RD CVS formatted Flashcards

1
Q
  1. A patient is due for a fistula in his left arm, best place for the vascath is
    a. Left internal jugular vein
    b. Right internal jugular vein
    c. Left subclavian vein
    d. Right subclavian vein
    e. Left femoral vein
A

b. Right internal jugular vein

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2
Q
  1. Subclavian arterial thrombosis (LAS – thoracic outlet syndrome), young painter, pain. Which is not associated.
    a. Dissection (Subclavian artery dissection)
    b. Aneurysm (Subclavian artery aneurysm)
    c. Stenosis (Subclavian artery stenosis)
    d. Venous thrombosis (Subclavian vein thrombosis)
    e. Arterial mural thrombus (Subclavian artery wall haematoma)
A

a. Dissection (Subclavian artery dissection)
2. Subclavian arterial thrombosis (LAS – thoracic outlet syndrome), young painter, pain. Which is not associated.
a. Dissection (Subclavian artery dissection)
b. Aneurysm (Subclavian artery aneurysm) T – SCA aneurysm
c. Stenosis (Subclavian artery stenosis) T – narrowing of SCA which is positional (abduction)
d. Venous thrombosis (Subclavian vein thrombosis) T – may be occlusive or non-occlusive
e. Arterial mural thrombus (Subclavian artery wall haematoma) T – mural thrombi

StatDx:
• TO consists of interscalene triangle, costoclavicular space, and retropectoralis minor space (subcoracoid tunnel)
o Compression of neural, arterial, or venous structures crossing these tunnels → TOS
o Narrowing of costoclavicular distance may be most important abnormality in symptomatic patients
• Neuropathic TOS: Symptomatology 2° to brachial plexus compression (most symptomatic patients)
o Up to 98% symptomatic patients have plexus compression; minority 2° to arterial or venous impingement
• Vascular TOS: Compression of subclavian vessels o Repetitive arterial trauma → focal stenosis, aneurysm formation, micro-embolization, tissue loss
o Venous compression → SCV thrombosis

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3
Q
  1. A 45 yo man with intermittent claudication on walking. Angiography showed 3cm long stenosis of less than 50% in the mid SFA. What is the most appropriate treatment:
    a. Exercise
    b. Angioplasty
    c. Bypass graft
    d. Stent-graft
A

a. Exercise Based on AHA/ACC guidelines for peripheral arterial disease 2006:
• Incomplete information – depends on impact on life of disease & comorbidities
• Try supervised claudication exercise therapy & pharmacotherapy first, as well as risk factor modificationTASC-II 2007 guidelines:

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4
Q
  1. Young man in MVA, CT shows smooth lobulated bulge anteromedial aortic arch near isthmus. No mediastinal blood or other injury. Most likely cause of appearances
    a. Ductus diverticulum
    b. Pseudo-aneurysm
    c. Traumatic aneurysm
    d. Acute dissection
    e. Injury to the mediastinal veins
A

Ductus

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5
Q
  1. AV fistula shows stenosis of arterial anastomosis. Best option for long term patency?
    a. Bare metal stent
    b. Covered stent
    c. Self-expanding stent
    d. Angioplasty
A

d. Angioplasty T angioplasty if upper forearm or upper arm; surgery if lower forearm

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6
Q
  1. Feature of HOCM: a. Diastolic dysfunction
    b. Aortic level stenosis
    c. Interatrial septal thickening
    d. Normal mitral valve
A

a. Diastolic dysfunction T abnormal LV stiffness → impaired LV relaxation → poor early diastolic filling

  1. Feature of HOCM:
    a. Diastolic dysfunction T abnormal LV stiffness → impaired LV relaxation → poor early diastolic filling
    b. Aortic level stenosis F subaortic stenosis (septal thickening + SAM)
    c. Interatrial septal thickening F asymmetric form (most common) has interventricular septal thickening
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7
Q
  1. In ‘Power Doppler’ the intensity of colour denotes:
    a. Angle of insonation
    b. Velocity
    c. Amplitude
    d. Direction of flow.
A

c. Amplitude

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8
Q
  1. Back pain in a 50yo male most likely:
    e. Aortic dissection
    f. Penetrating atherosclerotic ulcer
    g. Aortic aneurysm
A

e. Aortic dissection peak age 60 years, range 13-87 years (Dahnert)

  1. Back pain in a 50yo male most likely:
    e. Aortic dissection peak age 60 years, range 13-87 years (Dahnert)
    f. Penetrating atherosclerotic ulcer elderly with HTN/lipids/atheroma (Dahnert)
    g. Aortic aneurysm AAA usually age > 60 years M»F (Dahnert)
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9
Q

colour doppler, coding depends on …. what??

A
Colour displayed within BVs on colour Doppler function of:
•	Flow velocity
•	Doppler angle
•	Presence of aliasing
•	Colour map utilized
•	Phase of cardiac cycle
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10
Q

guy with US with thick walled aneurysm with increased ESR. likely??

a. inflammatory aneurysm
b. mycotic aneurysm

A

inflammatory A = idiopathic inflammatory aortic aneurysm = dense perianeurysmal fibrosis & a thickened aortic wall; accounts for 5-25% of all AAAs; CECT reveals delayed enhancement of soft tissue component; often fusiform

B = mycotic aneurysm = infected aortic aneurysm = uncommon (0.06-2.6% of all aneurysms); usually saccular rather than fusiform, with perianeurysmal gas, stranding & fluid +/- vertebral body & psoas involvement

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11
Q

which is not associated with azygous continuation of IVC

a. dextrocardia
b. polysplenia
c. left sided SVC
d. gonadal vein into renal vein
e. hepatic vein into RA

A

E = F hepatic veins drain directly into RA

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12
Q

Young woman with hypertension and narrowing of renal ostia. Most likely a. FMD

b. Wegners
c. PAN

A

C = T/F = aneurysms at bifurcation points (up to 1cm); renal infarcts; renal/retroperitoneal haemorrhage; however is listed in StatDx as cause of RAS- Maybe real answer was neurofibromatosis (aneurysm; narrowing of proximal RA) or Takayasu

Causes of RAS
• Atherosclerosis (most common cause, 70%; renal artery ostium or proximal 2cm; elderly)
• FMD (25%; mid-distal RA or hilar branches, may be multifocal; young adults; R>L; bilateral in 2/3)
• Congenital/inheritedo Congenital stenosis (childhood)o Neurofibromatosis (children; proximal renal artery)o Ehlers-Danlos or Williams syndrome
• Arteritiso Takayasuo PANo Buerger disease
• Other
o Abdominal aortic coarctation
o Thromboembolico Radiation therapy
o Aortic dissectiono Phaeochromocytoma
o Infrarenal AAA
o Retroperitoneal fibrosis

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13
Q
  1. Coronary artery dominance defined by the coronary artery that supplies:
    a. The obtuse artery
    b. The posterior interventricular artery
    c. AV nodal artery
    d. The conal artery
A

b. The posterior interventricular artery T
• Refers to the coronary artery that supplies the diaphragmatic surface of LV & the posterior diaphragmatic portion of the interventricular septum – i.e. the dominant artery gives the posterior interventricular (descending) branch (PDA) & the posterolateral branch (PLB)
• Right dominance denotes RCA origin of flow (80-85%)
• Left dominance denotes LCA origin of flow (15-20%) - in this case the PDA & PLB arise from the LCx artery
• Mixed dominance refers to an intermediate pattern, e.g. PDA comes from RCA & PLB comes from LCx; branches of both arteries run in or near the posterior interventricular groove
• Notes:o The LCA almost always supplies a greater volume of tissueo The non-dominant system is usually smaller in calibre c.f. the dominant system

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14
Q
  1. 50 female presents with headache and hypertension. Angiography reveals multiple renal aneurysms. Which is MOST likely?
    e. Aortic dissection
    f. Fibromuscular dysplasia
    g. Polyarteritis nodosa
    h. Takayasu’s arteritis
    i. Wegener’s granulomatosis
A

c. Polyarteritis nodosa T kidneys involved in 70-80% with multiple peripheral small aneurysms; CNS involved in 10% (microaneurysms; most common systemic vasculitis to affect the CNS)
2. 50 female presents with headache and hypertension. Angiography reveals multiple renal aneurysms. Which is MOST likely?
a. Aortic dissection F no renal aneurysms
b. Fibromuscular dysplasia F can cause hypertension, can also involve craniocervical arteries, but aneuryms usually post-stenotic, although multiple aneurysms can be seen
c. Polyarteritis nodosa T kidneys involved in 70-80% with multiple peripheral small aneurysms; CNS involved in 10% (microaneurysms; most common systemic vasculitis to affect the CNS)
d. Takayasu’s arteritis predilection for aorta esp. AA & its branches (esp. SCA); RAS may occur; can involve proximal carotid arteries; may cause aneurysms
e. Wegener’s granulomatosis F? typically causes GN, but can cause microaneurysms by its small vessel vasculitis; may cause intracerebral & meningeal granulomas or vasculitis

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15
Q
  1. CXR shows upward bowing of cardiac apex, rib notching and retrosternal mass, most likely? (+ VIC – young male with HTN, indentation of left lateral aortic border)
    t. Coarctation of aorta
    u. TAPVR
    v. Aortic stenosis
    w. Dissection
A

a. Coarctation of aorta T = get rounded elevated apex; rib notching; prominent ascending aorta

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16
Q
23.	Old dude with known coronary artery disease.  Ovoid mass with areas of calcification adjacent to left sphenoid sinus.  Most likely
\:i)	Fusiform basilar artery aneurysm
ii)	Fusiform ICA aneurysm 
iii)	CoW berry aneurysm
 iv)	Micotic MCA aneurysm
A

ii) Fusiform ICA aneurysm T on MR look for pulsation artifact!

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17
Q
  1. Middle aged woman. End stage renal failure. AV fistula thrombosed and needs access. Decompensating badly with encephalopathy etc. Multiple previous Subclavian, IJ and femoral vascaths/lines. Treating team failed insertion IJ line on ward. Best option:
    i) Peritoneal dialysis
    ii) Doppler venous mapping
    iii) Post con DSA venous mapping
    iv) Post con CT venous mapping
    v) Post con MR venous mapping
A

vi) Doppler venous mapping T with aim of doing US/fluoro guided central line insertionv
ii) Post con DSA venous mapping T if planning for new AVFIf in ESRF, further contrast would not be good (e.g. conventional venography) – can use Gadolinium for DSA (although this is against the RANZCR contrast guidelines!). No good evidence as yet for MRA.

Not sure what question means – if put in new AVF, would need to wait until matures anyway. Needs temporary central vein access & would assess with ultrasound in angio suite.If absolutely no access, could plan for peritoneal dialysis.Vascular access society guidelines for pre-op evaluation:

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18
Q
  1. 30 female left neck pain, 10 hrs of diplopia and dysarthria. Normal non contast CT head and neck. The next investigation should be:
    a. Lumbar puncture
    b. Contrast enhanced CT head
    c. DSA
    d. Carotid US
    e. MRI brain
A

e. MRI brain T if with T1 fat sat neck and MRA neck/brain, although according to RG 08 has quite poor sens/spec for vertebral artery dissection. MRI brain to exclude other causes other than dissection.
4. 30 female left neck pain, 10 hrs of diplopia and dysarthria. Normal non contast CT head and neck. The next investigation should be:
a. Lumbar puncture F
b. Contrast enhanced CT head F would be T if CTA head/neck
c. DSA ?F invasive, but “gold standard”
d. Carotid US F
e. MRI brain T if with T1 fat sat neck and MRA neck/brain, although according to RG 08 has quite poor sens/spec for vertebral artery dissection. MRI brain to exclude other causes other than dissection.

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19
Q

50 yo mande, long hx of worsening claudication. 5cm long segment SFA occlusion. Best tx.

a. angioplasty
b. stent graft
c. bypass
d. exercise programme
e. cryotherapy

A

Still considered limited disease as < 10cm length. Infrainguinal. Best choice is endovascular revascularisation.RCT shows significantly higher patency rates of stenting over angioplasty alone for femoropopliteal artery lesions, however most reserve stent placement for acute failure of PTA. Therefore best answer probably A, angioplasty

.From TASC II 2007 guidelines (JVascSurg 2007)
• Acute limb ischaemia (ALI): Infrainguinal causes of ALI, such as embolism or thrombosis, are often treated with endovascular methods. Initial therapy with catheter-based thrombolysis should be considered in cases of acute thrombosis due to vulnerable atherosclerotic lesions or late bypass graft failures. When thrombolysis reveals underlying localized arterial disease, catheter-based revascularization becomes an attractive option. Stenoses and occlusions are rarely the sole cause of ALI or even severe chronic symptoms but these commonly lead to superimposed thrombosis and, therefore, should be treated to avoid recurrent thrombosis.

  • Claudication: The initial approach to the treatment of limb symptoms should focus on structured exercise and, in selected patients, pharmacotherapy to treat the exercise limitation of claudication (risk factor modification and antiplatelet therapies are indicated to decrease the risk of cardiovascular events and improve survival). Failure to respond to exercise and/or drug therapy would lead to the next level of decision making, which is to consider limb revascularization. However, in patients in whom a proximal lesion is suspected (findings of buttocks claudication, reduced or absent femoral pulse) the patient could be considered for revascularization without initially undergoing extensive medical therapy.
  • Revascularisation: Endovascular treatment of infrainguinal disease in patients with intermittent claudication is an established treatment modality. The low morbidity and mortality of endovascular techniques such as PTA makes it to the preferred choice of treatment in limited disease such as stenoses/occlusions up to 10 cm in length. For diffuse aortoiliac (suprainguinal) disease, bypass has better long-term patency, however the risks of surgery are greater and patient factors may lead towards PTA which has a 90% success rate
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20
Q

Left SVC drains into

A

coronary sinus orleft atrium

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21
Q
  1. Churg Strauss syndrome extrathoracic manifestations include?
    a. Renal artery stenosis
    b. Cerebral hemorrhage
    c. Osteosarcoma
    d. Hepatosplenomegaly
    e. Mesenteric ischaemia
A

e. Mesenteric ischaemia T mesenteric vasculitisCSS = triad of asthma, hypereosinophilia & systemic small vessel granulomatous necrotizing vasculitis. Major involvement is of the heart, lungs & skin. (Dahnert – variant of PAN in asthmatic patients). Criteria for Dx (4 of 6) (1) asthma (wheezing, expiratory rhonchi), (2) eosinophilia of more than 10% in peripheral blood, (3) paranasal sinusitis, (4) pulmonary infiltrates (may be transient), (5) histological proof of vasculitis with extravascular eosinophils, and (6) mononeuritis multiplex or polyneuropathy.

    • Strong association with allergic rhinitis, asthma, eosinophilia
  • Vessels in lung, heart, spleen, peripheral nerves & skin involved by intravascular & extravascular granulomas, with infiltration of vessels & perivascular tissues by eosinophils
  • Severe renal disease infrequent
  • Coronary arteritis and myocarditis usual cause of morbidity and mortality
  • Histologically may be identical to PAN and microscopic angiitis
  • Both arteries and veins involved
  • p-ANCA present in 40-70%
  • Gastrointestinal symptoms (31%) - Symptoms related to GI vasculitis, eosinophilic gastritis, colitis (This includes abdominal pain [59%], diarrhea [33%], and GI bleeding [18%].)
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22
Q
  1. Which is NOT a recognised cause of Budd-Chiari syndrome
    a. Chronic pancreatitis
    b. Bone marrow transplantation
    c. Chemotherapy
    d. Systemic lupus erythematosus
    e. Oral contraceptives
A

a. Chronic pancreatitis F (but does cause PV thrombosis!)

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23
Q
  1. Regarding tunneled haemodialysis catheters, which is LEAST correct?
    a. Femoral catheters can remain in situ for several months
    b. Tunneled catheters have a higher rate of infection than non-tunneled catheters
    c. Internal jugular vein puncture is preferred to subclavian vein puncture
    d. Fibrin sheath is best treated by thrombolysis
    e. Optimal tip position is in the upper SVC.
A

a, c and e…

  1. Regarding tunneled haemodialysis catheters, which is LEAST correct? SK/Kandarpa p469
    a. Femoral catheters can remain in situ for several months F (med comp femoral catheter is intended for use for < 30 days (product info)) Kandarpa – femoral catheters have higher incidence of infection, limits mobility & risk of iliac vein stenosis
    b. Tunneled catheters have a higher rate of infection than non-tunneled catheters F non-tunnelled catheters have lower rates of blood flow, a higher incidence of infection & shortened survival c.f. tunneled catheters
    c. Internal jugular vein puncture is preferred to subclavian vein puncture T preference is R IJV > L IJV or R EJV – avoid use of subclavian veins (if for later AVF) & avoid insertion on side of maturing AVF
    d. Fibrin sheath is best treated by thrombolysis T
    e. Optimal tip position is in the upper SVC. (F atriocaval junction or into the RA to ensure optimum flow); red lumen medial & distal (venous/blue) end hole lateral
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24
Q
  1. The most correct statement about colour Doppler US is?
    a. Doppler colour coding depends on the amplitude of flow
    b. Doppler colour coding depends on the vessel type
    c. Doppler colour coding depends on the velocity of blood flow
    d. Doppler colour coding depends on the angle of isonisation
A

c. Doppler colour coding depends on the velocity of blood flow T brighter colours (or different colour shades) are used to display mean velocities

d.	Doppler colour coding depends on the angle of isonisation  T in colour Doppler the format of transducer determines direction of Doppler beam.  The Doppler angle may change with vessel orientation &amp; produce colour changes related only to changes in the Doppler angle &amp; not to changes in blood flow.Colour displayed within BVs on colour Doppler function of (Brant, US core curriculum)
\:•	Flow velocity
•	Doppler angle
•	Presence of aliasing
•	Colour map utilized
•	Phase of cardiac cycle
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25
Q
  1. Re: lower limb angiography, which is LEAST correct?
    a. Peroneal artery terminates above ankle
    b. 5Fr catheter adequate for diagnostic studies
    c. Adductor canal is in the lower thigh
    d. The profunda femoris origin is best seen with leg in external rotation
A

d. The profunda femoris origin is best seen with leg in external rotation F this will bring the postero lat origin behind the SFA (can’t find a reference)

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26
Q
  1. Left Atrial enlargement, which is false:
  2. VSD
  3. endocardial fibroelastosis
  4. HOCM
  5. TOF.
  6. Atrial myxoma.
A

4.TOF. F – have small left heart chambers due to ↓ blood returning from lungs (RVOT)

  1. Left Atrial enlargement which is false (JS)
  2. VSD - T - Increased pulmonary venous return leads to volume overload of the LA and LV, leading to dilation.
  3. Endocardial fibroelastosis T – focal or diffuse fibroelastic endocardial thickening of LV +/- LA from deposition of collagen and elastic tissue, causes CHF during first 6mths of life and if diffuse is often fatal by 2 years of age (Dahnert). Get enlarged LA & LV, pulmonary venous congestion. Accompanied by aortic valve obstruction & other CHD in one-third (Robbins). A cause of restrictive cardiomyopathy.
    * *LJS opinion: atria dilated due to pressure overload b/c can’t fill ventricles
  4. HOCM. T - LV hypertrophy leads to rapid blood flow through the outflow tract and anterior displacement of the anterior leaflet of the MV causing mitral regurgitation and subsequent LA enlargment (Dahnert)
  5. TOF. F – have small left heart chambers due to ↓ blood returning from lungs (RVOT)
  6. Atrial myxoma. T - typically causes enlargement of the LA without enlargement of the atrial appendage
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27
Q
  1. In lower limb DVT, which is true:
  2. Isolated calf vein thrombosis in ambulatory patients has an incidence of PE of <5%.
  3. Approx 40% of calf vein thrombi propagate superiorly to involve at least the popliteal or femoral veins.
  4. Clinical diagnosis is accurate in 80%.
  5. Vein diameter typically increases in chronic thrombosis.
  6. A phasic change with respiration on Doppler of implies thrombosis.
A
  1. Isolated calf vein thrombosis in ambulatory patients has an incidence of PE of <5%. - T - risk factors: surgery (esp. legs/pelvis), severe trauma, prolonged immoblisation, malignancy, pregnancy, meds (OCP), previous DVT… UTD: Distal calf vein thrombosis is felt to be of lesser clinical importance than proximal vein thrombosis and its optimal treatment has yet to be defined. If anticoagulation is not administered for isolated asymptomatic distal venous thrombosis, serial noninvasive studies of the lower extremity should be performed over the next 10 to 14 days to assess for proximal extension of the thrombus, which has a higher incidence of pulmonary embolism.
  2. In lower limb DVT, which is true: (GC) CME00.08 and 03.42 (mixture)
  3. Isolated calf vein thrombosis in ambulatory patients has an incidence of PE of <5%. - T - risk factors: surgery (esp. legs/pelvis), severe trauma, prolonged immoblisation, malignancy, pregnancy, meds (OCP), previous DVT… UTD: Distal calf vein thrombosis is felt to be of lesser clinical importance than proximal vein thrombosis and its optimal treatment has yet to be defined. If anticoagulation is not administered for isolated asymptomatic distal venous thrombosis, serial noninvasive studies of the lower extremity should be performed over the next 10 to 14 days to assess for proximal extension of the thrombus, which has a higher incidence of pulmonary embolism.
  4. Approx 40% of calf vein thrombi propagate superiorly to involve at least the popliteal or femoral veins. - F - up to 20% propagate. Serial evaluation every 3-5 days is therefore important in patients who remain symptomatic with conservative therapy to dx clot propagation and prevent PE. [B&H pg 1052]
  5. Clinical diagnosis is accurate in 80%. - F - The clinical presentation and physical examination findings are unreliable in making the diagnosis [B&H]. 2/3 of DVT are clinically silent and clinically suspected DVT is accurate in only 26-45% [Dahnert].
  6. Vein diameter typically increases in chronic thrombosis. - F - chronic clot does not expand the lumen of the vein and appears more echogenic than an acute clot. The walls appear thickened, irregular and echogenic and the vein is incompletely compressible. Collaterals can be seen on colour Doppler. [B&H]
  7. A phasic change with respiration on Doppler of implies thrombosis. - F - normally there is a cyclic variation in flow velocity with respiration - should decrease in expiration and increase in inspiration. Absence of phasicity (ie. continuous venous signal) is suspicious for proximal obstruction. [Dahnert pg 634]
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28
Q
  1. Vascular US, T/F:
  2. In the femoral artery a doubling of the peak systolic velocity in a zone of stenosis (cf. the normal vessel proximal to the stenosis) indicates that the stenosis is about 50%.
  3. 55% reduction in cross sectional area is equivalent to 70% diameter stenosis
  4. Power Doppler gives information regarding the direction of flow but is less sensitve to low velocities than is colour Doppler.
  5. Doppler evaluation of renal artery stenosis may be performed by interrogation of the intrarenal (parenchymal) branches.
  6. Evaluation of the sapheno-femoral junction for venous incompetence is performed with the patient supine
A

true 1,4

  1. Vascular US, T/F: (GC/TW)
  2. In the femoral artery a doubling of the peak systolic velocity in a zone of stenosis (cf. the normal vessel proximal to the stenosis) indicates that the stenosis is about 50%. - T - A ratio of 2 (ie. a doubling of the PSV) represents a hemodynamically significant stenosis with a greather than 50% lumen narrowing (see below about measurements).
  3. 55% reduction in cross sectional area is equivalent to 70% diameter stenosis. - F - the new remaining radius % squared (ie 70% = 30% radius or 0.3) multipled by the initial CSA = new CSA. Therefore the reduction is (1-remaining radius squared). See below.
  4. Power Doppler gives information regarding the direction of flow but is less sensitve to low velocities than is colour Doppler. - F - power doppler is more sensitive at detecting flow, particularly slow flow, but is unable to demonstrate direction or velocity of flow.
  5. Doppler evaluation of renal artery stenosis may be performed by interrogation of the intrarenal (parenchymal) branches. - T - Two approaches are used to detect RAS with Doppler US: direct visualization of the renal arteries and analysis of intrarenal Doppler waveforms. The segmental renal arteries are evaluated by means of a translumbar approach; the different segments must be scanned systematically to detect a stenosis of a segmental or accessory RA. A dampened appearance (pulsus tardus) of an intrarenal Doppler waveform indicates stenosis. The presence of an early systolic peak can be interpreted as a sign of normality; however, its absence does not necessarily indicate stenosis. [Renovascular HTN, RG 2000]
  6. Evaluation of the sapheno-femoral junction for venous incompetence is performed with the patient supine. - F - examination of the CFV/SFV is performed in the supine postion with a linear 5-7.5MHz transducer in a slight reverse Trendelenburg position. [B&H pg 1051]
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29
Q
  1. Renal vein thrombosis, not a risk factor:
  2. Dehydration
  3. Membranous GN
  4. Amyloid
  5. Scleroderma
  6. Nephrotic syndrome
A
  1. Scleroderma - F - Scleroderma affects the renal arterioles and causes cortical necrosis.
  2. Renal vein thrombosis, not a risk factor: (TW)
  3. Dehydration - T - Renal vein thrombosis in infants most commonly due to dehydation/sepsis.
  4. Membranous GN - T - see ans 5.
  5. Amyloid - T
  6. Scleroderma - F - Scleroderma affects the renal arterioles and causes cortical necrosis.
  7. Nephrotic syndrome - T - In adults, most commonly due to nephrotic syndrome (which in turn is most commonly due to membranous glomerulonephritis
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30
Q
  1. Atrial myxoma, which is false:
  2. Low T2
  3. Assoc with Carney’s complex
  4. Arises left side of the interatrial septum
  5. Usually pedunculated
A

1.Low T2

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31
Q
  1. Which is true re cardiac MRI:
  2. Gradient sequences used for dark blood
  3. Contrast used for cine
  4. Short anterior oblique (SAO) view shows aortic valve en face
  5. Retrospective gating better than prospective for diastolic function
  6. 50% R-R gating for assessing systolic function (this recall a bit hazy)
A
  1. Retrospective gating better than prospective for diastolic function - T - although prospective gating is more common, given the trigger window is typically 10-15% of the R-R window, prospective gating sequences will exclude late diastole. Retrospective gaiting is more computationally intensive, but is also helpful in patients with arrhythmias. In retrospective gating there is no trigger window and the whole cardiac cycle is imaged.
  2. Which is true re cardiac MRI: (TW)
  3. Gradient sequences used for dark blood - F - T2* weighted coherent GE sequences used so that blood ro CSF appears bright. GE sequences are flow sensitive, as gradient reversl is not slice selective (as in spine echo). Therefore, a flowing nucleus produces signal after gradient rephasing, regardless of its slice location during excitation. T1WI has moving blood produce a signal void.
  4. Contrast used for cine - F - most cardiac cine acquisitions are generally acquired with gradient echo sequence with retrospective gating techniques. Since cine is performed with a gradient echo sequence, flowing blood appears bright.
  5. Short anterior oblique (SAO) view shows aortic valve en face - F - horizontal long-axis plane / 4-chamber view. LVOT view used to look at aortic valve in perpendicular plane.
  6. Retrospective gating better than prospective for diastolic function - T - although prospective gating is more common, given the trigger window is typically 10-15% of the R-R window, prospective gating sequences will exclude late diastole. Retrospective gaiting is more computationally intensive, but is also helpful in patients with arrhythmias. In retrospective gating there is no trigger window and the whole cardiac cycle is imaged.
  7. 50% R-R gating for assessing systolic function (this recall a bit hazy) - F - peak fo the R wave is used to trigger each pulse sequence because, electrically, it has the greatest amplitude (prospective gating). Retrospective gating (performed during many cardiac cine acquisitions) acquires image data and times to the cardiac cycle during reconstruction (after the scan acquisition). The trigger window is typically 10-15% of the R-R window. The acquisiton window is the duration of the data aquisition (wiht standard trigger window and no trigger delay, this would be 85-90% of the R-R window). Because of the trigger window, prospectively gating sequences will exclude late diastole.
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32
Q

18.Peripheral haemangiomas in infants, which is false:

  1. More common in premature infants
  2. Embolism is the most common treatment
  3. Increased size after 12 months is atypical
  4. More common in the head and neck
  5. Sequester platelets
A
  1. Embolism is the most common treatment – F – usually require no treatment. Treatment depends on type and sequelae. Embolisation often used pre-resection
  2. Peripheral haemangiomas in infants, which is false: (TW)
  3. More common in premature infants – T – hemangiomas are the most common tumor of childhood occurring in 12% of infants. UTD: the incidence of hemangiomas is increased in preterm infants; the most signficiant risk factor appears to be low birth weight.
  4. Embolism is the most common treatment – F – usually require no treatment. Treatment depends on type and sequelae. Embolisation often used pre-resection
  5. Increased size after 12 months is atypical - T – characteristically 2-stage process of growth and regression. At birth lesionas are often small and inconspicuous. Shortly after birth, perior of rapi proliferation that lasts several months, and typically, involution begins at approximately 10 months of age. 50% lesions completely resolved by 5yo. UTD: the spontaneous involution phase typically begins in the latter part of the 1st year
  6. More common in the head and neck – T – have a predilection for head and neck, although they can occur anywhere in the skin, mucous membranes, or internal organs
  7. Sequester platelets – T – Kasabach-Merritt syndrome = hemorrhagic diathesis due to platelet sequestration by tumor / disseminated intravascular coagulation; characterised by an associateion of hemangioma or hemangioendothelioma, or angiosarcoma with thrombocytopenia and purpura (secondary to increased systemic fibrinolysis). There is an increased incidence of hemangiomas in females and in premature infants weighing less than 1500 grams Over half of all hemangiomas occur in the cervicofacial region
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33
Q
  1. Renovascular hypertension, which is false:
  2. Systolic – diastolic / systolic equals resistive index
  3. Aortorenal ratio of 2.5 means greater than a 70% stenosis
  4. Hyperpulsatility means a more distant stenosis
  5. 0.12 sec acceleration time intrarenal arteries indicates proximal stenosis
A

2.Aortorenal ratio of 2.5 means greater than a 70% stenosis - F - >3.5 for >60% (Dahnert 6) increased renal arterial resistive index (RI): a cut-off value of 0.7 may be a good approximation in clinical practice (RI difference between kidneys > 0.05 - 0.07 )

increased peak systolic velocity (PSV): some advocate 180cm/s 4increased renal-interlobar ratio (RIR): some advocate values greater than 5 3increased renal/aortic ratio (RAR) i.e. PSVrenal/PSVaorta: usually taken as >3.5, although some advocate >3 4turbulent flow in a post-stenotic areapulsus parvus et tardus waveform (slow-rising) due to stenosisintraparenchymal resitive indices > 0.8intraparenchymal acceleration time > 0.07 s

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34
Q
  1. Regarding TIPS, which is true:
  2. Ascites is a contraindication
  3. Increased velocity by 50cm/sec compared with baseline on a follow up study indicates possible stenosis
  4. Demonstration of flow reversal (ie retrograde flow) in the intrahepatic portal veins indicates stenosis
  5. Need to have the same pressures as SVC for best results
  6. Left common femoral approach is best
A

2.Increased velocity by 50cm/sec compared with baseline on a follow up study indicates possible stenosis - T – a change of >50cm/s (increase or decrease) relative to the baseline study can indicate stenosis. in addition to looking for a narrowing, elevated maximum and depressed minimum stent velocities are signs of stent stenosis (one system uses 90cm/sec and 190cm/sec as the lower and upper limits, of normal stent velocities). Additional signs of dysfunction are low PV velocity, a temporal increase or decrease in max and min stent velocities on sequential examinations, and reversal of flow in the draining hepatic vein (US requisites).

  1. Regarding TIPS, which is true: (TW)
  2. Ascites is a contraindication - F - if it was, there probably wouldn’t be many TIPS procedures done. See below for contraindications.
  3. Increased velocity by 50cm/sec compared with baseline on a follow up study indicates possible stenosis - T – a change of >50cm/s (increase or decrease) relative to the baseline study can indicate stenosis. in addition to looking for a narrowing, elevated maximum and depressed minimum stent velocities are signs of stent stenosis (one system uses 90cm/sec and 190cm/sec as the lower and upper limits, of normal stent velocities). Additional signs of dysfunction are low PV velocity, a temporal increase or decrease in max and min stent velocities on sequential examinations, and reversal of flow in the draining hepatic vein (US requisites).
  4. Demonstration of flow reversal (ie retrograde flow) in the intrahepatic portal veins indicates stenosis - F - this could potentially be true if saying ‘reversal of flow from the ‘normal’ post TIPS flow’ which itself is reversed. When first placing the TIPS, the stent decompresses the portal system directly into the low pressure hepatic venous system, portal flow in the right and left portal vein usually reverses after stent placement and is directed into the stent instead of into the liver
  5. Need to have the same pressures as SVC for best results
  6. Left common femoral approach is best - F - transjugular. Wire through heart into MHV. Then ream through the liver to where you expect the PV to be, and if you miss - try again. Some use a transcutaneous needle into PV and leave a little marker or wire to provide a target for the ‘reaming’, some use US.
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35
Q
  1. Budd Chiari syndrome, which is true:
  2. Spider like appearance of portal veins on portal venography is diagnostic
  3. 70% are idiopathic
  4. TIPS is not an option for treatment
  5. Central increased uptake is seen on sulphur colloid scans
A
  1. Central increased uptake is seen on sulphur colloid scans - T – (Sulphur-colloid was used previously, but has generally been replaced by other imaging modalities). Hypertrophy of the caudate lobe associated with BCS is demonstrated by its preferential uptake of the radionuclide. However, more than half of patients with BCS do not demonstrate this pattern (UTD). Sulfur colloid liver scan may show a central area of increased activity believed to be secondary to enlargement of the caudate lobe (AJR). See below.
  2. Budd Chiari syndrome, which is true: (TW)
  3. Spider like appearance of portal veins on portal venography is diagnostic - F – “Spider web” pattern of hepatic venous collaterals.
  4. 70% are idiopathic – Previously T, but now is F - in approx 75% of pts, a hematological abnormality or a cause of thrombotic diathesis can be identified that predisposes the patient to the occurrence of BCS (Radiographics 2009). Underlying disorcer can be identified in over 80% of patients with BCS (UTD). (Dahnert says 66% idiopathic)
  5. TIPS is not an option for treatment - F - TIPS is a good alternative method for relieving liver congestion, with lower mortality and morbidity than those assoc with open surgical procedures. Other options: medical, thrombolysis, angioplasty + stent of stenoses.
  6. Central increased uptake is seen on sulphur colloid scans - T – (Sulphur-colloid was used previously, but has generally been replaced by other imaging modalities). Hypertrophy of the caudate lobe associated with BCS is demonstrated by its preferential uptake of the radionuclide. However, more than half of patients with BCS do not demonstrate this pattern (UTD). Sulfur colloid liver scan may show a central area of increased activity believed to be secondary to enlargement of the caudate lobe (AJR). See below.

BCS is a heterogeneous group of disorders characterised by hepatic venous outflow obstruction at the level of the hepatic veins, IVC or right atrium. BCS is not a primary condition of the liver parenchyma; it is the result of partial or complete obstruction of hepatic venous outflow.

The “classic” scintigraphic pattern is caudate lobe hypertrophy, at expense of the rest of the liver, in which uptake may be normal, reduced, absent or patchy. Often colloid shift to spleen and bone marrowis seen. Caudate has own venous efferent connections directly with the IVC, so even so maintains good function cf rest of the liver - and maintains good tracer uptake and significant compensatory hypertrophy.This question could be answered as 2. correct (if using old numbers) and 4. incorrect using the argument that there is ‘normal’ (not increased) uptake centrally with relative decreased uptake around it.

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36
Q
  1. Regarding fibromuscular dysplasia of the renal artery:
  2. Most common at osteum
  3. Recurs post dilation
  4. Osteal stenosis
  5. Bilateral in 50%
  6. Intimal fibroplasia is the most common type and causes the classic stenoses alternating with aneurysms
A

4.Bilateral in 50% - T

  1. Regarding fibromuscular dysplasia of the renal artery: (JS)
  2. Most common at osteum - F - most commonly occurs in the middle and distal renal artery, causing “string of beads” appearance.
  3. Recurs post dilation - F - FMD classically responds well to angioplasty with success rates approaching 98% (B&H). Dahnert mentions 90% success rate with very low restenosis rates. Restenosis 12-25% over 6months to 2y, but restenosis is not necessarily associated with HTN.
  4. Osteal stenosis - F - more common with atherosclerotic disease
  5. Bilateral in 50% - T
  6. Intimal fibroplasia is the most common type and causes the classic stenoses alternating with aneurysms - F - This is Type 2
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37
Q
  1. AAA stent graft, which is true:
  2. Kinking = moved
  3. Not possible if AAA >8cms in length
  4. Endoleak lumbar artery needs fixing
  5. Endoleak needs immediate fixing
  6. Best grade stent with angio catheter and angiogram
A
  1. Kinking = moved - T most correct – diminished diameter of the aneurysm after stent – graft implantation also decreases length of aneurysm – associated with distal migration of graft.
  2. AAA stent graft, which is true: (TW)
  3. Kinking = moved - T most correct – diminished diameter of the aneurysm after stent – graft implantation also decreases length of aneurysm – associated with distal migration of graft.
  4. Not possible if AAA >8cms in length - F - for example the Zenith AAA grafts range from 82mm to 149mm in length.
  5. Endoleak lumbar artery needs fixing -?T (controversial) - = most common endoleak (type II). Significance and management of type II endoleaks is controversial. Some argue that as spontaneous resolution occurs 30-100% of cases, a “wait and see” approach is preferable. UTD recommendations are occluding type II endoleaks that have not spontaneously thrombosed in one month (as systemic pressures have been noted in aneuyrsm sac in the presence of type II endoleaks).
  6. Endoleak needs immediate fixing - - type I endoleak (ie incompetent seal at either proximal or distal attachment site) must be repaired as soon as possible. Type III endoleaks represtn flow into sac from separation between components of a modular system, or tears in the endograft - these are repaired with an additional endograft. Type IV leaks are due to egress of blood through the pores of the fabric - these heal spontaneously.
  7. Best grade stent with angio catheter and angiogram
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38
Q
  1. Carotid Doppler:
  2. 280cm/sec is >70% stenosis
  3. Maximal velocity is proximal to stenosis
A
  1. Carotid Doppler: (TW)
  2. 280cm/sec is >70% stenosis - T - >230cm/s equals >70% stenosis, ICA/CCA ratio >4.0. 125-230cm/s equals 50-69% stenosis, ICA/CCA ratio 2.0-4.0. <125cm/s equals <50% stenosis, ICA/CCA ratio <2.0. (US requisites)
  3. Maximal velocity is proximal to stenosis - F - maximal velocity is at stenosis. Calculating a ratio of PSV at stenosis vs PSV proximal to stenosis is also used as a calculation of % stenosis, where as ratio of 2 (ie., double PSV) equals >50% stenosis.
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39
Q
  1. Small renal artery aneurysm, which is not true:
  2. Diabetes
  3. Polyarteritis Nodosa
  4. IVDU
  5. SLE
  6. RCC
A
  1. Diabetes - F - causes diabetic nephropathy (diffuse glomerulosclerosis); other GU manifestations include renal a. stenosis, papillary necrosis, renal/perirenal abscess, emphysematous pyelonephritis/cystitis, XGP, fungal infection.
  2. Small renal artery aneurysm, which is not true: (GC) CME 03.40
  3. Diabetes - F - causes diabetic nephropathy (diffuse glomerulosclerosis); other GU manifestations include renal a. stenosis, papillary necrosis, renal/perirenal abscess, emphysematous pyelonephritis/cystitis, XGP, fungal infection.
  4. Polyarteritis nodosa - T - microaneurysms in 50%, esp. at branch points.
  5. IVDU - T - drug-abuse vasculitis may be due to immunologic injury from circulating hepatitis Ag-Ab complexes, bacterial endocarditis, direct toxicity, impurity-related. Methamphetamine, heroin, LSD. Mulitple small aneurysms in interlobar branches near corticomedullary jxn.
  6. SLE - T - aneurysms in interlobar and arcuate aa. (similar to but less frequent than PAN). Kidneys involved in 100% of cases (focal membranoproliferative GN).
  7. RCC - T - in 14% (also adult Wilm’s). Other neoplasms that may cause RAAs include AML (in 50%), metastatic arterial myxoma.
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40
Q
  1. Which is false re transjugular intrahepatic portosystemic shunt (TIPS)
  2. It is a recognized treatment of choice for refractory ascites
  3. Contraindicated in the presence of right heart failure
  4. May cause biliary dilatation acutely
  5. IJV thrombosis precludes performance of TIPS
A
  1. IJV thrombosis precludes performance of TIPS - F - RIJV usually used, LIJV can be used if right side can’t be used. Femoral venous approach techniques have also been described, but are used less commonly, and are technically more demanding (eMed).
  2. Which is false re transjugular intrahepatic portosystemic shunt (TIPS) (TW)
  3. It is a recognized treatment of choice for refractory ascites - T
  4. Contraindicated in the presence of right heart failure - T - right-sided heart failure with increased central venous pressure (eMed). Pulmonary HTN and hepatopulmonary syndrome is a contraindication.
  5. May cause biliary dilatation acutely - T - potential complication of fistula to biliary tree. Studies have also shown biliary epithelial proliferation with creation of large cystlike spaces (but this is not acute).
  6. IJV thrombosis precludes performance of TIPS - F - RIJV usually used, LIJV can be used if right side can’t be used. Femoral venous approach techniques have also been described, but are used less commonly, and are technically more demanding (eMed).
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41
Q
  1. SLE which is false?
  2. less likely to cause lower lobe fibrosis than Rheumatoid arthritis
  3. Liebman-Sachs nodules do not cause valve destruction
  4. pancreatitis secondary to vasculitis
  5. 30% of antiphospholipid syndrome has SLE
A
  1. Libman Sachs nodules do not cause valve destruction - F - Libman-sacks (verrucous) endocarditis. The verrucae, most common on the aortic and mitral valves. Accumulations of immune complexes, mononuclear cells, hematoxylin bodies, and fibrin and platelet thrombi. Typically asymptomatic, however they can fragment and produce systemic emboli (UTD). Spectrum of valvular disease in SLE ranges from valve leaflet thickening to Libman-Sacks endocarditis. The latter is characterised by formation of small single or multiple, sterile, granular pink vegetations ranging from 1-4mm that may be associated with intense valvulitis and lead to valve destruction (Radiographics 2004). Intense valvulitis and fibrinoid necrosis of the valve substance (Robbins).
  2. SLE which is false? (TW)
  3. Less likely to cause lower lobe fibrosis than RA - T - pulmonary fibrosis is less common relative to other collagen vascular diseases.
  4. Libman Sachs nodules do not cause valve destruction - F - Libman-sacks (verrucous) endocarditis. The verrucae, most common on the aortic and mitral valves. Accumulations of immune complexes, mononuclear cells, hematoxylin bodies, and fibrin and platelet thrombi. Typically asymptomatic, however they can fragment and produce systemic emboli (UTD). Spectrum of valvular disease in SLE ranges from valve leaflet thickening to Libman-Sacks endocarditis. The latter is characterised by formation of small single or multiple, sterile, granular pink vegetations ranging from 1-4mm that may be associated with intense valvulitis and lead to valve destruction (Radiographics 2004). Intense valvulitis and fibrinoid necrosis of the valve substance (Robbins).
  5. Pancreatitis secondary to vasculitis - T - GIT is often involved with SLE, but more commonly from medication side effects than from active SLE. SLE vasculitis can lead to pancreatitis, peritonitis, and colitis (UTD).
  6. 30% of antiphospholipid syndrome has SLE - T - APS is defined by 2 major components: presence in plasma of at least one type of autoantibody known as antiphospholipid antibody (aPL); occurrence of at least one clinical feature from a diverse list of potential disease manifestations. 34% of patients with aPL have SLE. About 50% of individuals with lupus anticoagulants meed the Am College of Rheum criteria for classification of SLE. Previously had 3. as False, rest True.
42
Q
  1. With respect to ventilation / perfusion scintigraphic lung scans:
  2. Using the PIOPED criteria for classification of results, a high probability scan is defined as showing one or more unmatched segmental perfusion defects
  3. Classification of a lung scan as low probability excludes the diagnosis of pulmonary embolism
  4. Complete unilateral loss of perfusion is more commonly seen in extrinsic compression by bronchogenic carcinoma than in massive pulmonary embolism
  5. Pregnancy is an absolute contraindication for performing a scintigraphic V/Q scan
  6. something else which is false
A

3.Complete unilateral loss of perfusion is more commonly seen in extrinsic compression by bronchogenic carcinoma than in massive pulmonary embolism - T - Acutally not sure about this one - but was True in the CME 03.37. Dahnert says 2% incidence of unilateral lung perfusion of which PE 23%, Bronchogenic carcinoma 23%. A paper from1987 (Radiographics, Cho et al) said PE is one of the least common causes, which was in agreement with another series.

  1. With respect to ventilation / perfusion scintigraphic lung scans: (TW)
  2. Using the PIOPED criteria for classification of results, a high probability scan is defined as showing one or more unmatched segmental perfusion defects - F - 2 or more large (segmental) perfusion defects without match
  3. Classification of a lung scan as low probability excludes the diagnosis of pulmonary embolism - F - Low probability of PE accounted for 34% cases, and 16% of these were positive for PE on angiogram. Even normal VQ (14% cases) had angiogram positive findings in 9%.
  4. Complete unilateral loss of perfusion is more commonly seen in extrinsic compression by bronchogenic carcinoma than in massive pulmonary embolism - T - Acutally not sure about this one - but was True in the CME 03.37. Dahnert says 2% incidence of unilateral lung perfusion of which PE 23%, Bronchogenic carcinoma 23%. A paper from1987 (Radiographics, Cho et al) said PE is one of the least common causes, which was in agreement with another series.
  5. Pregnancy is an absolute contraindication for performing a scintigraphic V/Q scan - F - pregnancy has 5x increase risk of VTE, and PE is leading preventable cause of maternal death. Mixed recommendations - it is VQ is favored by PIOPED II investigators as a means of imaging in pregnancy, has lower breast dose and lower nondiagnostic rate in pregnant population. Can reduce dose by eliminating the ventilation portion of examination in patients with normal perfusion (plus whack an IDC in to stop the bladder-fetus exposure). Of note - ther test: D-dimer can have false-positive results as pregnancy progresses, however NPV remains accurate regardless of trimester (but PE has still been found in normal D-dimers).
  6. something else which is false
43
Q
  1. Regarding aortic dissection, which is true?
  2. non-contrast CT is needed to evaluate
  3. type B starts proximal to left subclavian artery
  4. tear in ascending aorta mostly posterolateral
  5. intramural thrombus not a precusor to aortic dissection
A
  1. non-contrast CT is needed to evaluate T - Unenhanced CT can be helpful to diagnose acute haemorrhage and intramural haematoma and displacement of intimal calcifications - Not sure about “needed to evaluate” but it is helpful….
  2. Regarding aortic dissection, which is true? (JS)
  3. non-contrast CT is needed to evaluate T - Unenhanced CT can be helpful to diagnose acute haemorrhage and intramural haematoma and displacement of intimal calcifications - Not sure about “needed to evaluate” but it is helpful….
  4. type B starts proximal to left subclavian artery - F - Stanford type B involves the descending aorta only (ie beyond the brachiocephalic vessels)
  5. tear in ascending aorta mostly posterolateral - F – anterior and right lateral wall of ascending aorta, just distal to aortic valve in 65%
  6. intramural thrombus not a precusor to aortic dissection - F - this represents a localised haematoma within the aortic wall which may represent a controlled dissection and can progress to dissection (especially type A)
44
Q

39.With regards to imaging of the extracranial carotid arteries which of the following statements is TRUE:

  1. Echogenic plaque on US is more likely to be associated with cerebral transient ischaemic events than hypoechoic plaque
  2. Conventional angiography is a reliable predictor of plaque ulceration
  3. Peak systolic velocity in the internal carotid artery of >270 cm/sec suggests a stenosis of >70%
  4. The intimal flap is visible on US imaging in approximately 80% of cases presenting with internal carotid artery dissection
  5. Diastolic flow is lower in the internal carotid artery than the external carotid artery
A
  1. Peak systolic velocity in the internal carotid artery of >270 cm/sec suggests a stenosis of >70% - T - >230cm/s equals >70% stenosis, ICA/CCA ratio >4.0. 125-230cm/s equals 50-69% stenosis, ICA/CCA ratio 2.0-4.0. <125cm/s equals <50% stenosis, ICA/CCA ratio <2.0. (US requisites)
  2. With regards to imaging of the extracranial carotid arteries which of the following statements is TRUE: (TW)
  3. Echogenic plaque on US is more likely to be associated with cerebral transient ischaemic events than hypoechoic plaque - F - heterogeneous plaques, especially those with focal hypoechoic regions, tend to be unstabel. Homogeneous plaques tend to be stable.
  4. Conventional angiography is a reliable predictor of plaque ulceration - F
  5. Peak systolic velocity in the internal carotid artery of >270 cm/sec suggests a stenosis of >70% - T - >230cm/s equals >70% stenosis, ICA/CCA ratio >4.0. 125-230cm/s equals 50-69% stenosis, ICA/CCA ratio 2.0-4.0. <125cm/s equals <50% stenosis, ICA/CCA ratio <2.0. (US requisites)
  6. The intimal flap is visible on US imaging in approximately 80% of cases presenting with internal carotid artery dissection - F - detection of the intimal flap has not been reliable with US and the intimal tear may be too high in the ICA to be assessed with carotid US.
  7. Diastolic flow is lower in the internal carotid artery than the external carotid artery, - F - Like other parenchymal organs, the brain has a low resistance to arterial flow; therefore, waveforms from the ICA have broad systolic peaks and well-maintained dyastolic flow throughout the cardiac cycle. The ECA supplies the scalp, muscles, and face, all of which have a high resistance to arterial inflow. This results in a high-resistance arterial waveform with narrower systolic peaks and decreased or absent diastolic flow. CME 01.30 (30)
45
Q
  1. Regarding lower limb deep venous thrombosis, which is false:
  2. Failure of superficial femoral vein Doppler signal to augment on calf compression indicates thrombus distal to the point of interrogation
  3. Diameter of the thrombosed vein is not typically increased in chronic thrombosis.
  4. DVT in the leg most often begins in the sinuses of the soleal veins of the calf.
  5. Approximately 40% of calf vein thrombi propagate superiorly to involve at least the popliteal or femoral veins.
A
  1. Approx 40% of calf vein thrombi propagate superiorly to involve at least the popliteal or femoral veins. - F - up to 20% propagate. Serial evaluation every 3-5 days is therefore important in patients who remain symptomatic with conservative therapy to dx clot propagation and prevent PE. [B&H pg 1052]
  2. Regarding lower limb deep venous thrombosis, which is false: (GC) CME 03.42 and CME 00.08
  3. Failure of superficial femoral vein Doppler signal to augment on calf compression indicates thrombus distal to the point of interrogation. - T - augment by squeezing calf or plantarflexing foot; indicates venous occlusion/compression in intervening venous segments.
  4. Diameter of the thrombosed vein is not typically increased in chronic thrombosis. - T - chronic clot does not expand the lumen of the vein and appears more echogenic than an acute clot. The walls appear thickened, irregular and echogenic and the vein is incompletely compressible. Collaterals can be seen on colour doppler. (B&H)
  5. DVT in the leg most often begins in the sinuses of the soleal veins of the calf. - T
  6. Approx 40% of calf vein thrombi propagate superiorly to involve at least the popliteal or femoral veins. - F - up to 20% propagate. Serial evaluation every 3-5 days is therefore important in patients who remain symptomatic with conservative therapy to dx clot propagation and prevent PE. [B&H pg 1052] Changed option b from “is typically” so only 1 false; changed option c from “Isolated calf thrombosis occurs least often in the peroneal veins” to CME stem.
46
Q
  1. VSD which is true?
  2. Membranous > muscular
  3. Muscular > membranous
A

43.VSD (TW) 1.membranes > muscular - T - multiple factos are involved in closure of the region encompassing the membranous septum, thus this is the most common site of VSDs (75% are membranous (component 3 with extension into component 2 - see below)). Membranous VSDs like just beneath the AV and behind septal leaflet of the TV. 10-15% of VSDs are muscular defects (located along the RV free wall-septal junction, central, or in the apical septum). 3 main components of the interventricular septua are 1) the septum of the AV canal, 2) muscular septum, 3) pareital band or distal conal septum. VSDs may occur at various locations in any of these components. Embyrologically, closure of the IV septum depends on 3 factors: projections into the AV canal from the right-sided endocardial cushions (component 1); continued growth of connective tissue on the crest of the muscular septum (component 2); and downward growth of ridges dividing the conus (component 3).

47
Q
  1. Bowel Ischaemia: t/f
  2. Can be related to superior mesenteric vein thrombosis
  3. Is associated with paroxysmal nocturnal haemoglobinuria
  4. Vasospasm indicates underlying atherosclerosis and stenosis
  5. Occlusion is typically 10cm distal to the SMA origin
  6. Plain film changes are only seen after bowel infarction
A

t 1, 2 4

  1. Bowel Ischaemia: (TW)
  2. Can be related to superior mesenteric vein thrombosis - T - venous occlusion <10%. SMV > IMV > PV.
  3. Is associated with paroxysmal nocturnal haemoglobinuria - T - PNH is a disorder characterised by a defect in the GPI anchor due to an abnormality in th PIG-A gene. Result in abnormalities in hemopoietic function, including hemolytic anemia, a hypercoagulabel state, and diminished hematopoiesis.
  4. Vasospasm indicates underlying atherosclerosis and stenosis - F
  5. Occlusion is typically 10cm distal to the SMA origin - F - SMA thrombosis (20-40%) at origin + site of atherosclerotic narrowing. Embolus (40-50%) just distal to middle colic artery.
  6. Plain film changes are only seen after bowel infarction - F - ischaemia, oedematous bowel, thumb printing. Could also have bowel obstruction as cause of ischaemia (pre-infarction).
48
Q
  1. Aortic Stent Grafts: t/f
  2. Sac size greater than 8 cm is a contraindication
  3. The neck of the aneurysm is defined as the distance from the inferior most renal artery to the start of the aneurysm
  4. Immediate endoleak always needs further intervention
  5. Retro leak from lumbar arteries needs further intervention
  6. Luminal diameter is best measured via angiography with a graded catheter
A

t 2

  1. Aortic Stent Grafts: (TW)
  2. Sac size greater than 8cm is a contraindication - F - for example the Zenith AAA grafts range from 82mm to 149mm in length.
  3. The neck of the aneurysm is defined as the distance from the inferior most renal artery to the start of the aneurysm - T - the proximal neck is defined as the segment of aorta between the origin of the lowest renal artery and superior aspect of the aneurysm. Most endographs require a length of greater than 15mm to ensure adequate proximal seal.
  4. Immediate endoleak always needs further intervention - F - depends on type. type I endoleak (ie incompetent seal at either proximal or distal attachment site) must be repaired as soon as possible. Type III endoleaks represtn flow into sac from separation between components of a modular system, or tears in the endograft - these are repaired with an additional endograft. Type IV leaks are due to egress of blood through the pores of the fabric - these heal spontaneously. Type II enodleak (most common) - management is controversial. Some argue that as spontaneous resolution occurs 30-100% of cases, a “wait and see” approach is preferable. UTD recommendations are occluding type II endoleaks that have not spontaneously thrombosed in one month (as systemic pressures have been noted in aneuyrsm sac in the presence of type II endoleaks
  5. Retro leak from lumbar arteries needs further intervention - ?T/F - controversial, see ans c.
  6. Luminal diameter is best measured via angiography with a graded catheter - ?F
49
Q
  1. Regarding Cervico Cephalic Vessel Dissection: t/f
  2. Causes 5% to 20% of CVAs in young to middle aged patients
  3. Has a rim of T1 hyperintensity surrounding a void in the vessels
  4. Imaging identifies vasculopathy in the majority
  5. The location of vertebral artery dissections is most often proximal (between C2 and C6)
  6. The location of an ICA dissection is most often just immediately distal to the bulb
A

t 1, 2, 5

not sure about 3

  1. Regarding Cervico Cephalic Vessel Dissection: (GC)
  2. Causes 5% to 20% of CVAs in young to middle aged patients - T - 5-20% in those aged 40-60yrs [Dahnert]; up to 1/4 of strokes,with a peak prevalence in the 5th decade [RG].
  3. Has a rim of T1 hyperintensity surrounding a void in the vessels - T - subacute hematoma (7days-2mths) on T1 + fat sat appears as a bright crescent-shaped area around an eccentric flow void. Note that in the early and chronic stage, the haematoma is usually isointense to surrounding structures on T1.
  4. Imaging identifies vasculopathy in the majority
  5. The location of vertebral artery dissections is most often proximal (between C2 and C6) - F - at the level of C1/2 in 65% [Dahenrt]. ie. predominantly located in the pars transversaria (V2, 35%) or the atlas loop (V3, 34%) [RG]. Bilateral vertebal artery dissections in 5%.
  6. The location of an ICA dissection is most often just immediately distal to the bulb - T - extracranial ICA dissection affects the cervical part of the artery distal to the carotid bulb and tends not to extend beyond its entry into the petrous portion. [Craniocervical a. dissection, RG 2008]
50
Q
  1. Fixed inferior defects in a thallium scan are caused by:
  2. Diaphragmatic attenuation
  3. Mastectomy
  4. Right coronary artery infarct
  5. Pacemaker leads
  6. Left bundle branch block
A

1, 3, 4, probably 5

  1. Fixed inferior defects in a thallium scan are caused by: (GC)
  2. Diaphragmatic attenuation - T - variation in tracer intensity by 15-20% btn regions on planar images may be normal (due to soft tissue attentuation artifacts from subdiaphragmatic abdominal contents or breast tissue).
  3. Mastectomy - F - implants could cause attentuation artifact.
  4. Right coronary artery infarct - T - RCA territory is 5-8 o’clock on the short axis (oblique coronal).
  5. Pacemaker leads - T - attentuation artifact.
  6. Left bundle branch block - ?T
51
Q
  1. Pulmonary Emboli: t/f
  2. Septic emboli most commonly arise from the pelvic veins
  3. The defect on chest x-rays is often larger than the V/Q defect
  4. Matched defects on V/Q scans exclude PE
  5. PE is associated with pulmonary infarction in 30%
  6. The presence of a pleural effusion indicates pulmonary infarction
A

everything is false

  1. Pulmonary Emboli: (GC/TW)
  2. Septic emboli most commonly arise from the pelvic veins - F - most common cause of septic emboli in IVDU is tricuspid valve endocarditis. Other causes include septic thrombophlebitis, pelvic thrombophlebitis, infected lines, AV fistula, skin infection… Can’t find anything more specific than this.
  3. The defect on chest x-rays is often larger than the V/Q defect - F - An upright PA and lateral CXR should ideally be obtained as close as possible to the V/Q scan. Perfusion defects substantially larger than the corresponding CXR abnormalities are suggestive of PE, whereas perfusion defects substantially smaller than corresponding CXR abnormalities are not commonly associated with PE (Thoracic Imaging).
  4. Matched defects on V/Q scans exclude PE - F - a PE presents as a segmentally hypoperfused but normally ventilated lung (V/Q mismatch). A normal perfusion scan excludes a PE for practical purposes. A perfusion defect requires further evaluation with ventilation scan and CXR - if both (V and CXR) are normal, suspect PE. Matched V and Q defects + normal CXR = low prob. Matched V and Q and CXR defect = indeterminate.
  5. PE is associated with pulmonary infarction in 30% - F – false if using Path notes. If use Dahnert numbers (10-60%) then true. More likely to develop if cardiopulmonary disease with obstruction of pulmonary venous outflow.
  6. The presence of a pleural effusion indicates pulmonary infarction - F - pleural effusions are non specific - present in 48% of those with PE vs. 31% of those with no PE. Pulmonary infarction = any opacity developing as a result of thromboembolic disease. [Dahnert p524]
52
Q
  1. With regard to cerebral aneurysms: t/f
  2. In children are associated with trauma and infection
  3. Multiple aneurysms are strongly associated with male gender
  4. A truly azygos anterior cerebral artery is associated with lobar holoprosencephaly and saccular aneurysms
  5. Are multiple in 15% to 20%
  6. Occur in the posterior circulation in 40%
A

t 1, 3, 4
50.With regard to cerebral aneurysms: (TW)

  1. In children are associated with trauma and infection - T - Aneuyrsms in children may be congenital or idiopathic (77%), inflammatory or mycotic (11%), or traumatic (11%).
  2. Multiple aneurysms are strongly associated with male gender - F - Female > Male (Neuroradiology 2004). Female preponderance has been reported in up to 70% of multiple aneurysms and a 2.4:1 ratio of females > males was reported in the Cooperative Study of Intracranial Aneurysms and SAH.
  3. A truly azygos anterior cerebral artery is associated with lobar holoprosencephaly and saccular aneurysms - T - azygos ACA is a rare variation of the COW in which the A2 segments of both ACAs are represented by a singl common vessel from which arise all the major vessels supplying most of both anterior cerebral hemispheres, as well as the corpus callosum (ie a true azygos). Associated with holoprosencephaly. High indicence of berry aneurysms. Abnormal medial and intimal elements in the vessel wall of this developmental variant may account for the increased prevalence of associated saccular aneurysms.
  4. Are multiple in 15% to 20% - T
  5. Occur in the posterior circulation in 40% - F - 90-95% of aneurysms arise from COW - 90% from anterior circulation, 10% from posterior circulation. ACom 30-35%, PCom 30-35%, MCA 20-30%, Basilar apex 5-10%, other posterior 1-3%. Variations of the distal ACA: trus azygos artery, from which all major branches are given off to both cerebral hemispheres; a bihemispheric ACA, where both right and left ACAs are present, but one is rudimentary and most of the major branches to both hemispheres arise from the other ACA; a triple ACA, with the accessory ACA arising from the anterior communcating artery.
53
Q
  1. Cerebral angiography:
  2. The supraclinoid internal carotid artery is best seen in a caudal (Waters) projection
  3. The origin of the opthalmic artery is intradural in the majority of people
  4. Internal carotid injections are of 8mls at 2mls per second
  5. Cavernous haemangiomata are angiographically occult
  6. The enhancement of meningiomas persist late into the venous phase
A

true 2,3,4,5

  1. Cerebral angiography: (TW)
  2. The supraclinoid internal carotid artery is best seen in a caudal (Waters) projection - ?F - ICA/ophthalmic: transorbital oblique (15-30 degree rotation, and 7 degrees cephalad); Caldwell’s oblique (15-30 degrees rotation, and 7 degrees caudad). Waters is ~30 degrees caudad?
  3. The origin of the opthalmic artery is intradural in the majority of people - T - The origin of the ophthalmic artery is intradural in approx 90% of anatomic dissections (Diagnostic cerebral angiography, AG Osborn).
  4. Internal carotid injections are of 8mls at 2mls per second - T - CCA 4-5ml/s for 2s (ie total 8-10mls)
  5. Cavernous haemangiomata are angiographically occult - T - cavernous malformation: DSA is usually normal “angiographically occult vascular malformation”
  6. The enhancement of meningiomas persist late into the venous phase - T - mother-in-law - “comes early, stay late” - could always remember this as the pre-mature ejaculator who wants to cuddle afterwards.
54
Q
  1. Dural venous sinus thrombosis is not associated with:
  2. Pregnancy
  3. Meningioma
  4. Gastroenteritis
  5. Trauma
  6. Nephritic syndrome
A

5.Nephritic syndrome - F - haematuria, oliguria + azotemia, hypertension +/- some proteinuria. Nephrotic syndrome (proteinuria >3.5g/day) is one of the rarer causes of hypercoagulable state that can cause DST.

  1. Dural venous sinus thrombosis is associated with: (GC)
  2. Pregnancy - T - hypercoagulable state.
  3. Meningioma - T - tumour compressing sinus.
  4. Gastroenteritis - T - dehydration (low-slow states).
  5. Trauma - T - hfracture through sinus wall, cranial surgery, IJV catheterisation.
  6. Nephritic syndrome - F - haematuria, oliguria + azotemia, hypertension +/- some proteinuria. Nephrotic syndrome (proteinuria >3.5g/day) is one of the rarer causes of hypercoagulable state that can cause DST. Causes: Idiopathic Septic (esp. kids) - sinusitis, otitis, mastoiditis, meningitis, septicaemia etc. Aseptic causes - tumour (compression), trauma, low-flow states, hypercoagulability, chemotherapy. Unusual causes - Behcet’s disease, AIDS, UC, SLE, nephrotic syndrome, sarcoidosis. [Dahnert] Added options d and e.
55
Q

52.Regarding Dural spinal AVM: 1.Is usually associated with increased cord signal

A

yes

56
Q
  1. Regarding DVT, which is false:
  2. Lack of augmentation indicates thrombus distal to the point of interrogation
  3. There is a phasic change with respiration on Doppler of the normal femoral vein.
  4. Usually begin in the sinuses of the soleal veins.
  5. Acute thrombus is highly hyperechoic in the majority of cases.
  6. Thrombus in a duplicated femoral vein is a recognised cause of a false negative study.
A
  1. Acute thrombus is highly hyperechoic in the majority of cases. - F - a significant no. of clots are isoechoic to flowing blood, such that visualisation of intraluminal thrombus is not a reliable finding. Other findings are: loss of compressibility, distension, colour Doppler defect or void, lack of augmentation on spectral Doppler, loss of respiratory phasicity. [B&H]
  2. Regarding DVT, which is false: (GC) CME03.42
  3. Lack of augmentation indicates thrombus distal to the point of interrogation. - T - augment by squeezing calf or plantarflexing foot; indicates venous occlusion/compression in intervening venous segments.
  4. There is a phasic change with respiration on Doppler of the normal femoral vein. - T - normally there is a cyclic variation in flow velocity with respiration - should decrease in expiration and increase in inspiration. Absence of phasicity (ie. continuous venous signal) is suspicious for proximal obstruction. [Dahnert pg 634]
  5. Usually begin in the sinuses of the soleal veins. - T
  6. Acute thrombus is highly hyperechoic in the majority of cases. - F - a significant no. of clots are isoechoic to flowing blood, such that visualisation of intraluminal thrombus is not a reliable finding. Other findings are: loss of compressibility, distension, colour Doppler defect or void, lack of augmentation on spectral Doppler, loss of respiratory phasicity. [B&H]
  7. Thrombus in a duplicated femoral vein is a recognised cause of a false negative study. - T Changed option b from “the 40% propagate” stem (repeated elsewhere); changed option d from “Most common isolated vein is the peroneal vv.” to CME option.; added option e from CME.
57
Q
  1. Enlarged pulmonary artery is seen in:
  2. ASD
  3. TOF
A

1.ASD - T - congenital left to right shunts cause enlarged PA. Other causes of enlarged pulmonary trunk are: pulmonary valve stenosis with post-stenotic dilatation, pulmonary regurgitation, pulmonary arterial hypertension and aneurysms.

58
Q
  1. Enlarged L atrium is seen in: t/f
  2. HOCM
  3. TOF
  4. Ebstein’s Anomaly
  5. Endocardial fibroelastosis
A

1 and 4

  1. Enlarged L atrium is seen in:
  2. HOCM T - LV hypertrophy leads to rapid blood flow through the outflow tract and anterior displacement of the anterior leaflet of the MV causing mitral regurgitation and subsequent LA enlargment (Dahnert)
  3. TOF - F
  4. Ebstein’s Anomaly - F - enlarged right atrium
  5. Endocardial something - T (I presume they are referring to endocardial fibroelastosis) - diffuse endocardial thickening of LV and LA from deposition of collagen and elastic tissue, causes CHF during first 6mths of life and is fatal by 2 years of age Causes of left atrial enlargement - volume overload (mitral incompetence, VSD, PDA or ASD with shunt reversal), pressure overload (mitral stenosis, myxoma of left atrium) secondary to left ventricular failure. (Chapman)
59
Q
  1. Regarding Renal artery stenosis: t/f
  2. Peak velocity of 100cm/sec is normal
  3. In renal artery stenosis the aortic PSV is less than the renal artery PSV
  4. There is increased RI in subcapsular haematoma
  5. Increased RI excludes ureteric obstruction
A

t 1, 3

  1. Regarding Renal artery stenosis: (GC)
  2. Peak velocity of 100cm/sec is normal - T - PSV in normal RAs averages 120cm/s ±12. RAS if >150cm/s for angles <60, or 180cm/s for angles >70 (many false positives due to suboptimal Doppler angles).
  3. In renal artery stenosis the aortic PSV is less than the renal artery PSV - F
  4. There is increased RI in subcapsular haematoma - T - perinephric / subcaspular fluid collection. Elevated RI (>0.70) may also be seen in significant systemic HTN, markedly decreased heart rate, neonates and infants. [Dahnert p895]
  5. Increased RI excludes ureteric obstruction - FThere is a biphasic haemodynamic response to complete ureteral obstruction - short period of Pg-mediated vasodilatation, followed by vasoconstriction (latter initially thought to be due to increased blood flow and collecting system pressures; now suggested that complex interactions btn several regulatory pathways are responsible). The potential role of Doppler sonography in the evaluation of renal colic is controversial. In two initial series, either an RI greater than 0.70 or a difference of >0.06–0.10 in mean RI values between kidneys was found to be highly specific and sensitive for acute obstruction. Perhaps more important, several cases of obstruction were identified before the development of collecting system dilatation. Unfortunately, to our knowledge, these results were not duplicated in later series. [RI in renal Doppler US, AJR 2003].
60
Q
  1. Regarding Vascular USS:
  2. Coeliac artery high resistance in fasting
  3. SMA high resistance in fasting
A

2.SMA high resistance in fasting - T - normal preprandial (fasting) waveform for the SMA is high resistance, and the normal postprandial (after eathing a meal) waveform is low resistance. Normal flow resistances: Aorta = high; Renal artery = low; Celiac artery = low; SMA = high (preprandial), low (postprandial); splenic artery = low

61
Q
  1. Regarding Aberrant Left pulmonary artery – which is true:
  2. Goes behind trachea
  3. Causes a posterior impression on the oesophagus
  4. Presents 6-8 yrs
A
  1. Goes behind trachea - T - arises from the posterior aspect of the RPA and passes btn the trachea & oesophagus to reach the left hilum; forms a sling around the distal trachea and proximal RMB.
  2. Regarding Aberrant Left pulmonary artery - which is true: (GC)
  3. Goes behind trachea - T - arises from the posterior aspect of the RPA and passes btn the trachea & oesophagus to reach the left hilum; forms a sling around the distal trachea and proximal RMB.
  4. Causes a posterior impression on the oesophagus - F - forms an anterior indentation on oesophagogram.
  5. Presents 6-8 yrs - F - those affected may be classified generally into 2 groups: normal bronchial pattern - high mortality and morbidity during infancy. malformations of the tracheobronchial tree - eg. long segment tracheal stenosis, “napkin-ring trachea” (absence of pars membranacea); CVS abnormalities (PDA, ASD, persistent left SVC); this group includes very few asymptomatic adults. [RG 2006]
62
Q
  1. Which of the following compress the trachea?
  2. CCAM
  3. Aberrant L SCA
  4. Aberrant R SCA
  5. Normal thymus
A
  1. Aberrant L SCA - T - with right aortic arch + left ductus/ligamentum arteriosus.
  2. Aberrant R SCA - T - with left aortic arch + right ductus/ligamentum arteriosusBoth b and c cause anterior tracheal indentation + large posterior oesophageal impression.Posterior tracheal indentation + anterior oesophageal impression - aberrant L pulmonary a.Anterior tracheal indentation only - innominate a. with origin more distal along Ao arch; L CCA with origin more proximal to arch; common origin of innominate and L CCA.[Dahnert p592]
63
Q
  1. SLE
  2. dsDNA
  3. arterial and venous involvement
A

yap

64
Q
  1. Systemic sclerosis

1. vasculitis late

A

yap

65
Q
  1. Which finding makes it less likely to be Wegener’s granulomatosus ?
  2. lack of sinus involvement
  3. negative for cANCA
  4. lack of renal involvement
A
  1. negative for cANCA - approximately 90-95% of patients with active, Wegener’s granulomatosis are ANCA-positive.
  2. Which finding makes it less likely to be Wegener’s granulomatosus ? (TW)
  3. lack of sinus involvement - essentally all patients with classic or limited Wegener’s granulomatosis have upper airway OR pulmonary involvement, and the majority have both.
  4. negative for cANCA - approximately 90-95% of patients with active, Wegener’s granulomatosis are ANCA-positive.
  5. lack of renal involvement - a “limited” form, with clinical findings isolated to the upper respiratory tract or lungs, occurs in approximately 1/4 of cases. These however, eventually develop systemic involvement.
66
Q

63.4y.o. in ICU with cardiomegaly. Discharged, then one month later - left atrial enlargement. Cause?

A

1.Rheumatic fever

67
Q
  1. Atrial myxoma - atypical feature
  2. 3cm papillary soft tissue mass
  3. 8cm lobulated mass pedunculated
  4. atrial septum
  5. can prolapse into ventricle
  6. more common in right atrium
A
  1. more common in the right atrium - F - left to right ratio is 4:1 with 90% located in the atria 65.Atrial myxoma - atypical feature (JS)
  2. 3cm papillary soft tissue mass sessile - T - sessile or pedunculated masses that vary from hard globular masses mottled with haemorrhage to soft, translucent, papillary or villous lesions having a gelatinous appearance
  3. 8 cm globular mass pedunculated - T - size range is 1 to 10cm and they are usually solitary
  4. atrial septum - T - fossa ovalis in the atrial septum is a common site
  5. can prolapse into ventricle - T - pedunculated form mobile enough to move into or through the AV valves during systole causing intermittent and often position dependent obstruction or “wrecking ball” effect
  6. more common in the right atrium - F - left to right ratio is 4:1 with 90% located in the atria
68
Q
  1. Aortic dissection t.f
  2. Can occur without an intimal flap
  3. Longitudinal
  4. 30-60 cm long
  5. aortic valve prevents involvement of the coronary arteries
A

1 true? 3 true

  1. Aortic dissection (JS)
  2. Can occur without an intimal flap - T - There is usually (but not always) an intimal tear that extends into but not through the media of the ascending aorta (Robbins). According to Primer, intimal flap is detectable in 85-90%.
  3. Longitudinal - F - tears are usually transverse or oblique, 1-5cm in length with sharp jagged edges
  4. 30-50cm long ? - not sure if they mean the length of the tear (1-5cm) or the length of the dissection which is variable
  5. Aortic valve prevents involvement coronary arteries - F - occlusion of coronary aa in 8%
69
Q

69.ASD septum secundum, the most correct statement is:

  1. An isolated finding
  2. Close to AV junction
  3. Left ventricular failure
A
  1. An isolated finding - T - Isolated secundum atrial septal defects account for approximately 7% of congenital cardiac defects; occasionally demonstrates familial inheritance in an autosomal dominant pattern, esp. when assocd with prolonged AV conduction (ie, prolonged PR interval on ECG). Familial secundum ASD also occurs in Holt-Oram syndrome. May be assocd with prolpasing MV (20-30%), PV stenosis, tricuspid atresia, TAPVR, hypoplastic left heart, interrupted Ao arch. (cf. Ostium primum ASD which is almost always assocd with anomalies, including cleft MV and Down’s syndrome).
  2. An isolated finding - T - Isolated secundum atrial septal defects account for approximately 7% of congenital cardiac defects; occasionally demonstrates familial inheritance in an autosomal dominant pattern, esp. when assocd with prolonged AV conduction (ie, prolonged PR interval on ECG). Familial secundum ASD also occurs in Holt-Oram syndrome. May be assocd with prolpasing MV (20-30%), PV stenosis, tricuspid atresia, TAPVR, hypoplastic left heart, interrupted Ao arch. (cf. Ostium primum ASD which is almost always assocd with anomalies, including cleft MV and Down’s syndrome).
70
Q
  1. IV contrast reaction 4-12 hours afterwards, it results in skin necrosis. It’s a repeatable response. What type of reaction is it?
  2. Type I hypersensitivity
  3. Type II hypersensitivity
  4. Type III hypersensitivity
  5. Type IV hypersensitivity
  6. Not immune reaction
A

3.Type III hypersensitivity - T - Immunocomplex disease. Induced by antigen-antibody complexes that produce tissue damage as a result of their capacity to active the complement system. Can be generalized (immune complexes formed in circulation adn deposited in many organs etc), or localized to particular organs such as kidney (GN), joints (arthritis) or the small blood vessels of the skin if the complexes are formed an deposited locally (the local Arthus reaction). See below. eg serum sickness

  1. IV contrast reaction 4-12 hours afterwards, it results in skin necrosis. It’s a repeatable response. What type of reaction is it? (TW)
  2. Type I hypersensitivity - F- Anaphylactic type. Rapidly developing immunologic reaction developing within minutes after combination of antigen with antibody bound to mast cells or basophils in individuals previously sensitized to antigen
  3. Type II hypersensitivity - F - Cytotoxic type. Mediated by antibodies directed toward antigens present on surface of cells or other tissue component (subtypes: complement-dependent reactions; antibody-dependent cell mediated cytotoxicity; antibody mediated cellular dysfunction)- eg ABO
  4. Type III hypersensitivity - T - Immunocomplex disease. Induced by antigen-antibody complexes that produce tissue damage as a result of their capacity to active the complement system. Can be generalized (immune complexes formed in circulation adn deposited in many organs etc), or localized to particular organs such as kidney (GN), joints (arthritis) or the small blood vessels of the skin if the complexes are formed an deposited locally (the local Arthus reaction). See below. eg serum sickness
  5. Type IV hypersensitivity - F - Cell mediated (delayed). Initiated by specifically sensitized T lymphocytes. Eg TB
  6. Not immune reaction - F - unless someone is repeatedly extravasating a lot of contrast! Maybe fun, but not ethical.
71
Q
  1. A prominent aortic arch is seen with the following. t/f
  2. PDA
  3. ASD
  4. Mitral stenosis.
  5. Syphilis.
  6. Hypertension.
A
  1. A prominent aortic arch is seen with the following. (GC)
  2. PDA - T
  3. ASD - F
  4. Mitral stenosis - F
  5. Syphilis - T
  6. Hypertension - T
72
Q

75.Calcified valves
.1.Are consistently seen in severe aortic stenosis on plain films.
2.Occur in aortic incompetence with rheumatic heart disease.
3.Indicate progressive mitral valve degeneration.
4.Is seen in 10% of congenital aortic stenosis

A
  1. Are consistently seen in severe aortic stenosis on plain films. - T - good correlation btn amount of Ca2+ and degree of stenosis:- heavy Ca2+ = significant stenosis; none = AS unlikely.
  2. Calcified valves. (GC)
  3. Are consistently seen in severe aortic stenosis on plain films. - T - good correlation btn amount of Ca2+ and degree of stenosis:- heavy Ca2+ = significant stenosis; none = AS unlikely.
  4. Occur in aortic incompetence with rheumatic heart disease. - F - AR is rare in RHD, most commonly MS (70%), then MS+AS (25%). Isolated rheumatic AS is seen as a dense cluster of calcific deposits without a bicuspid contour (as in BAV). In patients 30-60yo, AV Ca2+ suggest RHD.
  5. Indicate progressive mitral valve degeneration. - F - mitral annular calcification is degenerative (physiologic in elderly). Mitral valve Ca2+ is virtually always due to RHD (see below).
  6. Is seen in 10% of congenital aortic stenosis. - F - in patients <30yo, AV Ca2+ are mostly due to bicuspid AV; usually extensive cluster of dense calcific deposits (nearly circular Ca2+ with interior linear bar DIAGNOSTIC; also get poststenotic dilatation). There is valvular calcification in 60% of patients >24yo.Aortic valve: Ca2+ best seen on lateral view. Causes: congenital BAV (<30yo), isolated rheumatic AS (30-60yo), degenerative AS (>65yo).Mitral valve: RHD, infective endocarditis, tumour attached to MV, MVP. Pulmonary valve: tetralogy of Fallot, PS, ASDTricuspid valve: RHD, septal defect, TV defect, IE.[Dahnert p595]
73
Q
  1. Bowel Ischaemia: t/f
  2. Can be related to superior mesenteric vein thrombosis
  3. Is associated with paroxysmal nocturnal haemoglobinuria
  4. Vasospasm indicates underlying atherosclerosis and stenosis
  5. Occlusion is typically 10cm distal to the SMA origin
  6. Plain film changes are only seen after bowel infarction
A

t 1, 2 45.Bowel Ischaemia: (TW)

  1. Can be related to superior mesenteric vein thrombosis - T - venous occlusion <10%. SMV > IMV > PV.
  2. Is associated with paroxysmal nocturnal haemoglobinuria - T - PNH is a disorder characterised by a defect in the GPI anchor due to an abnormality in th PIG-A gene. Result in abnormalities in hemopoietic function, including hemolytic anemia, a hypercoagulabel state, and diminished hematopoiesis.
  3. Vasospasm indicates underlying atherosclerosis and stenosis - F
  4. Occlusion is typically 10cm distal to the SMA origin - F - SMA thrombosis (20-40%) at origin + site of atherosclerotic narrowing. Embolus (40-50%) just distal to middle colic artery.
  5. Plain film changes are only seen after bowel infarction - F - ischaemia, oedematous bowel, thumb printing. Could also have bowel obstruction as cause of ischaemia (pre-infarction).
74
Q
  1. Aortic Stent Grafts: t/f
  2. Sac size greater than 8 cm is a contraindication
  3. The neck of the aneurysm is defined as the distance from the inferior most renal artery to the start of the aneurysm
  4. Immediate endoleak always needs further intervention
  5. Retro leak from lumbar arteries needs further intervention
  6. Luminal diameter is best measured via angiography with a graded catheter
A

t 2 46.Aortic Stent Grafts: (TW)

  1. Sac size greater than 8cm is a contraindication - F - for example the Zenith AAA grafts range from 82mm to 149mm in length.
  2. The neck of the aneurysm is defined as the distance from the inferior most renal artery to the start of the aneurysm - T - the proximal neck is defined as the segment of aorta between the origin of the lowest renal artery and superior aspect of the aneurysm. Most endographs require a length of greater than 15mm to ensure adequate proximal seal.
  3. Immediate endoleak always needs further intervention - F - depends on type. type I endoleak (ie incompetent seal at either proximal or distal attachment site) must be repaired as soon as possible. Type III endoleaks represtn flow into sac from separation between components of a modular system, or tears in the endograft - these are repaired with an additional endograft. Type IV leaks are due to egress of blood through the pores of the fabric - these heal spontaneously. Type II enodleak (most common) - management is controversial. Some argue that as spontaneous resolution occurs 30-100% of cases, a “wait and see” approach is preferable. UTD recommendations are occluding type II endoleaks that have not spontaneously thrombosed in one month (as systemic pressures have been noted in aneuyrsm sac in the presence of type II endoleaks
  4. Retro leak from lumbar arteries needs further intervention - ?T/F - controversial, see ans c.
  5. Luminal diameter is best measured via angiography with a graded catheter - ?F
75
Q
  1. Regarding Cervico Cephalic Vessel Dissection: t/f
  2. Causes 5% to 20% of CVAs in young to middle aged patients
  3. Has a rim of T1 hyperintensity surrounding a void in the vessels
  4. Imaging identifies vasculopathy in the majority
  5. The location of vertebral artery dissections is most often proximal (between C2 and C6)
  6. The location of an ICA dissection is most often just immediately distal to the bulb
A

t 1, 2, 5 not sure about 3

  1. Regarding Cervico Cephalic Vessel Dissection: (GC)
  2. Causes 5% to 20% of CVAs in young to middle aged patients - T - 5-20% in those aged 40-60yrs [Dahnert]; up to 1/4 of strokes,with a peak prevalence in the 5th decade [RG].
  3. Has a rim of T1 hyperintensity surrounding a void in the vessels - T - subacute hematoma (7days-2mths) on T1 + fat sat appears as a bright crescent-shaped area around an eccentric flow void. Note that in the early and chronic stage, the haematoma is usually isointense to surrounding structures on T1.
  4. Imaging identifies vasculopathy in the majority
  5. The location of vertebral artery dissections is most often proximal (between C2 and C6) - F - at the level of C1/2 in 65% [Dahenrt]. ie. predominantly located in the pars transversaria (V2, 35%) or the atlas loop (V3, 34%) [RG]. Bilateral vertebal artery dissections in 5%.
  6. The location of an ICA dissection is most often just immediately distal to the bulb - T - extracranial ICA dissection affects the cervical part of the artery distal to the carotid bulb and tends not to extend beyond its entry into the petrous portion. [Craniocervical a. dissection, RG 2008]
76
Q
  1. Fixed inferior defects in a thallium scan are caused by:
  2. Diaphragmatic attenuation
  3. Mastectomy
  4. Right coronary artery infarct
  5. Pacemaker leads5.Left bundle branch block
A

1, 3, 4, probably 5

  1. Fixed inferior defects in a thallium scan are caused by: (GC)
  2. Diaphragmatic attenuation - T - variation in tracer intensity by 15-20% btn regions on planar images may be normal (due to soft tissue attentuation artifacts from subdiaphragmatic abdominal contents or breast tissue).
  3. Mastectomy - F - implants could cause attentuation artifact.
  4. Right coronary artery infarct - T - RCA territory is 5-8 o’clock on the short axis (oblique coronal).
  5. Pacemaker leads - T - attentuation artifact.
  6. Left bundle branch block - ?T
77
Q
  1. Pulmonary Emboli: t/f
  2. Septic emboli most commonly arise from the pelvic veins
  3. The defect on chest x-rays is often larger than the V/Q defect
  4. Matched defects on V/Q scans exclude PE
  5. PE is associated with pulmonary infarction in 30%
  6. The presence of a pleural effusion indicates pulmonary infarction
A

everything is false

  1. Pulmonary Emboli: (GC/TW)
  2. Septic emboli most commonly arise from the pelvic veins - F - most common cause of septic emboli in IVDU is tricuspid valve endocarditis. Other causes include septic thrombophlebitis, pelvic thrombophlebitis, infected lines, AV fistula, skin infection… Can’t find anything more specific than this.
  3. The defect on chest x-rays is often larger than the V/Q defect - F - An upright PA and lateral CXR should ideally be obtained as close as possible to the V/Q scan. Perfusion defects substantially larger than the corresponding CXR abnormalities are suggestive of PE, whereas perfusion defects substantially smaller than corresponding CXR abnormalities are not commonly associated with PE (Thoracic Imaging).
  4. Matched defects on V/Q scans exclude PE - F - a PE presents as a segmentally hypoperfused but normally ventilated lung (V/Q mismatch). A normal perfusion scan excludes a PE for practical purposes. A perfusion defect requires further evaluation with ventilation scan and CXR - if both (V and CXR) are normal, suspect PE. Matched V and Q defects + normal CXR = low prob. Matched V and Q and CXR defect = indeterminate.
  5. PE is associated with pulmonary infarction in 30% - F – false if using Path notes. If use Dahnert numbers (10-60%) then true. More likely to develop if cardiopulmonary disease with obstruction of pulmonary venous outflow.
  6. The presence of a pleural effusion indicates pulmonary infarction - F - pleural effusions are non specific - present in 48% of those with PE vs. 31% of those with no PE. Pulmonary infarction = any opacity developing as a result of thromboembolic disease. [Dahnert p524]
78
Q
  1. With regard to cerebral aneurysms: t/
  2. In children are associated with trauma and infection
  3. Multiple aneurysms are strongly associated with male gender
  4. A truly azygos anterior cerebral artery is associated with lobar holoprosencephaly and saccular aneurysms
  5. Are multiple in 15% to 20%
  6. Occur in the posterior circulation in 40%
A

t 1, 3, 4

  1. With regard to cerebral aneurysms: (TW)
  2. In children are associated with trauma and infection - T - Aneuyrsms in children may be congenital or idiopathic (77%), inflammatory or mycotic (11%), or traumatic (11%).
  3. Multiple aneurysms are strongly associated with male gender - F - Female > Male (Neuroradiology 2004). Female preponderance has been reported in up to 70% of multiple aneurysms and a 2.4:1 ratio of females > males was reported in the Cooperative Study of Intracranial Aneurysms and SAH.
  4. A truly azygos anterior cerebral artery is associated with lobar holoprosencephaly and saccular aneurysms - T - azygos ACA is a rare variation of the COW in which the A2 segments of both ACAs are represented by a singl common vessel from which arise all the major vessels supplying most of both anterior cerebral hemispheres, as well as the corpus callosum (ie a true azygos). Associated with holoprosencephaly. High indicence of berry aneurysms. Abnormal medial and intimal elements in the vessel wall of this developmental variant may account for the increased prevalence of associated saccular aneurysms.
  5. Are multiple in 15% to 20% - T
  6. Occur in the posterior circulation in 40% - F - 90-95% of aneurysms arise from COW - 90% from anterior circulation, 10% from posterior circulation. ACom 30-35%, PCom 30-35%, MCA 20-30%, Basilar apex 5-10%, other posterior 1-3%. Variations of the distal ACA: trus azygos artery, from which all major branches are given off to both cerebral hemispheres; a bihemispheric ACA, where both right and left ACAs are present, but one is rudimentary and most of the major branches to both hemispheres arise from the other ACA; a triple ACA, with the accessory ACA arising from the anterior communcating artery.
79
Q
  1. Cerebral angiography:
  2. The supraclinoid internal carotid artery is best seen in a caudal (Waters) projection
  3. The origin of the opthalmic artery is intradural in the majority of people
  4. Internal carotid injections are of 8mls at 2mls per second
  5. Cavernous haemangiomata are angiographically occult
  6. The enhancement of meningiomas persist late into the venous phase
A

true 2,3,4,55

  1. Cerebral angiography: (TW)
  2. The supraclinoid internal carotid artery is best seen in a caudal (Waters) projection - ?F - ICA/ophthalmic: transorbital oblique (15-30 degree rotation, and 7 degrees cephalad); Caldwell’s oblique (15-30 degrees rotation, and 7 degrees caudad). Waters is ~30 degrees caudad?
  3. The origin of the opthalmic artery is intradural in the majority of people - T - The origin of the ophthalmic artery is intradural in approx 90% of anatomic dissections (Diagnostic cerebral angiography, AG Osborn).
  4. Internal carotid injections are of 8mls at 2mls per second - T - CCA 4-5ml/s for 2s (ie total 8-10mls)
  5. Cavernous haemangiomata are angiographically occult - T - cavernous malformation: DSA is usually normal “angiographically occult vascular malformation”
  6. The enhancement of meningiomas persist late into the venous phase - T - mother-in-law - “comes early, stay late” - could always remember this as the pre-mature ejaculator who wants to cuddle afterwards.
80
Q
  1. Dural venous sinus thrombosis is associated with:
  2. Pregnancy
  3. Meningioma
  4. Gastroenteritis
  5. Trauma
  6. Nephritic syndrome
A

5.Nephritic syndrome - F - haematuria, oliguria + azotemia, hypertension +/- some proteinuria. Nephrotic syndrome (proteinuria >3.5g/day) is one of the rarer causes of hypercoagulable state that can cause DST.

  1. Dural venous sinus thrombosis is associated with: (GC)
  2. Pregnancy - T - hypercoagulable state.
  3. Meningioma - T - tumour compressing sinus.
  4. Gastroenteritis - T - dehydration (low-slow states).
  5. Trauma - T - hfracture through sinus wall, cranial surgery, IJV catheterisation.
  6. Nephritic syndrome - F - haematuria, oliguria + azotemia, hypertension +/- some proteinuria. Nephrotic syndrome (proteinuria >3.5g/day) is one of the rarer causes of hypercoagulable state that can cause DST. Causes: Idiopathic Septic (esp. kids) - sinusitis, otitis, mastoiditis, meningitis, septicaemia etc. Aseptic causes - tumour (compression), trauma, low-flow states, hypercoagulability, chemotherapy. Unusual causes - Behcet’s disease, AIDS, UC, SLE, nephrotic syndrome, sarcoidosis. [Dahnert] Added options d and e.
81
Q

52.Regarding Dural spinal AVM: 1.Is usually associated with increased cord signal

A

yes

82
Q
  1. Regarding DVT, which is false:
  2. Lack of augmentation indicates thrombus distal to the point of interrogation
  3. There is a phasic change with respiration on Doppler of the normal femoral vein.
  4. Usually begin in the sinuses of the soleal veins.
  5. Acute thrombus is highly hyperechoic in the majority of cases.
  6. Thrombus in a duplicated femoral vein is a recognised cause of a false negative study.
A
  1. Acute thrombus is highly hyperechoic in the majority of cases. - F - a significant no. of clots are isoechoic to flowing blood, such that visualisation of intraluminal thrombus is not a reliable finding. Other findings are: loss of compressibility, distension, colour Doppler defect or void, lack of augmentation on spectral Doppler, loss of respiratory phasicity. [B&H]
  2. Regarding DVT, which is false: (GC) CME03.42
  3. Lack of augmentation indicates thrombus distal to the point of interrogation. - T - augment by squeezing calf or plantarflexing foot; indicates venous occlusion/compression in intervening venous segments.
    * AJL need to be careful with the use of ‘distal’. If meaning distal leg (as in inferior) this question is correct. If meaning distal vein (as in superior) this question is incorrect. (I hate proximal and distal with blood veins)
  4. There is a phasic change with respiration on Doppler of the normal femoral vein. - T - normally there is a cyclic variation in flow velocity with respiration - should decrease in expiration and increase in inspiration. Absence of phasicity (ie. continuous venous signal) is suspicious for proximal obstruction. [Dahnert pg 634]
  5. Usually begin in the sinuses of the soleal veins. - T
  6. Acute thrombus is highly hyperechoic in the majority of cases. - F - a significant no. of clots are isoechoic to flowing blood, such that visualisation of intraluminal thrombus is not a reliable finding. Other findings are: loss of compressibility, distension, colour Doppler defect or void, lack of augmentation on spectral Doppler, loss of respiratory phasicity. [B&H]
  7. Thrombus in a duplicated femoral vein is a recognised cause of a false negative study. - T Changed option b from “the 40% propagate” stem (repeated elsewhere); changed option d from “Most common isolated vein is the peroneal vv.” to CME option.; added option e from CME.
83
Q
  1. Enlarged pulmonary artery is seen in:
  2. ASD
  3. TOF
A

1.ASD - T - congenital left to right shunts cause enlarged PA. Other causes of enlarged pulmonary trunk are: pulmonary valve stenosis with post-stenotic dilatation, pulmonary regurgitation, pulmonary arterial hypertension and aneurysms.

84
Q
  1. Enlarged L atrium is seen in: t/f
  2. HOCM
  3. TOF
  4. Ebstein’s Anomaly
  5. Endocardial fibroelastosis
A

1 and 4

  1. Enlarged L atrium is seen in:
  2. HOCM T - LV hypertrophy leads to rapid blood flow through the outflow tract and anterior displacement of the anterior leaflet of the MV causing mitral regurgitation and subsequent LA enlargment (Dahnert)
  3. TOF - F
  4. Ebstein’s Anomaly - F - enlarged right atrium
  5. Endocardial something - T (I presume they are referring to endocardial fibroelastosis) - diffuse endocardial thickening of LV and LA from deposition of collagen and elastic tissue, causes CHF during first 6mths of life and is fatal by 2 years of age Causes of left atrial enlargement - volume overload (mitral incompetence, VSD, PDA or ASD with shunt reversal), pressure overload (mitral stenosis, myxoma of left atrium) secondary to left ventricular failure. (Chapman)
85
Q

56.Regarding Renal artery stenosis: t/f

  1. Peak velocity of 100cm/sec is normal
  2. In renal artery stenosis the aortic PSV is less than the renal artery PSV
  3. There is increased RI in subcapsular haematoma
  4. Increased RI excludes ureteric obstruction
A

t 1, 3

  1. Regarding Renal artery stenosis: (GC)
  2. Peak velocity of 100cm/sec is normal - T - PSV in normal RAs averages 120cm/s ±12. RAS if >150cm/s for angles <60, or 180cm/s for angles >70 (many false positives due to suboptimal Doppler angles).
  3. In renal artery stenosis the aortic PSV is less than the renal artery PSV - F
  4. There is increased RI in subcapsular haematoma - T - perinephric / subcaspular fluid collection. Elevated RI (>0.70) may also be seen in significant systemic HTN, markedly decreased heart rate, neonates and infants. [Dahnert p895]
  5. Increased RI excludes ureteric obstruction - FThere is a biphasic haemodynamic response to complete ureteral obstruction - short period of Pg-mediated vasodilatation, followed by vasoconstriction (latter initially thought to be due to increased blood flow and collecting system pressures; now suggested that complex interactions btn several regulatory pathways are responsible). The potential role of Doppler sonography in the evaluation of renal colic is controversial. In two initial series, either an RI greater than 0.70 or a difference of >0.06–0.10 in mean RI values between kidneys was found to be highly specific and sensitive for acute obstruction. Perhaps more important, several cases of obstruction were identified before the development of collecting system dilatation. Unfortunately, to our knowledge, these results were not duplicated in later series. [RI in renal Doppler US, AJR 2003].
86
Q

57.Regarding Vascular USS:

  1. Coeliac artery high resistance in fasting
  2. SMA high resistance in fasting
A

2.SMA high resistance in fasting - T - normal preprandial (fasting) waveform for the SMA is high resistance, and the normal postprandial (after eathing a meal) waveform is low resistance. Normal flow resistances: Aorta = high; Renal artery = low; Celiac artery = low; SMA = high (preprandial), low (postprandial); splenic artery = low

87
Q

58.Regarding Aberrant Left pulmonary artery – which is true
:1.Goes behind trachea
2.Causes a posterior impression on the oesophagus
3.Presents 6-8 yrs

A

1.Goes behind trachea - T - arises from the posterior aspect of the RPA and passes btn the trachea & oesophagus to reach the left hilum; forms a sling around the distal trachea and proximal RMB.

  1. Regarding Aberrant Left pulmonary artery - which is true: (GC)
  2. Goes behind trachea - T - arises from the posterior aspect of the RPA and passes btn the trachea & oesophagus to reach the left hilum; forms a sling around the distal trachea and proximal RMB.
  3. Causes a posterior impression on the oesophagus - F - forms an anterior indentation on oesophagogram.
  4. Presents 6-8 yrs - F - those affected may be classified generally into 2 groups: normal bronchial pattern - high mortality and morbidity during infancy. malformations of the tracheobronchial tree - eg. long segment tracheal stenosis, “napkin-ring trachea” (absence of pars membranacea); CVS abnormalities (PDA, ASD, persistent left SVC); this group includes very few asymptomatic adults. [RG 2006]
88
Q
  1. Which of the following compress the trachea?
  2. CCAM
  3. Aberrant L SCA
  4. Aberrant R SCA
  5. Normal thymus
A
  1. Aberrant L SCA - T - with right aortic arch + left ductus/ligamentum arteriosus.
  2. Aberrant R SCA - T - with left aortic arch + right ductus/ligamentum arteriosusBoth b and c cause anterior tracheal indentation + large posterior oesophageal impression.Posterior tracheal indentation + anterior oesophageal impression - aberrant L pulmonary a.Anterior tracheal indentation only - innominate a. with origin more distal along Ao arch; L CCA with origin more proximal to arch; common origin of innominate and L CCA.[Dahnert p592]
89
Q
  1. SLE
  2. dsDNA
  3. arterial and venous involvement
A

yap

90
Q

61.Systemic sclerosis1.vasculitis late

A

yap

91
Q
  1. Which finding makes it less likely to be Wegener’s granulomatosus ?
  2. lack of sinus involvement
  3. negative for cANCA
  4. lack of renal involvement
A
  1. negative for cANCA - approximately 90-95% of patients with active, Wegener’s granulomatosis are ANCA-positive.
  2. Which finding makes it less likely to be Wegener’s granulomatosus ? (TW)
  3. lack of sinus involvement - essentally all patients with classic or limited Wegener’s granulomatosis have upper airway OR pulmonary involvement, and the majority have both.
  4. negative for cANCA - approximately 90-95% of patients with active, Wegener’s granulomatosis are ANCA-positive.
  5. lack of renal involvement - a “limited” form, with clinical findings isolated to the upper respiratory tract or lungs, occurs in approximately 1/4 of cases. These however, eventually develop systemic involvement.
92
Q

63.4y.o. in ICU with cardiomegaly. Discharged, then one month later - left atrial enlargement. Cause?

A

1.Rheumatic fever

93
Q
  1. Atrial myxoma - atypical feature
  2. 3cm papillary soft tissue mass
  3. 8cm lobulated mass pedunculated
  4. atrial septum
  5. can prolapse into ventricle
  6. more common in right atrium
A
  1. more common in the right atrium - F - left to right ratio is 4:1 with 90% located in the atria
  2. Atrial myxoma - atypical feature (JS)
  3. 3cm papillary soft tissue mass sessile - T - sessile or pedunculated masses that vary from hard globular masses mottled with haemorrhage to soft, translucent, papillary or villous lesions having a gelatinous appearance
  4. 8 cm globular mass pedunculated - T - size range is 1 to 10cm and they are usually solitary
  5. atrial septum - T - fossa ovalis in the atrial septum is a common site
  6. can prolapse into ventricle - T - pedunculated form mobile enough to move into or through the AV valves during systole causing intermittent and often position dependent obstruction or “wrecking ball” effect
  7. more common in the right atrium - F - left to right ratio is 4:1 with 90% located in the atria
94
Q
  1. Aortic dissection t.f
  2. Can occur without an intimal flap
  3. Longitudinal
  4. 30-60 cm long
  5. aortic valve prevents involvement of the coronary arteries
A

1 true? 3 true

  1. Aortic dissection (JS)
  2. Can occur without an intimal flap - T - There is usually (but not always) an intimal tear that extends into but not through the media of the ascending aorta (Robbins). According to Primer, intimal flap is detectable in 85-90%.
  3. Longitudinal - F - tears are usually transverse or oblique, 1-5cm in length with sharp jagged edges
  4. 30-50cm long ? - not sure if they mean the length of the tear (1-5cm) or the length of the dissection which is variable
  5. Aortic valve prevents involvement coronary arteries - F - occlusion of coronary aa in 8%
95
Q
  1. ASD septum secundum, the most correct statement is:
  2. An isolated finding
  3. Close to AV junction
  4. Left ventricular failure
A
  1. An isolated finding - T - Isolated secundum atrial septal defects account for approximately 7% of congenital cardiac defects; occasionally demonstrates familial inheritance in an autosomal dominant pattern, esp. when assocd with prolonged AV conduction (ie, prolonged PR interval on ECG). Familial secundum ASD also occurs in Holt-Oram syndrome. May be assocd with prolpasing MV (20-30%), PV stenosis, tricuspid atresia, TAPVR, hypoplastic left heart, interrupted Ao arch. (cf. Ostium primum ASD which is almost always assocd with anomalies, including cleft MV and Down’s syndrome).
  2. An isolated finding - T - Isolated secundum atrial septal defects account for approximately 7% of congenital cardiac defects; occasionally demonstrates familial inheritance in an autosomal dominant pattern, esp. when assocd with prolonged AV conduction (ie, prolonged PR interval on ECG). Familial secundum ASD also occurs in Holt-Oram syndrome. May be assocd with prolpasing MV (20-30%), PV stenosis, tricuspid atresia, TAPVR, hypoplastic left heart, interrupted Ao arch. (cf. Ostium primum ASD which is almost always assocd with anomalies, including cleft MV and Down’s syndrome).
96
Q
  1. IV contrast reaction 4-12 hours afterwards, it results in skin necrosis. It’s a repeatable response. What type of reaction is it?
  2. Type I hypersensitivity
  3. Type II hypersensitivity
  4. Type III hypersensitivity
  5. Type IV hypersensitivity
  6. Not immune reaction
A
  1. Type III hypersensitivity - T - Immunocomplex disease. Induced by antigen-antibody complexes that produce tissue damage as a result of their capacity to active the complement system. Can be generalized (immune complexes formed in circulation adn deposited in many organs etc), or localized to particular organs such as kidney (GN), joints (arthritis) or the small blood vessels of the skin if the complexes are formed an deposited locally (the local Arthus reaction). See below. eg serum sickness
  2. IV contrast reaction 4-12 hours afterwards, it results in skin necrosis. It’s a repeatable response. What type of reaction is it? (TW)
  3. Type I hypersensitivity - F- Anaphylactic type. Rapidly developing immunologic reaction developing within minutes after combination of antigen with antibody bound to mast cells or basophils in individuals previously sensitized to antigen
  4. Type II hypersensitivity - F - Cytotoxic type. Mediated by antibodies directed toward antigens present on surface of cells or other tissue component (subtypes: complement-dependent reactions; antibody-dependent cell mediated cytotoxicity; antibody mediated cellular dysfunction)- eg ABO
  5. Type III hypersensitivity - T - Immunocomplex disease. Induced by antigen-antibody complexes that produce tissue damage as a result of their capacity to active the complement system. Can be generalized (immune complexes formed in circulation adn deposited in many organs etc), or localized to particular organs such as kidney (GN), joints (arthritis) or the small blood vessels of the skin if the complexes are formed an deposited locally (the local Arthus reaction). See below. eg serum sickness
  6. Type IV hypersensitivity - F - Cell mediated (delayed). Initiated by specifically sensitized T lymphocytes. Eg TB
  7. Not immune reaction - F - unless someone is repeatedly extravasating a lot of contrast! Maybe fun, but not ethical.
97
Q
  1. A prominent aortic arch is seen with the following. t/f
  2. PDA
  3. ASD
  4. Mitral stenosis.
  5. Syphilis.
  6. Hypertension.
A
75.A prominent aortic arch is seen with the following. (GC
)1.PDA - T 
2.ASD - F 
3.Mitral stenosis - F 
4.Syphilis - T 
5.Hypertension - T
98
Q
  1. Calcified valves.
  2. Are consistently seen in severe aortic stenosis on plain films.
  3. Occur in aortic incompetence with rheumatic heart disease
  4. Indicate progressive mitral valve degeneration.
  5. Is seen in 10% of congenital aortic stenosis
A
  1. Are consistently seen in severe aortic stenosis on plain films. - T - good correlation btn amount of Ca2+ and degree of stenosis:- heavy Ca2+ = significant stenosis; none = AS unlikely.
  2. Calcified valves. (GC)
  3. Are consistently seen in severe aortic stenosis on plain films. - T - good correlation btn amount of Ca2+ and degree of stenosis:- heavy Ca2+ = significant stenosis; none = AS unlikely.
  4. Occur in aortic incompetence with rheumatic heart disease. - F - AR is rare in RHD, most commonly MS (70%), then MS+AS (25%). Isolated rheumatic AS is seen as a dense cluster of calcific deposits without a bicuspid contour (as in BAV). In patients 30-60yo, AV Ca2+ suggest RHD.
  5. Indicate progressive mitral valve degeneration. - F - mitral annular calcification is degenerative (physiologic in elderly). Mitral valve Ca2+ is virtually always due to RHD (see below)

.4.Is seen in 10% of congenital aortic stenosis. - F - in patients <30yo, AV Ca2+ are mostly due to bicuspid AV; usually extensive cluster of dense calcific deposits (nearly circular Ca2+ with interior linear bar DIAGNOSTIC; also get poststenotic dilatation). There is valvular calcification in 60% of patients >24yo.Aortic valve: Ca2+ best seen on lateral view. Causes: congenital BAV (<30yo), isolated rheumatic AS (30-60yo), degenerative AS (>65yo).Mitral valve: RHD, infective endocarditis, tumour attached to MV, MVP. Pulmonary valve: tetralogy of Fallot, PS, ASDTricuspid valve: RHD, septal defect, TV defect, IE.[Dahnert p595]

99
Q
  1. Rheumatic heart disease. t/f
  2. Antibiotics should be used when performing a barium enema.
  3. Affects the pulmonary valve greater than the triscupid valve.
  4. Increase in size of the left atrial appendage is greater with rheumatic compared with non-rheumatic heart disease.
  5. Pericardial effusions are seen acutely.
A
  1. Affects the pulmonary valve greater than the triscupid valve. - F - mitral valve alone in 70%; MV and AV in 25%.
  2. Rheumatic heart disease: (GC)
  3. Antibiotics should be used when performing a barium enema. - T - there is approx 10% incidence of transient bacteraemia with Ba enema; pts with acquired valvular dysfunction (ie. chronic RHD) are considered at moderate risk of IE, whilst those with a previous hx of IE are high risk. However, despite accepted recommendations for prophylaxis and the decrease in the incidence of RHD, the number of reported cases of IE has remained fairly constant. [American Society of Colon & Rectal Surgeons]
  4. Affects the pulmonary valve greater than the triscupid valve. - F - mitral valve alone in 70%; MV and AV in 25%.
  5. Increase in size of the left atrial appendage is greater with rheumatic compared with non-rheumatic heart disease. - T - enlargement of the LAA is rare to uncommon in the wide range of nonrheumatic cardiac lesions which can lead to enlargement of the body of the LA (eg. L-R shunts, endocardial cushion defects, MVP). There is a very good correlation btn the presence of a dilated LAA and clincial/lab evidence of rheumatic MV disease, esp in severe enough cases that cause some degree of pulmonary venous obstruction. Proposed that this is a consequence of myocardial inflammation rather than mere haemodynamic factors (MV and LAA emb. derived from cardiac tissue, while LA body derived from pulmonary vein). [Significance of LAA in RHD, Radiology 1975]
  6. Pericardial effusions are seen acutely. - T - RHD is a pancarditis (any of the 3 layers can be affected). Causes a fibrinous or serofibrinous pericardial exudate, which generally resolves without sequelae. [Robbins]
100
Q

77.Ebsteins anomaly includes or is associated with

  1. Mitral regurgitation
  2. Atrial septal defect
  3. Enlarged aortic knuckle
  4. Right heart failure in infancy
  5. Cyanosis in all cases
A

2 and 4 true

  1. Ebsteins anomaly includes or is associated with (JS)
  2. Mitral regurgitation - F - Tricuspid regurgitation
  3. Atrial septal defect - T - PDA or ASD nearly always present, with right to left shunt (80%)
  4. Enlarged aortic knuckle - F - hypoplastic aorta and pulmonary trunk
  5. Right heart failure in infancy - T - tends to present in infancy
  6. Cyanosis in all cases - F - +/- cyanosis depending on the degree of right to left shunt
101
Q

78.The following are features of Marfan’s syndrome: t/f

  1. Autosomal recessive
  2. Aneurysm of the descending tharacic aorta
  3. Aortic incompetence
  4. Aneurysms of the pulmonary arteries
  5. Tricuspid incompetence
A

t 3,4

  1. The following are features of Marfan’s syndrome (JS)
  2. Autosomal recessive - F - 70-85% are familial with autosomal dominant inheritence, the remainder are sporadic and arise from new mutations.
  3. Aneurysm of the descending thoracic aorta - F - aneurysms occur in the ascending aorta due to cystic medial dilation
  4. Aortic incompetence - T - loss of connective tissue support in the aortic valve ring and root of the aorta give rise to aortic incompetence.
  5. Aneurysms of the pulmonary arteries - T - Marfans is associated with aortic sinus dilatation, aortic aneurysm, aortic insufficiency and pulmonary aneurysm (Dahnert)
  6. Tricuspid incompetence - F - Mitral valve prolapse and Aortic regurgitation are the only valve probs I could find
102
Q
  1. Features of Kawasaki’s disease (muco cutaneous lymph node syndrome) t/f
  2. Gallstones
  3. Hydrops of the gallbladder
  4. Coronary artery Anuerysms
  5. Desquamation of the skin
  6. Cataracts
A

2,3, 4 true

  1. Features of Kawasaki’s disease (mucocutaneous lymph node syndrome) (JS)
  2. Gallstones - F
  3. Hydrops of the gallbladder - T
  4. Coronary artery Anuerysms - T - approximately 20% develop CVS sequelae including coronary artery aneurysms
  5. Desquamation of the skin - T - erythema of palms and soles with desquamation (88%)
  6. Cataracts - F

KAWASAKI SYNDROME (MUCOCUTANEOUS LYMPH NODE SYNDROME) arteritis involving large, medium-sized, and small arteries (often the coronary arteries) associated with the mucocutaneous lymph node syndrome, usually in young children and infants (80% younger than 4 years old). The acute illness is manifested by fever, conjunctival and oral erythema and erosion, edema of the hands and feet, erythema of the palms and soles, a skin rash often with desquamation, and enlargement of cervical lymph nodes It is usually self-limited Epidemic in Japan, the disease has also been reported in Hawaii and increasingly in the United States Approximately 20% of patients develop cardiovascular sequelae, with a range of severity from asymptomatic vasculitis of the coronary arteries, coronary artery ectasia, or aneurysm formation to giant coronary artery aneurysms (7 to 8 mm) with rupture or thrombosis, myocardial infarction, or sudden death. Kawasaki syndrome is the leading cause of acquired heart disease in children in the United States Acute fatalities occur in approximately 1% of patients owing to coronary arteritis with superimposed thrombosis or ruptured coronary artery aneurysm. Pathologic changes outside the cardiovascular system are rarely significant. Although the vasculitis resembles that of polyarteritis nodosa, with necrosis and pronounced inflammation affecting the entire thickness of the vessel wall, fibrinoid necrosis is usually less prominent in Kawasaki syndrome