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Vascular Dan Flashcards

1
Q

How is ABPI performed?

How is it interpreted?

A

Systolic BP in ankle (highest of either DP or PT) ÷ systolic BP in arm (brachial arteries) while patient is in resting supine position for right and left
Normal 0.91 to 1.30
PVD at rest ≤ 0.9
Mild to mod PVD 0.41-0.90
Severe PVD ≤0.4
Falsely elevated ABI can occur in some limbs if vessels are very calcified and fail to compress - diabetes, arterioclerosis
Need ABPI >0.8 to undergo compression therapy

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2
Q

What is Thromboangitis Obliterans (Buergers disease)?

How is it treated?

A

Type of small vessel vasculitis affecting the upper limb and sometimes the lower limb
As names suggests there is thrombosis and luminal occlusion followed by fibrosis of vessels
Esp young men who are heavy smokers esp middle and Far East, and Indian subcontinent
Causes claudication, rest pain, red/cyanotic acral colour changes and can develop chronic painful paronychia or ischaemia esp of digits
Claudication in arch of foot is characteristic a sis intolerance to COLD
Mx
Essential to stop smoking
Bosentan can help
Vasc surgeon and physician

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3
Q

What is erythromelalgia?

what are key features and major types?

A

Episodic attacks of erythema and burning pain of extremety during which skin feels hot to touch
Attacks are precipitated by exercise or heat and are relieved by rapid cooling. Lasts from a few minutes to several hours and can become almost continuous
Cause unknown, some familial AD cases
Can be primary (idiopathic) or secondary
secodnary Dx due to thrombocythaemia is usually unilateral and may be relieved by aspirin
Other secondary types related to PVD or CTD eg SLE or rarely tiggered by drugs; Ca channel blockers, CsA

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4
Q

What are diagnostic criteria for erythromelalgia?

A

BARE Heat

  1. Burning pain in extremities
  2. pain Aggravated by warming
  3. pain Relieved by cooling
  4. Erythema of affected skin
  5. increased temperature of affected skin
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5
Q

What is the prognosis and management of erythromelalgia?

A

30% each: worsening, no change, improvement;
+ 10% complete resolution
No effective treatment and it gets worse with time.
Avoid exacerbating factors
Thrombocythaemia type may be relieved by aspirin + may give some relief in other types
Elevation to decrease oedema
Clopidogrel
Prostaglanding E infusion or oral misoprostol (prostaglandin E analogue)
Try propranolol, amitriptyline, gabapentin, SSRI’s

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6
Q

T/F

telangiectasia are new vessels

A

F

Dilations of pre-existing vessels without any new vessel growth

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7
Q

T/F

spider angiomas/naevi, angiokeratomas and angiomas and including cherry angiomas are all types of telangiectasia

A

T

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8
Q

What are the causes of Spider Telangiectasias?

How are they treated?

A

Idiopathic - common; 15% normal population esp kids
pregnancy (disappear after delivery) and OCP use
Liver disease
Rx
reassure - esp if pregnant (recur in later pregs)
treat cause if possible
Fine tip hyfrecator
Laser - PDL, KTP
2mm punch excise

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9
Q

What are causes of primary telangiectasia?

A 
AASONG
Ataxia telangiectasia
Angiomas, Angiokeratomas, Angioma serpiginosum
Spider naevi
Osler weber rondu (HHT)
Naevi; 
•	Naevus anaemicus
•	CMTC
Generalised essential telys and variants e.g. 
•	Unilateral naevoid telangiectasia
•	Hereditary benign telangiectasia
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10
Q

What are causes of secondary telangiectasia?

A 
EXTRACT and varicose veins
Environmental; - solar, XRT
XP
Trauma (scar)
Raynauds, Rosacea
Atrophy (TCS, poikiloderma), AIDS
CREST/Scleroderma/morphoea/LE*/Dermatomysoitis, Ca channel bockers
TMEP
* inc lupus erythematosis telangiectoides and rosacea-like lupus (both DLE variants)
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11
Q

What is solitary circumscribed angiokeratoma?

A

Small warty black papule on legs mainly (but can occur anywhere)
may be several
Result from trauma or chronic irritation of venule wall
Can be confused with melanoma

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12
Q

What is Angiokeratoma circumscriptum?

A

Plaque of multiple discrete coalescing papules, or hyperkeratotic papules and nodules that become confluent
Arise on trunk or limbs usually unilaterally in childhood
Resembles pseudokaposis sarcoma
Benign; cosmetic treatments

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13
Q

What is Angiokeratoma of Mibelli?

A

AD with variable penetrance
develop agminated region of flat or papular red angiokeratomas on dorsal/lateral aspects of fingers/toes (also dorsa of hands and feet and rarely elbows and knees)
onset age 10-15
May be chilblains and acrocyanosis

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14
Q

What are the associations of Angiokeratoma of Fordyce in men and women?

A

M
thrombophlebitis, varicoeles, inguinal hernias
F
vulvar varicosities, haemorrhoids, OCP’s or increased venous pressure in pregnancy

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15
Q

What conditions are associated with Angiokeratoma corporis diffusum?

A 
Fabry's most characteristically; XLR α-galactosidase A deficiency
Fucosidosis
Sialidosis
Galactosialidosis
Multiple others
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16
Q

What causes eruptive cherry angiomas?

A

assoc w/ lymphoproliferative disease eg multicentric Castleman’s disease

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17
Q

T/F

angiomas are more common in middle and old age but dissappear in extreme old age

A

T

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18
Q

What are venous lakes?

where do they occur?

A

Greatly dilated thin walled venules without proliferation of vascular tissue
Due to degeneration of supporting connective tissue
face, lips, and ears of elderly patients
Rx
Cryo - conatct freeze to empty with pressure
Hyfrecate
Laser - NdYAG preferred; can use diode, Alex, Ruby
Excision

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19
Q

What is Angioma serpiginosum?

A

Rare benign naevoid disorder
females (90%) in childhood
grouped areas or sheets of tiny angiomas
can be mistaked for petechiae but blanch (although not completely) and magnification shows vessels
lower limbs, buttocks; starts unilateral and often becomes bilateral
Can spontaneously resolve or persist
treat w/ vasc laser

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20
Q

What is Hereditary Haemorrhagic Telangiectasia (Osler-Rendu-Weber syndrome)?

A

AD disease causing telangiectasia, epsitaxis and visceral vascular malformations
2 types w/ different genes affected and slightly different risks;
HHT1 or endoglin gene (ENG) = higher risk of pulmonary and cerebral AVMs
HHT2 or activin receptor-like kinase 1 gene (ACVRL1) = higher risk of liver AVMs

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21
Q

What are diagnostic criteria for Hereditary Haemorrhagic Telangiectasia (Osler-Rendu-Weber syndrome)?

A

For definite diagnosis need all 3 of;
Epistaxis - onset around age 12
Telangiectasias - onset teens/after puberty
Visceral AV malformations
If 2 present is suspected diagnosis - highly likely if family history

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22
Q

What are features of the telys in HHT?

A 
Onset at/after puberty
anywhere but usually upper half of body esp face
Mucosa usually involved
Often lips, oral cavity, fingers, nose 
skin lesions rarly bleed
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23
Q

What is the management of pt with HHT/suspected HHT?

A

Hx
nose bleeds, tiredness/SOB(anameia), haemoptysis, cyanosis, malena, stroke
FHx - ?known HHT
consider other causes of telys
Ix and make referrals;
FBC – low Hb and haematocrit - microcytic/normocytic anemia in GIT AVMs
Fe studies – iron deficiency
FOB – positive in GIT AVMs
TTE(bubble study) – detect pulmonary AVMs which lead to right-to-left shunting
HRCT lungs, CXR
Brain MRI – cerebral AVMs
Upper endoscopy/capsule endoscopy
Colonoscopy
Doppler USS or CT liver – hepatic AVMs
Genetic testing
Mx
Education very important
PDL/IPL for telangiectasia
Iron for anaemia +/- RBC transfusions
Antibiotic prophylaxis for procedures with risk of bacteremia
Precautions to avoid air bubbles during IV cannulation
Avoid scuba diving
Be aware of epistaxis/internal bleeding- can be a big emergency!
Refer for lifelong screening program for pt and family to detect AVMs of brain or lung
Ca need liver Tx if sever liver disease
Disease does not usually shorten life; mortality

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24
Q

What are the main features of Ataxia telangiectasia?

A

Rare, AR mutation in ATM gene; AAATM
AR, Progressive cerebellar ataxia, low IgA
Telangiectases - face, conjunctivae>trunk>hand/ feeet
Marked susceptibility to cancer, particularly lymphoma and leukaemia
- Combined immunodeficiency w/ low IgA

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25
Apart from telys what skin findings are seen in Ataxia telangiectasia?
90% get Progeric changes of skin and hair - Grey hair, fat atrophy on face Granulomatous plaques on skin that ulcerate Nevoid hyper- and/or hypopigmentation (large segmental CALMs) Poikiloderma Eczematous dermatitis Seborrheic dermatitis KP Vitiligo Acanthosis nigricans
26
T/F | Pts with Ataxia telangiectasia should avoid ionizing radiation including medical imaging
T increased sensitivity to ionizing radiation and cancer risk keep scans to minimum and chose MRI if possible
27
What is cause of naevus anaemicus?
Congenital pale patch 5-10cm esp on trunk Within the patch the blood vessels are permanently vasosonstricted due to sensitivity to endogenous catecholamines May have islands of sparing within Histo normal
28
What is Generalized Essential Telangiectasia?
Large sheets of telangiectasias on limbs/body esp legs can be widespread or more localised starts in older children/young adults; F>M Lesions usually linear, but can have small angiomas Can have recurrent haemorrhages into skin and mucosa and eyes No associations R/o other telys syndromes eg. HHT, Angioma serpiginosum, benign hereditary telangiectasia, Unilateral naevoid telangiectasia syndrome
29
What is benign hereditary telangiectasia?
AD inherited pattern of telangiectasia vary variable clinical appearnce; onset in early childhood most often on sun=exposed sites Always asympmtomatic
30
What is Unilateral naevoid telangiectasia syndrome?
Rare Congenital or acquired syndrome Telangiectasia usually confined to trigeminal or upper cervical dermatomes and may follow lines of Blaschko most apparent when increaed Oe - preg, puberty, OCP, liver disease
31
T/F | Arteriovenous malformations are the most benign type of vascular malformations
F | most dangerous
32
what are the stages of change of AVMs?
Stage 1: Quiescent/dormant phase Stage 2: Progressive stage Stage 3: Destructive Stage 4: Cardiac decompensation
33
What can trigger an AVM to progress/worsen?
Puberty (75%), pregnancy (25% of women), and trauma | can push from stage 1 to stage 2
34
What is pseudo-kaposi’s sarcoma? | what are the triggers?
Acroangiodermatitis (of Mali) a chronic dermatosis triggered by various conditions which resuts in neovascularization and fibroblast proliferation Purpuric elsions wish coalesce into plaques esp on legs with a yellow-brown (ochre) colour + often eczema tous surface triggers; Chronic venous insufficiency vascular malformations such as klippel-trenaunay AVMs Paralysed limbs Can occur on amputation stumps
35
What are the DDs of Acroangiodermatitis?
Stasis dermatitis Schamberg’s disease/PPD Kaposi’s sarcoma Angiokeratoma circumscriptum
36
what vascular malformations are associated with | Klippel-Trenaunay syndrome ?
Capillary-venous (CVM) or capillary-lymphatic-venous malformation (CLVM) malformation sometimes described as a PWS low flow and has no arterial component CVM type tends to cause Pink-red blotchy stain in a haphazard distribution over the limb CVL
37
Whic blood abnormalities predispose to thrombosis?
``` Factor V Leiden mutation anticardiolopin, antiphospholipid, lupus anticoagulant antibodies antithrombin 3 deficiency protein C and S deficiency hyperhomocysteinaemia APC resistance methylene tetra-hydrofolate reductase gene mutation (MTHFR) Prothrombin gene mutation B12/folate deficiency ```
38
What are Thrombophlebitis migrans (migratory thrombophlebitis) Trousseau’s syndrome/ Trousseau’s sign of malignancy and Mondor’s disease?
All are recurrent episodes of thrombosis of the superficial veins; Cause crops of tender, linear or oval subcutaneous lumps/streaks Thrombophlebitis migrans can occurs at any site esp legs and abdomen; seen in Bechets disease should triger a seerahc fro malignancy and if found it may be called Trousseau’s syndrome/ Trousseau’s sign of malignancy Mondor's is a particular thrombophlebitis of the superficial chest veins seen mainly in women. Results in a fibrous inflamed cord which resolves in wks-months need to rule out breast cancer (12%)
39
What is Axillary Web Syndrome?
palpable cords that ‘bowstring’ across the axilla- creating ‘web of skin’ after mastectomy and lymphadenectomy for Ca breast usually resolve in 6months physio to keep movement range
40
T/F Corona phlebectatica paraplantaris with mild oedema represents stage 3 of the Widmer Classification of chronic venous insufficiency
F stage 1 this is lots of tortuous green-blue veins around the ankles stage 2 is Hyperpigmentation, lipodermatosclerosus, atrophie blanche, oedema, eczema stage 3 is a venous ulcer
41
T/F | Lipodermatosclerosus is pathognomonic of venous and lymphatic hypertension
T
42
What are the associations of atrophie blanche?
``` 40% people with chronic venous insufficiency Livedoid vasculopathy - characteristic of healing phase SLE scleroderma vasculitis cryoglobulinaemia polycythemia leukaemia ```
43
T/F | atrophie blanche is due to healed venous ulcers
F Due to obstruction of capillaries by thrombi and subsequent degeneration of surrounding matrix causing atrophic, ivory white depressed skin on the legs and surrounding brown discolouration But can also be caused by healing of vasculitic ulcers in Livedoid vasculopathy
44
What are the types of Livedoid vasculopathy?
Primary - no significnat venous disease or predisposition to thrombosis Secondary - chronic venous insufficiency - CTD eg SLE - thromobotic tendency e.g. factor V Leiden, hyperhomocysteinemia, antiphospholipid syndrome, altered fibrinolysis or platelet activation etc Should do CTD screen too
45
What is the appearance and course of Livedoid vasculopathy?
Mainly young-mid aged women Usually bilateral Can be livedo reticularis with Summer/Winter ulceration Multiple recurrent, punched out painful ulcers on the lower legs surrounding livedoid vasculitis clinically Ulcers heal slowly leaving atrophie blanche scars Rarely progresses to retiform purpura
46
What is the management of Livedoid vasculopathy?
Exclude other causes of ulcers and of livedo work up for venous disease and thrombophilias Treat cause if found Protect from trauma Debride slough, standard ulcer care Treat secondary infection if present Elevate legs Compression hosiery Stop smoking Antiplatelet agents - Aspin, dipyridamole Fibrinolytics – danazol, tPA (can work well then warfarinize) Anticoagulation – heparin, warfarin, rivaroxiban Anti-inflammatories – prednisolone, IVIg Pentoxifylline (alters blood viscosity and RBC flexibilty) Anabolic steroids – danazol, stanozolol
47
What are the classes of compression stockings? whta pressure do they suppply (mmHg)? what are the indications?
Class I 20-30 Simple varicose veins, mild oedema, leg fatigue, VTE prophylaxis Class II 30-40 Severe varicosities, moderate oedema, mod venous insufficiency, post sclerotherapy or thrombotic surgery Class III 40-50 Severe venous insufficiency, severe oedema, post thrombotic lymphoedema, established post-thrombotic limb Class IV 50-60 Severe lymphoedema, elephantiasis
48
Which surgical technique has the best outcome for varicose veins?
Phlebectomy (high tie and multiple stab avulsions) | Risks are DVT, neuralgia, haematoma, infection, phlebitis
49
What are the various methods to treat varicose veins?
``` Sclerotherapy - liquid sclerosant - foam sclerosant Endovascular laser or RFA Laser - Nd:YAG, Ruby, Alex, PDL IPL Surgery - Open high tie and Surgical stripping - SEPS (subfacial endoscopic perforator surgery) - Phlebectomy (high tie and MSA) ```
50
T/F | venous ulcers often begin on the foot
F v unusual medial gaiter area of leg most common
51
T/F | if an arterial ulcer does not respond to compression need to rethink the diagnosis
F | this is true of venous ulcers
52
What are the methods to debride chronic venous ulcers?
Sharp debridement (scalpel, scissors, curette) most rapid and precise Autolytic or enzymatic debridement (moisture-donating dressings or protease preparations) slow Vacum-assited closure (VAC) – topical negative pressure Maggots Ultrasonic debridement
53
T/F Surgical removal of superficial incompetent varicose veins in patients with normal deep veins doesn’t improve ulcer healing BUT significantly reduces incidence of ulcer recurrence
T
54
Outline Rutherfords classification of PVD
0 - Asymptomatic 1 - Mild claudication 2 - Moderate claudication 3 - Severe claudication 4 - Rest pain 5 - Ischemic ulceration not exceeding ulcer of digits of foot 6 - Severe ischaemic ulcers or frank gangrene
55
What is Martorell’s ulcer?
Hypertensive ulcer F>M Setting of poorly controlled longstanding HTN Heals with appropriate antihypertensive medications Usually bilateral esp on legs May be initiated by trauma Characteristically Pain disproportionate to the size of ulcer Small macular cyanotic lesion livid blue edge resolves when BP managed - also should modify other CVD risk factors
56
T/F | prolidase deficiency is a rare AR disorder which may present with chronic leg ulcers
T 50% pts have recurrent leg ulcers Skin fragility, purpura, bruising, and skin break down arises May have fine scarring, telangiectasias, and eczematous lesions Facies: hypertelorism with a saddle nose, mental retardation Can have dental caries, splenomegaly, hyperextensible ligaments, osteoporosis, respiratory infections, corneal opacities, amblyopia, optic atrophy
57
T/F | Rheumatoid ulcers usually start in the gaiter region
T
58
T/F | 'peau d’orange’ is a sign of subcutaneous oedema, pitting is a sign of dermal oedema
F | other way around
59
T/F | Primary lymphoedema always presents before age 35
F most cases present at or soon after puberty Of the rest; 10% present at birth 80% present before age 35 (lymphedema praecox) 10% present after age 35 (lymphedema tarda)
60
T/F regarding secondary lymphoedema; More common than primary Developed countries – cancer treatment is major cause Developing countries in tropical climates – infection dominates
T
61
What is Lymphedema-distichiasis syndrome?
A form of lymphoedema tarda (presents after age 35) AD mutation in FOXC2 (MFH-1) gene Distichiasis presents at birth or soon after (accessory eyelashes along posterior borders of lid margins in the position of the Meibomian glands); can led to corneal irritation, conjunctivitis, photophobia Lymphedema develops after puberty and up to 40s Others: ptosis, congenital heart defects, varicose veins
62
Which genetic or developmental conditions are associated with primary lymphoedema presenting in infancy?
``` Milroy's disease Turner's Noonan's Proteus Klippel-Trenaunay Maffuci's syndrome ```
63
What is Milroy's disease?
Milroy’s disease (primary congenital lymphedema) inactivating AD mutations in VEGFR-3 gene Failure of lymphangiogenesis Swelling confined to below knees Often brawny (no pitting) +/- hydrocele; superficial vein incompetence
64
What is Kaposi-Stemmer sign?
pathognomonic for lymphoedema; | cannot pinch skin at base of 2nd toe because too thick
65
T/F | chronic oedema that does not reduce significantly after overnight elevation is likely to be lymphatic in origin
T
66
What is Stewart-Treves syndrome?
lymphangiosarcoma developing from well-established post-mastectomy oedema but can occur in any region with chronic lymphedema
67
What causes Morbihan’s disease or solid facial oedema?
usually rosacea
68
T/F | calcium cahnnel blockers are a common cause of lymphoedema
T | 50% of pts prescribed them
69
What is Lipoedema?
Fatty, non-pitting swelling is confined to legs, thighs, hips and sometimes arms overlying triceps Almost always women Bilateral and symmetrical Tenderness and easy bruising Absence of pitting and lack of benefit from elevation Lack of improvement from weight loss (weight loss from other body sites but not from these) Treatment: liposuction at speacialist centre

Medical dermatology Dan (41 decks)

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