1
Q
What happens when tissue cells or blood cells are injured and exposed to blood
A
Blood coagulates and forms a clot
2
Q
What is a clot?
A
A tough and tenacious structure consisting of a meshwork of fibrin strands and platelets that have clumped together.
3
Q
During coagulation, what is plasma fibrinogen converted into?
A
Fibrin (via thrombin + Ca ions)
4
Q
Name the 2 systems or pathways of the clotting mechanism.
A
Intrinsic (Intravascular) System and Extrinsic (Extravascular) System
5
Q
What are the features of the Intrinsic System?
A
a. Trauma to the blood itself initiates clotting and activation of Factor XII (Hageman Factor)
b. Requires platelet phospholipid
c. Slow process – clotting occurs in minutes
6
Q
What are the features of the Extrinsic System?
A
a. Initiated when blood contacts traumatized vascular wall or extravascular tissue
b. Requires tissue thromboplastin
c. Rapid process – clotting occurs in seconds
7
Q
What substance is responsible for the lysis of blood clots and controls blood clotting?
A
Plasmin (Fibrinolysin)
8
Q
What is the function of blood vessels in the circulatory system?
A
Act as channels for blood to carry nutrients to various cells.
9
Q
What else is the circulatory system responsible for?
A
Removing metabolic waste products
10
Q
Too much blood; a change in the volume and flow of blood.
A
hyperemia
11
Q
In how many ways does hyperemia occur, and what are they?
A
2 ways:
a. Active hyperemia
b. Passive hyperemia
12
Q
What occurs in active hyperemia? (MAIN DEFINITION)
A
Arterioles are engorged or filled with blood.
13
Q
Describe the microscopic appearance of active hyperemia.
A
Capillaries, arteries, and arterioles are dilated and filled with blood.
14
Q
Describe the **gross appearance* of active hyperemia
A
Hyperemic area is bright red in color, and warmer to touch due to arterial blood.
15
Q
What occurs in passive hyperemia?
A
Blood accumulates in venous circulation due to decreased venous drainage.
And when too little blood is being removed by the venules
16
Q
Describe the microscopic appearance of passive hyperemia.
A
Capillaries and veins are dilated and filled with blood.
17
Q
Describe the gross appearance of passive hyperemia.
A
Congested tissue is swollen with bluish-red color;
during necropsy, blood is released when cut.
18
Q
What is physiologic hyperemia?
A
Increased blood flow due to increased demand by certain tissues.
19
Q
Give examples of physiologic hyperemia:
A
a. Increased blood flow to stomach and intestines during digestion
b. Congestion of erectile tissues during stimulation
c. Increased physiologic activity in certain body parts
20
Q
What is pathological hyperemia?
A
Alterations in blood flow due to underlying pathological processes.
21
Q
Name the 3 factors to consider in classifying pathological hyperemia.
A
a. Duration of hyperemia
b. Extent of hyperemia
c. Mechanism by which it occurred
22
Q
Classification of Pathological Hyperemia
Classification based on duration with meaning:
A
a. Acute – abrupt onset, rapid development
b. Chronic – slow developing, long duration or present for long time
23
Q
Classification of Pathological Hyperemia
Classification based on extent:
A
a. General – throughout an organ or system
b. Local – confined to a small area
24
Q
Classification of Pathological Hyperemia
Classification based on mechanism:
A
a. Active – increased arteriolar inflow
b. Passive – engorgement of vascular bed; venous obstruction
25
Name the 4 basic patterns of hyperemia.
1. Acute Local Active Hyperemia
2. Acute Local Passive Hyperemia
3. Chronic Local Active Hyperemia (pero sa inexplain ni doc Passive siya for some reason)
4. Chronic General Passive Hyperemia
26
What causes acute local active hyperemia?
Engorgement of vascular bed following increased arterial blood flow.
27
**Engorgement of vascular bed** following increased arterial blood flow.
Opens **new capillary beds** (angiogenesis) and **extends arteriolar blood pressure** to **smaller vascular channels.**
**Chemically mediated response via histamine, bradykinins,** and other vasoactive substances (as in inflammation).
Acute Local Active Hyperemia
28
What **mediates the microvascular response** in acute local active hyperemia?
**Chemically mediated response** via **histamine, bradykinins, and other vasoactive substances** (as in inflammation).
29
What does increased arterial blood flow do in this condition? (Acute Local Active Hyperemia)
**Opens new capillary beds** (angiogenesis) and **extends arteriolar blood pressure** to smaller vascular channels.
30
What causes **acute local passive hyperemia?**
Obstruction to venous drainage
31
What is the result of acute local passive hyperemia?
Backflow of poorly oxygenated blood,
local venous engorgement, and
black lesions in compressed tissue.
32
What does acute local passive hyperemia result in?
Backflow of poorly oxygenated blood to microvasculature with local venous engorgement.
33
Give an example where acute local passive hyperemia is seen
**Strangulated intestine** compressing vessels
34
What accumulates in veins during acute local passive hyperemia and how do lesions appear?
Blood accumulates in veins; lesions become black.
35
Chronic inflammatory lesions leading to fibrosis and eventually obstruction in tissue venous drainage.
Chronic Local Passive Hyperemia
36
What are the results of chronic local passive hyperemia?
Edema, development of collateral venous channels, and dilated/tortuous arterio-venous anastomoses.
37
Give an example disease where chronic local passive hyperemia is seen
**Cirrhosis of the liver** wherein blood may not readily pass the liver → congestion of portal venous system.
38
Which organs are involved in **chronic general passive hyperemia?**
Lung or heart
39
What is chronic general passive hyperemia called if cardiac involvement is present?
Congestive heart failure
40
Enumerate the 2 forms of congestive heart failure.
a. Right-sided heart failure
b. Left-sided heart failure
41
What causes right-sided heart failure?
Defective heart valve (e.g., **tricuspid valvular disease**) → leads to backflow of blood into vena cava →results to liver congestion.
42
What happens when **blood accumulates in systemic venous circulation?** (Right-Sided Heart Failure)
Fluid accumulates in tissues
(under skin, extremities, body cavities such as **abdomen = ascites**).
43
What happens when blood pools in the liver in right-sided heart failure? In right sided heart failure
Results to pooling of blood in liver then causes liver congestion, which causes hypoxia/anoxia in central veins in periacinar distribution.
44
What does severe anoxia in right-sided heart failure lead to?
Necrosis of hepatocytes and RBCs which are occupying hepatocyte space with fibrosis of central veins.
45
What is the gross description of liver in right-sided heart failure?
Nutmeg appearance or nutmeg liver = these areas appear red or reddish blue
This is because of degeneration and necrosis of hepatocytes
Sinusoids are dilated and filled with blood giving them reddish color
Periportal hepatocyte undergoes fatty degeneration so they became yellowish, wich results to marked lobular pattern
46
What happens to pulmonary circulation in **left-sided heart failure?**
Blood from pulmonary circulation is not pumped out, accumulates in lungs.
47
What may escape from distended lung vessels in left-sided heart failure?
RBCs may escape from distended vessels into lung alveoli and engulfed by macrophages eventually results to lysis of RBC hemoglobin
Released from rbc is converted into hemosiderin
48
What engulfs escaped RBCs in lungs during left-sided heart failure?
Macrophages
49
What happens after RBC lysis in the lungs in left-sided heart failure?
Hemoglobin is converted to hemosiderin
50
What are macrophages containing hemosiderin called?
“Heart failure cells”
51
What is defined as the escape of blood from the cardiovascular system into tissues or body cavities?
Hemorrhage
52
Hemorrhage is defined as?
escape of blood from the cardiovascular system into tissues or body cavities
53
By how many processes does hemorrhage occur and what are they?
a. **Hemorrhage by rhexis** – escape of RBCs from a cut blood vessel wall
b. **Hemorrhage by diapedesis** – escape of RBCs from intact vessel walls (as seen in hyperemia or inflammation)
54
Name the 4 causes of hemorrhage.
1. Trauma or injury to blood vessels
2. Toxic injury to capillary endothelium (due to bacterial toxins, plant, and chemical poisons)
3. Systemic damage to vascular structures (due to septicemia, and viremia)
4. Hemorrhagic disorders of the clotting mechanism (due to deficiency in clotting factors) example is prothrombin deficiency in liver disease
55
Give example of hemorrhagic disorders due to clotting factor deficiency.
Prothrombin deficiency
56
Give an example of hereditary deficiency of clotting factors.
Hemophilia
57
What is thrombocytopenia?
Decreased platelets due to disease processes (e.g., Ehrlichiosis)
58
Decreased platelets due to disease processes as in Ehrlichiosis
Thrombocytopenia
59
The severity of hemorrhage depends on which factors?
a. Location or site of hemorrhage = critical sites are cns and heart
b. Volume of blood loss
c. Rate of blood loss
60
Give examples of critical sites of hemorrhage and their consequences.
a. Hemorrhage in Pericardial cavity → cardiac tamponade → death
b. Brain → blood clot compression → permanent disability
c. Trachea → asphyxiation
61
Under severity of effects of hemorrhage depends on:
B. Volume of blood loss = What is the effect of losing 20-40% of total blood volume?
Hemorrhagic shock or circulatory collapse
Severe blood loss through the GIT
Chronic blood loss
62
What may result from severe blood loss through the GIT? Under hemorrhage
Poor prognosis, may be fatal
63
What is the effect of chronic blood loss? In hemorrhage
Chronic blood loss leads to decrease in iron then anemia
64
Rate of blood loss in hemorrhage can lead to
Rapid loss can lead to Shock
65
What is the effect of chronic blood lost in hemorrhage?
Decreased iron and anemia
66
What are the 2 mechanisms by which hemorrhage resolves?
**Reabsorption** – extravascular clots may be reabsorbed; body cavity hemorrhage is drained by lymphatic vessels
**Organization** – fibrous tissue formation and phagocytosis; RBCs and fibrin from hemorrhage are surrounded by vascular connective tissue
67
What are clots formed in flowing blood containing normal blood components like platelets, fibrin, RBCs, and WBCs called?
Thrombus/ Thrombi (also called **ante-mortem clots**)
68
What is the process of thrombus formation called?
Thrombosis
69
Name the 3 major determinants in the pathogenesis of thrombosis.
**Damage to vessel wall endothelium**
**Changes in blood components** leading to **coagulability**
**Hemodynamic and rheological changes**
70
Thrombosis is also known as?
Virchow's Triad
71
**Damage to Vessel Wall Endothelium**
Why does a normal endothelium not promote clotting?
It does not activate clotting or make blood cells sticky
72
**Damage to Vessel Wall Endothelium**
Explain the Glycocalyx Theory
The **non-thrombogenic property** of **endothelial lining** is due to **glycocalyx** (CHO-rich cell coat)
73
Damage to Blood vessel endothelia is explained by the three following
A. Glycocalyx theory
B. Surface Negative theory
C. Survaillance System Theory
74
Explain the Surface Negativity Theory.
Both endothelial cells and RBCs are negatively charged → 2 negatively charged surface leads to **electrostatic repulsion**
75
Explain the Surveillance System Theory.
Is explained by the ability of Endothelial cells synthesize **prostacyclin (prostaglandin I2)** → this substance prevents platelet aggregation by converting **platelet aggregating factors (Endoperoxidase & Thromboxane A2)** into unstable substances in case of enthothelial injury.
Prostacyclin is absent because damaged endothelium cannot synthesize the substance
76
Under surveillance system theory of thrombus
What happens to prostacyclin in endothelial injury?
It is absent because damaged endothelium cannot synthesize it.
77
Name 4 causes of endothelial damage.
a. Trauma
b. Electrical injury
c. Chemical injury
d. Inflammatory infectious agents and their toxins
78
How does the endothelium respond to injury? In thrombi
**Damaged vessel reacts with platelets, blood cells, and fibrinolytic factors** to produce a series of reactions → leading to vasoconstriction and formation of coagulum **(platelets + fibrin).**
79
2. Changes in blood itself, under Thrombus
What causes blood to become sticky?
a. **Increased activation of clotting factors**
(e.g., ↑ fibrinogen during pregnancy, ↑ factors VII, VIII, X, postpartum)
b. **Decreased activity of these inhibitors:**
i. Anticoagulants
ii. Anti-thrombin
iii. Irreversible inhibitors (destroy clotting factors immunologically)
iv. Reversible inhibitors (interfere with coagulation but do not destroy clotting factors)
80
3. Hemodynamic Factors (Thrombus)
How is normal blood flow in vessels described?
Laminar – innermost stream moves fastest, succeeding layers slower toward vessel wall
81
Under thrombus
What prevents contact between endothelial cells and blood cells?
Thin layer of plasma next to endothelium
82
Take a break
🩷
83
Thrombus
3. Hemodynamic Factors
What are the effects of turbulent blood flow?
a. Accelerates reactions important for thrombus formation
b. May cause further injury to vessel wall
84
5 Different Classifications of Thrombi Based on Location in **Vascular system**
1. Cardiac thrombi
2. Arterial Thrombi
3. Venous Thrombi
4. Lymphatic
5. Capillary
(C°A°V°L°C)
85
Name the thrombus type found in the heart.
Cardiac thrombi
86
Name the thrombus type found in arteries.
Arterial thrombi
87
Name the most common type of thrombus found in veins.
Venous thrombi
88
Name the thrombus type found in lymphatic vessels.
Lymphatic
89
Name the thrombus type found in capillaries.
Capillary
90
6 Different Thrombi Based on Location **within the Heart or Blood Vessels**
1. Mural Thrombi
2. Valvular Thrombi
3. Occluding Thrombi
4. Canalized Thrombi
5. Saddle Thrombi
6. Obturating Thrombi
91
Name the thrombus attached to the endocardial wall.
Mural thrombi
92
Name the thrombus attached to a heart valve.
Valvular thrombi
93
Name the thrombus that occupies the entire circumference of a blood vessel.
Occluding thrombi
94
Name the thrombus that allows partial blood flow.
Canalized thrombi
95
Name the thrombus that straddles the bifurcation of blood vessels.
Saddle thrombi
96
Name the thrombus with one end attached to the vessel wall and the other end freely moving.
Obturating thrombi
97
Three Different Thrombi Based on Content or **Presence of Pathogenic Agents**
1. Septic
2. Aseptic
3. Parasitic
98
Name the thrombus containing bacteria.
Septic Thrombi
99
Name the thrombus without pathogenic agents.
Aseptic Thrombi
100
Name the thrombus containing parasites
Parasitic thrombi **(filarial nematode)**
101
Three Thrombi Based on Color
1. Red thrombi
2. Pale or White thrombi
3. Laminated or Mixed Thrombi
102
Name the thrombus color composed of all types of blood cells.
Red thrombi
103
Name the thrombus composed only of platelets.
Pale or white thrombi
104
Name the thrombus composed of alternating layers of red and white thrombi components.
Laminated or mixed thrombi
105
What are the components seen microscopically in a thrombus?
(Microscopic Description)
Contains various components of blood like Erythrocytes, leucocytes, precipitated proteins, and platelets
106
Microscopic Description of Thrombi
How do platelets appear microscopically in a thrombus?
Adhere to each other and the vessel wall **forming amorphous pink or gray masses** with a **laminated appearance**
107
What causes the laminated or layered appearance in a thrombus?
**Microscopic description**
**Alternating layers of fibrin and leucocytes, fibrin and erythrocytes, or fibrin alone**
108
What type of fibrils are seen in a thrombus microscopically?
Thick or heavy fibrils of fibrin
109
What is the color of arterial thrombi?
Pale, gray-tan
110
What causes the pale or gray-tan appearance in arterial thrombi?
Alternating layers of fibrin and platelets mixed with few coagulated erythrocytes in concentric arrangements
111
Why do arterial thrombi have a laminated appearance?
Due to rapid blood flow in arteries
112
How is the surface of arterial thrombi described?
Friable, dull, irregularly roughened
113
Describe the gross appearance of venous thrombi.
Dark red, moist, gelatinous, and like intravenous clots of whole blood due to slow flow;
components randomly arranged;
occlusive and rarely mural;
easier to dislodge.
114
Describe the gross appearance of arterial thrombi.
Pale, gray-tan in color, consisting of alternating layers of fibrin and platelets mixed with few coagulated erythrocytes in concentric arrangement;
friable with dull and irregularly roughened surface;
laminated appearance due to rapid arterial blood flow.
115
What are the effects of arterial thrombi on tissue blood supply?
Thrombi may completely or partially obstruct blood flow to the tissue supplied.
116
What can happen if fragments of a thrombus break off?
They may be carried in the blood as emboli
117
Effects of Thrombosis
Thrombi in arteries may completely or partially obstruct blood flow to the tissue supplied.
Fragments of clot or thrombus may break off and may be carried in the blood as **emboli.**
118
Enumerate the possible fates of a thrombus.
Answer:
1. Propagation – thrombus becomes larger and may eventually obstruct the vessel.
2. Fragmentation – formation of thromboemboli.
3. Removal by fibrinolysis/thrombolysis via the fibrinolytic system or phagocytosis.
4. Organization – thrombus may be invaded by fibroblasts, leading to fibrous tissue growth or recanalization and restoration of blood flow.
119
Where do post-mortem clots usually form?
In the venous system following death.
120
Why is little blood left in arteries during post-mortem clot formation?
Arteries contract during rigor mortis.
121
Microscopic Description of Post-Mortem Clots
How do post-mortem clots differ microscopically from thrombi in terms of components?
Same components as thrombus except platelets are absent.
122
Microscopic Description of Post-Mortem Clots
How are the components arranged in a post-mortem clot?
Uniformly mixed, or erythrocytes may settle at the lowest part of a vessel and be covered by leucocytes and precipitated proteins.
123
Microscopic Description of Post-Mortem Clots
How do fibrils of fibrin appear in post-mortem clots?
Fine and barely visible under light microscope.
124
**Gross Appearance of Post-Mortem Clots**
Describe a “currant-jelly” post-mortem clot.
Dark red, smooth, shiny, jelly-like appearance, uniform texture, unattached to vessel wall.
125
**Gross Appearance of Post-Mortem Clots**
Describe a **“chicken fat”** post-mortem clot.
Results from **settling and separation of red cells from plasma;**
commonly found in **heart chambers when post-mortem clotting is delayed;**
**smooth and shiny surface like currant-jelly clot but yellow color of plasma;**
**unattached to vessel wall but may be entangled in cardiac valves** and **chordae tendinae**
126
Microscopic description of Post mortem clots
* Contains same components as a thrombus except for the absence of platelets
* Components are uniformly mixed or the erythrocytes may have settled to the lowest part of a vessel and covered by leucocytes and precipitated protein
* Fibrils of fibrin are fine and barely visible under the light microscope
127
Name the PM clot that is yellow (plasma), smooth, shiny, found in heart chambers.
| Gross Appearance of PM Clots
Chicken fat clot
128
Name the PM clot that is dark red, smooth, shiny, and jelly-like.
| Gross Appearance of PM Clots
Currant-jelly clot
129
What causes the yellow color in chicken fat clots?
Separation of plasma from red cells
130
Can chicken fat clots be entangled in cardiac valves?
Yes
131
**Comparison Between PM Clot and Thrombus**
Formation: Ante-mortem vs post-mortem?
Thrombus – ante-mortem;
PM clot – post-mortem
132
Cause of formation?
| Comparison Between PM Clot and Thrombus
Thrombus – endothelial injury;
PM clot – stagnant blood of dead animal
133
Attachment?
| Comparison Between PM Clot and Thrombus
Thrombus – vessel wall;
PM clot – none
134
Consistency?
| Comparison Between PM Clot and Thrombus
Thrombus – dry;
PM clot – moist
135
Surface?
| Comparison Between PM Clot and Thrombus
Thrombus – granular, rough;
PM clot – smooth, glistening
136
Endothelium of vessel?
| Comparison Between PM Clot and Thrombus
Thrombus – damaged and rough;
PM clot – smooth and intact
137
Organization?
| Comparison Between PM Clot and Thrombus
Thrombus – partly organized;
PM clot – none
138
Structure?
| Comparison Between PM Clot and Thrombus
Thrombus – laminated;
PM clot – homogenous
139
**Gross Appearance** of PM
**a. Currant-jelly clot**
* It is **dark red in color, smooth and shiny** on the outside with a jelly-like appearance
* Has a **uniform texture** and is unattached to the vessel wall
**b. Chicken fat clot**
* A **result of the settling and separation of the red cells **from the fluid part of the blood
* Commonly found in the **chambers of the heart when post-mortem clotting** is delayed
* Has a smooth and shiny surface of a currant-jelly clot but has the yellow color of plasma
* **Unattached to the vascular lining but may be entangled** in the cardiac valves and chordae tendinae
140
What is the process by which a solid mass is transported from one part of the body to another?
Embolism
141
What is the solid mass that moves in embolism called?
Emboli
142
Types of Emboli
a. **Simple or Fibrinous emboli**
b.**Fatty emboli**
c. **Gas emboli or Air emboli**
d. **Septic emboli**
e. **Parasitic emboli**
f. Others - *emboli from **neoplastic cells, bone marrow cells, amniotic cells and other foreign bodies***
143
are **fragments of thrombi or thrombo emboli** carried by blood;
resembles thrombi microscopically and grossly;
can block small arteries and again become organized into a thrombus
a. Simple or Fibrinous emboli
144
What is the effect of simple/fibrinous emboli?
Can block small arteries and again become organized into a thrombus
145
Name emboli caused by release of adipose cells from body fat, e.g., after long bone fracture.
Fatty emboli
146
due to release of adipose cells from body fat e.g. following fracture of a long bone (due to car accidents) and **can cause pulmonary and brain embolism**
b. Fatty emboli
147
Name emboli seen during venipuncture or IV air injection.
Gas emboli / Air emboli
148
seen during venipuncture or when large amount of air is injected during IV injection **(in rabbits, euthanasia is done by injecting 10mL of air into the ear vein)**
Gas emboli / Air emboli
149
– **composed of clumps of bacterial cells or fungal agents or skin hair** *injected during venipuncture;*
may come from septic thrombus on left heart valve which can be disseminated throughout the body or
in case of a septic thrombus on right heart valve it may be disseminated into the lung
Septic emboli
150
What is the origin of septic emboli from **left heart valve?**
Disseminated throughout the body
151
What is the origin of septic emboli from **right heart valve?**
Disseminated into the lungs
152
Name emboli resulting from heartworm fragments or migration of *Strongylus vulgaris* larvae.
Parasitic emboli
153
may be fragments of heartworm or it may result from migration of Strongylus vulgaris larvae in walls of celiac and cranial mesenteric arteries =
**thrombosis and emboli dissemination to intestines** *causing colic in horses which is fatal*
Parasitic emboli
154
Effect of parasitic emboli in horses?
**Thrombosis and emboli dissemination to intestines** causing colic (fatal)
155
Name other sources of emboli?
* Neoplastic cells,
* bone marrow cells,
* amniotic cells, and
* other foreign bodies
156
Common sites of embolism?
Organs with **end artery supply** (**brain, kidneys, spleen, myocardium**)
157
Effects of Embolism:
* Emboli in organs with end-artery supply = **ischemia or infarction**
* In organs with collateral blood supply = **atrophy**
* In veins (rare in occurrence) = **congestion which favors thrombogenesis**
* **Allows for spread of infectious organisms** throughout the body
158
Emboli in organs with collateral blood supply cause what?
| Effects of Embolism
Atrophy
159
Emboli in organs with end-artery supply cause what?
| Effects of Embolism
schemia or infarction
160
Emboli in veins (rare) cause what?
| Effects of Embolism
Congestion, favors thrombogenesis
161
* **Decrease flow of arterial blood** to a certain area; local anemia
Ischemia
162
What may **result from ischemia**, either as partial or complete reduction of oxygen supply?
Hypoxia (partial) or Anoxia (complete)
163
What is the ultimate consequence of prolonged ischemia leading to tissue death?
Necrosis
164
Effects of Ischemia depends on:
a. Organ involved – if supplied by an end-artery = necrosis
b. Degree of occlusion or anoxia – gradual loss of oxygen supply = atrophy
c. Degree of collateral circulation
d. Size of the vessel involved
165
The effects of ischemia depend on which factor relating to the organ?
Organ involved (end-artery supply may cause necrosis)
166
The effects of ischemia depend on which factor relating to oxygen supply?
Degree of occlusion or anoxia (gradual loss causes atrophy)
167
The effects of ischemia depend on which factor relating to alternate pathways of blood flow?
Degree of collateral circulation
168
Causes of Ischemia?
Causes:
1. **Compression of blood vessels** from without as seen in tumor growth, pregnancy, etc.
2. **Complete or partial obstruction to blood vessels** = thrombi formation
169
Name the **four functional causes of ischemia.**
1. Stagnant anoxia,
1. Anoxic anoxia,
1. Anemic anoxia,
1. Histotoxic anoxia
170
Which type of functional ischemia occurs due to **decreased flow of oxygenated blood as in shock?**
Stagnant anoxia
171
Which type occurs **due to insufficient oxygenation of blood**, e.g., severe pneumonia?
Anoxic anoxia
172
Which type occurs **due to decreased oxygen-carrying capacity of blood** or low hemoglobin, e.g., carbon monoxide poisoning?
Anemic anoxia
173
Which type occurs when **tissues cannot utilize oxygen despite normal oxygenation,** e.g., cyanide poisoning?
Histotoxic anoxia
174
- an area of necrosis caused by ischemia; caused by an obstruction to an artery or vein following thrombosis or embolism
Infarction/Infarct
175
What is defined as an area of necrosis caused by ischemia?
Infarct
176
What is the process of infarct formation?
Infarction
177
Which **tissues are susceptible to infarction** due to their high biological activity? (Enumerate)
Brain, Renal tubular epithelia, Cardiac muscles, Parenchymal tissues
178
Which tissues are resistant to infarction?
Mesenchymal cells (e.g., fibroblasts)
179
Review of the **basic anatomic patterns of the arterial system** in organs
Functional end-artery
Parallel system
Dual blood supply
180
What is a single vessel that gives off small branches at its end, e.g., i**n brain, kidney, spleen, heart?**
Functional end-artery
181
**has separate blood supply with several anastomotic channels** e.g. skeletal muscles and most tubular organs like the intestines and uterus
* Thrombotic or embolic occlusion rarely leads to infarction but in case occlusion occurs near the origin of the artery from the abdominal aorta = i**nfarction such as in thrombo-emboli colic in horses** caused by *Strongylus vulgaris* resulting to verminous arteritis of cranial mesenteric artery
Parallel system
182
In the parallel system, when does thrombotic or embolic occlusion cause infarction?
**When occlusion occurs near the origin of the artery** (e.g., abdominal aorta – thromboembolic colic in horses from Strongylus vulgaris)
183
What is the blood supply type with two vessels supplying an organ from different sources, e.g., lungs or liver?
Dual blood supply
184
When is infarction rare in organs with dual blood supply?
Except in chronic passive congestion affecting both supplies
185
when 2 blood vessels supply an organ from different sources
e.g. **lungs – pulmonary and bronchial**
**arteries, liver – hepatic artery and portal vein**
Dual blood supply
186
Based on Bacterial Contamination
| Classification of Infarcts based on the following:
Bacterial contamination
a. Septic infarct
b. Bland infarct
Color
a. White or anemic
b. Red or hemorrhagic
187
1. Which infarcts are darkly hemorrhagic?
1. Which infarcts are pale?
1. Venous infarcts
1. Arterial infarcts (except lungs)
188
Which solid parenchymatous organs **present pale infarcts?**
Heart, Kidney
189
What is the shape of infarcts in the kidneys?
Triangular
190
arterial infarcts are generally pale except in ?
in the lungs which show hemorrhagic infarcts
191
What happens if arterial obstruction is gradual?
| Infarcts
Blood is shunted to other arteries (e.g., carotid obstruction → vertebral artery via basilar artery)
192
* **Infarction often results from arterial obstruction**; if *gradual in development, blood is shunted to other arteries*
e.g. **obstruction of carotid arteries to the brain**; *blood is shunted to the vertebral artery via the basilar artery*
basahin nalang josko
193
What is defined as the accumulation of fluid in tissue or interstitial spaces?
Edema
194
* Interaction of various forces involved in the microcirculatory bed is described by
| Review of Fluid dynamics in the capillary bed:
starling equilibrium
195
* This equilibrium is achieved by the balance of filtering pressure exerted across the filtering membrane which is the ?
capillary endothelia
196
What is the **pressure difference across capillary endothelia** allowing fluid balance?
Net filtration pressure
197
What is the **difference between plasma colloid osmotic pressure and tissue hydrostatic pressure** at venous end?
Net absorption pressure
198
* It means that a balance exists between the net filtration pressure and net absorption pressure so that all fluid that is filtered out of the capillary endothelia to the interstitium is again reabsorbed and returned to the circulation
“starling equilibrium”
199
Plasma colloid osmotic pressure depends on what?
Plasma protein concentration
200
How does plasma protein concentration compare to interstitial fluid?
3-4x greater
201
What happens if the balance of forces is disrupted in capillaries?
Fluid accumulates in interstitial spaces → edema
202
* Change in balance of forces can = accumulation of fluid in interstitial spaces
| edema
ayan basahin yan
203
**Mechanisms** in Edema formation:
a. Decrease plasma colloid osmotic pressure
b. Increase in blood hydrostatic pressures (II)
c. Increase vascular permeability
d. Lymphatic obstruction
204
* Occurs when there is a decrease in plasma protein concentration in the blood e.g. albumin
* Any disease that results to increase loss of plasma proteins/albumin with accompanying decrease in synthesis = edema
a. Decrease plasma colloid osmotic pressure
205
* E.g. of disease conditions are:
| . Decreased Plasma Colloid Osmotic Pressure
a. Liver disease = *hypoalbuminemia*
b. Starvation
c. Renal disease = *loss of albumin especially with glomerular lesions*
d. Enteric diseases and parasitism
206
What causes edema due to increased venous pressure?
Increased blood hydrostatic pressure
207
* Occurs due to disease that results to increase venous (II) that eventually leads to increase capillary (II) (II at capillary level is influenced by the venous II)
* Increase venous II = decrease absorptive function of venous end so that the fluid that goes out from capillary endothelium at the arterial end will not be absorbed in the venous end
Increased blood hydrostatic pressure
208
* Causes diseases that result to obstruction in venous blood flow which may be local or generalized e.g.:
| b. Increase in blood hydrostatic pressures (II)
a. Local – occlusion of veins by thrombosis or emboli; compression as in pregnancy
b. Generalized – heart failure with leakiness of the blood vessel and increase Na retention due to increase aldosterone secretion
209
Name generalized causes of increased venous pressure leading to edema.
Heart failure, Increased Na retention (via aldosterone)
210
Name local causes of increased venous pressure leading to edema.
Occlusion of veins by thrombosis/emboli, Compression (e.g., pregnancy)
211
* Occurs during localized inflammation; due to increased vascular permeability in response to chemical mediators which are vasoactive and also due to toxins (e.g. bee sting venom)
* Edema fluid contains increase protein concentration because water and plasma proteins leak out of damaged endothelial wall
c. Increase vascular permeability
212
Which mediators increase vascular permeability?
Vasoactive chemical mediators, toxins (e.g., bee sting venom)
213
d. Lymphatic obstruction
* Result to local edema
basahin diko alam pano itatanong
214
* Causes:
| d. Lymphatic obstruction
* Causes:
a. Obstruction of lymphatics by growing neoplasms
b. Obstruction by emboli
c. Damage to lymphatics after surgery
215
Microscopically, what changes are seen in tissues with edema?
* Enlargement of spaces between adjacent cells, fibrils and other structures
* Faint, pink-staining residue of precipitated albumin and other proteins in the plasma fluid; lymphatic vessels are dilated
* Few RBC and WBC; presence of strands of fibrin
216
Gross Description of Edema
* Organs are wet and heavy
* Swollen edematous area has a firm and doughy consistency that pits on pressure
* Cut surface contain pale yellowish fluid in between tissue spaces
* Fluid may drip form cut surface or may be squeezed out when pressure is applied on tissues
* Affected area is cool to touch with no sign of pain
* In case of lung edema – cut area will release water with a slight tinge of blood
; appears distended and has a firm consistency
* In kidney edema – not readily seen; kidney is swollen but no fluid is observed
217
What occurs in chronic edema?
Formation of fibrous connective tissue → thickened organ/tissue
218
Terms associated with Edema:
Name edema that collects in lowermost parts of the body.
Dependent edema
219
when edema is generalized and severe so that when pressure is applied on the area a dent or depression results
2. Pitting edema
220
Terms associated with Edema:
1. Dependent edema
2. Pitting edema
3. Ascites
4. Hydrothorax
5. Hydropericardium
6. Hydroperitoneum
7. Pericardial effusion
8. Hydrocele
9. Anasarca
221
Name edema with fluid accumulation in the abdomen.
Ascites
222
Name edema with fluid in the thoracic cavity.
Hydrothorax
223
Name edema with fluid in pericardial sac.
Hydropericardium / Pericardial effusion
224
Name edema with fluid in the peritoneum.
Hydroperitoneum
225
Name edema in the scrotum.
Hydrocele
226
Name generalized massive edema throughout the body.
Anasarca
227
What is the pathological formation of blood clots within the body?
Disseminated Intravascular Coagulation (DIC)
228
* Due to defects in clotting mechanism/hemostasis
Disseminated Intravascular Coagulation (DIC)
229
Mechanisms Involved in DIC:
1. Activation of the intrinsic clotting mechanism independent of tissue damage
2. Activation of the extrinsic clotting mechanism following vascular injury with release of tissue thromboplastin e.g. widespread neoplasms, tissue necrosis, infectious diseases, surgery and severe trauma
3. Direct activation of prothrombin by proteolytic enzymes e.g. when trypsin is released in the circulation following pancreatitis and in snake bites
230
Stages of Reaction in DIC
**a. Hypercoagulable stage** – associated with thrombin formation that results to platelet aggregation and fibrin formation =
thrombosis of capillaries, arterioles and venules and infarction in many organs
**b. Hypocoagulable stage –**
results from:
1. Activation of the fibrinolytic system with release of fibrin and fibrinogen degradation products that suppress fibrin formation
2. Depletion of platelets
3. Depletion of clotting factors e.g. fibrinogen and F-VIII
231
Effects of DIC:
**1. Hemorrhagic diatheses/consumption coagulopathy/defibrination syndro**me
* Bleeding occurs due to depletion of platelets and other clotting factors
**2. Shock**
* A result of the release of vasoactive substances from platelets, interaction of the clotting mechanism with kallikrein-kinin system that leads to vascular dilation, hypotension and vasomotor collapse
232
* Acute peripheral circulatory failure due to impaired circulatory control or loss of circulatory fluid caused by sudden or severe injury
Shock
233
* There is insufficient blood that goes back to the heart, there’s decrease blood pressure and blood flow
Shock
234
* Results to cell damage due to hypoxia causing decrease oxidation phosphorylation and ATP production; cells obtain energy thru anaerobic glycolysis = increase lactate and metabolic acidosis
Shock
235
Stages of Shock
**1. Stage of ischemia hypoxia** = reflex arterial vasoconstriction
**2. Stage of stagnant hypoxia** associated with:
a. Gradual decrease of precapillary vasoconstriction
b. Pooling of blood in the capillary
c. Decline in venous return
d. Decrease cardiac output
e. Diminished blood pressure
**3. Stage of irreversibility** – fluid shift from intravascular to extravascular space and microembolism of capillaries
236
Regulatory mechanisms that control Shock
**a. Sympathetic nervous system** – produce peripheral vasoconstriction, tachycardia and redistribution of blood to vital organs
**b. CNS** – activated when hypoxia is present due to decrease ventilation as a result of hemodynamic changes in lungs
**c. Adrenal glands** – stimulated to release catecholamine (epinephrine and norepinephrine) and glucocorticoids
**d. Stimulation of Renin-Angiotensin-Aldosterone Axis System** – cells are stimulated in kidneys = increase renal tubular reabsorption to conserve water and sodium ions in order to increase systemic BP
237
Effects of Shock
**1. Effects on blood vessels**
a. Spasms of blood vessels with increase in blood pressure following activation of rein-angiotensin-aldosterone axis system
b. Decrease blood supply to renal cortex = damage
c. Ischemic injury
**2. Systemic pH changes (metabolic acidosis**)
**3. DIC**
238
Lesions of Shock
* Usually observed during necropsy
239
Gross lesions Shock:
1. Severe edema and congestion of the lungs (congestive atelectasis)
2. Visceral pooling of blood and fluids e.g. fluid in GIT, acute ulcerations and hemorrhages in the GIT
3. Hemorrhages in the heart specifically in the subendocardium
240
Microscopic lesions:
1. Microthrombi in lungs and kidney glomeruli due to DIC
2. Fatty changes or necrosis of hepatocytes
3. Hemorrhage and necrosis of cortical cells in the adrenal glands
4. Acute renal tubular necrosis
241
Name the gross lesions observed in necropsy during shock.
* Severe edema and congestion of lungs (congestive atelectasis)
* Visceral pooling of blood and fluids (e.g., GIT fluid, acute ulcerations, hemorrhages)
* Hemorrhages in the subendocardium of the heart
242
Name the effects on blood vessels in shock. (Enumerate)
a. Spasms of blood vessels with increased BP (after renin-angiotensin-aldosterone activation)
b. Decreased blood supply to renal cortex → damage
c. Ischemic injury
d. Systemic pH changes (metabolic acidosis)
243
Which system produces peripheral vasoconstriction, tachycardia,
| Regulatory Mechanisms Controlling Shock
Sympathetic nervous system
244
Which organ system is activated when hypoxia is present due to hemodynamic changes in lungs?
| Regulatory Mechanisms Controlling Shock
Central Nervous System (CNS)
245
Which glands are stimulated to release catecholamines and glucocorticoids during shock?
| Regulatory Mechanisms Controlling Shock
Adrenal glands
246
What system is stimulated in kidneys to increase water and sodium reabsorption in shock?
| Regulatory Mechanisms Controlling Shock
Renin-Angiotensin-Aldosterone Axis System
247
What occurs during stagnant hypoxia? (Enumerate)
| Stages of Shock
a. Gradual decrease of precapillary vasoconstriction
b. Pooling of blood in capillaries
c. Decline in venous return
d. Decrease cardiac output
e. Diminished blood pressure
248
What is the stage associated with reflex arterial vasoconstriction?
Stage of ischemia hypoxia
249
What are the four main mechanisms of edema formation?
1. Decrease plasma colloid osmotic pressure
2. Increase in blood hydrostatic pressures
3. Increase vascular permeability
4. Lymphatic obstruction
250
What causes decrease plasma colloid osmotic pressure? In edema
I
A decrease in plasma protein concentration in the blood (e.g., albumin).
251
What happens in diseases with increased loss of plasma proteins/albumin and decreased synthesis?
Edema develops
252
Give examples of disease conditions that cause decrease plasma colloid osmotic pressure.
In edema
a. Liver disease → hypoalbuminemia
b. Starvation
c. Renal disease → loss of albumin, especially with glomerular lesions
d. Enteric diseases and parasitism
253
When does increased blood hydrostatic pressure occur?
In edema
In diseases that result in increased venous pressure, eventually leading to increased capillary pressure.
254
What is the effect of increased venous pressure at the venous end?
In edema
Decreased absorptive function, so fluid that exits the arterial end is not reabsorbed at the venous end.
255
What are the causes of increased blood hydrostatic pressure?
Diseases that obstruct venous blood flow, either local or generalized.
256
Give examples of local venous obstruction.
a. Occlusion of veins by thrombosis or emboli
b. Compression as in pregnancy
257
Give examples of generalized venous obstruction.
Heart failure with leakiness of the blood vessels
Increased sodium retention due to increased aldosterone secretion
258
What are the causes of lymphatic obstruction?
a. Obstruction of lymphatics by growing neoplasms
b. Obstruction by emboli
c. Damage to lymphatics after surgery
259
What are the microscopic descriptions of edema?
Enlargement of spaces between adjacent cells, fibrils, and other structures
Faint, pink-staining residue of precipitated albumin and other proteins in plasma fluid
Dilated lymphatic vessels
Few RBCs and WBCs present
Strands of fibrin may be observed
260
What are the gross characteristics of organs with edema?
Organs are wet and heavy.
Swollen edematous area has a firm and doughy consistency that pits on pressure
• Cut surface contain pale yellowish fluid in between tissue spaces
• Fluid may drip form cut surface or may be squeezed out when pressure is applied
on tissues
• Affected area is cool to touch with no sign of pain
• In case of lung edema – cut area will release water with a slight tinge of blood;
appears distended and has a firm consistency
261
262
not readily seen; kidney is swollen but no fluid is observed
In edema
kidney edema
263
What happens in chronic edema?
Formation of fibrous connective tissue that leads to thickening of the organ or tissue.
264
Edema fluid collects in the lowermost portions of the body, such as the limbs and abdomen.
dependent edema
265
Generalized and severe edema where pressure applied to the area produces a dent or depression.
pitting edema
266
Accumulation of fluid in the peritoneal cavity.
ascites
267
Accumulation of fluid in the pleural cavity
hydrothorax
268
Accumulation of fluid in the pericardial sac.
hydropericardium
269
Another term for fluid accumulation in the peritoneal cavity.
hydroperitoneum
270
Abnormal collection of fluid in the pericardial cavity.
pericardial effusion
271
Accumulation of fluid in the scrotum (tunica vaginalis).
hydrocele
272
Severe, generalized edema throughout the body.
anasarca
Pathology 141
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