passmed Flashcards

1
Q

long QT - what is normal

A

QT interval in females = <450ms and in males <430ms

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2
Q

causes of long QT syndrome

A

Inherited mutations - Jervell Lange Nielsen, Romano Ward
Acquired causes:
-Electrolyte imbalance - HYPOKALAEMIA, HYPOCALCAEMIA, HYOPMAGNAESAEMIA
-Meds - tramadol, amiodarone, TCAs, SSRIs, erythmocyin, methadone, chloroquine, terfenadine etc
-CNS lesions: SAH + ischaemic stroke
-Malnutrition
-Hypothermia

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3
Q

what can long QT syndrome lead to

A

VT / TdP –> collapse/sudden death

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4
Q

cholesterol of 5.1 + QRISK score of 11%

what is the mx

A

statins - atorvastatin 20mg 1st line for primary prevention

  • INCREASE DOSE IF NON-HDL has not REDUCED by >40%
  • atorvastatin 80mg for secondary prevention
  • simvastatin for those who can’t tolerate it
  • save dietary measures for those with qrisk <10%
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5
Q

statins MoA and adverse effects (3)

A

HMG CoA reductase INHIBITOR , rate-limiting enzyme, in hepatic CHOLELSTEROL synthesis
Adverse effects:
-MYOPATHY - myalgia, myositis, rhabdomyolysis + asympt raised CK
-LIVER IMPARIMENT - check LFTs at baseline, 3m, 12m
-STATINS - can incr risk of ICH in pts who hv had previous stroke - effect not seen in primary prevention

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6
Q

statins CI (2)

A

Macrolides = stop statins till pt course complete

pregnancy

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7
Q

difference between primary and secondary preventio

A

primary - measures to prevent onset of illness before disease process begins eg QRISK >10% OR most T1DM pts OR CKD eGFR<60 —> ATORVASTATIN 20mg
secondary - measures that lead to early dx and prompt tx of disease eg known IHD OR CVD OR PAD –> ATORVASTATIN 80mg OD

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8
Q

ECG changes for thrombolysis or PCI

A

ST elevation of > 2mm (2 small squares) in 2 or more consecutive anterior leads (V1-V6) OR

ST elevation of greater than 1mm (1 small square) in greater than 2 consecutive inferior leads (II, III, avF, avL) OR

New Left bundle branch block

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9
Q

how do loop diuretics work

A

furosemide and bumetanide are loop diuretics that act by INHIBITING NA-K-Cl cotransporter in the thick ascending LoH, reducing the absorption of NaCl

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10
Q

Loop diurtics adverse effeects

A

LOW BP, Na+, K+, Mg+, Cl
LOW Ca2+ –> excess PTH secretion –> more calcium released from bone –> weakens structure
RENAL IMPAIRMENT (from dehydration + direct toxic effect)
HIGH GLUCOSE (less common than with thiazides)
GOUT

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11
Q

posterior MIs ECG findings

A

cause reciprocal changes in V1-3 (anterior leads) as these leads are directly opposite posterior surface

  • ST depression
  • tall broad R waves
  • upright T waves
  • dominant R wave in V2
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12
Q

complete heart block following an MI, where is the lesion

A

commonly RCA lesion

-AVN is supplied by a branch of the RCA, posterior interventricular artery

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13
Q

aortic stenosis mx

A
  • observe pt is general rule
  • if symptomatic then valve replacement
  • if asymptomatic but valvular gradient >40mmHg and features eg LV systolic dysfunction then consider surgery
  • as CVD can coexist, often do angiogram before surgery so procedures can be combined with PCI
  • BALLOON VALVULOPLASTY limited to pts with critical aortic stenosis
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14
Q

acute pericardits acute mx

A

NSAIDs + colchicine used 1st line - for pts with acute idiopathic or viral pericarditis

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15
Q

thiazides affect on calcium levels - in blood + urine

A

BLOOD - HYPERCALCAEMIA

URINE - HYPOCALCIURIA

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16
Q

MX for bradycardia + signs of shock

A

require 500micrograms of IV atropine (repeated up to max 3mg)

  • bradycardia only req tx when HR is less than 60 + SYMPTOMATIC/signs of haemodynamic compromise
  • if this fails then consider TCPacing
  • NB. amiodarone is a RF for dev severe bradycardai
17
Q

cardiac tamponade becks triad

A

HYPOTENSION
RAISED JVP
MUFFLED HEART SOUNDS

18
Q

cardiac tamponade : JVP, Pulsus Paradoxus, Kussmauls sign

A

JVP - absent Y descent - TAMpaX
PP - present
K..Sign - Rare

19
Q

Constrictive pericarditis: JVP, Pulsus paradoxus, Kussmauls, Char Feat

A

JVP - X+Y present
PP - absent
Kussmauls- present - JVP rises on inspiration
Char feat - pericardiac calcification on CXR

20
Q

trifascicular block

A

RBBB + left anterior or posterior hemiblock + 1st-degree heart block = trifasicular block

21
Q

bifascicular block

A

combination of RBBB with left anterior or posterior hemiblock
e.g. RBBB with left axis deviation

22
Q

how to reduce the risk of sudden cardiac death in HOCM

A

ICD

23
Q

can LBBB be normal in athletes

A

NO NEVER NORMAL - means underlying ischaemic or structural heart disease

24
Q

what are cannon a waves and when do they occur

A

due to atria and ventricles contracting together –> RA contracts against closed tricuspid valve , column of blood shoots up the SVC into the jugular vein
-COMPLETE HEART BLOCK

25
Q

what JVP waveform is seen in TR

A

Large V waves

-ventricular contraction causing blood to surge through an incompetent TV through RV into Jugular vein

26
Q

what is Kussmaul sign + what is it caused by

A

paradoxical rise in JVP on inspiration
-caused by conditions that impari ventricular filling
eg CONSTRICTIVE PERICARDITIS

27
Q

what JVP waveform is seen with tricuspid stenosis

A

Slow Y descent

28
Q

what happens to JVP in SVCO

A

raised JVP with ABSENT PULSATION

29
Q

what is dresslers syndrome

A

PERICARDITIS after MI (can cause pericardial effusion)
2-10 weeks later due to production of AUTOANTIBODIES after MI
DIFFERENT to simple post-MI pericarditis 2-4 DAYS after MI