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Medicine year 3 ANNA > AAA > Flashcards

AAA Flashcards

1
Q

What differentials might you consider in a patient with;

Sudden severe abdo pain + back pain, pale hands + feet, clammy hands, vomiting, HR 124, BP 90/60, cap refill 5 seconds

A
  1. Perforated viscera e.g. perforated gastric/duodenal ulcer
  2. Acute pancreatitis
  3. Biliary colic or acute cholangitis
  4. Acute mesenteric ischaemia (possibly due to an embolus)
  5. Ruptured or leaking AAA
  6. Rarely: above diaphragm pathology can present with severe abdo pain e.g. basal pneumonia or inferior MI
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2
Q

What possible complications can occur as part of blood transfusions? x7

A
  1. Dilutional coagulopathy:
    • If pt is given packed RBCs only (which don’t contain coagulation factors or platelets) –> thus blood volume ↑ and the concentration of clotting factors ↓
  2. Hypocalcaemia:
    • ​​Citrate (used in blood product storage solutions) binds Ca2+ ions in blood –> hypocalcaemia
    • FFP and platelets contain more citrate than packed RBCs
  3. Hypothermia:
    • RBCs are stored at ~4 degrees
    • Hypothermia –> ↓ metabolism of citrate and lactate –> ↑ likelihood of hypocalaemia, metabolic acidosis and arrhythmias
  4. Haemolytic reactions:
    • Most common complication of massive blood transfusion
    • Incompatibility between donors RBC antigens and host antibodies –> complement activation + intravascular haemolysis
    • Immediate reactions:
      • More severe + due to ABO incompatibility
    • Delayed reactions:
      • Reaction due to minor RBC antigens e.g. Rhesus
  5. Allergy
    1. Anaphylaxis
    2. Minor allergy (uticaria)
    3. Febrile reaction
  6. Transfusion-associated circulatory overload (TACO) (HF made worse)
  7. Transfusion-related acute lung injury (TRALI)
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3
Q

Describe TRALI (transfusion-related acute lung injury)

A
  • Complication of blood transfusion within 6 hrs
  • Characterised by;
    • Acute
    • non-cardiogenic pulmonary oedema
    • SoB
    • Hypoxemia
    • Hypotension/hypertension
  • TRALI = often hypotension + minimal response to diuretics
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4
Q

Describe TACO (transfusion associated circulatory overload)

A
  • Is a transfusion reaction that can occur during rapid transfusion of large vol. of blood – can also occur in a single RBC transfusion
  • Characterised by;
    • SoB
    • Orthopnoea
    • Peripheral oedema
    • Rapid ↑ in BP
  • Suspect TACO if pt has signs of respiratory ditress < 12 hrs post transfusion
  • TACO = often hypertension + strong response to diuretics
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5
Q

Which drugs are ‘P2Y12 inhibitor’ and what do they do?

A

Clopidogrel and Ticagrelor and Ticlodipine

  • Irreversibly inhibits the P2Y12 subtype of ADP-receptor on platelets –> this inhibits platelet activation and aggregation
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6
Q

Which drug is used as an antiplatelet via its inhibition of COX enzymes?

A

Aspirin

  • inhibits COX enzymes required for prostaglandin and thromboxane synthesis
  • Low-dose aspirin irreversibly inhibits COX1 –> thus inhibiting prostaglandin H2 formation – required for formation of thromboxane A2 in platelets –> which is needed for platelet aggregation and activation
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7
Q

Eptifibatide and tirofiban are anti-platelet drugs frequently used during PCI, what class of antiplatelet drug are they?

A

Glycoprotein IIb/IIIa inhibitors

  • Anything with -fib- in the name = glycoprotein inhibitor
  • Inhibit platelet aggregation via inhibiting Gp IIa/IIIb receptor on platelets
  • Used during PCI
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8
Q

Peripheral arterial disease can be divided in acute vs chronic forms - what are the main causes of each?

A

Chronic:

  • Progressive degeneration of arterial walls –> atherosclerotic occulsion

Acute:

  • Atherosclerosis + thrombus
  • Embolus
  • Aneurysm
  • Dissection
  • Trauma
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9
Q

What are the 6 P’s of acute limb-threatening ischaemia?

A
  • Present at 4 hours + reversible by vascular surgeon:
    • Pale
    • Perishingly cold
    • Pulseless
    • Pain
  • 4-6 hours (limb threatened) –> paraesthesia
  • 6-8 hours (limb non-viable) –> paralysis (numb + mottled)

NOT SWOLLEN, HOT OR TENDER!! - These indicate acute venous disease e.g. DVT

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10
Q

What are some risk factors for peripheral arterial disease (PAD)?

A
  • ↑ Age
  • Men > women
  • FHx of PAD
  • Smoking
  • HTN
  • Hypercholesterolemia
  • Diabetes
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11
Q

Which classifcation system is used for severity of chronic peripheral arterial disease/ischaemia?

A

Fontaine Classification

  • Fontaine I – asymptomatic
  • Fontaine II – claudication (IIa = mild, IIb = moderate)
    • Claudication = aching muscles on exertion
    • Is predictable – will occur on each instance of activity
    • Worse on hills, with loads or at speed
    • Settles quickly with rest
  • Fontaine III – rest pain
    • Icy, burning, constant aching pain in foot
    • Worse on elevation or at night
    • Often requires opiates
  • Fontaine IV – tissue loss
    • E.g. ulcers, necrosis, gangrene
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12
Q

How is chronic PAD managed?

A
  1. Lifestyle:
    • Smoking cessation
    • Weight loss (if obese)
    • Regular exercise
    • ↓ Cholesterol in diet
  2. Pharmacology:
    • Antiplatelet therapy e.g. Aspirin 75mg OD or Clopidogrel 75mg (NICE 1st line)
    • Blood pressure control (aim = sBP <140 mmHg)
    • Cholesterol reduction e.g. Atorvastatin 80mg (aim = < 5 mmol/L)
    • Diabetes control (aim = HbA1c < 7% i.e. 53 mmol/mol or <6.5% i.e. 48 mmol/mol)
    • Cilostazol - phosphodiesterase III inhibitor - vasodilator + antiplatelet - licensed for use in intermittent claudication to improve walking distance in patients without peripheral tissue necrosis who do not have pain at rest
  3. Surgery:
    • Angioplasty
    • Stenting
    • Bypass surgery
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13
Q

What is the prognosis of chronic type PAD?

A
  • Generally improves over 6-12 months with smoking cessation and lifestyle changes
  • Lifetime amputation risk = ~1% (if following medical advice)
  • Risk of MI in 5-years = ~30%
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14
Q

What symptoms are present in a patient with leg claudication?

A
  • Aching or burning in leg muscles following walking
  • Pts typically walk for a predictable distance before symtpoms start
  • Relieved within minutes of stopping
  • Pain not present at rest
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15
Q

How would you interpet ABPI results?

A
  • > 1.2 = abnormally hard vessels e.g. calcification in diabetes - can’t assess using ABPI as pt may have peripheral arterial disease being obscured by calcification
  • 1.0 -1.2 = normal
  • 0.5-0.9 = intermittent claudication
  • 0.3 -0.5 = rest pain
  • < 0.3 = gangrene, ulceration, critical ischaemia
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16
Q

Define a AAA.

A
  • AAA is a swelling/dilation of the aorta to > 1.5 times its normal size – usually due to underlying weakness of aortic wall – it can remain asymptomatic for long periods
    • Ectasia = dilation up to 50% (i.e. 1-1.5 times)
  • AAA should be viewed as a ‘local manifestation’ of generalised arterial disease – hence pts often have;
    • Ischaemic heart disease (i.e. CAD)
    • Cerebrovascular disease
    • Poor mesenteric/renal circulation
    • Atherosclerosis of abdominal aortic branches
17
Q

Define the following terms relating to aneuryms.

  1. Fusiform
  2. Saccular
  3. True
  4. False
A
  1. Fusiform aneurysm = general dilation on all sides of blood vessel
  2. Saccular aneurysm = asymmetrical dilation (balloon on one side)
  3. True = dilation is composed of all layers of arterial wal
  4. False = collection of blood between two outer layers (tunica media + tunica adventitia)
18
Q

What are some common risk factors for AAA?

A
  • Smoking
  • FHx (1st degree relative with AAA = double risk)
  • Men >>>> women (4-6 times more prevalent)
  • Connective tissue disorders e.g. Marfan’s syndrome
  • Age:
    • Men > 55yrs = most frequently diagnosed group
    • AAA discovered ~ 10 years later in women
    • AAA rupture rarely occurs < 65yrs
    • AAA rupture in women >>> men
      *
19
Q

What signs / symptoms might be seen in a patient with AAA?

A
  • Sudden onset severe central abdominal pain radiating to back = ruptured AAA
  • Shock state e.g. hypotension + tachycardic –> ruptured AAA
  • Sudden collapse –> ruptured AAA
  • Bilateral leg ischaemia (shock + unilateral leg ischaemia –> think dissection or PVD)
  • Triad of ruptured AAA:
    1. Collapse
    2. Hypotension
    3. Sudden severe abdominal or lower back/flank pain
  • Triad of inflammatory AAA:
    1. Abdominal or back pain
    2. Weight loss
    3. ↑ ESR
  • Examination:
    • Tender abdomen
    • Palpable, expansile mass above + lateral (left) to umbilic
20
Q

A ruptured AAA is often misdiagnosed as other pathologies, including; renal colic (24%), Diverticulitis (13%), GI bleed (13%), MI (9%) and musculoskeletal pain (9%)

Thus, in men > 60yrs + 1st presentation of renal colic style pain –> what should you suspect?

In pts with GI bleeding + Hx of aortic surgery –> What should you suspect?

A
  • Men > 60yrs + 1st presentation of renal colic –> ALWAYS suspect ruptured AAA
  • Pts with GI bleeding + Hx of aortic surgery –> suspect aorto-enteric fistula (until proven otherwise)
21
Q

How reliable is a peripheral vascular exam in picking up AAA?

How good are AXRs at identifying AAA?

A

Exams = Quite poor ~40-50% of AAA are identified on exam

  • Made more difficult in obesity
  • False positives can occur in thin patients
  • Examine all limbs as AAA pts have ↑ incidence of other aneurysmal arteries

AXR = quite poor

  • DO NOT diagnose a AAA on AXR!
  • Some signs of AAA/rupture:
    • Loss of lateral border of ilio-psoas shadow –> sign of ruptured AAA
    • Line of calcification can indicate edge of AAA
22
Q

Decided whether the following AAA scenarios warrent intervention or surveillance.

  1. Aortic diameter < 5.5cm and is symptomatic
  2. Aortic diameter
  3. Aortic diameter > 5.5cm and is not symptomatic

What does intervention involve?

A
  1. Intervene - if patient has AAA and is symptomatic ALWAYS inervene
  2. < 5.5 cm + asymptomatic = surveillance US scans + optimise CV risk factors
  3. > 5.5 cm = intervene on risk balance

Intervention involves: endovascular repair (EVAR) or open repair if unsuitable

  • EVAR = a stent is placed into the abdominal aorta via the femoral artery to prevent blood from collecting in the aneurysm
23
Q

What does open surgery for unruptured AAA often involve?

What about the surgery conveys major risk?

A
  • Open surgery involves replacing affected aortic segment with plastic graft, tube or bifurcated tube under general anaesthesia
  • Major risk = placement of cross-clamp
    • ↑ stress on heart
    • Cause ischaemia of organs distal to clamp
    • Mortality rate = 5% and up
24
Q

Define an aortic dissection.

A
  • Separation of the aortic wall such that blood penetrates the intima and enters the tunica media layer. The high pressure flow often splits the tunica media (inner 2/3rds from outer 1/3rd) creating a false lumen for blood to flow
  • Blood flow through false lumen can occlude branches of aorta e.g. coronary, renal, iliac etc.
  • Aortic dissection = acute IF process is < 14 days old
25
Q

What are some risk factors for Aortic Dissection?

A
  • Hypertension
  • Men >>> women (3 times)
  • Age (peak incidence 50-65yrs without connective tissue disorder)
  • Smoking
  • Connective tissue disorder: Marfan’s or Ehlers-Danlos syndrome
  • Turner’s and Noonan’s syndrome
  • Bicuspid aortic valve
  • Pregnancy
  • Annulo-aortic ectasia (dilation of ascending aortia + aortic annulus)
  • FHx of aortic aneurysm or dissection
26
Q

What are some common signs/symptyoms of aortic dissection?

A
  • Severe chest pain - ripping/tearing + radiates to the back
    • Anterior pain can suggest dissection in ascending aorta
    • Interscapular / lower back = descending aorta
  • ↑ BP (hypertension)
  • BP difference between L/R arm - subject to location of dissection
  • Specific features subject to location of dissection and BVs affected e.g. coronary –> angina, distal aorta –> limb ischaemia
  • Features of Marfan’s; tall, arachnodactyly (spider fingers), pectus excavatum, hypermobile joints, high arched palate, narrow face
  • Features of Ehlers-Danlos (type IV): translucent skin, easy bruising, hypermobility of small joints, and premature ageing of the skin
  • Turner’s, Noonans
27
Q

What 2 classification systems exist for aortic dissection?

A
  1. Standford
    1. Type A = ascending aorta, 2/3 of cases (with or without involvement of arch of aorta)
    2. Type B = descending aorta, distal to left subclavian origin, 1/3 of cases
  2. DeBakey
    1. Type I = originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally
    2. Type II = originates in and is confined to the ascending aorta
    3. Type III = originates in descending aorta, rarely extends proximally but will extend distally
28
Q

What tests might you use to diagnose an aortic dissection?

A
  1. Transoesophageal echo
    1. Quick, cheap, but only useful for imaging aortic valve, ascending and thoracic aorta
  2. CT with contrast = gold standard
  3. Magnetic resonance angiogram
    1. 100% sesnsitive + specific for aortic dissection
    2. But more risky that CT with contrast
29
Q

Define Shock.

A

An acute syndrome caused by ineffective perfusion + cellular hypoxia –> resulting in severe dysfunction of organs vital to survival

30
Q

What are the signs of shock?

A
  • Narrow pulse pressure
    1. Diastolic increases due to vasocontriction
    2. Systolic tries to go up due to ↑ HR + ↑ contractiltiy BUT due to loss of blood vol. it stays ~same
  • Pale + cool skin
  • ↑ Capillary refill time
  • Oliguria (↓ urine output below <400 ml/day)
  • Cerebral hypo-perfusion –> cognitive changes
  • Anaerobic metabolism –> causes metabolic acidosis with ↑ serum [lactate]
31
Q

Shock is associated with a fall in blood pressure and cardiac output, what 3 cardiovascular parameters affect these?

A
  1. Peripheral vascular resistance i.e. vascular tone
    1. CO x PVR = mean arterial BP
  2. Stroke volume –> affects cardiac output
  3. Heart rate –> affects cardiac ouput
32
Q

What are the 4 classifications of shock?

A
  1. Hypovolemic - characterised by ↓ intravascular volume
    • Haemorrhage
    • Burns
    • GI losses (vomiting, diarrhoea, fistula)
    • Dehydration (heat exposure, polyuria i.e. DKA)
  2. Cardiogenic - characterised by intrinsic cardiac (pump) failure
    • MI
    • Arrhythmia
    • Acute valvue pathology
  3. Distributive - characterised by vasodilation + impaired organ perfusion
    • SIRS related - triggered by sepsis, pancreatitis, trauma, burns
    • Neurogenic - spinal cord injury
    • Anaphylaxis - causes profound vasodilation + circulatory collapse
  4. Obstructive - characterised by impairment of blood flow
    • Tension pneumothorax
    • Pericardial tamponande
    • PE
33
Q

A patient who is in hypovolemic shock has the following clinical signs:

Heart rate 120 beats/minute, systolic blood pressure 80mmHg and urine output 20mL. After administering an IV fluid bolus, which of these is the best indication of improved tissue perfusion?

  1. Heart rate decreases to less than 100 bts/min
  2. Systolic Blood Pressure improves to 90 mmHg
  3. Urine output improves to 30 mls/hour
A

Option 3: Urine output improves to 30 mls/hour

  • Whilst improvement in HR and BP reflect improvement in cardiac output and effective circulating volume respectively, urine output is the best indication of tissue perfusion
  • Kidney’s well perfused –> ↑ urine output (kidney’s have reduced blood supply in shock so ↑ blood supply is reassuring)
34
Q

The same patient with hypovolaemic shock is transfused 2 units of blood. What measurement indicates his plasma volume is adequately restored to prevent a cardiac arrest?

  1. Haemoglobin
  2. Oxygen saturations > 90%
  3. Lactate less than 2 mmol/l
A

3. Lactate less than 2 mmol/l

  1. No – serum haemoglobin is an unreliable indicator of haemorrhagic shock
  2. No – less oxygen delivery caused by haemorrhagic shock means tissues switch to anaerobic respiration and therefore lactate levels increase
  3. Yes – less oxygen delivery caused by haemorrhagic shock means tissues switch to anaerobic respiration and therefore lactate levels increase. A return to < 2 is a good sign.

Medicine year 3 ANNA (30 decks)

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