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Surgery > Vascular > Flashcards

Vascular Flashcards

1
Q

whats peripheral arterial disease

A

narrowing of arteries that supply the limbs and peripheries so reducing the blood supply to these areas

usually refers to the lower limbs that results in claudication symtpoms

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2
Q

what is included in peripheral arterial disease

A

intermittent claudication
critical liumb ischemia= end stage of peripheral arterial disease
acute limb ischmia = like an mi where clot stuck and ishcmeia acutely

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3
Q

whats intermittent claudication and s and s

A

symotom of ichemia in a limb
athleroscleoriss in the limb and so not enough blood supply to the limb on exertion
occurs on exertion and relived by rest
crampy achy pain
calf, buttocks, thighs

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4
Q

whats critical limb ischemia

A

end stage of peripheral arterial disease
have inadequate blood supply to limb to allow it to function normally even at rest
pain at rest- burning pain worse at nigh (no gravity to help)
ulcers that dont heal
gangrene
6ps:
pain
pallor
perishingly cold
pulsless parlysis
paraestheisa

have sign risk of loosing a limb

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5
Q

what acute limb ischemia

A

due to peripheral arterial disease
have a rapid onset of ischemia in a limb
typically due to a thombus - clot - blocking the arterial supplying distal lumb

like a thrombus blocking a coronary artery causing MI

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6
Q

whats atheleroscleorisis and the end results of athelroscleorisis

A

fatty depsits in arterial walls
medium- large arteries
get hardening and stiffening of blood vessel
casued by chroninc inflammatio and acitvation of immune system and depisots of lipids casuing a fibrous atherloscelrotic plaque

plaques cause:
stiffenng => ht, strain on heart
stenoiss => reduced blood flow- angina
plaque rupture=> thrombus block distal vessel= acs

resutls in
angina
MI
TIA
stroke
peripheral arterial disease
chronic mesenteric ischemia

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7
Q

risk factors atherloscleorisis

A

non modifiable= male, age, fam hist

modifiable=
obestiy
smoking
alcohol
sedentary-no exercise
diet- high fats low veg
stress
poor sleep

medical co morbitis increase risk of getting athelroscletisis if not managed well
hypertesnion
CKD
inflammatory conditions =RA
diabtetes
atypical antipsycotic medication

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8
Q

pt has claducation in thigh/buttock
male impotence
absent femoral pulse

A

leriche syndrome =
occulsion of dital arota/proximal common iliac artery

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9
Q

signs of periheral arterial disease

A

look for risk factors (atherloesclorisis risk factors cus this casues peripheral arterial disease) :
tar staining
xanthomata
cvd:
missing limb/digit already
midline sternomty - cabg
scar on calf- cabg
wakenss- stroke

signs of PAD:

weak peirpheral pulses - use hand hel[ doppler to asess properly
hair loss
cyanosisi
pallor
ulcers
dependent rubor - deep red limb whe. below body
poor wound healing
muscle wasting
gangrene

low skin temp
prlonged capillary refil time
changes in beurgers test
decreased snesation

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10
Q

whats beurgers test

A

Buerger’s test is used to assess for peripheral arterial disease in the leg. There are two parts to the test.

The first part involves the patient lying on their back (supine). Lift the patient’s legs to an angle of 45 degrees at the hip. Hold them there for 1-2 minutes, looking for pallor. Pallor indicates the arterial supply is not adequate to overcome gravity, suggesting peripheral arterial disease. Buerger’s angle refers to the angle at which the leg is pale due to inadequate blood supply. For example, a Buerger’s angle of 30 degrees means that the legs go pale when lifted to 30 degrees.

The second part involves sitting the patient up with their legs hanging over the side of the bed. Blood will flow back into the legs assisted by gravity. In a healthy patient, the legs will remain a normal pink colour. In a patient with peripheral arterial disease, they will go:

Blue initially, as the ischaemic tissue deoxygenates the blood
Dark red after a short time, due to vasodilation in response to the waste products of anaerobic respiration

The dark red colour is referred to as rubor.

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11
Q

peropheral arterial disease can get leg ulcers due to skin and tossue not having adequate blood suplly to heal opropelry

how differntiate between venous and arterial leg ulcers

A

arterial:
smaller
deeper
well defined
punched out apperance
distally- toes, dorsum foot
reduced bleeding
painful - more
pale = decreased blood to it
pain worse at night- horozontally
oain worse on elevation and improve when lower leg

venous;
larger
more superficial
occur after a minory injury to leg
irregular and sloping bprder
gaiter area of leg
less painful
occur with other signs of chronic venous insufficiency : haemosiderin staining, venous ezcema, lipodermatoslcerosis (inverted champagne bottle legs)
more likly to bleed
pain relieved on elevation and worse lowering elg

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12
Q

when do arterial ulcers occur

A

ishcemia 2dry to inadequate blood supply

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13
Q

when do venous ulcers occur

A

impaired drainage and pooling of blood in legs

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14
Q

deep
painful
quite small
ulcer
type?

A

arterial

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15
Q

investigations an do for peripheral arterial disease

A

ankle brachail pressure index
duplex US
angiogrpahy- contrast involved

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16
Q

how do you do ankle brachial pressure index and values mean

A

measure ankle systolic BP
brachial systolic bp using dopple probe

ankle/brachial systolic BP = ratio
eg. 80/100=0.8

0.9-1.3 normal
0.6-0.9= mild pAD
0.3-0.6=mod - severe PAD
less 0.3= severe PAD- critical limb ischemia

above 1.3= calcification- hard to compress bv- in diabtetics

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17
Q

management of intermitent claudication

A

modify risk facotrs -
lifestyle changes
exercise training - w;aking till hurt the rest

meds:
atorvastatin 80mg
clopidogrel 75mg OD(aspirin if clopiudogrel CI)
naftiodrofuryl oxalate- 5HT R antagonist= peripheral vasodialtor

surgical:
endarvascualr angioplasty and stening
endarectomy = remove plaque
bypass surgery

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18
Q

magament critical limb ischemia

A

urgent referal vascualr team
analgesia
urgent revascualrisation:
endovascualr angiop;asty and steniting
endarterectomy
bypass
amputation

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19
Q

management acute limb ischemia

A

urgernt referal oncall vascualr team
enovacualr thrombolyisis
endovacualr thromectomy
surgical thromectomy
endaertectomy
bypass
amputation

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20
Q

VTE

A

dvt and PE
dvt can embolise and cause PE
if atrial septal defect can go into ssytemic and have stroke

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21
Q

risk fctors DVT

A

stagnation of blood and hypercoagualbility:
immobility
recernt surgery
pregnacy
long haul flight
oestrogen- COCP, HRT
maligancy
polycythaemia
thrombophilia
SLE

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22
Q

what thrombophilias increase risk of VTE

A

antiphospholid sydnrome
factor V leiden
antithrombin deficiency
protien C or S deficiency
hyperchromocystiameia
prothrombin gene variant
actuvcated protein c resitance

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23
Q

what vte prophylaxis is there

A

all pt in hosp asses for need

LMWH = enoxaparin
ci= active bleeding, already o anticoagulation

anti-embolic compression stockings
ci= SIGNIFICANT PERIPHERAL ARTERIAL DISEASE

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24
Q

DVT PRESENTATION

A

unilatral
calf weliing- more 3cm diff is sign= measure 10cm below tibila rubersotiy
dilated superfical veins
tenderness
oedema
colour changes t leg

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25
Q

investigations for vte
inital
diagnostic

A

wells score

inital= D dimer

diagnostic for dvt= doppler US (if negative and psotive d dimer and wells score re do in 6-8 days)

diagnotic for pe= CTPA (if contrast allergy/renal impairement do VQ scan)

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26
Q

when can d dimer be rasied

A

sensitive but not specific for vte
also raised in:
PE
DVT
pregancy
heart failure
maligancy
pneumonia
surgery

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27
Q

management inital fir dvt/pe

A

is susepcted confirmed inital start immediate anticoagulation:
DOAC= apixaban/ rivaroxaban

if dvt in ileofemoral and less tha14 days can maybe do catherter directed thrombolysis

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28
Q

loing term management for dvt/pe

A

first line for most (including cancer) = DOAC= apixaban, rivaroxaban, edoxaban/ dabigatran

pregnacy first line= LMWH= enoxaparin

antiphospholipid syndrome first line is warfarin- INR aim 2-3

duration=
reversible casue 3months
cancer 3-6 months
uknown casues/ not reversible/ recurrent vte= more than 3 monhts (usulally 6)
then review them all

can use IVC filter if anticoagualtion CI

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29
Q

if unprovocked VTE what can you do for managment after anticoagulation

A

test for antiphosphlipid syndrome- antbpdies

if forst degree relative has thrombophilia test [t for herediatary thrombophilias

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30
Q

whats varicose veins

A

distended superficial veins measuring more tha 3mm in diameter
usually in legs

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31
Q

whats dialted bv in skin that are 1-3mm in diameter

A

reticular veins

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32
Q

whats dilated veins in skin that are less than 1mm in diameter

A

telangiectasia / thread veins/ spider veins

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33
Q

how do varicose veins develop

A

incompetnet valves
blood drains down towards gravity and pools in veins and feet

perforating veins connect deep and superficial veins
these valves in these veins become incompetnant and so blood flowd backwards from deep vein into superficial veins and so get dilitation and egorgement

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34
Q

whats signs of chronic venous innufficiecy

A

skin changes- brown= haemosiderin staining = due to blood pooling in the dital veins, the pressure in veins causes the blood to leak a bit and the hb in the tissues gets broken down to haemosiderin and the haemosiderin gets deposited aorund the shins

venous eczema = the blood pools in dital veins that causes inglammation and so skin becomes dry and inflammed

lipodermatoscleorisis =
skin and soft tissue becomes fibrotic and tight so legs become narrowed and hard

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35
Q

risk facotrs of varicose veins

A

obesity
long periods standing - ask re occupation
pregnancy
female
fam hist
DVT- damage the valves
increased age

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36
Q

presentation of varicose veins

A

engorged and dilated superficial veins
can be asymptomatic
heavy dragging feeling
itching
burning
aching
oedema
muscle. cramps
restless leg

may also have signs of chronic venous insufficniecny - skin colour changes and ulcers

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37
Q

investigations for varicose veins

A

tap test
cough test= thrill at SFT then dilated at SFJ and means saphenous varix
trendelburg test
perthes test
duplex US - SEE EXTENT OF VARIOCSE VEINS SEE FLOW AND VOLUME

Tap test – apply pressure to the saphenofemoral junction (SFJ) and tap the distal varicose vein, feeling for a thrill at the SFJ. A thrill suggests incompetent valves between the varicose vein and the SFJ.

Cough test – apply pressure to the SFJ and ask the patient to cough, feeling for thrills at the SFJ. A thrill suggests a dilated vein at the SFJ (called saphenous varix).

Trendelenburg’s test – with the patient lying down, lift the affected leg to drain the veins completely. Then apply a tourniquet to the thigh and stand the patient up. The tourniquet should prevent the varicose veins from reappearing if it is placed distally to the incompetent valve. If the varicose veins appear, the incompetent valve is below the level of the tourniquet. Repeat the test with the tourniquet at different levels to assess the location of the incompetent valves.

Perthes test – apply a tourniquet to the thigh and ask the patient to pump their calf muscles by performing heel raises whilst standing. If the superficial veins disappear, the deep veins are functioning. Increased dilation of the superficial veins indicates a problem in the deep veins, such as deep vein thrombosis.

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38
Q

managmenet of varicose veins

A

pregnancy normally go back to normal after delviery
weight loss
physically active
rasie legs when can
compression stockings- once excluded arterial disease using ankle brachial pressure index

endothermal ablation - catheter in and use radiofrequency ablation
sclerotherpay- irritaitng foam injected to casue vein to close
stripping

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39
Q

complciations of treatment of varicose veins

A

dvt
prlonged/ heavy bleeding after trauma
chronic venous insufficney symptoms
superficial thrombophelbititd = thormbosis and inflammation in superficial veins

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40
Q

what eed check before givng patient compression stockings

A

dont have peripheral arterial disease = check measuring ankle brachial pressure index
0.9-1.3 normal

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41
Q

whats chronic venous insufficiency

A

blood doesnt efficiently drain from legs to heart
usually result of damage of valves in the veins

asocaited with varicose veins

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42
Q

what can damage the valves in the veins of legs causing chronic venous insufficiency

A

dvt
obesity
prolonged stadning
immobility
increased age

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43
Q

presentation of chronic venous insufficency

A

skin changes in gaiter area:

haemosiderin staining - red/brown discolouration (poolsing blood leaks into tissue hb broken down to haemosidering and deposited in tissues)

lipodermatosclerosis=> harfdening and tigheting of skin and tissue => inverted champagne bottle appearance (chronic infallamtion casues fibrosis of the subcutaenous tissue (infalm of subcutaneous tissue is called panniculitis) )

venous eczema= dry, itchy, scaly, flaky, red, cracked skin (due to chroninc inflammation due to blood pooling)

atrophie blanche = pathes smooth white scar tissue often surrounded by areas of hyperpigemntation

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44
Q

chronic venous insufficency can lead to what

A

cellulits
pain
poor healing after injury
skin ulcers

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45
Q

managment of chronic venous insufficney

A

skin healthy:
regular emolients = double base, diprobase, cetraben, oliatum

topical steroids for venous eczema flares

v potent topical steroids for lipodermatoscleorisis flares

monitor and avoid damage

improve venous drainage:
loose weight
active
raise legs when can
compression stockings = once ruled out arterial disease using ankle brachial pressure index

manage complications :
antibiotics for cellulits - when look at patients legs and look like chronic venous insufficeny dont think defo cellulits as bilateral cellulitis is rare and abx wont help chronic venous insufficency so make sure it is actually they also have an ifection- cellulitis

anaglesia for pain
wound care for ulceration

46
Q

why do arterial ulcers occur

A

insufficeint blood supply to skin due to periheral arterial disease

47
Q

why do venous ulcers occur

A

due to pooling of blood and waste products
secondary to venous insufficency

48
Q

type of ulcers

A

diabetic foot ulcers
arterial
venous
pressure

49
Q

why do diabetic fppt ulcers occur

A

loos sensation = diabetic neuropahty= dont feel foot as well so less likely relasie injuried it/ tight fitting shoes

large nad small bv are damaged so impairs blood supply for wound healing

high blood glcuose, high immune system, autonomic neuropahty=> ulceration and poor wound healing

50
Q

complication of diabetic foot ulcers

A

osteomyeloitis

51
Q

why do pressure ulcers occur and how to prevent them

A

pt with reduce mobility- prlonged pressure on certain area

skin breaks down due to:
decreased blood supply and locaslised ischemia
decreased lymph drainagae
abdmoal change to shape of tissues

prevetn:
risk asses= waterflow score
regular turns
special inflating matress
regular ski checks
protective dressings and creasm

52
Q

investigfations for leg ulcers

A

ankle bracial pressure index= do for arterial and venous as need excluse not arterial when treating = assesing for arterial disease

bloods= inflammation, co morbidits- hba1c(diabaeted), albumin (malnutirtion)

swabs- infection
skin biospy- suspect other eg. skin cancer

53
Q

management arterial ulcers

A

urgent referal to vascualr
consider surgical revascualrisation
same as periheral arterial disease - meds, lifestule etc.
not using compression or debridment

54
Q

managment for venous ulcers

A

may refer to:
vascualr if mixed
tissue viability clinics if not healing. complex
dermatology suspect other
pain cliic
diabetic ulcer services
district nurses/ tissue viability nurses: clean wound. debridement(remove dead tissue0 dressing

compression- once exclude not arterial using ABPI
pentoxifylline orally - not licensed
abx
anaglesia - nsaids make it worse

55
Q

what medication ca make venous ulcers worse

A

NSAIDs

56
Q

whats lymohoedema

A

chronic condition
caused bu impaired lymphatic draiange of area

lymph system drains excess fkuid and so if impaired get swoellen with protein rich fluid

57
Q

taking blood/cannula/ bp/ injection on pt with lymphoedema need think what

A

prone to infection on area of lymphoeema so dont do injection/cannulation/bloods/bp on this area

58
Q

whats primary lymphoeodema

A

rare, genti consition
usuallt present before 30s
faulty development of lymph system

59
Q

whats seondary lymphoedema

A

anothe conditions that affects the lymph system

eg. breast cancer have removal of axially nodes leads to pt developing lymphoedema in the arm

60
Q

whats a differential for lymphodema and signs of it

A

lipodema = abmnorla build up of fat tissue in the limbs- often legs

women more
feet are spared (unline lymphoedema)
pain
psyco distress

61
Q

swollen right leg
foot spared

A

lipoedema

62
Q

swollen left leg
what can casues be

A

lymphoedema
something blocking blood vessels so blood cant drain out eg. lymoh tumour

63
Q

investigfations for lymphoedema

A

stemmers sign = 2nd toe or mid finger - pinch the skin and if lift and tent negative. if cant lift and tent skin the postive and suggestive of lymphoedmea

limb volume calcuations- water displacement
circumferntial
perometry

bioelectric impedance spectrometry - electric current passed

lymphoscintography= nuclear med scan- see structure of lymphatics

64
Q

stemmers sign postive
sugegstive of what

A

lymohedema

65
Q

managment of lymphoedema

A

specialist
manual lymohatic drainage- massage
weight loss
exercises
compression bandages

lymphaticovenular anastamosisis- connect lymph and nearby veins so can drain via veibs

abx if celluitis develops
cbt / anti depresants

66
Q

pt been recent to africa
swollen left leg
akin thickened

A

elephatiasis

67
Q

what lymphatic filariasis

A

infectious disease
caused by parastic worms spread by mosquitos

worms live in lyphatics and damage it => severe lymphoedema

asscociated with thickening and fibrosis of skin= elephantiasis

68
Q

whats an abdominal aortic aneurysm

A

dilation of abdominal aorta more than 3cm

69
Q

risk facotros of AAA

A

men
increase age
smoking
hypertension
hyperlipidameia
cvd
fam hist

70
Q

what age and who can have screeing for aaa
what scan is it

A

all men 65 can have US scan to screen for asymptomatic AAA

women over 70 who have riskfacotrs- cvd, copd, hypertension, hyperlipidameia, fam hist, smoking

71
Q

presntaion of AAA

A

most are asymptomatic
seen on screening/ investigatios for other things- ct, abdo xray, us

non specific abdo pain
pulsatile and expansile mass in abdo on palpation

72
Q

investigations for AAA

A

intial US
detail in pic and to help for elective surgery - ct angiogram

73
Q

classiication of aaa

A

under 3cm normal
3-4.4 cm = small aneursym
4.5-5.4cm= medium aneursy
5.5 above = large aneurysm

74
Q

management of aaa

A

if aorta diameteter over 3cm - refer to vasuclar

if aorta over 5.5 cm need urgent referal to vascualr

decrease risk of progression of aaa by:
stop smoking
healthy diet and exercise
optomise rx of ht, diabetes, hyperlipidaemia

follow up scan to monitor:
yearly if small- 3cm-4.4cm
3 monthly if med size 4.5-5.4cm

elective repair - do for:
all over 5.5cm diameter
symtpoamtic
diameter grow more than 1cm per year
repiar via grafting - lapartomy or by endovascualr aneurysm repiar via stent into the femoral a

75
Q

when do pt need iinvolve dvla they have an aaa

A

anyeusrm over 6cm then inform dvla
stop driving if aneurysm over 6.5cm

stricter if drive heavy vehicle

76
Q

when to do elecetive repiar of aaa

A

symtpomatic
over 5.5.cm diameter
grows diameter more than1cm/year

77
Q

presentaion of ruptured aaa

A

severe abdo pain- can radiate to back/groin
haemodynamically unstable - low bp, high hr
pulsatile and exapnsile mass in abdo on palpation
collapse
loss consiousness

78
Q

treat ruptured aaa

A

mortalilty 80%
surgical emergency
if haemodynamically ustbale straight to thetatre (not even imaging)

if haemodynamically stable can do ct angiogram to diagnose/exlcude ruptured aaa

permissive hypotension- allow a lower than normal bp when giving fluid resus as thoght as increasing bp can increase blood loss

79
Q

pt has severe abdo pain
radiates to groin
they then collapse

what could it be

A

ruputured aaa

80
Q

whats aortic dissection

A

tear of inner layer of aorta
blood enters between intima and media creating false lumen

81
Q

type A aortic dissection

A

start in asecinding aorta
before brachiaocephalic artery

82
Q

typeB aortic dissection

A

start in descinding aorta
after left subclavian artery

83
Q

type 1 aortic dissection

A

begin in ascending aorta and involves at least the arch of aorta if not whole of it

84
Q

type 2 aortic dissection

A

beigns in asceinding aorta and is isolated to the asceidning aorta

85
Q

type 3a aortic dissection

A

begins in descending aorta
onoly involves section above diaphragm

86
Q

type 3b aortic dissection

A

begins in descending aorta and involes the aorta belo the diaphrgam

87
Q

risk facrtors aortic dissection

A

same peripheral arterial disease
male
increase age
hypertension!= big one - sudden increase in bp(trigger) can cause dissection eg. weight lifting/ cocaine use
amoking
poor diet
low activity
high cholesterol
bicuspid aortic valve
coarctation of aorta
aortic valve repalcement
cabg
marfans syndrome
ehlers danlos syndrome = both are connective tissue disorders

88
Q

diagnose aortic dissection

A

inital use ct angiogram - relativel quick
in ed can use bedisde us - quick and easy
ecg and cxr to exclude other casues - but can have mi and aortic dissection
mri angiogram- more detail but takes longer

89
Q

pt has stemi on ecg but suspect aortic dissection
what need think

A

can have them both occur
can have mi and also aortic dissection so need be careful cus if got aortic dissection and treat the mi with thrombolysis that casues progression of dissection worse

90
Q

presentation of aortic dissection

A

suden onset, tearing/ripping severe chest pain
can have no chest pain
chest pain and abdominal pain together
back pain- descinding aorta
chest pain - ascending aorta
pain may migrate
hypertension
diffin arm bp= more 20mmhg sign
radial pulse defecit = once is decreased/absent/ doesnt match apex beat
diastolic murmur
focal nuerological defecit-paraestheisa/ weaknes
syncope
hypotension as progresses

91
Q

managemnt of aortic dissection

A

surgical emergency
need control bp and heart rate as want to decrease stress on aortic walls= Bblockers

type A= open surgery and graft
type B = thoracic endovascualr aortic reapia- TEVAR- and stent graft inserted- may need open if complex

92
Q

complications of aortic dissection

A

mi
stroke
paraplegia- sensation/motor in legs
cardiac tamponade
death
aortic valve regurgitation

93
Q

man 60
ht
presents with sudden onset tearing chest pain

A

aortic dissection

94
Q

carotid arterty stenosis

A

narrowing of carotid arteires

95
Q

casue of carotid stenosis

A

usually secondary to athleroscleorsis

96
Q

whats the risk of carotid arteru stensois

A

plaque can break off- embolus and go to brain and casue embolic stroke

97
Q

risk facvtors carotid artery stneosis

A

same as peripheral arterial disease ad athlerosclerosis

increase age
male
smoke
ht
poor diet
high cholesterol
decreased pysical activity

98
Q

patients who have a tia/ stroke will be investigated for carotid artery stneosis how

A

carotid us

99
Q

classification of caarotid artery stenosis

A

mild= less than 50% redcution in diameter
moderate= 50-69% reduction in daimeter
severe= 70% or more reduction in diameter

100
Q

presentation of carotid artery stenosis

A

usually asymptoamtic
usually found after stroke/tia

may hear carotid bruit =whooshing over stenosis during systole

101
Q

investigfations carotid artery stensois

A

carotid us - inital
ct /mri angiogram to see better detail beofre surgery

102
Q

managemnt of carotid artery stenosis

A

conservcative:
stop smoking
better healthy diet and exercise
manage comorbidities-diabetes, ht
antiplatelets- aspirin, clopidogrel, ticagrelor
lipid lowering= atrovastatin

surgical:
carotid endarterectomy - first line
angioplassty and stening - into femoral artery and balloon and stent

103
Q

whats the complciations of carotid endaerterectomy

A

stroke
damage nerve: permenat or tmeporary:

facial nerve= facial weakenss- often marginal mandibular nerve= lower lip drooping

glossopharyngeal nereve=> diff swallowing

recurrent laryngeal nerve=> hoarse voice

hypoglossal nerve=> unilateral tongue paralysis

104
Q

if pt has carotid artery stneois what other illness think may have

A

v likely have arterial disease and athlerosclerosis elsewhere in body => at risk of cornary artery disease and MI

105
Q

whats buerger disease

A

inflammatory condition that casues thrombus formation in small and medium bv in distal arterial system = hands and feet

106
Q

antoher name for buerger disease

A

thromboangittis olbiterans

107
Q

diagnostic criteria for buerger disease

A

under 50
no other ahtleroscletorric risk factors other than smoking

108
Q

presentation of buerger disease

A

typically men 25-35
painful
blue discolouration of fingertips and tips of toes
pain worse at night
mag progress to ulcers, gangrene and amputation

109
Q

whats buerger disease very strongly asscoaited with

A

smoking

110
Q

what investigations for diangosis do for buerger idsease

A

mainly clinical diagnosis
can do angiogram- show corkscrew collaterals - new bv that have grown to bypass affected ones

111
Q

management of buerger disease

A

main component= stop smoking!!! - completley stop- not enough to reduce or nicotine patches

can give iv iloprost = prostacylin analouge that dialtes bv

112
Q

risk factros for buerger disease

A

men
strong association with smoking

Surgery (7 decks)

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