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introductory clinical sciences > thrombis, embolism, ischemia, infarction > Flashcards

thrombis, embolism, ischemia, infarction Flashcards

1
Q

define thrombus and embolism

A
  • thrombus - vein or artery is blocked by a blood clot
  • embolism - a blood clot that breaks off, travels around the body and blocks a vessel
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2
Q

define ischemia and infarction

A
  • ischemia - reduced blood flow to a certain tissue
  • infarction - complete cut off of blood flow to a tissue
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3
Q

what are the steps in a normal clotting cascade and briefly explain what happens at each stage.

A
  • vascular spasm - smooth muscle in the vessel wall contracts to reduce blood flow to the injured area
  • platelet plug formation - platelets stick to collagen at the wound site, forming a platelet plug
  • clotting cascade
  • fibrin mesh formation
  • clot retraction and fibrinolysis - break down of clot
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4
Q

what is primary and secondary haemostasis?

A
  • primary - platelet aggregation
  • secondary - coagulation cascade
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5
Q

outline what happens during a platelet plug formation?

A

platelet adherance
- platelets bind to collagen
- VWF is released which causes for platelet activation - change shape

platelet activation
- platelet releases cytokines such as ADP, VWF, thromboxane A2, platelet-derived growth factor, vascular endothelial growth factor, serotonin and coagulation factors
- this activates and attracts nearby platelets

platelet aggregation
- fibrin mesh from the coagulation cascade is produced and connects the platelets together in a mesh
- VWF and fibrin binds to receptor GP11b-111a on platelets

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6
Q

what are the steps of the extrinsic coagulation pathway?

A

Tissue factor III is released from damaged tissues
This forms a complex with factor VII, which activates factor X

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7
Q

What are the steps of the intrinsic coagulation pathway?

A

Initiated by exposure of negatively charged surfaces to blood
This triggers the activation of factor XII, which leads to the activation of factor XI
Factor XI then activates factor IX, which combines with factor VIII to form the tenase complex
The tenase complex then activates factor X

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8
Q

What do both the intrinsic and extrinsic pathways of coagulation lead to?

A

The activation of factor X

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9
Q

What does thrombin do?

A

It converts fibrinogen to fibrin, which forms the basis of a clot

It also activates factor XIII, which stabilises the fibrin clot by cross-linking the fibrin strands

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10
Q

What is the common pathway of the coagulation cascade?

A

The activated factor X combines with factor V to form prothrombinase
This then converts prothrombin to thrombin

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11
Q

how is the clot broken down?

A
  • plasmin gradually breaks down the fibrin
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12
Q

describe the role of endothelium during normal blood flow?

A
  • maintains vascular haemostasis
  • regulates blood flow
  • prevents inappropriate clotting
  • supports vessel health
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13
Q

How does the endothelium prevent spontaneous clot formation?

A

It releases anticoagulants like heparan sulfate and thrombomodulin, which inhibit clotting factors and thrombin.

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14
Q

What role does nitric oxide (NO) play in endothelial function?

A

NO is a vasodilator that relaxes smooth muscle, prevents platelet adhesion, and maintains vessel patency for smooth blood flow.

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15
Q

Which two substances released by the endothelium help to prevent platelet aggregation and adhesion?

A

Nitric oxide (NO) and prostacyclin (PGI₂).

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16
Q

What is endothelin-1, and how does it function in blood flow?

A

Endothelin-1 is a potent vasoconstrictor produced by the endothelium, which helps regulate blood pressure and local blood flow, especially during stress or injury.

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17
Q

Describe the endothelium’s barrier function.

A

The endothelium acts as a selective barrier, allowing essential nutrients and gases to pass while preventing harmful substances from entering tissues.

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18
Q

How does the endothelium contribute to the anti-inflammatory response in blood vessels?

A

It inhibits leukocyte adhesion with NO and prostacyclin and only expresses adhesion molecules (e.g., selectins, ICAMs) during injury or infection.

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19
Q

What role does the endothelium play in smooth muscle cell growth?

A

The endothelium prevents excessive smooth muscle growth through NO and prostacyclin, reducing the risk of vascular remodeling.

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20
Q

How does the endothelium modulate platelet behavior?

A

It prevents platelet adhesion and activation in healthy vessels and releases von Willebrand factor (vWF) at injury sites to initiate clotting when needed.

21
Q

In what way does the endothelium contribute to blood pressure regulation?

A

The endothelium releases vasodilators (like NO) and vasoconstrictors (like endothelin-1) to adjust vessel diameter and maintain stable blood pressure.

22
Q

What are the key factors that influence blood flow and hemodynamics?

A

Cardiac output and vascular resistance primarily influence blood flow. Normal flow is smooth (laminar), but conditions like atherosclerosis create turbulent flow, increasing resistance and causing endothelial damage.

23
Q

How does vascular resistance affect blood flow?

A

Vascular resistance is influenced by vessel diameter, length, and blood viscosity. Small changes in vessel radius can significantly impact resistance, affecting blood pressure and flow.

24
Q

What role does endothelial dysfunction play in blood flow pathophysiology?

A

Endothelial dysfunction reduces nitric oxide production, leading to increased vascular tone, inflammation, and risk of thrombosis. It is a key factor in diseases like atherosclerosis.

25
Q

What is atherosclerosis and how does it affect blood flow?

A

Atherosclerosis is plaque buildup within arterial walls, narrowing arteries and increasing resistance. Plaque rupture can lead to clot formation and blockages, causing ischemia and potential infarction.

26
Q

How does hypertension contribute to blood flow pathophysiology?

A

Hypertension increases vascular resistance due to narrowed vessels or arterial stiffness, putting strain on the heart and blood vessels, and raising the risk of atherosclerosis, heart disease, and stroke.

27
Q

What are ischemia and hypoxia, and how are they related to blood flow?

A

Ischemia is reduced blood flow, limiting oxygen delivery to tissues. Hypoxia is the resulting oxygen deficiency, leading to tissue damage and dysfunction (e.g., angina or stroke).

28
Q

Explain vascular remodeling and its impact on blood flow.

A

Vascular remodeling occurs in response to chronic stressors (like hypertension), resulting in vessel wall changes that increase resistance, worsen hypertension, and disrupt blood flow.

29
Q

What are the major contributors to abnormal blood flow and tissue damage in blood flow pathophysiology?

A

Key contributors include endothelial dysfunction, atherosclerosis, hypertension, thrombosis, and heart failure, all of which can lead to compromised oxygen delivery and tissue injury.

30
Q

what is Virchow’s triad used to describe, and what are the 3 main components?

A

a model describing the 3 factors which contribute to abnormal thrombus formation

  • endothelial injury
  • stasis or turbulent blood flow
  • hypercoagulability

each factors can increase risk of thrombosis but with all 3 - chances are highly increased

31
Q

How does endothelial injury contribute to thrombosis?

A

Endothelial injury disrupts the blood vessel lining, reducing anticoagulant production and promoting platelet adhesion and clot formation.

32
Q

Give examples of conditions that cause endothelial injury.

A

Examples include atherosclerosis, trauma or surgery, and hypertension, all of which damage the endothelium and increase thrombosis risk.

33
Q

What is the role of stasis or turbulent blood flow in Virchow’s Triad?

A

Stasis or turbulence allows clotting factors to accumulate or causes endothelial injury, both of which increase the likelihood of clot formation

34
Q

What are some examples of stasis or turbulent blood flow leading to thrombosis?

A

Examples include deep vein thrombosis (DVT) from immobility, atrial fibrillation, which causes turbulent flow, and varicose veins that increase stasis

35
Q

Define hypercoagulability in Virchow’s Triad.

A

Hypercoagulability is an increased tendency for blood to clot due to genetic or acquired factors, raising the risk of thrombosis.

36
Q

What are some examples of conditions that cause hypercoagulability?

A

Examples include genetic disorders like Factor V Leiden, pregnancy or hormone therapy, cancer, and chronic inflammatory diseases.

37
Q

Why are patients with atrial fibrillation at higher risk for thrombus formation?

A

Atrial fibrillation causes turbulent blood flow in the atria, which promotes thrombus formation and increases the risk of stroke.

38
Q

What are the potential complications of pathological thrombosis?

A

Pathological thrombosis can lead to serious conditions like deep vein thrombosis (DVT), pulmonary embolism, stroke, and myocardial infarction.

39
Q

why don’t blood clots form all the time?

A
  • laminar flow - cells travel in the centre of the arterial vessels and dont touch the sides
  • endothelial cells which line vessels arent sticky when healthy
40
Q

what are some causes of an embolism?

A
  • air into an iv
  • deep vein thrombosis
  • cholesterol crystals of atherlosclerosis plaques
41
Q

Q: Why can’t a venous embolus reach the arterial circulation?

A

A: The lungs act as a filter, as the pulmonary blood vessels narrow to capillary size, allowing only single red blood cells to pass.

42
Q

Q: What path does an embolus take if it enters the venous system?

A

A: It travels from the vena cava, through the right side of the heart, and lodges in the pulmonary arteries.

43
Q

Q: What is the function of the lungs in relation to venous emboli?

A

A: The lungs filter out venous emboli by preventing them from passing through the small capillaries into the arterial circulation.

44
Q

Q: Where can an arterial embolus travel?

A

A: An arterial embolus can travel anywhere downstream of its entry point in the systemic circulation.

45
Q

describe the role of endothelium in normal blood flow

A
  • barrier function - controls the passage of things in and out of the blood
  • regulation of vascular tone - release vasoactive substances causing vasodilation or vasoconstriction
  • anti-thrombic properties - prevents unwanted clotting by producing factors which inhibit this
  • anti-inflammatory roll - produces chemicals to reduce inflammation by preventing leukocytes sticking to its walls
  • regulation of blood clotting - release vwf and tissue factor
  • regualtion of permeability of blood vessels
  • angiogenesis - formation of new blood vessels
46
Q

what is haemodynamics?

A

the physiology of blood flow

47
Q

you can probs read this - outline the different factors contributing to blood flow

A
  • pressure gradient - blood flows from an area of high pressure to an area of low pressure
  • cardiac output - the volume of blood the heart pumps per minute - effected by heart rate and stroke volume
  • vascular resistance opposes blood flow and is massively influenced by the diamater of vessels
  • blood viscosity
  • laminar vs turbulent flow - laminar is normal with minimal friction - turbulent is when its abnormal
  • role of endothelium
  • elasticity of blood vessels
  • capillary exchange - blood flows slower to allow time for gas exchange
  • venous return and muscle pump - muscle contractions
  • autoregulation of blood control - tissues regulate blood flow based on metabolic needs
  • neurohormonal control - effects blood flow
48
Q

explain what Virchow’s triad is, and the different factors of it

A

Virchow’s Triad explains the main factors that can lead to a blood clot (also called a thrombus) forming inside a blood vessel. It’s named after a German doctor, Rudolf Virchow, who described the three main things that make clots more likely. Here’s an easy breakdown:

Blood Stasis (Slowed or Stopped Blood Flow):
Blood needs to keep moving to stay healthy. When it slows down or pools in one area, it becomes more likely to clot.
This can happen if someone is immobile for a long time, like during a long plane ride, bed rest, or after surgery. Blood can start to pool in the legs or other areas where it isn’t moving as much.
Endothelial Injury (Damage to the Blood Vessel Wall):
The lining inside blood vessels (called the endothelium) usually keeps blood flowing smoothly. When this lining is damaged, the blood is more likely to form clots there.
Damage can happen from physical injury (like a cut or bump), high blood pressure, surgery, or even from smoking. When the lining is damaged, it triggers clotting to stop potential bleeding—but it can also start clots in places where they’re not needed.
Hypercoagulability (Increased Tendency of Blood to Clot):
This means that the blood is “stickier” than normal and clots more easily.
Some people have conditions that make their blood naturally more prone to clotting. This can be due to genetic factors, certain medications (like birth control pills), pregnancy, or diseases like cancer.

49
Q

give examples of some reasons why the factors of Virchow’s hierarchy could be disrupted, making a thrombus more likely

A

blood stasis:
- prolongues immobolisation
- long flights or car rides
- heart failure

endothelial injury:
- athlersoclerosis
- trauma or surgery
- smoking

hypercoagulability:
- genetic clotting disorders
- pregnancy
- cancer
- hornome replacement therapy or birth control pills

introductory clinical sciences (12 decks)

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