Disturbances in circulation pt2 Flashcards
(239 cards)
1
Q
Activation of the sympathetic nervous system produces (2) to redistribute blood to vital organs
A
- peripheral vasoconstriction
- tachycardia
2
Q
Activation of the apneustic and pneumotaxic areas of the brain
A
Stimulation of the respiratory centers in the brain
3
Q
Stimulation of adrenal gland releases these chemicals
A
- Adrenal medulla - catecholamines (epinephrine and norepinephrine)
- Adrenal cortex - glucocorticoids
4
Q
result toconservation of sodium ions and water by increasing kidney tubular
reabsorption
A
Activation of the Renin-Angiotensin-Aldosterone Axis
5
Q
Counter Regulatory Mechanisms operating at early stages of shock
A
- Activation of Sympathetic Nervous System
- Stimulation of the respiratory centers in the brain
- Stimulation of adrenal gland
- Activation of the Renin-Angiotensin-Aldosterone Axis
6
Q
Hypovolemic Shock
A
includes hemorrhage and traumatic shock; inadequate blood or plasma volume
7
Q
Cardiogenic Shock
A
shock resulting from myocardial infarction; failure of myocardial pump due to intrinsic myocardial damage
8
Q
shock associated with toxemia and septicemia, including endotoxemia
A
septic or toxic shock
9
Q
Neurogenic Shock
A
resulting from severe fright, pain and trauma without hemorrhage
10
Q
as a result of massive degranulation of mast cells following antigen-antibody interaction
A
anaphylactic shock
11
Q
Stages of shock
A
- Stage of ischemic hypoxia
- Stage of stagnant hypoxia
3.. Stage of irreversibility
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
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
14
Q
shift of fluid from the intravascular space to the extravascular space and microembolization of capillaries
A
stage of irreversibility
15
Q
phase that the counter regulatory mechanisms are activated
A
stage of ischemic hypoxia
16
Q
state of peripheral circulatory failure caused by sudden and severe injury
A
shock
17
Q
shock is a syndrome of?
A
diminishing blood pressure in the capillary bed
18
Q
anaerobic glycolysis results in accumulation of this acid which cause acidosis
A
Lactic acid/lactate
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.
19
Q
DIC phase associated with subsequent formation of
thrombin
A
hypercoagulable phase
20
Q
leads to platelet aggregation and fibrin formation resulting to microthrombosis of vascular capillaries, and infarction in many organs
A
hypercoagulable phase
21
Q
Clotting factors depleted during hypocoagulable phase
A
- fibrinogen
- Factor VIII (anti-hemophilic factor)
- Factor V (proaccelerin)
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
23
Q
area of coagulative necrosis caused by ischemia and is due to obstruction of the blood supply following thrombosis or embolism
A
infarct
24
process of infarct called
infarction
25
cells and tissues most susceptible to infarction
▪ brain,
▪ renal tubular epithelia,
▪ heart muscles, and
▪ most parenchymal tissues
26
resistant to infarction such that the
stromal support of infracted tissues survives while the parenchyma succumb to
infarction
fibroblasts
27
artery ramifies into smaller branches as it ends
Functional End-Artery
28
Functional end artery organs where infarction are commonly seen
1. kidneys
2. heart muscles
3. brain
4. spleen
29
there are separate blood supply that often has several functional anastomotic channels
Parallel system
30
pulmonary and hepatic infarctions rarely occur but may happen if dual blood supply is compromised, such as in?
chronic passive venous congestion
31
organs that have two separate blood
supply originating from different points (dual blood supply)
1. lungs (pulmonary artery and bronchial artery)
2. liver (hepatic artery and portal vein)
32
thrombo-embolic colic in the horse is cause by ___ obstructing the
cranial mesenteric artery
Strongylus vulgaris
33
Thrombotic or embolic occlusion
rarely leads to infarction in organs with parallel system, but happens so when?
occlusion occurs at the root of the blood vessel
34
localized anemia
ischemia
35
ischemia results to infarction if it lodges in organs with so called
end arteries
36
if ischemia is partial or gradual it results to
atrophy
37
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
histotoxic anoxia
38
caused by low hemoglobin or reduced capacity of blood to carry oxygen as in carbon monoxide poisoning
anemic anoxia
39
result from insufficient oxygenation of blood as may occur in severe pneumonia
anoxic anoxia
40
ischemia due to reduced flow of oxygenated blood as in hypovolemic shock
stagnant anoxia
41
reduction of blood supplies maybe partial called
hypoxia
42
anoxia
complete reduction in the oxygen supplied to tissues
43
reduction in the flow of arterial blood to an organ or tissue result to
ischemia
44
end result of ischemia depend on
1. organ involved
2. degree of occlusion/anoxia
3. presence of collateral circulation
4. size of blood vessels
45
Causes of ischemia
1. Compression of blood vessels
2. Obstruction
3. Functional lesion
46
stagnant anoxia example
hypovolemic shock
47
anoxic anoxia may occur in
severe pneumonia
48
Anemic Anoxia example
carbon monoxide poisoning
49
histotoxic anoxia example
cyanide poisoning
50
solid mass transported from one part of the body to another through the circulatory system
emboli
51
process of a solid mass being transported from one part of the body to another
through the circulatory system
embolism
52
embolus can be:
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
53
produces emboli of pieces of skin or hair
venipuncture
54
One of the notorious “seeders” of emboli that causes multiple embolisms in the
kidneys
bacterial valvular endocarditis
55
Valvular thrombosis of the left chamber of the heart usually produces emboli in the
systemic circulation
56
valvular thrombosis in the left chamber of the heart cause emboli at the?
Systemic circulation
57
organs with end artery
brain, kidneys, spleen and myocardium
58
detachment of thrombi in the vessel wall can cause
emboli
59
thrombi become larger and larger eventually obstructing the lumen of the blood vessel where they are formed
propagation
60
portions of the thrombi break and
are carried into the circulation
fragmentation to form thrombo-emboli
61
lysis of the thrombi by plasma-derived
fibrinolytic system or through slow phagocytosis by phagocytic cells
dissolution by fibrinolysis
62
invasion and growth of fibrous tissue could happen, along with recanalization and restoration of blood flow
fibrous tissue organization
63
Once thrombi are formed, there are four possible outcomes
1. Propagation
2. Fragmentation to form thrombo-emboli
3. Dissolution by fibrinolysis
4. Fibrous tissue organization
64
Thrombi are clinically important for two reasons
a) they cause obstruction of blood vessels
b) they can be a source of emboli
65
in cat species, thrombosis at this site cause hind limb paralysis
distal aorta
66
in horse species, thrombosis at this site is usually caused by strongyle infection
cranial mesenteric arteries
67
trailing thrombi with one end attached and
the other freely moving
obturating thrombi
68
straddles the bifurcation of blood vessels
saddle thrombi
69
Canalized thrombi
allows partial flow of blood
70
Occluding thrombi
blocks the entire lumen of the blood vessel
71
Valvular thrombi
attached to the valves of the heart
72
Mural thrombi
attached to the endocardial wall of heart
73
Based on location of thrombi:
a. Cardiac thrombi
b. Arterial thrombi
c. Venous thrombi
d. Lymphatic thrombi
e. Capillary thrombi or hyaline thrombi
74
septic thrombi
contains bacteria
75
aseptic thrombi
no pathogenic agent present
76
parasitic thrombi
contains parasites such as filarial worms
77
red thrombi
composed of all blood cell components
78
pale or white thrombi
composed entirely of platelets
79
layered red and white thrombi
laminated or mixed thrombi
80
pale gray-tan mass consisting of bands of fibrin and platelets mixed with coagulated red blood cells
arterial thrombi
81
when arterial thrombi builds up, head and tail are in what colors?
Head - pale
Tail - darker red
82
During propagation concentric laminations are formed
lines of Zahn
83
they are dark red, moist or gelatinous and are easier to dislodge
venous thrombi
84
resemble intravascular clots of whole blood due to slow blood flow and as influenced by gravity
venous thrombi
85
It is the carbohydrate-rich cell coat present in endothelial lining cells which prevents circulating cells from adhering to the surface
glycocalyx
86
negatively-charged surface of
endothelial lining lead to a mutual electrostatic repulsion between two sets
of negatively charged cells
surface negativity theory
87
prostaglandin that prevent platelet
aggregation by converting platelet aggregation factors into unstable substances
Prostacyclin (PG12)
88
Theories on Non-thrombogenic Vascular Endothelia
1. Glycocalyx theory
2. Surface negative theory
3. Surveillance system theory
89
prostacyclin convert these platelet aggregation factors to unstable forms
1. endoperoxidase
2. thromboxane A2
90
hemostasis steps
1. vascular contraction
2. stasis of blood
3. endothelial adhesion
4. blood coagulation
5. platelet aggregation
91
formation of ante mortem clot within the blood vessels
thrombosis
92
2 mechanisms of blood coagulation
1. intrinsic clotting mechanism
2. extrinsic clotting mechanism
93
intrinsic clotting mechanism
involves the components normally present in the plasma
94
extrinsic clotting mechanism
involves tissue component in addition to the components from the blood
95
two systems of coagulation both activate this factor which lead to fibrin formation
(Factor X) stuart-prower factor
96
Diseases that result in marked bleeding tendencies
hemorrhagic diathesis
97
indicates former hemorrhage
1. hemosiderin-laden macrophages
2. erythrophagocytosis
98
clinical term applied to an animal that has extensive petechial and ecchymotic hemorrhages on serous and mucous surfaces
purpura
99
usually occur on serosal or mucosal surfaces and are visible but cannot be palpated
Petechiae, ecchymosis, paint-brush hemorrhages
100
Metrorrhagia
Passage of blood through the uterus
101
Hemothorax
Hemorrhage into the thoracic cavity
102
Hemoptysis
Coughing out of blood
103
hemoperitoneum
Hemorrhage into the peritoneal cavity
104
hemopericardium
Hemorrhage into the pericardial sac
105
hematochezia
defecation of blood
106
three-dimensional collection of blood coagula
hematocyst/hematoma
107
hematocyst/hematoma
sufficient red cells come out in one area to form lump
108
hematemesis
vomition of blood
109
hemarthrosis
hemorrhage into joint spaces
110
extravasation
Extensive hemorrhage within the substance of the tissue
111
Nasal bleeding or bleeding from the nostrils
epistaxis
112
entorrhagia
passage of blood to alimentary tract (digestive tract)
113
paint brush hemorrhage
Linear or streaked appearance of hemorrhage
114
Blotchy or irregular areas of hemorrhage up to 3 centimeters in diameter
ecchymosis
115
Minute, pin-point foci of hemorrhage up to 2 millimeter in diameter
petechiae
116
critical sites of hemorrhage
brain and heart
117
effect of hemorrhage depend on
1. location of hemorrhage
2. volume of blood lost
3. rate of blood lost
118
blood escapes from the vasculature
hemorrhage
119
implies rupture of a blood vessel
rhexis
120
hemorrhage by diapedesis
passive process where blood
escapes from minute pores of the vascular endothelia as observed in events of hyperemia of inflammation
121
causes of hemorrhagic diathesis
1. Liver disease
2. Deficiencies in blood coagulation factors
122
deficiency of this vitamin cause deficiency of prothrombin
Vit. K
123
condition in dogs where deficiency of platelets caused by infectious agents
canine ehrlichiosis
124
thrombocytopenia
deficiency of platelets
125
hemorrhagic diathesis can be seen in hereditary anomaly such as in?
congenital hemophilia
126
classification of pathological hyperemia
1. Duration of hyperemia (acute or chronic)
2. Extent of hyperemia (general or local)
3. The underlying mechanism (active or passive)
127
occurs as a manifestation of some alterations in blood flow characteristics
pathological hyperemia
128
True or false
Pathological hyperemia is a result of some underlying pathological process, not a cause of alteration.
True
129
Hyperemia can be observed in?
1. Inflammation
2. Cardiac failure
3. Obstructive venous disease
130
due to engorgement of the vascular bed following an increase in arteriolar flow into the area
Acute local active hyperemia
131
passive engorgement of the drainage area due to obstruction in the venous drainage
acute local passive hyperemia
132
tissues involved are dark red in color grossly than bright red, as they are engorged with poorly oxygenated blood
acute local passive hyperemia
133
organ or organ system develops chronic inflammatory lesions which progress to fibrosis and obstruction tissue’s venous drainage
chronic local passive hyperemia
134
Examples of physiological hyperemia
1. Exercise
2. Stomach and intestine digestion
3. stimulation of erectile tissues
4. blushing
135
refers to a local increase in the volume of blood in
tissues due to dilation of the small blood vessels
hyperemia
136
refers to the damming of blood in an area due to diminished venous outflow, and is considered
a form of passive hyperemia
congestion
137
Characteristics of exudate (active process)
* high protein content
* increased specific gravity
* increased number of inflammatory cells
138
Characteristics of transudate (passive process)
* Low protein content
* Low specific gravity
* Low or absence on inflammatory cells
139
fixative of choice to retain edema lesion
Bouin's fluid or solutionq
140
gives a characteristically homogenous, pink-staining lesion
edema lesion
141
Gut edema is caused by
Escherichia coli
142
Malignant edema is caused by
Clostridium septicumin
143
common lesion affecting lungs and is often the immediate cause of death in many different disease conditions
pulmonary edema
144
Anasarca
generalized edema or extreme edema in the entire body, as occurs in some aborted fetuses
145
arises from leakage of surface pleural lymphatic vessels in very edematous lungs
hydrothorax
146
arises from excess flow of lymph within the myocardium
hydropericardium or pericardial effusion
147
edema in peritoneal cavity
Ascites or hydroperitoneum
148
Ascites or Hydroperitoneum occurs in conditions such as?
1. Chronic passive congestion or heart failure
2. Chronic liver diseases
3. Chronic renal diseases
4. Hypoproteinemia
5. Tumors implanted in abdominal cavity
149
deficiency of protein level in the blood such as in nephrotic syndrome
hypoproteinemia
150
edema is severe and generalize which produce a dent when pushed by a finger
pitting edema
151
dependent edema
a fluid collects in lowermost portion:
1. ventral abdomen
2. limbs
152
causes pinkish precipitates in the area of edema during examination
high amount of protein content
153
True or false.
Edema is more evident grossly than microscopically.
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
Edema is most evident in?
1. Subcutaneous
2. Lungs
3. Brain
155
takes the form of fluid collections that may be tinged red with blood
subcutaneous edema
156
fills the alveolar spaces such that the lung tissue becomes heavy and filled with fluid
edema in lungs
157
When edema in the brain occurs, it pushes brain out into?
Foramen magnum, characteristically seen as herniation or “coning” of the cerebellum.
158
changes associated with edema are dependent on
* the severity of edema
* the rapidity of onset
* the extent
* the anatomic location
* the underlying cause of edema
159
True or false.
Lymphatic obstruction usually results to local edema.
True.
160
a parasite that can cause obstruction and lymphatic damage
elephantiasis
161
condition may occur following impediments in lymphatic flow by growing neoplasms, emboli, and
damage to the lymphatic channels following surgical interventions
lymphatic obstruction
162
Mechanisms of Edema
1) Decreased plasma colloid osmotic pressure
2) Increased blood hydrostatic pressure
3) Increased vascular permeability
4) Lymphatic obstruction
163
most important plasma protein, and is principally produced in the liver
albumin
164
results when there is a decrease
in plasma protein concentration in the blood
decreased plasma colloid osmotic pressure
165
occurs when there is a disease condition that increases the venous capillary pressure
Increase blood hydrostatic pressure
166
occurs as edema of inflammation and is characteristically local
increased vascular permeability
167
mechanism of edema which fluid is high in protein content and leaks out of the damaged endothelial walls
Increased vascular permeability
168
accumulation of an excessive amount of extracellular water in the interstitial fluid spaces
edema
169
True or false
Edema is a lesion and not a specific disease
True
170
nutrient / waste exchange between blood and extravascular tissue
microcirculation system
171
collection system
lymphatic and veins
172
distribution system
arteries
173
pumps blood
heart
174
Approximately 60% of the total lean body weight is composed of
water
175
water percentage present in intracellular space
40%
176
water percentage present in extracellular compartment
15%
177
water percentage retained in the plasma
5%
178
Net filtration pressure
difference between plasma hydrostatic pressure and interstitial tissue colloid
osmotic pressure at the arteriolar end
179
Net absorption pressure
difference between the plasma colloid osmotic pressure and the tissue fluid osmotic pressure
180
plasma proteins in the blood
albumin and globulin ( alpha, beta, and gamma)
181
release of protein into the urine is called
nephrotic syndrome
182
relationship between the various forces at work in the microcirculatory bed
starling equilibrium
183
generalized passive hyperemia results to
Congestive Heart Failure
184
liver generalized congestion and could result to necrosis of periacinar (or centrilobular) hepatocytes
Right sided CHF
185
congestion with characteristic gross appearance as “nutmeg liver”
Right sided CHF
186
lungs will show severe congestion and edema, and in some, hydrothorax could be seen
Left sided CHF
187
deficiency in platelets
thrombocytopenia
188
dogs with canine ehrlichiosis is deficient in
platelets
189
True or false.
More rapid the blood is lost, less is the
total volume of blood that must be lost before shock comes in
True
190
percentage of critical amount of blood lost that can lead to circulatory collapse and
shock
20-40% of the total blood volume in any given species
191
What is expected from a dog whose feces are with digested or frank blood that appears either black or dark violet in color?
low chance of recovery from a disease (poor prognosis) due to great blood lost in GIT
192
skin lesion as a result of hemorrhage
bruise
193
arrest of hemorrhage
hemostasis
194
In intrinsic clotting mechanism, Activated Christmas Factor (Factor IX) combines with (3) to activate Factor X
a. antihemophilic factor (Factor VIII)
b. Phospholipid
c. divalent calcium (Factor IV)
195
In extrinsic clotting mechanism, tissue thromboplastin combines with (2) to activate Stuart-Prower Factor
a. Proconvertin (Factor III)
b. divalent calcium (Factor (IV)
196
they do not promote activation of either the intrinsic or extrinsic clotting mechanisms, and do not promote the adherence of platelets and leucocytes
intact vascular endothelial cells
197
major determinants in the pathogenesis of thrombosis (virchow's triad)
1. vascular damage
2. Hypercoagulability of blood
3. Hemodynamic and Rheological Changes
198
promote platelet adhesion
1. collagen
2. elastin
3. basement membrane
4. microfilament
5. Amorphous ground substance (AGS)
199
Hydrolytic enzymes released at Phase 2 of platelet reaction
1. Beta-glucuronidase
2. Cathepsin
3. beta nitro acetyl glucosaminidase
200
accelerate thrombogenesis
PF3, PF4
201
Most critical organs in obstruction of blood flow
brain and heart
202
In cats, thromboses at the distal aorta are the usual cause of
hind limb paralysis
203
organs with end artery
a. brain
b. heart
c. kidney
d. spleen
204
If the occlusion of thrombi is limited it results to
atrophy
205
if there is complete blockage of blood flow it results to
infarction
206
etiology of post mortem clot
Stagnated blood as in downer
animal
207
a normal component of serum, and is activated during stress, infection or shock
plasminogen
208
Plasmin is formed from
beta globulin (i.e. plasminogen)
209
this is used in some species as a means of euthanasia
occlusion of cerebral vessels (through venipuncture)
210
significant cause of death in human after
serious car accident
1. Pulmonary emboli
2. Cerebral Fat emboli
211
causes of ischemia
1. compression of blood vessels
2. obstruction
3. functional lesion
212
Infarcts are classified based on
1. presence or absence of bacterial contamination
2. color
213
intensely hemorrhagic as blood backs up into the affected tissue behind the obstruction
venous infarcts
214
generally pale, except in loose tissues such as the lungs that tend to be hemorrhagic
arterial infarcts
215
organs with arterial infarcts
heart and kidneys
216
considered one of the “silent” killers of humans
myocardial infarction (heart attack)
217
infarction of brain result to
encephalomalacia
218
normal blood pH
7.35-7.45
219
normal pH is maintained by
bicarbonate and carbonic acid
220
cause of alkylosis (pH = 7.8)
excess bicarbonate, decrease carbonic acid
221
leads to acidosis at a pH of about 7.0
deficient bicarbonate, excess carbonic acid
222
slowing down of the circulation, settling out of red cells from plasma and increased stickiness of blood
sludging
223
visceral pooling
Blood fall resultant of diapedeses or rbcs
224
Some lesions found postmortem may be very suggestive, or in some cases diagnostic, of severe shock
congestive atelectasis (shock lung)
225
disease states that have accompanying
sepsis, minute thrombi form and are widely dispersed in the microcirculation
microcirculatory thrombosis or disseminated intravascular coagulation (DIC)
226
not a primary disorder, rather a complication of some underlying
cause, and is essentially a defect in hemostasis
DIC
227
DIC
disseminated intravascular coagulation
228
DIC mechanism
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
Direct Activation of Prothrombin or Factor X (Stuart-Power Factor)
proteolytic enzymes that include snake venoms, and trypsin during
episodes of acute pancreatitis activate these factors
230
widespread neoplasm, tissue necrosis due to infectious diseases, surgical
interventions, and severe trauma to tissues
Activation of the Extrinsic Clotting Mechanism
231
independent on tissue
damage through the
direct activation of Factor
XII
Activation of the
Intrinsic Clotting
Mechanism
232
DIC phase wherein thrombocytes are depleted
hypocoagulable phase
233
occurs following prolonged vomiting with loss of acid
metabolic alkylosis
234
occurs following prolonged vomiting with loss of acid
metabolic alkylosis
235
Lesion indicative of shock
1. Congestive atelectasis
2. Visceral pooling
3. Acute renal tubular necrosis
4. Sludging
5. Disseminated intravascular coagulation
236
In most disease conditions where widespread vascular damage is a
feature, it is the immediate cause of death when left unattended
DIC
237
Platelet Release reaction in Phase 1 (2)
1. Adenosine nucleotide (ADP)
2. 5-hydroxytryptamine (5-HT) or serotonin
238
Thromboxane A2
Promote platelet aggregation
