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Vascular Flashcards

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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
investigations for vte inital diagnostic
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)
26
when can d dimer be rasied
sensitive but not specific for vte also raised in: PE DVT pregancy heart failure maligancy pneumonia surgery
27
management inital fir dvt/pe
is susepcted confirmed inital start immediate anticoagulation: DOAC= apixaban/ rivaroxaban if dvt in ileofemoral and less tha14 days can maybe do catherter directed thrombolysis
28
loing term management for dvt/pe
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
29
if unprovocked VTE what can you do for managment after anticoagulation
test for antiphosphlipid syndrome- antbpdies if forst degree relative has thrombophilia test [t for herediatary thrombophilias
30
whats varicose veins
distended superficial veins measuring more tha 3mm in diameter usually in legs
31
whats dialted bv in skin that are 1-3mm in diameter
reticular veins
32
whats dilated veins in skin that are less than 1mm in diameter
telangiectasia / thread veins/ spider veins
33
how do varicose veins develop
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
34
whats signs of chronic venous innufficiecy
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
35
risk facotrs of varicose veins
obesity long periods standing - ask re occupation pregnancy female fam hist DVT- damage the valves increased age
36
presentation of varicose veins
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
37
investigations for varicose veins
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.
38
managmenet of varicose veins
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
39
complciations of treatment of varicose veins
dvt prlonged/ heavy bleeding after trauma chronic venous insufficney symptoms superficial thrombophelbititd = thormbosis and inflammation in superficial veins
40
what eed check before givng patient compression stockings
dont have peripheral arterial disease = check measuring ankle brachial pressure index 0.9-1.3 normal
41
whats chronic venous insufficiency
blood doesnt efficiently drain from legs to heart usually result of damage of valves in the veins asocaited with varicose veins
42
what can damage the valves in the veins of legs causing chronic venous insufficiency
dvt obesity prolonged stadning immobility increased age
43
presentation of chronic venous insufficency
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
44
chronic venous insufficency can lead to what
cellulits pain poor healing after injury skin ulcers
45
managment of chronic venous insufficney
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
why do arterial ulcers occur
insufficeint blood supply to skin due to periheral arterial disease
47
why do venous ulcers occur
due to pooling of blood and waste products secondary to venous insufficency
48
type of ulcers
diabetic foot ulcers arterial venous pressure
49
why do diabetic fppt ulcers occur
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
complication of diabetic foot ulcers
osteomyeloitis
51
why do pressure ulcers occur and how to prevent them
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
investigfations for leg ulcers
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
management arterial ulcers
urgent referal to vascualr consider surgical revascualrisation same as periheral arterial disease - meds, lifestule etc. not using compression or debridment
54
managment for venous ulcers
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
what medication ca make venous ulcers worse
NSAIDs
56
whats lymohoedema
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
taking blood/cannula/ bp/ injection on pt with lymphoedema need think what
prone to infection on area of lymphoeema so dont do injection/cannulation/bloods/bp on this area
58
whats primary lymphoeodema
rare, genti consition usuallt present before 30s faulty development of lymph system
59
whats seondary lymphoedema
anothe conditions that affects the lymph system eg. breast cancer have removal of axially nodes leads to pt developing lymphoedema in the arm
60
whats a differential for lymphodema and signs of it
lipodema = abmnorla build up of fat tissue in the limbs- often legs women more feet are spared (unline lymphoedema) pain psyco distress
61
swollen right leg foot spared
lipoedema
62
swollen left leg what can casues be
lymphoedema something blocking blood vessels so blood cant drain out eg. lymoh tumour
63
investigfations for lymphoedema
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
stemmers sign postive sugegstive of what
lymohedema
65
managment of lymphoedema
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
pt been recent to africa swollen left leg akin thickened
elephatiasis
67
what lymphatic filariasis
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
whats an abdominal aortic aneurysm
dilation of abdominal aorta more than 3cm
69
risk facotros of AAA
men increase age smoking hypertension hyperlipidameia cvd fam hist
70
what age and who can have screeing for aaa what scan is it
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
presntaion of AAA
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
investigations for AAA
intial US detail in pic and to help for elective surgery - ct angiogram
73
classiication of aaa
under 3cm normal 3-4.4 cm = small aneursym 4.5-5.4cm= medium aneursy 5.5 above = large aneurysm
74
management of aaa
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
when do pt need iinvolve dvla they have an aaa
anyeusrm over 6cm then inform dvla stop driving if aneurysm over 6.5cm stricter if drive heavy vehicle
76
when to do elecetive repiar of aaa
symtpomatic over 5.5.cm diameter grows diameter more than1cm/year
77
presentaion of ruptured aaa
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
treat ruptured aaa
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
pt has severe abdo pain radiates to groin they then collapse what could it be
ruputured aaa
80
whats aortic dissection
tear of inner layer of aorta blood enters between intima and media creating false lumen
81
type A aortic dissection
start in asecinding aorta before brachiaocephalic artery
82
typeB aortic dissection
start in descinding aorta after left subclavian artery
83
type 1 aortic dissection
begin in ascending aorta and involves at least the arch of aorta if not whole of it
84
type 2 aortic dissection
beigns in asceinding aorta and is isolated to the asceidning aorta
85
type 3a aortic dissection
begins in descending aorta onoly involves section above diaphragm
86
type 3b aortic dissection
begins in descending aorta and involes the aorta belo the diaphrgam
87
risk facrtors aortic dissection
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
diagnose aortic dissection
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
pt has stemi on ecg but suspect aortic dissection what need think
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
presentation of aortic dissection
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
managemnt of aortic dissection
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
complications of aortic dissection
mi stroke paraplegia- sensation/motor in legs cardiac tamponade death aortic valve regurgitation
93
man 60 ht presents with sudden onset tearing chest pain
aortic dissection
94
carotid arterty stenosis
narrowing of carotid arteires
95
casue of carotid stenosis
usually secondary to athleroscleorsis
96
whats the risk of carotid arteru stensois
plaque can break off- embolus and go to brain and casue embolic stroke
97
risk facvtors carotid artery stneosis
same as peripheral arterial disease ad athlerosclerosis increase age male smoke ht poor diet high cholesterol decreased pysical activity
98
patients who have a tia/ stroke will be investigated for carotid artery stneosis how
carotid us
99
classification of caarotid artery stenosis
mild= less than 50% redcution in diameter moderate= 50-69% reduction in daimeter severe= 70% or more reduction in diameter
100
presentation of carotid artery stenosis
usually asymptoamtic usually found after stroke/tia may hear carotid bruit =whooshing over stenosis during systole
101
investigfations carotid artery stensois
carotid us - inital ct /mri angiogram to see better detail beofre surgery
102
managemnt of carotid artery stenosis
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
whats the complciations of carotid endaerterectomy
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
if pt has carotid artery stneois what other illness think may have
v likely have arterial disease and athlerosclerosis elsewhere in body => at risk of cornary artery disease and MI
105
whats buerger disease
inflammatory condition that casues thrombus formation in small and medium bv in distal arterial system = hands and feet
106
antoher name for buerger disease
thromboangittis olbiterans
107
diagnostic criteria for buerger disease
under 50 no other ahtleroscletorric risk factors other than smoking
108
presentation of buerger disease
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
whats buerger disease very strongly asscoaited with
smoking
110
what investigations for diangosis do for buerger idsease
mainly clinical diagnosis can do angiogram- show corkscrew collaterals - new bv that have grown to bypass affected ones
111
management of buerger disease
main component= stop smoking!!! - completley stop- not enough to reduce or nicotine patches can give iv iloprost = prostacylin analouge that dialtes bv
112
risk factros for buerger disease
men strong association with smoking

Surgery (7 decks)

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