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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
Q

Chronic peripheral arterial occlusive disease causes

A

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
Q

Intermittent claudication symptoms & signs

A

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
Q

Ischaemic pain indicative of critical lower limb ischaemia

A

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
Q

Chronic peripheral arterial occlusive disease investigations

A

Bloods: FBC (rule out anaemia), HbA1c, lipids

ABPI

29
Q

Effects of peripheral neuropathy (diabetics) on development of chronic peripheral arterial disease

A

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
Q

Pathophysiology of intermittent claudication

A

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
Q

Leg pain differentials

A

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
Q

Causes of acute arterial occlusion

A

Embolus (40%)
Thrombus (40%)
Trauma (incl. angioplasty)

33
Q

Thrombosis predispositions (Virchow’s triad)

A

Endothelial dysfunction: trauma, inflammation, atheroma
Changes in blood flow: stasis/slow flow
Changes in coagulation: inflammatory response/congenital causes

34
Q

Embolic occlusion pathophysiology

A 
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
Q

Clinical symptoms of the acute ischaemic limb

A

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
Q

Embolic occlusion features

A

Sudden severe onset due to lack of collaterals
Source normally identifiable
Pulses previously normal, contralateral pulses
No history of arterial disease

37
Q

Thrombotic occlusion features

A

Insidious onset due to advanced collaterals
No obvious source
Long-standing decreased pulses bilaterally
Previous history of intermittent claudication, stroke, MI

38
Q

Difference between Raynaud’s phenomenon/syndrome

A

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
Q

Secondary causes of Raynaud’s syndrome

A

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
Q

Raynaud’s phenomenon phases and clinical characteristics

A

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
Q

Types of varicose veins

A

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
Q

Varicose veins symptoms

A 
Unsightly appearance
Tired/aching/throbbing legs
Ankle oedema
Itching/nocturnal cramps
Signs of deep venous insufficiency: hameosiderosis, eczema, lipodermatosclerosis
43
Q

Deep venous insufficiency pathophysiology

A

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
Q

Deep venous insufficiency presentation

A 
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
Q

Deep venous insufficiency investigations

A

Duplex sonography/venography

46
Q

Deep venous insufficiency investigations

A

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
Q

DVT anatomical location

A 
Deep veins in leg, originating around the valves
Anterior tibial
Posterior tibial
Perineal
Superficial femoral
Popliteal
48
Q

DVT risk factors

A 
Stasis &amp; coagulability = main risk factors
Age/immobility
Pregnancy/oral contraceptive pill
Malignancy
Obesity
Post-op (week 2)
Previous DVT
49
Q

DVT presentation

A

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
Q

Pulmonary embolism presentation

A 
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
Q

DVT investigations

A

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
Q

Types of PE

A 
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
Q

PE investigations

A

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
Q

Lymphoedema definition

A

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
Q

Primary vs secondary lymphoedema

A

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
Q

Lymphoedema investigations

A

Lymphoscintography: confirm diagnosis

Exclude other forms of oedema: CCF, renal disease, deep venous insufficiency

CP1 (12 decks)

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