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S1.2 Cardiovascular > Pathophysiology of Thrombosis/Embolism and Ischaemia/Infarction > Flashcards

Pathophysiology of Thrombosis/Embolism and Ischaemia/Infarction Flashcards

1
Q

What factors affect blood flow?

A 
Pressure gradient
Resistance
Viscosity
Velocity
Compliance
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2
Q

What effects might abnormal factors have on blood flow?

A

Cause stasis or turbulent flow

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3
Q

What are some endogenous causes of thromboembolism?

A 
Atheroma
Hyperviscosity
Spasm
External compression
Vasculitis
Vascular steal
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4
Q

What is Virchow’s Triad?

A

Three factors contributing to thrombosis:

  • changes in vessel wall
  • changes in blood constituents
  • changes in pattern of blood flow
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5
Q

What is a typical atheromatous pathogenesis of a thrombus?

A

Turbulent blood flow
Loss of intimal cells, denuded plaque
Collagen exposed, platelets adhere
Fibrin meshwork, RBCs trapped

Alternating bands - lines of Zahn
Further turbulence and platelet deposition
Propagation
> consequences

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6
Q

What are the consequences of a thromboembolism?

A

Depend on site, extent, collateral circulation

Common - DVT, ischaemic limb, MI

Resolution via organisation/recanalisation
Death

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7
Q

What are some types of embolus?

A 
Thrombus
Fat
Gas
Tumour
Trophoblast (pregnancy)
Septic material
Amniotic fluid
Bone marrow
Foreign bodies
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8
Q

What are some risk factors for DVT and resultant PE?

A 
Cardiac failure
Severe trauma/burns
Post-op/post-partum
Nephrotic syndrome
Disseminated malignancy
Oral contraceptive
Increased age
Bed-rest/immobility
Obesity
PMH of DVT

Prophylaxis?

  • TEDs
  • S/C heparin
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9
Q

What is ischaemia?

A

Relative lack of blood supply to tissue/organ leading to inadequate O2 supply

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10
Q

What are the various types of hypoxia?

A

Hypoxic
- low inspired O2/PaO2

Anaemic
- abnormal blood

Stagnant
- normal inspired but abnormal delivery e.g. occlusion

Cytotoxic
- abnormal at tissue level

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11
Q

What factors affect O2 supply?

A 
Inspired O2
Pulmonary function
Blood constituents
Blood flow
Integrity of vasculature
Tissue mechanisms
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12
Q

What can cause ischaemic heart disease?

A

Various supply issues:

  • coronary artery atheroma
  • cardiac failure
  • pulmonary disorder
  • anaemia
  • previous MI

Demand issues
- exertion, stress

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13
Q

What are some clinical consequences of atheroma?

A 
MI
TIA
Cerebral infarction
Abdominal aortic aneurysm
Peripheral vascular disease
Cardiac failure
Coronary artery disease (> MI)
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14
Q

What is infarction?

A

Ischaemic necrosis

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15
Q

What are some examples of causes of infarction?

A

Thrombosis/Embolism
Strangulation e.g. gut
Trauma - damaged vessel

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16
Q

What factors affect the scale of damage in ischaemia?

A

Time period
Tissue/organ
Pattern of blood supply
Previous disease

17
Q

What is the short-term progression of events in maintained myocardial ischaemia?

A

Seconds = anaerobic metabolism, ATP depletion
< 2 minutes = loss of myocardial contractility
A few minutes = ultrastructural changes (cell swelling, relaxation, glycogen depletion)
20-30 minutes = irreversible damage
20-40 minutes = myocyte necrosis (troponin positive at this stage)
>1 hour = injury to microvasculature

18
Q

How does the appearance of an infarct change with time?

A

<24 hours

  • no visual changes
  • 12 hours post - swollen mitochondria

24-48 hours

  • pale infarct (myocardium, spleen, kidney, solid tissues)
  • red infarct (lung, liver, loose tissues)
  • acute inflammation at edge of infarct

72 hours +

  • pale infarct goes to yellow/white and red
  • red infarct little changes
  • chronic inflammation, macrophages remove debris, granulation tissue, fibrosis

End result
- scar replaces area of damage

19
Q

What are the long term progression of events in myocardial infarction?

A

4-12 hours
- early coagulation necrosis, oedema, haemorrhage

12-24 hours
- ongoing necrosis, myocyte changes, early neutrophilic infiltrate

1-3 days
- necrosis, loss of nuclei and striations, brisk neutrophilic infiltrate

3-7 days
- disintegration of dead myofibres, dying neutrophils, early phagocytosis

7-10 days
- well established granulation tissue with new blood vessels and collagen deposition

2-8 weeks
- increased collagen deposition

> 2 months
- dense collagenous scar

20
Q

What is a transmural infarction?

A

Ischaemic necrosis affecting the full thickness of the myocardium

21
Q

What is a subendochondral infarction?

A

Ischaemic necrosis mostly limited to a zone of myocardium under the endocardial lining of the heart.

22
Q

What are some complications of an MI?

A

Can be immediate or later

Sudden death
Arrhythmias
Angina
Cardiac faiure
Cardiac reupture
Reinfarction
Pericarditis
PE secondary to PE
Papillary muscle dysfunction > mitral incompetence
Ventricular aneurysm
Dressler's syndrome

S1.2 Cardiovascular (20 decks)

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