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Group 4 General Pathology of Ischemia

Ischemia is insufficient blood supply to tissues caused by obstruction of blood vessels, resulting in hypoxia and tissue damage. Key cellular defects in ischemic cells include decreased ATP generation due to mitochondrial damage and accumulation of reactive oxygen species. Loss of ATP fails ion pumps and protein synthesis, depleting glycogen stores and lowering pH through lactic acid buildup. Ischemia is more fatal than hypoxia alone as it also compromises substrate delivery for anaerobic glycolysis once stores are exhausted. Reperfusion injury occurs when blood flow returns, paradoxically damaging viable cells through enhanced reactive oxygen species generation and inflammation.

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Sufyan Mirza
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106 views13 pages

Group 4 General Pathology of Ischemia

Ischemia is insufficient blood supply to tissues caused by obstruction of blood vessels, resulting in hypoxia and tissue damage. Key cellular defects in ischemic cells include decreased ATP generation due to mitochondrial damage and accumulation of reactive oxygen species. Loss of ATP fails ion pumps and protein synthesis, depleting glycogen stores and lowering pH through lactic acid buildup. Ischemia is more fatal than hypoxia alone as it also compromises substrate delivery for anaerobic glycolysis once stores are exhausted. Reperfusion injury occurs when blood flow returns, paradoxically damaging viable cells through enhanced reactive oxygen species generation and inflammation.

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Sufyan Mirza
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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GENERAL PATHOLOGY

OF ISCHEMIA
GROUP 4

• Hammad Afzal 6630


• Muhammad Hammas 6634
• Sufyan Iqbal 6644
• Abubakar Asghar 6653
• Sarfraz Ahmad 6659
ISCHEMIA

• Insufficient blood supply to an organ or area of the body by


the obstruction of blood vessels is called ischemia.
• It is a common cause of acute cell injury underlying human
disease.
• It results in tissue damage because of hypoxia (lack of
oxygen). Ischemia also causes discomfort, pain and tissue
death.
MAJOR CELLULAR DEFECTS IN ISCHEMIC
CELLS

Decreased
DecreasedATP
ATPgeneration
generation

Mitochondrial
Mitochondrialdamage
damage

Accumulation
AccumulationofofROS
ROS
BIOCHEMISTRY OF ATP IN ISCHEMIA
EFFECTS OF ATP DEFICIENCY

Loss of ATP results in failure of many energy dependent cellular systems, such as:
1. Ion pumps (leading to cell swelling, and influx of Ca2+, with its deleterious
consequences)
2. Depletion of glycogen stores and accumulation of lactic acid, thus lowering the
intracellular pH
3. Reduction in protein synthesis.
WHY IS ISCHEMIA MORE FATAL THAN
HYPOXIA?
• In contrast with hypoxia, in which energy generation by anaerobic glycolysis can
continue (even if less efficiently than by oxidative pathways), ischemia, because
of reduced blood supply, also compromises the delivery of substrates for
glycolysis.
• Consequently, anaerobic energy generation also ceases in ischemic tissues after
potential substrates are exhausted or when glycolysis is inhibited by the
accumulation of metabolites that would normally be removed by blood flow.
• Therefore, ischemia injures tissues faster and usually more severely than does
hypoxia.
ISCHEMIA-REPERFUSION INJURY

• The restoration of blood flow to ischemic but viable tissues results,


paradoxically, in the death of cells that are not irreversibly injured,
this phenomenon is called as ischemia-reperfusion injury.
• It leads to tissue damage in myocardial and cerebral ischemia.
MECHANISMS OF CELL INJURY IN REPERFUSION
1.1.Enhanced
Enhancedgeneration
generationofofROS
ROS

 When oxygen supply is increased, there may be increase in the


production of ROS, because mitochondrial damage leads to incomplete
reduction of oxygen, and because of the action of oxidases in
leukocytes, endothelial cells, or parenchymal cells.
 Cellular antioxidant defense mechanisms may also be compromised by
ischemia, favoring the accumulation of free radicals.
MECHANISMS OF CELL INJURY IN REPERFUSION
2.2.Inflammation
Inflammation

 The inflammation that is induced by the products of activated


leukocytes and activation of the complement system may also
contribute to ischemia-reperfusion injury.
 Complement proteins may bind in the injured tissues, or to antibodies
that are deposited in the tissues, and subsequent complement activation
generates by-products that exacerbate the cell injury and inflammation.

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