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MBBS - Year 2 > Vascular System - Acute & Chronic Ischaemia > Flashcards

Vascular System - Acute & Chronic Ischaemia Flashcards

1
Q

What is the Circulatory system transport for

A

Oxygen
Nutrients
Waste products

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2
Q

What does the circulatory system consist of

A

Heart
Vessels (arteries, capillaries, veins)
Lymphatics (to a lesser extent)

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3
Q

General structure of arteries and veins

A

Composed of 3 layers - tunics
Tunica intern, tunica media, tunica externa
Lumen

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4
Q

Lumen

A

Central blood-containing space surrounded by tunics

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5
Q

What are capillaries composed of

A

Endothelium with sparse basal lamina

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6
Q

Structure of elastic (conducting) arteries

A

Large lumen allows low-resistance conduction of blood

Contains elastin all 3 tunics

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7
Q

Where are elastic (conducting) arteries found

A

Thick-walled arteries near the heart; the aorta and its major branches

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8
Q

Function of elastic (conducting) arteries

A

Withstand and smooth out large blood pressure fluctuations

Allows blood to flow fairly continuously through the body

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9
Q

Structure of muscular (distributing) arteries and arterioles

A

Have thick tunica media with more smooth muscle and less elastic tissue
Active in vasoconstriction

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10
Q

Arterioles

A

Smallest arteries; lead to capillary beds

Control flow into capillary bed via vasodilation and constriction

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11
Q

When are veins formed

A

When venules converges

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12
Q

What are veins composed of

A

3 tunics, with a thin tunica media and thick tunica externa consisting of collage fibres and elastic networks

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13
Q

Veins as capacitance vessels

A

Blood reservoirs

Contains 65% of the blood supply

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14
Q

Special adaptations of veins

A

Large diameter BP, which offer little resistance to flow

Valves, which prevent back flow of blood

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15
Q

Venous sinuses

A

Specialised, flattened veins with extremely thin walls (e.g. coronary sinus of the heart and dural sinuses of the brain)

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16
Q

Anastomosis

A

Connection between two structures that are normally diverging e.g. arteriovenous

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17
Q

What is blood flow equivalent to

A

Cardiac output (CO), considering the entire vascular system

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18
Q

What is blood flow, or tissue perfusion, involved in

A

Delivery of oxygen and nutrients to, and removal of waste from tissue cells
Gas exchange in the lungs
Absorption of nutrients from the digestive system

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19
Q

What is blood pressure

A

Force per unit area exerted on the wall of a blood vessel by its contained blood

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20
Q

Main factors influencing BP

A 
Cardiac output (CO)
Peripheral resistance (PR)
Blood volume
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21
Q

Blood pressure eqn

A

CO x PR

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22
Q

What is blood flow directly proportional to

A

The difference in bp between two points in the circulation

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23
Q

What is blood flow inversely proportional to

A

Resistance

R is more important than difference in bp between 2 points in the circulation

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24
Q

Systolic pressure

A

Pressure exerted on arterial walls during ventricular contraction

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25
Q

Diastolic pressure

A

Lowest level of arterial pressure during a ventricular cycle

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26
Q

Pulse pressure

A

The difference between systolic and diastolic pressure

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27
Q

Calculating MAP

A

Diastolic pressure + 1/3 pulse pressure

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28
Q

Venous BP throughout cardiac cycle

A

Steady and changes little during the cardiac cycle

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29
Q

Factors aiding venous return

A

Respiratory pump
Muscular pump
Valves prevent back flow during venous return

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30
Q

APBI

A

Ankle: Brachial Pressure Index

An objective vascular measurement of the vascular supply to the lower limbs

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31
Q

Body sites to palpate pulse

A 
Temporal artery 
Facial artery
Common carotid artery 
Brachial artery 
Radial artery 
Femoral artery 
Popliteal artery 
Posterior tibial artery 
Dorsalis pedis artery
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32
Q

Autoregulation

A

Automatic adjustment of blood flow to each tissue in proportion to the requirements at any given point in time

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33
Q

What does atherosclerotic disease have a predilection for

A 
Carotid bifurcation
LAD 
Aortic bifurcation 
Common bifurcation 
Superficial femoral 
Aorta just distal to left (subclavian)
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34
Q

Vascular disease - arterial

A

Narrow and block
Expand and pop
Embolus

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35
Q

What points does an aneurysm have a predilection for

A

Abdominal aorta
Popliteal Arteries
All the vessels

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36
Q

Embolus

A

A mass of clotted blood or other material

Brought by the blood from one vessel and forced into a smaller one, obstructing the circulation

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37
Q

What does a decrease in tissue perfusion promote

A

Compensatory mechanisms e..g vasodilation, development of collateral vessels and anaerobic metabolism

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38
Q

True aneurysm

A

When an aneurysm involves an intact attenuated arterial wall or thinned ventricular wall of the heart
Involves all 3 layers

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39
Q

When does an arterial dissection arise

A

Tear in the intima

When blood enters the arterial wall itself, a haematoma dissecting between its layers

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40
Q

False aneurysm (pseudo-aneurysm)

A

Defect in the vascular wall leading to an extravascular haematoma
Does not consist of the true layers of the arterial wall

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41
Q

Saccular aneurysms

A

Spherical out pouching
Vary from 5-20 cm in diameter
Often contain thrombus

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42
Q

Fusiform aneurysms

A

Involve diffuse, circumferential dilation of a long vascular segment
Vary in diameter (up to 20cm)

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43
Q

Factors of pathogenesis of aneurysms

A

The intrinsic quality of the vascular wall connective tissue is poor
The balance of collagen degradation and synthesis is altered
The vascular wall is weakened through loss of smooth muscle cells

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44
Q

Examples of poor intrinsic quality of the vascular wall

A
  1. Marfan syndrome – defective synthesis of fibrillin
  2. EDS – defective type III collagen causing weak vessel wall
  3. Vit C deficiency – altered collagen cross-linking
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45
Q

When does ischaemia of the inner media occur

A

When there is atherosclerotic thickening of the intima “increases the distance that oxygen and nutrients must diffuse”

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46
Q

Factors predisposing weakening of arterial wall

A 
Atherosclerosis 
HTN 
Trauma 
Vasculitis 
Congenital defects 
Infections
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47
Q

How can mycotic aneurysms originate

A

From embolisation of a septic thrombus, usually as a complication of infective endocarditis
By circulating organisms directly infecting the arterial wall

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48
Q

Syphilitic aneurysms

A

3’ syphilis is now a rare cause of aortic aneurysms

Ischaemic injury can be caused by obliterative endarteritis

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49
Q

What are AAA’s associated with

A

Atherosclerotic plaque in the intima compresses the underlying media

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50
Q

Risk factors for AAA

A

Men
Smokers
Age 50+
Atherosclerosis

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51
Q

Where are AAA’s usually found

A

Usually positioned below the renal arteries and above the bifurcation of the aorta
Can be saccular or fusiform

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52
Q

Consequences of AAA

A

Rupture into the peritoneal cavity or retroperitoneal tissues with potentially fatal haemorrhage
Obstruction of a branch vessel resulting in ischaemic injury of downstream tissue
Embolism forms atheroma or mural thrombus

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53
Q

Px of AAA

A

Abdominal mass (pulsating) that simulates a tumour

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54
Q

When can aortic dissection be catastrophic

A

If the dissection then ruptures through the adventitia and haemorrhages into adjacent spaces

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55
Q

Aortic dissection classification

A

Type A dissection

Type B dissection

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56
Q

Type A dissection - aortic dissection

A 
More common (dangerous) proximal lesions
Involving either both ascending & descending aorta or just the ascending aorta
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57
Q

Type B dissection - aortic dissection

A

Distal lesions usually beginning distal to the L subclavian artery

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58
Q

Classical clinical symptoms of aortic dissection

A

Sudden onset of excruciating pain:
Beginning in the anterior chest
Radiating to the back between the scapulae
Moving downward as the dissection progresses
Confused with that of MI

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59
Q

Pathogenic mechanisms of vasculitis

A

Immune-mediated infl
Direct invasion of vascular walls by infectious pathogens
Infections can indirectly induce non-infectious vasculitis - by generating immune complexes or triggering cross-reactivity

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60
Q

Types of vasculitis

A

Large vessel
Medium vessel
Small vessel

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61
Q

Thromboangitis Obliterans (Buerger disease)

A

Distinctive disease that often leads to vascular insufficiency
Segmental, thrombosing, acute and chronic infl of medium-sized and small arteries

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62
Q

Epidemiology of Buerger disease

A

Occurs almost exclusively in heavy cigarette smokers, usually before the age of 35

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63
Q

Pathogenesis of Buerger disease

A

Strong rship to cigarette smoking

Genetic influences - certain HLA halotypes

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64
Q

Clinical features of Buerger’s disease

A

Cold sensitivity of the Raynaud type in the hands
Pain in the instep of the foot
Severe pain, related to the neural involvement
Chronic ulcerations of the toes, feet or fingers

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65
Q

What can bring drastic relief from further attacks of Buerger’s diesase

A

Abstinence of cigarette smoking

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66
Q

Varicose veins

A

Abnormally dilated, tortuous veins

The superficial veins of the upper and lower leg are typically involved

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67
Q

What are varicose veins produced by

A

Prolonged, increased intraluminal pressure

Loss of vessel wall support

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68
Q

What can happen when legs are dependent for prolonged periods

A

Venous pressure in these sites can be markedly elevated (up to 10x) and can lead to venous stasis and pedal oedema

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69
Q

Why is there a higher incidence of varicose veins in females

A

A reflection of the elevated venous pressure in lower legs caused by pregnancy

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70
Q

Most disabling sequelae of varicose veins

A

Incl persistent oedema in the extremity and ischaemic skin changes manifesting as stasis dermatitis and ulcerations

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71
Q

Where do venous ulcers usually occur

A

Gaiter areas

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72
Q

Thrombosed deep veins vs superficial

A

Embolism from the superficial veins is rare but thromboembolism is relatively frequent in thrombosed deep veins

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73
Q

Venous leg ulcers pathophysiology

A

80-85% of all cases develop when persistently high bp in the veins of the legs (venous htn) causes damage to the skin, which eventually breaks down and forms an ulcer

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74
Q

Interchangable names for venous thrombosis and infl

A

Thrombophlebitis

Phlebothrombosis

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75
Q

Portal vein thrombosis

A 
Peritoneal infections (peritonitis, appendicitis, salpingitis and pelvic abscesses)
Thrombophilic condn associated with platelet hyperactivity (e.g., polycythaemia vera)
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76
Q

Mechanical factors that slow venous return and promote DVT

A

Congestive heart failure
Pregnancy
Obesity

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77
Q

Trousseau sign

A

Venous thromboses classically appear at one site, disappear and then reoccur in other veins – migratory thrombophlebitis

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78
Q

Local manifestations of thrombi in legs incl

A 
Distal oedema 
Cyanosis 
Superficial vein dilation 
Heat 
Tenderness 
Redness 
Pain
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79
Q

PE as a serious complication of DVT

A

Fragmentation/ detachment of the whole venous thrombus
Can be 1st manifestation of thrombophlebitis
Outcome ranges from no symptoms to death

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80
Q

What does Raynaud’s phenomenon result from

A

Exaggerated vasoconstriction of digital arteries and arterioles

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81
Q

What does secondary Raynaud’s refers to

A

Vascular insufficiency of the extremities 2’ to arterial disease caused by SLE, scleroderma, Buerger disease or even atherosclerosis

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82
Q

Peripheral Arterial Disease

A

Term used to describe a narrowing or occlusion of the peripheral arteries, affecting the blood supply to the lower limbs

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83
Q

What is PAD most caused by

A

Atherosclerosis which narrows the affected arteries. This limits blood flow to the affected limb

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84
Q

Epidemiology of PAD

A

More common in males

Prevalence rises with age

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85
Q

What diseases are PAD associated with

A

Coronary artery disease

Cerebrovascular disease

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86
Q

Fontaine classification of PAD

A 
Stage I - Asymptomatic 
Stage IIa - mild claudication 
Stage IIb - moderate to severe (short distance) claudication
Stage III - ischaemic rest pain 
Stage IV - ulceration or gangrene
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87
Q

Most common symptom of PAD

A

IC

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88
Q

Intermittent claudication

A

Exercise–induced muscle pain
Most commonly in the calf, thighs, buttocks
Worse walking uphill or hurrying
Relieved by rest <10 mins

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89
Q

Possible Intermittent Claudication sites

A

Buttock and hip
Thigh
Calf
Foot claudication

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90
Q

IC site - buttock and hip

A

Aortoiliac disease (Leriche syndrome triad)

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91
Q

IC site - thigh

A

Aortoiliac or common femoral artery

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92
Q

IC site - upper 2/3 of the calf

A

Superficial femoral artery

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93
Q

IC site - lower 1/3 of the calf

A

Popliteal artery

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94
Q

IC site - foot claudication

A

Tibial or peroneal artery

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95
Q

Types of ddx of PAD

A

Vascular
Neurological pain
MSK

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96
Q

Vascular ddx for PAD

A 
Aneurysm
Limb trauma
Radiation exposure
Vasculitis or ergot use for migraines
Popliteal entrapment syndrome
Chronic venous disease
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97
Q

Neurological ddx for PAD

A 
Neurospinal (e.g. disc disease, spinal stenosis, tumour) 
Neuropathic causes (e.g. DM, alcohol abuse)
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98
Q

Prevalence of Chronic Limb Threatening Ischaemia

A

1 - 2%

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99
Q

When is Chronic Limb Threatening Ischaemia seen

A

When two or more levels of arterial tree are diseased

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100
Q

Ischaemic rest pain

A

Severe pain at rest due to inadequate oxygen perfusion

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101
Q

Chronic limb threatening ischaemia and Critical limb threatening ischaemia

A

Chronic limb threatening limb ischaemia can develop into Critical Limb ischaemia

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102
Q

Where do ischaemic ulcers form

A

At sites of increased focal pressure
Malleoli, tips of toes, metatarsal heads, heels
Usually dry and punctuate

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103
Q

What condn is dry gangrene most likely seen in

A

DM

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103
Q

When does dry gangrene develop

A

When blood flow to the affected area is impaired
The tissue dries up and may be brown to purplish-blue to black in colour
Can be left to auto-amputate or can be amputated after revascularisation

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104
Q

Wet gangrene

A

Liquefactive necrosis due to infection

The tissue swells and blisters and is called ‘wet’ because of pus

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105
Q

Why is wet gangrene v serious

A

Infection from wet gangrene can spread quickly throughout the body

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106
Q

Treatment of wet gangrene

A

Needs IV high dose Abx

Revascularisation, debridement +-/- amputation

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107
Q

Clinical exam for PAD

A 
Inspection (scars, ulcers, gangrene, venous guttering)
Buerger's test 
Palpation of pulses 
Auscultation for bruits 
APBI measurement
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108
Q

Vascular ix for PAD

A

Duplex ultrasound
CT angiography
Magnetic resonance angiography

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109
Q

Lifestyle modifications for asymptomatic PAD pts or mild claudication

A

Smoking cessation
Exercise
Diet control

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110
Q

Pharmacological therapy for asymptomatic PAD pts and mild claudication

A

Risk factor modification (control BP, diabetes, dyslipidaemias)
Antiplatelet therapy (clopidogrel 75mg OD)
Cholesterol lowering medication (atorvastatin 80mg OD)

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111
Q

Mx for short distance claudication - Lifestyle modification

A

Supervised exercise classes

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112
Q

Mx for short distance claudication - Pharmacological

A

BP/ DM/ Cholesterol control
Antiplatelet and statins
Naftidofuryl/ cilostazol

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113
Q

Mx of short distance claudication - endovascular

A

Angioplasty +/- stent placement

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114
Q

Mx of short distance claudication - Surgical

A

Endarterectomy

Peripheral bypass graft: autologous vein, prosthetic (long blockages of vessels)

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115
Q

Angioplasty

A

Pressure controlled balloon inflation to fracture arterial plaque and remodel the artery

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116
Q

What’s angioplasty most effective for

A

Short focal stenoses without heavy calcification

Excessive calcification is resistant to angioplasty

117
Q

Complications of angioplasty

A 
Arterial puncture site haemorrhage 
Arterial rupture 
Dissection 
Distal embolism 
Contrast induced nephropathy
118
Q

Stents

A

Supportive framework that apply radial force to diseased arteries and promotes vessel remodelling

119
Q

What are stents made from

A

Stainless steel or Nitinol

120
Q

2 types of stents

A

Balloon expandable

Self-expanding stents

121
Q

Surgical revascularisation

A

Endarterectomy

Surgical bypass

122
Q

When is endarterectomy used in surgical revascularisation

A

For lesions in readily accessible sites, such as common femoral artery

123
Q

Which surgical bypasses require a prosthetic graft

A

Infra-inguinals bypasses
Aorta-iliac
Femoral-femoral crossover
Axillo-bifemoral

124
Q

Complications of surgical revascularisation

A 
Bleeding 
Infection 
Distal embolism 
Limb loss
Heart/ lung/ kidney complications 
DVT 
Death
125
Q

Mx of CLTI

A 
Lifestyle modification 
Pharmacological therapy 
Wound care - conservative mx 
Revascularisation 
Amputation
126
Q

Leading cause of amputation in western world

A

PAD

127
Q

How many more times likely are diabetics to suffer amputation

A

8-12x

128
Q

What must be considered before amputation

A

Rehabilitative potential of the pt
Level and pattern of vascular disease
Likely healing

129
Q

Common amputation sites

A 
Toe amputation 
Ray amputation 
Tran-metatarsal amputation
Below knee amputation
Above knee amputation
130
Q

Toe amputation

A

Removal of toe through proximal phalanx

131
Q

Ray amputation

A

Removal of toe through metatarsal bone

132
Q

Trans-metatarsal amputation

A

Amputation of all the toes through mid-metatarsal bones

133
Q

Below knee amputation

A

Through tibia 10-12 cm distal to tibial tuberosity

Through fibula 2cm proximal to tibia

134
Q

Above knee amputation

A

At mid-femoral level >15 cm from tibial plateau

135
Q

Amputation complications

A 
Failure of wound to heal 
Flap necrosis 
Wound infection 
Post amputation pain 
Stump haematoma 
Flexion contractures 
Psychological problems
136
Q

Why should rehab be started ASAP after amputationn

A

Prevents flexion contractures

137
Q

What happens after stump heals - amputation

A

Elasticated compression, stump socks fitted to shrink stump to an acceptable size for fitting for prosthesis

138
Q

When is limb fitting usually delayed until

A

> 6/52 post-op to allow stump oedema to subside

139
Q

Prognosis for IC

A

Variable, over 5-years most people continue to have stable claudication
10-20% develop worsening symptoms
5-10% develop critical limb ischaemia
Amputation in required in 1-2%

140
Q

Prognosis of CLTI

A

High risk of amputation and premature death
50 - 90% will have a revascularisation procedure
1/3 require LL amputation if no revascularisation
5-yrs all cause mortality of 50%

141
Q

ALI

A

A sudden decrease in limb perfusion that causes a potential threat to limb viability in pts who present within 2 weeks of the acute event
Surgical emergency

142
Q

Incidence of ALI

A

1.5 cases per 10,000 people per yr but is a frequent missed or delayed dx

143
Q

Aetiology of ALI

A

Embolus
Thrombosis
Trauma

144
Q

Aetiology of ALI - Embolus

A

Cardiac source - AF, MI, endocarditis, valvular disease, atrial myxoma, prosthetic valves
Arterial source - aneurysms, atherosclerotic plaque

145
Q

Aetiology of ALI - thrombosis

A 
Vascular grafts 
Atherosclerosis 
Thrombosis of aneurysm
Entrapment syndrome 
Hypercoaguable state 
Low flow state
146
Q

Aetiology of ALI - Trauma

A

Blunt
Penetrating
Iatrogenic

147
Q

6P’s of acute ischaemia

A 
Pain 
Pulselessness 
Pallor
Paresthesia 
Paralysis 
Poikilothermic (perishingly cold)
148
Q

Imaging for ALI

A

CT angiography - distinguishes between thrombosis and embolism
Bedside Doppler ultrasound scan

149
Q

Initial mx for ALI

A 
ABC 
Analgesia 
FBC 
U&Es
Baseline clotting profile 
Heparin
IV access and IV resus
ECG
Catheterise and hourly UO
150
Q

Giving heparin for ALI

A

Once the dx of acute arterial occlusion has been made the pt should immediately receive an IV-heparin bolus of 5,000 units followed by continuous infusion

151
Q

What does mx of ALI depend on

A

Type of occlusion (thrombosis or embolus)
Location
Duration of ischaemia
Neurological deficit
Co-morbidities
Type of conduit (artery or graft, the risks of treatment and the viability of the limb)

152
Q

Endovascular therapies for ALI

A

Percutaneous catheter-directed thrombolytic therapy

Percutaneous mechanical thrombus extraction

153
Q

Surgical mx for ALI - emboli cause

A

Surgical embolectomy
Bypass surgery (if there is insufficient flow back)
Local intra-arterial thrombolysis
Amputation if limb is unsalvageable

154
Q

Thromboembolectomy

A

Balloon connected to Fogarty catheter inflated removing thrombi

155
Q

Complications of ALI

A

Compartment syndrome

Reperfusion injury

156
Q

Compartment syndrome - complication of ALI

A

Reperfusion of ischaemic muscles can cause oedema and increased compartmental pressure

157
Q

Reperfusion injury - complication of ALI

A

Products of cell death (e.g K, CO2 and myoglobin) are released when blood flow to ischaemic limb is restored

158
Q

What can reperfusion injury result in

A 
Rhabdomyolysis 
Cardiac dysrhythmia 
AKI 
Multi-organ failure 
Disseminated IV coagulation
159
Q

Mortality of ALI

A

15 - 20% with about a 1/3 of deaths resulting from metabolic complications associated with revascularisation e.g. acidosis and hyperkalemia

160
Q

Limb prognosis of ALI

A

Related to the severity of arterial disease, the acuteness of ischaemia onset, and how rapidly perfusion is restored

161
Q

Causes of lower limb loss in less developed countries

A

Industrial, railway, farming accidents where safety measures are poor

162
Q

Causes of lower limb loss in western world

A

90% vascular (60% PVD/ 30% DM)
Trauma - 5%
Neoplasm - 1%
Other (infection/ psychiatric ) - 4%

163
Q

Levels of lower limb amputation

A 
Hemi- pelvictomy 
Hip disartictlatrion 
Transfemoral 
Through knee 
Transtibial
Symes (Ankle disarticulation)
Chopart (mid-tarsal)
Lisfrank (traso-metatrsal)
164
Q

What does the energy required after amputation depend on

A

Level of amputation
Length of stump
Pt’s health/ commodity
Reason for amputation

165
Q

Which level of amputation has the biggest increase in energy needed for gait above normal

A

Bilateral transfemoral - 200%

166
Q

ICF

A

International Classification of Functioning, Disability and Health Framework
Forms basis of rehab med

167
Q

What does ICF demonstrate the rship between

A

Health (disorder/ disease)
Function - body functions & structure, activity, participation
Disability - impairment, activity limitation, participation restriction

168
Q

Role of rehab - pre-amp

A

Pt education
Defining expectations (ICE)
Determining suitability for artificial limb
Phantom limb prophylaxis

169
Q

Determining suitability for artificial limb

A

Energy needed
Contratures
Allodynia
Cognition

170
Q

PLP prophylaxis

A

PLP is associated with pre-operative pain and can be reduced with analgesia at least 72 hrs before surgery and 48 hrs after

171
Q

Role of rehab immediately post-amp

A

Reduce complications
Maximise independence
Minimise pain and discomfort
Co-ordination and better use of resources

172
Q

Role of amp rehab on the ward

A

Post-op care
Artificial limb fitting and training
Long term follow up

173
Q

What does artificial limb fitting and training involve

A

Goal establishment
Stump casting and measurement and limb prescription from week 3 post-op
Gait retraining
Education on skincare, and artificial limb maintenance

174
Q

Long-term follow up - rehab

A

Checking if new limb is required
Checking for changes in stump size and condn
Checking for changes in residual
Pain management and medical complications

175
Q

Early walking aids (EWAs)

A

Used as early 5-7 days post amp
Temporary devices
Useful as part of the assessment process for suitability of artificial limb

176
Q

Examples of EWA

A

Post-amputation mobility aid for TT

Femurett for TF

177
Q

Gait retraining sequence

A

Full wt-bearing and transfer
Walking with 2 parallel bars
Walking with 2 stick between parallel bars
Walking with 1 stick outside bars

178
Q

Gait challenges for an amputee

A

Ground clearance
Times initial (Heel) contact without proprioception
Loss of ability to aboard energy
Maintaining mid-stance on the prosthetic limb
Loss of foot eversion/ inversion AKA stopping knee from buckling
Transmit centre of gravity
Loss of push off in terminal stance

179
Q

Phantom sensation

A

Feeling the missing part

180
Q

Phantom pain

A

Pain in missing part

181
Q

Superadded Phantom

A

Tight band, tight shoes, tight wristwatch over the missing part

182
Q

Incidence of PLP

A

54% of all amputees

100% of all LL amputees

183
Q

Mechanism of PLP

A

Unknown
Lacking peripheral input
Central cortical reorganisation
Psycho factors - grieving, depression

184
Q

Why is PLP not a peripheral nervous phenomenon

A

Changes with time (telescoping)

Changes with interceptive stimuli e.g. micturition

185
Q

Pharmacological mx of PLP

A

Analgesic ladder - paracetamol, NSAIDs, opioids
Anticovulsants
Low dose amitriptyline - 10mg then increase gradually up to 50mg
Treatment of clinical depression (if applicable)
Misc - baclofen, botulinum, beta-blockers

186
Q

Examples of anticonvulsants

A

Gabapentin
Pregabalin
Carbamazepine

187
Q

Physical mx of PLP

A 
Massage
Heat 
Accupuncture
Electromagnetic 
TENS 
Electro-accupunture
188
Q

Psychotherapy as mx for PLP

A

Distrcation
Relaxation
Autogenic hypnosis (controlling the phantom hypnosis)
Biofeedback (Ramachandran’s Mirror Box)

189
Q

Local stump complications after amp

A

Skin breakdown/ ulcers

Pressure areas

190
Q

What causes local stump complications

A 
Poor donning technique 
Poor socket 
Associated neuropathy 
Change in stump volume 
Change in gait pattern 
Infection with or without ischaemia
191
Q

Mx for local stump complications

A

Establish cause
Minimise prothetic use
Dynamic socket fitting/ repeat casting
Abx, regular dressing and reviews

192
Q

Components of TT artificial limb

A 
Socket 
Suspension mechanism 
Adaptor 
Shin tube 
Shock/ torque absorber 
Foot
193
Q

Factors that would influence unemployment after amputation

A

Occupational ability

Work environment

194
Q

What affects occupational ability after amputation

A

Individual - psychology, physical

Social factors - family support, organisational support

195
Q

Work environment affecting employment after amputation

A 
Legislations
Social security system 
Welfare rights 
Labour market
Employer - size of firm, work force flexibility
196
Q

How does ionised state of drug affect passive diffusion

A 
Unionised = lipid soluble = easy passage 
Ionised = water soluble = difficult passage
197
Q

What does level of ionisation depend on

A

Dissociation constant Ka acid or base

pH of bodily fluid

198
Q

Recommended treatment for aspirin overdose

A

NaHCO3

199
Q

Examples of unionised drugs

A

Digoxin (for AF)

Prednisolone

200
Q

Major rate-limiting factor for drugs

A

BBB - blood brain barrier

201
Q

First order kinetics - exponential

A

As conc of drugs increases, rate of reaction (or breakdown of drugs) goes up
Has predictable half life

202
Q

Zero order kinetics

A

Saturation = rate limited
Limited capacity of body to process drug
Dose increase - sudden toxicity

203
Q

Bioavailability

A

Proportion of parenteral drug that passes into systemic circulation after administration

204
Q

Improving bioavailability

A

Change in formulation
Route
Concurrent use of inhibitor

205
Q

Apparent volume of distribution

A

Reflects amount of drug in plasma after being taken up

Total amount of drug in body/ plasma conc

206
Q

Clearance of drugs

A

Amount of plasma totally cleared of drug

Elimination of drug from plasma

207
Q

Main parameters of half-life

A

Clearance

Volume of distribution

208
Q

How does clearance affect half life

A

High clearance = shorter half life

209
Q

How does volume of distribution affect half life

A

High volume volume of distribution - longer half life

210
Q

When will a drug reach a steady state

A

When drugs are given at a constant rate and after 5 half-lives
Either continuous infusion or intermittent chronic dosing

211
Q

When do you use a large priming or loading dose

A

Quicker effect

Useful in urgent situation e.g Abx for sepsis

212
Q

What if drug t 1/2 is short

A

Give larger dose frequently
Inhibit clearance
Reduce movement of drug to plasma
Modify formulation

213
Q

Examples of modified release formulations

A

Sustained release tablets

Depot injectables

214
Q

Atheroma

A

Cholesterol plaque

215
Q

Risk factors of ALI

A 
DM 
HTN 
Increased cholesterol & triglycerides 
AF (a/c blood clots)
Obesity 
Fhx of PVD
Trauma (immobilised --> DVT can embolise)
Male sex
216
Q

Spinal stenosis as ddx of IC

A

Pain gets better when walking uphill due to simian posture (extension) but worse in IC

217
Q

Why are IC pts advised to exercise to point of pain and past

A

Hypoxia promotes angiogenesis

218
Q

Sex difference of venous ulcers

A

F > M

219
Q

Sex difference of arterial ulcers

A

M < F

220
Q

Sex difference of neuropathic ulcers

A

F = M

221
Q

Risk factors of venous ulcers

A

Previous DVT
Varicose veins
Incompetent valve

222
Q

Risk factors of arterial ulcers

A

Smoking
HTN
DM

223
Q

Risk factor of neuropathic ulcers

A

DM

224
Q

Pain levels of different ulcers

A

Venous - not painful
Arterial - pressure areas
Neuropathic - usually painless, nerves are dead

225
Q

Site of venous ulcers

A

Gaitar areas

226
Q

Site of arterial ulcers

A

Pressure areas e.g. in between toes, heel

227
Q

Vein in venous ulcers

A

Full, dilated

228
Q

Veins in arterial ulcers

A

Not visible

Guttering

229
Q

Veins in neuropathic ulcers

A

Veins are normal

230
Q

Temperature of venous ulcers

A

Normal to warm

231
Q

Temp of arterial ulcers

A

Cool

232
Q

Temp of neuropathic ulcers

A

Warm or cold

233
Q

Appearance of venous ulcers

A

Shallow and flat
Irregular margin
Slough at base
Moderate to heavy exudate

234
Q

Appearance of arterial ulcers

A

Punched out
Regular shape
Presence of necrotic tissue

235
Q

Apperance of neuropathic ulcers

A

Callous
Trophic
Insensate
Macerated

236
Q

Site of neuropathic ulcers

A

Plantar aspect of foot
Tip of toe
Lateral to 5th metatarsal

237
Q

Condn of leg when venous ulcer is present

A

Hemosiderin staining
Thickening and fibrosis
Eczematous and itchy skin
Normal CRT

238
Q

Condn of leg when arterial ulcer is present

A

Thin, shiny skin
Pallor on leg elevation
Absent/ weak pulses
Delayed CRT

239
Q

Treatment of venous ulcers

A

Compression stockings - check ABPI
Leg elevation
Surgical mx

240
Q

Treatment of arterial ulcers

A

Revascularisation
Anti-platelet med
Mx of risk factors

241
Q

Treatment of neuropathic ulcers

A

Off-loading of pressure

Topical growth factors

242
Q

Features of asymptomatic PAD

A

Abnormal/absent pedal pulses
Age 70+
Age 50-69 and hx of smoking and DM

243
Q

Tunica interna composition

A

Thin single layer of endothelium

244
Q

Tunica media composition

A

Thicker contractile tissue made from circularly arranged elastic fibres, connective tissue and smooth muscle cells

245
Q

Tunica externa composition

A

Connective tissue

246
Q

Bifurcation

A

Where an artery splits into 2, common site for cholesterol build up and thrombus formation

247
Q

Mural thrombus

A

Thrombus attaching two chamber walls

248
Q

Where is mitral valve found

A

Between left atrium and left ventricle

249
Q

Claudication hx

A

Exercise tolerance - how far can they work
How long to rest for
Rest pain?

250
Q

When should duplex ultrasound not be done when investigating ischaemia

A

Absent limb pulses

251
Q

Pre op work for vascular surgery

A

NTProBNP
LFT
Fibroscan
Consultant anaesthetic review

252
Q

How is chronic limb ischaemia clinically defined

A

Ischaemic rest pain for greater than 2 weeks duration, requiring opiate analgesia
Presence of ischaemic lesions or gangrene
ABPI less than 0.5

253
Q

Acute-on-chronic ischaemia

A

There is an acute often embolic event in a pt w/ previous PAD

254
Q

What can cause a falsely high ABPI

A

Calcification and hardening of the arteries so any ABPI value >1.2 should be interpreted with caution

255
Q

What can chronic limb ischaemia result in

A

Sepsis (2’ to infected gangrene)
Acute-on-chronic ischaemia
Amputation
Reduced mobility and QoL

256
Q

Signs of Chronic Limb Ischaemia

A 
Pale and cold limbs 
Weak/ absent pulses
Limb hair loss 
Skin changes (atrophic skin, ulceration or gangrene)
Thickened nails
257
Q

Sensitive sign of ALI caused by emboli occlusion

A

A normal, pulsatile contralateral limb

258
Q

What can cause a mural thrombus

A

Recent MI

259
Q

Surgical mx for ALI - thrombotic cause

A

Local intra-arterial thrombolysis
Angioplasty
Bypass surgery
Thrombolectomy

260
Q

Irreversible limb ischaemia

A

Mottled, non-blanching appearance

Requires urgent amputation or taking a palliative approach

261
Q

What can release of substances in reperfusion injury cause

A

K+ - hyperkalemia
H+ - acidosis
Myoglobin - significant AKI

262
Q

Leriche syndrome triad

A

Claudication
Absent femoral pulses
Erectile dysfunction

263
Q

Conditions for use of compression stockings (venous)

A

Patent arteries and ABPI above 0.8

264
Q

What does an ABPI of 1.3+ indicate

A

Abnormally hard vessel e.g. calcification

Common in diabetics

265
Q

When would we hear biphasic signals on the Doppler

A

Beginning of arterial disease

Old age - vessels losing elasticity

266
Q

Lipodermatosclerosis

A

Induration, pigmentation and infl of skin

267
Q

When does an ulcer become chronic

A

4 weeks

268
Q

Ulcers in which areas suggest pressure sores

A

Sacrum
Greater trochanter
Heel

269
Q

Slough

A

Mixture of fibrin, cell breakdown products, serous exudate, leukocytes and bacteria

Does not always imply infection

270
Q

Granulation tissue

A

Deep, pink, gel-like matrix contained within a fibrous collagen network
Evidence of a healing wound

271
Q

What does associated lymphadenopathy w/ ulcers suggest

A

Infection or malignancy

272
Q

Signs of high cholesterol in eyes

A

Corneal arcus

Xanthelasma

273
Q

Signs of central cyanosis

A

Blue tongue and mouth

274
Q

What can radio-radial delay be caused by

A 
Aortic dissection (Type A)
Difference in bp (>20 mmHg)
275
Q

What can radio-femoral delay be caused by

A

Type B aortic dissection

Coarctation of the aorta

276
Q

Differentiating between thrombotic and embolic cause of ALI

A

Pts with cardiac sources will have no hx of IC or PAD, and ABPI will not be low in both limbs

277
Q

ABCDE approach - A

A

Voice, breath sounds

278
Q

ABCDE approach - treatment of A

A

Head tilt, chin lift
Oxygen (15 litres)
Suction

279
Q

ABCDE approach - B

A 
Resp rate 
Chest wall movements 
Chest percussion 
Lung auscultation 
Pulse oximetry
280
Q

ABCDE approach - treatment of B

A

Rescue breaths

Bag-mask ventilation

281
Q

ABCDE approach - C

A 
Skin colour, sweating 
CRT 
Pulse rate 
Heart auscultation 
BP 
ECG
282
Q

ABCDE approach - treatment of C

A

Cannulate:
Give 500ml IV bolus for hypotension (saline or Hartmann’s)
Take bloods - FBC, cross-match, LFTs, U&E’s, ESR/CRP, ABG/VBG

283
Q

ABCDE approach - D

A

Level of consiousncess - GCS
AVPU
Limb movements
Blood glucose

284
Q

ABCDE approach - E

A

Expose skin - looking for lesions, erythema, wounds, fractures, rashes etc
Temp

285
Q

What is key in ABCDE approach

A

Checking to see if interventions have helped

286
Q

Leriche syndrome triad

A

IC
Erectile dysfunction
Absence of femoral pulse

287
Q

Types of thrombotic ischaemia

A

Incomplete

Complete

288
Q

Mx of incomplete ischaemia - thrombotic

A

Angiography to map out occlusion and plan intervention

289
Q

Mx of complete ischaemia - thrombotic

A

Surgical bypass

Angio and thrombolysis delays mx - takes too long

MBBS - Year 2 (20 decks)

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