Vascular 1 Flashcards
What is the protocol if blood pressure is measured above 140/90 in clinic?
Offer ABPM to confirm diagnosis
What is stage 1 HTN?
Clinic >140/90
ABPM >135/85
What is stage 2 HTN?
Clinic >160/100
ABPM/HBPM >150/95
What is Severe HTN?
SBP >180
or DBP >110
What is the causes of primary HTN?
Unknown… likely to be multifactorial
What are the causes of secondary HTN?
Adrenal cortical disease: primary hyperaldosteronism (e.g. Conn’s) - most common secondary cause
Cushing’s / Acromegaly
Renal artery stenosis - second most common cause
CKD
PCC: rare - HTN initially paroxysmal, presenting with sweating, pallor and palps
CoA: congenital narrowing of the aorta, leading to peripheral vascular resistance
Neurogenic: raised ICP
Pregnancy
What is benign hypertension?
Gradual elevation of blood pressure over years
This leads to gradual hypertrophy of the muscular media in artery walls, reducing their capacity to expand and increasing their fragility
What is malignant hypertension?
Rapid sustained increase in blood pressure
leads to intimal proliferation, reducing the luminal size and leading to cessation of blood flow through the small vessels
Foci of tissue necrosis e.g. in the glomeruli
Carries an untreated 1 year mortality of 20%
How is malignant hypertension diagnosed?
SBP >200 or DBP >120 AND bilateral retinal haemorrhages/exudates
papilloedema may be present
What are the pathological consequences of HTN?
Heart: left ventricular hypertrophy with dilation and eventual failure
Aorta: AAA and aortic dissection
Brain: intracerebral haemorrhage due to vessel rupture
Kidney: CKD due to progressive nephron ischaemia and glomerular destruction
Eyes: Hypertensive retinopathy
How should a hypertensive patient be assessed?
Full Hx: any features of malignant HTN? Headaches, epistaxis, fits, LOC
Any sx of secondary causes: PCC/CKD/Conn’s/IHD
Examination: funsocopy, CV exam
Hypertensive: AV nipping/flame shaped haemorrhages/cotton wool spots
Malignant HTN: bilateral papilloedema
Features of LVH/LVF
Assess for secondary causes (RAS, CKD, radio femoral delay)
What further investigations should be done following initial assessment for HTN?
Urine dip: renal damage
ECG: LVH
Echo: LVF
Assess for secondary causes
RAS - renal artery doppler
CKD: U&Es, eGFR
PCC: 3x 24 hour urine collections for free met adrenaline and normetadrenaline
Assess overall CV risk: HbA1c, lipids for Qrisk2
What is the first line treatment for HTN?
Lifestyle: weight loss, increasing exercise, decreasing alcohol, caffeine, sodium intake and stopping smoking
When should medication be started for HTN?
All with stage 2 HTN
Under 80 with stage 1 and one of the following:
10 year CV risk >20%
Other co-morbidities such as renal disease, known CV disease and organ damage
What is the target blood pressure following medical control?
<140/90
<150/90 if over 80
Home: 135/85
145/85 if aged >80
What is the treatment algorithm for HTN?
- <55 and non/black: ACEi (unless diabetic in which case ACEi regardless of age)
Older >55 or black: CCB - A+C or D
- A+C+ diuretic
- Add alpha blocker / spironolactone / other diuretic / beta blocker
If potassium <4.5 spironolactone, if <4.5, another drug
ACEi e.g.s
mode of action?
Ramipril, lisinopril
Act by RAAS antagonism
Who are ACEi used in?
<55
diabetics (renoprotective) regardless of age
What are the side effects of ACEi?
dry cough (due to potentiation of bradykinin) Switch to AT1 receptor antagonists e.g. candesartan/losartan
(block action of AT2 at AT1 receptor)
HYPERKALAEMIA
First dose hypotension
Worsened renal failure in those with previously ‘normal’ GFR
Monitor U+Es when initiating
contraindicated in renal artery stenosis
Can occasionally cause angioedema
CCB e.g.s?
MOA
Amlodipine / nifedipine - dihydropyridines
peripheral vasodilatation
Who are CCBs used in?
> 55
Afro-caribbean descent
What are the side effects of CCB?
Peripheral oedema (ankle swelling)
Postural hypotension
Reflex tachycardia
What if monotherapy is ineffective?
combined ACEi and CCB or Diuretic
Then add loop diuretic e.g. furosemide
then, if potassium <4.5 - spironolactone
if potassium >4.5, thiazide/thiazide like drug will be used (bendroflumothiazide)
What is hyperlipidaemia?
abnormally high levels of one/more lipoproteins in the plasma
What is primary hyperlipidaemia caused by?
due to a genetic predisposition to abnormal lipid metabolism e.g. familial hypercholesterolaemia
What is secondary hyperlipidaemia caused by?
a systemic metabolic disturbance e.g. obesity, alcoholism, diabetes
What is serum cholesterol a reflection of?
Serum LDL - predisposes to atheroma if serum cholesterol is >4
Association less strong with triglyceride / VLDL levels
What are xanthomata?
Lipid deposits on the eyelids, cornea, tendons as a result of raised cholesterol levels
What is the first line treatment for high LDL/low HDL cholesterol?
Lifestyle changes
Statins can be started if the lifestyle changes show no effect
Fibrates = second line - reserved for those with FH/co-morbid hypertryglyceridaemia
What is the Qrisk2 score?
10 year cardiovascular risk Age sex BMI BP lipid levels smoking + diabetes
gives 10 year risk of heart attack/stroke
What is the indication for a statin in Qrisk2 score?
Any patient with a score >10% as they have been shown to reduce mortality REGARDLESS of serum cholesterol
What is the MoA of a statin?
HMG-CoA reductase inhibitor - thus stop the first step in the cholesterol synthesis pathway
Increases LDL receptor expression by hepatocytes, leading to decreased LDL levels in circulation
What are the advantages of statins?
Reduce LDL, reduce mortality, morbidity from strokes and stabilise atherosclerotic lesions
When are statins taken?
At night (40-80mg)
What are the interactions/monitoring requirements for statins?
variety of interactions: metabolism by P450 enzymes
Care taken in liver disease: always monitor LFTs
Muscle pain = common side effect but should always be reported
Rhabdomyolysis can occur rarely, dip urine.
Stop if CK 5x upper limit of normal
e.g.s of fibrates?
Mode of action?
Bezafibrate / gemofibrozil
PPAR Alpha activators, with the main effect of reducing triglycerides
Also cause small increases in HDL and decreases in LDL
In combination with statins, may cause rhabdomyolysis
What other lipid lowering therapies are there?
Cholestyramine - decrease fat absorption
cholesterol absorption inhibitors such as ezetimibe
What is an aneurysm?
Focal dilation of an artery >150% of its normal diameter
What is the presentation of an aneurysm?
mass effects: pressuring adjacent structures
Embolic events: due to development of mural thrombi
Haemorrhage: due to rupture
What are the causes of aneurysm?
Atherosclerotic e.g. aortic, popliteal
Developmental e.g. berry aneurysm - Marfans/Ehlers-Danlos
Infective e.g. mycotic in endocarditis, syphilitic in tertiary syphilis
Trauma
What is an AAA?
Dilation of the abdominal aorta >3cm
Who gets AAA?
Males over 60
Suspect AAA in any male >50 presenting with renal colic
What screening programme is in place for AAA?
USS screening to males at aged 65
What is the presentation of AAA rupture?
Severe continuous / intermittent epigastric pain
radiating to the back/groin
Pulsatile/expansile abdominal mass
Signs of shock
What is the management of AAA?
EMERGENCY A-E
taken to theatre as soon as stabilised
Clamp the aorta above the leak, then insert a graft
Only 50% of ruptured AAAs make it to hospital
Of these patients, 50% will not survive the operation
What is the management of unruptured AAA?
<3cm: normal - no further acttion
3-4.4 - small aneurysm: rescan every 12 months
4.5-5.4: medium - rescan every 3 months
>5.5 = large aneurysm: Refer within 2 weeks to vascular surgery for probable intervention
Only found in 1 per 1,000 screened patients
What are the indications for surgery of AAA?
AAA >6cm: risk of rupture increases from 1% to 25% at 6cm
AAAs expanding at >1cm/year
Symptomatic aneurysms
In which patients is rupture of AAA more likely?
Patients with hypertension, family history of rupture, smokers and females
Therefore, operation may be performed at an earlier stage
What is EVAR?
Endovascular aneurysm repair:
Most common surgery, using the femoral arteries to access and stent the aorta under fluoroscopic guidance
What are the advantages of EVAR?
Lower mortality rate than the conventional open operation
Lower post-operative morbidity and shorter hospital stay, ITU not required
What kind of pre/post op management is needed with EVAR?
Lifelong monitoring is required and re-intervention is not uncommon
Endoleaks = common reason for re-intervention
Thorough pre-op assessment: co-existing cardiorespiratory/kidney disease that can affect decision to operate
Why is a CKD a particular risk for EVAR?
Contrast used in EVAR is nephrotoxic, and in the open procedure, there is prolonged ischaemia to the kidneys after the aorta is clamped
What aneurysm is a common finding if patients have other aneurysms?
Popliteal aneurysm
10% of AAA patients will also have popliteal aneurysm
What is the presentation of a popliteal aneurysm?
Asymptomatic or may present with complications
Acute limb ischaemia - due to rupture/thrombosis of the aneurysm or distal emboli
Chronic limb ischaemia: gradual occlusion of the aneurysm
DVT: if occluding popliteal veins
What ix are done for popliteal aneurysm?
USS: to determine the size of the aneurysm
Angiography: prior to surgery to assess distal arterial tree
What is the management of popliteal aneurysm?
Femoral to distal popliteal bypass grafts
Intra-vascular thrombolysis or embolectomy may occur at the time of surgery for distal emboli
What is a true aneurysm?
All layers of the arterial wall are involved
What is a false/pseudoaneurysm?
the surrounding soft tissues lined by thrombus form teh wall of the aneurysm, mainly following trauma
e.g. femoral artery puncture with inadequate compression
Describe how an aortic dissection occurs
A tear in the intima leads to blood tracking into the arterial media
the arterial media splits, forming a false channel
Most commonly occurs in the aorta
What are the possible outcomes of an aortic dissection?
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
What are the cause of Aortic dissection?
Hypertension
Atheroma
Congenital disease (Marfan’s/Ehler’s Danlos)
What are the two patterns of Aortic dissection?
Type A (70%): involve the ascending aorta Type B (30%) do not involve the ascending aorta
What is the presentation of aortic dissection?
Severe, very sudden onset central chest pain, described as ‘tearing’
May radiate down the arm / to the back (mimicking MI)
Patient is shocked
blockage of distal arterial trunks
What are the investigations for aortic dissection?
CXR: mediastinum is classically widened
CT: confirms diagnosis
ECG: patterns similar to MI
Transoesophageal echocardiography (TOE) if patient is unstable and can’t go to CT
What does retrograde spread of Aortic dissection lead to?
Cardiac tamponade
What does distal spread of aortic dissection lead to?
Origins of main arterial branches become blocked, leading to symptoms depending on the arteries involved
Coronary arteries: MI
Brachiocephalic trunk: unequal arm pulses and central neurological symptoms
Same if left common card and LSA occlusion
Renal arteries: haematuria, anuria, AKI
SMA/IMA: acute mesenteric ischaemia
Iliac arteries: acute lower limb ischaemia
What is the management of aortic dissection?
A-E resuscitation with urgent cardiothoracic advice
Type A
surgical management, but blood pressure should be controlled to a target systolic of 100-120 mmHg whilst awaiting intervention
Type B*
conservative management
bed rest
reduce blood pressure IV labetalol to prevent progression
