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PGY 5 > Miscellaneous: FMD, other aneurysms, AV malformation, peds, tumours > Flashcards

Miscellaneous: FMD, other aneurysms, AV malformation, peds, tumours Flashcards

1
Q

What vessels does fibromuscular dysplasia affect?

A

Most medium sized arteries - e.g. internal carotid and renals

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2
Q

What layer of the vessel does fibromuscular dysphasia affect?

A

Media

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3
Q

What is the prevalence of fibromuscular dysphasia?

A

Unknown

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4
Q

Who gets fibromuscular dysphasia? (Age, sex)

A

Young females

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5
Q

What is the theory for pathogenesis of fibromuscular dysplasia?

A

Ischemia of vasovasorum. Arteries affected are internal carotid, vertebral and renals that have long segments without branch points thus less vasovasora.

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6
Q

What is the definition of nutcracker syndrome?

A

Compression of left renal vein by SMA. Nutcracker syndrome = constellation of symptoms. NC phenomenon if asymptomatic.

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7
Q

What are risk factors of nutcracker syndrome?

A

Low BMI, young female

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8
Q

How can low BMI lead to nutcracker syndrome?

A

Paraspinal muscle wasting and low mesenteric/retroperitoneal fat means that SMA is at a more acute angle <16 degrees vs normal 35-40 degrees

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9
Q

What are the 3 anatomical types of nutcracker syndrome?

A

Anterior and posterior. Also “atypical” circumaortic renal vein or congenital malformations e.g. left IVC

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10
Q

What is posterior nutcracker syndrome

A

Usually with retroaortic vein, compression of left renal vein against vertebral body

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11
Q

What are symptoms of nutcracker syndrome?

A

Hematuria and left flank pain. Also genital varices, pain with menses/sex/urination, protienuria and abdo pain

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12
Q

What is the duplex criteria for nutcracker syndrome?

A

Flow velocities/diameter proximal and distal to stenosis ratio > 5

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13
Q

What is the most common open operation for nutcracker syndrome?

A

Renal vein transposition onto the IVC more caudally. Gonadal and adrenal veins often have to be ligated.

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14
Q

What are open options for anterior nutcracker syndrome?

A

Left renal vein transposition +/- patch or saphenous vein cuff. Gonadal vein transposition. Saphenous vein bypass from LRV to IVC.

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15
Q

What open operations can be used for both anterior and posterior nutcracker syndrome?

A

Gonadal vein transposition, saphenous vein bypass from LRV to IVC

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16
Q

What is the rate of migration for renal vein stenting?

A

7%. Can possibly migrate to right atrium and require open heart surgery!

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17
Q

What are the differences between hemangiomas and congenital malformations?

A

Hemangioma = tumour, grows rapidly, involutes by age 12, originates from proliferative endothelium

Congenital vascular malformations - inborn error, grow steadily in parallel with childs growth, never disappear or regress, quiescent endothelium

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18
Q

What are the 6 types of congenital malformations according to the Hamburg classification?

A

1-Arterial

2- Venous

3-Arteriovenous shunting

4-Lymphatic

5-Combined hemolymphatic

6-Capillary

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19
Q

What are the congenital vascular malformation embryologic subtypes?

A
  • Extratruncular:
    • infiltrating/diffus,
    • limited/localized
  • Truncular:
    • stenosis or obstruction (hypoplasia, aplasia, hyperplastia, membrane congenital spur),
    • dilation (localized = aneurysm, diffuse = ectasia)
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20
Q

What abnormality is depicted here?

A

Portwine stain - Klippel Trenaunay syndrome. Limb swelling and leg length discrepancy. Hemolymphatic malformation.

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21
Q

Who gets congenital vascular malformations more? Men or women?

A

1:1, M:F

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22
Q

What is the most common type of congenital vascular malformation?

A

Venous

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23
Q

What are 5 types of risk factors during pregnancy that are associated with congenital vascular malformations?

A

1) Exposure to chemicals
2) Infections: rubella, herpes, toxoplasmosis
3) Drugs: thalidomide, anticonvulsants, quinine
4) Rec Drugs: EtOH, Cocaine, smoking
5) Diseases: DM, thyroid disease, TB, hypoxia, lead/carbon monoxide

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24
Q

When do extratruncular congenital malformations arrest development?

A

Early embryonic life while vascular system is in the reticular stage.

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25
Q

What stmulates extratruncular CVMs to grow and proliferate?y,

A

Internal stimulation: menarche, pregnancy hormonal release

External: trauma, surgery

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26
Q

Why do extratruncular CVMs behave like an infiltrating process/invade surrounding structures?

A

Arrested growth in early embryonic life. Bones, muscle, soft tissue and blood vessels all originate from same mesoderm and no plane of partition between them.

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27
Q

What has a higher rate of recurrence - extratruncular or truncular CVM?

A

Extratruncular

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28
Q

What type of CVMs are associated with more serious hemodynamic consequences? Truncular or extratruncular?

A

Truncular

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29
Q

When do truncular CVMs arise?

A

Arrested development later, during vascular trunk formation stage when truncular lesions have lost the characteristics of mesenchymal cells. All appear as formed vessels with various degrees of development.

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30
Q

What are the differences between a vascular birthmark and capillary malformations?

A

1- Colour: CM = port wine, birthmark = pinkish

2- Location: CM = anywhere on body, birthmark = nuchal “stork bite” or face “angel’s kiss”

3- CM accompanied by other abnormal findings beneath the skin (e.g. CM of face = warning sign of intracranial CVM Sturge Weber Syndrome with ipsilateral ocular and leptomeningeal vascular malformation)

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31
Q

What is Sturge Weber syndrome?

A

Neurologic syndrome that presents as port wine stain of face. Ipsilateral ocular and leptomeningeal vascular malformation may result in seizures, increased pressure in the eye (glaucoma), developmental delays, and weakness on one side of the body

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32
Q

What type of CVM is this? Soft bluish swelling. Easily compressible. Enlarge with dependency/valsalva. Respond to compression therapy.

A

Venous

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33
Q

What type of CVM is this? Ischemic changes, distal gangrene, high output heart failure

A

Arteriovenous

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34
Q

What is the marginal vein?

A

An embryonic tissue remnant that fails to involute - usually on lower leg and looks like a large dilated lateral vein. Often heralds coexisting deep venous anomalies which should be investigated.

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35
Q

What is the name of the prominent vein on the back of this patients leg?

A

Marginal vein (embryonic remnant failed to involute). Parker weber syndrome.

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36
Q

What is transarterial lung perfusion scintigraphy (TLPS)?

A

A scan with radioisoptope tagged albumin microspheres to measure the percentage of blood shunted by AVMs. Can be used to detect microshunting common in Park weber syndrome

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37
Q

Which type of congenital vascular malformations need to be treated aggressively?

A

Extratruncular. They grow and will recur unless the lesion nidus is completely destroyed

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38
Q

Which type of congenital vascular malformations can be handled conservatively unless they become hemodynamically significant?

A

Truncular lesions. They lack the potential for proliferation.

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39
Q

What are 10 indications to treat extratruncular vascular malformations?

A

1-Hemorrhage

2-High output heart failure

3-Cosmetically deforming

4-Vascular bone syndrome

5-Near vital structures: airway, sight/eat/hear regions

6-Recurrent sepsis

7-Disabling pain

8-Lymph leak

9-High risk regions: hemartrhrosis, DVT, PE

10-Secondary ischemic complications

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40
Q

What is congenital vascular bone syndrome?

A

Long bone abnormal growth caused by congenital vascular malformation

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41
Q

What do congenital vascular malformations contribute to leg length descrepency to make the affected limb longer?

A

AV shunts cause arterial hypertrophy and hypervascularization of the bone

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42
Q

What do congenital vascular malformations contribute to leg length descrepency to make the affected limb shorter?

A

Bone compression from vascular mass or reduction of arterial inflow from arterial hypoplasia will cause bone shortening.

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43
Q

How does the marginal vein relate to congenital vascular bone syndrome?

A

It causes angio-osteo hypertrophy and limb overgrowth

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44
Q

What are 4 clinical features of Klippel Trenaunay Syndrome?

A

1-port wine stain localized to a small area

2-limb overgrowth/gigantism

3-large cluster of varicose veins

4-large lateral venous collector (Marginal Vein)

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45
Q

What type of congenital vascular malformations do Klippel Trenanay patients get? Arteriovenous, venous or lymphatic?

A

All KTS patients get venous, lymphatic and combined hemolymphatic

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46
Q

How do you treat the majority of Klippel Trenaunay Syndrome patients?

A

Compression stockings (35-45) and sclerotherapy

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47
Q
A
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48
Q

What is the difference between park weber syndrome and klippel trenaunay syndrome?

A

Very similar. PWS associated with arteriovenous malformations that require embolization in symptomatic patients.

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49
Q

What is “Localized Intravascular Coagulopathy”?

A

Extratruncular venous malformations associated with coagulopathy due to stasis of blood within abnormal structures

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50
Q

What are phleboliths?

A

Microthrombi from localized intravascular coagulopathy associated with venous malformation that take on a “stone like” structures that you can see on plain x-rays. May be an indication to anticoagulate.

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51
Q

Why do congenital malformation patients need to be followed life long?

A

Menarche, pregnancy, hormonal therapy, trauma, or surgery can trigger activity in previously quiet lesions and they can grow rapidly

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52
Q

What are “high flow” congenital vascular malformations?

A

arteriovenous fistulas

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53
Q

What are “low flow” congenital vascular malformations?

A

Venous, lymphatic, capillary

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54
Q

How do you treat capillary malformations for cosmesis?

A

Flashlamp pulse dye laser therapy

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55
Q

How are macrocystic lymphatic malformations treated differently from microcystic?

A
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56
Q

Name 3 signs and symptoms of large vessel vasculitis

A
  1. Bruit
  2. Asymmetrc BP
  3. Claudication
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57
Q

Name 5 signs and symptoms of medium vessel vasculitis

A
  1. Cutaneous nodules
  2. Livedo reticularis
  3. Digital gangrene
  4. Mononeuritis multiplex
  5. Renovascular HTN
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58
Q

Name 4 signs or symptoms of small vessel vasculitis

A
  1. Palpable purpura
  2. Pulmonary renal syndromes (glomerulonephritis, alveolar hemorrhage)
  3. urticarial skin rashes
  4. scleritis.
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59
Q

Name 2 large vessel vasculitis

A

“Giant Samurai”

  1. Giant cell arteritis
  2. Takayasu
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60
Q

Name 3 medium vessel vasculitis

A

“Obliterating your cow in a medium sized pan”

  1. Thromboangitis obliterans
  2. Kawasaki
  3. Polyarteritis Nodosa
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61
Q

Name 5 small vessel vasculitis

A

Small German men who Cryo

  1. Henoch Schonlen Purpura (IgA vasculitis)
  2. Wegners (Granulomatosis w Polyangitis)
  3. Cryoglobunimeic vascultis
  4. Churg Strauss (Eosinophilic granulomatosis w polyangitis)
  5. Microscopic polyangitis
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62
Q

Is giant cell arteritis more common in men or women?

A

Women (life time risk 1% for women, 0.5% for men)

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63
Q

What are the diagnostic criteria for giant cell arteritis?

A

3 of 5:

  1. Elevated ESR
  2. Age > 50
  3. Temporal abnormality (e.g. tenderness or decreased pulsation)
  4. New headache
  5. Abnormal biopsy (predominance of mononuclear cell infiltration or granulomatous inflammation with multinucleated giant cells)
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64
Q

What is the treatment for giant cell arteritis?

A

Give Cortocosteroids Always! (GCA)

IV methylprednisolone 1000 mg/day x 3 days if visual loss.

Otherwise 40-60 mg po daily.

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65
Q

What are classic CT findings of Ormond Disease (Idiopathic retroperitoneal fibrosis)?

A

Homogenous mass around the aorta following the iliac bifurcation with associated medial deviation of the mid part of the ureter and secondary hydronephrosis.

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66
Q

What are typical symptoms of Ormond Disease (idiopathic retroperitoneal fibrosis)?

A

Pain in lower back, abdomen, flank and scrotum

HTN

Systemic symptoms (fever, anorexia, malaise)

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67
Q

Which vasculitis is associated with a “hairy kidney”?

A

Erdheim Chester Disease

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68
Q

What feature distinguishes Erdheim Chester Disease from Ormond and IgG4 related systemic disease?

A

Bony lesions often of the lower extremeties that present with juxta-articular pain

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69
Q

What are the diagnostic criteria for polyarteritis nodosa?

A

3 of 10: ABCDEFGHI

  1. Arteriographic abnormality (aneurysms or occlusions, string of pearls)
  2. Biopsy of small or medium arteries showing polymorphic neutrophils.
  3. Cr or BUN elevated
  4. dBP > 90

5/6. Extremity pain (myalgia) incl. testicular pain

  1. Florid Livedo reticularis
  2. Gross weight loss > 4kg
  3. Hep B infection
  4. Impaired sensation (Mono or poly neuropathy)
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70
Q

Name 5 conditions that mimic polyarteritis nodosa

A
  1. Segmental arterial mediolysis (SAM)
  2. Pseudoxanthoma elasticum
  3. Neurofibromatosis
  4. Vascular type Ehlers Danlos (defect in Type 3 Collagen)
  5. Adenosine deaminase 2
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71
Q

What are arteriographic findings consistent with Thromboangiitis obliterans?

A

“Corkscrew collaterals” around areas of occlusion with normal proximal arteries without evidence of atherosclerosis or emboli

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72
Q

What are 2 histologic features of thromboangiitis obliterans that distinguishes it from other vasculitis?

A
  1. IEL is preserved
  2. Venulitis also often seen
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73
Q

What are treatments for thromboangiitis obliterans?

A
  1. Total cessation of all nicotine
  2. Calcium channel blockers
  3. IV iloprost
  4. Sympathectomy
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74
Q

What percentage of patients with thromboangiitis obliterans that continue to smoke require an amputation?

A

50%

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75
Q

Which vasculitis involves small vessels, associated with pANCA and associated with pulmonary renal syndrome?

A

Microscopic polyangitis

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76
Q

What is the diagnostic criteria for Eosinophilic Granulomatosis with Polyangiitis (Churg Strauss)

A

APE MEN (4 of these 6)

  1. A - asthma
  2. Paranasal sinusitis
  3. Eosinophilia
  4. Migratory pulmonary infiltrates on CXR
  5. Extravascular accumulation (e.g. nasal polyps)
  6. Neuropathy
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77
Q

What are clinical features of Bechets Disease (focus on vascular symptoms)?

A

BOOGIE PANTS

  1. Budd chiari
  2. Oral ulcers
  3. Ocular ulcers
  4. Genital ulcers
  5. Intracranial aneurysms
  6. Extremity aneurysms (popliteal/femoral/brachial/iliac)
  7. Pulmonary aneurysms - can have fatal hemoptysis
  8. Aortic aneurysm
  9. Neurologic symptoms
  10. Thrombosis of veins (mesenteric, hepatic, renal)
  11. Stomach/GI inflammation
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78
Q

What percentage of rheumatoid arthritis patients develop vasculitis?What percentage of rheumatoid arthritis patients develop vasculitis?

A

10-15%

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79
Q

Which vasculitis is a rare autoimmune disease manifested with recurrent inflammation of cartilaginous tissues? What vessels are involved?

A

Relapsing polychondritis, large-vessel (thoracic and AAA)

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80
Q

Which condition is an inherited systemic disease that can cause early and diffuse arteriopathy in absence of traditional risk factors?

A

Pseudoxanthoma Elasticum

81
Q

Which size vessels does pseudoxanthoma elasticum affect?

A

Small and medium

82
Q

How do patients with pseudoxanthoma elasticum present?

A

Lower extremity claudication

83
Q

How can you treat pseudoxanthoma elasticum patients with claudication?

A

Surgical bypass and angioplasty has been effective. NB higher risk of bleeding with antiplatelet and anticoagulation due to risk of arterial rupture in GI and GU tracts.

84
Q

What is the mechanism behind exercise related external iliac arteriopathy?

A

Usually in competitive cyclists. Repetitive bending and compression of EIA between psoas branch, circumflex iliac and internal epigastric arteries leads to vessel wall fibrosis, smooth muscle proliferation and intimal thickening.

85
Q

Name 4 different vasculitis mimics.

A
  1. Fibromuscular dysplasia
  2. Radiation arteritis
  3. Neurofibromatosis type 1
  4. Drug induced/hypersensitivity vasculitis
86
Q

Which vessels do Buerger’s disease/thromboangiitis obliterans primarily affect?

A

Small and medium sized infrapopliteal and infrabrachial arteries and veins

87
Q

Why did the 2012 Chapel Hill consensus guidelines remove thromboangiitis obliterans from list of vasculitides?

A

Absence of inflammation markers and antibodies makes TAO unique from other forms of vasculitis

88
Q

Which condition is characterized by segmental inflammatory cell infiltration of vessel wall and arterial or venous thrombotic occlusion. The thrombus formation tends to be hypercellular and the vessel wall architecture including the IEL is preserved.

A

Buerger’s (TAO)

89
Q

What is the diagnostic criteria for Buergers (5)

A

Diagnosis of exclusion. No universally accepted criteria.

Shionoya Criteria:

  1. smoking history
  2. age of onset < 50
  3. infrapopliteal arterial occlusive lesions
  4. either upper limb involvement or phlebitis migrans
  5. no other atherosclerotic risk factors.
90
Q

What is this image depicting? Which diagnosis is this a hallmark feature?

A

Corkscrew collateral (“dot sign”) - Buerger’s disease

91
Q

Which investigations should you order for Buerger’s patients?

A
  1. Vasc lab: BP/ABI/Toe pressures, tcPO2, arterial duplex, digital hypothermic challenge
  2. Angio: MRA/CTA or XA
  3. Labs (r/o other conditions): CBC Lytes, Bun Cr, Liver enzymes, Glc. ,
  • coags, thyroid, lipid profile, homocysteine, vit b12, coags: PTT, aPTT, protein C&S, ATIII, Factor V leiden, APLA, ACLA,
  • autoimmune: ESR, CRP, ANCA, RF, ANA, cryoglbulins
  • serologic markers for CREST
  • Hep B&C serology
  • Tox screen: cocaine, amphetamine, cannabis
  1. Exclude embolic sources: echo, tele, abdo ultrasound, angio
  2. Consider biopsy if unusual features (e.g. age > 50)
92
Q

What are 5 angiographic findings in Buerger’s disease?

A
  1. Small and medium sized arteries, digital arteries
  2. Segmental occlusive lesions (normal appearing segmeets interspersed)
  3. More severe distally
  4. Tapering or abrupt occlusion with corkscrew collateral around occlusion
  5. Normal proximal arteries (no aneurysms, atherosclerosis or sources of emboli)
93
Q

What is the rate of major amputation with Buerger’s disease at 5, 10 ad 20 years? If you stop smoking, how long until risk of amputation is eliminated?

A

5 years - 10%

10 years - 20%

20 years - 23%

Risk eliminated after 8 years of no smoking

94
Q

Name 8 pharmcologic treatments for Buerger’s. Do they work?

A
  1. Calcium channel blockers - no evidence written in chapter

2. Prostacyclin - iloprost infusion showed better ulcer healing and relief of ischemic rest pain compared with ASA

  1. Prostaglandin E1 - limaprost - no significant difference
  2. Phophodiesterase inhibitors: cilastozol (PDE-3), viagra (PDE-5) - few reported cases showing some benefit
  3. Endothelin receptor antagonists - RCTs still needed
  4. Thrombolytics - high bleeding rate, RCT needed
  5. Folate - no difference in amputation rate
  6. Statins - RCT needed
95
Q

Do men or women typically get Takayasu’s? Old or young?

A

Young women - often of childbearing age

96
Q

Which layers of the vessel wall are affected by Takayasu’s?

A

Panarteritis affecting all 3 layers

97
Q

SLE diagnostic criteria?

A

PRUNE RASH (4 of 11)

  1. Photosensitivity
  2. and 3. Rashes (ie, 2. Discoid rash; 3. Malar rash)
  3. Ulcers in mouth
  4. Neurologic (ie, seizures, psychosis)
  5. and 7. Elevated blood tests (ie, 6. raised antinuclear antibody; 7. positive SLE cells seen, positive anti-double-stranded DNA antibody, positive antismooth muscle antibody, false-positive VDRL test)
  6. Renal (ie, proteinuria, hematuria, cellular casts)
  7. Arthritis (non-erosive)
  8. Serositis (ie, pleuritis, pericarditis, peritonitis)
  9. Hematologic (ie, hemolytic anemia, leukopenia, thrombocytopenia)
98
Q

Which condition is this CTA depicting?

A

Takayasu’s arteritis - skip lesion with inflammation of aortic wall (low attenuation ring)

99
Q

How is Takayasu’s classified?

A

6 types (1994 Tokyo Conference)

  1. Aorotic branches
    2a. Aortic arch + branches
    2b. Aortic arch + branches + thoracic aorta
  2. Descending thoracic and abdo aorta + branches
  3. Abdo aorta + branches
  4. Entire aorta + branches

Add C or P for coronary or pulmonary involvement

100
Q

What is the first line treatment for Takayasu’s?

A

Glucococorticoids - oral can be started. Many will relapse and require additional agents (cyclophosphamide, azathioprine, methotrexate, or mycophenolate mofetil).

101
Q

Name 7 indications for surgical revascularization for Takayasu’s

A
  1. HTN due to renal artery stenosis
  2. Lifestyle limiting claudication
  3. Cerebral ischemia or > 70% symptomatic stenosis of cerebral vessels
  4. Moderate aortic regurg
  5. Cardiac ischemia with coronary artery stenosis
  6. Severe aortic coarctation
  7. Progressive aneurysmal enlargement and dissecting aneurysm
102
Q

What is the locus for marfans syndrome? What mutation? What is its genetic transmission pattern?

A

Locus: 15q21.1

Mutation: FNB1

Autosomal dominant with complete penetrance

103
Q

How do Marfan’s patients die?

A

Cardiovascular mortality ~90%. Aortic root aneurysm risks life threatening aortic dissection and rupture. Advances in surgery has returned life expectancy of marfans to near normal (before ~37 years).

104
Q

Which condition is associated with aortic root aneurysm?

A

Marfan’s

105
Q

What are 7 features of Marfan’s syndrome?

A

Mitral prolapse

Aortic root dilatation/dissection

Retinal detachment

Fibrillin abnormality

Arachnodactyly

pNeumothorax/blebs

Skeletal abnormalities

106
Q

Name 4 differential diagnoses for Marfans

A

Other conditions associated with FBN1 mutations:

  1. MASS phenotype - usually meets 1 but not other Ghent criteria for Marfan’s
  2. Shprintzen-Goldberg syndrome - more phenotypic heterogeneity. Still associated with aortic root enlargement but also mental retardation.
  3. Homocystinuria - also have mental retardation, history of VTE, and CAD
  4. Congenital contractural arachnodactyly - shares skeletal features with Marfans but no ocular or cardiovascular manifestations
107
Q

How do you survey Marfans patients?

A

Life long optholomagy, cardiology and orthopedic assessments. Lifelong transthoracic echo monitoring.

108
Q

When should you surgically intervene on Marfans?

A

Children: >1cm growth per year or 2-3 SD above nomogram “z score”

Adults: >50 mm

109
Q

How do you medically manage Marfans?

A

Avoid burst exercise (sprinting, weightlifting etc)

B-blockers or Losartan equally effective.

110
Q

Which type of ehlers danlos is vascular subtype? How is it inherited?

A

4, autosomal dominant

111
Q

Which mutation do vascular Ehlers Danlos patients have? What does it code for?

A

COL3A1 gene, which codes for type 3 procollagen. The abnormal type 3 collagen molecule cannot fold into a triple helix, and is slowly degraded. “protein suicide”.

112
Q

What are the 9 minor diagnostic criteria for Vascular EHDS?

A

CHEAT FANG:

  1. Club foot
  2. Hypermobility of small joints
  3. Early onset varicose veins
  4. AV carotid-cavernous fistula
  5. Tendon/muscle rupture
  6. Family history (suddent death in one or more close relatives)
  7. Acrogeria (taut thin skin)
  8. pNeumothorax
  9. Gingival recessession
113
Q

What are the 4 major diagnostic criteria for Vascular EHDS?

A

FABS:

  1. Facial characteristic appearance (thin delicate nose, thin lips, hollow cheeks)
  2. Arterial/uterine/GI rupture
  3. Bruising
  4. Skin thin/translucency
114
Q

How can you confirm the diagnosis of ED IV?

A
  1. Collagen testing - structurally abnormal collagen 3
  2. Serum/blood testing of COL3A1 gene
115
Q

Where do ruptures and dissections of ED IV patients occur? What about Marfan’s?

A

ED IV = medium sized vessels

Marfan’s = aorta

116
Q

Name 3 differentials for ED IV?

A

Disorders of bruisability and woundhealing e.g. “battered child”

  1. Von Willebrand’s disease
  2. Platelet disorders
  3. Scurvy
117
Q

How can you mitigate the risk of suture line bleeding when repairing ED IV vessels?

A
  1. Felt pleged
  2. Bioglue
118
Q

Name 2 non-vascular but common complications of ED IV

A
  1. GI perforation - 25% of all ED IV complications. Sigmoid colon most common location
  2. Uterine and pregnancy related complications.
119
Q

What medical treatment options are available for ED IV?

A
  1. Celiprolol (controversial study) - 5 year decreased risk of rupture from 50% to 20%
  2. Factor 7 transfusion for spontaneous abdo bleed
120
Q

What 3 features are associated with Loeys Dietz, “classic triad”?

A
  1. Aortic aneurysm/vascular tortuosity
  2. Craniofacial abnormality - bifid uvula or cleft palate
  3. Hypertelorism
121
Q

How many types of Loeys Dietz are there?

A
  1. Severe craniofacial and aortic aneurysms
  2. Less severe craniofacial (only a bifid uvula or high palate) and aortic aneurysms
  3. Aneurysms and early osteoarthritis
  4. Aneurysm of aorta and cerebral tortuoustiy - aortic root can dissect or rupture at small diameter in childhood unlike EDSIV and Marfan’s
122
Q

What type of LDS dies earliest?

A

Type 1 - 23 years old (type 2 = 32, other types later onset)

123
Q

What type of connective tissue disorder is associated with ectopia lentis

A

Lens dislocation - Marfan’s

124
Q

When should aneurysms of the thoracoabdominal and infrarenal aorta be repaired prophlyactically in LDS patients?

A

4 cm +.

Lower threshold compared with EDS IV because tissue fragility are dramatically more fragile in EDS IV. Loeys Dietz has much better tissue handling and can make better anastomoses.

125
Q

What is the conservative/medical management of Loeys Dietz patients?

A
  1. Beta blockade
  2. Avoid “burst” activities

Similar to Marfan’s. No RCT data to support initiating Losartan.

126
Q

What is the difference between primary and secondary Raynaud’s phenomenon?

Which is more common?

What is Raynaud’s disease?

A

Primary - idiopathic

Secondary - associated with an underlying disease like rheumatoid arthritis, systemic sclerosis

Primary more common.

Raynaud’s disease = old nomenclature

127
Q

What is the “hunting response”?

A

Maximum vasoconstriction in responce to cold happens at 10-20 degrees Celsius. Beyond that there is a rhythmic fluctuation in finger flow caused by periods f vasoconstriction and vasodilation q 30s to 2 mins. The cold induced dilation protects the fingers from freezing in a cold environment and is impaired in secondary Raynaud’s phenomenon because of occlusive arterial disease.

128
Q

What are medical treatment options for Raynauds (5)?

A
  1. Calcium channel blockers (nifidepine)
  2. Prostaglandins (prostacyclins, iloprost)
  3. Alpha adrenergic blockers (prazosin)
  4. PDE5 inhibitors (sildenafil)
  5. Endothelin inhibitors (bosentan)
  6. Others: fluoxetine, ACE, nitrates, ARB (losartan)
129
Q

Name 6 surgical/invasive therapies for Raynaud’s phenomenon.

A
  1. Botox
  2. Sympathetic block
  3. Thoracoscopic sympathectomy
  4. Lumbar sympathectomy
  5. Digital sympathectomy
  6. Spinal cord stimulators.
130
Q

Which renal artery is more affected in FMD - right or left? Any theories as to why?

A

Right - it’s longer.

Theory that FMD may be caused by vessel wall ischemia due to vasa vasora damage because it happens in long vessels away from branch points which are prone to stretching and further away from where vasa vasorum originate. Right is longer than left renal artery.

131
Q

Name 4 differential diagnoses for FMD and distincitive features that separate them?

A
  1. Neurofibromatosis-1: characteristic skin lesions
  2. ED IV: acrogeric dysmorphism, skin elasticity, distal joint laxity
  3. Williams syndrome: facial dysmorphism, supraaortic stenosis, behaviour
  4. Vasculitis: FMD is not inflammatory and has no associated increase in acute phase reactnatns, anemia, or thrombocytopenia
132
Q

How is FMD classified?

A
  1. Angiographically: multifocal - “string of beads” or focal
  2. Histologically: intimal, medial or adventitial - not used as frequently since FMD patients undergo less surgery
133
Q

When should you investigate for secondary causes of hypertension? 7 indications

A
  1. > 3 antihypertensive agents
  2. Flash pulmonary edema
  3. Suddem acceleration of serum Cr
  4. Spontaneous hypokalemia
  5. Bruit
  6. Young < 50 yrs
  7. Worsening of previously well controlled hypertension
134
Q

What is a hemodynamically significant renal artery stenosis?

A
  1. Pressure gradient > 10 mm Hg
  2. Renal to aortic pressure ratio < 0.9
135
Q

What is the treatment of choice for FMD patients with uncontrollable hypertension due to renovascular hypertension?

A

Balloon angioplasty for renal vessels. Stenting is usually not required. Vessels respond well to angioplasty because the septae are broken. Also patients are young.

136
Q

How are aortorenal bypasses approached (type of incision)?

A

Transverse subcostal - kidney can be exposed retroperitoneally or transperitoneally depending on extent of aorta needed to be exposed.

137
Q

At what size should renal artery aneurysms be excluded/treated in patients with FMD?

138
Q

What is the treatment of choice for carotid FMD?

A

PTA with flow reversal for distal protection. Stenting not ideal because of kinked arteries. Also difficult to find landing zone for other distal embolic protection devices.

139
Q

What are the 2 most common causes of popliteal artery disease that is not atherosclerotic?

A
  1. Popliteal entrapment
  2. Adventitial cystic disease
140
Q

What are the 6 types of popliteal entrapment syndrome?

A
  1. Popliteal completes development before migration of medial head of gastroc. Gastroc is situated normally but pushes popliteal artery medially.
  2. Popliteal artery is displaced medially because the medial head of gastroc has an abnormal insertion site on the femoral condyle.
  3. Abnormal muscle slip or fibrous band from either medial or lateral femoral condyle
  4. Persistence of axial artery as the mature distal popliteal artery - remains in its embryologic position deep to the popliteus.
  5. Both popliteal artery and vein are entrapped by any of the type 1-4
  6. Anatomic variant not known, possible gastroc hypertrophy
141
Q

Name 7 non-atherosclerotic causes of peripheral artery disease

A
  1. Popliteal entrapment
  2. Adventitial cystic
  3. Iliac artery endofibrosis
  4. Fibromuscular dysplasia
  5. Buerger’s disease
  6. Vasculitis (Takayasu, Giant Cell Arteritis, Behcets)
  7. Chronic exertional compartment syndrome
142
Q

How can you tell angiographically between popliteal entrapment syndrome and popliteal adventitial cystic disease?

A

Adventitial cystic disease popliteal stenosis should be visible when foot in a neutral position. Provacative maneuvers should unmask a popliteal entrapment.

143
Q

Which types of popliteal entrapment are best approached from a medial vs. posterior approach?

A

Medial - I and II

Posterior - III and IV

144
Q

When should you replace the popliteal artery vs. just release muscle/fibrous bands in popliteal entrapment syndrome?

A

Abnormal artery:

  • PSV 250-275
  • Velocity ration > 2
  • Occluded
  • Stenoses
  • Post steotic dilatation/aneurysm
145
Q

Name 4 classes of infected aneurysms

A
  1. Microbial arteritis - noncardiac source bacteremia or local spread
  2. Septic emboli
  3. Post-traumatic (e.g. illicit drugs)
  4. Bacteremia of pre-existing atheroscerlotic aneurysm
146
Q

Name 5 ways of dealing with an infected femoral pseudoaneurysm

A
  1. Ligate & wide debridement (illicit drug use can ligate the femoral if SFA/profunda intact, test occlusion and see if you maintain a pedal doppler signal first)
  2. In-situ reconstruction with vein or cryopreserved allograft and sartorius muscle flap
  3. Obturator bypass
  4. Latera femoral bypass from external to distal SFA
  5. Axillary to distal SFA bypass.
147
Q

Name 8 conditions associated with secondary Raynauds

A

COLD HAND

  1. Cancer: multiple myeloma, leukemia
  2. Occupational: hypothenar hammer, vibration
  3. Lupus and other connective tissue diseases: scleroderma, rheum arthritis, Sjogrens
  4. Drugs: vasopressors, cocaine, ergot
  5. Hematologic: polycythemia rubra vera, thrombocytosis
  6. Arterial: TAO, atherosclerosis, GCA
  7. Nasty infections: Hep B & C
  8. Diabetes
148
Q

Why do you need to exercise caution in administering ASA to children?

A

Potential for Reye syndrome - a rapidly progressing encephalopathy

149
Q

Name 6 causes for pediatric aneurysms

A
  1. Infection
  2. Aortitis - takayasu
  3. Arteritis - Behcet, SLE, kawasaki, PAN
  4. Genetic - EDIV, LDS, Tuberous sclerosis, Marfans
  5. Developmental/idiopathic
  6. Traumatic
150
Q

Name 4 major types of pediatric vascular tumours

A
  1. Infantile hemangioma
  2. Congenital hemangioma
  3. Kaposiform hemangioendothelioma
  4. Pyogenic granuloma
151
Q

What anomalies can lower body infantile hemangiomas be associated with?

A

LUMBAR

  1. Lumbar/spinal
  2. Urogenital

3, Myelopathy

  1. Bone deformities
  2. Anorectal/arterial anomalies
  3. Renal
152
Q

What anomalies can a facial infantile hemangioma be associated with?

A

PHACES syndrome

  1. Posterior fossa brain malformation
  2. Hemangioma
  3. Arterial abnormalities
  4. Coarctation of aorta/Cardiac deficits
  5. Eye abnormalities
  6. Sternal clefting, supraimbulical raphe
153
Q

What is the difference between a congenital hemangioma and infantile hemangioma?

A

Congenital hemangiomas are fully formed at birth and does not have the postnatal growth seen in infantile hemangioma

154
Q

What is the hallmark histopathologic feature of infantile hemangiomas?

A

GLUT-1 positivity

155
Q

How do you treat infantile hemangiomas that cannot be treated with observation alone or with topical agents?

A

Propanolol. Systemic steroids are given if patients cannot tolerate or have a contraindication to beta blockers.

156
Q

Name the Neves and Zincke classification of this tumour thrombus

A

Level 3 - retrohepatic but still below the diaphragm without extension into the right atrium

157
Q

Name the Neves and Zincke classification of this tumour thrombus

A

Level 2 - cephalad extent is more than 2 cm above the left renal vein but still infrahepatic

158
Q

Name the Neves and Zincke classification of this tumour thrombus

A

Level 1 - cephalad extent is confined to less than 2 cm above the left renal vein

159
Q

During an “en bloc ” resection of a colon cancer fecal contamination occurs and the IVC is resected 5 cm longitudinally and 50% circumferentially. List 5 ways to repair the IVC:

A
  1. Lateral venorapphy with 3-0 or 4-0 Prolene if less than 50% stenosis
  2. Patch repair (saphenous; prosthetic if no contamination). Patch repair preferred over interposition graft
  3. Interposition graft (deep femoral vein or spiral saphenous vein graft; 16 mm PTFE if no fecal contamination)
  4. Ligation of infrarenal IVC (unstable patient with severe injuries or when repair produces major stenosis or cancer patients with chronically obstructed IVC and developed collaterals)
  5. Reconstruction of IVC with cuff of abdominal aorta and subsequent aortic reconstruction with ax-fem graft or rifampin coated graft (if no fecal contamination then regular Dacron tube graft repair)
160
Q

Why should you reimplant the renal vein when doing IVC reconstruction/interposition grafting?

A

Maintains patency of IVC. (Usually doesn’t affect renal function that much).

161
Q

What are 2 methods to improve IVC reconstruction patency?

A

1) Renal vein reimplantation
2) Create AV fistulas (renal art/vein, SFA/GSV, renal art/gonadal vein)

162
Q

When performing IVC reconstructions - which patients should you consider creating an AV fistula in?

A

High risk of graft thrombosis:

1) Infrarenal IVC (lower flow than suprarenal)
2) Long grafts/multilevel IVC recon
3) Small diameter grafts < 16 mm in diameter

163
Q

When do you need to use veno-venous bypass for IVC reconstructions? (5)

A
  1. Pt unable to tolerate IVC clamping due to tenuous cardiopulmonary status or old age
  2. Level 3 extension of tumour thrombous
  3. Complex multilevel IVC involvement
  4. Need full graft replacement
  5. Adequate oncologic resection cannnot be achieved without bypass support
164
Q

If you plan to embolize a splenic artery aneurysm, which vaccines do you need to give patients?

A
  1. Pneumococcal
  2. Meningococcal
  3. Hemophilus influenza B
165
Q

When repairing splanchnic aneurysms open, when can you ligate the celiac and common hepatic artery (what needs to be open for collaterals?)

A

Gastroduodenal artery, pancreaticoduodenal arteries, portal vein

166
Q

When ligating vessels for a hepatic artery aneurysm, when do you also need to perform a cholecystectomy?

A

If the proper or right hepatic artery is ligated, a cholecystectomy should also be performed

167
Q

What type of vascular injury is associated with pediatric fall on outstretched hand?

A

Brachial artery injury in context of supracondylar fracture

168
Q

How should you manage pediatric patients with a pulseless pink hand?

A

Controversial - Rutherford’s authors recommend exploring in stable patients and repair vessel as needed

169
Q

What are the KDOQI guidelienes for when to place permanent HD access in pediatric patients?

A

KDOQI guidelines recommend placeing permanent HD access in all patients aged 0 to 19 who are greater than 20 kg and are not expected to receive a kidney transplant within 1 year

170
Q

What are the 4 most common causes of ESRD in pediatric patients?

A
  1. Glomerular sclerosis
  2. Renal hypoplasia/dysplasia
  3. Congenital obstructive uropathies
  4. Lupus nephritis
171
Q

What is the difference between chronic regional pain syndrome type 1 and type 2?

A

CRPS type II is distinguished by evidence of peripheral nerve injury.

172
Q

Name 5 major theories about the pathogenesis of chronic regional pain syndrome

A
  1. Exaggerated inflammatory response - inflammatory mediators TNF-a and IL-6 are elevated in affected limbs. Red/hot/swollen affected limb are all signs of inflammation. Some benefit of IVIG.
  2. Sympathetically mediated syndrome
  3. Limb ischemia and reperfusion injury
  4. Central sensitization theory
  5. Secondary to nerve damage
  6. Autoimmune disorder
  7. Cortical reorganization theory
173
Q

Name the Stanton Hicks diagnostic criteria for complex regional pain syndrome

A
  1. Clinical symptoms:
  • burning, hyperpathia, allodynia
  • Temperature or color changes edema
  • Hair or nail growth changes
  1. Laboratory results
  • Thermometry or thermography bone radiography
  • 3 phase bone scan quantitative sweat test response to sympathetic block

Interpretation: > 6 reflex sympathetic dystrophy probable, 3-5 RSD possible, <3 RSD unlikely

174
Q

Name the Budapest clinical diagnostic criteria for complex regional pain syndrome

A

1. Ongoing pain out of proportion to inciting event

2. 1 symptom in 3/4 categories:

i) vasomotor: tempreature asymmetry/skin colour
ii) sensory: hyperesthesia, allodynia
iii) Motor/trophic
iv) Sudomotor/edema

3. One sign in 2+ categories:

i) vasomotor: temp asymmery
ii) sensory: hyperalgesia to pin prick and/or allodynia to light touch
iii) motor/trophic: decreased ROM or motor dysfunction or trophic changes
iv) Sudomotor/edema

4. No other diagnosis better explains signs/symptoms

175
Q

A 3 phase bone scan with accelerated blood flow in the disease limb combined with increased diffuse activity during the blood-pool phase and increased periartericular uptake in the delayed statis phase is pathognomonic for which condition?

A

Chronic regional pain syndrome. However a meta-analysis states bone scans have a sensitivity of 50% therefore many believe are not accurate for diagnosing CRPS.

176
Q

Name 9 medications that can be used in the treatment of chronic regional pain syndrome

A
  1. Opoids
  2. Tricyclic antidepressants
  3. GABA agonists (e.g. gabapentin)
  4. Alpha adrenergic blocking agents (e.g. IV phentolamine)
  5. Beta blockers - propanolol
  6. Calcium channel blockers
  7. Bisphosphonates
  8. NSAID
  9. Steroids
177
Q

What is the timeline and treatment for stage 3 chronic regional pain syndrome?

A

Timeline: >6 months

Treatment recommendation:

  1. Steroid therapy or sympathetic blockade should be considered but may be unsuccessful.
  2. Neuromodulation (e.g. spinal cord stimulation) may be used.
  3. Manipulation of joint contractures under general anesthesia
  4. Antidepressants
  5. Vocational guidance
178
Q

What is the timeline and treatment for stage 2 chronic regional pain syndrome?

A

Timeline: 3-6 months

Treatment recommendation:

  1. Physical therapy, TENS and steroids combined.
  2. If fails, consider sympathetic blockade and surgical sympathectomy
179
Q

What is the timeline and treatment for stage 1 chronic regional pain syndrome?

A

Timeline: 0-3 months

Treatment recommendation:

  1. Physical therapy +/- TENS.
  2. Local nerve or sympathetic block for patients w severe pain unable to undergo PT.
  3. If fails: give steroids.
180
Q

What are the indications for cervicothoracic sympathectomy?

A
  1. Essential hyperhidrosis
  2. Selected cases of hand ischemia
  3. Complex regional pain syndrome
  4. Clinically refractory long QT syndrome
  5. Rare cases of Raynaud syndrome
181
Q

What are the indications for a lumbar sympathectomy?

A
  1. Essential plantar hyperhidrosis
  2. Selected cases of chronic critical leg ischemia with no conditions or revascularization options
182
Q

What are the denervation level(s) for: Long QT syndrome

A

Stellate ganglion, G2 and G3

183
Q

What are the denervation level(s) for: Raynaud syndrome

A

Stellate ganglion, G2 and G3

184
Q

What are the denervation level(s) for: Vascular disease

A

Stellate ganglion, G2 and G3

185
Q

What are the denervation level(s) for: Complex regional pain syndrome?

A

Stellate ganglion, G2 and G3

186
Q

What are the denervation level(s) for: plantar hyperhidrosis?

187
Q

What are the denervation level(s) for: facial rubor?

188
Q

What are the denervation level(s) for: craniofacial hyperhidrosis?

189
Q

What are the denervation level(s) for: axillary hyperhidrosis?

190
Q

What are the denervation level(s) for: palmar hyperhidrosis?

191
Q

Name 6 rare (< 1%) causes of complications associated with thoracoscopic sympathectomy

A
  1. Horner syndrome
  2. Hemothorax
  3. Pleural effusions
  4. Injury to vagus nerve
  5. Injury to phrenic nerve
  6. Injury to subclavian artery and vein
192
Q

Name 4 common causes of complications associated with thoracoscopic sympathectomy

A
  1. Compensatory sweating 70-100%
  2. Segmental atelectasis 1-5%
  3. Pneumothorax 1-5%
  4. Subcutaneous emphysema 1-2%
193
Q

What are 3 causes of failure of thoracic sympathectomy?

A
  1. Incomplete denervation
  2. Functional reorganization (collateral nerve sprouting)
  3. Regeneration of new fibers from the ganglion cell
194
Q

Name 7 secondary IVC tumours that may have tumour thrombus

195
Q

Name 7 secondary IVC tumours

196
Q

Name 7 secondary SVC tumours

197
Q

What is the most common primary tumour of the IVC?

A

Primary leiomyosarcoma

198
Q

If you are resecting an IVC tumour and planning to patch angioplasty, how large should the diameter of your patch be?

A

D x 3 x % of caval wall to be replaced

E.g. IVC 20 mm with 50% resected - 20 x .5 x 3 = 30 mm

PGY 5 (25 decks)

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