Vasculopathies - Aortic Aneurysm, Peripheral Vascular Disease, Ulcers Flashcards

1
Q

Pathophysiology of atherosclerosis

A

Endothelium damaged by sheer stress

Monocytes adhere and penetrate to damage => macrophages

  • absorb oxLDL => foam cells => die and form lesion core
  • cytokine release => aggregation of more macrophages, SM proliferation

SM forms fibrous cap

Plaque rupture => thrombosis, coronary artery block

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2
Q

Peripheral arterial disease
- disease progression and presentation
- diagnosis and investigations
- management

A

SMOKING - GREATEST RISK FACTOR

Intermittent claudication - 0.5-0.8
- pain on exertion (few mins) relieved by rest
-feet, calf, thigh, bottom
- cold, dry skin, no hair
- weak pulses

Management
- CV risk optimisation (statin, smoking cessation, clopidogrel)
- supervised exercise programme
- angioplasty/bypass surgery

Critical limb ischemia - U0.5
- burning pain on rest
- arterial ulcers, gangrene
- cold, dry skin, no hair
- no pulses

Management
- analgesia
- angioplasty if U10cm stenosis
-bypass if 10cm+
-amputation if ganrgenous

Pulse check
ABPI - ankle BP:brachial BP
Duplex US - confirm diagnosis

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3
Q

Aortic dissection
- pathophysiology
- risk factors

A

Tear in intima => weakens aortic wall => rupture
-occlusion of branching vessels => ischemia of affected areas

STRONGEST - HTN, connective tissue disorders
-CV risk factors

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4
Q

Aortic dissection
- presentation and signs
- investigation and diagnosis

A

Sudden, severe tearing pain between shoulder blades
Chest/back pain
SOB

RR/RF delay
BP difference between both arms

If unstable => ALS, A-E resus
HOE
B
- ECG - can be some non specific changes
B
-FBC, U&E, G&S and crossmatch
I
-CXR - wide mediastinum
-CT angio - false lumen
-Transesophageal echo if too unstable for CT

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5
Q

Aortic dissection

-types and the management

A

Type A (most common) - proximal to LSC
SURGICAL REPLACEMENT OF AA
-permissive hypotension, IV labetolol
- transfusion

Type B - distal to LSC
CONSERVATIVE MANAGEMENT
- bedrest, analgesia, IV labetolol
- consider TEVAR

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6
Q

Abdominal aortic aneurysm
- pathophysiology
- risk factors

A

Dilation of all 3 layers => 3cm+
MOST COMMONLY - infrarenal

CV risk factors
Connective tissue disorders

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7
Q

Abdominal aortic aneurysm
- presentation and signs
- investigation and diagnosis

A

Back, abdo pain
Abdo pulsation

Bruit on auscultation
Grey-Turners
SHOCKED => RUPTURE!

Diagnostic - Abdo USS

HOE
B
-ECG
B
-FBC, U&E, CRP, G&S and crossmatch
I
-CT angio, MRI

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8
Q

Abdominal aortic aneurysm
- screening
- management

A

Screening
65+ males US
U3cm - :)
3-4.4cm - yearly
4.5-5.5 - 3monthly
5.5+ - 2w vascular referral

Surveillance - CV risk optimisation
Elective surgical repair
-5.5+, asymptomatic
-4cm+ and grown by 1cm in 1 year
Urgent surgical repair
-symptomatic/ruptured

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9
Q

What are ulcers

A

Abnormal breaks in skin or mucous membranes

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10
Q

Venous ulcers
-risk factors
-pathophysiology

A

Most common ulcer
Increased venous pooling => reduced venous return => uneven, impaired tissue perfusion => ulceration, delayed healing

Age
Existing/Hx venous problems
-VTE
-varicose veins
Pregnancy, obesity, physical inactivity
Leg trauma

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11
Q

Venous ulcer
-presentation

A

Before ulcers appear - Aching, itching

Painful
Superficial, irregular borders
Gaiter region
Leg edema
Varicose veins
Infection prone (cellulitis)
Hemosiderin staining - hemosiderin pools in veins
Venous eczema
Lipodermatosclerosis - wine bottle
Atrophie blanche - white scar after ulcer heals

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12
Q

Venous ulcer
-investigations

A

Clinical diagnosis
Investigation only confirms findings
-insufficiency confirmed by duplex
-ABPI to check whether there is sufficient arterial flow

If infection present - swabs and ABx

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13
Q

Venous ulcer
-management

A

Definitive - compression bandaging

Conservative - leg elevation, increased physical activity
-weight reduction

ABx if infection found

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14
Q

Arterial ulcer
-risk factors
-pathophysiology

A

CV risk factors

Reduction in arterial blood flow => reduced perfusion and poor healing

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15
Q

Arterial ulcer
-presentaton

A

Existing intermittent claudication or critical limb ischemia
Develops over long period of time with v little healing

Small deep lesions
Well demarcated
Long CRT
Patient may sleep in a chair, increase blood flow to legs
Distal to trauma sites
Pressure areas
Cold limbs
Reduced/no pulse
Thick, necrotic toes
Hair loss
Shiny taut skin

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16
Q

Arterial ulcer
-investigations

A

Clinical diagnosis but confirm location and severity with investigations

ABPI - measure severity of PAD

1 = :)
0.5+ = PAD
U0.5 = critical limb ischemia
Duplex => assess location of arterial disease leading to distal ischemia

17
Q

Arterial ulcer
-management

A

Vascular review needed if ulcers present (critical limb ischemia)

Conservative - CV risk lifestyle changes
Medical - lipid modification, aspirin, HTN, DM
Surgical - if extensive disease
-angioplasty, stenting if U10cm
-femoral artery bypass if 10cm+

18
Q

Neuropathic ulcer
-risk factors
-pathophysiology

A

Result of peripheral neuropathy
-loss of protective sensation => unnoticed injuries resulting in painless ulcers on pressure points
Healing complicated by concurrent vascular disease

Most common causes
-DM
-B12 deficiency
Ulcer risk made worse by existing foot deformity, PVD

19
Q

Neuropathic ulcer
-presentation

A

Hx of peripheral neuropathy
-burning, tingling, pain in legs
-weakness, balance issues
-length dependent neuropathy
Hx of PVD
Punched out appearance of ulcers on pressure sites
Warm feet, pulses unless concurrent arterial disease

20
Q

Difference between wet and dry gangrene
-management

A

Gangrene - tissue death from ischemia

Management - debridement, amputation if needed

Dry - chronic ischemia without infection
-cannot be saved

Wet - ischemia leading to necrosis + bacterial infection

21
Q

Neuropathic ulcers
-investigations

A

Glucose check
B12 check
Assess for arterial disease - ABPI, duplex

If infection - swab
Assess extent of peripheral neuropathy with tuning fork

22
Q

Neuropathic ulcers
-management

A

Optimise diabetic control
-HbA1c
-diet, exercise
Optimise CV risk factors

Regular chiropody

foot hygiene
good footwear
Signs of infection - ABx
Ischemic/necrotic tissue - debride or amputate

23
Q

What is Charcot’s Foot

A

Loss of joint sensation => continuous joint trauma leading to foot deformity
-increased risk of neuropathic ulcers

Swollen, distorted, painful foot

Specialist review needed

offload abnormal weight
immobilise joint in plaster

24
Q

Lymphodema
-causes
-investigations and diagnosis
-management

A

Cancer treatment
Cellulitis - damages lymphatics
Inflammatory conditions
Venous insufficiency
Obesity, immobility, trauma
Clinical diagnosis
-confirmed with lymphoscintigram

Supportive - skin care
Definitive - compression garments
-elevation, exercise, weight reduction

25
Q

Mesenteric ischemia
-presentation
-definitive diagnosis

A

Minimal clinical signs

Distended abdo
Diffuse tenderness
No guarding => no peritonitis
Tympanic abdo
Abdo pain out of proportion to clinical findings

High LACTATE!

CT angiogram

26
Q

Mesenteric ischemia
-management

A

Quick restoration of blood flow
-keep laparotomy open for 2nd look
Remove necrotic bowel
Manage ends of healthy bowel with stoma
Short gut syndrome management

27
Q

Peripheral arterial disease
-3 types

A

Intermittent claudication
Critical limb ischemia
Acute limb-threatening ischemia

28
Q

Acute limb-threatening ischemia
-presentation
-investigations

A

6Ps
-pale
-pulseless
-pain
-paralysed
-paraesthetic
-perishingly cold

Handheld arterial Doppler
ABPI

29
Q

Differentiating between thrombus and embolus in acute limb ischemia

A

Thrombus
-known claudication with sudden deterioration
-no clear source of emboli
-reduced/no pulses in other limb
-evidence of widespread CVD

Embolus
-sudden onset pain
-no Hx of claudication, PAD
-clear source of emboli

30
Q

Acute limb ischemia
-initial management
-definitive management

A

Initial
-A-E
-IV opioids, heparin
-vascular review

Definitive
-intra-arterial thrombolysis
-surgical embolectomy
-angioplasty
-bypass
-amputation is irreversible