AP: Aneurysms and vasculitis Flashcards

1
Q

DEEPSIT: Berry aneurysms

D: where are they often found?

E: What type of defects are in the smooth muscle layer of the artery? What type of factors are often stressors that make the berry aneurysm increase in size? What two disorders lead to an increased risk of berry aneurysm formation?

E: Age group? Gender preference?

P: What sort of defect leads to berry aneurysms to develop? What does this lead to in the vessel wall?

S: Rupture of aneurysms are the most common cause of clinically significant non-traumatic ____ ______? What sort of headache? Sx pre/post rupture?

I: What three different types of imaging can be done? What is a characteristic feature of the CSF?

T: What surgical procedure?

A

Definition:

  • A type of aneurysm that resembles a berry.
  • Found at branch points of the large intracranial arteries in the Circle of Willis.

Etiology:

  • Form in areas where there are congenital defects in the smooth muscle layer of the artery.
  • LIFESTYLE FACTORS: Haemodynamic stress eg hypertension, smoking, cause aneurysm to expand over time.
  • Increased risk in polycystic kidney disease, Ehlers-Danlos syndrome.

Epidemiology:

  • Adults aged 30-60.
  • F > M.

Pathophysiology:

  • Aneurysms occur at points of weakness in the vessel wall.
  • Congenital defect ► vessel wall is attenuated.

Signs, Symptoms and Sequelae:

  • SUBARACHNOID HAEMORRHAGE → 50% risk of death.
    • Usually traumatic causes.
  • Can spontaneously rupture, leading to intracerebral haemorrhage.

Before rupture

  • Vomiting.
  • Double vision.
  • Usually asymptomatic.
  • Seizures.

With rupture and SAH

  • Thunderclap headache.
  • Vomiting, collapsing, seizures, confusion.
  • Death.

Investigations and Diagnosis:

  • Imaging of the brain and the blood vessels → angiogram, CT, MRI.
  • Blood detected throughout the CSF sample.

Treatment, Management and Prevention:

  • Surgical clipping.
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2
Q

What are three causes of aortic aneurysms?

A
  1. Atherosclerosis.
  2. Non-inflammatory degeneration eg connective tissue disorders.
  3. Inflammation eg syphilis, giant cell aortitis.

Anything that causes abnormality in the aortic wall → destroys the capacity of the tissue to resist the haemodynamic forces of systole.

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3
Q

What is this?

A

Abdominal aortic aneurysm.

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4
Q

DEEPSIT for abdominal aortic aneurysms.

D: What sort of aneurysm is an AAA? Where is it often located? (below what/above what).

E: What disease commonly leads to AAA? What other factors? How can circulating microorganisms be a risk factor for AAA?

E: Gender preference? Age group? What mortality rate if rupture occurs?

P: How do atherosclerotic arteries lead to AAA?

S: Before rupture? After rupture (triad)?

I: What imaging will help diagnose AAA?

T: What two surgical modes of repair are indicated for AAAs?

A

Definition:

  • Can be saccular or fusiform aneurysm.
  • Below the level of renal arteries and above the level of the aortic bifurcation (where it branches into common iliac arteries).

Etiology and Risk Factors:

  • Atherosclerosis.
  • Lifestyle factors: SMOKING, alcohol, hypertension.
  • Genetic influences.
  • Mycotic AAAs
    • Circulating microorganisms (as in bacteremia from a Salmonella gastroenteritis) seed the aneurysm wall or the associated thrombus; the resulting suppuration accelerates the medial destruction and may lead to rapid dilation and rupture.

Epidemiology:

  • Common in Caucasian population.
    • 2-4% of autopsies.
  • Males > females
  • Usually 65-75 years old.
  • 90% mortality associated with AAA rupture.

Pathophysiology:

Most often:

  • Excess ECM degradation mediated by local inflammatory infiltrates in atherosclerotic arteries and the destructive proteolytic enzymes produced at these sites.
  • Atherosclerotic plaques compromise the diffusion of nutrients and wastes between the vascular lumen and the arterial wall, and also directly compress the underlying media.
  • As a result, the media undergoes degeneration and necrosis, which results in arterial wall thinning.

Signs, Symptoms and Sequelae:

Before rupture

  • Usually asymptomatic.
  • Can feel back or abdominal pain.
  • Throbbing sensation.

Rupture

  • Triad of
    • Abdominal pain.
    • Hypovolaemic shock.
    • Pulsatile abdominal mass (simulates a tumour).
  • Pain is of sudden onset, excruciating and is felt in the abdomen, flank or groin.
  • Obstruction of a vessel branching off the aorta, resulting in distal ischemia of the kidneys, legs, spinal cord, or GIT, respectively.
  • Embolism.
  • Impingement on adjacent structures.
  • Rupture into peritoneal cavity.

Investigations and Diagnosis:

  • Diagnosis can be made off of clinical finding or imaging studies eg CT scan.

Treatment, Management, and Prevention:

  1. Open aortic surgery.
  2. Endovascular aneurysm repair.
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