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

Vascular System - VV, DVT, Leg Ulcers Flashcards

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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
How does AF cause changes to blood flow
Irregularly irregular rhythm of heart can cause blood to pool in atria --> thrombus formation Can also embolise into systemic circulation
26
How can rheumatic heart disease cause changes to blood flow
Following Group A strep infection, can destruct mitral valve Turbulent flow as blood passes through slit like valve
27
Causes of altered blood flow - veins
Usually stasis
28
What can cause stasis in veins
Immobilisation Compressed veins e.g. bed rest Varicose veins Increased blood viscosity e.g. sickle cell, dehydration
29
Factors causing endothelial cell injury
Ischaemia hypoxia Infection of blood vessels Physical - atheroma, crushed veins, HTN Chemical - lipid, cigarette Immunological deposition of immune complexes
30
Genetic changes in constituents in blood leading to thrombosis
Antithrombin II deficiency | Protein C
31
Acquired changes in constituents in blood leading to thrombosis
``` Tissue damage Post-op Malignancy Cigarette smoke Elevated blood lipids Oral contraceptives ```
32
What are the options of a thrombus remains attached
Lysis Retraction and recanalisation Organisation Infection
33
What happens if a thrombus detaches
Embolises - either sterile, infected or septic
34
Embolus
Abnormal mass of undisolved material which is transported from one part of circulation to another
35
Types of emboli
``` Thrombus Gas - air, nitrogen Fat Tumour Misc - foreign bodies (drug addicts), amniotic fluid ```
36
What can happen if emboli lodge in pulmonary artery
``` Hypoxia Reduced cardiac output Pulmonary infarction Pulmonary HTN Right heart failure Death ``` Size of thromboembolism determines symptoms
37
Sequelae to PE
``` Sudden death R sided heart failure - 60% of circulation is obstructed Organisation of embolism Pulmonary infarction Pulmonary HTN ```
38
PE - saddle embolus
Occludes both pulmonary arteries
39
PE - paradoxical embolus
Passes through interatrial or interventricular cardiac defect to gain access to systemic circulation
40
Effects of emboli - arterial
Emboli from L side of heart will enter systemic arterial system Iscahemia/ infarction occurs Bacterial endocarditis vegetation on inner surface of aortic valves
41
What may infected emboli give rise to
Pyaemia and access formation
42
Pyaemia
Type of sepsis leading to widespread abscesses of metastatic nature Caused by pus-forming bacteria
43
How may air enter circulation
During obstetric procedures | In chest wall injuries
44
When does air in the circulation have a clinical effect
More than 100cc
45
Effect of air embolus
Bubbles coalesce to form frothy masses with may occlude major vessels
46
Who do nitrogen emboli occur in
Deep sea divers on rapid ascent
47
When can fat globules be found in circulation
Fracture of long bones Soft tissue trauma Burns
48
Symptoms of fat embolism
``` Tachypnoea Tachycardia Dyspnea Irritability and restlessness Diffuse petechial rash (20-50%) Thrombocytopenia ```
49
What is seen with amniotic fluid embolus
Dyspnoea, cyanosis, HTN DIC, seizures, shock Mortality >80%
50
Leg ulcer definition
Loss of skin below the knee on the leg/foot, which takes >2 wks to heal Break in continuity of covering epithelium
51
Epidemiology of ulcers
1% will suffer from leg ulceration at some point | Prevalence 1.5 to 3 per 100 and increases with age
52
Aetiology of leg ulcers
``` Venous insufficiency (60-85%) PAD (10-20%) Mixed arterial and venous disease Neuropathic diabetic ulcer RhA Systemic vasculitis Lymphoedema Trauma Malignant ulcer Infection ```
53
Vascular causes of leg ulcerations
Venous Arterial Mixed arterial and venous aetiology Lymphatic
54
Vascular causes of leg ulceration - venous
Venous insufficiency Varicose veins Post-phlebitis post sclerotherapy
55
Vascular causes of leg ulceration - arterial
``` Atherosclerosis Buerger's disease Vasculitis Raynaud's Diabetic foot ulceration ```
56
Types of veins in LL
Superficial Deep Perforator
57
Superficial veins of LL
Long saphenous vein | Short saphenous vein
58
Deep veins of LL
Anterior & posterior tibial veins Peroneal veins Popliteal vein Femoral veins (Profunda femoris and superficial femoral vein)
59
VV definition
Dilated, tortuous,superficial veins > 2mm diameter
60
Main cause of VV
Increased venous pressure --> valvular incompetence
61
What can cause post-ambulatory HTN
Ineffective calf muscle contraction Incompetent valve Veins that aren't patent
62
Normal post-ambulatory venous pressure
<25mmHg As the pressure increases as does incidence of venous leg ulcers
63
Causes of venous HTN
Superficial venous reflux Deep venous reflux & occlusion Perforating vein reflux
64
Cause of primary deep venous reflux & occlusion
Idiopathic
65
Cause of secondary deep venous reflux & occlusion
Caused by DVT or injury
66
Causes of perforating vein reflux
Abnormal calf pump Neurological MSK
67
What do incompetent valves in the calf lead to
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
Venous insufficiency
Irreversible skin damage as the result of sustained ambulatory venous HTN
69
In which group of people, do venous ulcers take longer to heal
People from lower socioeconomic groups | Also have higher recurrence rates
70
When do venous leg ulcers become chronic
If they remain unhealed after 4 weeks
71
Risk factors for venous leg ulcers
``` 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
Most important factors causing venous HTN
Venous insufficiency Obesity Immobility
73
Causes of secondary valvular incompetence
``` Post-phlebitis Venous obstruction Muscle pump dysfunction Aging/ leg pathologies Valvular hypoplasia/agenesis ```
74
Hypothesis of microvascular pathophysiology of venous ulcers
White cell trapping hypothesis | Fibrin cuff hypothesis
75
Atherosclerosis development and progression
Fatty streak Fibrous plaque Complicated plaque - haemorrhage, ulcerated plaque, calcified plaque
76
Neuroischaemic (diabetic) foot ulcers are seen in what % of DM pts
1--25%
77
Pathophysiology of diabetic foot ulcers
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
Link between sensory neuropathy and ulceration
Increase risks of ulceration by 7x
79
Motor neuropathy and ulceration
Motor neuropathy --> weakness and atrophy of foot muscle --> altering foot structure --> deformity and altered biomechanics
80
Autonomic neuropathy and ulceration
Autonomic neuropathy is associated with dry skin --> fissures, cracking, and callus
81
Clinical hx of leg ulcers
``` Mode of onset/ precipitating event Duration of ulcer Symptoms (pain, discharge, systemic features) Risk factors Peripheral ischaemic symptoms Previous interventions ```
82
Clinical assessment of leg ulcers
Hx Clinical exam of ulcer and surroundings Vascular system exam (arterial and venous) Neurological examination if diabetic foot ulcer suspected
83
Clinical exam of ulcer and surroundings
``` 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
Venous hx for ulcer
``` VV DVT/ thrombophlebitis Previous ulceration Previous treatments (e.g. foam sclerotherapy) Oedema Pain or lack of? Precipitating factors Co-existence - PVD, DM, RhA ```
85
Arterial hx for ulcer
IC Ischaemic rest pain Risk factors for PAD Previous arterial intervention
86
Stages of venous leg ulcers
Exudative phase Granulation stage Chronic infl and scar formation
87
What are you looking for in a venous clinical exam
``` VV Oedema Skin changes Healed ulcers Active ulcers ```
88
Skin changes seen in venous disease
Varicose eczema Haemosiderin staining Lipodermatosclerosis Atrophie blanche
89
Neuroischaemic clinical exam
Inspection - dry skin, absence of hair, ingrown nails, calluses, fissures Hammer toe deformity Charcot's deformity 10g monofilament test 128Hz tuning fork
90
Ix - venous ulcer suspected
Venous duplex CT venogram MR venography Standard venography
91
Ix - arterial ulcer suspected
Arterial duplex CT peripheral angiogram MR angiography DSA
92
Mainstay of ulcer management
Treat underlying cause
93
Mx of venous leg ulcer
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
Surgery for superficial venous ulcers
Endovenous radio frequency ablation Endovenous laser ablation Endovenous foam sclerotherapy
95
What does mx of venous leg ulcer involve
``` 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
Deep venous procedures
Catheter-directed thrombolytic therapy for DVT | Self-expandable metallic stent placement of pt has significant post-thrombotic complications
97
Complications of venous leg ulcers
``` Immobility due to pain Infection Sepsis Contact dermatitis Sinus formation and fistula -ve impacts of QoL OM ```
98
What is suggestive of sepsis in ulcer pt
Tachycardia Fever Chills
99
What is suggestive of OM in an ulcer pt
Fever Disproportionate pain Systemically unwell Bone at base at wound
100
Mx of arterial ulcers
Revascularisation
101
Treating mixed aetiology leg ulcers
Arterial component must be treated first | ABPI<0.8 means pts needs lower levels of compression (modified compression)
102
Mx of diabetic foot ulcers
``` MDT approach Good BM control Treat infection Revascularise Off-load ulcer ```
103
Preventing recurrence of venous ulcers
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
Preventing recurrence of arterial/ neuroischaemic ulcers
``` Report worsening symptoms Keep skin moist Never walk barefoot Ensure shoes are well fitting Give up smoking Exercise ```
105
Prognosis of venous ulcers
Healing rates of 70% have been achieved
106
Factors associated with failure of venous ulcer to heal within 24 wks
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
When is the prognosis of arterial ulcers good
If revascularisation procedures are successful, pt modifies lifestyle and takes antiplatelets and statins
108
What do we call thrombosis in superficial veins
Superficial thrombophlebitis
109
Treatment of DVT in pregnancy
LWMH as DOACs and warfarin can cross placenta
110
Where does the long saphenous vein start
In front of MM
111
Does the SSV run behind or in front of LM
Behind
112
SFJ
Sapheno-femoral junction Where long saphenous vein drains into femoral vein
113
SPJ
Sapheno-popliteal junction Where the short saphenous veins drains into popliteal vein Found posterior
114
Where can valvular incompetence in the leg be
4 diff areas SFJ Mid thigh perforators SPJ Mid calf perforators
115
When can you not refer a DVT to VTE clinic
If there is a suspected PE
116
Most common artery to stenose in leg
SFA
117
Leg cellulitis vs a/c DVT
Much warmer Redness expands over time If limited to anterior aspect, most likely leg cellulitis
118
How can impacts of serious illnesses be grouped
``` Practical and domestic Emotional Social Spiritual Financial ```
119
Kubler-Ross grief
``` Denial Anger Bargaining Depression Acceptance ```
120
Open family systems
Communicate freely Flexible boundaries Rules are up to date and promote growth
121
Closed family systems
Indirect/ restricted communication Overly dependent on one another Inflexible rules
122
Roles of carers for those w/ terminal illnesses
ADL Mediating Nursing tasks
123
Issues of concern for carers
``` Ability to provide care Stress Uncertainty Fear Conflict Altered role and lifestyle Own physical health Finances ```
124
Problems faced by carers
Extra demands on time/ energy Changing roles/ responsibilities Changing ability to work Pressure to continue caring and have life outside
125
Effective palliative care
``` Symptom control Psychological support Communication Info Practical support End of life care Bereavement support ```
126
Families at risk of struggling with being a carer
``` Other children/ family members already disabled Single parent families Families separating/ divorcing 'Dysfunctional families' PMH mental health problems Cultural/ lang difficulties ```
127
Signs of a struggling family
``` 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
Recommendation for carers
``` Take breaks Take care of self Understand limits Get help Professional support e.g. palliative care ```
129
Where can families get help with symptom control
GP Specialist nurse Palliative care specialists
130
Where can families get help with Nursing
District/ community nurse
131
Where can families get domestic support from
Social services
132
Where can families get psychosocial support
GP Macmillan nurse Bereavement counsellors
133
Where can families get support with aids and appliances
OT/ PT
134
Where can families get financial support from
Social worker | Macmillan benefits officer
135
Condns caused by thrombotic problems
MI Stroke PAD Deep venous occlusion
136
Major risk factors for venous thrombosis
``` Major surgery Late pregnancy LL fracture Malignancy Reduced mobility Previous DVT ```
137
Minor risk factors for venous thrombosis
``` Congenital heart disease Cardiac failure HTN Central venous catheter Oral contraceptives option/ HRT Thrombotic disorder Obesity, COPD ```
138
LL DVT clinical features
Painful, swollen hot LL Prominent superficial veins Acute onset
139
Ddx of DVT
``` Cellulitis Ruptured popliteal cyst Muscle tear/ haematoma Fracture Lymphoedema Hypoproteinaemia ```
140
Where else can DVTs occur
Cerebral sinuses Arms Retina Mesentery
141
Ix for LL DVT
Ascending venography Ultrasound Nuclear med, CT, MR plethysmography D-dimer
142
Ultrasound for DVT
Normal veins are compressible and demonstrate venous pattern flow Thrombus may be visible
143
When would you repeat a CT for a suspected DVT if unsure
3-5 days
144
What is D-dimer
Degradation products of cross-linked fibrin
145
When is D-dimer released
When the fibrinolytic system attacks the fibrin matrix of fresh venous theromboemboli
146
What does the absence of a raised conc of D-dimer imply
There is no fresh thromboembolic material undergoing dissolution in the deep veins/ pulmonary artery tree
147
What can cause false +ve in D-dimer test
``` Cancer PAD Many infl/ infective conditions Post-op Increasing age ```
148
Clinical features part of Well's score
``` 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
Measuring calf swelling in DVT
Measure circumference 10cm below tibial tuberosity | Significant is >3cm difference
150
Wells' score of 1 or 2
Moderate possibility of DVT | Check D-dimer, if high venous duplex ultrasound
151
Well's score of 3/3+
High probability of DVT | LL ultrasounds requested without need for D-dimer
152
Low Well's score and low D-dimer
No ultrasound GP informed Telephone follow up @ 3/12
153
Cause of PE
Venous thrombus breaks off from LL veins and moves through venous circulation Can get stuck in pulmonary arteries and cause pulmonary infarction
154
Symptoms of PE
``` Breathlessness Pleuritic chest pain Haemoptysis Arrhythmias Sudden death ```
155
What's seen in PE
Zone of lung which is ventilated but not perfused
156
PE - ix
``` ECG ABG D-dimer Chest radiograph Ventilation-perfusion (VQ) scan CT pulmonary angiogram Catheter pulmonary angiography ```
157
Treatment of PE
Anti-coagulate
158
Possible edges/margins of ulcers
Punched out (arterial) Sloping (venous) Heaped-up (cancerous) Undermined (pressure)
159
What might the surrounding skin of ulcers look like
Cellulitis (red) Haemosiderin staining (brown) Congested (blue) Ischaemic (pale)
160
Best ix for suspected neuroischaemic ulcer
MR angiography
161
What is CTangio contraindicated in
Those with poor renal function e.g. CKD | Dye used is nephrotoxic
162
What can venous ultrasound duplex scans show you
``` Thrombosis Valvular incompetence (reflux) ```
163
When is catheter-directed thrombolytic therapy used for DVT
Acute ilio-femoral DVT to prevent post-phlebitic limb | Women on OCP are good candidates due to possible complications
164
What is the sign of complete occlusion in DVT
Cyanotic discolouration of limb | Severe oedema
165
What location of DVT is more likely to cause of PE
Iliofemoral compared to DVT below knee
166
Post phlebitis syndrome and its link to DVT
Ulceration of a limb caused by chronic venous obstruction (DVT) Presents with single swollen limb

MBBS - Year 2 (20 decks)

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