Path 12: Thrombosis, embolism, and infracion Flashcards

1
Q

Thrombosis is described as?

A

Pathologic formation of a blood clot. Solid structure formed by components of the blood within the circulatory system

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2
Q

What can form thrombosis?

A

platelets

fibrin

leucocytes

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3
Q

What are the necessary conditions for the Virchow triad?

A

Endothelial damage

Alteration of blood flow

Alteration of blood composition

you just need one to have thrombosis

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4
Q

What are the requirements for thrombosis?

A

Blood must flow (stagnant blood clots, but do not form thrombi)

Decreased flow rate (permits contact of thrombocytes with endothelium)

Once attached to the endothelium, thrombocytes resist blood flow and current by forming “eddies” which allows more thrombocytes to adhere ad form a mass -> Thrombus

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5
Q

Analyze this image

A
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6
Q

Endothelial damage

A

Endothelial damage leading to platelet activation almost inevitably underlies thrombus formation in the heart and arterial circulation, where the high rates of blood flow impedes clot formation.

Endothelial damage or change to prothrombotic status (endothelial activation) > exposure of vWF and TF.

Endothelial activation: Physical injuries, infectious agents, abnormal blood flow, inflammatory mediators, metabolic abnormalities (hypercholesterolemia), toxins > prothrombotic state

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7
Q
A

Endothelial damage: Most important factor. Endothelium must be damaged, physically ruptured, or dysfunctional to contribute to the development of thrombosis. Dysfunction eg: produce more clotting factors and less anticoagulants (hypertension, turbulent flow, endotoxins, radiation, hypercholesterolemia

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8
Q

Alterations of the normal blood flow

A

Turbulence > endothelial injury or dysfunction and countercuurents, contributing to local formation of stasis
-Promotes endothelial activation (shift in genetic expression)
-Breaks laminar flow (platelets touch the endothelium)
-Promotes «washing» of activated clotting factors.

Stasis: major contributor to formation of venous thrombus

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9
Q

Hypercoagubility
aka thrombophilia

A

Any disorder of the blood that predisposed to thrombosis

Important role in venous thrombosis

Primary (gnetic) and seconday (acquired)
P: factor V mutation, prothrombin mutation
S: prolonged immolization, myocardial infraction, atrial fibrillation, tissue injury, cancer, prosthetic cardiac valves, DIC, cardiomyopathy, nephrotic syndrome, Hyper-estrogenic states, others)

mass tissue destruction > release of large amounts of tissue thromboplastin

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10
Q

Thrombi can develop where?

A

Anywhere in the cardiovasular system. Focally attached to underlying vascular surface

-arterial or cardiac: sites of turbulence or endothelial injury, tend to grow downstream from the site of attachment

-venous: characteristically occur at sites of statsis, tend to extend upstream from their point of origin

BOTH GROW AWAY FROM THE HEART

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11
Q

Arterial or cardiac thrombi

A

Usually at sites of endothelial injury (atheroscerotic plaques) or turbulence (vessel bifurcation)

Tend to grow in downstream from point of attachment

Tend to be *occlusive**

Thrombi development on heart valves
- infective endocarditis: bacterial/ fungal infection
- sterile endocarditis: hyper coagulable states

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12
Q

Analyze the photo

A

Spirocerca lupi

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13
Q

Venous thrombi

A

Typically at sites of STASIS: contain more RBCs

Tend to grow against the direction of blood flow

Tend to be occlusive

May be confused with postmortem clots

More frequent than arterial thrombi. Hepatic abscesses >Thrombosis of caudal vena cava > pulmonary emboli.

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14
Q

look at bottom of image

A

Abscess
-green

Happened from the outlined red line which is a venous thrombus

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15
Q

Fate of thrombi?

A

If patient survives immediate effects of thrombotic vascular obstruction, thrombi may under one or more events

Propagation
Embolization
Dissolution
Organization & Recanalization

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16
Q

What is occuring?

A

Recanalization Process

-Ingrowth of endothelial cells, smooth muscle cells, and fibroblasts

Formation of capillary channels -> channels anastomose to create conduits that re-establish limited blood flow continuity

With time -> contraction of mesenchymal cells -> connective tissue of organized thrombus incorporated as a subendothelial swelling of vessel wall

17
Q

Effects of Thrombosis (3)

A

Negligible no adverse effects (occurs in vessels that are not critical for life)

Beneficial it is needed to stop bleeding (important in hemostasis)

Damaging thrombosis in areas with inadequate collateral circulation > ischemia or infract

18
Q

How can you remember what occurs with DIC ?

A

Death is coming!!

not a disease but a CONSEQUENCE

19
Q

Embolism is described as?

A

Detached intravascular solid, liquid, or gaseous mass that is carried by blood to a site distant from its point of origin

ischemic necrosis of distal tissue = INFRACTION

20
Q

Embolism etiology is?

A
  1. Thrombus (95%)
  2. Fibrin
  3. Bacteria
  4. Parasites
  5. Neoplasia
  6. Fat embolism (in lungs due to fractures)
  7. Gas embolism
21
Q

Describe Embolus and Embolism?

A

Embolus: Any foreign body (solid, liquid or gaseous) that circulates in the vascular or lymphatic system.

Embolism: An embolus is carried by the circulation, and is trapped in small caliber vessel > ischemia > infarct

22
Q

Infract is described as?

A

an area of schemic necrosis caused by occlusion of either arterial supply or venous drainage in a particular tissue

23
Q

Infractions can be caused by?

A

Nearly 99% of all infarcts result from thrombotic or embolic events, and almost all result from arterial occlusion
-Venous infarcts rare: bypass channels rapidly open after venous thrombosis
- Venous infarction more likely in organs with single venous outflow channels (kidney, heart, spleen, brain)

24
Q

How do you recognize of ATE?

A

Pain

Paralysis

Pulselessness

Poikilothermy

Pallor

25
Q

what is this?

A

Chronic infart