passmed Flashcards
long QT - what is normal
QT interval in females = <450ms and in males <430ms
causes of long QT syndrome
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
what can long QT syndrome lead to
VT / TdP –> collapse/sudden death
cholesterol of 5.1 + QRISK score of 11%
what is the mx
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%
statins MoA and adverse effects (3)
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
statins CI (2)
Macrolides = stop statins till pt course complete
pregnancy
difference between primary and secondary preventio
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
ECG changes for thrombolysis or PCI
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
how do loop diuretics work
furosemide and bumetanide are loop diuretics that act by INHIBITING NA-K-Cl cotransporter in the thick ascending LoH, reducing the absorption of NaCl
Loop diurtics adverse effeects
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
posterior MIs ECG findings
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
complete heart block following an MI, where is the lesion
commonly RCA lesion
-AVN is supplied by a branch of the RCA, posterior interventricular artery
aortic stenosis mx
- 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
acute pericardits acute mx
NSAIDs + colchicine used 1st line - for pts with acute idiopathic or viral pericarditis
thiazides affect on calcium levels - in blood + urine
BLOOD - HYPERCALCAEMIA
URINE - HYPOCALCIURIA