6916459
Beschreibung
Mindmap von Ella Middlemiss, aktualisiert more than 1 year ago
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Erstellt von Ella Middlemiss
vor etwa 8 Jahre
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Atherosclerosis
and CHD
- What is atherosclerosis
- The disease process
that leads to CHD
and strokes
- Fatty deposits can
either block an artery
directly or increase its
chance of being
blocked by a blood clot
(thrombosis)
- The blood supply can
be blocked completely
and if not restored
quickly, the affected
cells are permanently
damaged
- In the coronary
arteries, this
results in a heart
attack (myocardial
infarction)
- In the arteries
supplying the brain
it results in a stroke
- In the coronary
arteries, this
results in a heart
attack (myocardial
infarction)
- An artery can burst
where blood builds
up behind an artery
that's been
narrowed as a result
of atherosclerosis
- The disease process
that leads to CHD
and strokes
- What happens in atherosclerosis?
- Endothelium
becomes damaged
and dysfunctional
- Endothelial
damage results in
HBP, which puts
extra strain on the
layer of cells
- It might also occur
due to some of the
toxins from
cigarette smoke in
the bloodstream
- Once the inner
lining of the artery
is breached, there's
an inflammatory
response
- White blood cells
leave the blood
vessel and move
into the artery wall
- These cells
accumulate
chemicals from the
blood, particularly
cholesterol
- A fatty deposit
builds up, called an
atheroma
- Calcium salts and fibrous
tissue also build up at the
site, resulting in a hard
swelling called a plaque on
the inner wall of the artery
- The build up of fibrous
tissue means that the
artery wall loses some
of its elasticity - it
hardens
- Plaques leads to the lumen
narrowing - makes it more difficult
to pump blood around the body
can lead to a rise in blood pressure
- Positive
feedback
- HBP and more plaques
- Endothelial
damage in other
areas more likely
- Endothelial
damage in other
areas more likely
- HBP and more plaques
- The fast flowing blood in arteries is
under high pressure so there is a
significant chance of damage to the walls.
The low pressure in he veins means there
is less chance of damage to the walls
- Positive
feedback
- Plaques leads to the lumen
narrowing - makes it more difficult
to pump blood around the body
can lead to a rise in blood pressure
- The build up of fibrous
tissue means that the
artery wall loses some
of its elasticity - it
hardens
- Calcium salts and fibrous
tissue also build up at the
site, resulting in a hard
swelling called a plaque on
the inner wall of the artery
- A fatty deposit
builds up, called an
atheroma
- These cells
accumulate
chemicals from the
blood, particularly
cholesterol
- White blood cells
leave the blood
vessel and move
into the artery wall
- Once the inner
lining of the artery
is breached, there's
an inflammatory
response
- It might also occur
due to some of the
toxins from
cigarette smoke in
the bloodstream
- Endothelial
damage results in
HBP, which puts
extra strain on the
layer of cells
- Endothelium
becomes damaged
and dysfunctional
- Blood Clotting
- Vital when a blood
vessel is damaged
- The blood clot seals the
break in the blood
vessel and limits blood
loss and prevents entry
of pathogens through
any open wounds
- When platelets (a type of
blood cell without a
nucleus), come into contact
with the damaged vessel
wall they change from
flattened disks to spheres
with long thin projections
- Their cell surfaces change,
causing them to stick to
exposed collagen in the wall and
to each other to form a
temporary platelet plug. They
also release substances that
activate more platelets
- The direct contact of
blood with collagen
triggers a cascade of
chemical changes
- Usually blood
doesn't clot inside
blood vessels
- Platelets don't stick to the endothelium of blood vessels.
- It is very smooth and has substances on its
surface that repel the platelets. However, if
there is atherosclerosis and the endothelium is
damaged, the platelets come into contact with
the damaged surface and any exposed collagen.
- The clotting cascade
results in a clot
- The clotting cascade
results in a clot
- It is very smooth and has substances on its
surface that repel the platelets. However, if
there is atherosclerosis and the endothelium is
damaged, the platelets come into contact with
the damaged surface and any exposed collagen.
- Platelets don't stick to the endothelium of blood vessels.
- Usually blood
doesn't clot inside
blood vessels
- The direct contact of
blood with collagen
triggers a cascade of
chemical changes
- Their cell surfaces change,
causing them to stick to
exposed collagen in the wall and
to each other to form a
temporary platelet plug. They
also release substances that
activate more platelets
- Platelets stick to damaged
wall and to each other,
forming a platelet plug
- Thromboplastin
release triggers
clotting cascade
- Thromboplastin is
released from
damaged tissue
and from platelets
- Ca2+ and vitamin K in
plasma must also be present
- Thromboplastin activates
an enzyme that catalyses
the conversion of the
protein prothrombin into
a enzyme called thrombin
- Thombin catalyses the
conversion of soluble
plasma protein,
fibrinogen, into the
insoluble protein, fibrin
- A mesh of fibrin forms
that traps more
platelets and red blood
cells to form a clot
- A mesh of fibrin forms
that traps more
platelets and red blood
cells to form a clot
- Thombin catalyses the
conversion of soluble
plasma protein,
fibrinogen, into the
insoluble protein, fibrin
- Thromboplastin activates
an enzyme that catalyses
the conversion of the
protein prothrombin into
a enzyme called thrombin
- Ca2+ and vitamin K in
plasma must also be present
- Thromboplastin is
released from
damaged tissue
and from platelets
- Thromboplastin
release triggers
clotting cascade
- Vital when a blood
vessel is damaged
- Coronary Heart Disease
- Narrowing of the
coronary arteries
limits the amount
of oxygen-rich
blood reaching the
heart muscle
- The result may be a
chest pain (angina)
- Angina is usually
experienced during exertion
when the cardiac muscle is
working harder and needs
to respire more
- Because the heart muscle
lacks oxygen, it's forced to
respire anaerobically
- Results in
chemical changes
that trigger pain
- Results in
chemical changes
that trigger pain
- Because the heart muscle
lacks oxygen, it's forced to
respire anaerobically
- Angina is usually
experienced during exertion
when the cardiac muscle is
working harder and needs
to respire more
- The result may be a
chest pain (angina)
- If a fatty plaque ruptures,
collagen is exposed which
leads to rapid clot formation
- The blood supply to the
heart may be blocked
completely
- The heart muscle supplied by these
arteries doesn't receive blood so it's
said to be ischaemic (without blood)
- If the affected muscle
cells are starved of
oxygen for long they will
be permanently damaged
- Heart attack or myocardial infarction
- Heart attack or myocardial infarction
- If the affected muscle
cells are starved of
oxygen for long they will
be permanently damaged
- The heart muscle supplied by these
arteries doesn't receive blood so it's
said to be ischaemic (without blood)
- The blood supply to the
heart may be blocked
completely
- Narrowing of the
coronary arteries
limits the amount
of oxygen-rich
blood reaching the
heart muscle
- Stroke
- Supply of blood to the
brain briefly interrupted
is a mini-stroke
- Blood clot blocks
one of the arteries
leading to the brain
is a full stroke, may
be fatal
- Supply of blood to the
brain briefly interrupted
is a mini-stroke
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