The Great Vessels Flashcards

1
Q

The three layers of blood vessels

A

tunica intima, tunica media, tunica adventitia

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2
Q

What is the abnormal measurement of the AO?

A

Greater than 3.0cm

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3
Q

What does the celiac axis branch off into?

A

Hepatic artery, left gastric artery, and splenic artery

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4
Q

What are the wings of a seagull?

A

Hepatic artery / splenic artery

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5
Q

What is the nutcracker phenomenon?

A

Compression of the left renal vein between the superior mesenteric artery/aorta.

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6
Q

What is the portal triad?

A

Portal vein, hepatic artery, and bile duct

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7
Q

What is the portal confluence?

A

Junction of superior mesenteric vein and splenic vein to make main portal vein, posterior to pancreas

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8
Q

What is Arteriovenous Fistulas and what causes them?

A

Abnormal connection between an artery and a vein. Most commonly trauma but can be complication of AAA or RCC.

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9
Q

What is aortic dissesction?

A

Separation of the layers of the arterial wall by blood or hemorrhage.

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10
Q

What are the risk factors, signs and symptoms, and sonographic appearances for aortic dissection?

A

Risk factors: hyper tension, Marfan syndrome
S/S: intense chest pain, abdominal/back/arm/leg pain, vomiting, paralysis
SA: thin linear flap within lumen with motion during cardiac cycle, blood flow on both sides of flap

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11
Q

If the posterior wall and anterior wall can’t be seen on a vein but there is acoustic shadowing distal, what is likely to be missed?

A

Atherosclerosis; wall calcification will create shadowing

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12
Q

What is atherosclerosis and its SS, risk factors, SA?

A

Accumulation of fat and funk in the intima and media layers of the artery. Associated with aneurysms. More commonly seen at areas of bifurcation or branching.
Risk factors: hyperlipidemia, hypertension, smoking
SS: Asymptomatic until stenosis develops
SA: Luminal irregularities, wall calcifications, wall irregularities

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13
Q

What is a AAA? What are the 3 types?

A

Abnormal focal dilation (greater than 3.0cm) of blood vessel caused by a weakness in the wall.

Saccular: sac like protrusion toward one side
Fusiform: most common, gradual dilation of complete circumference of vessel
Dissecting: when a longitudinal tear in the wall allows bleeding to occur into wall

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14
Q

What are the risk factors of AAA?

A

Tobacco, hypertension, vascular disease, COPD, family history. More common in men over 65 than women. Atherosclerosis has huge correlation.

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15
Q

What is a pseudoaneurysm (aka a false aneurysm)?

A

Extravascular pulsating hematoma communicating with the intravascular space, most commonly caused by trauma

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16
Q

Aortic rupture most common place and S/S?

A

Most commonly ruptures into peritoneal space.

S/S: central back pain, hypotension

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17
Q

Splenic Artery Aneurysms, S/S, SA

A

Most common splanchnic vessel aneurysm but rare. Most commonly ruptures into peritoneal cavity. Most commonly seen in females.
Risk factor: portal hypertension, multiple pregnancies
S/S: varied, asymptomatic, LUQ pain, nausea

18
Q

Hepatic Artery Aneurysm

A

Most common extrahepatic. Most common in males.
Comes from systemic infection, arteriosclerosis, blunt abdo trauma
S/S: asymptotic until large enough to cause symptoms

19
Q

Renal Artery Aneurysm

A

Most commonly extrarenal. Surgery needed is bigger than 1.5cm. Comes from atherosclerosis.
S/S: Palpable mass, hypertension, flank pain, hematuria

20
Q

When an AAA is diagnosed, what other arteries should be checked?

A

Common Iliacs

21
Q

What is an aortic graft?

A

A structure used to repair an aortic aneurysm by preventing recurrent flow into aneurysm sac.

22
Q

What is EVAR?

A

Endovascular repair of abdominal aortic aneurysms. A stent graft deployed into aorta.
SA: Very echogenic walls with ribbing and are straighter than native vessels

23
Q

What kind of complications can an aortic graft (EVAR) create?

A

Pseudoaneurysms (most common complications), graft aneurysms, hematomas, abscesses, occlusion, endoleaks.

24
Q

What are the four types of Endoleaks and which is most common?

A

I: incomplete seal
(Most Common) II: IMA or lumbar artery haven’t been exluded by device and continues to provide flow into aneurysm
III: Rare, endograft failure due to disconnection or fabric disruption
IV: rare, endograft failure due to graft porosity

25
Describe IVC thrombus and its SA.
Clot in the IVC. | SA: avascular isochoic/echogenic foci within lumen. Prefers to occur at iliac bifurcation below renal veins.
26
Describe Vena Caval Obstruction (etiology, S/S, SA)
Etiology: Right sided heart failure (most common) SS: Abdominal pain, ascites, tender hepatomegaly, lower extremity edema SA: IVC dilates below level of obstruction, decreased or absent respiratory variations
27
What is the most common IVC tumour?
Leiomyoma or leiomyosarcoma (primary tumours). Most common in women with median age of 61yrs.
28
What is mets most common for in the IVC?
Most commonly occurs from RCC.
29
Describe renal vein enlargement.
Etiology: splenorenal or gastrorenal shunts in pts with portal hypertension or portal thrombosis. S/S: no distinguishing clinical features except arteriovenous malformation. SA: RV dilation greater than 1.5cm
30
What is the most common type of visceral venous aneurysm?
Portal vein aneurysm
31
What is the most common cause of renal vein thrombosis? Describe its SS and SA.
Nephrotic syndrome, renal tumors. SS: flank pain, leg swelling, proteinuria, hematuria SA: Renal vein dilation proximal to occlusion, isoechoic/echogenic intraluminal focus kidney enlargement
32
Describe Budd-Chiari Syndrome. Describe SS. What is the classic triad?
Occlusion of some or all of the hepatic veins and/or occlusion of the inferior vena cava. Primary: occlusion of HV or IVC by congenital web or fibrous cord Secondary: occlusion of HV and/or IVC by tumour or thrombus Risk factors: Oral Contraceptive Pill use, HCC SS: Abdominal pain, jaundice, ascites, hepatomegaly, splenomegaly. CLASSIC SS TRIAD: ascites, hepatomegaly, abdominal pill
33
Describe Budd-Chiari's SA.
Depends on degree of obstruction. HV may not be visible. Hypertrophic caudate lobe (due to direct venous drainage into IVC). Acute - hypoechoic liver parenchyma Chronic - hyperechoic and inhomogenous liver parenchyma
34
Describe Portal Venous Thrombosis' SA.
Varies depending on stage of disease process. Isoechoic/echogenic intraluminal thrombus seen first then collaterals. These collaterals grow, and are a way of the body making new paths to get around the occlusion. Portal vein gains worm-like vessels near it. Lack of normal PV landmarks. MPV may dilate bigger than 13mm. The SMV and SV will also be dilated.
35
What is Portal Hypertension?
An increase in portal venous pressure due to increased resistance to venous flow through liver.
36
What causes portal venous hypertension?
Cirrhosis, HV + PV + IVC thrombosis and or occlusion, mets
37
What are the signs and symptoms of Portal Venous Hypertension?
Ascites, GI bleeding, jaundice, hematemesis, elevated liver enzymes. Complications can include: variceal hemorrhage and ascites
38
What are the two types of Portal Venous Hypertension?
1. Presinusoidal portal hypertension - results of elevated pressure in portal-splenic venous system (extrahepatic) 2. Intrahepatic portal hypertension - result of disease that affect the portal zones of the liver
39
What's the caput medusa sign?
Severe cases where the paraumbilical veins dilate and can be clinically seen around the umbilicus.
40
What is the SA of Portal Venous Hypertension?
Comma shaped portal trunk, increased periportal echogenicity, dilated SMV and SV, ascites, splenomegaly. Potential hepatofugal flow in PVs. Collateral vessel development (commonly gastroesophageal)
41
What is a TIPS?
Transjugular intrahepatic portosystemic shunt: connection between HV and PV inserted via transcatheter route