AAA abdominal aortic aneurysm Flashcards

1
Q

Definition

A

A permanent dilation to 1.5-2x the size of the aorta’s original diameter

True- goes through2 layers, outer layer makes up the wall of the aneurysm

Flase- goes through all 3 layers, surrounding tissues make up the wall off the aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Aetiology

A

Caused by a number of bacterias and infections like:
– salmonella- can begin its life cycle in the intestines and then move into the bloodstream and become fatal
– sylphilis

– atherosclerotic changes (almost all are caused by this)
– can be caused by hypertension and high blood pressure
– inflamed blood vessels
– marfans syndrome (causes weakening of the lining of the aorta)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Epidemiology

A

3-8% of the population
Mortality rate of a ruptured aneurysm is around 50% (around 2/3 patients rupture before making it to the hospital)

Peak age of incidence- 75 (starts usually in the 50s)

Men are 5x more likely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Risk factors

A

Age
Smoking
Hypertension
Atherosclerosis
Genetic predisposition (Marfans syndrome and Ehlers danlos syndrome)
25% of cases there is a first degree relative with AAA
Patients with popliteal artery aneurysms frequently have AAA (25-50% of cases)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Pathophysiology

A

The presence of proteolytic enzymes in the aorta, lead to aneurysmal change

There may also be a presence of the matrix metalloproteinases. These are known to degrade elastin which may lead to further aneurysmal change.

Pathophysiology is poorly understood.
– in the aorta there is decreasing collagen and elastin content from proximal to distal (matrix metalloproteinases)
– elastin fragmentation and degeneration are seen in aneurysm walls

– also appears to be a local inflammatory and immune response associated with the process that is further influenced by familial molecular genetics
—- 90% found below renal arteries
—- 80% are said to be readily palpable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Clinical presentation

A

Unruptured:
– asymptomatic in 50-75% of cases until the rupture occurs
– most are discovered incidentally on a scan for another reason
– may see of feel a pulsatile mass in the abdomen
– if there is symptoms there may be:
—– back pain (70%)
——– may simulate that of a herniated disc or facet syndrome pain

—- groin pain may be present with retroperitoneal expansion and pressure on the right or left femoral nerve

—- abdominal pain (58%)
—- syncope (30%)
—- vomiting (22%)
—— if these 2 symptoms or the back pain becomes progressive, then it may be a sign of an imminent rupture

—- possible intermittent lower limb claudication

Rupture:
– Medical emergency
– presents with severe epigastric pain radiating to the back and groin
– hypotension
– tachycardia
– profound anaemia
– sometimes loss of consciousness and sudden death
– symptoms may mimic that of:
—– renal colic, diverticulitis and severe lower abdominal and testicular pain
—– lumbar disc herniation is a differential diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Investigations

A

Abdominal ultrasound is the most common method for detection (sensitivity 95% with specificity of 100%)

Once diagnosis is made further imaging with:
– CT, MRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Sizes

A

Normal 3cm- wouldn’t require treatment or further scans

Small 3-4.4cm- will require annual ultrasound (unless symptoms change)

medium 4.5-5.4cm- requires quarterly ultrasound

large >5.5cm- will need to be referred

How well did you know this?
1
Not at all
2
3
4
5
Perfectly