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CP1 > Vascular > Flashcards

Vascular Flashcards

1
Q

Diagnosis of hypertension

A

If lowest BP in clinic is >140/90, offer ambulatory BP monitoring (2 measurements/h, average used)
Home blood pressure used if APBM not tolerated (2x a day)

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2
Q

Stages of hypertension

A

Stage 1: clinic BP >140/90 & ABPM >135/85
Stage 2: clinic BP>160/100 & ABPM >150/95
Severe HTN: clinic SBP>180 or DBP>110

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3
Q

Prevalence of HTN

A

20-30% of adult population
Isolated systolic hypertension affects >50% >60s
Doubles the risk of MI

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4
Q

Types of hypertension

A

Primary (essential): 95% of cases, unknown cause
Secondary: adrenal cortical diseases (primary hyperaldosteronism, Cushing’s, acromegaly), renal artery stenosis (bruit), CKD, pheochromocytoma (initially paroxysmal HTN), aortic coarction, neurogenic (raised ICP), pregnancy
Primary & secondary HTN can be…
Benign: gradual elevation of BP, hypertrophy of muscular media reducing capacity to expand & increasing fragility
Malignant: rapid sustained increase in BP, intimal proliferation, reduced luminal size, cessation of blood flow through small vessels –> foci of tissue necrosis
1y mortality = 20%
SBP>200 or DBP>120 & bilateral retinal haemorrhages/exudates +/- papilloedema

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5
Q

Pathological consequences of HTN

A

Heart: LVH, dilation & eventual failure
Aorta: AAA/dissection
Brain: Intracerebral haemorrhage
Kidney: CKD, progressive nephron ischaemia & glomerular destruction
Eyes: hypertensive retinopathy

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6
Q

Taking a HTN history

A

Malignant HTN? Headaches, epistaxis, fits, level of consciousness
Secondary causes? Signs of pheochromocytoma/CKD/Conn’s
Ischaemic heart disease may suggest renal artery stenosis

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7
Q

HTN examination

A 
Fundoscopy: hypertensive retinopathy (AV nicking, flame shaped haemorrhages, cotton wool spots, bilateral papilloedema)
CV examination: LVH/LVF
Renal bruits: renal artery stenosis
CKD features
Radiofemoral delay: aortic coarction
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8
Q

HTN investigations

A 
Urine dip: renal damage
ECG: LVH
Echo: LVF
Renal artery doppler: RAS
U&Es & eGFR: CKD
3x 24h urine collections for free metadrenaline & normetadrenaline: pheochromocytoma
HbA1c, lipids: for Qrisk2 CV risk
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9
Q

Types of hyperlipidaemia

A

Primary: genetic predisposition to abnormal lipid metabolism (e.g. familial hypercholesterolaemia)
Secondary: systemic metabolic disturbance (e.g. obesity, alcohol, diabetes)

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10
Q

Links between cholesterol and CV risk

A

Raised serum cholesterol: reflection of serum LDL –> predisposes to atheroma if levels >4
Less strong association with VLDL & triglycerides
High HDL levels are protective against atheroma
Hypercholesterolaemia –> xanthomata (eyelids/cornea/tendons)

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11
Q

Aneurysm definition

A

Focal dilation of an artery >150% of its normal diameter

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12
Q

How can an aneurysm present

A

Mass effects: pressuring adjacent structures
Embolic events: development of mural thrombi
Haemorrhage: rupture

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13
Q

Aneurysm causes

A

Atherosclerotic: aortic, popliteal
Developmental: berry, Marfan’s, Ehlers-Danlos
Infective: mycotic in endocarditis, syphylitic in tertiary syphilis
Trauma: false aneurysm?

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14
Q

AAA aetiology

A 
Dilation of the abdominal aorta >3cm
5% males >60y
USS screening offered to males >65y
5x more common in men
Mainly asymptomatic
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15
Q

AAA rupture presentation

A

Severe continuous/intermittent epigastric pain
Radiating to back/groin
Signs of shock

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16
Q

Unruptured AAA management

A

AAAs <5.5cm: monitored by regular USS/CT, modification of risk factors, 75% eventually require surgery
Indications for surgery…
AAAs>6cm: risk of rupture increases to 25%
AAAs expanding >1cm/y
Symptomatic
Rupture is more likely: HTN, FH, smokers, females

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17
Q

Aortic dissection pathophysiology

A

A tear in the intima leads to blood tracking into the arterial media
The media splits, forming a false channel
Most commonly occurs in the aorta
External rupture: massive fatal haemorrhage
Internal rupture: rare, blood tracks back into the lumen to produce a double-channelled aorta
Cardiac tamponade: retrograde spread into the pericardial cavity

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18
Q

Aortic dissection causes

A

Hypertension
Atheroma
Congenital: Marfan’s, Ehlers-Danlos

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19
Q

Types of aortic dissection

A 
Type A (70%): involves ascending aorta
Type B (30%): does not involve the ascending aorta
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20
Q

Aortic dissection presentation

A

Severe, sudden onset central chest pain, ‘tearing’
Radiates down arm/to the back (mimics MI)
Shocked patient
Signs of blockage of distal arterial trunks

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21
Q

Aortic dissection investigations

A

CXR: mediastinum is classically widened
CT: confirm diagnosis
ECG: pattern similar to MI

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22
Q

Aortic dissection complications

A

Retrograde spread: cardiac tamponade
Distal spread blocks origins of main arteries…
Coronary: MI
Brachiocephalic trunk: unequal arm pulses and CNS symptoms
Renal arteries: haematuria, anuria, AKI
Superior/inferior mesenteric: acute mesenteric ischaemia
Iliac: acute lower limb ischaemia

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23
Q

Fontaine classification of chronic lower limb arterial disease

A
  1. Asymptomatic
  2. Intermittent claudication
  3. Ischaemic rest pain
  4. Ulceration/gangrene
24
Q

Ankle-brachial pressure index to assess arterial disease

A

ABPI<0.8: arterial disease present
ABPI<0.4: critical limb ischaemia
ABPI >1.2: may be false negative due to calcification giving abnormally stiff vessels (more common in diabetics)

25
Chronic peripheral arterial occlusive disease causes
Atherosclerosis: most common Fibromuscular dysplasia: non-inflammatory arterial wall thickening Buerger's disease (thromboangiitis obliterans): acute inflammation and thrombosis of lower limb arteries/veins: young heavy smokers
26
Intermittent claudication symptoms & signs
Ischaemic 'cramping' muscle pain on walking, relieved by rest Pain reproducible at a similar level: 'claudication distance' Commonly in calf: femoral disease Thigh/buttock: ileal disease, often bilateral, ask about penile function (aortoiliac occlusive disease/Leriche syndrome) Absent pulses Cold, pale legs Atrophic, hairless, shiny skin Beurger's test: angle <20 degrees, observe for reactive hyperaemia Arterial ulcers
27
Ischaemic pain indicative of critical lower limb ischaemia
Classically at night in the forefoot Pain wakes patient Relief by swinging leg over the side of the bed/walking on a cold floor Hx of intermittent claudication & signs of arterial insufficiency Ulcers likely to form from minor injury --> infection of ulcers can lead to rapidly spreading gangrene (more common with DM)
28
Chronic peripheral arterial occlusive disease investigations
Bloods: FBC (rule out anaemia), HbA1c, lipids | ABPI
29
Effects of peripheral neuropathy (diabetics) on development of chronic peripheral arterial disease
Sensory neuropathy: reduces protective reactions to minor injury, reduces awareness of infection/ischaemia Autonomic neuropathy: anhydrosis --> dry, fissured skin, allowing entry of bacteria Motor neuropathy: wasting of small muscles of the foot leads to loss of arches and development of abnormal pressure areas on feet
30
Pathophysiology of intermittent claudication
Femoral artery most commonly becomes atheromatous: calf most often affected At rest: 02 requirements met by collateral system of deep femoral artery Exercise: 02 demand not met, calf muscle becomes ischaemic
31
Leg pain differentials
Intermittent claudication Spinal stenosis: osteophyte formation compressing lumbar nerve root/cauda equina. Pain relieved by spine flexion. Pulses will be present. MRI diagnosis. Venous claudication: iliofemoral occlusion, gradual onset of pain, affects whole leg. Relieved by elevation. Signs of venous disease/Hx DVT Musculoskeletal: osteo/rheumatoid arthritis Peripheral neuropathy Popliteal artery entrapment: young, normal pulses
32
Causes of acute arterial occlusion
Embolus (40%) Thrombus (40%) Trauma (incl. angioplasty)
33
Thrombosis predispositions (Virchow's triad)
Endothelial dysfunction: trauma, inflammation, atheroma Changes in blood flow: stasis/slow flow Changes in coagulation: inflammatory response/congenital causes
34
Embolic occlusion pathophysiology
``` Occlusion by a mass of material transported in the bloodstream, commonly fragments of thrombus (thromboemboli) Thromboemboli arise from... Left atrium: AF Left ventricle: post-MI Heart valves: endocarditis Mural thrombi: AAA ```
35
Clinical symptoms of the acute ischaemic limb
Pulseless Painful Pallor Perishingly cold Paralysis: threatened limb Paraesthesia (prickling/tingling): threatened limb Fixed staining of the leg + rigid muscles indicate a non-viable limb
36
Embolic occlusion features
Sudden severe onset due to lack of collaterals Source normally identifiable Pulses previously normal, contralateral pulses No history of arterial disease
37
Thrombotic occlusion features
Insidious onset due to advanced collaterals No obvious source Long-standing decreased pulses bilaterally Previous history of intermittent claudication, stroke, MI
38
Difference between Raynaud's phenomenon/syndrome
Raynaud's phenomenon: episodic digital vasospasm in the absence of an identifiable associated disorder Raynaud's syndrome: episodic digital vasospasm occuring secondary to another condition
39
Secondary causes of Raynaud's syndrome
Connective tissue disorders: systemic sclerosis, mixed connective tissue disease, SLE, Sjogren's syndrome, polyarteritis nodosa Macrovascular disease: atherosclerosis, thoracic outlet obstruction, Buerger's disease Occupational trauma: vibration white finger, repeated extreme cold or chemical exposure Drugs: beta-blockers, cytotoxic drugs Malignancy Atrio-ventricular fistula
40
Raynaud's phenomenon phases and clinical characteristics
Phase 1: pallor due to digital artery spasm 2: cyanosis: accumulation of deoxygenated blood 3: rubor: erythema due to reactive hyperaemia Numbness/burning/pain upon return to normal. Attacks usually <45mins
41
Types of varicose veins
Varicose veins: abnormally dilated and lengthened superficial veins Primary (idiopathic): 2x as common in women Pregnancy accentuates symptoms Likely a primary superficial valve defect + familial elements No deep venous incompetence Secondary: superficial varicosities occur secondary to deep venous incompetence Previous DVT Raised systemic venous pressure due to compression (pregnancy, pelvic tumour), AVF, severe tricuspid incompetence
42
Varicose veins symptoms
``` Unsightly appearance Tired/aching/throbbing legs Ankle oedema Itching/nocturnal cramps Signs of deep venous insufficiency: hameosiderosis, eczema, lipodermatosclerosis ```
43
Deep venous insufficiency pathophysiology
Postphlebitic limb Incompetent valves of deep venous system Soleal pump no longer efficient at returning blood to the thoracic cavity Primary: congenital absence of valves Secondary: DVT causing valvular damage/AVF raising venous pressure
44
Deep venous insufficiency presentation
``` Lower limb aching pain/discomfort Lower leg oedema Superficial varicose veins (raised central pressure causes perforator incompetence) Haemosiderin deposition in gaiter area Eczema over pigmented area: pruritis Atrophie blanche Lipodermatosclerosis: subcut tissue replaced by thick fibrous tissue, giving inverted champagne bottle appearance Ulceration ```
45
Deep venous insufficiency investigations
Duplex sonography/venography
46
Deep venous insufficiency investigations
Hand-held doppler: identify reflux at saphenofemoral/saphenopopliteal junctions Duplex sonography: diagnose valvular and perforating vein incompetence, large vein occlusion Venography: tourniquet placed around the ankle to occlude superficial veins, contrast injected into foot Fluoroscopy then used to see the progress through the deep system Deep vein occlusion & perforating vein reflux readily detected
47
DVT anatomical location
``` Deep veins in leg, originating around the valves Anterior tibial Posterior tibial Perineal Superficial femoral Popliteal ```
48
DVT risk factors
``` Stasis & coagulability = main risk factors Age/immobility Pregnancy/oral contraceptive pill Malignancy Obesity Post-op (week 2) Previous DVT ```
49
DVT presentation
Asymptomatic Calf tenderness & firmness Oedema Erythema & calor (heat) Superficial vein distension Superficial thrombophlebitis: tender, erythematous, palpable superficial vein Homan's sign: pain on dorsiflexion of ankle (should not be tested for as may dislodge thrombus) Atypical presentations... Ilio-femoral thrombosis: severe pain, few physical signs Complete occlusion of large vein: cyanotic discolouration
50
Pulmonary embolism presentation
``` More common with iliofemoral thrombosis Sudden onset unexplained dyspnoea Pleuritic chest pain Haemoptysis Increased pulmonary artery pressure/right heart strain Ischaemia of the lung V/Q mismatch Raised JVP Cyanosis Evidence of a DVT ```
51
DVT investigations
D-dimer: sensitive, non-specific for DVT (infection, pregnancy, malignancy, post-op) Compression USS: Non-collapsing veins indicate presence of DVTs Thrombophilia screen: Prior to commencing anticoagulant
52
Types of PE
``` Massive PE (5%): >60% pulmonary circulation is blocked, rapid CV collapse Major PE (10%): middle-sized pulmonary arteries blocked, leading to breathlessness, pleuritic chest pain, haemoptysis Minor PE (85%): small peripheral vessels are blocked, may be asymptomatic, or present as major Massive PE may ensue following a minor PE = 'premonitory embolus' ```
53
PE investigations
Bloods: FBC, U&E, clotting, d-dimer ABG: type 1 respiratory failure CXR: normal/dilated pulmonary artery, wedge shaped opacities ECG: tachycardia, RBBB, RV strain, S1Q3T3 Echo: confirm right heart strain CTPA: gold standard (V/Q if this is unavailable)
54
Lymphoedema definition
Swelling resulting from an increased quantity of fluid in the interstitial space of soft tissues, due to failure of lymphatic drainage Chronic non-pitting oedema, commonly affecting the legs
55
Primary vs secondary lymphoedema
Primary: presents early in life, result of inherited deficiency of lymphatic vessels (e.g. Milroy's) Secondary: obstruction of lymphatic vessels: filaria infection, repeated cellulitis, malignancy, post-operative
56
Lymphoedema investigations
Lymphoscintography: confirm diagnosis | Exclude other forms of oedema: CCF, renal disease, deep venous insufficiency

CP1 (12 decks)

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