Pathophyiology PEBC - Part IV

Consequences of Ischemia/Hypoxia:
 Cell Death:
o Necrosis: Due to severe ATP depletion, membrane breakdown,
and loss of cell structure, leading to unregulated cell death.
o Apoptosis: In some cases, prolonged ischemia or hypoxia can
trigger programmed cell death via apoptotic pathways.
 Tissue Injury: Prolonged ischemia or hypoxia leads to tissue necrosis,
organ dysfunction, and inflammation.
Diseases Associated with Ischemia/Hypoxia:
 Myocardial Infarction (Heart Attack): Ischemic injury to heart

tissue due to blockage of coronary arteries.
 Cerebrovascular Accidents (Stroke): Ischemic injury to brain tissue
due to blockage of cerebral blood vessels.
 Chronic Obstructive Pulmonary Disease (COPD): Hypoxia due to
impaired lung function.
 Renal Failure: Ischemia of renal tissue leads to kidney damage.
Exam Relevance (PEBC EE):
 Understanding Ischemia and Hypoxia: Be able to distinguish

between ischemia (lack of blood flow and oxygen) and hypoxia (lack of
oxygen) and explain their respective impacts on cellular and tissue
function.
 Mechanisms of Injury: Focus on how ATP depletion, membrane
dysfunction, acidosis, calcium accumulation, and ROS contribute to
cellular injury and death.
 Reperfusion Injury: Understand how the restoration of blood flow can
worsen tissue damage due to oxidative stress and inflammation.
 Clinical Applications: Recognize how ischemic and hypoxic injuries
are central to common clinical conditions such as heart attacks,
strokes, and kidney failure.
Free Radicals and Mechanism of Cell Injury
Key Concepts:
 Free Radicals: Highly reactive molecules with unpaired electrons,

often formed during cellular metabolism or in response to external
factors (radiation, toxins, etc.).
 Oxidative Stress: A state where the production of free radicals
exceeds the body's ability to neutralize them, leading to cellular
damage.
Pathophysiology of Free Radical-Induced Injury:
1. Generation of Free Radicals:

o Normal Cellular Processes: Mitochondrial respiration produces
reactive oxygen species (ROS) like superoxide anions (O2•−).
o External Factors: Pollution, UV radiation, smoking, and toxins
can increase ROS production.
2. Damaging Effects on Cellular Components:

o Lipid Peroxidation: Free radicals attack unsaturated fatty acids
in cell membranes, leading to membrane damage, increased
permeability, and loss of cell function.
o Protein Oxidation: Free radicals damage proteins by oxidizing
amino acid residues, leading to protein misfolding, degradation,
and loss of function.
o DNA Damage: ROS can cause DNA strand breaks, base
modifications, and mutations, contributing to cancer and cell
death.
3. Oxidative Stress:
o Imbalance: Excess free radicals overwhelm antioxidant
defenses.
o Cellular Damage: Persistent oxidative stress results in
inflammation, tissue injury, and activation of cell death pathways
(apoptosis or necrosis).
Cellular Defense Mechanisms:
 Antioxidants: Enzymes like superoxide dismutase (SOD), catalase,

and non-enzymatic antioxidants (e.g., Vitamin C) neutralize free
radicals.
 DNA Repair: Mechanisms that repair oxidative DNA damage (e.g.,
base excision repair).
 Protein Repair: Chaperones refold misfolded proteins due to oxidative
damage.
Outcomes of Free Radical Damage:
 Cell Death:
o Necrosis: Uncontrolled cell death due to severe damage.
o Apoptosis: Programmed cell death triggered by extensive DNA
or protein damage.
 Inflammation: Oxidative stress promotes inflammatory responses,
worsening tissue damage.
Diseases Associated with Free Radical Damage:
 Cancer: Oxidative damage to DNA can cause mutations, leading to

carcinogenesis.
 Cardiovascular Diseases: Oxidation of LDL contributes to
atherosclerosis and cardiovascular disease.
 Neurodegenerative Diseases: Alzheimer's, Parkinson's, and other
conditions are linked to oxidative damage in neurons.
 Aging: Accumulation of oxidative damage contributes to the aging
process.

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Consequences of Ischemia/Hypoxia:

Diseases Associated with Ischemia/Hypoxia:

 Myocardial Infarction (Heart Attack): Ischemic injury to heart

Exam Relevance (PEBC EE):

 Understanding Ischemia and Hypoxia: Be able to distinguish

 Free Radicals: Highly reactive molecules with unpaired electrons,

Pathophysiology of Free Radical-Induced Injury:

1. Generation of Free Radicals:

2. Damaging Effects on Cellular Components:

Cellular Defense Mechanisms:

 Antioxidants: Enzymes like superoxide dismutase (SOD), catalase,

Diseases Associated with Free Radical Damage:

 Cancer: Oxidative damage to DNA can cause mutations, leading to

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