Reno-vascular hypertension Flashcards

1
Q

Causes of secondary hypertension

A
  1. Endocrine: Cushing’s, Conn’s, Phaeochromocytoma, hyperthyroidism, hyperparathyroidism, adreno-genital syndrome
  2. Renal parenchymal disorders: Nephroblastoma
  3. Renovascular disorders: Renal artery stenosis, coarctation of the aorta, the middle aortic syndrome
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2
Q

Clinical features that suggest secondary hypertension

A
  • Early onset of hypertension (<30 y.o)
  • Late onset hypertension
  • Severe hypertension (>160/100)
  • Malignant hypertension (>180/120)
  • Multi-drug requiring therapy for hypertension
  • Medically refractory hypertension
  • epigastric bruits
  • Grade 3 or 4 hypertensive retinopathy
  • Flash pulmonary oedema (non-cardiogenic)
  • Refractory angina in the elderly
  • Clinical stigmata of endocrine disorders
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3
Q

What does an endocrine screen entail in a patient with suspected secondary hypertension

A
  • 9 am or midnight serum cortisol
  • 24 hour urinary cortisol levels
  • serum aldosterone levels
  • Plasma renin assays
  • 24 hour urinary metanephrines/ catecholamines
  • Plasma catecholamines
  • Thyroid function tests
  • parathyroid hormone levels
  • Serum calcium and phosphate levels
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4
Q

What imaging options are available based on the endocrine screen for secondary hypertension

A
  • CT abdomen, brain or chest
  • ultrasound of the thyroid gland
  • Radio-isotope scans
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5
Q

Which renal investigations are available?

A
  • Duplex ultrasound of the kidneys: renal masses/ tumours; discrepant renal lengths
  • MAG 3 renogram with GFR
  • Captopril renogram
  • Vascular imaging (aortic and renal): DSA, CTA, MRA
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6
Q

How does angiotensin II produce hypertension

A
  • Acts on Angiotensin II receptors resulting in vasoconstriction
  • Promotes the production and release of aldosterone which results in fluid retention and volume expansion
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7
Q

What are the three Goldblatt models and how do they each present?

A
  • Single renal artery stenosis (RAS)/ two kidney model: Hypertension but no volume expansion
  • Bilateral RAS/ two kidney model: hypertension and volume expansion
  • RAS in solitary kidney model: hypertension and volume expansion
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8
Q

What is ACE-I intolerance and what does it suggest?

A
  • Patient taking ACE-I, loses vasoconstriction of the efferent arteriole, resulting in decreased glomerular pressure and subsequent filtration.
  • Represents a subtle clinical clue that RAS may be cause of patient’s severe hypertension
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9
Q

The anatomical classification of RAS

A
  • Ostial
  • Parostial
  • Truncal
  • Accessory
  • Segmental
  • Mixed type
  • Renal artery occlusion
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10
Q

Pathological classification of RAS

A
  • Atherosclerotic

- non- Arthersclerotic

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11
Q

Causes of non-artherosclerotic RAS

A
  • Fibromuscular dysplasia
  • Takayasu’s disease
  • Renal artery dissection
  • Developmental (neurofibromatosis)
  • Renal artery aneurysm
  • Trauma
  • Juxta-renal saccular aortic aneurysm
  • Radiation induced RAS
  • Anastomotic RAS involving transplant kidneys
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12
Q

What is haemodynamically significant RAS?

A

Has been estimated at >60% stenosis

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13
Q

Treatment modalities of RAS

A
  • Medical therapy
  • Percutaneous transluminal renal angioplasty
  • Percutaneous transluminal renal angioplasty and stenting
  • Surgical revascularisation
  • Nephrectomy
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14
Q

Which two ways can atherosclerosis manifest?

A
  • severe hypertension

- Ischaemic nephropathy

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15
Q

Clinical presentation of atherosclerotic RAS

A
  • Elderly
  • Usually with risk factors: smoking, hypertension, diabetes meillitus, hyperlipidaemia and obesity
  • May have associated ischaemic heart disease, absent leg pulses or carotid bruits. May have epigastric bruit on auscultation of the abdomen
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16
Q

Treatment of mild- moderate atherosclerotic RAS

A
  • Risk factor reduction
  • Anti-platelet therapy
  • Statins
  • Anti-hypertensive treatment
  • ACEIs reccommended in treatment regimens
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17
Q

What is the first line treatment in people with co-morbidities

A

Percutaneous renal angioplasty and stenting (PTRAS)

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18
Q

what are the surgical options for atherosclerotic RAS

A
  • Aorto-renal bypass procedure
  • Renal endarterectomy
  • Extra axial bypass procedures (Hepato-renal bypass, spleno-renal artery bypass)
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19
Q

Indications for surgical treatment of atherosclerotic RAS

A
  • Patients requiring direct aortic reconstruction
  • Patients with aorto-iliac occlusive disease
  • Renal artery occlusion
  • Sub-optimum PTRAS
  • Complicated PTRAS
  • small caliber renal artery < 4 mm
  • Length of RAS > 2 cm
  • Ras extending up to renal bifurcation
  • Truncal RAS with segmental RA involvement
20
Q

Requirements for nephrectomy

A
  • Small, shrunken, scarred kidny <8 cm in length

- Single kidney GFR < 10/mls/min/1.73 m2

21
Q

What percentage of RAS is due to fibro muscular dysplasia

A

It is the pathology found in 10- 20 % RAS

22
Q

How can fibromuscular dysplasia be classified pathologically?

A
  • medial type (75-80%): medial fibroplasia, perimedial fibroplasia, medial hyperplasia
  • Adventitial type
  • intimate type
23
Q

What is the DSA findings that help to diagnose fibro muscular dysplasia

A
  • Aorta is normal on angio- imaging
  • the string of beads appearance is classical
  • the disease profile usually affects the mid and distal thirds of the renal artery
24
Q

Mainstay of treatment for fibro muscular dysplasia

A

Percutaneous transluminal balloon angioplasty

25
When is surgical revascularisation done for fibromuscular dysplasia?
- Intimal type FMD - complicated or suboptimal balloon angioplasty - associated significant renal branch vessel disease
26
What type of RAS (an atomic classification) typically occurs with takayasu's disease
It is generally the Ostial or mixed type | It is not unusual to have bilateral RAS and/or renal artery occlusion
27
Clinical features of takayasu's disease
- prodromal symptoms (fever, headaches, joint pains, muscle aches, carotidynia) - absent or diminished upper limb pulses (subclavian artery stenosis or occlusion) - patients may present with coronary artery disease, aortic or mitral regurgitation or pulmonary hypertension
28
CTA findings in takayasu's disease
- features of aortitis (thick- walled aorta) - occlusive disease of the aorta and aortic branched vessels - RAS/ renal artery occlusion
29
Histological features of takayasu's disease
- pan- arteritis | - giant cell granulomas (non-caseating)
30
Treatment of choice in young patients with takayasu's disease
Surgical revascularisation
31
When should PTRAS or percutaneous transluminal renal balloon angioplasty be performed in patients with takayasu's disease
May be considered as a bridge to surgery in patients needing to be optimized
32
Medical treatment of takayasu's disease
- steroid therapy - methotrexate - folic acid - vitamin D supplements - alternative immunosuppressive drugs may be considered
33
What level does coarctation of the aorta usually occur
Level of the ligamentum ateriosum
34
How may coarctation of the aorta present
- asymptomatic - symptomatic (headaches, syncope, claudication) - complicated (cardiac failure, stroke) - radio- radial delay or radio- femoral delay - bruit over the precordium
35
Findings on ecg in coarctation of the aorta
Features of LVH
36
Findings on X-ray chest in coarctation of the aorta
- cardiomegaly | - posterior inferior rib notching (dilated torturous intercostal arteries)
37
Findings on CTA, MRA or DSA in coarctation of the aorta
- aortic stenosis at or distal to left subclavian artery - dilated proximal aorta and left subclavian artery - dilated tortuous intercostal arteries - post- stenotic dilatation of the aorta
38
Anatomical classification of coarctation of the aorta
1. Post ductal 2. Pre ductal 3. Interrupted aorta
39
Medical treatment of coarctation of the aorta
Anti hypertensive treatment: - beta blockers - calcium channel blockers
40
Surgical treatment of coarctation of the aorta
- patch aortoplasty - interposition bypass graft - resection and re- anastomosis
41
Interventional treatment of coarctation of the aorta
- balloon angioplasty - aortic stent ( bare metal stent) - aortic stentgrafting (covered stent)
42
What is mid aortic syndrome?
Acquired vascular condition where various disease processes result in narrowing of the descending aorta resulting in renin- dependent hypertension. The abdominal branches, including the renal arteries may or may not be involved
43
Pathologies associated with mid aortic syndrome
- takayasu's disease - atherosclerosis - congenital hypoplasia - Von Recklinghausens disease - fibromuscular dysplasia - tuberculous aortitis
44
Clinical features of mid aortic syndrome
- upper limb hypertension - radio femoral delay - inter scapular and/ or abdominal Bruits - patients may present with Lower extremity claudication
45
Treatment of mid aortic syndrome
1. Surgical: thoraco- abdominal aortic bypass, with or without visceral or renal revascularisation 2. Endovascular: aortic stenting