04/11/2024 Flashcards

(61 cards)

1
Q

What are the 2 types of AAA true aneurysms and which is more likely to rupture?

A

Saccular - more likely to rupture
Fusiform

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2
Q

Pathophysiology of AAA?

A

Weakening of the Aortic Wall over time due to age, high blood pressure, or genetic factors. Conditions like atherosclerosis further damage the wall, making it prone to dilation.

Chronic inflammation and an increase in enzymes that break down structural proteins (like elastin and collagen) within the aortic wall contribute to this weakening.

As the wall weakens, the aorta starts to bulge out due to the constant pressure of blood flowing through it.
With each heartbeat, the pressure on this weakened area causes it to enlarge progressively, forming an aneurysm.

If the aneurysm continues to grow, the aortic wall may become too thin to handle the pressure, leading to a rupture.

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3
Q

Triad of AAA?

A

Hypotension
Tearing back or abdominal pain
Painful pulsatile mass

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4
Q

Investigations for AAA?

A

US is first line
CT angiography for detailed assessment, especially for pre-surgery

In haemodynamically unstable patients the diagnosis is clinical, these patients are not stable enough for a CT scan etc to confirm the diagnosis and should be taken straight to theatre.

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5
Q

What is the mortality rate of a ruptured AAA?

A

80%

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6
Q

Management of asymptomatic AAA?

A

Rusk factors - statins, aspriin 75mg OD, antihypertensives, stop smoking & screening
Surgery - open surgical repair or EVARif more comobidities, women or men >70

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7
Q

If a pt has an AAA found at 4.7cm how often do they need to be screened?

A

3 monthly

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8
Q

What is a small, medium and large AAA?

A

3-4.4cm = small
4.5-5.4cm = medium
>=5.5cm = large

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9
Q

What are the 2 different types of surgery for AAA?

A

Open surgical repair - large laparotomy, clam aorta, remove aneurysm all segment and replace it with a synthetic graft.
EVAR - stent graft is inserted through femoral arteries and places within the aneurysm to reinforce the aortic wall

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10
Q

OSR vs EVAR for AAA?

A

OSR has good long term durability, is good for younger pts or those with complex anatomy
More invasive, longer recovery time and higher postoperative risk

EVAR requires lifelong surveillance due to potential for endoleak. It’s also not suitable for all anatomies.

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11
Q

What can trigger Raynaud’s disease?

A

Cold temperature or emotional stress

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12
Q

Pathophysiology of raynayds disease?

A

Excessive arterial vasoconstriction in response to cold temperatures or stress

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13
Q

What can cause raynaud syndrome i..e secondary raynaud phenomenon?

A

Vasospasms due to arteriolar changes in fingers which may be precipitated by the following:
Drugs - oral contraceptives
Cervical rib
leukaemia
type I cryoglobulinaemia, cold agglutinins
Smoking
Ioccupation trauma e.g. handling vibrating tools
Hyperviscocity
CTD e.g. scleroderma, SLE, sjogrens etc
Arterial disease
Neurological diseases e.g. carpal tunnel syndrome

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14
Q

Which area of the hand is typically spared in primary raynauds diseases but not in secondary?

A

The thumb!
Due to it having better blood flow

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15
Q

Clinical presentation of raynauds?

A

Finger & toes B/L
White -> blue -> red
Livedo reticularis may occur during episodes
Rewarming is associated with transient numbness, pain or paraesthesia in the affected areas

In primary you may get Sx of systemic vasospasm e.g. migraine or IBS
In secondary you may get pain, ulceration or necrosis due to critical ischaemic, signs of associated systemic disease.

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16
Q

Managament of raynauds?

A

Prevent cold to hands/feet & stress management & minimise vibration exposure & smoking cessation & discontinue causative drugs
Nifedipine or other CCB

If severe or complicated pt may be admitted and given IV prostcyclin infusions: effects may last several weeks/months e.g. iloprost

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17
Q

Pathophysiology of hammer toes and claw toes in diabetic foot disease?

A

Muscle wasting of the intrinsic pedal muscles leads to overpowering of the spared extrinsic muscles = Thickening of plantar aponeurosis = sole of foto contracts

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18
Q

Triad of Leriche syndrome?

A

Absent femoral pulses
Impotence
Claudication

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19
Q

What ABPI suggests critical limb ischaemic?

A

<0.5

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20
Q

Trophic changes from peripheral arterial disease?

A

Hair absent
Thickened nails
Dry scaly skin
Shiny skin

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21
Q

Imaging for PAD

A

ABPI (if too high due to calcification then toe brachial index may be done)
Handheld Doppler is the best initiat test for detecting blood flow if acute limb ischaemia
CT angiography with contrast to look for thr site of stenosis or occlusion

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22
Q

What options for surgery are there for PAD/

A

Endovascular revascularisation- percutaneous transluminal angioplasty +/- stent placement or atherectomy
Peripheral artery bypass surgery or endarterectomy (opening vein up ans scraping off plaque)

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23
Q

Wet vs dry gangrene

A

dry gangrene – where the blood flow to an area of the body becomes blocked - chronic
wet gangrene – caused by a combination of an injury and bacterial infection - more of an emergency in terms of vascular surgeons as will spread quickly!!

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24
Q

What is autonomic dysreflexia?

A

A clinical syndrome that occurs in pts who have had a spinal cord injury at or above level of T6
This causes a sympathetic spinal reflex via thoracolumbar outflow and the usual parasympathetic response is prevented by the cord lesion = imbalanced sympathetic response causing extreme hypertension, flushing and sweating above the level of the cord lesion

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25
What are the 2 most common causes of autonomic dysreflexia?
Faecal impaction Urinary retention
26
If you have a pt with an ischaemic stroke of unknown origin and the ECG shows sinus rhythm what should you do?
A 24 hour tape for paroxysmal AF If this shows sinus rhythm then you can do a 7 day patch ECG
27
What is leptomeningeal disease?
When cancer cells are found in the leptomeninges & CSF
28
Pros and cons of biologic and mechanical heart valves?
Biological dont necessarily need long term anticoagulation but low dose aspirin is given long term. Structural deterioration and calcification can happen over time so better suited for pts over 65 if aortic and over 70 if mitral Mechanical valves have a low failure rate, last longer. But increased risk of thrombosis so they need long term warfarin
29
What is a hypometric saccadic eye movements?
Eye movements that undershoot a visual target so have to make small additional saccades to adjust and finally reach the target
30
What is past-pointing called?
Dysmetria
31
Most common form of brain tumours?
Metastasis
32
Most common tumours that spread to the brain?
lung (most common - up to 50% of cases) breast bowel Melanoma kidney
33
What is the most common primary brain tumour in adults?
Glioblastoma
34
Prognosis of glioblastoma?
~1 year
35
What is the most common primary brain tumour in adults?
Pilocytic astrocytoma (aka a glioma)
36
Imaging findings in a glioblastoma?
On imaging they are solid tumours with central necrosis and a rim that enhances with contrast. Disruption of the blood-brain barrier and therefore are associated with vasogenic oedema.
37
Which age group has the highest indecence of brain tumours in adults?
85-89byear olds
38
Which type of thyroid cancer has the highest mortality rate?
Anaplastic thyroid cancer
39
What proportion of pts with postpartum thyroiditis end up as hypothyroid and require thyroid hormone replacement therapy?
1/3rd
40
Most common type of thyroid cancer?
Papillary
41
Commonest causes of dilated cardiomyopathy?
Chronic alcohol use Coxsackie B virus wet beri beri doxorubicin
42
Causes of aortic stenosis?
Degenerative calcification - MC cause in >65s Bicuspid aortic valve - MC cause in <65s Williams syndrome causing supravalvular aortic stenosis Post rheumatic disease HOCM
43
Management of symptmatic aortic stenosis?
Valve replacement
44
Management of asymptomatic aortic stensois?
Observe is the general rule! But if valvular gradient >40mmHg and there are features such as left ventricular systolic dysfunction then consider surgery Options for surgery are surgical AVR, trans catheter AVR or balloon valvuloplasty (latter mostly used in children with no aortic valve calcification)
45
ABG features of salicylate overdose?
First you get a respiratory alkalosis due to raised RR and then later the direct effects of the salicylates can lead to acidosis so it leads to a mixed respiratory alkalosis and metabolic acidosis
46
Management of renal stones if <5mm?
Watchful waiting if asymptomatic (most will pass within 4 weeks of Sx onset) If severe causes then lithotripsy and nephrolithotomy may be used
47
Management of renal stones if 5-10mm?
Shockwave lithotripsy
48
Management of renal stones if 10-20mm?
Shockwave lithotripsy or ureteroscopy
49
Management of renal stones if >20mm?
Percutaneous nephrolithotomy
50
Prevention of renal stones?
High fluids, add lemon to water, avoid carbonates drinks, limit salt intake. Can use potassium citrate or thiazide diuretics Oxalate stones - use cholesturamine or pyridoxine Uric acid stones - allopurinol, urinary alkalinization with oral bicarbonate
51
SSRIs in pregnancy risk?
First trimester - congenital heart defects Third trimester - persistent pulmonary hypertension of the newborn (Paroxetine also has an increased risk of congenital malformations)
52
What are the red features on the traffic light system for paediatrics?
Pale/mottled/ashen/blue No response to social cues Appears ill to a healthcare professional Does not wake or if roused cannot stay awake Weak, high pitched or continuous cry Grunting RR >60 Moderate or severe chest indrawing Reduced skin turgor <3 months and temp >=38 degrees Non-b;arching rash Bulging fontanelle Neck stiffness Status epilepticus Focal neurological signs Focal seizures
53
Causes of 2nd degree AV block mobitz type 1?
Drugs: BB, CCB, digoxin, amiodarone Increased vagal tone e.g. in athletes Inferior MI Myocarditis Following cardiac surgery
54
What is sick sinus syndrome?
A disease characterized by abnormal sinus node functioning with resultant bradycardia and cardiac insufficiency. Often occurs due to age-related degeneration of the SAN Can lead to arrhythmias, arrests, AF, bradycardia
55
Features of chronic mesenteric ischaemia?
Central colicky abdominal pain about 30 minutes after eating Weight loss due to food avoidance Abdominal bruit may be heard on auscultation
56
How is chronic mesenteric ischaemia diagnosed?
CT angiography
57
Features of acute mesenteric ischaemia?
Acute non specific abdominal pain disproportionate to examination findings Shock, peritonitis and sepsis
58
Ischaemic colitis vs mesenteric ischaemia?
Ischaemic colitis is the large intestine, particuarly watershed areas e.g. splenic flexure. More gradual onset with abdominal pain and blood diarrhoea Mesenteric ischaemia most commonly affects the small intestine and involves larger vessels like the superior or inferior mesenteric artery. It’s usually of sudden onset with pain out of proportion to signs due to it being most commonly due to thromboembolic disease
59
Which lipid-lowering treatment should I offer for the primary prevention of cardiovascular disease?
High intestnsity statin treatment with atorvastatin 20mg to all people If statins are CI or not tolerate consider ezetimibe
60
Management of NSTEMI?
Aspirin 300mg If no immediate PCI planned give fondaparinux Calculate GRACE score. If <=3% give ticagrelor If >3% PCI within 72 hours. Give prasugrel or ticagrelor, unfractionated heparin
61
Management of chronic HF with reduced ejection fraction?
First-line: ACEi and a beta blocker (bisoprolol, carvedilol, nebivolol) - start 1 at a time Secondary: Aldosterone antagonist e.g. spironolactone and eplerenone SGLT2i if reduced ejection fraction Specialists: Ivabradine - if left ventricular fraction <35% and sinus rhythm >75 Sacubitril-valsartan - if left ventricular fraction <35% Hydralazine & nitrate - particuarly if Afro-caribbean Digoxin - if coexisting AF Cardiac resynchronisation if widened QRS