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MBBS - Year 2 > Vascular System - VV, DVT, Leg Ulcers > Flashcards

Vascular System - VV, DVT, Leg Ulcers Flashcards

1
Q

Thrombus definition

A

Mass of normal blood constituents formed inappropriately within the circulation during life

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2
Q

What are thrombus’ composed of

A

Fibrin
Platelets
Entrapped R/WBC

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3
Q

Where can thrombus’ form

A

Cardiac chamber

Vessels

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4
Q

Microscopy of thrombus’

A

Laminations visible, called Lines of Zahn

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5
Q

Haemostasis vs thrombosis production

A

Haemostasis is a physiological response to injury of blood vessels
Thrombus production is a pathological repose (activated inappropriately)

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6
Q

Mechanisms of haemostasis

A

Injury –> loss of lining endothelial cells
Exposure of underlying ECM, activates platelets –> 1’ haemostatic plug
Coagulation cascade activates
Thrombin and fibrin produce 2’ haemostatic plug

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7
Q

Main components of controlled haemostasis

A

Endothelial cells
Platelets
Coagulation cascade

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8
Q

Anti-thrombotic properties of endothelial cells

A

Antiplatelet
Anticoagulant
Profibrinolytic

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9
Q

Antiplatelets in endothelial cells

A

Prostacyclin

NO

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10
Q

Anticoagulants in endothelial cells

A

Antithrombin III

Thrombomodulin-activated proteins C/S

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11
Q

Profibrinolytic in endothelial cells

A

Tissue plasminogen activator

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12
Q

When do endothelial cells exert a prohaemostatic effect

A

If injured or activated

Pro-platelet
Pro-coagulant
Anti-fibrinolytic

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13
Q

Pro-platelet factors in endothelial cells

A

Von-Willebrand factor

Platelet activating factor

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14
Q

Pro-coagulant factors in endothelial cells

A

Tissue factor

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15
Q

Anti-fibrinolytics in endothelial cells

A

Plasminogen activator inhibitors

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16
Q

What are platelets produced by

A

Megakaryocytes in blood

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17
Q

What are platelets activated by

A

Exposure to sub endothelial ECM

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18
Q

What happens after platelets are activated

A

Adhesion
Platelet release reaction
Platelet aggregation

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19
Q

Types of coagulation pathways

A

Intrinsic
Extrinsic
Common

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20
Q

Virchow’s Triad

A

Change in blood flow
Change in vessel wall
Change in blood constituents

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21
Q

What does disruption to laminar flow cause

A

Platelets to come into contact with endothelium
Injury or activation of endothelium
Impaired removal of pro-coagulant factors/ impaired delivery of anti-coagulant factors

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22
Q

Causes of altered blood flow

A 
Atherosclerosis (narrowing)
Aneurysm 
Infarcted myocardium 
Abnormal cardiac rhythm 
Valvular heart disease
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23
Q

Changes in blood flow are seen in which condns

A

Following MI
AF
Rhemuatic heart disease, following Group A strep infection

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24
Q

How does an MI change the blood flow

A

Fibrotic (healed) myocardium may dilate forming ventricular aneurysm and turbulent blood flow

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25
Q

How does AF cause changes to blood flow

A

Irregularly irregular rhythm of heart can cause blood to pool in atria –> thrombus formation
Can also embolise into systemic circulation

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26
Q

How can rheumatic heart disease cause changes to blood flow

A

Following Group A strep infection, can destruct mitral valve
Turbulent flow as blood passes through slit like valve

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27
Q

Causes of altered blood flow - veins

A

Usually stasis

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28
Q

What can cause stasis in veins

A

Immobilisation
Compressed veins e.g. bed rest
Varicose veins
Increased blood viscosity e.g. sickle cell, dehydration

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29
Q

Factors causing endothelial cell injury

A

Ischaemia hypoxia

Infection of blood vessels

Physical - atheroma, crushed veins, HTN

Chemical - lipid, cigarette

Immunological deposition of immune complexes

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30
Q

Genetic changes in constituents in blood leading to thrombosis

A

Antithrombin II deficiency

Protein C

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31
Q

Acquired changes in constituents in blood leading to thrombosis

A 
Tissue damage 
Post-op
Malignancy 
Cigarette smoke 
Elevated blood lipids 
Oral contraceptives
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32
Q

What are the options of a thrombus remains attached

A

Lysis
Retraction and recanalisation
Organisation
Infection

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33
Q

What happens if a thrombus detaches

A

Embolises - either sterile, infected or septic

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34
Q

Embolus

A

Abnormal mass of undisolved material which is transported from one part of circulation to another

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35
Q

Types of emboli

A 
Thrombus 
Gas - air, nitrogen 
Fat
Tumour 
Misc - foreign bodies (drug addicts), amniotic fluid
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36
Q

What can happen if emboli lodge in pulmonary artery

A 
Hypoxia
Reduced cardiac output 
Pulmonary infarction 
Pulmonary HTN 
Right heart failure 
Death

Size of thromboembolism determines symptoms

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37
Q

Sequelae to PE

A 
Sudden death 
R sided heart failure -  60% of circulation is obstructed 
Organisation of embolism 
Pulmonary infarction 
Pulmonary HTN
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38
Q

PE - saddle embolus

A

Occludes both pulmonary arteries

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39
Q

PE - paradoxical embolus

A

Passes through interatrial or interventricular cardiac defect to gain access to systemic circulation

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40
Q

Effects of emboli - arterial

A

Emboli from L side of heart will enter systemic arterial system
Iscahemia/ infarction occurs
Bacterial endocarditis vegetation on inner surface of aortic valves

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41
Q

What may infected emboli give rise to

A

Pyaemia and access formation

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42
Q

Pyaemia

A

Type of sepsis leading to widespread abscesses of metastatic nature
Caused by pus-forming bacteria

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43
Q

How may air enter circulation

A

During obstetric procedures

In chest wall injuries

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44
Q

When does air in the circulation have a clinical effect

A

More than 100cc

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45
Q

Effect of air embolus

A

Bubbles coalesce to form frothy masses with may occlude major vessels

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46
Q

Who do nitrogen emboli occur in

A

Deep sea divers on rapid ascent

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47
Q

When can fat globules be found in circulation

A

Fracture of long bones
Soft tissue trauma
Burns

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48
Q

Symptoms of fat embolism

A 
Tachypnoea 
Tachycardia 
Dyspnea 
Irritability and restlessness 
Diffuse petechial rash (20-50%)
Thrombocytopenia
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49
Q

What is seen with amniotic fluid embolus

A

Dyspnoea, cyanosis, HTN
DIC, seizures, shock
Mortality >80%

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50
Q

Leg ulcer definition

A

Loss of skin below the knee on the leg/foot, which takes >2 wks to heal
Break in continuity of covering epithelium

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51
Q

Epidemiology of ulcers

A

1% will suffer from leg ulceration at some point

Prevalence 1.5 to 3 per 100 and increases with age

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52
Q

Aetiology of leg ulcers

A 
Venous insufficiency (60-85%)
PAD (10-20%)
Mixed arterial and venous disease 
Neuropathic diabetic ulcer 
RhA
Systemic vasculitis 
Lymphoedema 
Trauma 
Malignant ulcer
Infection
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53
Q

Vascular causes of leg ulcerations

A

Venous
Arterial
Mixed arterial and venous aetiology
Lymphatic

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54
Q

Vascular causes of leg ulceration - venous

A

Venous insufficiency
Varicose veins
Post-phlebitis
post sclerotherapy

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55
Q

Vascular causes of leg ulceration - arterial

A 
Atherosclerosis 
Buerger's disease 
Vasculitis 
Raynaud's 
Diabetic foot ulceration
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56
Q

Types of veins in LL

A

Superficial
Deep
Perforator

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57
Q

Superficial veins of LL

A

Long saphenous vein

Short saphenous vein

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58
Q

Deep veins of LL

A

Anterior & posterior tibial veins
Peroneal veins
Popliteal vein
Femoral veins (Profunda femoris and superficial femoral vein)

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59
Q

VV definition

A

Dilated, tortuous,superficial veins > 2mm diameter

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60
Q

Main cause of VV

A

Increased venous pressure –> valvular incompetence

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61
Q

What can cause post-ambulatory HTN

A

Ineffective calf muscle contraction
Incompetent valve
Veins that aren’t patent

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62
Q

Normal post-ambulatory venous pressure

A

<25mmHg

As the pressure increases as does incidence of venous leg ulcers

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63
Q

Causes of venous HTN

A

Superficial venous reflux
Deep venous reflux & occlusion
Perforating vein reflux

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64
Q

Cause of primary deep venous reflux & occlusion

A

Idiopathic

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65
Q

Cause of secondary deep venous reflux & occlusion

A

Caused by DVT or injury

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66
Q

Causes of perforating vein reflux

A

Abnormal calf pump
Neurological
MSK

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67
Q

What do incompetent valves in the calf lead to

A

Backflow of blood and the veins elongate and become tortuous
Increase in pressure –> leakage of blood particles and fluid
Overload of lymphatic system –> oedema
Leads to lymphovenous oedema

68
Q

Venous insufficiency

A

Irreversible skin damage as the result of sustained ambulatory venous HTN

69
Q

In which group of people, do venous ulcers take longer to heal

A

People from lower socioeconomic groups

Also have higher recurrence rates

70
Q

When do venous leg ulcers become chronic

A

If they remain unhealed after 4 weeks

71
Q

Risk factors for venous leg ulcers

A 
Obesity 
Immobility 
Personal of Fhx of VV
Personal hx of DVT 
Arteriovenous fistula
Increasing age
Hx of leg fracture or trauma 
Prolonged standing 
Late pregnancy
72
Q

Most important factors causing venous HTN

A

Venous insufficiency
Obesity
Immobility

73
Q

Causes of secondary valvular incompetence

A 
Post-phlebitis 
Venous obstruction
Muscle pump dysfunction 
Aging/ leg pathologies 
Valvular hypoplasia/agenesis
74
Q

Hypothesis of microvascular pathophysiology of venous ulcers

A

White cell trapping hypothesis

Fibrin cuff hypothesis

75
Q

Atherosclerosis development and progression

A

Fatty streak
Fibrous plaque
Complicated plaque - haemorrhage, ulcerated plaque, calcified plaque

76
Q

Neuroischaemic (diabetic) foot ulcers are seen in what % of DM pts

A

1–25%

77
Q

Pathophysiology of diabetic foot ulcers

A

Neuropathy predisposed foot to ulceration through its effect on the sensory, motor and autonomic nerves
Loss of protective sensation (pressure, pain & temp) render pt vulnerable to physical, thermal and chemical trauma

78
Q

Link between sensory neuropathy and ulceration

A

Increase risks of ulceration by 7x

79
Q

Motor neuropathy and ulceration

A

Motor neuropathy –> weakness and atrophy of foot muscle –> altering foot structure –> deformity and altered biomechanics

80
Q

Autonomic neuropathy and ulceration

A

Autonomic neuropathy is associated with dry skin –> fissures, cracking, and callus

81
Q

Clinical hx of leg ulcers

A 
Mode of onset/ precipitating event 
Duration of ulcer 
Symptoms (pain, discharge, systemic features)
Risk factors 
Peripheral ischaemic symptoms 
Previous interventions
82
Q

Clinical assessment of leg ulcers

A

Hx
Clinical exam of ulcer and surroundings
Vascular system exam (arterial and venous)
Neurological examination if diabetic foot ulcer suspected

83
Q

Clinical exam of ulcer and surroundings

A 
Number 
Site 
Size 
Shape 
Floor
Edge/ margin 
Base 
Discharge?
Depth
Surrounding skin 
Exam of arterial, venous and neurological systems 
Exam of nutritional status or anything that may prolong healing
84
Q

Venous hx for ulcer

A 
VV 
DVT/ thrombophlebitis 
Previous ulceration 
Previous treatments (e.g. foam sclerotherapy)
Oedema 
Pain or lack of?
Precipitating factors 
Co-existence - PVD, DM, RhA
85
Q

Arterial hx for ulcer

A

IC
Ischaemic rest pain
Risk factors for PAD
Previous arterial intervention

86
Q

Stages of venous leg ulcers

A

Exudative phase
Granulation stage
Chronic infl and scar formation

87
Q

What are you looking for in a venous clinical exam

A 
VV
Oedema 
Skin changes 
Healed ulcers 
Active ulcers
88
Q

Skin changes seen in venous disease

A

Varicose eczema
Haemosiderin staining
Lipodermatosclerosis
Atrophie blanche

89
Q

Neuroischaemic clinical exam

A

Inspection - dry skin, absence of hair, ingrown nails, calluses, fissures
Hammer toe deformity
Charcot’s deformity

10g monofilament test
128Hz tuning fork

90
Q

Ix - venous ulcer suspected

A

Venous duplex
CT venogram
MR venography
Standard venography

91
Q

Ix - arterial ulcer suspected

A

Arterial duplex
CT peripheral angiogram
MR angiography
DSA

92
Q

Mainstay of ulcer management

A

Treat underlying cause

93
Q

Mx of venous leg ulcer

A

Compression for 3/12 (only if no arterial insufficiency and no infection)
Determine whether deep, superficial or functional problem
Consider surgery if superficial
Consider skin grafting if fails to heal

94
Q

Surgery for superficial venous ulcers

A

Endovenous radio frequency ablation
Endovenous laser ablation
Endovenous foam sclerotherapy

95
Q

What does mx of venous leg ulcer involve

A 
Cleaning and dressing the ulcer 
Compression therapy
Wound swab and abx - if infected
Arranging follow up for reassessment 
Referring to specialist if hasn't healed after 2 wks in primary care
96
Q

Deep venous procedures

A

Catheter-directed thrombolytic therapy for DVT

Self-expandable metallic stent placement of pt has significant post-thrombotic complications

97
Q

Complications of venous leg ulcers

A 
Immobility due to pain 
Infection 
Sepsis 
Contact dermatitis 
Sinus formation and fistula 
-ve impacts of QoL
OM
98
Q

What is suggestive of sepsis in ulcer pt

A

Tachycardia
Fever
Chills

99
Q

What is suggestive of OM in an ulcer pt

A

Fever
Disproportionate pain
Systemically unwell
Bone at base at wound

100
Q

Mx of arterial ulcers

A

Revascularisation

101
Q

Treating mixed aetiology leg ulcers

A

Arterial component must be treated first

ABPI<0.8 means pts needs lower levels of compression (modified compression)

102
Q

Mx of diabetic foot ulcers

A 
MDT approach 
Good BM control 
Treat infection 
Revascularise 
Off-load ulcer
103
Q

Preventing recurrence of venous ulcers

A

Education and lifestyle changes
Wearing appropriate compression stockings for 5 hrs
Follow up every 6/12 - 12/12 to identify risk factors
Doppler APBI every 6/12

104
Q

Preventing recurrence of arterial/ neuroischaemic ulcers

A 
Report worsening symptoms 
Keep skin moist 
Never walk barefoot 
Ensure shoes are well fitting 
Give up smoking 
Exercise
105
Q

Prognosis of venous ulcers

A

Healing rates of 70% have been achieved

106
Q

Factors associated with failure of venous ulcer to heal within 24 wks

A

Initial size of ulcer Longer ulcer duration at px
Hx of surgical treatment for VV
Hx of hip or knee replacement
ABPI < 0.8

107
Q

When is the prognosis of arterial ulcers good

A

If revascularisation procedures are successful, pt modifies lifestyle and takes antiplatelets and statins

108
Q

What do we call thrombosis in superficial veins

A

Superficial thrombophlebitis

109
Q

Treatment of DVT in pregnancy

A

LWMH as DOACs and warfarin can cross placenta

110
Q

Where does the long saphenous vein start

A

In front of MM

111
Q

Does the SSV run behind or in front of LM

A

Behind

112
Q

SFJ

A

Sapheno-femoral junction

Where long saphenous vein drains into femoral vein

113
Q

SPJ

A

Sapheno-popliteal junction

Where the short saphenous veins drains into popliteal vein

Found posterior

114
Q

Where can valvular incompetence in the leg be

A

4 diff areas

SFJ
Mid thigh perforators
SPJ
Mid calf perforators

115
Q

When can you not refer a DVT to VTE clinic

A

If there is a suspected PE

116
Q

Most common artery to stenose in leg

A

SFA

117
Q

Leg cellulitis vs a/c DVT

A

Much warmer
Redness expands over time
If limited to anterior aspect, most likely leg cellulitis

118
Q

How can impacts of serious illnesses be grouped

A 
Practical and domestic 
Emotional 
Social 
Spiritual 
Financial
119
Q

Kubler-Ross grief

A 
Denial 
Anger 
Bargaining 
Depression 
Acceptance
120
Q

Open family systems

A

Communicate freely
Flexible boundaries
Rules are up to date and promote growth

121
Q

Closed family systems

A

Indirect/ restricted communication
Overly dependent on one another
Inflexible rules

122
Q

Roles of carers for those w/ terminal illnesses

A

ADL
Mediating
Nursing tasks

123
Q

Issues of concern for carers

A 
Ability to provide care 
Stress 
Uncertainty 
Fear 
Conflict 
Altered role and lifestyle 
Own physical health 
Finances
124
Q

Problems faced by carers

A

Extra demands on time/ energy
Changing roles/ responsibilities
Changing ability to work
Pressure to continue caring and have life outside

125
Q

Effective palliative care

A 
Symptom control 
Psychological support
Communication 
Info
Practical support 
End of life care 
Bereavement support
126
Q

Families at risk of struggling with being a carer

A 
Other children/ family members already disabled 
Single parent families 
Families separating/ divorcing 
'Dysfunctional families' 
PMH mental health  problems 
Cultural/ lang difficulties
127
Q

Signs of a struggling family

A 
Frequent call outs to GP or district nurse
Illness of carer 
Rship breakdowns within family 
Symptoms not responding to treatment 
Psychological distress in carers or pt 
'I can't cope'
128
Q

Recommendation for carers

A 
Take breaks 
Take care of self 
Understand limits 
Get help 
Professional support e.g. palliative care
129
Q

Where can families get help with symptom control

A

GP
Specialist nurse
Palliative care specialists

130
Q

Where can families get help with Nursing

A

District/ community nurse

131
Q

Where can families get domestic support from

A

Social services

132
Q

Where can families get psychosocial support

A

GP
Macmillan nurse
Bereavement counsellors

133
Q

Where can families get support with aids and appliances

A

OT/ PT

134
Q

Where can families get financial support from

A

Social worker

Macmillan benefits officer

135
Q

Condns caused by thrombotic problems

A

MI
Stroke
PAD
Deep venous occlusion

136
Q

Major risk factors for venous thrombosis

A 
Major surgery 
Late pregnancy 
LL fracture 
Malignancy 
Reduced mobility 
Previous DVT
137
Q

Minor risk factors for venous thrombosis

A 
Congenital heart disease 
Cardiac failure 
HTN 
Central venous catheter 
Oral contraceptives option/ HRT 
Thrombotic disorder 
Obesity, COPD
138
Q

LL DVT clinical features

A

Painful, swollen hot LL
Prominent superficial veins
Acute onset

139
Q

Ddx of DVT

A 
Cellulitis 
Ruptured popliteal cyst 
Muscle tear/ haematoma 
Fracture 
Lymphoedema 
Hypoproteinaemia
140
Q

Where else can DVTs occur

A

Cerebral sinuses
Arms
Retina
Mesentery

141
Q

Ix for LL DVT

A

Ascending venography
Ultrasound
Nuclear med, CT, MR plethysmography
D-dimer

142
Q

Ultrasound for DVT

A

Normal veins are compressible and demonstrate venous pattern flow
Thrombus may be visible

143
Q

When would you repeat a CT for a suspected DVT if unsure

A

3-5 days

144
Q

What is D-dimer

A

Degradation products of cross-linked fibrin

145
Q

When is D-dimer released

A

When the fibrinolytic system attacks the fibrin matrix of fresh venous theromboemboli

146
Q

What does the absence of a raised conc of D-dimer imply

A

There is no fresh thromboembolic material undergoing dissolution in the deep veins/ pulmonary artery tree

147
Q

What can cause false +ve in D-dimer test

A 
Cancer 
PAD
Many infl/ infective conditions 
Post-op 
Increasing age
148
Q

Clinical features part of Well’s score

A 
Active cancer 
Paralysis/ LL immobilisation 
Bedridden/ major surgery <4 wks
Localised tenderness along deep venous system 
Calf swelling 
Pitting oedema 
Dilated collateral superficial veins 
Pregnancy

Lose 2 points if alternative dx is as likely

149
Q

Measuring calf swelling in DVT

A

Measure circumference 10cm below tibial tuberosity

Significant is >3cm difference

150
Q

Wells’ score of 1 or 2

A

Moderate possibility of DVT

Check D-dimer, if high venous duplex ultrasound

151
Q

Well’s score of 3/3+

A

High probability of DVT

LL ultrasounds requested without need for D-dimer

152
Q

Low Well’s score and low D-dimer

A

No ultrasound
GP informed
Telephone follow up @ 3/12

153
Q

Cause of PE

A

Venous thrombus breaks off from LL veins and moves through venous circulation
Can get stuck in pulmonary arteries and cause pulmonary infarction

154
Q

Symptoms of PE

A 
Breathlessness
Pleuritic chest pain 
Haemoptysis 
Arrhythmias 
Sudden death
155
Q

What’s seen in PE

A

Zone of lung which is ventilated but not perfused

156
Q

PE - ix

A 
ECG
ABG 
D-dimer 
Chest radiograph 
Ventilation-perfusion (VQ) scan 
CT pulmonary angiogram 
Catheter pulmonary angiography
157
Q

Treatment of PE

A

Anti-coagulate

158
Q

Possible edges/margins of ulcers

A

Punched out (arterial)
Sloping (venous)
Heaped-up (cancerous)
Undermined (pressure)

159
Q

What might the surrounding skin of ulcers look like

A

Cellulitis (red)
Haemosiderin staining (brown)
Congested (blue)
Ischaemic (pale)

160
Q

Best ix for suspected neuroischaemic ulcer

A

MR angiography

161
Q

What is CTangio contraindicated in

A

Those with poor renal function e.g. CKD

Dye used is nephrotoxic

162
Q

What can venous ultrasound duplex scans show you

A 
Thrombosis 
Valvular incompetence (reflux)
163
Q

When is catheter-directed thrombolytic therapy used for DVT

A

Acute ilio-femoral DVT to prevent post-phlebitic limb

Women on OCP are good candidates due to possible complications

164
Q

What is the sign of complete occlusion in DVT

A

Cyanotic discolouration of limb

Severe oedema

165
Q

What location of DVT is more likely to cause of PE

A

Iliofemoral compared to DVT below knee

166
Q

Post phlebitis syndrome and its link to DVT

A

Ulceration of a limb caused by chronic venous obstruction (DVT)
Presents with single swollen limb

MBBS - Year 2 (20 decks)

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