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Gen Surgery > Reno-vascular hypertension > Flashcards

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
Q

When is surgical revascularisation done for fibromuscular dysplasia?

A
  • Intimal type FMD
  • complicated or suboptimal balloon angioplasty
  • associated significant renal branch vessel disease
26
Q

What type of RAS (an atomic classification) typically occurs with takayasu’s disease

A

It is generally the Ostial or mixed type

It is not unusual to have bilateral RAS and/or renal artery occlusion

27
Q

Clinical features of takayasu’s disease

A
  • 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
Q

CTA findings in takayasu’s disease

A
  • features of aortitis (thick- walled aorta)
  • occlusive disease of the aorta and aortic branched vessels
  • RAS/ renal artery occlusion
29
Q

Histological features of takayasu’s disease

A
  • pan- arteritis

- giant cell granulomas (non-caseating)

30
Q

Treatment of choice in young patients with takayasu’s disease

A

Surgical revascularisation

31
Q

When should PTRAS or percutaneous transluminal renal balloon angioplasty be performed in patients with takayasu’s disease

A

May be considered as a bridge to surgery in patients needing to be optimized

32
Q

Medical treatment of takayasu’s disease

A
  • steroid therapy
  • methotrexate
  • folic acid
  • vitamin D supplements
  • alternative immunosuppressive drugs may be considered
33
Q

What level does coarctation of the aorta usually occur

A

Level of the ligamentum ateriosum

34
Q

How may coarctation of the aorta present

A
  • asymptomatic
  • symptomatic (headaches, syncope, claudication)
  • complicated (cardiac failure, stroke)
  • radio- radial delay or radio- femoral delay
  • bruit over the precordium
35
Q

Findings on ecg in coarctation of the aorta

A

Features of LVH

36
Q

Findings on X-ray chest in coarctation of the aorta

A
  • cardiomegaly

- posterior inferior rib notching (dilated torturous intercostal arteries)

37
Q

Findings on CTA, MRA or DSA in coarctation of the aorta

A
  • 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
Q

Anatomical classification of coarctation of the aorta

A
  1. Post ductal
  2. Pre ductal
  3. Interrupted aorta
39
Q

Medical treatment of coarctation of the aorta

A

Anti hypertensive treatment:

  • beta blockers
  • calcium channel blockers
40
Q

Surgical treatment of coarctation of the aorta

A
  • patch aortoplasty
  • interposition bypass graft
  • resection and re- anastomosis
41
Q

Interventional treatment of coarctation of the aorta

A
  • balloon angioplasty
  • aortic stent ( bare metal stent)
  • aortic stentgrafting (covered stent)
42
Q

What is mid aortic syndrome?

A

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
Q

Pathologies associated with mid aortic syndrome

A
  • takayasu’s disease
  • atherosclerosis
  • congenital hypoplasia
  • Von Recklinghausens disease
  • fibromuscular dysplasia
  • tuberculous aortitis
44
Q

Clinical features of mid aortic syndrome

A
  • upper limb hypertension
  • radio femoral delay
  • inter scapular and/ or abdominal Bruits
  • patients may present with Lower extremity claudication
45
Q

Treatment of mid aortic syndrome

A
  1. Surgical: thoraco- abdominal aortic bypass, with or without visceral or renal revascularisation
  2. Endovascular: aortic stenting

Gen Surgery (31 decks)

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