Introduction to Pathology
Cellular Adaptations and Injuries
Pharm D 3rd Prof
Bahauddin Zakariya University Multan
Waseem Ashraf
Learning Objectives
After this lecture, students will be able to
• Define Infarction
• Describe types of Infarction
Recommended Books:
• Robbins and Cotran PATHOLOGIC BASIS OF DISEASE Seventh Edition
• Text Book of Phathology by Harsh Mohan Seventh Edition
Infarction
An infarct is an area of ischemic necrosis caused by occlusion of either the arterial supply or the
venous drainage.
Arterial Obstruction >90% of cases Ischemic Necrosis
Venous Occlusion mostly in organs with single venous outflow Stagnant Hypoxia
Testis, Ovary
Limited usually to congestion
Opening of bypass channels to drain the blood
Causes of Infarction
• Thrombus / Emboli Events (Majorly)
• Local Vasospasm
• Extrinsic Compression (Tumor, edema etc.)
• Expansion of Atheroma (Hemorrhage within a plaque)
• Twisting of Vessels (Testicular torsion)
• Traumatic rupture
Classification of Infarction
1. According to their color:
i) Pale or anemic, due to arterial occlusion and are seen in compact organs e.g. in the kidneys, heart, spleen.
ii) Red or hemorrhagic, seen in soft loose tissues and are caused either by pulmonary arterial obstruction (e.g. in the
lungs) or by arterial or venous occlusion (e.g. in the intestines).
2. According to their age:
i) Recent or fresh
ii) Old or healed
3. According to presence or absence of infection:
i) Bland, when free of bacterial contamination
ii) Septic, when infected.
Morphology of Infarction
Red Infarction
• Venous occlusion (e.g. Ovarian torsion)
• Loose tissues or organs (such as lungs) which allow blood to be collected in infarcted zone
• Tissues with dual circulation of blood (lungs, small intestines etc) allowing perfusion of blood to
necrotic zone through alternative channels
• Tissues previously congested with sluggish flow of blood
• Sites of previous occlusion and necrosis when flow of blood is re-established
Morphology of Infarction
Pale or White Infarction
• with arterial occlusions in solid organs with end-arterial circulation (e.g., heart, spleen, and kidney), and where tissue
density limits the seepage of blood from adjoining capillary beds into the necrotic area.
Morphological & Histological Features
Wedge shaped
• Occluded vessel at the apex and the periphery of the organ is at the base
• Often covered with fibrinous exudate, if the base is serosal membrane
• Lateral margins can be irregular depending upon the adjacent blood
supply and can become distinct with the passage of time
Ischemic coagulative necrosis
• Initial inflammatory response (few hrs to days)
• Reparative response (days to weeks)
• Scars
Liquefactive necrosis (brain)
Septic infarction
Factors influencing the development of Infarction
Anatomic pattern of vascular supply (availability of alternative supply
• Dual circulation (lungs, liver)
• Anastomosing circulation (radial & ulnar arteries)
• End arterial vessels (kidneys or spleen)
Rate of development of occlusion
Slow development can give time for alternative blood supply development
Vulnerability of tissues to Hypoxia
Neurons 3 – 4 mins
Myocardial cells 20 – 30 mins
Fibroblasts till hours
Oxygen content of blood