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MLA content map > MLA: Medicine > Flashcards

MLA: Medicine Flashcards

1
Q

How does the Resus Council UK define anaphylaxis?

A
  1. sudden onset and rapid progression
  2. AB and C problems - swelling of tongue and throat, respiratory wheeze and dyspnoea, hypotension and tachycardia
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2
Q

what are the skin and mucosal changes seen in anaphylaxis?

A

generalised pruritus and widespread erythematous/urticarial rash

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3
Q

what is the dose of adrenaline for a child <6 months?

A

0.1 - 0.15ml 1 in 1000

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4
Q

what is the adrenaline dose of a child 6 months - 6 years?

A

0.15ml 1 in 1000

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5
Q

what is the adrenaline dose a child aged 6-12 years for anaphylaxis?

A

0.3ml 1 in 1000

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6
Q

what is the adrenaline dose for adults and children aged >12 years for anaphylaxis?

A

0.5ml 1 in 1000

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7
Q

how often can adrenaline be administered in anaphylaxis?

A

can be repeated every 5 minutes if necessary

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8
Q

what is refractory anaphylaxis?

A

defined as respiratory and/or CV problems despite 2 doses of IM adrenaline

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9
Q

what is an abdominal aortic aneurysm?

A

a dilatation of the abdominal aorta greater than 3cm in diameter

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10
Q

what is the peak incidence of AAA?

A

70+ years and is more common in males 2:1

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11
Q

what is the incidence of AAA?

A

10 cases per 100,000 persons

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12
Q

what are the risk factors for AAA?

A
  1. female = although it is much more prevalent in males, the risk of rupture is much higher in women and will occur at smaller diameters
  2. 70+ years (age)
  3. smoking
  4. HTN
  5. existing vascular disease
  6. FHx
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13
Q

what are the clinical features of AAA?

A
  1. pain - back or loin pain - some described as abdominal pain which radiates through to the back
  2. CV failure - although posteriorly located, ruptures can tamponade - rapidly progressive tachycardia and hypotension
  3. distal ischaemia
  4. death - 33% of patients with AAA die
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14
Q

what is the gold standard investigation for AAA once diagnosed/rupture?

A

CT angiogram

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15
Q

which investigation must always be considered in patients over 50 presenting with acute and severe back pain?

A

consider an abdominal USS in case of AAA

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16
Q

management of a ruptured AAA is dependent on which factors?

A
  1. anatomy of the aneurysm
  2. baseline health of the patient
  3. clinical state of the patient on admissionw
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17
Q

what are some of the complications of ruptured AAA?

A
  1. acute limb ischaemia -> embolus of clot from the site or injury to the lower limb vessels, especially in endovascular repair
  2. open and EVAR require sacrifice/occlusion of the inferior mesenteric artery, which can lead to bowel ischaemia
  3. abdominal compartment syndrome = rising intra-abdominal pressure which causes a fall in renal perfusion, compression of the inferior vena cava and reduces cardiac preload
  4. graft infection!
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18
Q

when does screening for AAA occur?

A

consists of a single abdominal USS for males over the age of 65

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19
Q

when should a patient be re-scanned if their AAA is 3-4.4cm?

A

every 12 months

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20
Q

when should a patient be rescanned if their AAA is 4.5-5.4cm?

A

every 3 months

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21
Q

what is the immediate action of a patient presenting with AAA >5.5cm

A

refer immediately to vascular surgery for probable intervention

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22
Q

generally, what causes arrhythmias?

A

they result from an interruption to the normal electrical signals that coordinate the contraction of the heart muscle

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23
Q

which are the shockable rhythms?

A

ventricular tachycardia and ventricular fibrillation

24
Q

what are the non-shockable rhythms?

A
  1. pulseless electrical activity (PEA)
  2. asystole
25
Q

what is a narrow complex tachycardia?

A

refers to a fast heart rate with a QRS duration of less than 0.12 seconds (fits within 3 small squares)

26
Q

what are the four main differentials of a narrow complex tachycardia?

A
  1. sinus tachycardia
  2. supra ventricular tachycardia
  3. atrial fibrillation
  4. atrial flutter
27
Q

how does supraventricular tachycardia appear on ECG?

A

looks like a QRS complex followed immediately by a T wave, then another QRS, then a T wave. There are P waves but they are often buried by the T waves

28
Q

how can you distinguish between SVT and sinus tachycardia?

A

SVT has an abrupt onset and a very regular pattern without variability. Sinus tachycardia has a more gradual onset and more variability in the rate. The Hx is also important - where sinus tachycardia usually has an explanation (pain or fever), SVT can appear at rest with no apparent cause

29
Q

how can AF be identified on ECG?

A

absent P waves and an irregularly irregular ventricular rhythm

30
Q

how does atrial flutter appear on ECG?

A

300 beats per minute and gives a sawtooth pattern. The QRS occurs at regular intervals depending on how often there is conduction form the atria. This often results in two atrial contractions for every one ventricular contraction, giving a ventricular rate of 150bpm

31
Q

what is the treatment of narrow complex tachycardias with life-threatening features e.g. LOC?

A

they are treated with synchronised DC cardioversion under sedation or GA. IV amiodarone is also administered if initial DC shocks are unsuccessful

32
Q

what is a broad complex tachycardia?

A

refers to a fast heart rate with QRS duration of more than 0.12 seconds or more than 3 small squares on an ECG

33
Q

how does the resus guidelines break down broad complex tachycardias?

A
  1. ventricular tachycardia of unclear cause - treated with IV amiodarone
  2. polymorphic ventricular tachycardia (Torsades) - treated with IV magneiusm
  3. AF with BBB - treated as AF
  4. Supraventricular tachycardia with BBB - treated as SVT
34
Q

what is the mechanism of action of Amiodarone for SVT?

A

it blocks potassium currents that cause repolarisation of the heart muscle during the third phase of the cardiac action potential - thereby slowing down the electrical activity of the heart, slowing down HR

35
Q

what happens in atrial flutter?

A

normally, electrical signal passes through the atria once, stimulating a contraction, then disappears through the AV node into the ventricles. In atrial flutter, there is a re-entrant rhythm in either atrium. This signal re-circulates in a self-perpetuating loop due to an extra electrical pathway in the atria. The signal goes round the atrium continuously with no interruption, making the atrial rate around 300 beats per minute

36
Q

what is the treatment of atrial flutter?

A

it is similar to AF, including anticoagulation based on the CHADVASc score and radiofrequency ablation of the re-entrant rhythm can be a permanent solution

37
Q

what is the QT interval?

A

it is from the start of the QRS complex to the end of the T wave

38
Q

what is prolonged QT interval?

A

presents a prolonged depolarisation of the myocytes after a contraction. Repolarisation is a recovery period before the muscle cells are ready to depolarise again. Waiting a long time for depolarisation can result in spontaneous depolarisation in some cells - these can spread throughout the ventricles, causing a contraction before proper repolarisation = this is Torsades

39
Q

what is Torsades de pointes?

A

type of polymorphic ventricular tachycardia - translates to twisting of the spikes - on the ECG, it looks like standard VT with the appearance that the QRS complex is twisting around the baseline. The height of the QRS gets progressively smaller, then larger, then smaller and so on

40
Q

what are the causes of prolonged QT?

A
  1. long QT syndrome (inherited)
  2. medications - antipsychotics, citalopram, flecainide, sotalol, amiodarone and macrolide antibiotics
  3. electrolyte imbalances, such as hypokalaemia, hypomagnesemia and hypocalcameia
41
Q

what is the management of prolonged QT interval syndromes?

A
  1. stopping and avoiding medications that prolong QT interval
  2. correcting electrolyte disturbances
  3. Beta-blockers (not Sotalol)
  4. Pacemakers or implantable cardioverter defibrillators
42
Q

what is the acute management of torsades de pointes?

A
  1. correct the underlying cause (electrolyte disturbances or medications)
  2. magnesium infusion
  3. defibrillation if VT occurs
43
Q

what are ventricular ectopics?

A

premature ventricular beats causes by random electrical discharges outside of the atria - patients often present complaining of random extra or missed beats

44
Q

how do ventricular ectopics appear on an ECG?

A

they appear as isolated, random, abnormal broad complexes on an otherwise normal ECG

45
Q

what is bigeminy?

A

refers to when every other beat is a ventricular ectopic. The ECG will show a normal beat, followed immediately by an ectopic beat, then a normal beat, then an ectopic and so on…

46
Q

what is first degree heart block?

A

this occurs when there is delayed conduction through the AV node. Despite this, every atrial impulse leads to a ventricular contraction, meaning every P wave is followed by a QRS complex.

47
Q

how does first degree heart block appear on an ECG?

A

it presents as a PR interval greater than 0.2 seconds (5 small or 1 big square)

48
Q

what is second degree heart block?

A

this is where some atrial impulses do not make it through the AV node to the ventricles. There are instances were P waves are not followed by QRS complexes. There are two types: Mobitz 1 (Wenckebach) and Mobitz type 2

49
Q

what is Mobitz type 1 (Wenckebach)?

A

a type of second degree heart block where the conduction through the AV node takes progressively longer until it finally fails, after which it resets, and the cycle restarts. On an ECG, there is an increasing PR interval until a P wave is not followed by a QRS complex. The PR then returns to normal and the cycle repeats itself

50
Q

what is Mobitz type 2?

A

a type of second degree heart block where there is intermittent failure of conduction through the AV node, with an absence of QRS complexes following P waves. The PR interval remains the same. There is a risk of asystole

51
Q

what is 3:1 block?

A

there is usually a set ratio of P waves to QRS complexes (3 P waves to every QRS)

52
Q

what is 2:1 block?

A

this is where there are two P waves for every QRS complex - every other P wave does not stimulate a QRS

53
Q

what is third degree block?

A

this is also known as complete heart block - there is no observable relationship between the P waves and QRS complexes. There is a significant risk of asystole

54
Q

what is the management of unstable patients and those at risk of asystole?

A
  1. IV atropine (first line)
  2. Inotropes (isoprenaline or adrenaline)
  3. temporary cardiac pacing
  4. permanent implantable pacemaker
55
Q

what is atropine?

A

antimuscarinic medication that works by inhibiting the PNS. Therefore, by inhibiting the PNS, side effects can include pupil dilation, dry mouth, urinary retention and constipation

56
Q

what is atropine used for?

A

mainly in the management of patients with bradycardia - it works by increasing the heart rate and improve the AV conduction by blocking the parasympathetic influences on the heart

57
Q
A

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