Renovascular Hypertension Flashcards

1
Q

Definition of renovascular hypertension?

A

Any vascular pathology that produces hypoperfusion of the kidney/s, resulting in the development of systemic hypertension

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2
Q

What proportion of hypertensive patients have primary vs secondary hypertension?

A

Primary - 95%

Secondary - 5%

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3
Q

What is the significance of diagnosing hypertension as being due to secondary cause?

A

It may be treated, either surgically or otherwise, rather than just symptomatically managing the patient with anti-hypertensive medications

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4
Q

Types/categories/causes of secondary hypertension?

A
- Endocrine disorders:
  ~ Cushing's syndrome
  ~ Conn's syndrome
  ~ Phaeochromocytoma
  ~ Hyperthyroidism
  ~ Hyperparathyroidism
- Renal parenchymal disorders:
  ~ Nephroblastoma
- Renovascular disorders:
  ~ Renal artery stenosis
  ~ Coarctation of the aorta
  ~ Middle aortic syndrome
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5
Q

Clinical features suggestive of secondary hypertension?

A
  • Early onset of HPT ( 160/100), malignant HPT (>180/120)
  • Multi-drug requiring HPT, refractory HPT
  • Epigastric bruits
  • Grade 3,4 hypertensive retinopathy
  • Non-cardiogenic flash pulmonary oedema
  • Clinical stigmata of endocrine disorder + severe HPT
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6
Q

Pathogenesis of renovascular HPT?

A
  • Decreased perfusion of kidney
  • Stimulation of RAAS
  • Angiotension 1 (weak) and 2 (strong) vasocntrict blood vessels
  • Production and release of aldosterone results in fluid retention
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7
Q

Pathology in single renal artery stenosis?

A
  • Hypertension due to Angiotensin etc

- NO volume overload, because normal kidney compensates with a diuresis

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8
Q

Pathology in bilateral renal artery stenosis?

A
  • Hypertension + volume overload, because no normal kidney to excrete excess fluid which is retained
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9
Q

Why do ACE-inhibitors worsen HPT in renal artery stenosis?

A

Angiotensin 2 acts on the efferent arteriole of the glomerulus to increase glomerular pressure, thus an ACEI removes this protective mechanism and the patient has decreased glomerular pressure and filtration, and has worsening creatinine clearance

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10
Q

Goals of treatment for renovascular HPT?

A
  • Control BP
  • Preserve renal function
  • Limit treatment-related complications
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11
Q

Anatomical classification of renal artery stenosis?

A
  • Ostial: involves origin of renal artery
  • Parostial: stenosis commences 10mm from origin of renal artery
  • Accessory: occurs in an accessory renal artery
  • Segmental: occurs in a segmental branch of the artery
  • Mixed-type
  • Complete renal artery occlusion
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12
Q

Pathological classification of renal artery stenosis?

A
  • Atherosclerotic (90%)
  • Fibromuscular dysplasia
  • Takayasu’s disease
  • Renal artery dissection
  • Renal artery aneurysm
  • Trauma
  • Juxta-renal saccular aortic aneurysm
  • Radiation-induced
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13
Q

Severity grading of renal artery stenosis?

A
  • Mild: 70%
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14
Q

When is renal artery stenosis haemodynamically significant?

A

When it is >60% stenosed

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15
Q

What are the treatment options for renal artery stenosis?

A
  • Medical therapy
  • Percutaneous transluminal renal angioplasty
  • Percutaneous transluminal renal angioplasty and stenting
  • Surgical revascularisation
  • Nephrectomy
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16
Q

Clinical presentations of atherosclerotic RAS?

A
  • Severe hypertension: newly-diagnosed, or rapidly worsening HPT
  • Ischaemic nephropathy: rapidly-progressive renal dysfunction
17
Q

Where (anatomically) does the stenosis occur in the majority of atherosclerotic RAS?

A
  • Ostium: generally an extension of an aortic plaque
18
Q

Treament of mild-moderate RAS?

A
  • This is ~95% of patients with RAS
  • Medical treatment:
    ~ Risk factor reduction: smoking, hypertension, diabetes, hyperlipidaemia, obesity)
    ~ Drugs: antiplatelet therapy, statins, anti-HPT,ACEI (!)
19
Q

Why are ACEI incorporated into the medical treatment regime of RAS if they are known to worsen the HPT?

A

Initially worsen HPT and decrease creatinine clearance, but this can be managed symptomatically in the meantime
ACEI have been shown to be reno-protective in the long run, compared to the natural history of the disease

20
Q

What is fibromuscular dysplasia?

A

A degenerative condition that involves branchless vessels, classically the renal, subclavian, carotid and iliac arteries

21
Q

Pathological classification of fibromuscular dysplasia?

A
  • Medial type (80%):
    ~ Medial fibroplasia: alternating areas of stenosis with areas of dilatation (“string of beads” - larger than diameter of renal artery)
    ~ Perimedial fibroplasia: “string of beads” - same diameter as renal artery
    ~ Medial hyperplasia: focal, smooth stenosis
  • Adventitial type:
    ~ Adventitial fibroplasia
  • Intimal type:
    ~ Intimal fibroplasia: diffuse narrowing
22
Q

What is Takayasu’s arteritis?

A

Non-specific large vessel vasculitis, affecting the aorta and its branches, predominantly occurring in females

23
Q

What is a common diagnostic feature of Takayasu’s arteritis?

A

Stenosis of the subclavian arteries (pulseless disease in a young woman)

24
Q

Common history/examination findings in Takayasu’s disease?

A
  • Female
  • Prodome (headaches, fever, joint and muscle pains, carotidynia)
  • Diminshed upper limb pulses (subclavian stenosis)
  • Coronary artery disease, aortic or mitral regurgitation, pulmonary HPT
25
Q

Investigations and findings in Takayasu’s arteritis?

A
  • CTA: aortitis (thick-walled), occlusive disease of aorta and aortic branches)
  • Bloods: raised ESR and CRP
  • Histology: pan-arteritis, giant-cell granulomas
26
Q

What is coarctation of the aorta?

A

Congenital narrowing of the thoracic aorta at the level of the ligamentum arteriosum
Commonest congenital cause of hypertension

27
Q

Clinical features of coarctation of the aorta?

A
  • Asymptomatic
  • Symptomatic: headaches, claudication, syncope
  • Complicated: cardiac failure, stoke
  • Radio-radial or radio-femoral delay
  • Praecordial bruit
28
Q

Anatomical classification of coarctation of the aorta?

A
  • Post-ductal: commonest type, associated with bicuspid aortic valves in ~40% of patients, good prognosis
  • Pre-ductal: associated with early death, multiple associated cardiac anomalies
  • Interrupted aorta: most severe form, most are still-born
29
Q

What is the middle-aortic syndrome?

A

An acquired vascular condition where various disease processes result in narrowing of the descending aorta, resulting in renin-dependent HPT

30
Q

Pathologies associated with middle aortic syndrome?

A
  • Takayasu’s disease (most commonly)
  • Atherosclerosis
  • Congenital hypoplasia
  • Von Recklinghausen’s disease (neurofibromatosis type 1)
  • Fibromuscular dysplasia
  • Tuberculous arteritis
31
Q

Clinical features of middle aortic syndrome?

A
  • Upper limb hypertension
  • Radio-femoral delay
  • Inter-scapular and/or abdominal bruits
  • Lower extremity claudication