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JL Cardiovascular > Vascular and Ischaemic Heart Disease > Flashcards

Vascular and Ischaemic Heart Disease Flashcards

1
Q

Where do the right and left coronary arteries arise from?

A

The base of the aorta

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2
Q

Where does most coronary venous blood drain into?

A

The coronary sinus and then into the right atrium

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3
Q

What area of the heart becomes deprived of blood supply if the left coronary artery becomes blocked?

A

Left ventricle

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4
Q

Give four special adaptations of coronary circulation?

A
  1. High capillary density
  2. High basal blood flow
  3. High oxygen extraction (75% compared to 25%)
  4. Extra oxygen can only be supplied by increasing coronary blood flow
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5
Q

What does decreased PO2 do to the coronary arteries?

A

Causes vasodilatation

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6
Q

What is an intrinisc mechanism of coronary blood flow, and matches flow to demand?

A

Metabolic hyperaemia

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7
Q

What is a potent vasodilator for coronary blood flow (intrinsic mechanism)?

A

Adenosine from ATP

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8
Q

What type of nerves are coronary arterioles supplied by?

A

Sympathetic vasoconstrictor nerves

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9
Q

What are sympathetic vasoconstrictor nerves in coronary arterioles over-ridden by?

A

Metabolic hyperaemia as a result of increased heart rate and stroke volume

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10
Q

What does sympathetic stimulation of the heart result in?

A

Coronary vasodilatation despite direct vasoconstrictor effect

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11
Q

What substances activates beta-2-adrenoceptors, which causes vasodilatation?

A

Adrenaline

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12
Q

What receptors does sympathetic stimulation act on in relation to coronary blood flow?

A

Alpha receptors

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13
Q

What do increased metabolites such as K, PCO2 and H+ do to coronary blood flow?

A

Increase it

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14
Q

What does an increase in adenosine, do to coronary blood flow?

A

Increases it

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15
Q

When does peak left coronary flow occur?

A

During diastole

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16
Q

What does shortening diastole (e.g. very fast heart rate) do to coronary flow?

A

Decreases it

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17
Q

What gives blood supply to the brain?

A

Internal carotids and vertebral arteries

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18
Q

What is very sensitive to hypoxia in the brain?

A

Grey matter

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19
Q

What two arteries form the basilar?

A

Two vertebral arteries

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20
Q

What arteries anastomose to for the circle of Willis?

A

Basilar and carotid arteries

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21
Q

Where do the major cerebral arteries arise from?

A

The circle of Willis

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22
Q

What is caused by an interruption/cut-off of blood supply to a region of the brain?

A

Stroke

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23
Q

What are the two main types of stroke?

A
  1. Haemorrhagic bleeding

2. Ischaemic stroke

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24
Q

What type of stroke is described - blood leaks out of artery wall which is damaged?

A

Haemorrhagic stroke

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25
Q

What type of stroke is dewscribed - blood clot forms on atheroma on artery wall or comes from another part of body and gets stuck, blood cannot flow past?

A

Ischaemic stroke

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26
Q

What is autoregulation of cerebral blood flow guard against?

A

Changes in cerebral blood flow if mean arterial blood pressure changes within a range (60 - 160 mmHg)

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27
Q

In relation to autoregulation of cerebral blood flow: what happens to resistance vessels automatically when MABP rises?

A

Resistance vessels constrict to limit blood flow

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28
Q

When does autoregulation fail in relation to MABP falling?

A

Below 60mmHg

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29
Q

What does MABP below 50 mmHg, result in?

A

Confusion, fainting and brain damage if not quickly corrected

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30
Q

What does increased PCO2 do to cerebral vessels?

A

Causes cerebral vasodilatation

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31
Q

What does decreased PCO2 do to cerebral vessels?

A

Cause vasoconstriction (which is why hyperventilation could lead to fainting)

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32
Q

What is the term for blood flow increasing to active parts of the brain?

A

Regional hyperaemia

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33
Q

What is normal intracranial pressure (ICP) within the skull?

A

8 - 13 mmHg

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34
Q

What is the equation for cerebral perfusion pressure (CPP)?

A

CCP = MAP - ICP

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35
Q

What two things could increase ICP?

A
  1. Head injury

2. Brain tumour

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36
Q

What does increasing ICP, do to CPP and cerebral blood flow?

A

Decreases it

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37
Q

What are tight intercellular junctions called in cerebral capillaries?

A

The blood brain barrier

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38
Q

What are cerebral capillaries highly permeable to?

A

O2 and CO2

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39
Q

How does glucose cross the blood brain barrier?

A

By facilitated diffusion using specific carrier molecules

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40
Q

What three hydrophilic substances is the blood brain barrier exceptionally impermeable to?

A
  1. Ions
  2. Catecholamines
  3. Proteins
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41
Q

What are the metabolic needs of the airways met by?

A

Systemic bronchial circulation

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42
Q

What is pulmonary artery BP typically?

A

20-25/ 6-12 mmHg

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43
Q

What is the pulmonary capillary pressure like compared to the systemic cappilary pressure?

A

Low

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44
Q

What special adaptation of the pulmonary circulation protects against pulmonary oedema?

A

Absorptive forces exceed filtration forces

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45
Q

What causes vasoconstriction of pulmonary arterioles?

A

Hypoxia

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46
Q

Why is resting blood flow in skeletal muscle low?

A

Because of sympathetic vasoconstrictor tone

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47
Q

In relation to skeletal muscle blood flow: during exercise what overcomes sympathetic vasoconstrictor activity?

A

Metabolic hyperaemia

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48
Q

In skeletal muscle blood flow, what does circulating adrenaline cause?

A

Vasodilatation (beta-2-areniceptors)

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49
Q

What does contraction of muscle aid in relation to veins?

A

Venous return

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50
Q

What does skeletal muscle pump reduce the chance of?

A

Postural hypotension and fainting

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51
Q

What is the term for blood pooling in lower limb veins if venous valves become impotent?

A

Varicose veins

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52
Q

Why do varicose veins not lead to a reduction of CO?

A

Because of compensatory increase in blood volume

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53
Q

What is the term for the result of imparied vascular perfusion depriving the affected tissue of nutrients (including oxygen). It can be reversible on multiple factors including speed of onset, local demand and duration?

A

Ischaemia

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54
Q

What term refers to ischaemic necrosis of a dtissue or organ secondary to occlusion/reduction of the arterial supply or venous drainage. Recovery depends on a tissue regenerative ability?

A

Infarction

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55
Q

What is the term for a set of well regulated processes that accomplish functions (1. maintaing blood in a fluid, 2. induce rapid, localised haemostatic plug at site of vascular injury)?

A

Haemostasis

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56
Q

What is pathological/ corruption of haemostasis?

A

Thrombosis

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57
Q

What is the term for the formation of a solid or semi-solid mass from the constituents of blood, within the vascular system, during life?

A

Thrombosis

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58
Q

What are the three components of Virchow’s triad?

A
  1. Changes in vessel walls (endothelial injury)
  2. Changes in blood constituents (hypercoaguability)
  3. Changes in blood flow
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59
Q

What close small breaches in vessel walls and if activated in a vessel cause thrombus?

A

Platelets

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60
Q

Name the two components of platelets?

A
  1. Alpha granules (adhesion componenets, e.g. fibrinogen, fibronection, PDGF, anti-heparin)
  2. Dense granules (aggregation, ADP)
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61
Q

What do platelets cause when contacting collagen or fibrin?

A

Temporary patching

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62
Q

What maintains a permeability barrier and elaborates anticoagulant, antithrombotic, fibrinolytic regulators?

A

The endothelial cell

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63
Q

What four anticoagulant, antithrombotic and fibrinolytic regulators are elaborated in the endothelial cells?

A
  1. Prostacyclin
  2. Thrombomodulin
  3. Heparin-like molecules
  4. Plasminogen activator
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64
Q

What three prothrombotic molecules does the endothelial cell elaborate?

A
  1. VWF
  2. Tissue factor
  3. Plasminogen activator inhibitor
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65
Q

What does the endothelial cell use to modulate blood flow and vascular reactivity?

A
  1. Vasoconstrictors - endothelin, ACE

2. Vasodilators - NO, prostacylcin

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66
Q

What three substances are used in regulation of inflammation and immunity in the endothelial cell?

A
  1. IL-1, IL-6, chemokines

2. Adhesion molecules - VCAM-1, ICAM-1, E-selectin, P-selectin

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67
Q

Give three growth stimulators that regulate cell growth in endothelial cells?

A
  1. PDGF
  2. CSF
  3. FGF
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68
Q

Name two growth inhibitors that regulate cell growth in endothelial cells?

A
  1. Heparin

2. TNF-beta

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69
Q

What are important contributory factors in thrombosis that disrupt laminar blood flow?

A

Turbulence and stasis

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70
Q

What refers to any alteration in the coagulation pathway which predisposes to thrombosis?

A

Hypercoagulability

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71
Q

What two groups can conditions causing hypercoaguability be split into?

A

Acquired and Genetic

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72
Q

What are MI, immobilisation, tissue damage, cancer, prosthetic heart valves, DIC, heparin induced thrombocytopenia and antiphospholipid syndrome?

A

Acquired high risk hypercoaguable states

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73
Q

What are AF, cardiomyopathy, nephrotic syndrome, hyperoestrogenic states, oral contraceptive use, late pregnancy, sickle cell anaemia and smoking?

A

Lower risk aquired hypercoaguable states

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74
Q

Give three examples of genetic hypercoaguable states?

A
  1. Factor V mutations
  2. Defects in anticoagulant pathways - antithrombin III deficiency, protein C or S deficiency
  3. Defects in fibrinolysis
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75
Q

What show lines of Zahn?

A

Arterial thrombi

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76
Q

What two areas do mural thrombi take place?

A

Ventricles (heart) - MI, arrhythmias

Aorta (aneurysms) - atheroma

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77
Q

What thrombi are laminated due to alternating pale (platelet and fibrin) and dark (RBC/WBC) bands?

A

Mural thrombi

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78
Q

What is the term for a venous thrombi evoking inflammation?

A

Phlebothrombitis

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79
Q

What thrombi is most important in DVT of calf?

A

Venous thrombi (phlebothromboses)

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80
Q

What are large vessel thrombi prone to do?

A

Embolise

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81
Q

What thrombi form reddish/blue casts and are adherent to the wall?

A

Venosu thrombi

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82
Q

Give four fates of thrombi?

A
  1. Propagation proximally (small to large vessel)
  2. Embolisation
  3. Resolution (fibrinolysis)
  4. Organisation (granulation tissue, recanalisation)
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83
Q

What is the term for a detached intravascular solid, liquid ot gaseous mass which is carried by the bloodstream to a site distant from the point of origin?

A

Embolism

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84
Q

Name a fluid embolism?

A

Amniotic fluid embolism

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85
Q

What travels via IVC to pulmonary circulation?

A

Pulmonary thromboembolism

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86
Q

What can cause acute sudden death vs. segmental infarction (red infarcts), contrast with white infarcts?

A

Pulmonary thrombo embolism

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87
Q

How would you describe wedge shaped infarcts?

A

Wedge-shaped and firm

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88
Q

What is it important to remember in relation to venous emboli?

A

They do not cause infarcts in peripheral arterial circulation unless, atrial/ventricular septal defect, paradoxical embolus

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89
Q

What kind of embolism follows major soft tissue trauma and major bone fractures?

A

Fat embolism

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90
Q

Give two steps/features of fat emboli?

A
  1. Fatty marrow enters venules most globules arrest in lungs = dyspnoea
  2. Some reach peripheral circulation = skin rashes, CNS confusion
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91
Q

What embolism can result from barotrauma (occurs in divers) and during delivery/abortion or iatrogenic?

A

Gas/air embolism

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92
Q

How are vessels occluded in gas/air embolism?

A

Frothy bubbles occlude major vessels e.g. pulmonary artery

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93
Q

What embolism causes DIC (Disseminated intravascular coagulation), marked oedema and is post-partum?

A

Amniotic fluid embolism

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94
Q

How do amniotic fluid embolisms work?

A

Amniotic fluid and debris enters torn veins and embolises to lungs

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95
Q

What is a prostaglandin rich fluid?

A

Amniotic fluid

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96
Q

What three disease patterns is arteriosclerosis a generic term for?

A
  1. Atherosclerosis
  2. Monckeberg Medial Calcific Sclerosis
  3. Arteriosclerosis
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97
Q

What arteriosclerosis type occurs in >50 years and involes calcification of medium sized arteries?

A

Monckeberg Medial Calcific Sclerosis

98
Q

What can an atherosclerosis, ischaemic encephalopathy lead to?

A

Dementia

99
Q

What is the basic lesion in an atherosclerosis disease?

A

A plaque

100
Q

What two things occur as plaque size increases in atherosclerosis?

A
  1. Luminal diameter decreases

2. Blood flow reduces

101
Q

In atherosclerosis, what is a cause of more easily ingested by macrophages, acts as cehmotactic factors for monocytes, increase monocyte adhesion, induce antibody response, directly damage endothelial and smooth muscle cells and inhibit macrophage motility and trapping?

A

Lipoprotein oxidation

102
Q

During atherosclerosis, when hypercholesterolaemia persists, smooth muscle proliferation and collagen deposition convert the fatty streak into what?

A

A mature fibrofatty atheroma

103
Q

Which area of the aorta typically displays severe atheroma?

A

Bifurcation into iliac arteries

104
Q

Give 4 complications of atherosclerosis?

A
  1. Ulceration of athermatous plaque and thrombosis
  2. Haemorrhage into plaque with plaque rupture and embolism of plaque contents
  3. Ongoing narrowing = critical stenosis
  4. Aneurysm formation
105
Q

What results from inadequate systemic perfusion as a result of cardiac dysfunction?

A

Cardiogenic shock

106
Q

In the clinical diagnosis of angina, what is the pain like and what is it from?

A

Visceral pain from myocardial hypoxia - hard to describe

107
Q

What do provocation, relief and timing all lead to the clinical diagnosis of?

A

Angina

108
Q

Pressing, sqeezing, heaviness, a weight. Radiating to arms, back, neck, jaw, teeth. Exertion, stress, cold wind, after meals. Few minutes, relieved by rest, GTN.

A

Angina

109
Q

Give three features of peptic ulcer pain?

A
  1. Epigastric
  2. Boring and point of finger gesture
  3. Relief by antacids/foods
110
Q

What type of chest pain is focal, exacerbated by breathing, sharp and catching?

A

Pleuritic pain

111
Q

What is the pain like in dissection of aorta?

A

Tearing, excruciating, severe then eases

112
Q

What is the gold standard investigation for CHD?

A

Angiography

113
Q

What two methods of revascularisation are there for reducing risk and symptoms of CHD?

A
  1. CABG

2. PCI

114
Q

What four drugs are there for CHD?

A
  1. Aspirin
  2. Bblockers
  3. Statin
  4. ACE inibitor
115
Q

What is there a risk of 8-10 years post-op in coronary artery bypass?

A

Graft disease

116
Q

Give 4 complications of CABG?

A
  1. death
  2. stroke
  3. MI
  4. AF
117
Q

What do these steps describe: vascular access, antiplatelet/coagulation, catheter to ostium of coronary, guidewire down vessel, balloons threaded over wire, stents implanted, balloon catheter and wires removed?

A

PCI technique

118
Q

What are two indications for angiography?

A
  1. Severe symptoms

2. High risk

119
Q

What are 4 indications for aborting revascularisation?

A
  1. Multi-vessel disease
  2. Diabetes
  3. Left main disease
  4. Co-morbidities
120
Q

What revascularisation is done in a STEMI?

A

Primary PCI

121
Q

What revascularisation is done in acute coronary syndrome?

A

Angiography with a view to revascularisation

122
Q

What revascularisation is done in chronic stable angina?

A

Revascularisation for severe symptoms or high risk

123
Q

What 2 vasculitis diseases can be risk factors for DVT/PE?

A
  1. SLE and lupus anticoagulant

2. Behcet’s disease

124
Q

Give 4 things related to drugs and medications that can be risk factors for DVT/PE?

A
  1. IV drug abuse
  2. Oestrogens - ORP and HRT
  3. Tamoxifen
  4. Chemotherapy
125
Q

What blood test would you do to investigate DVT?

A

D-dimer

126
Q

What are di-dimers?

A

Fibrin breakdown products

127
Q

What five other conditions can raise d-dimers?

A
  1. Infection
  2. MI
  3. Surgery
  4. Liver disease
  5. Pregnancy
128
Q

What imaging would you use to investigate DVT?

A

Ultrasound

129
Q

What technique for investigating DVT involves: strain gauge around affected limb, venous emptying by compression, measure refill time (fast = not much, empty = clot)?

A

Venous plethysomography

130
Q

What should be done when diagnosing DVT if there is high PTP score, but negative d-dimer and USS?

A

No DVT, consider other differentials

131
Q

What should be done when diagnosing DVT if there is a high PTP score, positive d-dimer but negative USS?

A

Repeat assessment, repeat USS later

132
Q

What are two treatment methods for DVT?

A
  1. anticoagulation with LMWH and warfarin

2. Compression stockings

133
Q

What is phlegmasia dolens and what can it cause?

A

DVT causing obstruction of arterial inflow - severe DVT, background PAOD
Can cause venous gangerene

134
Q

Give three treatments for Phlegmasia dolens?

A
  1. IVC filter
  2. Femoral arterial line
  3. tPA intra-arterially
135
Q

What are SOB, collapse, pleuritic chest pain, haemoptysis and sudden death causes of?

A

Pulmonary thromboembolism

136
Q

What is oligemia on CXR and what can it be a sign of?

A

Segmental loss of pulmonary vasculature - PE

137
Q

What heart sounds can be heard in PE?

A

Fourth heart sound or accentuated pulmonic component of the second heart sound

138
Q

What can a pleural rub, tachypnea, hypotension, cardiorespiratory arrest, wheeze, tachycardia and signs of pleural effusion all be found in?

A

PTE

139
Q

What, on the ECG is only seen in 20% of PE cases?

A

S1, Q3, T3

140
Q

What are four main investigations for PTE?

A
  1. Arterial blood gases
  2. CXR
  3. V/Q scan
  4. CTPA
141
Q

When should a V/Q scan be performed to investigate a PE?

A

Within 48 hours

142
Q

What investigation for PE is poor for more peripheral lesions and involves breath holding/IV contrast?

A

CT pulmonary angiogram

143
Q

What can potentially be the four main treatments for PE?

A
  1. Anticoagulants
  2. Thrombolytic therapy
  3. IVC interupption - IVC filter/surgery
  4. Surgical removal
144
Q

What is the treatment for a massive PE with shock or syncope?

A

Thrombolysis or surgery

145
Q

What is the treatment for a major PE with right-ventricular dysfunction?

A

Anticoagulants and thrombolysis

146
Q

What is the treatment for a major PE without reight-ventricular dysfunction?

A

Anticoagulants

147
Q

What is the treatment for a minor PE?

A

Anticoagulants

148
Q

What anticoagulant is used for initial treatment of PE?

A

LMWH

149
Q

What induction period with heparin is associated with a lower rate of recurrent PE?

A

5 days

150
Q

What would be used for PTE treatment in these cases: recurrent PTE despite adequate anticoagulation, PTE when coagulation cannot be used (post-op) and high risk patients (phlegmasia dolens)?

A

IVC filter

151
Q

Give an indication for surgery (pulmonary embolectomy) in PTE?

A

Chronic thromboembolism pulmonary hypertension

152
Q

Name two anticoagulation vitamin K antagonists for PTE?

A

Wrfarin and phenindione

153
Q

Name an antithrombin drug used as anticoagulation therapy in PTE?

A

Dabigatran

154
Q

Name two anti Xa drugs used as anticoagulation in PTE?

A

Apixaban and rivaroxaban

155
Q

Where are the four vitamin K dependent clotting factors synthesised?

A

In the liver

156
Q

What are the four vitamin K dependent clotting factors?

A
  1. II
  2. X
  3. IX
  4. VII
157
Q

What drug acts as an anticoagulant by blocking the ability of vitamin K to carboxylate the vitamin K dependent clotting factors, therefore reducing their coagulant activity?

A

Warfarin

158
Q

What three things is warfarin used in teh prophylaxis/and or treatment of?

A
  1. Venous thrombosis and its extension
  2. Pulmonary embolism
  3. Thromboembolic complications associated with AF and cardiac valve replacement
159
Q

What is a mathematical correction that normalises the PT ratio by adjusting for the variablity in the sensitivity of the different thromboplastins?

A

INR ratio

160
Q

Give four conditions where warfarin therapy is contraindicated?

A
  1. Pregnancy
  2. Bleeding diathesis
  3. Uncontrolled alcohol/drug abuse
  4. Unsupervised dementia/physhosis
161
Q

What does heparin bind directly to, to inactivate it?

A

Thrombin

162
Q

What factors does heparin inactivate?

A

Xa
IXa
XIa

163
Q

How is heparin dosing monitored?

A

By activated partial thromboplastin time (APTT)

164
Q

What is a large molecule, cross links thrombin with antithrombin, thrombin inhibition 4 fold compared to action on factor Xa, unpredictable and needs monitored?

A

UFH

165
Q

What is a small molecule, no cross links, thrombin inhibition 1 to 1 with action of factor Xa, predictable by weight and needs no monitoring?

A

LMWH

166
Q

Which has less osteopenia, LMWH or UFH?

A

LMWH

167
Q

Give four cautions and caveats of LMWH?

A
  1. Dosing in obesity and in renal insufficiency
  2. Dosing in pregnancy
  3. Protamine reversal
  4. Interchangeability of different preperations
168
Q

How long is the duration of therapy for PE in a temporary risk factor?

A

4-6 weeks

169
Q

How long is the duration of therapy for PTE in an idiopathic PE?

A

3-6 months

170
Q

How long is the duration of therapy for PTE in a second idiopathic event?

A

LIFELONG

171
Q

What are inherited thrombophilia (not factor V Leiden or prothrombin mutation), antiphospholipid syndrome, recurrent idiopathic VTE, malignancy and thromboembolic pulmonary hypertension?

A

Potential indications for indefinite anticoagulant therapy

172
Q

For oral anticoagulation, what remains the only option?

A

Vitamin K antagonists

173
Q

Give three things you would monitor with anti-thrombin drugs?

A
  1. Monitor aPTT
  2. Thrombin time for DTIs
  3. Ecarin clotting time
174
Q

What is used to reverse dabigatran?

A

Recombinant factor VIIa, FFP and dialysis

175
Q

How do you reverse FXa inhibitors?

A

Prothrombin complex concentrate (PCC)

176
Q

What occurs when insufficient blood reaches exercising muscle?
The patient is pain-free at rest, but after exercise develops ischaemic pain in the affected limb, which is relieved by rest.

A

Intermittent claudication

177
Q

Name a protective factor for intermittent claudication?

A

Alcohol

178
Q

List two non-invasive investigations for lower limb ischaemia?

A
  1. Measurement of ABPI

2. Ultrasound scanning

179
Q

Name 3 invasive investigations for lower limb ischaemia?

A
  1. Magnetic resonance angiography
  2. CT angiography
  3. Catheter angiography
180
Q

What does ABPI stand for?

A

Ankle Brachial Pressure Index

181
Q

What is the equation for ABPI?

A

Ankle pressure / brachial pressure

182
Q

What is a normal ABPI level?

A

0.9 - 1.2

183
Q

What is a claudication ABPI level?

A

0.4 - 0.85 (-1)

184
Q

What is a severe ABPI level?

A

0 - 0.45

185
Q

Give four ways of improving claudication symptoms?

A
  1. Exercise training
  2. Drugs
  3. Angioplasty/stenting
  4. Surgery
186
Q

What intensity of exercise should you be doing with intermittent claudication?

A

1 hour per day

30 minutes 3 times per week for 6 months

187
Q

Name a drug used for intermittent claudication?

A

Cilostozol

188
Q

Give two types of critical limb ischaemia?

A
  1. Rest pain - toe/foot ischaemia (nerve ending pain)

2. Ulcers/gangrene = severe ischaemia + damage

189
Q

What is rest pain, in toes and forefoot, worse at night, helped by sitting and putting the leg in a dependent position and helped by getting up and walking about?

A

Critical limb ischaemia

190
Q

What are two major risk factors for amputation in critical limb ischaemia?

A
  1. Smoking

2. Diabetes

191
Q

What are 3 methods of treatment for critical limb ischaemia?

A
  1. Analgesia
  2. Angioplasty/stenting
  3. Surgical reconstruction/amputation
192
Q

What patients are more likely to develop intermittent claudication and critical limb ischaemia?

A

Males > 55 years

193
Q

What does this pathogenesis describe: medial degeneration, regulation of elastin/collagen in aortic wall, aneurysmal dilatation, increase in aortic wall stress and progressive dilatation (law of laplace)?

A

Abdominal Aortic Aneurysm

194
Q

What size are true arterial aneurysms?

A

50% increase in normal diameter (1.2 - 2cm)

195
Q

What are the three main risk factors for abdominal aortic aneurysm?

A

Female, smoker, hypertensive

196
Q

What are these symptoms of: tachycardia, hypotensive, pulsatile, expansile mass +/- tender, transmitted pulse and perihperal pulses?

A

Symptomatic AAA

197
Q

What two investigations are done for AAA?

A
  1. Ultrasound

2. CT scan

198
Q

What investigation only tells us if there is an AAA, not its AP diameter?

A

Ultrasound scan

199
Q

What investigation for AAA, allows identification of shape, size, iliac movement and allows for management planning? It is also the only method to identify ruptured AAA?

A

CT scan

200
Q

What type of operations are elective aneurysm repairs?

A

Prophylactic

201
Q

What type of operation is an emergency aneurysm repair?

A

Therapeutic

202
Q

What can be done during intervention of an abdominal aortic aneurysm?

A

Endovascular aneurysm repair (EVAR)

203
Q

In open/laparotomy repair of an abdomoinal aortic aneurysm, what graft is used?

A

Dacron graft

204
Q

What patients are abdominal aortic aneurysms commonly found in?

A

Males > 60

205
Q

What three veins are part of the deep system in the leg?

A
  1. Tibials
  2. Popliteal
  3. Femoral
206
Q

What two veins are part of the superficial system in the leg?

A
  1. Saphenous

2. Perforators

207
Q

What is the term for dilated, tortuous superficial veins, due to transmission of deep vein pressure?

A

Varicose veins

208
Q

What can you get varicose veins following?

A

A DVT

209
Q

What two conditions increase the deep veins pressure and can cause varicose veins?

A
  1. Deep vein obstruction

2. Deep valve incompetence

210
Q

What are 4 signs of varicose veins?

A
  1. Dilated and tortuous superficial veins
  2. More prominent with standing
  3. Arising in groin or behind the knee
  4. Complications of varicose veins
211
Q

What are three clinical features of chronic venous insufficiency?

A
  1. Haemosidering deposits
  2. Lipodermatosclerosis
  3. Ulceration
212
Q

What are bleeding and bruising, superficial thrombophlebitis and chronic venous insufficiency all complciations of?

A

Varicose veins

213
Q

What is thrombophlebitis?

A

Inflammation of a vein caused by a blood clot

214
Q

What is the term for irreversivle skin damage as a result of sustained ambulatory venous hypertension?

A

Chronic venous insufficiency

215
Q

What is a break in the skin, between malleoli and tibial tuberosity, presumed to be due to venous disease?

A

Chronic venous ulcer

216
Q

What are haemosiderin deposits caused?

A

Red cell leakage, red cell breakdown and haemosiderin (iron)

217
Q

What can superficial reflux (LSV and/or SSV), deep reflux, deep venous occlusion, mixed superficial and deep disease, perforating vein reflux and abnormal calf pumps cause?

A

Venous hypertension

218
Q

What are the two main issues ultrasound focuses on in relation to varicose veins?

A
  1. State of the deep veins (occlusions or impotence)

2. Saphenofemoral or saphenopopliteal incompetence

219
Q

What is graduated compression as a management for varicose veins contraindicated in?

A

Low ABPI

220
Q

Name three types of interventional, endovenous management methods for varicose veins?

A
  1. Foam sclerotherapy
  2. Endovenous ablation
  3. Surgical - high tie, stripping or foam, multiple stab avulsions or foam
221
Q

Give four complications of intervention of varicose veins?

A
  1. Thrombophlebitis
  2. Skin staining
  3. Local ulceration
222
Q

What is acute onset of focal neurological symptoms and signs due to disruption of blood supply?

A

Stroke

223
Q

In a haemorrhagice stroke: what two factors can weaken blood vessel walls?

A
  1. Structural abnormalities like aneurysm, arteriovenous malformation (AVM)
  2. Inflammation of vessel wall (vasculitis)
224
Q

What are three modifiable risk factors for stroke?

A
  1. Hypertension
  2. Hyperlipidaemia
  3. Smoking
225
Q

What is homocysteinemia a rare cause of?

A

Stroke

226
Q

What can protein S, C and antithromboin III deficiency cause (rarely)?

A

Stroke

227
Q

What 4 genetic causes of stroke are there?

A
  1. Factor V Leiden mutation
  2. Common prothrombin mutation
  3. MELAS + CADASIL
  4. Fabry’s disease
228
Q

What can hypoglycaemia, siezure and migraines mimic?

A

Stroke

229
Q

What is the only way of differentiating between ischaemic and haemorrhagic stroke?

A

Brain imaging

230
Q

What are three brain imaging techniques used for stroke?

A
  1. CT Brain +/- angiography
  2. MRI with DWI +/- angiography
  3. MRI with GRE - looks for old haemosiderin deposits
231
Q

What does LVH on an ECG suggest?

A

Uncontrolled hypertension which is common cause of AF

232
Q

What embolism infarcts in same side as affected carotid artery?

A

Atheroembolism

233
Q

What embolism infarcts in more than one arterial territory, bilateral?

A

Cardioembolism

234
Q

If there is a haemorrhagic stroke in a young patient, what two underlying conditions will you investigate for?

A
  1. Aneurysm

2. AVM

235
Q

If there is a haemorrhagic multiple bleed, what two conditions would you look for?

A

Vasculitis
Moya Moya disease
(using cerebral amyloid angiopathy

236
Q

What two drugs do you give for initial management of TIA/stroke?

A

Aspirin 75mg + dipyridamole MR 200mg twice daily/clopidogrel 75mg daily

237
Q

What along with antiplatelets, what three drugs would you give for TIA/stroke managmenet?

A
  1. Statins
  2. Anticoagulate if AF
  3. Antihypertensives
238
Q

What are three surgical managements for TIA/stroke?

A
  1. Haematoma evacuation
  2. Relief of raised intracranial pressure
  3. Carotid endarterectomy
239
Q

What surgical management would you do for obstructive hydrocephalus and large total MCA infarctions?

A

Relief of intracranial pressure

240
Q

What surgical management would you do for a patient with >70% stenosis in same sided internal carotid artery?

A

Carotid endarterectomy

241
Q

In emergency management of TIA what is done?

A

Thrombolysis

JL Cardiovascular (18 decks)

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