Pathomorphology - circulatory disorders Flashcards
(113 cards)
1
Q
ARTERIAL or ACTIVE HYPEREMIA is
A
Active engorgement of vascular beds with a normal or decreased outflow of blood resulting in an excess amount of blood in an organ (refers to both volume and flow)
2
Q
TYPES of hyperemia (2)
A
- Physiologic hyperemia
- Pathologic hyperemia
3
Q
Give 4 examples of physiologic hyperemia
A
blood flow to the stomach and intestines during digestion
blood flow in the muscles of athletes during exercise
blood flow in skin to dissipate heat
neurovascular hyperemia (blushing)
4
Q
Give examples of pathologic hyperemia
A
-Response to an inflammatory stimuli (NOT THE CAUSE of the hyperemia)
-Result of an underlying pathologic process
- Engorgement of the vascular bed due to increased arteriolar blood flow into an area
- Cardinal sign of inflammation = “Hyperemia of inflammation”
5
Q
4 mechanisms for pathogenesis of hyperemia
A
- angioneurotic
- collateral
- postanemic
- inflammatory hyperemia
6
Q
VENOUS or PASSIVE HYPEREMIA or CONGESTION is
A
Passive engorgement of a vascular bed generally caused by a decreased outflow with normal or increased inflow of blood.
7
Q
2 factors used in defining the types of congestion
A
- DURATION: acute/chronic
Acute: implies abrupt onset with rapid development
Chronic: slowly developing and/or present for a long time - EXTENT: localized/generalized
Local: change confined to a discrete area (localized or limited)
Generalized: indicates a systemic change or generalized within an organ
8
Q
Acute local congestion:
A
Local obstruction to venous drainage
- Passive engorgement of the drainage area
- Blood backs up into the microvascular bed
- Local venous engorgement results
9
Q
Acute generalized congestion:
A
Occurs following euthanasia or acute heart failure
10
Q
Chronic local congestion:
A
Differs from acute local congestion by the time frame required.
E.g. A slowly developing tumour or abscess enlarges that eventually compresses adjacent veins can produce congestion.
Or - A chronic inflammatory lesion that progresses to fibrosis and can lead to venous outflow obstruction.
e.g. Hepatic cirrhosis
11
Q
Chronic generalized congestion:
A
(passive hyperemia) is most often associated with pathology of either the heart or lungs.
12
Q
APPEARANCE of congestion:
Grossly:
A
Cut surfaces of congested tissues are dark red to brown and wet.
Blood oozes on cut section.
Wet - due to edematous tissue.
13
Q
APPEARANCE of congestion:
Histologically:
A
acute - associated with capillaries engorged with blood, usually some edema
chronic -
- engorgement by poorly oxygenated venous blood
- degree of chronic local hypoxia
- degeneration, atrophy or even necrosis of parenchymal cells
14
Q
4 consequences - of chronic pulmonary congestion (hyperemia)
A
- Microhemorrhages
Small capillaries rupture¸ intra-alveolar hemorrhages¸ extravascular red cells are phagocytized by alveolar macrophages¸ hemosiderin pigment “heart failure cells” - Pulmonary edema causes interference with gaseous exchange
- fibrosis of interstitium (fibroblasts secrete excess collagen)
- pulmonary arteries subject to pulmonary hypertension
15
Q
a cardiac cause of pulmonary congestion
A
Chronic failure of left ventricle impedes the flow of blood from the lungs to the heart results in chronic passive congestion in alveolar capillaries and alveolar capillaries become engorged with blood. coupled with edema
16
Q
2 causes of liver congestion
A
right heart failure
pulmonary hypertension
17
Q
gross appearance of liver congestion
A
mottled appearance - “nutmeg liver”
Dark red appearance of the zones around the central veins and yellow-brown appearance of less affected parenchyma around the portal areas.
- increased hepatic size/hepatomegaly (acute) due to volume and mass of added blood
- Chronic, low-grade hypoxia and pressure¸ atrophy and death of central hepatocytes
18
Q
HEMORRHAGE VS HYPEREMIA/CONGESTION:
A
Hemorrhage involves blood outside vessel wall ie: extravascular
Hyperemia involves blood inside of vessel wall ie: intravascular
19
Q
chronic centrilobular fibrosis also known as
A
“Cardiac cirrhosis”
Hemosiderin-filled fixed macrophages (Kupffer cells) due to erythrocyte phagocytosis.
- blood filled central veins¸ fibrous connective tissue
- dilation of sinusoids, pressure atrophy and necrosis of
centrilobular hepatocytes, dilated centrally located lymphatics
20
Q
4 stages to teh developement of chronic passive hepatic congestion
A
Stage I: centrilobular stasis
Stage II: centro- and mediolobular stasis with mediolobular steatosis and extension of stasis
Stage III: changes in lobules, enlarged area of stasis
Stage IV: centrolobular stasis, mediolobular fibrosis, cardiac cirrhosis of the liver
21
Q
What are “heart failure cell” in pulmonary induration?
A
hemosiderin-pigmented macrophages in alveolar macrophages
22
Q
Local insufficient supply of blood or ischemia is
A
reduction or lack of blood flow in a tissue, organ or body part due to insufficient flow or obstruction of arterial blood.
23
Q
oligaemia
A
General insufficient supply of blood that is caused by decrease in the amount of blood, for example due to massive loss of blood, is called oligaemia or hypovolemia.
24
Q
Angiospastic
A
A sudden constriction of a blood vessel, causing a reduction in blood flow.
25
Angiospastic or refractory ischemia develops as a result of
of reflex constriction of the vasomotor centres and blood vessels under the influence of various stimuli.
26
Obstructive ischemia is caused by
obstruction of arterial lumen with a thrombus or an embolus, or constriction of arterial lumen due to their pathological thickening.
27
Compression ischemia develops when
the artery is compressed from the outside (scar tissue, tumor, ligature).
28
Collateral ischemia can occur in organs where
blood outflow may be fast.
29
Thrombosis is
the formation, development or presence of a solid mass within the blood vessels or heart.
Adherent to the vascular endothelium and must be differentiated from a simple (post mortem) blood clot.
30
What is a thrombus?
An aggregation of blood factors, primarily platelets and fibrin with entrapment of cellular elements, which frequently causes vascular obstruction at the point of its formation or embolism (detachment and travel).
Arterial thrombi are attached and grow away from the heart.
Venous thrombi are attached and grow in the direction of blood flow (to heart).
Arterial and venous thrombi differ in appearance.
31
Pathogenesis of thrombosis, 3 primary mechanisms:
1. Endothelial injury
2. Alterations in normal blood flow
3. Hypercoagulability (thrombophilia)
32
Endothelial injury in the pathogenesis of thrombosis
Dominant influence = can lead to thrombosis by itself
e.g: inflammation of heart valves
Exposure of subendothelial ECM (extracellular matrix),
platelet adherence,
release of tissue factor,
depletion of prostacyclin,
primary and secondary hemostatic plug formation.
33
prostacyclin in coagulation
Prostacyclin is a potent but unstable vasodilator, and inhibitor of platelet aggregation.
Platelet aggregability may be constantly regulated in vivo by local or circulating prostacyclin.
34
Alterations in normal blood flow in the pathogenesis of thrombosis
turbulence or stasis
Normal blood flow is laminar - cellular elements in the middle, surrounded by plasma.
Disruption of normal laminar flow allows platelets to contact endothelium.
Stasis prevents dilution of activated clotting factors by freshflowing blood which allows the build up of thrombi (slows the inflow of anticoagulants such as prostacyclin).
Promotes endothelial cell activation and thus thombus formation.
35
Hypercoaguability in the pathogenesis of thrombosis
Definition: any alteration of the coagulation pathways that predisposes to thombosis.
Involving:
Coagulation factors
Coagluation-inhibitory factors
36
Virchow's triad
Virchow's triad or the triad of Virchow describes the three broad categories of factors that are thought to contribute to thrombosis.
They include intravascular endothelial injury, abnormal(stasis) flow, and the presence of a hypercoagulable state.
37
Thrombi are divided (4)
White thrombus
Red thrombus
Mixed thrombi
Hyaline thrombus
38
A white thrombus is
white or greyish white and of thick consistency.
White thrombi mainly consist of thrombocytes, fibrin and leukocytes.
39
A red thrombus is
dark red. Red thrombi consist of fibrin and blood
components in about the same proportions as in circulating blood.
40
Mixed thrombi are
a combination of white and red thrombi.
41
A hyaline thrombus consists of
agglutinated blood components and hyaline mass of blood plasma precipitate.
42
According to lumen, thrombi are classified as: (2)
mural thrombus
occluding thrombus
43
Dissolving of thrombus may be (2)
aseptic (fibrinolytic dissolution by blood factors)
septic (by microbes that have penetrated thrombus mass, often producing pus).
44
fate of thrombus (5)
1. propagation
2. embolization
3. dissolution (fibrinolysis)
4. organization
(endothelial cells, smooth muscle cells, fibroblasts, capillaries)
5. recanalization (new small lumina)
45
Embolism =
detached intravascular solid, liquid or gaseous mass carried from point of origin by blood to distant site
46
6 types of embolism:
1. thrombembolism (99%)
pulmonary x systemic -> infarction
2. cellular - amniotic fluid, tumor cells
3. subcellular - debris
4. fat
5. air
6. foreign bodies - catheter
47
paradoxical embolism
occurs when a thrombus crosses an intracardiac defect into the systemic circulation.
48
saddle embolism
a rare type of acute pulmonary embolism
a visible thrombus located at the bifurcation of the main pulmonary artery
49
Systemic thromboembolism
emboli which travel through the systemic arterial circulatory system. The vast majority of these arise within the heart secondary to atrial fibrillation (altered flow) or thrombus formation over an area of myocardial infarction (altered wall).
can cause infarctions in various parts of the body such as brain (10%), bowel + kidney + spleen
50
Fat embolism sources (3)
fractures of bones with fatty bone marrow,
soft tissue trauma,
burns
51
Definition of infarction.
Definition: Infarction is a necrotic focus that has occurred in the organ, because blood circulation in the organ has stopped.
Extreme result of ischemia
52
Causes/ mechanisms of infarction.
Infarction occurs in organs, where the arteries have few anastomoses or they are not well-developed. That is why collateral circulation will not develop when the main branch of the artery is obstructed (kidneys, spleen, lungs, myocardium, brain, bowel)…
53
Infarction macroscopically (4)
white or ischemic infarction
red or hemorrhagic infarction
white or ischemic infarction with hemorrhagic borders
Venous infarction
54
describe white or ischemic infarction macroscopically
arterial occlusion, solid organs: heart, spleen, kidney,
55
describe red or hemorrhagic infarction macroscopically
venous occlusion, loose tissue (lung) blood collection, previously congested organs.
56
describe white or ischemic infarction with hemorrhagic borders macroscopically
develops, when the reflectory spasm that started with blocking the artery is replaced by paralytic widening in its branches, which results in blood filling the peripheral small vessels, leading to haemostasis and hemorrhagic diapedesis (kidneys and myocardium).
57
describe Venous infarction macroscopically
the vein is compressed fast or due to thrombosis
58
infarction outcomes depend on (5)
1. Degree/severity of injury to vascular supply
2. Size of artery affected
3. Degree of vascular occlusion
4. Collateral blood supply available
5. Vulnerability of cells to ischemia
59
Coagulative necrosis of the myocardium, with secondary myomalacia (softening) macrosopically (2)
Irregular in shape
White or white with hemorrhagic border
60
Coagulative necrosis of the kidneys macroscopically (2)
Pyramid shape necrosis
White or white with hemorrhagic border
61
Coagulative necrosis of the spleen macroscopically (2)
Pyramid shape necrosis
White
62
Coagulative necrosis of the lung macroscopically (2)
Pyramid shape necrosis
Red
63
Liquefactive necrosis of the bowel macroscopically (2)
Irregular
Red
64
Liquefactive necrosis of the brain macroscopically (2)
Irregular
white or red encephalomalacia (softening)
65
Definition of venous infarction.
Definition: obstruction or compression of vein - venous obstruction occurs, when the vein is compressed fast or due to thrombosis.
-may cause slowly developing stasis with engorgement of the tributary venous system (chronic passive hyperemia)
- Serious if anterior or posterior vena cava obstructed
- common cause of shock
66
consequence and sequelae of Acute Blockage of the Portal Vein:
infarction of the intestine
shock and death
Example: Gastric torsion in dogs, obstruction of the portal venous system, severe venous congestion, vascular stasis ischemia,
loss of endothelial integrity, hemorrhages, shock
67
Bronchiectasis
Bronchiectasis is a chronic condition where the walls of the bronchi are thickened from inflammation and infection.
68
Outcome of venous infarction
Fast changes, hemorrhagic necrosis
- Spleen hemorrhagic necrosis requires quick splenectomy.
- Hemorrhagic infarction of bowel segment requires enterectomy
69
Definition of hemorrhage.
Definition: Escape of blood from the cardiovascular system (extravasation).
Discharge of blood from the vascular compartment to the exterior of the body or
enclosed within a tissue. Capillary bleeding can occur under conditions of chronic congestion.
70
ecchymoses
“Ecchymosis” is the medical term for bruises.
71
HEMORRHAGIA PER RHEXIN:
hemorrhage due to a substantial tear present in the blood vessel (or heart)¸ moderate flow of blood out of vascular system.
72
HEMORRHAGIA PER DIABROSIN:
occurs when the wall of a blood vessel is damaged due to inflammations, ulcers, tumors.
73
HEMORRHAGIA PER DIAPEDESIN:
hemorrhage due to a small defect or red blood cells passing through the wall in hyperemia of inflammation.
74
extravasate
Escape of blood from vessels is also called extravasation and the blood outside the vessel is extravasate.
so hemorrhage
75
microscopically, older hemorrhages can be identified by
degraded erythrocytes and phagocytosed erythrocytes in macrophages
76
latin term for this type of hemorrhage
hemorrhagia per rhexin
77
latin term for this type of hemorrhage
hemorrhagia per diabrosin
78
latin term for this type of hemorrhage
hemorragia per diapedesin
79
Epistaxis
nosebleed
80
Hemoptysis
coughing up of blood or bloody sputum from
the lungs or airway
81
Hematemesis
vomiting of blood
82
Metrorrhagia
uterine bleeding
83
Melena
is the passage of black, tarry stools.
84
Hematochezia
is the passage of fresh blood per anus, usually in or with stool.
85
HEMARTHROSIS:
Blood in a joint space.
86
Cardiac tamponade
specific syndrome of acute cardiac failure which is caused by massive fluid accumulation within the pericardium usually blood, hemopericardium, which results in acute right heart failure.
87
EXTRAVASATION:
Escape of blood from a vessel into tissue (also used as extensive hemorrhage within the substance of a tissue).
88
PETECHIAL HEMORRHAGES:
PETECHIAE: minute, pin-point foci of haemorrhage up to 1-2 mm in size.
89
HEMORRHAGIC DIATHESIS:
Increased tendency to hemorrhage from usually insignificant injuries.
Seen in a wide variety of clinical disorders.
(A predisposition for abnormal bleeding).
Bleeding diathesis refers to an increased susceptibility to bleeding or bruising.
90
PURPURA:
Hemorrhages - 3mm. May be associated with diseases which cause petechiae, vascular inflammation or vascular damage. Often scattered on many body surfaces.
91
ECCHYMOTIC HEMORRHAGES:
ECCHYMOSES:
Larger than petechiae and usually blotchy or irregular areas up to >1-2 cm in size often seen
with trauma and other problems.
e.g. subcutaneous hematomas / bruises
92
SUFFUSIVE HEMORRHAGE:
Affected area is larger than ecchymosis and continuous.
93
PAINT BRUSH HEMORRHAGES:
Hemorrhages which look as though a paint brush dipped in red paint was hastily applied to the tisuse. Most commonly found on serosal or mucosal surfaces.
94
what gives a bruise its reb-blue color
hemoglobin
95
what gives a bruise its blue-green color
bilirubin
96
what gives a bruise its golden-brown color
hemosiderin / hematoidin
97
name 3 disturbances of lymph circulation
lymphostasis
lymphorrhagia
thrombosis of lymph vessels
98
Lymphatic blockage will result in
an inability of the lymphatics to remove normal fluid excess in the interstitium resulting in edema.
This may result from surgery or trauma damaging lymphatic system; neoplastic cells obstructing normal flow of lymph; parasites obstructing flow; or a hereditary malformation of the lymphatic system.
99
LYMPHANGIECTASIA:
Dilatation of lymphatic vessels.
100
LYMPHEDEMA:
Accumulation of lymph in subcutaneous tissues.
101
Thoracic duct obstruction and rupture will result in
chylothorax
lymph formed in the digestive system (chyle) accumulates in the chest cavity.
102
Definition of edema.
Definition: Abnormal accumulation of excess fluid in interstitial tissue spaces or in body cavities.
Edema fluid is outside the vascular fluid compartment and outside the cellular fluid compartment - in the interstitium.
103
Pathophysiologic mechanisms of edema (5)
1. Decreased plasma colloidal-osmotic pressure
2. Increased intravascular hydrostatic pressure
3. Lymphatic obstruction
4. Increased microvascular permeability
5. Sodium retention (both increased: vascular hydrostatic psi, plasma colloid osmotic psi)
Out of these only 4 is inflammatory.
104
edematous specimen microscopically?
Tissues are pale staining. Tissue spaces are distended by lightly staining eosinophilic fluid.
Blood vessels maybe filled with erythrocytes (hyperemia).
Lymphatics are dilated. The edema may be difficult to discern if the protein content
is low.
Collagen bundles of interstitial stroma are separated by an increase in intercellular space.
105
Inflammation of lymphatics can be called
lymphangitis
106
Pulmonary edema
Definition: accumulation of edema fluid in interstitium and alveoli of the lungs.
Sequence:
1. Fluid accumulates in interstitium
2. Fluid disrupts the basement membranes
of Endothelial cells & Pneumocytes
3. Leads to fluid within alveoli
4. Fluid drains via lymphatics
5. Result dilated pleural lymphatics
107
Name 3 potential causes of Cerebral edema
Trauma to the skull
Obstruction of venous outflow
Intracranial infections
(meningitis, brain abscess and encephalitis)
108
Cerebral coning
is herniation of the caudal cerebral
cortex through the tentorium cerebelli (horizontal projection of the meningeal dura mater separates the cerebellum from the cerebral hemispheres)
caused by cerebral edema
109
Cerebellar coning
is herniation of the cerebellum through
the foramen magnum
can be caused by cerebral edema
110
protein content of transudate
- low protein content < 30 g/L
- specific gravity below 1.017
- total nucleated cell count < 1.5 X 109/L
111
protein content of exudate
- Fluid Characteristics: "protein rich"
- high concentration of protein > 30 g/L
- specific gravity > 1.025
- total nucleated cell count > 7.0 X 109/L
112
Hydrops
a condition in which large amounts of fluid build up in tissues and organs, causing extensive swelling (edema).
Types of hydrops:
- abdominal cavity – ascites
- thoracic cavity – hydrothorax
- hydropericardium
- hydrocephaly
- hydrocele
- hydroarthrosis
113
anhydraemia
an abnormal reduction of water in the blood.
