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Medsci 203 (my own) > L21 Ischaemia and Infarction > Flashcards

L21 Ischaemia and Infarction Flashcards

1
Q

What is ischaemia and what does it cause?

A

Inadequate local blood supply to a tissue, causing reduced transfer of metabolic substances in and out of tissues.

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2
Q

What is hypoxia?

A

Deficiency of oxygen which causes cell injury by reducing aerobic respiration

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3
Q

What is anoxia?

A

Complete lack of oxygen

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4
Q

What is infarction?

A

Necrosis of a tissue due to ischaemia

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5
Q

Why do ischaemic tissues due via necrosis and not apoptosis?

A

Lack of ATP due to ischaemic conditions

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6
Q

What is external occlusion?

A

Tumors or bed sores

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7
Q

What is internal occlusion?

A

Atherosclerosis, thrombosis, embolism

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8
Q

Which cells are more susceptible to ischaemia than others?

A
  • Neurons are highly sensitive to O2, irreversibly damage within 3 mins
  • Myocardium is sensitive to ischaemia, damage after 20 mins
  • Skeletal muscle cells are slightly sensitive, can still do anoxic work
  • Fibroblasts and macrophages (stromal cells) are insensitive to oxygen levels.
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9
Q

Which cell’s activity is enhanced under hypoxic conditions?

A

Neutrophils

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10
Q

Explain how O2-related gene expression changes promote neutrophil survival in low O2 conditions.

A

Anoxia promotes HIF transcription system activity, which leads to increased NFkB activity, leading to pro-survival of target RNAs. Increased protein production and maintenance leads to increased survival chances.

Normoxia leads to apoptosis, due to sufficient levels of ATP

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11
Q

What are the effects of ischaemia on cells?

A
  • Ischaemia, not sufficinetly severe or of long duration to kill a cell may change the biology of a cell.
  • Reduced ATP availability to the cell
  • Activation of signalling cascades
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12
Q

What changes in the channel pumps are observed when a cell has low ATP? What does this lead to on an organelle level?

A
  • Decreased functional Na+ pump activity (ATPase pump)
  • Influx of Ca, H2O, efflux of K
  • Leads to ER swelling, cellular swelling, loss of microvilli.
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13
Q

What type of glycolysis occurs under low ATP? What does this lead to?

A
  • Anaerobic glycolysis - breakdown of glucose under anaerobic conditions
  • Leads to lower glycogen levels and lower pH (due to H+ production)
  • Leads to clumping of nuclear chromatin)W
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14
Q

What other effects are seen in the cells under low ATP conditions?

A
  • Detachment of ribosomes
  • Decreased protein synthesis
  • Lipid deposition
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15
Q

What is the difference between necrosis and apoptosis?

A
  • Apoptosis is regulated, ordered cell death, whereby the cell breaks off into smaller apoptotic fragments. The fragments are later phagocytosed.
  • Necrosis is a passive, emergency, messy cell death –> autolysis (cell lysis and release of enzymes which digest the cell), messy due to leak of contents into suroundings. Cleaned up by macrophages
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16
Q

What are the potential effects of ischaemia at tissue level?

A
  • Functional defects due to sub-optimal tissue perfusion –> less damage (i.e. myocardial dysrhythmia and renal insufficiency)
  • Adaptation (i.e. fatty change), atrophy, and shut down –> more damage
  • Apoptosis of isolated cells –> even more damage
  • Infarction (necrosis) of most/alll cells in a tissue due to overwhelming ischaemic injury –> most damage
17
Q

Which factors influence the outcome (of ischaemia) for tissues of vessel occlusion?

A
  • Anatomy of blood supply to organs (end organs- single route, collateral circulation - alternative routes)
  • Size of occluded vessel (larger area = larger area killed)
  • Speed and Duration of onset
  • Reperfusion –> further damage due to oxidative stress
  • Metabolic demands of the tissue at the time
  • Adequacy of circulatory system –> if px has anaemia, less O2 capacity to carry to tissues.
18
Q

How does reperfusion cause damage (via ROS)?

A
  • Attack double bonds of UFA (unsaturated fatty acids) –> lipid peroxidation
  • oxidise amino acid side chains –> enzyme damage
  • React with thymine to cause DNA damage
19
Q

What is infarction?

A

Necrosis of a tissue due to ischemia

20
Q

Autocatalytic reactions propagate….

A

…a chain of reactions

21
Q

What does infarction result from?

A

Infarction results from thrombosis or embolism, spasm, torsion, or extrinsic compression of vessels

22
Q

What is red infarct?

A

Haemoraggic –> when the major blood supply to the organ is compromised, but there are still other blood vessels bringing blood to the tissue. They do not bring in enough O2 so the cell still dies. However, there is still blood pumping in and out of the dead tissue.
i.e. in lungs

23
Q

What is white infarct?

A
  • Anaemic infarcts occur in single (end) arteries, with no haemorage (no blood coming out)
  • Coagulative necrosis is the usual pattern after infarction in solid organs
24
Q

What is ischaemic heart disease usually caused by?

A
  • Atherosclerotic narrowing of coronary arteries that supply myocardium
25
Q

What symptoms are seen in ischaemic heart disease?

A

Angina pectoris (least severe), myocardial infarction (MI), and cerebral ischaemic injury (most severe)

26
Q

What happens when you have angina pectoris?

A
  • Pain in chest due to inadequate blood supply (may be due to atherosclerotic plaque) to the heart during exercise. Transcient myocardial ischaemia –> enough O2 to myocardium at rest, but not with exercising.
  • Cell don’t die because px stops exercising due to pain. Once px stops exercising, px gets oxygenated blood again.
  • Chronic ischaemic heart condition (over time) can cause heart failure - progressive damage to heart cells so the heart can no longer pump blood successfully around the body.
27
Q

What happens in myocardial infarction?

A
  • When a slow growing atherosclerotic plaque in a coronary artery suddenly ruptures or has a thrombus on it. Previously silent atherosclerotic plaque generates symptoms.
  • Thrombus growing on top of plaque reduces blood flow to downstream areas of the heart, causing infarctino to parts of heart = endocardium or transmural infarction
  • Subendocardial infarction
28
Q

What happens in a cerebral ischaemic injury?

A

Stroke/blockage of blood to a region of the brain, leading to infarction of the part

29
Q

READ NOTES ON NOTION FOR WHAT HAPPENS IN THE TIMELINE BETWEEN 24 HRS TO 2 WEEKS AFTER OCCLUSION

A
30
Q

What are some treatments of myocardial infarction?

A

Thrombolytic agents - i.e. streptokinase or tissue-type plasminogen activator

Mechanical re-expansion of occluded vessel - angioplasty and stenting, or coronary artery bypass grafting

31
Q

Last bits near ROS

A

Medsci 203 (my own) (18 decks)

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