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TEST 3 - Advanced Pathophysiology Summer 2024/2025 UTA 5315 already graded A+
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TEST 3 - Advanced Pathophysiology Summer 2024/2025 UTA 5315 already graded A+
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TEST3
-
Advanced
Pathophysiology
Summer
2018
UTA
5315
Mitral
Valve
Stenosis
-
ANS-
Characterized
by
NARROWING
of
mitral
valve
-
Normal
is
4-6
cm
-Narrowed
is
less
than
2.5
cm
-
Caused
by
RHEUMATIC
FEVER
-More
common
in
WOMEN
-Oxygenated
blood
comes
back
into
heart
into
the
left
atrium
and
down
through
the
mitral
valve
to
the
left
ventricle
-
Complex:
Stenosis
leads
to
volume/pressure
in
left
atrium,
which
results
in
atrial
hypertrophy/dilation,
which
increases
pressure/volume
in
the
pulmonary
circulation
&
causes
PULMONARY
EDEMA
-
Simplified:
Skinny
mitral
valve
doesn't
let
blood
pass
through
easily,
so
blood
backs
up
into
the
left
atrium
and
causes
it
to
swell,
then
backs
up
into
the
lung
and
causes
resp.
symptoms
-S/sx:
dyspnea,
hemoptysis,
a-fib,
dysphagia,
pulmonary
hypertension
Mitral
Valve
Regurgitation
-
ANS-Characterized
by
INCOMPLETE
CLOSURE
of
mitral
valve
-Caused
by
MITRAL
VALVE
PROLAPSE
(flaps
don't
close
together
properly,
leaving
valve
ajar);
more
common
in
WOMEN;
STICKING
CHEST
PAIN
-Blood
in
left
ventricle
backs
up
to
left
ventricle
during
systole
(mitral
valve
should
be
closed
during
systole/contraction
of
heart)
-Leads
to
atrial
dilation/hypertrophy,
increased
pulmonary
vascular
pressure/volume,
PULMONARY
EDEMA
-S/sx:
Dyspnea,
rales,
pansystolic
murmur,
S3
&
S4
heart
sounds
Aortic
Valve
Stenosis
-
ANS-Most
common
valvular
disease
-Most
common
causes
are
aortic
valve
CALCIFICATION
(stiffening)
in
people
over
60;
congenital
aortic
valve
stenosis
in
people
less
than
30
-Normal
valve
3
cm;
symptoms
seen
when
valve
less
than
1
cm;
severe
when
valve
is
less
than
0.5
cm
-Narrowed
valve
prevents
outflow
from
left
ventricle
to
aorta.
This
backs
up
blood
to
the
left
atrium
and
ultimately
floods
the
lung
causing
PULMONARY
EDEMA
S/Sx:
Pulmonary
hypertension/edema,
poor
outflow
of
aorta
to
body
(aorta
sends
out
oxygenated
blood
to
body),
causing
fainting
or
chest
pain
Simplified:
Aorta
is
stiff
and
can't
send
out
oxygenated
blood
properly
to
the
body,
depriving
tissues
of
oxygen.
Blood
gets
backed
up
into
lungs,
causing
pulmonary
edema.
Aortic
Valve
Regurgitation
-
ANS-Valve
is
TOO
WIDE
or
TOO
NARROW,
blood
doesn't
pass
through
effectively,
causing
back
flow
of
blood
into
the
left
ventricle -Marked
by
EARLY
DIASTOLIC
MURMUR
(on
systole,
heart
contracts
and
pushes
blood
up
the
aorta,
but
on
diastole,
heart
relaxes
and
ineffective
aortic
valve
is
not
able
to
hold
blood
up
in
aorta,
so
blood
falls
and
makes
a
swish
sound,
which
is
the
murmur)
-Most
commonly
caused
by
AORTIC
ROOT
DILATION(starting
point
of
aorta
is
too
wide)
-Other
causes:
infective
endocarditis,
rheumatic
fever,
aortitis
from
syphilis,
coarctation
(congenital
narrowing
of
aorta),
aortic
dissection
(tear),
ankylosing
spondylitis
(inflammatory
arthritis)
-Acute:
increases
left
ventricular
end-diastolic
pressure
(LVEDP)
(increased
blood
back
down
in
the
left
ventricle
increases
pressure),
decreased
stroke
volume
(not
much
blood
is
being
pushed
from
left
ventricle
because
blood's
backed
up
and
overwhelming
left
ventricle),
normal
or
decreased
pulse
pressure,
decreased
cardiac
output
(aorta
is
not
effectively
pumping
blood
from
heart)
Chronic:
Body
adjusts;
LVEDP
normalizes,
systolic
bp
increases
(compensation:
harder
contraction
to
push
blood
out
of
aorta
before
it
falls
back
down
to
left
ventricle),
diastolic
bp
decreases
(compensation:
decreased
relaxation
of
heart
to
stop
blood
from
seeping
back
out
of
aorta),
cardiac
output
is
normal,
pulse
pressure
is
increase.
Blood
ultimately
is
backed
up
into
the
left
atrium
and
pulmonary
circulation.
Atherosclerosis
Causes
-
ANS-Begins
with
tissue
injury
Sources
of
injury:
CIGARETTES
(toxins)
Hypertension
(increased
force
of
the
blood
hitting
the
blood
vessel
can
weaken
it)
Diabetes
Hyperlipidemia
(lipids
take
place
of
endothelial
cells
lining
the
blood
vessel,
initiating
an
inflammatory
response)
Patho
of
Atherosclerosis
r/t
Hyperlipidemia
-
Inflammatory
Response
-
ANS1.
Tissue
injury
to
endothelial
cells
lining
the
blood
vessel.
2.
Endothelial
cells
become
inflammed
and
unable
to
produce
sufficient
antithrombotic
and
vasodilating
cytokines,
increasing
risk
for
clot
formation
and
creating
a
tighter
space
for
plaques
and
clots
to
grow.
3.
Macrophages
and
platelets
are
called
to
the
area
of
injury,
further
congesting
the
growing
plaque
area.
4.
LDL
replaces
endothelial
cells
in
the
lining
of
the
blood
vessel.
5.
Macrophages
engulf
the
LDL
particles.
6.
Macrophages
eat
too
much
LDL,
causing
them
to
burst
and
become
foam
cells
(under
a
microscope
they
look
like
sea
foam)
7.
Accumulation
of
foam
cells
causes
a
fatty
streak.
Fatting
streak
further
triggers
inflammatory
responses,
repeating
the
whole
cycle,
and
growing
the
fatty
streak.
8.
Smooth
muscle
hyperplasia
from
all
the
inflammation
grows,
produces
collagen,
and
covers
the
fatty
streak
to
create
a
fibrous
plaque. 9.
The
plaque
may
calcify,
protrude
into
the
vessel,
and
occlude
blood
flow,
resulting
in
ischemia
or
infarction.
Hyperlipidemia
-
ANSLeading
cause
of
coronary
artery
disease
Most
commonly
affects
promximal
portions
of
coronary
arteries,
larger
branches
of
carotid
arteries,
circle
of
Willis
(base
of
brain),
large
vessels
of
lower
extremities,
renal
arteries,
mesenteric
(intestinal)
arteries
Consequences
of
Atherosclerosis
-
ANSReduced
blood
flow
Coronary
artery
disease,
myocardial
infarction,
carotid
artery
disease,
cerebral
vascular
disease,
stroke,
mesenteric
ischemia,
peripheral
vascular
disease,
renal
artery
stenosis
Congenital
Heart
Disease
-
ANS-Most
common
heart
disease
affecting
children
-Etiology
is
unknown
in
90%
of
cases
Causes:
Genetic/environmental
factors
(multifactorial
factors)
Primary
genetic
factors
(single
gene
disorders,
chromosome
disorders)
Sole
environmental
factors
(Accutane/isotretinoin
for
acne,
alcohol,
maternal
rubella
infection)
Maternal
Risk
Factors:
Age
over
45,
prior
child
with
heart
defect,
poorly
controlled
diabetes
during
pregnancy,
alcohol,
congenital
infection
during
pregnancy
(rubella),
aspirin,
lupus,
Dilantin/phenytoin/diphenylhydantoin
for
seizures
LEFT
to
RIGHT
shunt
(Congenital
heart
defect)
-
ANS-Oxygenated
blood
from
the
left
side
of
the
heart
mixes
with
unoxygenated
blood
in
the
right
side
of
the
heart.
-Oxygen
saturation
on
left
side
is
usually
95%,
whereas
right
side
is
75%
-
As
blood
mixes,
right
side's
oxygen
saturation
increases
to
80%
or
more
-VOLUME
OVERLOAD
occurs
on
RIGHT
side
of
heart
occurs,
leading
to
PULMONARY
HYPERTENSION,
which
causes
RIGHT
VENTRICULAR
HYPERTROPHY,
(secondary
to
pulm.
hptn.),
and
LEFT
VENTRICULAR
HYPERTROPHY(secondary
to
blood
being
returned
to
left
ventricle)
Eisenmenger
Syndrome:
Reversal
of
left
to
right
shunt
to
a
right
to
left
shunt.
Eisenmenger
Syndrome
-
ANS1.
Increased
blood
flow
returns
to
lungs
rather
than
to
the
rest
of
the
body.
2.
Blood
vessels
become
stiff
and
narrow
-
permanent
damage.
3.
Increased
pressure
of
the
blood
flow
in
the
lung
becomes
so
great
that
the
direction
of
blood
flow
through
the
shunt
reverses.
4.
Oxygen-poor
(blue)
blood
from
the
right
side
of
the
heart
flows
into
the
left
ventricle
and
is
pumped
to
the
body
and
tissues
do
not
receive
enough
oxygen.
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