Carotid stenosis, renal artery stenosis, and mesenteric ischaemia Flashcards

1
Q

What is carotid stenosis?

A

Narrowing of carotid artery - e.g. due to atherosclerosis

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2
Q

Symptoms/signs of carotid stenosis

A
Symptoms of stroke or TIA
OR asymptomatic (e.g. picked up carotid bruit)
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3
Q

Investigaions

A

Duplex ultrasound scan done first, if narrowing then:

CT angiogram or MR angiography

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4
Q

Management of carotid stenosis

A

Determine risk
Optimise treatment + non-treatment
OR
Surgery - can be end-arterectomy or carotid stenting (determined by MDT)

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5
Q

Grading of carotid artery stenosis

A
Minor = 0-49% narrowed
Moderate = 50-69% narrowed
Severe = 70-99% blocked
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6
Q

Indications for surgery

A

1) Had stroke or TIA and have moderate or severe stenosis
or
2) Severe stenosis alone with no TIA/stroke

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7
Q

Pathophys of plaque formation

A

Endothelial dysfunction and high circulating LDLs

  • -> LDLs deposit in intima and become oxidised. This activates endothelial cells, causing them to express adhesion molecules for WBCs on surface.
  • -> monocytes and T helper cells move into tunica intima
  • -> monocytes become macrophages and take up oxidised LDLs and become foam cells
  • -> foam cells promote migration of smooth muscle cells from media to intima and promote their proliferation (and also attract more macrophages)
  • -> smooth cell proliferation increases synthesis of collagen (vessel hardening)
  • -> foam cells die and release their lipid content and proinflammatory cytokines, promoting inflammation and growth of the plaque.
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8
Q

Layers of blood vessels

A
Lumen
Endothelium
Intima
Media
Adventitia
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9
Q

How to distinguish between mesenteric ischaemia and ischaemic colitis?

A

Mesenteric ischaemia = typically small bowel, due to embolism, sudden onset, severe, high mortality, needs urgent surgery
Ischaemic colitis = large bowel, multifactorial, transient, less severe, bloody diarrhoea, thumbprinting, conservative management

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10
Q

Predisposing factors for bowel ischaemia

A

1) increasing age
2) atrial fibrillation
3) other causes of emboli - endocarditis, malignancy
4) CVD risk factors
5) Cocaine

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11
Q

Features of bowel ischaemia

A
sudden onset severe abdominal pain out of keeping with physical exam findings (mesenteric ischaemia)
rectal bleeding
diarrhoea
fever
elevated WBC
lactic acidosis
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12
Q

Investigation of choice for bowel ischaemia

A

CT

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13
Q

Cause of acute mesenteric ischaemia

A

embolism resulting in occlusion of an artery which supplies the small bowel, for example the superior mesenteric artery.

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14
Q

Management of acute mesenteric ischaemia

A

Urgent resus + early senior involvement
IV fluids, catheter, fluid balance chart, broad-spectrum abx, early ITU input
Urgent surgery is usually required - excision of necrotic/non-viable bowel or revascularisation of the bowel
poor prognosis

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15
Q

Features of chronic mesenteric ischaemia

A

Colickly intermittent abdo pain

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16
Q

Symptoms/signs of renal artery stenosis

A
Hypertension
CKD
Sudden or unexplained recurrent pulmonary oedema
Abdominal bruit
Other PVD
17
Q

Types of renal artery stenosis

A

Due to atherosclerosis (90%) - think if CVD risk factors, history of CVD etc.
Fibromuscular dysplasia - usually younger females

18
Q

Diagnosis of renal artery stenosis

A
Bloods - U&Es, urinalysis, aldosterone renin ratio
Duplex USS
MRA
CTA
Angiography
19
Q

Management of renal artery stenosis

A

Antihypertensive therapy and lifestyle modification
Statin
Antiplatelet
Second line = renal artery stenting
Third line = surgical reconstruction of renal arteries

20
Q

Why are ACE inhibitors used in caution in patients with (bilateral) renal artery stenosis?

A

Causes creatinine to increase dramatically since angiotensin II usually constricts the efferent arteriole and blocking it will cause the efferent arteriole to dilate and thus less filtration (lowers GFR).
Renal artery stenosis patients rely more upon that efferent constriction to maintain normal glomerular pressures for filtration.

21
Q

Stroke definition

A

Rapidly progressive clinical symptoms and signs of focal, and at times global, loss of cerebral function lasting more than 24hrs or leading to death with no apparent cause other than that of vascular origin.

22
Q

Total or partial anterior circulation infarct symptoms/signs

A
  • Unilateral motor deficit
  • Homonymous hemianopia
  • Higher cerebral function (e.g. dysphasia, neglect)
23
Q

Posterior circulation infarct symptoms/signs

A
  • Pure hemianopia
  • Cerebellar signs
  • Diplopia and CN palsy
  • Bilateral/crossed sensory-motor signs
24
Q

Lacunar infarct symptoms/signs

A
  • Pure motor (50%)
  • Pure sensory (5%)
  • Ataxic hemiparesis (10%)
  • Sensorimotor stroke (35%)
25
Q

Causes of ischaemic stroke

A
Arteriolarsclerosis
Atherosclerosis
Carotid stenosis
Carotid dissection
Vasculitis
AF
26
Q

Causes of haemorrhagic stroke

A

Primary i.e. hypertension (microaneurysm)

Secondary causes:
Trauma
AV malformation
Venous thrombosis
Vasculitis
Coagulopathy/anticoagulation/TPA
Drugs e.g. cocaine
Haemorrhagic transformation of infarct
27
Q

Management of long-term complications of stroke in primary care

A

Specialist stroke rehabilitation team - initial follow-up
Discuss any issues with a stroke specialist
Incontinence - management initiated by specialist stroke team, follow up by community continence services. Can include timed toileting, prompted voiding, bladder retraining, pelvic floor exercises, drug treatments in some cases.
Constipation - give advice on diet, fluid, exercise, review meds, consider toileting routines, laxatives
Fatigue — assess for depression, anxiety, thyroid, infection, meds, pain, sleep apnoea + treat. Give info about daily routines, modified tasks, planned exercise schedules, sleep hygiene.
Nutrition and hydration — monitor dietary intake and nutritional status, may need referral to dietician, discuss stroke specialist if unable to swallow, access to appropriate equipment and assistance
Cognitive dysfunction - screen with MMSE, may need referral for neuropsych assessment
Mood and wellbeing — consider depression, may need referral to psych or for psychology, motivational interviewing, problem-solving therapy, education groups, exercise, social interaction, antidepressants
Mouth care - at least 3 times a day.
Neuropathic pain - amitriptyline, gabapentin or pregabalin.
Musculoskeletal - assess, paracetamol, topical NSAIDS, TENS
Sexual dysfunction - assess for reversible causes, can use sildenafil ONLY 3 MONTHS AFTER STROKE, can refer to psychosexual specialist
Spasticity and contractures — may have splinting

28
Q

TIA definition

A

Transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction.

29
Q

TIA management

A

Aspirin 300 mg (unless bleeding disorder, on anticoag, on low-dose aspirin already, or aspirin contraindicated)
Discuss urgently with stroke specialist if has had more than 1 or has suspected cardioembolic source or severe carotid stenosis
Urgent assessment (within 24 hours) by stroke physician if within 7 days, or ASAP (within 7 days) if it happened more than week ago
Advise the person not to drive

Long-term - clopidogrel

30
Q

Stroke management

A

Aspirin 300mg ASAP if haemorrhagic stroke has been excluded
Thrombolysis with alteplase if within 4.5 hours of onset + haemorrhage excluded
Mechanical thrombectomy + thombrolysis if within 6 hours of onset
Mechanical thrombectomy alone if between 6-24 hours

31
Q

Secondary prevention of stroke

A

Clopidogrel 75mg daily
Carotid endartectomy in certain situations
Lifestyle
Atorvastatin 20-80mg daily
Antihypertensives - thiazide-like diuretic, long-acting calcium channel blocker or ACE inhibitor
Optimise management of other conditions e.g. diabetes
Warfarin or direct thrombin or factor Xa inhibitor if AF