pathology presentation

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2. INFARCTION
SIMRA SHABBIR
RIPHAH INSTITUTE OF PHARMACEUTICAL SCIENCES

3. CONTENTS :
 Definition
 Etiology
 Pathogenesis
 Types
 Morphological feature
 Factors
 Infarct of different organs
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4. INFARCTION
 Infarct is localized area of ischemic necrosis in an organ or
tissue resulting most often from reduction of arterial blood
supply or occasionally its venous drainage.
 Process by which such lesions form are termed as
INFARCTION.
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5. ETIOLOGY
Arterial obstruction Capillary occlusion Venous obstruction
Caused by Caused by Caused by
1. Ischemic necrosis Vasculitis Stagnant hypoxia
2. embolism Frost bite Traumatic repurture
There is another cause ‘non occlusive circulatory insufficiency’ due to
HERNIA
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6. PATHOGENISIS
Obstruction in vessels
Ischemia
hypoxia
Reduced oxygen
Thrombus formation
Necrosis
Infarction
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7. TYPES
 Infarction is classified on two basis :
1. On the basis of color of affected site
2. On the basis of presence or absence of microbial
infection
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8. On color
basis
Red
hemorrhagic
White
anemic
Color reflect the
amount of
hemorrhage
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9. Microbial infection
When Present
called septic
Absence of infection
called blend
Microbe seeds in
necrotic tissue
Infarct covert into
abscess
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10. Morphological feature
Type
/ sr.
no
Hemorrhagic or red infarct Anemic or pale infarct
1. Caused by artery or vein occlusion or
reperfusion.
caused by arterial occlusion
2. Observe in soft organs having loose tissue
such as brain, liver and GIT.
Observe in solid organs such as heart,
kidney and spleen.
3. These organs typically include dual blood
circulation.
Include single blood supply.
4. Loose texture tissue allows RBC released
from damaged vessels that will flood the
necrotic tissue and infarct will appear red.
These are referred to as ‘white’ because
lack of hemorrhaging and limited RBC.
5. Infarct grossly appear as wedged shape.
Apex of lesion is towards the blood vessels
and base toward the surface.
Infarct grossly appear as wedged shape
area of necrosis with hemorrhage border
zone.
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12. •In pale infarct, red cell lysed, with release of hemoglobin remaining in the form
of hemosiderin sharply define with time.
•In red infarct, hemorrhage is too extensive to permit the lesion ever to become
pale however it become firmer and browner with time reflecting the
accumulation of hemosiderin pigment.
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13. FACTORS
 Factors that influence infarct development:
1. Anatomy of vascular supply
2. Rate of occlusion
3. Tissue susceptibility to hypoxia
4. Hypoxemia
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14. Anatomy of vascular supply
 the blood supply may be single or it may dual.
 The dual blood supply mean that organ is receiving blood
by two means e.g. liver (hepatic artery and hepatic portal
vein)
 In single blood supple all have end arterial circulation e.g. in
heart and kidney.
 The presence or absence of dual circulation is important
because presence cause decrease chances of infarction.
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15. Rate of occlusion
 it may be slow or it may be fast.
 Increase chances with fast rate.
 Slowly developing occlusion are less likely to cause
infarction because they allow time for the development of
collateral blood supply.
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16. Tissue susceptibility to hypoxia.
 This mean that how much tissue resist after hypoxia.
 Neurons undergo irreversible damage when
deprived of their blood. (3 -4 min)
 Myocardial cells ------ hardier than neuron. (20-30min
minimum and 4-12 hr maximum)
 Fibroblast ------ within myocardium (many hrs)
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17. Hypoxemia
 It is decreased blood oxygen regardless of the cause.
 It increase both chances and extent of infarction.
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18. Infarct of different organs
Location Cause Gross
appearance
Complications
Myocardial
infarction
Arterial obstruction Pale Arrhythmia
Cardiogenic shock
Cerebral
infarction
vessel thrombotic
ischemic stroke.
May be hemorrhagic
or may be pale
Brain edema
Intestinal
infarction
Ischemia due to
previous surgery.
Hemorrhagic Peritonitis
Renal infarction Arterial obstruction Pale hypertension
Liver infarction Arterial or venous
occlusion
Pale Rare condition due
to dual blood
circulation 18

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