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Vascular 1 Flashcards

1
Q

What is the protocol if blood pressure is measured above 140/90 in clinic?

A

Offer ABPM to confirm diagnosis

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2
Q

What is stage 1 HTN?

A

Clinic >140/90

ABPM >135/85

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3
Q

What is stage 2 HTN?

A

Clinic >160/100

ABPM/HBPM >150/95

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4
Q

What is Severe HTN?

A

SBP >180

or DBP >110

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5
Q

What is the causes of primary HTN?

A

Unknown… likely to be multifactorial

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6
Q

What are the causes of secondary HTN?

A

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

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7
Q

What is benign hypertension?

A

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

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8
Q

What is malignant hypertension?

A

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%

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9
Q

How is malignant hypertension diagnosed?

A

SBP >200 or DBP >120 AND bilateral retinal haemorrhages/exudates

papilloedema may be present

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10
Q

What are the pathological consequences of HTN?

A

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

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11
Q

How should a hypertensive patient be assessed?

A

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)

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12
Q

What further investigations should be done following initial assessment for HTN?

A

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

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13
Q

What is the first line treatment for HTN?

A

Lifestyle: weight loss, increasing exercise, decreasing alcohol, caffeine, sodium intake and stopping smoking

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14
Q

When should medication be started for HTN?

A

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

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15
Q

What is the target blood pressure following medical control?

A

<140/90
<150/90 if over 80

Home: 135/85
145/85 if aged >80

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16
Q

What is the treatment algorithm for HTN?

A
  1. <55 and non/black: ACEi (unless diabetic in which case ACEi regardless of age)
    Older >55 or black: CCB
  2. A+C or D
  3. A+C+ diuretic
  4. Add alpha blocker / spironolactone / other diuretic / beta blocker

If potassium <4.5 spironolactone, if <4.5, another drug

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17
Q

ACEi e.g.s

mode of action?

A

Ramipril, lisinopril

Act by RAAS antagonism

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18
Q

Who are ACEi used in?

A

<55

diabetics (renoprotective) regardless of age

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19
Q

What are the side effects of ACEi?

A 
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

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20
Q

CCB e.g.s?

MOA

A

Amlodipine / nifedipine - dihydropyridines

peripheral vasodilatation

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21
Q

Who are CCBs used in?

A

> 55

Afro-caribbean descent

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22
Q

What are the side effects of CCB?

A

Peripheral oedema (ankle swelling)
Postural hypotension
Reflex tachycardia

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23
Q

What if monotherapy is ineffective?

A

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)

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24
Q

What is hyperlipidaemia?

A

abnormally high levels of one/more lipoproteins in the plasma

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25
What is primary hyperlipidaemia caused by?
due to a genetic predisposition to abnormal lipid metabolism e.g. familial hypercholesterolaemia
26
What is secondary hyperlipidaemia caused by?
a systemic metabolic disturbance e.g. obesity, alcoholism, diabetes
27
What is serum cholesterol a reflection of?
Serum LDL - predisposes to atheroma if serum cholesterol is >4 Association less strong with triglyceride / VLDL levels
28
What are xanthomata?
Lipid deposits on the eyelids, cornea, tendons as a result of raised cholesterol levels
29
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
30
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
31
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
32
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
33
What are the advantages of statins?
Reduce LDL, reduce mortality, morbidity from strokes and stabilise atherosclerotic lesions
34
When are statins taken?
At night (40-80mg)
35
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
36
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
37
What other lipid lowering therapies are there?
Cholestyramine - decrease fat absorption | cholesterol absorption inhibitors such as ezetimibe
38
What is an aneurysm?
Focal dilation of an artery >150% of its normal diameter
39
What is the presentation of an aneurysm?
mass effects: pressuring adjacent structures Embolic events: due to development of mural thrombi Haemorrhage: due to rupture
40
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
41
What is an AAA?
Dilation of the abdominal aorta >3cm
42
Who gets AAA?
Males over 60 | Suspect AAA in any male >50 presenting with renal colic
43
What screening programme is in place for AAA?
USS screening to males at aged 65
44
What is the presentation of AAA rupture?
Severe continuous / intermittent epigastric pain radiating to the back/groin Pulsatile/expansile abdominal mass Signs of shock
45
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
46
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
47
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
48
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
49
What is EVAR?
Endovascular aneurysm repair: | Most common surgery, using the femoral arteries to access and stent the aorta under fluoroscopic guidance
50
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
51
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
52
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
53
What aneurysm is a common finding if patients have other aneurysms?
Popliteal aneurysm | 10% of AAA patients will also have popliteal aneurysm
54
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
55
What ix are done for popliteal aneurysm?
USS: to determine the size of the aneurysm Angiography: prior to surgery to assess distal arterial tree
56
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
57
What is a true aneurysm?
All layers of the arterial wall are involved
58
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
59
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
60
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
61
What are the cause of Aortic dissection?
Hypertension Atheroma Congenital disease (Marfan's/Ehler's Danlos)
62
What are the two patterns of Aortic dissection?
``` Type A (70%): involve the ascending aorta Type B (30%) do not involve the ascending aorta ```
63
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
64
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
65
What does retrograde spread of Aortic dissection lead to?
Cardiac tamponade
66
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
67
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

CP3 Surgery (12 decks)

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