflammatory cells
139
Q

fixative of choice to retain edema lesion

A

Bouin’s fluid or solutionq

140
Q

gives a characteristically homogenous, pink-staining lesion

A

edema lesion

141
Q

Gut edema is caused by

A

Escherichia coli

142
Q

Malignant edema is caused by

A

Clostridium septicumin

143
Q

common lesion affecting lungs and is often the immediate cause of death in many different disease conditions

A

pulmonary edema

144
Q

Anasarca

A

generalized edema or extreme edema in the entire body, as occurs in some aborted fetuses

145
Q

arises from leakage of surface pleural lymphatic vessels in very edematous lungs

A

hydrothorax

146
Q

arises from excess flow of lymph within the myocardium

A

hydropericardium or pericardial effusion

147
Q

edema in peritoneal cavity

A

Ascites or hydroperitoneum

148
Q

Ascites or Hydroperitoneum occurs in conditions such as?

A
  1. Chronic passive congestion or heart failure
  2. Chronic liver diseases
  3. Chronic renal diseases
  4. Hypoproteinemia
  5. Tumors implanted in abdominal cavity
149
Q

deficiency of protein level in the blood such as in nephrotic syndrome

A

hypoproteinemia

150
Q

edema is severe and generalize which produce a dent when pushed by a finger

A

pitting edema

151
Q

dependent edema

A

a fluid collects in lowermost portion:

  1. ventral abdomen
  2. limbs
152
Q

causes pinkish precipitates in the area of edema during examination

A

high amount of protein content

153
Q

True or false.

Edema is more evident grossly than microscopically.

A

True.

Microscopically, it is extremely difficult to detect the increase in interstitial
fluid in the affected tissue, and the appearance of the section rather
unremarkable

154
Q

Edema is most evident in?

A
  1. Subcutaneous
  2. Lungs
  3. Brain
155
Q

takes the form of fluid collections that may be tinged red with blood

A

subcutaneous edema

156
Q

fills the alveolar spaces such that the lung tissue becomes heavy and filled with fluid

A

edema in lungs

157
Q

When edema in the brain occurs, it pushes brain out into?

A

Foramen magnum, characteristically seen as herniation or “coning” of the cerebellum.

158
Q

changes associated with edema are dependent on

A
  • the severity of edema
  • the rapidity of onset
  • the extent
  • the anatomic location
  • the underlying cause of edema
159
Q

True or false.

Lymphatic obstruction usually results to local edema.

160
Q

a parasite that can cause obstruction and lymphatic damage

A

elephantiasis

161
Q

condition may occur following impediments in lymphatic flow by growing neoplasms, emboli, and
damage to the lymphatic channels following surgical interventions

A

lymphatic obstruction

162
Q

Mechanisms of Edema

A

1) Decreased plasma colloid osmotic pressure
2) Increased blood hydrostatic pressure
3) Increased vascular permeability
4) Lymphatic obstruction

163
Q

most important plasma protein, and is principally produced in the liver

164
Q

results when there is a decrease
in plasma protein concentration in the blood

A

decreased plasma colloid osmotic pressure

165
Q

occurs when there is a disease condition that increases the venous capillary pressure

A

Increase blood hydrostatic pressure

166
Q

occurs as edema of inflammation and is characteristically local

A

increased vascular permeability

167
Q

mechanism of edema which fluid is high in protein content and leaks out of the damaged endothelial walls

A

Increased vascular permeability

168
Q

accumulation of an excessive amount of extracellular water in the interstitial fluid spaces

169
Q

True or false

Edema is a lesion and not a specific disease

170
Q

nutrient / waste exchange between blood and extravascular tissue

A

microcirculation system

171
Q

collection system

A

lymphatic and veins

172
Q

distribution system

173
Q

pumps blood

174
Q

Approximately 60% of the total lean body weight is composed of

175
Q

water percentage present in intracellular space

176
Q

water percentage present in extracellular compartment

177
Q

water percentage retained in the plasma

178
Q

Net filtration pressure

A

difference between plasma hydrostatic pressure and interstitial tissue colloid
osmotic pressure at the arteriolar end

179
Q

Net absorption pressure

A

difference between the plasma colloid osmotic pressure and the tissue fluid osmotic pressure

180
Q

plasma proteins in the blood

A

albumin and globulin ( alpha, beta, and gamma)

181
Q

release of protein into the urine is called

A

nephrotic syndrome

182
Q

relationship between the various forces at work in the microcirculatory bed

A

starling equilibrium

183
Q

generalized passive hyperemia results to

A

Congestive Heart Failure

184
Q

liver generalized congestion and could result to necrosis of periacinar (or centrilobular) hepatocytes

A

Right sided CHF

185
Q

congestion with characteristic gross appearance as “nutmeg liver”

A

Right sided CHF

186
Q

lungs will show severe congestion and edema, and in some, hydrothorax could be seen

A

Left sided CHF

187
Q

deficiency in platelets

A

thrombocytopenia

188
Q

dogs with canine ehrlichiosis is deficient in

189
Q

True or false.

More rapid the blood is lost, less is the
total volume of blood that must be lost before shock comes in

190
Q

percentage of critical amount of blood lost that can lead to circulatory collapse and
shock

A

20-40% of the total blood volume in any given species

191
Q

What is expected from a dog whose feces are with digested or frank blood that appears either black or dark violet in color?

A

low chance of recovery from a disease (poor prognosis) due to great blood lost in GIT

192
Q

skin lesion as a result of hemorrhage

193
Q

arrest of hemorrhage

A

hemostasis

194
Q

In intrinsic clotting mechanism, Activated Christmas Factor (Factor IX) combines with (3) to activate Factor X

A

a. antihemophilic factor (Factor VIII)
b. Phospholipid
c. divalent calcium (Factor IV)

195
Q

In extrinsic clotting mechanism, tissue thromboplastin combines with (2) to activate Stuart-Prower Factor

A

a. Proconvertin (Factor III)
b. divalent calcium (Factor (IV)

196
Q

they do not promote activation of either the intrinsic or extrinsic clotting mechanisms, and do not promote the adherence of platelets and leucocytes

A

intact vascular endothelial cells

197
Q

major determinants in the pathogenesis of thrombosis (virchow’s triad)

A
  1. vascular damage
  2. Hypercoagulability of blood
  3. Hemodynamic and Rheological Changes
198
Q

promote platelet adhesion

A
  1. collagen
  2. elastin
  3. basement membrane
  4. microfilament
  5. Amorphous ground substance (AGS)
199
Q

Hydrolytic enzymes released at Phase 2 of platelet reaction

A
  1. Beta-glucuronidase
  2. Cathepsin
  3. beta nitro acetyl glucosaminidase
200
Q

accelerate thrombogenesis

201
Q

Most critical organs in obstruction of blood flow

A

brain and heart

202
Q

In cats, thromboses at the distal aorta are the usual cause of

A

hind limb paralysis

203
Q

organs with end artery

A

a. brain
b. heart
c. kidney
d. spleen

204
Q

If the occlusion of thrombi is limited it results to

205
Q

if there is complete blockage of blood flow it results to

A

infarction

206
Q

etiology of post mortem clot

A

Stagnated blood as in downer
animal

207
Q

a normal component of serum, and is activated during stress, infection or shock

A

plasminogen

208
Q

Plasmin is formed from

A

beta globulin (i.e. plasminogen)

209
Q

this is used in some species as a means of euthanasia

A

occlusion of cerebral vessels (through venipuncture)

210
Q

significant cause of death in human after
serious car accident

A
  1. Pulmonary emboli
  2. Cerebral Fat emboli
211
Q

causes of ischemia

A
  1. compression of blood vessels
  2. obstruction
  3. functional lesion
212
Q

Infarcts are classified based on

A
  1. presence or absence of bacterial contamination
  2. color
213
Q

intensely hemorrhagic as blood backs up into the affected tissue behind the obstruction

A

venous infarcts

214
Q

generally pale, except in loose tissues such as the lungs that tend to be hemorrhagic

A

arterial infarcts

215
Q

organs with arterial infarcts

A

heart and kidneys

216
Q

considered one of the “silent” killers of humans

A

myocardial infarction (heart attack)

217
Q

infarction of brain result to

A

encephalomalacia

218
Q

normal blood pH

219
Q

normal pH is maintained by

A

bicarbonate and carbonic acid

220
Q

cause of alkylosis (pH = 7.8)

A

excess bicarbonate, decrease carbonic acid

221
Q

leads to acidosis at a pH of about 7.0

A

deficient bicarbonate, excess carbonic acid

222
Q

slowing down of the circulation, settling out of red cells from plasma and increased stickiness of blood

223
Q

visceral pooling

A

Blood fall resultant of diapedeses or rbcs

224
Q

Some lesions found postmortem may be very suggestive, or in some cases diagnostic, of severe shock

A

congestive atelectasis (shock lung)

225
Q

disease states that have accompanying
sepsis, minute thrombi form and are widely dispersed in the microcirculation

A

microcirculatory thrombosis or disseminated intravascular coagulation (DIC)

226
Q

not a primary disorder, rather a complication of some underlying
cause, and is essentially a defect in hemostasis

227
Q

DIC

A

disseminated intravascular coagulation

228
Q

DIC mechanism

A
  1. Activation of the Intrinsic Clotting
    Mechanism
  2. Activation of the Extrinsic Clotting Mechanism
  3. Direct Activation of Prothrombin or Factor X (Stuart-Power Factor)
229
Q

Direct Activation of Prothrombin or Factor X (Stuart-Power Factor)

A

proteolytic enzymes that include snake venoms, and trypsin during
episodes of acute pancreatitis activate these factors

230
Q

widespread neoplasm, tissue necrosis due to infectious diseases, surgical
interventions, and severe trauma to tissues

A

Activation of the Extrinsic Clotting Mechanism

231
Q

independent on tissue
damage through the
direct activation of Factor
XII

A

Activation of the
Intrinsic Clotting
Mechanism

232
Q

DIC phase wherein thrombocytes are depleted

A

hypocoagulable phase

233
Q

occurs following prolonged vomiting with loss of acid

A

metabolic alkylosis

234
Q

occurs following prolonged vomiting with loss of acid

A

metabolic alkylosis

235
Q

Lesion indicative of shock

A
  1. Congestive atelectasis
  2. Visceral pooling
  3. Acute renal tubular necrosis
  4. Sludging
  5. Disseminated intravascular coagulation
236
Q

In most disease conditions where widespread vascular damage is a
feature, it is the immediate cause of death when left unattended

237
Q

Platelet Release reaction in Phase 1 (2)

A
  1. Adenosine nucleotide (ADP)
  2. 5-hydroxytryptamine (5-HT) or serotonin
238
Q

Thromboxane A2

A

Promote platelet aggregation

Veterinary General Pathology (4 decks)

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