infarction Flashcards

1
Q

definition of infarction

A

Infarct
Is an area of ischemic necrosis (death of tissue due to lack of oxygen) due to abrupt cessation of the arterial supply (‘arterial infarction’) or venous drainage (‘venous infarction’)

Infarction
Is the process of formation of an infarct

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2
Q

causes of infarction

A

Blockage: an obstruction in the vessel (e.g. anarterial embolus,thrombus, atherosclerotic plaque)

Compression: by something outside of the vessel causing it to be compressed (e.g.tumor,volvulus,hernia)

Torsion: The twisting of an organ, obstructing blood flow (e.g. testicular torsion, ovarian torsion

Rupture: by trauma resulting in a loss of blood pressure downstream of the rupture

Vasoconstriction: narrowing of the blood vessel by contraction of the muscle wall rather than an external force (e.g.cocaine vasoconstriction)

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3
Q

examples of infarction

A

Myocardial infarction - myocardial cell death due to prolonged ischemia

Cerebral infarction - brain or retinal cell death due to prolonged ischemia

Pulmonary infarction - is usually a complication of another primary disease state, most commonly pulmonary embolism

Bowel infarction - is frequently fatal

Testicular infarction – caused by testicular torsion

Gangrene - life threatening condition, which arises when a considerable mass of living healthy tissue dies

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4
Q

types of infarction

A

Colour: based on amount of haemorrhage
‘Pale’ or ‘white’ infarct (A): solid organs e.g. heart

- ‘Red’ or ‘haemorrhagic’ infarct (V): in loose spongy tissue rich in blood supply or has dual blood e.g.lungs  
Age: 
	Fresh 
	Old
Infection: 
Infection – ‘Septic
- No infection – ‘bland’
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5
Q

infarct shape and appearance

A

Infarct is usually wedge shaped with occluded artery at apex and base at periphery (if serosa- fibrinous exudate)

Margins: early poorly defined slightly haemorrhagic but later well defined

Inflammatory response followed by reparative response - finally scar tissue

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6
Q

arterial infarction

A

Example - myocardial infarction: necrosis of heart muscle due to occlusion of the supplying coronary artery.

Outcomes of myocardial infarction:
Sudden death
Survival with infarct replaced by granulation tissue and, ultimately, fibrous scar
Death due to complications during the infarct healing process

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7
Q

stages in infarction

A

0-12 hours - early stages of cell death
12 - 24 hours -coagulative necrosis- necrotic muscle fibres apparent microscopically. tissue proteins are denatures, underlying architecture of the tissue is preserved
24 - 72 hours - acute inflammatory reaction to dead muscle- to remove cell debris from the area of MI. neutrophils are undergoing karyorrhexis
3 - 14 days - macrophagic removal of debris and vascular granulation tissue formation
14 - 21 days - fibrous granulation tissue formation
21 - 56 days - scar formation and cicatrisation

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8
Q

early complications of myocardial infarction

A

Sudden death due to cardiac dysrhythmia
Sudden death due to acute left ventricular failure
Rupture of myocardium -> haemopericardium
Rupture of papillary muscle -> acute valve failure->LVF
Mural thrombus on infarct -> embolism -> stroke & others
Fibrinous Pericarditis & extension of MI

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9
Q

haemopericardium

A

Haemopericardiumrefers to the presence of blood within thepericardial cavity.

The condition can be caused by full-thicknessnecrosis of themyocardium aftermyocardial infarction.

The fluid build-up can cause increased pressure within thepericardial sac.

If the pressure becomes greater than the intracardiac pressure, compression of the adjacent cardiac chambers can occur, restricting cardiac filling and decreasing cardiac output.

This compression is calledcardiac tamponade.

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10
Q

fibrinous pericarditis

A

Pericarditisis inflammation of the pericardium

The fibrous pericardium is the outer layer of the pericardium.
Injury to the pericardium leads to therelease of inflammatory cells, fibrin,and fluid

In fibrinous pericarditis, the pericardial texture is rough, granular and has many fibrous adhesions.

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11
Q

papillary muscle rupture

A

Papillary muscle rupture is a potentially fatal complication which can occur following a myocardial infarction

Can result insevere mitral valve regurgitation and subsequent acute life-threatening cardiogenic shock and pulmonary oedema.

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12
Q

mural thrombus

A

Mural thrombiarethrombithat attach to the wall of a blood vessel . They occur in large vessels such as the heart and aorta, and can restrict blood flow but usually do not block it entirely

the major risk of left ventricular thrombus is subsequent embolization

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13
Q

late complications

A
  • chronic LVF
  • ventricular aneurysm
  • > swelling of a weakened area in the muscular wall of the heart
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14
Q

venous infarction

A

Venous infarction can occur when the entire venous drainage from an organ or tissue is, and remains, completely obstructed.

examples:
Bowel infarction eg volvulus, hernial strangulation.
Testis infarction, due to torsion.
Ovarian infarction, due to torsion.

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15
Q

venous infarction- sequence of events

A

Veins become obstructed, usually by extrinsic pressure

Tissues become congested with blood, venules and capillaries being engorged with blood which cannot escape

Pressure in capillaries and venules rises so high that:
Many of them rupture, with leakage of blood
Arterial blood cannot enter, so hypoxia ensues

Tissues become congested, hypoxic and necrotic

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16
Q

volvulus

A

Avolvulusis when a loop of intestine twists around itself and the mesentery resulting in a bowel obstruction.

Delay in diagnosis and treatment of volvulus is associated with a highmorbidity and mortality.

17
Q

torsion of testis

A

Torsion of the testes occurs when the testis twists and rotates, trapping the spermatic cord, cutting off the blood supply to the testis.
It is imperative to make a prompt diagnosis because prolonged testicular torsion may cause irreversible damage or death to the testes.

18
Q

ovarian torsion

A

The twisting, or torsion, of the ovary around its ligamentous supports. This may result in loss of blood supply to both the ovary and the fallopian tube.
Correct diagnosis, as quickly as possible is critical in order to prevent adverse events that may result in the loss of the ovary or fallopian tube (or both)

19
Q

factors affecting development of infarction

A

Nature of vascular supply: end artery Vs dual blood supply

Rate of development of occlusion: abrupt Vs gradual

Type of tissue - 
Vulnerability to hypoxia (irreversible damage)
Neuron: 2-3 minutes
Myocardium: 20-40 minutes
Fibroblasts: many hours