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Year 3 > Clinical Skills > Flashcards

Clinical Skills Flashcards

1
Q

resp?

A

rate, sound regularity

12-20 breaths per min

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2
Q

SpO2?

A
  • scale 1: 94-100
  • nails: acrylic, nail polish (probe sideways)
  • check cap refill
  • only put in on their fingers
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3
Q

Recording BP on a NEWS chart?

A
  • systolic: arrow up, diastolic arrow down, diagonal line in between
  • is this normal for the patient
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4
Q

pulse?

A
  • manual for an AF patient
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5
Q

ECG = ?s per big square?

A

0.2 sec per big square (1 small sq is 0.04s)

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6
Q

ECG sticker placement

A
  • 3rd iCS right and left
  • left, 5th ICS and one in between the 2
  • shoulder or wrist
  • ankle
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7
Q

v4 placement?

A

5th ICS

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8
Q

ECG sticker placements

A
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9
Q

limb lead placement

A
  • red right arm
  • yellow left arm
  • green left leg
  • black right leg

RIDE YOUR GREEN BIKE

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10
Q

which type of hernias are more common in men?

A

inguinal

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11
Q

which type of hernias are more common in women?

A

femoral

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12
Q

test for appendicitis?

A

speedumb, almosy always lost their appetite

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13
Q

guarding?

A

tense their abd muscles when you’re about to palpate

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14
Q

rebound?

A

Rebound tenderness involves tenderness with the sudden withdrawal of manual pressure

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15
Q

what are the signs of peritonitis?

A

Blumberg’s sign (rebound tenderness) and guarding

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16
Q

air under D on a CXR?

A

perforation

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17
Q

PR interval should be?

A

5 small squares

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18
Q

Q wave?

A

LEFT DEPOLARISES B4 RIGHT SIDE

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19
Q

S wave?

A

purkinje fibres at the base going off

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20
Q

ST?

A

isoelectric line, not depolarsing, refractory period

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21
Q

aVR?

A

negative p and T bc directly opp direction of current

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22
Q

First degree HB?

A

BBs cause prolonger P-R interval

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23
Q

AF ecg?

A

no P wave, squiggly baseline and irregularly regular

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24
Q

p mitrale?

A

double P wave, L artrium enlargement or MS

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25
Q

tall P wave?

A

RA enlargement (P pulmonale - copd, PE)

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26
Q

which 2 drugs can’t be given together?

A

DON’T GIVE BBS and CBS together bc can cause 3rd degree HB

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27
Q

priceton heartblock poem

A
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28
Q

flattened p wave?

A

hyperkalaemia

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29
Q

RBBB?

A

2 R waves - r down then r again

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30
Q

ventricular tachycardia?

A

wide qrs and no p waves

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31
Q

tall tenting T waves?

A

hyperkalemia, widended qrs needs urgent tx

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32
Q

torsaides de points?

A

w Mg (key Tx for this), type of VT

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33
Q

LBBB?

A

axis deviation, septum activated right to left meaning depolarisation vector is not straight down (towards left)

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34
Q

V fib ecg?

A

should never be a 12 lead - unconcious patient - very random looking

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35
Q

v parkinson white?

A

p launches straight into qrs without the PR int of the isokinetic line

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36
Q

Breast exam - inspection?

A
  • inspect - arms in neutral
  • inspect - arms pressed into hips leaning forward - contracts pecs muscles
  • arms raised above head
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37
Q

palpation in a breast exam?

A
  • 45 degree angle
  • arm behind head
  • start w normal breast
  • use flats of fingers
  • axillary tail, axillary, supraclavicular and cervical LNs
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38
Q

Method of examining the breast?

A
  • quadrants, clock face methods
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39
Q

describing masses?

A
  • location (to nipple)
  • size and shape - round, oval, irregular
  • consistency
  • margins - smooth or irregular
  • mobile, fixed
  • tenderness
  • skin colour
  • note discharge
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40
Q

masses/ skin changes need triple assessment:

A
  • clinical
  • imaging - US or mammography
  • histology
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41
Q

Signs of breast pathology?

A
  • irregular lump and skin tethering
  • asymmetry
  • nipple inversion
  • discharge
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42
Q

RF for BC?

A

female, age, oestrogen exposure. BRCA, chest wall radiation

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43
Q

Breast cysts?

A
  • rounded smooth fluctulant lumps
  • sometimes tender
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44
Q

fibroadenoma?

A
  • develop from excessive division of a single lobule
  • mobile, non tender breast lump
  • doesn’t vary in size w menstrual cyccle
    * discrete, smooth,very mobile, rubbery swelling
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45
Q

who are fibroadenomas common in?

A

under 20s

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46
Q

which type of tumours can present similarly to fibroadenomas?

A

phyllodes tumours

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47
Q

fat necrosis

A
  • due to trauma with rupture of fat cells -> inflammation and calcification over time
  • signs - history of trauma, presents similar to cancer
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48
Q

BPH occurs in?

A
  • bph: transitional zone
  • sulcus in the middle flattens out
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49
Q

cauda equina?

A
  • bilateral leg weakness, inability to pass urine
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50
Q

position for PR exam?

A
  • lie on their LHS, knees to chest
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51
Q

asking them to cough in a PR exam?

A
  • cough - rectal prolapse, int haemorrhoids - dilated vascular cushions in anal canal
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52
Q

PR - palpation?

A
  • anal tone - 360 degrees
  • masses, stool, tenderness
  • prostate - walnut sized w palpable midline sulcus
  • rubbery but firm with smooth surface
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53
Q

BPH vs PC

A

bph - symmetrical enlargement

PC - HARD AND IRREGULAR LUMPS

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54
Q

What can falsely raise PSA?

A

PR exam

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55
Q
A
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56
Q

which lymph nodes drain the testis?

A

para-aortic lymph nodes for the testis due to embryological origin

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57
Q

peyronie disease?

A

fibrous scar tissue on penis, causing curved shape during erection + pain during erection

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58
Q

cemasteric reflex?

A

L1/L2 loss w torsion

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59
Q

palpation - prehn’s test?

A

lifting the painful testes reduces the pain in epididmymitis but not testicular torsion

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60
Q

palpation for a PR exam?

A
  • scrotum and scortal wall
  • testes - check both prrsent in the scrotum
  • inguinal canal and lymph nodes
  • abdomen - including para-aortic lymph node
  • reassess after getting the patient to stand (hernia at iC - mass that u can’t get above)
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61
Q

hydrocele?

A

when fluid builds up in tunica vaginalis of the testes

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62
Q

causes of scrotal masses?

A
  • hydrocele - non painful fluctulant swellling that transilluminates
  • usually idiopathic but can be 2’ to tumours, trauma, inflammation, pancreatitis, peritoneal dialysis
  • should be able to feel it sep from the testes
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63
Q

varicocele?

A
  • varicosires of the pampinoform plexus
  • normally on the left
  • if occurs suddenly exclude renal cancer
  • bag of worms in scortum when standing
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64
Q

RF for testocular tumours?

A

undescended testes

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65
Q

testicular tumours?

A
  • non tender solid mass in testes, irregular surface to the testes
  • assoc w abn sensation
  • haematospermia
  • secondary hydrocele
  • spread via PA LN not inguinal to lngs
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66
Q

markers of testicular tumours?

A
  • markers: B-HCG, LDH and a-FP
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67
Q

presentation of a testicular torsion?

A
  • unilateral severe testicular pain or abd pain
  • swollen, red hot testis
  • may lie high and transverse in scrotum
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68
Q

what can be lost w TT?

A
  • cremasteric reflex may be lost
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69
Q

treatment of torsion?

A

bilateral orchidopexy +/- orchidectomy if testis not viable

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70
Q

6 Ps of ischemia?

A
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71
Q

which nerves are first to become ischemic?

A
  • sensory nerves are small and unmeylinated so they’re first to become ischemic
  • first they get tingling from this - parasthesia without paralysis is reversible
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72
Q

why does paralysis occur later on in ischemia?

A
  • paralysis much later bc motor nerves are affected
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73
Q

ALI timeline?

A
  • 6 hour timeline
  • 2 hours: parasthesia
  • 4 hrs: paralysis from nerve damage
  • muscle tenderness indicated muscle damage = poor sign
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74
Q

saddle embolus?

A
  • saddle embolus: aorta blocked at the bifurcation
  • can present several hours later with completely rigid legs
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75
Q

rhabdomialysis?

A
  • condition where skeletal muscle breaks down rapidly releasing breakdown products into BS
  • myoglobin is harmful to kidneys
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76
Q

causes of rhabdo?

A
  • causes: extensive muscle damage e/g/ crush injury, prolonged immobilization, 3rd degree burns
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77
Q

medications that can cause rhabdo?

A

statins, propofol

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78
Q

toxins that can cause rhabdo?

A

snake venom, mushroom poisoning, bee stings, wasp stings

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79
Q

process of rhabdo?

A
  • influx of EC sodium and calcium into muscle cells
  • influx of water
  • sustained contraction and ATP deletion
  • inflammatory process leading to muscle necrosis and release of breakdown products
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80
Q

signs of rhabdo?

A
  • muscle pain
  • muscle weakness
  • dark urine
  • elevation in creatine kinase
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81
Q

most common ALI pres?

A
  • arrythmia - very high pulse
  • decompensate - low blood pressure
  • blockages can cause thumps higher up
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82
Q

where do blockages occur more?

A
  • blockages can cause thumps higher up
  • blockages occur more at the birfurcations - most common is at the common femoral artery - into superficial and deep arteries
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83
Q

what can cause a secondary ischemic episode?

A

Warm foot and pain -> compartment syndrome from reperfusing quickly after ischemia -> swelling -> reduced perfusion -> secondary ischemic episode

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84
Q

PVD features?

A
  • calf pain in both legs
  • come on when exercising
  • PVD claudication is alleviated by stopping activity and standing still
  • obs to BF of muscle during times of high demand
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85
Q

PVD clinical signs?

A
  • absent pulses
  • bruit - turbulent flow usually at the point of stenosis
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86
Q

PVD stents?

A
  • arteries are ballooned at the same time to avoid one artery occluding the other - kissing stents
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87
Q

Rf of PVD?

A
  • smoking
  • hypertension
  • IHD
  • hypercholesterolemia
  • diabetes
  • male
  • age
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88
Q

Spinal claudication?

A
  • spinal claudication also comes on when walking but it typically relieved by sitting down or flexing the spine
  • causes the same referred pain down the same leg muscles
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89
Q

critical limb ischemia?

A
  • defined as tissue loss either in the form or gangrene or an ulcer or rest pain for more than 2 weeks
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90
Q

burgers test for ischemia?

A

With the patient supine, elevate both legs to an angle of 45 degrees and hold for one to two minutes. Observe the color of the feet. Pallor indicates ischaemia. It occurs when the peripheral arterial pressure is inadequate to overcome the effects of gravity.

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91
Q

sunset foot?

A

critically ischaemic foot may appear red and ‘healthy’. This is known as a ‘sunset’ foot and occurs due to maximal skin capillary dilatation and is often mistaken for cellulitis

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92
Q

what causes sunset foot in critical ischemia?

A
  • due to SNS activiation to get blood to peripheries so there is perm vasodilation -> hot foot - sleeping in chair with foot hanging out
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93
Q

APBI values?

A

Peripheral arterial disease (PAD) is present if the ABPI is less than 0.95

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94
Q

APBI greater than 1?

A

in diabetes bc of arterial calcification or arteries can’t be compressed

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95
Q

chronic limb ischemia is ?

A

end stage PVD

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96
Q

Venous ulcers?

A
  • swelling, discoloration around it
  • AVPI >1.4 - inflexible arteries due to diabetes
  • elderly
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97
Q

venous ulcers respond to?

A

compression

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98
Q

Things that would make u consider a venous rather than arterial ulcer?

A
  • DVT history - causes scarring of valves in veins which increases pressure in veins
  • varicose veins - inc pressure (reflux)
  • palpable pulses excludes arterial disease
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99
Q

appearance of a venous ulcer?

A
  • shallow wet appearance of a venous ulcer
  • rusting of skin - hemosiderin deposition
  • capillary perfusion drives RBCs into subcutaneous space where they become brown caused by venous hypertension
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100
Q

venous ulcer - scarring?

A
  • proteins in ECM of blood and become hard and scar which causes the leg to shrink - lipodermatossclerosis (upside down champagne bottle)
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101
Q

how does venous hypertension cause ulceration

A
  • venous hypertension -> protein exudate leaks into capillary bed -> ischemia -> ulceration
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102
Q

what impairs ulcer healing?

A

diabetes

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103
Q

mixed aetiology ulcers?

A
  • 10% are venous ulcers
  • 10% are mixed
104
Q

mixed ulcers signs?

A
  • edematous feet
  • monophasic signals on doppler - should be triphasic or biphasic (this requires resistance)
  • varcicose veins and hemosiderin depositon
  • absent pulses
105
Q

what causes monophasic signals on doppler?

A
  • monophasic signals on doppler - should be triphasic or biphasic (this requires resistance)
106
Q

what do we treat first w mixed ulcers?

A
  • treat arteries first - can’t compress bc there is limited circulation so treating veins would cause more ischemia
107
Q

arterial vs venous ulcers?

A
108
Q

diabetic foot ulceration?

A
  • often younger patients
  • diabetes and microischemia causes poor healing from injury
  • microischemia kills nerves causing misshapen foot (clawed toes) as muscle groups imbalance due to lack of proprioception
109
Q

diabetic foot ulcer pres?

A
  • swollen foot, swollen lymph notes
  • boggy foot that feels like a balloon filled w water
  • toe has become black
110
Q

Tx of DFU?

A
  • emergency - will require amputation within 1 day
  • Tx - drainage of pus
111
Q

Pathogenesis of atherosclerosis?

A
  • Inflammation and accumulation of “foam cell” macrophages
  • Fibrosis and progressive luminal narrowing
  • Plaque rupture or ulceration
  • Thrombosis or thromboembolism
112
Q

athero steps

A
113
Q

non mod athero RF?

A
  • Age (risk increases with advancing age)
  • Sex (M>F)
  • Family history/ genetics / Race
114
Q

Modifiable athero RF?

A
  • Smoking
  • Hyperlipidaemia
  • Hypertension
  • Diabetes
  • Sedentary lifestyle
115
Q

Intermittent claudication?

A
  • Cramping muscular pain, which is brought on by exertion, relieved by rest and reproducible on walking that distance again.
  • It is due to inadequate oxygen delivery to the muscles.
116
Q

definition of CLI?

A
  • Defined as ischaemic rest pain for more than 2 weeks, despite analgesia, or the presence of tissue loss (ulcers / gangrene)
117
Q

recognising intermittent claudication: history

A
  • Site: symptoms evident distal to the level of disease (e.g. calf pain = SFA disease)
  • Onset: occurs during exertion e.g. walking; often worse on inclines
118
Q

Type of pain in intermittent claudication?

A

cramping, muscular pain

119
Q

assoc factors w IC?

A
  • Ask about skin changes and ulceration (critical limb ischaemia!)
120
Q

relieving factors in IC pain?

A
  • Relieved by rest within a few minutes. Unlike spinal stenosis it is not relieved by leaning forwards/bending over.
121
Q

Leriche Syndrome:

A
  • Aortoiliac occlusion manifesting in:
  • buttock & thigh claudication
  • impotence
122
Q

core feature of CLI?

A
  • The core feature of CLI is rest pain.
  • This pain is felt in the toes/forefoot as this is the most distal site.
123
Q

Pain in CLI often?

A
  • Pain often wakes the patient up at night, because of the loss of gravity’s help in perfusing the foot.
  • Patients typically hang their legs from the side of the bed, or just resort to sleeping in chairs.
124
Q

Examination in ischemia?

A
  • Inspection of the legs, comparing both sides, looking for pallor, mottling, skin changes, loss of hair, ulcers (active or healed), gangrene.
  • Palpation of temperature, comparing both legs/feet with the back of your hand, and checking the capillary refill time distally.
  • Pulses: for the lower limb, this begins with the abdominal aorta, moving distally.
125
Q

femoral bruit?

A

sign of occult aortoiliac disease.

126
Q

Buerger’s test?

A
  • Reported as the angle at which the leg becomes pale when you elevate it against gravity (which healthy limbs don’t do). You then swing the patient’s leg over the side and watch out for a “sunset foot” (arteriolar vasodilatation with foot reperfusion).
127
Q

falsely high APBI?

A

diabetes or CKD

128
Q

+ of computed tomographic angiography

A
  • rapid image acquisition (seconds)
  • Relatively high radiation dose
129
Q
  • of CTA?
A
  • Uses iodinated contrast
  • risk of causing/ worsening renal injury or failure
  • risk of allergic reaction
130
Q

Magnetic Resonance Angiography – aka MRA -?

A
  • Can take up to 40-60mins
  • claustrophobia sometimes an issue
  • the contrast used (gadolinium) can very rarely cause Nephrogenic Systemic Fibrosis in patients with existing renal impairment
131
Q

MRA is not possible in patients w?

A

pacemakers, ICDs

132
Q

+ of MRA?

A
  • No iodine-based contrast, therefore lower renal risk
  • No Radiation dose - uses magnetic excitement of water molecules
133
Q

PTA?

A
  • Percutanous Transluminal Angiography / Angioplasty – aka PTA
  • catheter in arterial tree
  • injection of contrast
134
Q

DSA?

A
  • “Digital Subtraction Angiography” (DSA) removes all background structures, such as bone, from the image to allow a more detailed view of the arteries
  • The “gold-standard’
135
Q

PTA uses?

A
  • Uses iodinated contrast – risk of causing/ worsening renal impairment
  • CO2 can sometimes be used as an alternative
136
Q

risks of pta?

A
  • Risks of damage to vessels, bleeding, emboli, dissection, pseudoaneurysm
137
Q

+ of PTA?

A

balloon angioplasty or stenting) - can be performed at the same time

138
Q

Tx for PAD?

A
  • Antiplatelet
  • statin
  • BP control
  • diabetes screening
139
Q

lifestyle for PAD?

A
  • smoking cessation advice +/- nicotine replacement therapy / further intervention
140
Q

Limb revascularisation in CLI?

A
  • An open surgical procedure (bypass, endarterectomy)
  • Autologous vein (e.g. great saphenous vein) is preferred to prosthetic (dacron/PTFE) graft wherever possible, particularly for below-the-knee disease
  • An endovascular procedure (angioplasty, stenting)
  • A Hybrid procedure (combination of both open and endovascular techniques)
141
Q

Indications for amputation:

A
  • PAD/ diabetes
  • Trauma and Military injuries: one of the most common causes worldwide, especially young men
  • Neoplasm
  • Venous ulcers
  • Congenital deformity
  • Chronic pain
  • Neurological injury resulting in a non-functional limb
142
Q

Minor amputation?

A
143
Q

major amputation?

A
144
Q

post op management for amputations?

A
  • psychological impact considered
  • risk of infection, ischemia, prevention of slump trauma, pressure injury
  • social input and home adaptations
145
Q

prognosis for amputation

A
  • major amputation reflects end stage PAD
  • mortality double for AKA than BKA
146
Q

thrombotic ALI?

A
  • Rupture of atherosclerotic plaque
  • Bypass graft thrombosis
  • Prothrombotic e.g. malignancy
  • Arteritis
  • Infection
  • States of low flow e.g. shock
147
Q

Embolic ALI?

A
  • Mural thrombus
  • Atrial fibrillation
  • Thoracic / abdominal aortic Aneurysm
  • Bacterial endocarditis
  • Cardiac tumour
148
Q

Rare causes of ALI?

A
  • Compartment syndrome
  • Dissection
  • Trauma
149
Q

Sx of ILA

A
  • Sudden onset painful, numb, weak and cold limb
  • atherosclerosis is predominant cause but can manifest in both thrombotic and embolic presentations
150
Q

Signs of ALI - 6 PS?

A
151
Q

Assessment of ALI?

A
  • sensory and motor function of the leg
  • assess muscle tenderness (late sign)
  • doppler US

ABPI for PAD

152
Q

Test for ALI?

A
  • ABPI
  • ECG – arrhythmia may precipitate an embolic event.
  • creatine kinase - marker of rhabdomyolysis
153
Q

Rutherford classification of acute limb ischemia?

A
154
Q

Initial Mx of ALI?

A
  • oxygen
  • UF heparin
155
Q

Categories of ALI?

A
156
Q

compartment syndrome?

A
  • Acute increase in pressure within a compartment which endangers the perfusion of tissues, requiring emergency decompression
157
Q

Causes of compartment syndrome?

A
  • Reperfusion injury post revascularisation in acute limb ischaemia
  • Other causes include fractures, crush injuries, burns
158
Q

symptoms of CS?

A
  • Disproportionate ’Crescendo pain’, unresponsive to analgesia
159
Q

Pathophys of CS?

A
  • Ischaemia-reperfusion injury
  • Release of free radicals, K+, Ca++, Toxins etc
  • Vascular leakage causing tissue swelling within fixed fascial compartment
  • Decreased perfusion pressure
160
Q

Signs of CS?

A
  • Pain on passive movement
  • Paraesthesia
  • Pulselessness (late)
  • Paralysis (late)
161
Q

Management of CS?

A
  • Urgent fasciotomy
  • remove constrictive dressings
162
Q

Rare causes of ALI

A
163
Q

CS most commonly affects the ?

A
  • CS most commonly affects the lower leg
  • most common causes: soft tissue injury and fractures
164
Q

what to be careful of in a fasciotomy?

A

saphenous nerve and vein

165
Q

chronic exertional compartment syndrome ?

A
  • higher resting intra-compartmental pressure
  • pressure rises steeply after intiation of exercise
  • burning, cramping or aching pain within 20 mins of exercise
166
Q

aortic aneurysm?

A
  • A permanent, focal dilation of an artery with at leasta 50% increase in diameter compared to normal
167
Q

AAA high risk group?

A
  • Highest incidence is in Caucasian men aged >65 years: 5%
  • The risk of rupture increases exponentially with increasing size
168
Q

AAA screening programme?

A
  • There is a screening programme in place in the UK NHS: the NAAASP
169
Q

RF for AAA?

A
  • PREV 4-5x higher in men
  • atherosclerosis predominant cayse
170
Q

Rare causes of AAA

A
  • rare causes: mycotic aneurysm (infection), CT disorders (Marfans and Ehlers-Danlos), arteritis
  • diabetes had a protective effect
171
Q

Risks for AAA

A
172
Q

National Abdominal Aortic Aneurysm Screening Programme (NAAASP)?

A
  • First invitation is at 65yrs of age for men
  • Abdominal USS, measures the anteroposterior (AP) infrarenal aortic diameter
173
Q

AAA clinical pres?

A
  • Generally asymptomatic until rupture
  • Some patients may report back or hip pain if large or rapidly expanding AAA
  • May compress surrounding structures – vague GI symptoms, DVT
174
Q

common features of an AAA rupture

A
  • abd pain radiating to back
  • shock
175
Q

management of an AAA rupture?

A
  • Urgent CT scan
  • proceed to either open or endovascular repair
176
Q

chronic venous disease?

A
  • Superficial venous incompetence
  • Deep venous disease
  • Which may manifest as obstruction or incompetence
177
Q

anatomy of leg veins

A
178
Q

normal physiology - veins?

A
  • Blood in deep veins returns to the heart due to pressure generated by the calf muscles.
  • 80% of venous return from the legs is via the deep veins.
179
Q

superficial and deep veins?

A
  • blood collected from superficial venous capillaries is directed upward and inward via one-way valves into superficial veins.
  • These in turn drain via junctions & perforator veins, which pass through muscular fascia into deeper veins
180
Q

pathology - veins?

A
  • unlike deep veins which are thicker and confined by fascia, superficial veins cannot withstand high pressure and eventually become dilated and tortous
181
Q

superficial venous incompetence?

A
  • men = women
  • more women present w symptoms
182
Q

RF for superficial venous incompetence?

A
  • Obesity
  • Increasing age
  • Family history / genetics
  • Pregnancy
  • hormonal factors increase the laxity of venous walls and valves
183
Q

Sx of superficial venous incompetence?

A
  • Itching, aching discomfort and heaviness of the legs
  • Leg swelling
  • “Restless” legs
184
Q

when are symptoms worse for SVI?

A
  • Symptoms typically worse after prolonged standing / towards end of day
  • Bleeding varicosities (typically after minor trauma)
185
Q

Aggrevating factors for SVI?

A
  • occupation: prolonged standing, lifting e.g. factory production lines etc
  • pregnancy
  • hormonal changes – endogenous or exogenous
  • menstruation
186
Q

Exam - varicose veins?

A
  • Varicose veins will typically empty when lying down or with application of pressure, and then refill when pressure is released or patient stands up
187
Q

Small vs great saphenous vein varicosites?

A
  • Great saphenous vein varicosities may run the whole length of the leg and are generally distributed medially
  • Varicosities of the small saphenous vein are seen below the knee and are distributed posterolaterally
188
Q

signs of advanced venous insufficiency?

A

include (healed) ulcers, lipodermatosclerosis, haemosiderin pigmentation, telangiectasia or eczema / atrophie blanche.

189
Q

typical site for change w venous insufficiency?

A
  • the typical site of skin change is around the ankle, the so-called “gaiter area”, particularly around the medial malleolus
190
Q

CEAP classification system?

A
  • clinical, aEtiologic, anatomic and pathophysiologic
191
Q

examples of venous insufficiency?

A
192
Q

management of varicose veins?

A
193
Q

investigations for varicose veins?

A

Duplex ultrasound (combination of Doppler and B-mode ultrasound) is the gold standard

194
Q

Tx for superficial venous incompetence - first line?

A
  • endovenous thermal ablation - sealing of the lumen of the incompetent vein by delivering thermal energy via catheter using US guidance
195
Q

2nd line for varicose veins?

A
  • Ultrasound-guided foam sclerotherapy - This is recommended if endothermal ablation is unsuitable. It involves injection of a sclerosant chemical into the veins.
  • Offered as 2nd line treatment to patients unsuitable for Thermal Ablation
196
Q

3rd line for varicose veins?

A
  • Conventional surgery: (junctional ligation, stripping and avulsions)
  • 3rd-line option if the above treatments not feasible
197
Q

mechanism of endovenous thermal ablation?

A

*Thermal injury to venous endothelium
* Luminal obliteration
* Contraction & fibrosis

198
Q

features of endovenous thermal ablation

A
  • daycase procedure performed under LA
  • lesser complications and lower recurrence rates comp to conventional surgery
199
Q

Ultrasound-guided Foam Sclerotherapy mechanism?

A
  • Chemical injury to venous endothelium
  • → Luminal obliteration
  • → Contraction & fibrosis
200
Q

featurs of UGFS?

A
  • Walk in procedure
  • local anaesthetic
201
Q

side effects of UGFS?

A
  • higher risk of DVT than surgery or EVTA
  • can cause transient migraine/ visual aura from bubbles in circ
  • higher failure and reccurence rates than EVTA/ surgery
202
Q

Surgery for venous insufficiency mechanism?

A
  • ligation of the saphenofemoral (or saphenopopliteal junction)
  • Stripping of the incompetent superficial vein (GSV/SSV)
  • Avulsion of the varicosities through stab incisions
203
Q
  • of surgery?
A
  • DVT/ PE, wound infection
  • delays at work
204
Q

causes of chronic leg ulceration?

A
205
Q

leg ulcers =

A
  • breach in epithelial integrity of the skin
  • chronic: present for > 6 weeks
206
Q

majority of chronic ulcers have a…

A
  • majority of chronic ulcers have a vascular cause
  • chronic venous hypertension is a primary cause
207
Q

venous ulcers?

A
  • very painful
  • relieved slightly by elevation
208
Q

appearance of venous ulcers?

A
  • most commonly affect medial perimalleolar (gaiter) areas
  • Ulcer is large, shallow and irregular with an exudative and granulating base
209
Q

venous insufficiency

assoc features w VI?

A
  • warm skin
  • normal peripheral pulses
  • varicose veins
  • leg oedema
  • haemosiderin pigmentation (leaching of iron from blood into the soft tissues)
  • venous eczema
  • lipodermatosclerosis and atrophie blanche
210
Q

risk factors for venous ulcers

A
  • Superficial venous incompetence (e.g. Varicose veins)
  • Previous deep vein thrombosis in the affected leg
  • Phlebitis in the affected leg
  • Previous fracture, trauma, or surgery to leg
211
Q

symptoms of venous incompetence?

A

include leg pain, aching, itching, swelling, pigmentation and eczema and ultimately ulceration.

212
Q

arterial ulcer features?

A
  • Painful and worse when legs are elevated
  • Most commonly affect pressure and trauma sites (pretibial and supra-malleolar) and distal points e.g. toes
213
Q

arterial ulcers appearance?

A
  • Lesion is typically small, deep, sharply defined (developing a “punched-out” appearance with time), often with a necrotic base
214
Q

Features associated with arterial ulcers?

A
  • Associated features: cold skin, weak or absent peripheral pulses, shiny pale skin, loss of hair
  • Represent advanced PAD – Critical Ischaemia
215
Q

RF for arterial ulcers?

A
  • Peripheral arterial disease.
  • Coronary heart disease.
  • History of stroke or transient ischaemic attack.
  • Diabetes mellitus.
  • Obesity and immobility.
216
Q

appearance of venous vs arterial ulcers?

A
  • shallow irregular exudative gaiter ulcer = venous
  • smaller punched out deep ulcers = arterial
217
Q

which areas are more affceted by diabeteic ulcers?

A
  • usually foot rather than leg
  • affects pressure sites more: soles, heels, toes, metatarsal heads
  • often painless with abn or absent sensation
218
Q

diabetic ulcers are caused by

A
  • caused by peripheral neuropathy secondary to diabetes
219
Q

Appearance of diabetic ulcers?

A

lesion usually punched out w variable size and depth with a granulating base

220
Q

features of DU?

A

warm skin, peripheral neuropathy, normal peripheral pulses

221
Q

Ix for a venous ulcer?

A
  • Venous: Venous duplex ultrasound to look for venous incompetence
222
Q

Ix for arterial ulcer?

A
  • Arterial: Arterial imaging – usually multilevel disease
223
Q

Ix for diabetic ulcers?

A
  • Diabetic: Assess sensation – monofilament test. Check HBA1C & optimise
  • Foot x-rays to look for underlying osteomyelitis.
224
Q

APBI >1.3?

A
  • > 1.3: generally indicates calcified, stiff arteries.
  • This may be seen with advanced age, diabetes or chronic kidney disease
225
Q

APBI which represents PAD?

A
  • < 0.8: PAD very likely
  • < 0.5 indicates severe PAD and should be referred urgently
226
Q

Management of venous vs arterial ulcers?

A
  • Venous: If ABPI >0.8 apply compression bandaging
  • Arterial: vascular reconstruction
227
Q

management of a mixed ulcer?

A
  • Mixed arterial/ venous: initially modified strength compression w close obs (+ revascularisation if needed)
228
Q

what is Raynaurd’s?

A
  • Episodic vasospasm of the arteries of the extremities resulting in digital ischaemia, can be induced by cold or emotional stress
  • idiopathic in 95% of cases
229
Q

who does Raynaurd’s affect?

A
  • older age, M=F
230
Q

aetiology of RS?

A
  • Associated with connective tissue disease especially Scleroderma,
  • Also SLE, RA, Sjogen’s Syndrome
231
Q

Drugs causing raynaurds?

A

amphetamines, cocaine, beta blockers, chemotherapy, COCP

232
Q

Vascular occlusive disease causing RS?

A

Buerger’s, Atherosclerosis, Thromboembolic
Haematological

233
Q

Haematological causes of RS?

A
  • Haematological e.g. polycythemia, leukaemia, Protein C, S or antithrombin III deficiency.
234
Q

Environmental/occupational causes of RS?

A
  • vibration, frostbite, ulnar aneurysm
235
Q

Anatomical cause of RS?

A

CTS

236
Q

infections causing RS?

A
  • Infections e.g. Hep B & C (cryoglobulinaemia), mycoplasma (cold agglutinins), parvovirus B19
237
Q

Endocrine causes of RS?

A

hypothyroidism, phaeochromocytoma, carcinoid syndrome

238
Q

Symptoms of RS?

A
  • Pallor of distal part of fingers
  • Numbness
  • Pain
  • Blue fingers (cyanosis)
  • Hyperaemic phase – red and warm fingers
239
Q

Symptoms assoc w RS?

A
  • Migraines
  • Dry Eyes etc (Sicca syndrome)
  • Joint/muscle pain
  • Gastro-oesophageal reflux
  • Weight loss
  • Rashes
240
Q

Signs of RS?

A
  • blanching then cyanosis (hyperamia can occur after)
241
Q

Imaging for Raynaurds?

A
  • Infrared thermography (cold provocation test)
  • Laser doppler flowmetry
  • Digital plethysmography
242
Q

diagnosis of RS?

A
  • At least one colour change e.g. cyanosis/erythema
  • Identified cold/emotion triggers
  • Exclude cervical rib/ thoracic outlet syndrome
243
Q

when to suspect secondary Raynaurds?

A
  • Onset >30yrs
  • Asymmetrical, Intense or painful episodes
  • Features of underlying condition
  • Digital ulcers
  • Positive autoimmune tests
244
Q

Tx of raynaurds?

A
  • Calcium channel blockers esp. Nifedipine
  • Consider antiplatelet
  • Consider immunosuppression for autoimmune associated raynaud’s
245
Q

3 management options for ALI?

A
  • analgesia
  • heparin
  • revascularisation
246
Q

Thrombolysis?

A
  • usually alteplase
  • percutaneous technique that involves obtaining vascular access with a catheter
247
Q

percutaneous mechanical thrombectomy/thrombo-aspiration ?

A
  • removal of thrombus
  • can be combined w catheter directed thrombolysis
248
Q

surgical thrombectomy?

A
  • vessel opened and thrombus removed
249
Q

surgical bypass?

A
  • bypass involves placing a graft connecting the vesse; proximal to the obstruction to the vessel and distal to it
250
Q

rehab following amputation?

A
  • exercises whilst sitting or lying
  • taught transfer techniques from wheelchair to bed
  • encouraged to move around ASAP using wheelchair
  • physio and OT
  • physio will teach them how to use prosthetic limb
251
Q

mobility aids post amputation?

A
  • OT: for adaptations required to home
  • e.g. wheelchair ramp or stairlift
252
Q

side effects of arterial reconst?

A
  • thrombosis
  • sepsis
  • disruption
253
Q

initial Tx of ALI?

A

The initial management of acute limb ischaemia includes analgesia, IV heparin and vascular review

254
Q

All ppts w PAD should take…

A

All patients with peripheral arterial disease should take clopidogrel and atorvastatin

255
Q

femoral vs iliac claudication?

A

Claudication affecting the femoral vessels is likely to present with calf pain rather than iliac claudication which causes buttock pain

256
Q
A

Year 3 (45 decks)

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