Vascular Flashcards

(53 cards)

1
Q

define acute arterial ischaemia

A

acute occlusion of a peripheral artery, usually without Hx of claudication

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2
Q

Risk factors for developing acute arterial ischaemia

A

Conditions that predispose to embolism: arrhythmias, endocarditis, arterial aneurysms
atherosclerosis
previous vascular grafts
hypercoagulable states

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3
Q

symptoms of acute limb ischaemia

A
pain
pallor
paraesthesia
paralysis
perishing cold
pulsless
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4
Q

investigations for acute ischiaemia

A
ECG
troponin
FBC
PT/INR, PTT
echo
CTA
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5
Q

treatment of acute limb ischaemia

A
heparin
embolectomy
thrombectomy
bypass graft
amputation
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6
Q

complications of reperfusion in acute ischaemia

A

compartment syndrome (with prolonged ischaemia)
arrhythmia and death
renal failure and multi-organ failure (toxic metabolites)

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7
Q

define chronic arterial occlusion/insufficiency

A

chronic ischaemia due to inadequate arterial supply to meet cellular metabolic demands

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8
Q

risk factors for chronic arterial insufficiency

A
smoking
DM
age
HTN
hyperlipidaemia
obesity
sedentary
PMHx, FHx of CAD/CVD
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9
Q

cause of chronic arterial insufficiency

A

atherosclerosis

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10
Q

clinical features of chronic arterial insufficiency: claudication

A

pain with exertion that is relieved by a short rest and is reproducible

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11
Q

clinical features of chronic arterial insufficiency: critical limb ischaemia

A
rest pain
night pain
tissue loss: ulercation, gangrene
pain over forefoot 
ABI < 0.4
absent pulses
signs of poor perfusion
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12
Q

DDx of claudication

A
  1. Vascular
    a. Atherosclerotic disease
    b. Vasculitis e.g. Buerger’s disease, Takayasu’s arteritis
    c. Diabetic neuropathy
    d. Popliteal entrapment syndrome
    1. Neurogenic
      a. Neurospinal disease e.g. spinal stenosis
      b. Complex regional pain syndrome
    2. MSK
      a. OA
      b. RA, connective tissue disease
      Remote trauma
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13
Q

list congenital hypercoagulable states

A
Group I (reduced anticoagulants)
antithrombin
Protein C
Protein S
Group II (increased coagulants)
Factor V Leiden
Prothrombin
Factor VIII
Hyper-homocysteinemia
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14
Q

list acquired hypercoagulable state

A
immobility
cancer
Pregnancy/systemic hormonal contraceptives/HRT
Antiphospholipid antibody syndrome
Inflammatory disorders (e.g. IBD)
Myeloproliferative disorders (e.g. ET)
Nephrotic syndrome (acquired deficit in Protein C and S)
DIC
HITT
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15
Q

type A vs B aortic dissection

A

A involves the ascending aorta but B does not

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16
Q

aetiology of aortic dissection

A
most common HTN
others:
connective tissue disease - Marfans, Ehlers-Danlos
cystic medial necrosis
atherosclerosis
congenital conditions - coarctation, bicuspid aortic valves, PDA
syphillis
trauma
takayasus arteritis
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17
Q

investigaitons of aortic dissection

A

CTA
ECG and troponin
CXR
transoesphageal echo

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18
Q

what will a CXR show in aortic dissection

A

pleural cap
widened mediastinum
left pleural effusion

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19
Q

treatment of type A aortic dissection

A

resection of segment and replacement of graft

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20
Q

post operative complications of aortic dissection repair

A
renal failure
intestinal ischaemia
stroke
paraplegia
persistent leg ischaemia
death
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21
Q

treatment of type B aortic dissection

A

IV antihypertensives
oral antihypertensives
b-blocker to decrease cardiac contractility

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22
Q

true vs false aneurysm

A

true - involves all vessel wal layers

23
Q

risk factors for aortic aneurysm

A
smoking
HTN
PVD
CAD
CVD
age > 70
FHx
male
24
Q

aetiology of aortic aneurysm

A
degeneraitve 
truamatic
mycotic - salmonella, staph
connective tissue disorder
vasculitis
infectious - syphilis, fungal
biscuspid aortic valves
25
where are mycotic aortic aneurysm commonly found?
suprarenal
26
what type of aortic aneurysms are associated with bicuspid aortic valves?
ascending thoracic aorta
27
clinical features of aortic aneurysm
``` asymptomatic syncope pain hypotension pulsatile, expansile mass ```
28
what is the classic triad of a ruptured AAA
hypotension back/abdo pain expansile, pulsatile abdo mass
29
investigations for an aortic aneurysm
FBC, U+E, creatinine, PTT, INR, group and save abdo USS CTA peripheral arterial duplex
30
conservative management of aortic aneurysm
cardiovascular risk factor reduction
31
when would you surgically repair an aortic aneurysm
> 5.5.cm
32
what does the risk of rupture of an aortic aneurysm depend on?
``` size FHx of rupture rate of enlargement symptoms comorbities smokin ```
33
what are the surgical options for repair of aortic aneurysm
open or EVAR
34
complications of open aortic aneurysm repair
Early: renal failure, spinal cord injury (paraparesis or paraplegia), impotence, arterial thrombosis, anastomotic rupture or bleeding, peripheral emboli Late: graft infection/thrombosis, aortoenteric fistula, anastomotic (psuedo) aneurysm
35
complications of EVAR
Early: immediate conversion to open, groin haematoma, arterial thrombosis, iliac artery rupture, thromboemboli Late: endoleak, graft kinking, migration. Thrombosis, rupture of aneurysm
36
what is carotid stenosis?
narrowing of the internal carotid lumen due to atherosclerotic plaque formation, usually near bifurcation
37
risk factors for carotid stenosis
``` HTN smoking DM CVD CAD dyslipidaemia age ```
38
clinical features of carotid stenosis
asymptomatic | hemispheric or ocular
39
investigations for carotid stenosis
FBC, PT/INR, PTT Fundoscopy – cholesterol emboli in retinal vessels (Hollenhorst plaques) Auscultation over bifurcation for bruits Carotid duplex – determines severity +/- cross sectional imaging with CT/M
40
treatment of carotid stenosis
Risk factor modification Dual antiplatelets Surgical carotid endarectomy or endovascular angioplasty +/- stenting
41
what are varicose veins?
distention of tortuous superficial veins resulting from incompetent valves in the deep, superficial or perforator systems
42
causes of varicose veins
``` age oral contraceptive prolonged standing pregnancy obesity Secondary: DVT, malignant pelvic tumours with venous compression, congenital anomalies, AV fistulae, trauma ```
43
clinical features of varicose veins
Diffuse aching, fullness/tightness, nocturnal cramping Aggravated by prolonged standing, premenstrual Visible long, dilated, tortuous superficial veins (great or small saphenous + tributaries) Ulceration, hyperpigmentation, and induration (ie lipodermatosclerosis)
44
complications of varicose veins
Recurrent superficial thrombophlebitis/superficial vein thrombosis Features of chronic venous insufficiency: ulceration, eczema, lipodermatosclerosis, stasis dermatitis and hyperpigmentation Bleeding or haematoma secondary to trauma
45
treatment of varicose veins
Cosmetic problem Compression stockings Indications for surgery: failure of conservative treatment, symptomatic varix (pain, bleeding, recurrent thrombophlebitis), tissue changes (hyperpigmentation, ulceration), cosmetic Surgical: high ligation and stripping of the long saphenous vein and its tributaries, Ultrasound guided foam sclerotherapy, endovenous laser therapy
46
what is chronic venous insufficiency?
Calf muscle pump dysfunction and valvular incompetence (reflux) due to phlebitis, varicositis, or DVT Venous obstruction
47
clinical features of chronic venous insufficiency
Pain, ankle and calf oedema – relieved by foot elevation Pruritis, brownish hyperpigmentation (haemosiderin deposits) Stasis dermatitis, SC fibrosis if chronic (lipodermatosclerosis) Ulceration: shallow, above medial malleolus, weeping, painless, irregular outline Signs of DVT/varicose veins/thrombophlebitis
48
treatment of chronic venous insufficiency
Compression stockings Ambulation Periodic rest elevation Avoid prolonged standing Ulcers: multilayer compression bandage, antibiotics Surgical ligation of perforators in region of ulcer Endovenous: laser or radiofrequency ablation, or foam sclerotherapy
49
what is lymphoedema
obstruction of lymphatic drainage resulting in oedema with high protein count
50
primary causes of lymphoedema
Milroy’s syndrome: congenital hereditary lymphedema Lymphoedema praecox (75% of cases): starts in adolescence Lymphoedema tarda: starts >35 yr
51
secondary causes of lymphoedema
Infection: filariasis (#1 cause worldwide) Malignant infiltration: axillary, groin or intrapelvic Radiation/surgery (axillary, groin lymph node removal)
52
clinical features of lymphoedema
Classically non-pitting oedema | Impaired limb mobility, discomfort/pain, psychological distress
53
treatment of lymphoedema
Avoid limb injury (can precipitate or worsen lymphedema) Cellulitis: treat early to avoid further lymphatic damage Skin hygiene Daily skin care with moisturizers Early medical assessment and treatment for infection (topical for fungal infection; systemic for bacterial infection) External support Intensive: compression bandages Maintenance: compression garment Exercise Gentle daily exercise of affected limb, gradually increasing ROM Must wear a compression sleeve/bandages when doing exercises Massage: manual lymph drainage therapy