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Medicine > Vascular > Flashcards

Vascular Flashcards

1
Q

Where are baroreceptors?

A

Carotid sinuses (glossopharyngeal) and aortic arch (vagus)

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2
Q

What is the average pulse pressure?

A

40 mm Hg

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3
Q

Why does the pulse pressure increase in ageing?

A

SBP increases due to less elastic aorta

DBP decreases due to lack of elastic recoil

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4
Q

When does the pulse pressure decrease?

A

haemorrhage

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5
Q

How often should BP be measured?

A

Every 5 years in adults

Annually over 80

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6
Q

How to investigate hypertension?

A

ECG - LVH
Fundoscopy - hypertensive retinopathy
Urinalysis

Cardiovascular risk assessment

Bloods: U&Es, glucose, lipids

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7
Q

NICE hypertension criteria

A

Stage 1: 140/90 clinic, 135/85 ABPM/ HBPM

Stage 2:160/100, 150/95

Stage 3: 180/110

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8
Q

If BP elevated in clinic, how is hypertension confirmed?

A

ABPM (2 readings every hour)

HBPM (2 readings daily)

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9
Q

What are the hypertensive crises?

A

MALIGNANT (ACCELERATED) HTN: stage 3 + accompanied with end-organ damage - refer hospital same day

SUSPECTED PHAECHROMOCYTOMA: refer same day

HYPERTENSIVE URGENCY: stage 3 without impending organ damage - refer within few days

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10
Q

Secondary causes of hypertension

A

Renal: intrinsic or renovascular

Endocrine: Cushing’s - Conn’s - thyroid - phaechromocytoma - acromegaly - hyperparathyroidism

Coarctation of the aorta

Obstructive sleep apnoea

Pre-eclampsia and HTN in pregnancy

Drugs: alcohol, cocaine, amphetamines, antidepressants, COCP, etc.

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11
Q

Management of hypertension

A

Young + non-black // Black or over 55

STEP 1: A (or B if contra-indicated) // C (or D if contra-indicated)

STEP 2: A + C (AIIRA in black)
B + C if initially started on B
A + D (if C contraindicated)

STEP 3: A + C + D

STEP 4: Consider fourth agent/ specialist

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12
Q

Mx HTN: HF

A

Normally already on A + B

Add D - refer to specialist for spiro

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13
Q

Mx HTN: DM

A

A is first-line, regardless of age/ race
Then add D
Then add C

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14
Q

Mx HTN: AF

A

If rate control needed, add B or CCB (diltiazem better than amlodipine)

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15
Q

MoA beta-blockers

A

B1 mainly in heart
B2 mainly smooth muscle of vessels and airway
Blockade reduces speed of contraction and speed of conduction

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16
Q

Five 5 indications for beta-blockers

A 
IHD (symptoms + prognosis)
HF (prognosis)
AF (reduce ventricular rate)
SVT (restores sinus rhythm)
HTN
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17
Q

Who requires a low dose of beta-blockers?

A

Hepatic failure

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18
Q

In whom should beta-blockers be avoided?

A

Asthma (in COPD use B1-selective, not propranolol)
Heart block
Avoid in haemodynamically unstable

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19
Q

Which medication should not be given with beta-blockers?

A

Non-dihydropyridine CCB (eg verapamil, diltiazem) –> HF, bradycardia, asystole

Needs specialist supervision

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20
Q

What are the classes of CCBs?

A

Dihydropyridines (more vasc-selective): nifedipine, amlodipine

Non-dihydropyridines (more heart-selective): diltiazem, verapamil

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21
Q

3 indications for CCBs

A

HTN (amlodipine, nifedipine less oftten)
Stable angina (beta-blockers main alternative)
Rate control in SVT arrhythmias (diltiazem and verapamil)

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22
Q

MoA CCBs

A

reduced calcium entry into vascular and cardiac muscle –> less contraction

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23
Q

ADRs of CCBs

A

Dihydropyridines: ankle swelling, flushing, headaches, palpitations (vasodilataion + compensatory tachycardia)

Verapamil: constipation - bradycardia, heart block, cardiac failure

Diltiazem has both as less selective

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24
Q

When should dihydropyridines not be given?

A 
Unstable angina (don't want to increase O2 demand of heart)
Severe AS (provokes collapse)
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25
Q

When should non-dihydropyridines not be given?

A

Avoid in AV nodal conduction delay

Caution in poor LV function

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26
Q

Total cholesterol healthy limit

A

< 4 mmol/L

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27
Q

How long after an acute cardiac event should cholesterol be measured?

A

8 weeks

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28
Q

What should raise suspicion of an inherited hyperlipidaemia?

A

Consider if values v high
FHx first-degree premature CHD
Premature corneal arcus, tendon xanthomata, xantholasma

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29
Q

Where are tendon xanthamata often found?

A

Knuckles and achilles tendon

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30
Q

Before starting a statin, what should be checked?

A

Thyroid levels: hypothyroidism causes hyperlipidaemmia

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31
Q

Causes of secondary hyperlipidaemia

A

Pregnancy
Obesity
Alcohol excess

Medical: hypothyroid, obstructive jaundice, Cushing’s, anorexia nervosa, nephrotic syndrome, DM, CKD

Drugs: thiazides, glucocorticoids, beta-blockers, ciclosporin, antiretrovirals, atypical antipsychotics

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32
Q

4 indications for statin therapy

A

Primary hyperlipidaemia
Familiar hypercholesterolaemia

Established atherosclerotc disease

Everyone over 40 with T1DM and T2DM

Diabetic 18-39 with:
poor glycaemic control
retinopathy, nephropathy
HTN
evidence of metabolic sx
FHx CVD (first-degree, premature)

NICE recommends everyone over 85

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33
Q

When should statins be taken?

A

Evening - greatest effect when diet reduced

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34
Q

MoA statins

A

Inhibit HMG CoA reductase (makes cholesterol) - also indirectly reduces TGs and increases HDLs

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35
Q

In whom should statins be avoided?

A

Pregnant/ BF (need cholesterol)

Caution in hepatic impairment

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36
Q

Who needs lower doses of statins?

A

Renal disease

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37
Q

How to manage interactions with statins?

A

Metabolism REDUCED by cytochrome P450 inhibitors –> accumulation of statins –> side effects

Reduce statin dose, or withhold if other drug only needed for short time

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38
Q

ADRs of statins?

A

Rare but: headache, GI disturbance, muscles (from aches to serious myopathy), drug-induced hepatitis

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39
Q

What are the 3 stages of peripheral vascular disease and their equivalents?

A

Intermittent claudication (stable angina)

Critical limb ischaemia (unsuable angina)

Acute limmb ichaemia (MI)

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40
Q

Pain in buttock is usually claudication where?

A

Iliac artery

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41
Q

Pain in calf is usually claudication where?

A

Femoral or popliteal artery

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42
Q

Mx intermittent claudication

A

Encourage aerobic exercise –> angiogenesis
Lifestyle advice
Monitor DM/ HTN
Statins
ACEi (though 25% will have renal artery stenosis)
Antiplatelets if symptomatic
Peripheral vasodilator therapy

Angioplasty to dilate stenosed vessel

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43
Q

Defining criteria for critical limb ischaemia

A

Pain at rest
Gangrene
ABPI <0.3

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44
Q

Mx critical limb ischaemia

A 
Usually bypass (greater saphenous), can be helped by angioplasty
Or amputation
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45
Q

6Ps of acute limb ischaemia

A 
Pallor
Pulselessness
Perishingly cold
Pain
Paraesthesia
Pulselessness
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46
Q

Causes of acute limb ischaemia

A

Thrombus (ruptured plaque)
Embolism (esp from AF, vegetations from infective endocarditis, thrombus within sac of aneurysm)
Raynaud’s syndrome (if excessive vasoconstriction)
Trauma
Compartment syndrome

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47
Q

Ix acute limb ischaemia

A

Hand-held Doppler ultrasound scan may help demonstrate any residual arterial flow

Bloods:
FBC (ischaemia is aggravated by anaemia).
ESR (inflammatory disease - eg, giant cell arteritis, other connective tissue disorders).
Glucose (diabetes).
Lipids.
Thrombophilia screen.

If diagnosis is in doubt, perform urgent arteriography.

Investigations to identify the source of embolus:
ECG.
Echocardiogram.
Aortic ultrasound.
Popliteal and femoral artery ultrasound.
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48
Q

Mx acute ischaemic limb

A

Hospital admission
Immediate heparinisation
Pain relief

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49
Q

Causes of claudication with normal pulses

A

Neurogenic claudication (spinal stenosis)
Anaemia
Beta-blockers

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50
Q

What is Leriche syndrome?

A

Common iliac disease

Bilateral buttock pain and impotence

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51
Q

Buerger’s disease

A

Thromboangiitis obliterans
Vessels become blocked and inflamed by thrombi
Associated with smoking

52
Q

Why are lower doses ACEi given in diabetic nephropathy and CKD?

A

Risk of hyperkalaemia

53
Q

MoA of ACEi

A

Prevents conversion of angiotensin I to angiotension II (potent vasoconstrictor that stimulates aldosterone)

ACEi promotes Na+/H2O excretion - reduces preload

54
Q

ADRs of ACEi

A

Hypotension (esp after first dose)
Persistent dry cough (increased bradykinin - usually inactivated by ACE)
Hyperkalaemia (reduced aldosterone)
Rare: angioedema (anaphylactoid)

55
Q

When should ACEi not be given?

A

Pregnant/ BF
Renal artery stenosis
AKI

56
Q

Caution interactions with ACEi

A

NSAID + ACEi –> predisposes to renal failure

potassium-sparing drugs + ACEi –> only under specialist advice, HF

57
Q

Name some ACEi and ARBs

A

Ramipril, lisinopril

Losartan, candesartan

58
Q

4 indications of aspirin

A

Treatment of ACS + acute ischaemic stroke (rapid inhibition of platelets aggregation)

Secondary prevention of thrombotic arterial events

Reduce thrombus formation in AF (where warfarin/ oral anticoags contra-indicated)

Pain (though not best NSA/iD)

59
Q

MoA aspirin

A

Irreversibly inhibits cyclooxygenase –> reduces production of thromboxane

60
Q

How long do the effects of aspirin last?

A

7-10 days (lifetime of plts)

61
Q

ADRs of aspirin

A

GI ulceration/ haemorrhage (co-prescribe omeprazole if has risk factors + on other damaging drugs, eg NSAIDs/ pred)

Hypersensitivity (inc bronchospasm)

Tinnitus if reg high doses

62
Q

Why should under 16s not be given aspirin?

A

Reye’s syndrome: liver + brain effects

63
Q

When should pregnant women not take aspirin?

A

3rd trimester: premature closure of ductus arteriosus

64
Q

Who should not be given aspirin?

A

Peptic ulceration

Gout (precipitates attack)

65
Q

Indications for clopidogrel

A

Usually with aspirin

Prevents occlusion of coronary stents

66
Q

What is the MoA of clopidogrel?

A

Binds irreversibly to ADP receptors on platelets

67
Q

When should clopidogrel be stopped before surgery?

A

7 days

if emergency, may need platelet transfusion

68
Q

Which gastro-protection should be avoided with clopidogrel?

A

Omeprazole can inhibit clopi

69
Q

TRUE ANEURYSM

A

All 3 layers involved

70
Q

2 types of aneurysm

A

Fusiform, saccular

71
Q

FALSE ANEURYSM (PSEUDO-)

A

contained by outer layers of vessel or surrounding connective tissue

72
Q

DISSECTING ANEURYSM

A

False lumen between intima and media due to tear

73
Q

Risk factors for aneurysmal disease

A

HTN- hyperlipidaemia - old - smoker - COPD
[NOT DM]

Family hx

Atherosclerosis
Connective tissue disorders
Congenital: Berry aneurysms in circle of Willis (rupture = subarachnoid)

Vasculitis predisposes
Infection: tertiary syphilis –> saccular aortic aneurysm

74
Q

The following vasculitides predispose to aneurysms where:

Kawasaki’s
GCA
Takayasu’s

A

K: coronary artery aneurysm
GCA: ascending aorta
T: all

75
Q

Complications of aneurysmal disease

A

Can be asymptomatic:

Rupture
Thrombus (turbulent flow)
Emboli (sent anywhere!)
Pressure on adjacent structures

76
Q

Investigations for aneurysmal disease

A

Bloods: FBC, U&Es, LFTs, clotting, group & save if needs surgery, ESR/ CRP if suspect inflammatory cause

ECG, CXR

USS
CT/ IV Contrast

77
Q

How is a ruptured thoracic aortic aneurysm usually diagnosed?

A

Usually leads to MI and/ or death - a post-mortem diagnosis

78
Q

Definition of AAA

A

More than 3 cm

normal is 2 cm

79
Q

Clinical features of unruptured AAA

A

Asymptomatic

Or
pressure symptoms
uterohydronephrosis
microembolic lower limb infarcts (+ good pulses should raise suspicion)
inflammation and retroperitoneal fibrosis may cause symptoms due to entrapment-related structures (eg back pain, weight loss)

80
Q

Monitoring AAA diameters

A
  1. 0 - 4.4 cm: annual US
  2. 5 - 5.4 cm: 3- monthly US
  3. 5+: SURGERY
81
Q

Management of AAA

A

Monitoring

Smoking cessation
Strict BP
Statins, anti-platelets

Surgery, if indicated: open-repair or EVAR (stent-graft via femoral)

82
Q

Presentation of ruptured AAA

A

Triad: back pain - hypotension - pulsatile mass

likely to look unwell, be cold + sweaty
rapid, weak + thready pulse
peritoneal bleeding –> acute abdomen

83
Q

Types of aortic dissection

A

Type A: ascending aorta

Type B: descending aorta (not immediately life-threatening)

84
Q

How does aortic dissection present?

A

Severe chest pain, ‘ripping’
Pain might be worse on onset and then improve (cf MI) - and may then rupture > tamponade
Radiates to the back

Difference in BP in both arms

May be other symptoms due to occlusion by dissecting arteries: 
angina (coronary arteries)
limb ischaemia (distal aorta)
paraplegia (spinal arteries)
neurological deficit (carotid arteries)
85
Q

How is aortic dissection best visualised?

A

MRI or TOE

86
Q

Mx of aortic dissection

A

HDU/ ITU > surgery

87
Q

How is dissection prevented in those with connective tissue disorders?

A

Periodic aortic diameter screening
Lifelong beta-blockade
Moderate restriction of physical activity

88
Q

What is carotid artery disease?

A

Atherosclerosis at bifurcation of carotid artery

89
Q

How might carotid artery disease present?

A

If bilateral: cerebral hypoperfusion

Can throw off emboli –> TIA

90
Q

How is carotid artery disease managed?

A

Doppler for degree of stenosis

If symptomatic: carotid endarterectomy (scrape out atheroma) or stenting

91
Q

Causes of varicose veins

A

Caused by valvular incompetence or compression of deep veins causing stasis

92
Q

Risk factors for varicose veins

A

pregnancy, obesity, prolonged standing, previous DVT, pelvic mass pressing on deep veins

93
Q

Complications of varicose veins

A

Poor circulation can cause….

Bleeding: mild trauma causes profuse bleeding (pressure is high but walls are thin)

Phlebitis: can be complicated by bacterial infection

Venous eczema: haemosiderin released as cells pushed into tissue by increased presure

Venous ulcers

Oedema

94
Q

Management of varicose veins

A

lifestyle
compression stockings

refer:
urgently if active bleeding
routine if complications
imaged via duplex

Endothermal ablation
Ultrasound-guided foam sclerotherapy (if ablation unsuitable)
others

95
Q

Where do DVTs tend to occur?

A

Usually lower limb but can be pelvic veins

96
Q

Clinical features of DVT

A

Can be hard to diagnose, esp if complicated by cellulitis

Limb pain + tenderness along line of deep vein
Swelling of calf or thigh (usually unilateral but if high up may cause bilateral leg oedema)
Pitting oedema
Distension of superficial veins
Hot, erythematous (sometimes cyanosed)

97
Q

Risk factors for DVT

A

Previous DVT - family hx - thrombophilia - immobility - dehydration - cancer - smoking - COCP/ HRT - antiphospholipid sx - HF - varicose veins

98
Q

DDx for soft and tender leg

A 
Superficial thrombophlebitis
Peripheral oedema
Venous/ lymphatic obstruction
Vasculitis
Ruptured baker's cyst
cellulitis
septic arthritis
compartment syndrome
99
Q

Investigations for DVT

A

Wells’ score gives likelihood + leg USS
D-dimer

If positive:
gold-standard is contrast venography (rarely used)

Full examination/ look for cancers, esp if under 40

100
Q

Management of DVT

A

LMWH or fondaparinux
UFH if GFR <30 or increased risk of bleeding

oral anticoags for 3 months

101
Q

POST-THROMBOTIC SYNDROME

A

Due to damage to deep veins and their valves

Chronic venous hypertension can cause pain, swelling, hyperpigmentation, ulcers, gangrene etc

102
Q

2 indications for heparins and fondaparinux

A

prophylaxis and initial DVT treatment

ACS: first-line to improve revascularisation

103
Q

What is used to reverse heparins?

A

Protamine

104
Q

3 indications for warfarin

A

Prevents clot extension + recurrence of VTE
Prevent embolic complications in AF
“ after heart valve replacement

105
Q

Why is warfarin not used in arterial thrombosis?

A

These are driven by platelets: need anti-platelets

106
Q

MoA of warfarin

A

Inhibits hepatic production of vit K-dependent coag factors

107
Q

ADRs or warfarin

A 
Bleeding!
Including spontaneous (eg epistaxis) and peptic ulcers
108
Q

What can increase/ decrease effects of warfarin?

A

cytochrome P450 inhibitors: inhibit warfarin
inducers: stimulate warfarin

many abx increase anticoag as kill the gut flora synthesising vit K

109
Q

How much INR to prescribe?

A

Initially 5-10 mg, then guided by yellow book

Changes in INR lag behind dose changes

110
Q

Describe typical appearance and location of ulcers

A

Venous: shallow, throbbing pain, exudate, skin changes - GAITOR REGION

Arterial: punched out, painful ++, associated with gangrene - FEET, TOES, MEDIAL MALLEOLUS

Neuropathic: painless - BOTTOM OF FEET + GOOD PULSES

111
Q

Management of ulcers

A

Venous: compression bandages to reduce venous hypertension + abx

arterial: not compression!, address risk factors, consider surgery

Neuropathic: foot care to remove callous + orthowedge

112
Q

Describe types of gangrene

A

Wet: death + infection
Dry: just death
Gas: bacterial infection causing gas in tissues

113
Q

What is Fournier’s gangrene?

A

Multiorganism infection of scrotum
Pts usually DM + catheterised
Sudden pain in scrotum - needs urgent abx and debridement

114
Q

Secondary prevention of PAD

A

75 mg clopidogrel

115
Q

Who should be offered ABPM?

A

More than 140/90

If severe: 180/110, no need to confirm with ABPM. Consider starting Mx. Check no red flags

116
Q

Who should be treated for HTN?

A

All stage 2+

For stage 1, if under 80 and:
target organ damage
CVD
DM
renal disease
10 year CVD risk >20%
117
Q

Which thiazide used in BP management?

A

Chlortalidone or indapamide, rather than bendroflumethazide or hydrochlorothiazide (but if already on, don’t need to change)

118
Q

Target BP in over 80s

A

<150/90 (ABP/HBPM <145/85)

119
Q

Red flags for hypercholesterolaemia

A

Chest pain

Leg pain

120
Q

Red flags for hypertension

A

Diastolic BP >120
Microscopic haematuria
Encephalopathy
Pregnant

Impending complications, eg TIA, LVF

Severe HTN: look for papilloedema, retinal haemorrhage

Phaechromocytoma: headache, palpitations, pallor, excessive sweating, fever, abdo pains

121
Q

What tests after initiating statins?

A

LFTs at 3 months and 12 months

122
Q

Statin first-line doses

A

Primary prevention: atorvastatin 20 mg
Secondary prevention: atorvastatin 80 mg (20 mg if CKD)

Aiming for 40% reduction in non-HDL cholesterol after 3 months

123
Q

?familial hypercholesterolaemia

A

Cholesterol over 7.5
Tendon xanthamata
FHx premature CHD (under 60)

124
Q

Red flags for intermittent claudication

A

Critical limb ischaemia (Ps)

125
Q

Red flags for varicose veins

A

DVT

Abdominal mass

126
Q

Definition postural hypotension

A

Drop in >20 systolic or >10 diastolic within 3 mins of standing

Medicine (30 decks)

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