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Semester 3 > General Pathology 300 (thrombi, emboli, infarcts) > Flashcards

General Pathology 300 (thrombi, emboli, infarcts) Flashcards

1
Q

thrombosis define

A

local coagulation or clotting of the blood in a part of the circulatory system.

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2
Q

thrombosis define.

A

Transformation of a fluid into a solid

Clotting of whole blood into an aggregate of blood cells & fibrin

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3
Q

fibrin define

A

Fibrin – a polymerized fibrinogen

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4
Q

fibrinogen define

A

a soluble protein present in blood plasma, from which fibrin is produced by the action of the enzyme thrombin.

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5
Q

fibrin function

A

Forms mesh network of thin filaments binding blood cells to form thrombus or hemostatic plug

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6
Q

thrombus define

A

a blood clot formed in situ within the vascular system of the body and impeding blood flow

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7
Q

“pathogenesis” of thrombi

A

..

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8
Q

where do thrombi form

A

Thrombi form only in living organisms

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9
Q

what is thrombi formation part of

A

End products of the coagulation sequence

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10
Q

what is normal function of thrombi

A

Normally activated to prevent blood loss from disrupted vessels

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11
Q

how does pathological thrombosis occur?

A

If coagulation sequence activated in intact vessels pathological thromboses develop

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12
Q

coagulation sequence activated in intact vessels

A

pathological thrombosis

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13
Q

normal blood?

A

consists of protein-rich fluid (plasma) and blood cells (formed elements)

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14
Q

blood circulating depends on

A

blood must be fluid and blood cells must be freely suspended

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15
Q

Fluidity results from

A

factors that promote coagulation and those that inhibit it

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16
Q

clotting vs anti-clotting –> homeostasis

A

Under normal conditions, clotting and anti-clotting are in balance

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17
Q

which mechanisms promote / counter-act thrombosis

A

Clotting factors and platelets promote thrombosis

and endothelial cells and plasmin counteract it

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18
Q

which THREE factors determine intravascular coagulation

A

Intravascular coagulation is the result of interaction between:

  1. Coagulation proteins
  2. Endothelial cells
  3. Platelets
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19
Q
  1. Coagulation proteins
A

Cascade sequence of activation

culminates in thrombin

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20
Q

what does thrombin do

A

Thrombin is a catalyst, promoting polymerization of fibrinogen into fibrin

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21
Q

what does fibrin do

A

Meshwork of fibrin is the framework for the clot which includes blood cells and proteins

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22
Q

intrinstic pathway, extrinsic pathway –> common pathway

A

..

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23
Q
  1. Endothelial Cells
A

Normal resting endothelial cells have antithrombotic function, but if activated will initiate coagulation.

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24
Q

resting vs activated endothelial cells

A

resting endothelial cells have antithrombotic function, but if activated will initiate coagulation.

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25
Q

how are endothelial cells “activated”

A

Can be activated by inflammation or trauma

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26
Q

what activates endothelial cells

A

Cytokines activate endothelial cells

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27
Q

E.g. of cytokines that activate endothelial cells

A

Can initiate thrombosis

E.g. IL-1 and TNF

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28
Q

IL-1

A

The Interleukin-1 family (IL-1 family) is a group of 11 cytokines that plays a central role in the regulation of immune and inflammatory responses

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29
Q

TNF

A

Tumor necrosis factor is a cytokine and member of the TNF superfamily, which consists of various transmembrane proteins with a homologous TNF domain

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30
Q
  1. Platelets
A

Neutralize heparin and other anticoagulation factors

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31
Q

heparin define

A

Heparin is an anticoagulant (“blood thinner”) that stops your blood from forming blood clots or making them bigger.

It can help a blood clot dissolve faster, but it can’t break it down

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32
Q

heparin vs warfarin

A

Heparin: Heparin works to inhibit the blood clotting reactions caused by thrombin and fibrin by inactivating these proteins.

Warfarin: Warfarin functions as a vitamin K antagonist. Vitamin K functions to regulate the production of the cofactors, and warfarin functions to prevent vitamin K from performing this function.

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33
Q

what do platelets release

A

Secrete thromboxane

Coagulation stimulation

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34
Q

thromboxane define

A

Thromboxanes, a substance produced by platelets, lead to occlusion of blood vessels by fueling blood clots inside the vascular system.

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35
Q

Thromboxane

A

Thromboxane is a member of the family of lipids known as eicosanoids. The two major thromboxanes are thromboxane A2 and thromboxane B2

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36
Q

what about small thrombi

A

Small thrombi wash away easily

Degraded by thrombolytic chemicals like plasmin

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37
Q

about pathologic thrombus formation

A

Virchow’s Triad (predisposing factors)

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38
Q

Virchow’s Triad

A

Virchow’s triad or the triad of Virchow describes the three broad categories of factors that are thought to contribute to thrombosis.

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39
Q

Virchow’s Triad:

A
  1. Endothelial cell injury
  2. Hemodynamic changes
  3. Hypercoagulability of whole blood
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40
Q
  1. Endothelial Cell Injury
A

Intact endothelium has anticoagulant properties

Under influence of inflammatory mediators, endothelium loses antithrombotic properties

(becomes coagulant)

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41
Q
  1. Hemodynamic Changes
A

Disturbed normal laminar flow resulting in turbulence and margination

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42
Q

laminar flow define

A

Laminar flow is the property of fluid particles in fluid dynamics to follow smooth paths in layers, with each layer moving smoothly past the adjacent layers with little or no mixing.

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43
Q

margination define

A
  1. : the act or process of forming a margin. specifically : the adhesion of white blood cells to the walls of damaged blood vessels.
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44
Q

velocity vs laminar flow

A

Slow blood flow results in sedimentation & blood eddies

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45
Q

blood eddies define

A

a circular movement of water, counter to a main current, causing a small whirlpool.

“An eddy is a movement of fluid that deviates from the general flow of the fluid. An example for an eddy is a vortex which produces such deviation.”

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46
Q

thrombi in slow/sluggish bloodstream

A

Small thrombi not dissolved by thrombolytic substances tend to persist or even grow in sluggish bloodstream

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47
Q
  1. Hypercoagulability
A

Blood is hypercoagulable in severe burn victims probably due to severe fluid loss and hemoconcentration

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48
Q

hemoconcentration

A

An increase in the concentration of blood cells resulting from the loss of plasma or water from the blood stream.

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49
Q

why else can blood be hypercoagulable

A

Also in cancer, chronic cardiac failure and pregnancy

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50
Q

pregnancy, hypercoagulability

A

Pregnancy-induced hypercoagulability is probably a physiologically adaptive mechanism to prevent post partum hemorrhage.

Pregnancy changes the plasma levels of many clotting factors, such as fibrinogen, which can rise up to three times its normal value.

Thrombin levels increase. Protein S, an anticoagulant, decreases.

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51
Q

cancer hypercoagulability

A

A hypercoagulable or prothrombotic state of malignancy occurs due to the ability of tumor cells to activate the coagulation system.

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52
Q

cardiac failure, hypercoagulability

A

Several studies have shown that patients with heart failure have increased plasma concentrations of beta-thromboglobulin, a marker of platelet activation.

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53
Q

Classification of thrombi: based on location

A

…

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54
Q

Intramural thrombi

A

mural endocardium – attached to wall of heart chambers and commonly found overlying myocardial infarction

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55
Q

mural define

A

MEDICINE
relating to or occurring in the wall of a body cavity or blood vessel.

56
Q

(intra)mural thrombi

A

Mural thrombi are thrombi that attach to the wall of a blood vessel and cardiac chamber.

Mural thrombus occurrence in a normal or minimally atherosclerotic vessel is a rare entity in the absence of a hypercoagulative state or inflammatory, infectious, or familial aortic ailments.

57
Q

Valvular thrombi

A

“attaches to valves”

fibrinous growths in debilitated persons

mimics endocarditis

aka non-bacterial (marantic) or sterile thrombotic endocarditis

58
Q

marantic endocarditis

A

Formerly known as marantic endocarditis, which comes from the Greek marantikos, meaning “wasting away”.

The term “marantic endocarditis” is still sometimes used to emphasize the association with a wasting state such as cancer.

Nonbacterial thrombotic endocarditis.

aka “sterile thrombotic endocarditis”

59
Q

what does Endocarditis do to heart valves

A

Bacterial endocarditis causes clumps of bacteria and cells start to form on the heart valves.

These clumps can break free into the bloodstream.

They can then cause damage by blocking other blood vessels.

They can also spread the infection to other organs.

60
Q

non-bacterial (thrombotic) endocarditis

A

Non-bacterial thrombotic endocarditis (NBTE) is a disease characterised by the presence of vegetations on cardiac valves, which consist of fibrin and platelet aggregates and devoid of inflammation or bacteria.

61
Q

Arterial thrombi

A

attached to arterial wall

cover ulcerated atheromas in aorta or coronary arteries

atherosclerosis / aneurysms

62
Q

atheroma define

A

Atheroma refers to the fatty material that clogs your arteries. It builds up over time and can lead to complications.

Atheroma (plaque) is the defining feature of a disease called atherosclerosis.

When you have atherosclerosis, you have plaque buildup in your arteries.

63
Q

venous thrombi

A

common in varicose veins

chronic may lead to organized granulation tissue and inflammation (thrombophlebitis)

64
Q

granulation tissue define

A

Granulation tissue is new connective tissue and microscopic blood vessels that form on the surfaces of a wound during the healing process.

Granulation tissue typically grows from the base of a wound and is able to fill wounds of almost any size.

65
Q

thrombophlebitis

A

thrombus
vein
inflammation

“Thrombophlebitis is swelling (inflammation) of a vein, often caused by a blood clot (thrombus) in the vein.”

66
Q

Microvascular thrombi

A

in arterioles, capillaries, venules

Typical of Disseminated Intravascular Coagulation (DIC)

67
Q

Disseminated Intravascular Coagulation (DIC)

A

“Disseminated intravascular coagulation is a condition in which blood clots form throughout the body, blocking small blood vessels.

Symptoms may include chest pain, shortness of breath, leg pain, problems speaking, or problems moving parts of the body.

As clotting factors and platelets are used up, bleeding may occur.”

68
Q

Thrombi can also be classified on the basis of their gross (external) appearance:

A

Red (conglutination) thrombi

Thrombi in small vessels are red

composed of tightly intermixed RBCs and fibrin

69
Q

conglutination

A

to unite by or as if by a glutinous substance.

to become conglutinated. blood platelets conglutinate in blood clotting.

70
Q

Layered (sedimentation) thrombi

A

distinct layering of cellular elements and fibrin

white lines – Lines of Zahn

Thrombi in large arteries, veins, mural thrombi

71
Q

Lines of Zahn

A

Lines of Zahn are a characteristic of thrombi.

They have layers,

with lighter layers of platelets and fibrin,

and darker layers of red blood cells.

72
Q

why in larger arteries/veins?

A

They are more present on thrombi formed with faster blood flow, more so on thrombi from the heart and aorta.

73
Q

Fate of thrombi – depends on:

A

Size, location, hemodynamics of vessel

Most small thrombi lysed without consequence

Larger thrombi remain attached to surface of vessel wall or endocardium

74
Q

what can happen? What is attachment initially mediated by?

A

Attachment initially mediated by adhesion molecules such as fibronectin or fibrin

75
Q

fibronectin atherosclerosis

A

Extra domain A of cellular fibronectin (FN-EDA) is known to cause insulin resistance, atherosclerosis, tissue fibrosis, ischemic stroke

76
Q

ATTACHMENT VIA

A

adhesion molecules such as fibronectin or fibrin

77
Q

what can thrombus stimulate

A

Eventually thrombus can stimulate ingrowth of inflammatory cells and vessels

78
Q

granulation tissue, anchor – “organization”

A

Granulation tissue forms firmer anchorage - organization

79
Q

“organization” define (thrombus)

A

Organization of the thrombus -

the vessel wall under the thrombus suffers hypoxia and undergoes necrosis, which is destroyed by reparative inflammation

(along the fibrin fibers penetrate blood vessels and fibroblasts, i.e. granulation tissue - the thrombus is organized by granulation tissue, resulting in thickening of the vessel wall under the thrombus).

80
Q

other possible events

A

Inflammatory cells of granulation tissue dissolve the thrombus

Granulation tissue replaced by collagenous fibrous tissue

Occlusive thrombi can be recanalized

Can become break of and become emboli

Can block b.v. leading to infarction

81
Q

granulation tissue vs fibrous (scar) tissue

A

During the next few weeks, the granulation tissue is gradually replaced by fibrous scar.

During this period, collagen type III is slowly replaced by collagen type I and the wound acquires tensile strength.

82
Q

thrombotic occlusions of cardiac and cerebral arteries

A

Thrombotic occlusions of cardiac and cerebral arteries are a major cause of death in US

83
Q

clinical Sx of thrombotic occlusion (?)

A

Clinical symptoms depend on site, extent of thrombi, rapidity with which they form, duration of thrombosis, widespread nature of disease, complications

84
Q

occlusion of lumen causes

A

Occlusion of lumen of blood vessel causes ischemia

85
Q

most common cause of Myocardial infarct

A

Sudden thrombotic occlusion of coronary arteries most common cause of myocardial infarction

86
Q

Chronic Heart Failure (Congestive Heart Failure)

occlusion over time

A

Slowly narrowing of lumen of blood vessel and decrease in blood flow results in hypoxia and reduced function of affected organ over time (chronic heart failure)

87
Q

thrombus vs embolus

A

Thrombus can become detached become free flowing in blood - embolus

88
Q

chronic heart failure

A

Chronic heart failure, otherwise known as congestive heart failure or heart failure

89
Q

what can emboli do

A

Emboli can become lodged in arteries and lead to infarct

90
Q

cerebral infarct

A

Cerebral infarct - stroke

91
Q

thrombus can accelerate the development of…

A

Thrombus can accelerate the development of atherosclerosis

92
Q

thrombus vs infection

A

Thrombus can become infected

93
Q

infected thrombus braeking off (?)

A

Can break off - septic emboli

94
Q

Emboli

A

Embolus - a freely movable, intravascular mass that is carried from one anatomical site to another by blood

Emboli – plural

95
Q

Embolism define

A

MEDICINE
obstruction of an artery, typically by a clot of blood or an air bubble.

“Embolism – infarct caused by embolus”

96
Q

Classification of emboli

A

Thromboemboli

Liquid emboli

Gaseous emboli

Solid particle emboli

97
Q

Thromboemboli

A

thrombi carried by venous or arterial blood

98
Q

Liquid emboli

A

fat emboli following bone fracture;

amniotic fluid emboli in veins

99
Q

amniotic fluid emboli

A

What is amniotic fluid embolism? Amniotic fluid embolism (AFE) is a rare and life-threatening complication that occurs when a pregnant person gets amniotic fluid into their bloodstream just before, during or immediately after childbirth.

100
Q

bone fracture emboli

A

When you break a bone, fat tissue from the bone marrow can leak into your blood.

“Fat embolism syndrome is a rare condition that usually follows breaking a major bone. It most often happens when you break your pelvis or a bone in your legs, but can rarely occur with other medical conditions or circumstances.”

101
Q

Gaseous emboli

A

air injected into veins;

air liberated under decreased pressure (caisson disease or decompression sickness)

102
Q

air embolism

A

When an air bubble enters a vein, it’s called a venous air embolism. When an air bubble enters an artery, it’s called an arterial air embolism.

These air bubbles can travel to your brain, heart, or lungs and cause a heart attack, stroke, or respiratory failure.

Air embolisms are rather rare.

103
Q

why air injected?

A

A syringe or IV can accidentally inject air into your veins.

104
Q

Decompression sickness (Caisson disease)

A

Decompression sickness (DCS; also called divers’ disease, the bends, aerobullosis, and caisson disease) is a medical condition caused by dissolved gases emerging from solution as bubbles inside the body tissues during decompression.

DCS most commonly occurs during or soon after a decompression ascent from underwater diving, but can also result from other causes of depressurisation, such as emerging from a caisson, decompression from saturation, flying in an unpressurised aircraft at high altitude, and extravehicular activity from spacecraft.

DCS and arterial gas embolism are collectively referred to as decompression illness.

105
Q

Solid particle emboli

A

cholesterol, tumour cells, bone marrow

106
Q

MOST COMMON EMBOLI (most clinically significant)

A

Thromboemboli are the only clinically significant emboli; all others are rare

107
Q

what can all emboli do

A

All emboli can occlude blood vessels resulting in decreased blood supply to organ (ischemia)

108
Q

VENOUS EMBOLI

A

Originate in veins

Carried by venous circulation

Typically lodge in pulmonary artery and cause pulmonary embolism

Smaller emboli cause pulmonary infarcts —> subpleural pain

109
Q

pulmonary embolism

A

A pulmonary embolism (PE) occurs when a blood clot gets stuck in an artery in the lung, blocking blood flow to part of the lung.

NOTE:
Different from Bronchial arteries (from descending aorta) that supply O2/nutrients to lung tissue itself

110
Q

pulmonary infarct

A

Pulmonary infarction is one of the key complications of pulmonary embolism (PE).

“It is important to note that infarction invariably occurs in a subpleural location, whilst malignancy or pneumonia can occur centrally.”

111
Q

Arterial emboli

A

Common cause of ischemia in spleen, kidney, intestines

Usually originate from cardiac A) mural or B) valvular thrombi

Can also originate from aorta

112
Q

ARTERIAL EMBOLI FRAGMENTATION

THEREFORE tend to…

A

Arterial emboli mechanically fragmented inside vessels because arterial blood flows fast and disrupts them

THEREFORE?
Therefore tend to lodge in small and medium-sized arteries

113
Q

THEREFORE, where is greatest risk?

A

Greatest risk in cerebral circulations

“mechanically fragmented”
—> “Therefore tend to lodge in small and medium-sized arteries”

114
Q

most common cerebral artery and infarct

A

Typically lodge in middle cerebral artery and cause infarcts of BASAL GANGLIA

115
Q

morality of “

A

Associated with high mortality and neurological defects

116
Q

Splenic emboli/infarcts can cause this SSx

A

Infarcts that develop from splenic emboli cause sharp subcostal pain

117
Q

Renal infarct/emboli

A

Renal infarcts are painful and associated with hematuria

(blood in urine)

118
Q

Intestinal infarct/emboli

A

Intestinal infarct – medical emergency; can cause gangrene of intestines

119
Q

renal infarct prognosis

A

Outlook. Renal infarction 30-day mortality was 11.4% in a retrospective analysis of 44 individuals with atrial fibrillation and renal infarction.

120
Q

pulmonary embolism SSx

A

dyspnea

hemoptysis (coughing blood)

pain

sudden death

121
Q

Infarction

A

Sudden insufficiency of blood supply resulting in an area of necrosis

122
Q

most infarction caused by

A

Most are caused by thrombi or thromboemboli

123
Q

classification of infarction (origin)

A

May be classified by origin as arterial or venous

124
Q

classificaiton of infarction (appearance)

A

Can be further classified by appearance as white or red

125
Q

White or pale infarcts

A

Typical of solid organs

E.g. heart, kidney, spleen

Ischemic necrosis paler than surrounding tissues

126
Q

marble skin / mottled appearance (White Infarcts)

A

Blood may infiltrate from collateral arteries resulting in mottled appearance

127
Q

mottled

A

mottle:
marked with spots or smears of color.

128
Q

Red infarct

A

Typical of venous infarction

E.g. Particularly of intestines or testes

Circulation can be interrupted by twisting organ

E.g. torsion of testes

129
Q

Why Red ?

A

It happens due to the inability of blood to exit the infarcted area.

The area becomes congested, causing an accumulation of blood around the site.

Red infarcts occur in organs with multiple blood supplies, such as the lungs, liver, intestines, and testes.

130
Q

E.g. of location (Red Infarct)

A

organs with multiple blood supplies,

such as lungs, liver, intestines, and testes.

131
Q

Fate of infarcts – depends on…

A

Anatomic site
Circulatory status
Capacity for repair

132
Q

mitotic vs post-mitotic tissue –> regeneration capabilities of necrotic tissue after infarct

A

Ischemic necrosis of post-mitotic cells (e.g. heart) cannot be repaired - only replaced with fibrous tissue (scarring)

Necrotic brain cells also not repaired, but liquefactive necrotic tissue resorbed

—-> leaves clear fluid-filled cyst

133
Q

mitotic tissues / facultative mitotic tissues – after infarcts

A

Mitotic tissues and facultative mitotic tissue heal with relatively few defects – e.g. liver

134
Q

exception even with mitotic tissues

A

However, large infarcts may be impossible to regenerate completely

—> Leaves scarring
—> Loss of function

135
Q
A

Semester 3 (32 decks)

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