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pathology > 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 of a normal thrombus formation, 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 meant by 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

How does the endothelium prevent spontaneous clot formation?

A
  • It releases anticoagulants like heparan sulfate and thrombomodulin, which inhibit clotting factors and thrombin.
  • anti-thrombic surface
  • vasodilators and prevention of aggregation - NO and prostocyclin
  • laminar flow
  • doesnt express ICAM and selectins unless nessesary
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13
Q

name the roles of nitric oxide released by endothelial cells

A

Vasodilation: Relaxes smooth muscle in blood vessel walls, reducing vascular resistance and blood pressure.
Inhibition of Platelet

Aggregation: Prevents platelets from sticking together, reducing the risk of clot formation.

Anti-Inflammatory Action: Suppresses the adhesion of inflammatory cells to the endothelium.

Antioxidant Effects: Limits oxidative stress by reducing free radical formation.
Maintenance of Vascular

Tone: Regulates the balance between vasoconstriction and vasodilation in the circulatory system.
Protection Against

Atherosclerosis: Inhibits processes that lead to plaque formation in arteries.

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14
Q

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

A

aggregation:
Nitric oxide (NO) and prostacyclin (PGI₂).

adhesion:
thrombomodulin and heparan sulfate

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15
Q

Describe the normal endothelium 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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16
Q

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

A

Release of Anti-Inflammatory Mediators:
Nitric Oxide (NO): Inhibits leukocyte adhesion and migration to the endothelial surface, reducing inflammation.

Prostacyclin (PGI₂): Prevents leukocyte adhesion and platelet aggregation, minimizing vascular inflammation.

Maintenance of a Non-Thrombogenic Surface:
Produces factors like thrombomodulin and heparan sulfate, which prevent clot formation and reduce inflammatory triggers.

Inhibition of Leukocyte Adhesion:
Endothelial cells express low levels of adhesion molecules (e.g., ICAM-1, VCAM-1) under normal conditions, limiting the recruitment of inflammatory cells to the blood vessel wall.

Barrier Function:
Maintains vascular integrity to prevent the leakage of inflammatory mediators and cells into surrounding tissues.

Regulation of Cytokine Release:
Modulates inflammatory cytokine production, balancing pro- and anti-inflammatory signals in the blood vessels.

Secretion of Anti-Inflammatory Cytokines:
Releases substances like interleukin-10 (IL-10) to suppress excessive inflammation.

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17
Q

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

A

under normal conditions:
endothelium prevents excessive SMC growth to maintain vessel structure so releases:
- NO - inhibits cell cycle
- prostocyclin
- transforming growth-factor beta

injury or disease:
stimulate SMC frowth in aid to repair tissue so releases:
- endothelin-1
- growth factors

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18
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.

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19
Q

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

A
  • Cardiac output and vascular resistance
  • Normal flow is smooth (laminar)
  • conditions like atherosclerosis create turbulent flow, increasing resistance and causing endothelial damage.
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20
Q

what vessel and blood factors affect vascular resistance?

A

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

21
Q

What role does endothelial dysfunction in producing NO 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.

22
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.

23
Q

How does hypertension contribute to blood flow pathophysiology?

A
  • Increased Afterload: Hypertension increases resistance in arteries, making it harder for the heart to pump blood, leading to left ventricular hypertrophy and potentially heart failure.
  • Arterial Remodeling: Chronic hypertension causes arteries to stiffen, reducing their ability to dilate and increasing vascular resistance.
  • Endothelial Dysfunction: High blood pressure damages endothelial cells, decreasing their ability to release nitric oxide, which impairs blood vessel dilation.
  • Atherosclerosis: Hypertension accelerates plaque buildup in arteries, narrowing vessels, increasing resistance, and raising the risk of cardiovascular events (heart attack, stroke).
  • Microvascular Disease: Damages small blood vessels in organs like kidneys, eyes, and brain, leading to nephrosclerosis, retinopathy, and increased stroke risk.
  • Acute Events: Increased shear stress from high blood pressure can rupture plaques, forming clots that block blood flow and cause heart attacks or strokes.
  • Disrupted Blood Flow Regulation: Hypertension impairs the body’s ability to regulate blood flow, leading to inconsistent blood supply to organs, particularly under stress or physical exertion.
24
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).

25
Q

Explain vascular remodeling and its impact on blood flow.

A
  • occurs in response to chronic stressors (like hypertension),
  • results in vessel wall changes that increase resistance, worsen hypertension, and disrupt blood flow.
  • make the vessel narrow and stiffened
  • increased risk of disease
26
Q

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

A
  • endothelial dysfunction,
  • atherosclerosis,
  • hypertension,
  • thrombosis,
  • heart failure,
27
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

28
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.

29
Q

Give examples of conditions that cause endothelial injury.

A
  • atherosclerosis,
  • trauma or surgery,
  • hypertension,
30
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

31
Q

What are some conditions which cause stasis or turbulent blood flow which can lead to thrombosis?

A
  • Examples include deep vein thrombosis (DVT) from immobility
  • atrial fibrillation, which causes turbulent flow,
  • varicose veins that increase stasis
32
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.

33
Q

What are some examples of conditions that cause hypercoagulability?

A
  • Examples include genetic disorders like Factor V Leiden,
  • pregnancy
  • hormone therapy,
  • cancer,
  • chronic inflammatory diseases.
34
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.

35
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.

36
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
  • nitroc oxide and prostocyclins inhibit platelet activation and aggregation
  • anticoagulant proteins circulate
37
Q

what are some causes of an embolism?

A
  • air into an iv
  • deep vein thrombosis
  • cholesterol crystals of atherlosclerosis plaques
38
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.

39
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.

40
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.

41
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.

42
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
43
Q

what is haemodynamics?

A

the physiology of blood flow

44
Q

outline the different factors which affect the rate of 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
45
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

46
Q

name the roles of prostacyclin released by endothelial cells

A

Vasodilation: Relaxes blood vessel walls to enhance blood flow and reduce blood pressure.
Inhibition of Platelet

Aggregation: Prevents platelets from clumping, reducing the risk of clot formation.

Anti-Inflammatory Effects: Reduces adhesion of leukocytes to the endothelium, limiting inflammation.

Maintenance of Vascular Homeostasis: Balances pro-thrombotic and anti-thrombotic factors in the circulatory system.

47
Q

What mechanisms regulate the clotting cascade to prevent excessive clot formation?

A

Endogenous Anticoagulants:
Antithrombin III: Inhibits thrombin and factors IXa, Xa, XIa, and XIIa, reducing clot propagation.
Protein C and Protein S: These proteins inactivate factors Va and VIIIa, limiting clot formation.
Fibrinolytic System:
Plasmin: Breaks down fibrin into degradation products, dissolving clots.
Tissue Plasminogen Activator (tPA): Converts plasminogen to plasmin, facilitating clot breakdown.
Endothelial Regulation:
Nitric Oxide (NO) and Prostacyclin (PGI₂): Inhibit platelet aggregation and prevent adhesion to intact endothelium.
Thrombomodulin: Binds thrombin, activating protein C to inhibit clotting factors Va and VIIIa.
Natural Flow Dynamics:
Laminar Blood Flow: Dilutes activated clotting factors and limits their activity.
Tissue Factor Pathway Inhibitor (TFPI):
Inhibits the tissue factor-factor VIIa complex, preventing excessive activation of the extrinsic pathway.
Negative Feedback Mechanisms:
High levels of thrombin promote activation of anticoagulant pathways like protein C.

48
Q

name the vasoconstrictors and vasodilators.

A

Vasoconstrictors
Endothelin-1 (ET-1)
Angiotensin II
Norepinephrine and Epinephrine (via α-adrenergic receptors)
Vasopressin (Antidiuretic Hormone, ADH)
Thromboxane A2 (TXA2)
Prostaglandin F2-alpha (PGF2α)
Serotonin (5-HT)
Leukotrienes (e.g., LTC4, LTD4)

Vasodilators
Nitric Oxide (NO)
Prostacyclin (PGI₂)
Atrial Natriuretic Peptide (ANP)
Bradykinin
Histamine
Epinephrine (via β2-adrenergic receptors)
Acetylcholine
Substance P
Vasoactive Intestinal Peptide (VIP)
Prostaglandin E2 (PGE2)

pathology (14 decks)

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