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MIDS 127 - abdo > The Great Vessels > Flashcards

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
Q

Describe IVC thrombus and its SA.

A

Clot in the IVC.

SA: avascular isochoic/echogenic foci within lumen. Prefers to occur at iliac bifurcation below renal veins.

26
Q

Describe Vena Caval Obstruction (etiology, S/S, SA)

A

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
Q

What is the most common IVC tumour?

A

Leiomyoma or leiomyosarcoma (primary tumours). Most common in women with median age of 61yrs.

28
Q

What is mets most common for in the IVC?

A

Most commonly occurs from RCC.

29
Q

Describe renal vein enlargement.

A

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
Q

What is the most common type of visceral venous aneurysm?

A

Portal vein aneurysm

31
Q

What is the most common cause of renal vein thrombosis? Describe its SS and SA.

A

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
Q

Describe Budd-Chiari Syndrome. Describe SS. What is the classic triad?

A

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
Q

Describe Budd-Chiari’s SA.

A

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
Q

Describe Portal Venous Thrombosis’ SA.

A

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
Q

What is Portal Hypertension?

A

An increase in portal venous pressure due to increased resistance to venous flow through liver.

36
Q

What causes portal venous hypertension?

A

Cirrhosis, HV + PV + IVC thrombosis and or occlusion, mets

37
Q

What are the signs and symptoms of Portal Venous Hypertension?

A

Ascites, GI bleeding, jaundice, hematemesis, elevated liver enzymes.
Complications can include: variceal hemorrhage and ascites

38
Q

What are the two types of Portal Venous Hypertension?

A
  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
Q

What’s the caput medusa sign?

A

Severe cases where the paraumbilical veins dilate and can be clinically seen around the umbilicus.

40
Q

What is the SA of Portal Venous Hypertension?

A

Comma shaped portal trunk, increased periportal echogenicity, dilated SMV and SV, ascites, splenomegaly.
Potential hepatofugal flow in PVs.
Collateral vessel development (commonly gastroesophageal)

41
Q

What is a TIPS?

A

Transjugular intrahepatic portosystemic shunt: connection between HV and PV inserted via transcatheter route

MIDS 127 - abdo (14 decks)

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