Unit 4 Case 3: Thoracic Aortic Aneurysm Flashcards
(102 cards)
1
Q
histology of blood vessels
A
tunica intima
tunica media
tunica adventitia
2
Q
tunica intima
A
innermost
simple squamous flat cells with flat nuclei
sit on the basal lamina
3
Q
tunica media
A
elastic circular smooth muscle
4
Q
tunica adventitia
A
outermost
fibroblasts
longitudinal and smooth muscle
vaso vasorum
5
Q
capillaries
A
endothelial cells
basement membrane and some pericytes
continuous: uninterrupted endothelium and reduced permeability
sinusodial: wider gaps for the movement of larger molecules/cells in the liver and the spleen
fenestrated: gap junctions allow the movement of fluid (real corpuscles)
6
Q
types of arteries
A
muscular
elastic
7
Q
muscular arteries
A
media is bound by internal and external elastic lamina
8
Q
elastic arteries
A
within the media layer has concentric layers of elastic fibres and smooth muscles
9
Q
lumen of arteries compared to veins
A
arteries are smaller
10
Q
wall of arteries compared to veins
A
thicker in arteries
11
Q
media layer in arteries compared to veins
A
thicker in arteries
12
Q
adventitia layer in arteries compared to veins
A
thinner in arteries
13
Q
other features arteries and veins have
A
arteries have internal and external elastic lamina
veins have valves
14
Q
how does the histology of vessels differ in the presence of an aneurysm
A
affects all layers of the vessel wall
degradation of extracellular elastin and collagen fibres
meidal degeneration
medial and adventitial infiltration by mononuclear lymphocytes and macrophages forming vascular associated lymphoid tissue
thickening of the vasa vasorum
vessel wall is weakened so the lumen is widened
15
Q
what occurs in the media of vessels during aneurysms
A
SMCs clonal expand and change to more phagocytic like phenotypes
MMP activity increases causing further aortic wall degradation and dilation
16
Q
what is laplaces law
A
the large the vessel radius the greater the wall tension required to withstand the given internal fluid pressure
P= (w/r) x T
p= inward pressure of the artery from the vessel wall
T= tensional stress within the wall of the vessel
W= thickness of the artery wall
17
Q
relationship between inward pressure and tensional stress and radius of the wall
A
inward pressure exerted by the vessel wall on the blood is directly proportional to the tensional stress in the wall and inversely proportional to the radius of the wall
18
Q
large thin walled vessels pressure
A
they are low pressure
e.g. veins
19
Q
larger the radius the what
A
greater the tension
20
Q
why can capillaries withstand larger pressures
A
due to their small diameter
21
Q
what is in the image and why
A
elastic artery
elastic fibres appear black
22
Q
what is shown by the yellow arrows
A
the adventitia of the vein
23
Q
what is shown by the black arrows
A
external elastic lamina
24
Q
what are the different categories for beta blockers
A
1st generation
2nd generation
3rd generation
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1st generation beta blockers
non selective
block beta 1 and beta 2 receptors n the heart
based on the blockade of beta 1 receptors, decreased heart rate and reduces contractility
treat hypertension angina
beta 2 receptors are predominant in the lungs so the blockade can lead to bronchoconstriction
not recommended in asthma
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examples of 1st generation beta blockers
propranolol
pindolol
nadolol
solatol
timolol
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2nd generation beta blockers
beta 1 selective
cardio selective
chronic diseases
at high enough doses can be lost and beta 2 receptor blockade may occur
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examples of 2nd generation beta blockers
atenolol
acebutolol
bisoprolol
esmolol
metoprolol
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3rd generation beta blockers
non selective and selective
act on blood vessels to cause vasodilation
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carvedilol and labetalol
non selective
cause vasodilation by blocking alpha and beta q
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nebivolol
beta 1 selective and released nitrous oxides from endothelial cells
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betaxolol
vasodilation by blocking calcium channels
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side effects of beta blockers
tiredness
dizziness]lightheaded
cold fingers or toes
difficulty sleeping/nightmares
nausea
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emergency side effects of beta blockers
shortness of breath
wheezing
tightening of chest
yellow skin
whites of eyes turn yellow
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beta blockers used in aneurysms
proanalol
lower blood pressure by slowing the heart rate
may reduce how fast the aorta is widening
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marfan syndrome
disorder of the body's connective tissue
autosomal dominant hereditary condition
gene leads to abnormal fibrillar production
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what is an aneurysm
budge in the wall of an artery
caused by constant high blood pressure, wearing the arteries
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different types of aneurysms
abdominal aortic
thoracic aortic
cerebral
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abdominal aortic aneurysms
most dangerous type
aorta is the largest vessel in the body
most common
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thoracic aortic aneurysm
largely asymptomatic
may get back pain and shortness of breath if symptoms do occur
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cerebral aneurysm
brain
not too dangerous unless they rupture causing a bleed on the brain
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risk factors for aneurysms
high blood pressure
smoking
family history
age
gender
genetic conditions
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high blood pressure as a risk factor
places increased pressure on the walls off the artery increasing the chances of an aneurysm
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smoking as a risk factor
harmful substances in tobaccos smoke can damage the walls of the blood vessels
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age as a risk factor
normally around age 40
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gender as a risk factor
women are more likely to develop
after menopause women have less oestrogen in their blood which helps with the elasticity of blood vessels
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genetic link as a risk factor
having a close relative that has aneurysms will increase your own chances
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genetic conditions as a risk factor
marfan syndrome
genetic condition that affects the connective tissue of the body will weaken the wall of the aorta
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aortic rupture
the all layers of the aorta wall tear
causing blood to leak out of the aorta due to the burst aneurysm
stops blood being pumped around the body and is life threatening
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aortic dissection
starts with a tear in the inner layer of the aortic wall of the thoracic aorta
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stage 1 of the response to internal bleeding
hypovalemia and cardiovascular compensation
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osmoreceptor response to internal bleeding
osmolality of the remaining fluid hasn't yet changed
osmoreceptors are ignorant of the volume reduction
vasopressin release is triggered by baroreceptors sensing loss of blood pressure
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categories of cardiovascular response to haemorrhage
autonomic effects
neurohormonal effects
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autonomic effects in the response to haemorrhage
arterial hypotension causes baroreflex activation
decreased cardiac output causes chemoreceptor activation
decreased vagal stimulus, increased heart rate
sympathetic activation which results in:
-increased peripheral vascular resistance
-redistribution of blood flow away from the cutaneous and splanchnic circulariotn
-stimulation of systemic catecholamine release from adrenal glands producing increased systemic effect in addition to peripheral sympathetic nervous system of solitary tract to hypothalamus
-stimulation of renin by sympathetic stimulation of the juxtaglomeraluar cells due to lower renal perfusion
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what causes baroreflex activation
arterial hypotension
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what causes chemoreceptor activation
decreased cardiac output
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neurohormonal effects to haemorrhage
renin secretion causes: vasoconstriction by angiotensin and increased sodium retention by aldosterone
vasopressin release causes:
vasoconstriction by V1 receptors and increased water retention by V2 receptors
venous hypotension decreases atrial natriuretic peptide secretion causing:
decreased renal blood flow and decreased urinary water and sodium excretion
net effect is decreased urine output and increased retention of sodium and water
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what does renin secretion cause
vasoconstriction by angiotensin
increased sodium retention by aldosterone
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what does vasopressin release cause
vasoconstriction by V1 receptors
increased water retention by V2 receptors
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what restores intravascular volume
transcapillary refill
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transcapillary refill
movement of fluid and protein (mainly albumin) from interstitial compartment into the intravascular compartments
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what describes the net movement of fluid in the capillaries
the starling equation
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what does the sympathetic response to haemorrhage result in
decrease in diameter of the arterioles and decrease in pressure at capillaries
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oncotic pressure after haemorrhage
remains same
as the fluid composition of the intravascular component is unchanged
no longer balanced by high capillary hydrostatic pressure
results in movement of free tea out of the interstitial space and into the intravascular space
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albumin movement
after movement of free water the capillary fluid is diluted
hydrostatic attraction into the capillary is balanced by the osmotic attraction out of the capillary
protein concentration gradient appears to be related to volume of interstitial compartment and pressure within it
interstitial albumin replenishes the intravascular albumin deficit
haemorrhage stimulates albumin synthesis by the liver
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compensatory mechanism
reduction in blood volume during acute blood loss causes a fall in central venous pressure and cardiac filling
leads to reduced cardiac output and arterial pressure
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what are examples of the body's compensatory mechanisms
baroreceptor reflexes
chemoreceptor reflexes
circulating vasoconstrictors
renal absorption of sodium and water
activation of thirst mechanisms
reabsorption of tissue fluids
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cariogenic shock
impaired coronary blood flow resulting from hypotension causes myocardial hypoxia and acidosis
depresses cardiac function and causes arrythmias
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sympathetic escape
Accumulation of tissue metabolic vasodilator substances impairs sympathetic-mediated vasoconstriction, which leads to loss of vascular tone, progressive hypotension and organ hypoperfusion
Loss of precapillary vascular tone increases capillary hydrostatic pressure and capillary fluid filtration, which reduces plasma volume
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Cerebral ischemia/hypoxia
Loss of sympathetic outflow from a hypoxic medulla leads to vasodilation, which further reduces arterial pressure and cerebral perfusion
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Metabolic acidosis
acidosis depresses cardiac muscle and vascular smooth muscle contraction, which further decreases arterial pressure
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Rheological factors
Reduced microcirculatory flow
increases tissue blood viscocity reduces perfusion
Plugging of the microcirculation by leukocytes and platelets, and intravascular coagulation reduce organ perfusion
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Systemic inflammatory response
Endotoxins released into systemic circulation from the ischemic gastrointestinal tract lead to cytokine production, and enhanced formation of nitric oxide and oxygen free radicals, which cause vasodilation, cardiac depression, and organ injury
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hypovolemic shock
occurs when the body starts to shut down due to large amount of fluid loss
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haemorrhage shock
type of hypovolemic shock
where the fluid lost is blood
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classes of haemorrhage shock
Class 1 – blood loss < 15% of total blood volume (up to 750mL of blood lost)
Class 2 - blood loss is 15-30% of total blood volume (750-1500 mL of blood lost)
Class 3 – blood loss is 30-40% of total blood volume (1500-2000 mL of blood lost)
Class 4 – blood loss > 40% (more than 2000 mL of blood lost)
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what is involved in initial haemorrhage shock resuscitation
primary survey, circulation
insert 2 large-bore IVs for fastest fluid administration
administer 20mL/kg bolus of normal saline
transfuse blood products at a 1:1:1 ratio
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how are TAAs diagnosed
CT
MRIU
X ray
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what does the image show
Ct scan with an iodine contrast
black arrow is an aneurysm of descending aorta
white arrow shows blood in the throat as a result of the aortic dissection
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chest x ray and aneurysms
demonstrates widening mediastinum
not sensitive enough to diagnose
CT required for more detailed imaging
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surgical processes used in the case
aortic root surgery
end-vascular aortic aneurysm repair
emergency surgery
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aortic root surgery
Open-chest surgery to treat and enlarged section of the aorta to prevent a rupture. Aortic aneurysms near the aortic root may be related to Marfan and other related condition.
Asurgeon removes part of the aorta and sometimes the aortic valve. A graft replaces the removed section of the aorta and a mechanical or biological valve. If the valve is not removed, the surgery is called valve-sparing aortic root repair.
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end vascular aortic aneurysm repair
catheter inserted into blood vessel
graft attached at the end and placed at the site of the aneurysm
reinforces the weakened section
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emergency surgery
ruptured TAA requires emergency open chest surgery
risky and high chance of complications
important to treat TAAs before rupturing
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difference between surgeries for ascending and descending aneurysm
Median sternotomy for ascending and aortic arch aneurysms or left thoractotomy or thoraco-retroperitoneal exposure for descending and thoracoabdominal aneurysms) and replacement with a synthetic graft.
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when is elective surgery indicated for aneurysms
Large in the case the diameter was 61mm which is large.
Rapidly enlarging (> 0.5 cm/year)
Causing bronchial compression
Causing aortobronchial or aortoesophageal fistulas(abnormal tunnel in the body)
Symptomatic
Traumatic
Mycotic(infection with a fungus or a disease caused by a fungus.)
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complications of open heart surgery
Bleeding.
Death.
Heart attack due to a blood clot after surgery.
Infection at the site of the chest wound.
Long-term need for a breathing machine.
Irregular heart rhythms, called arrhythmias.
Kidney problems.
Memory loss or trouble thinking clearly, which often is temporary.
Stroke.
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less invasive options for aneurysm treatment
transcatheter-placed end-vascular stent grafts
end-vascular surgery
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complications of TAA
rupture of aorta
aorta dissection
these may lead to death
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delayed mobilisation after surgery
associated with higher short term readmission and mortality
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early mobilisation after surgery
reduces risk of post operative complications
accelerates recovery of function walking capacity
reduces length of hospital stay
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positive impacts of early mobilisation post op
prevents blood clots
increased wound healing due to increased circulation
decreased gas and constipation
increased mood
prevents muscle weakness
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prevalence
number of individuals with the disease either at the specific point in time or over a specific period of time
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incidence
number of new cases of disease during a specified period
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mortality
related to the number of deaths caused by health event under investigation
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role of an agency carer
provide domestic care
no nursing care
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carer assessment
provided to individuals who care for someone to see what would make their lives easier
may be eligible for support
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psychological impact of being a full time carer
stress and worry
anxiety
isolated and lonely
less time for yourself
financial worries
lack of sleep
guilt frustration and anger
low self esteem
depression
physical impact
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fear of surgery
homophobia
where symptoms involve irrational fear, situational induced panic attacks
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acute stress
anxiety disorder develops in weeks after traumatic event
lasts at least 3 days
up to a month
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symptoms of acute stress
feeling numb
detached
experiencing derealisation
depersonalisation
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treatment of acute stress
psychiatric evaluation
medication such as antidepressants
