PR3154 > SPAF > Flashcards

SPAF Flashcards

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1
Q

AF sequelae

A

cardio-embolic stroke

  1. Uncoordinated contraction in LA
  2. Clot formation in appendages (LA)
    a. Circulatory stasis
  3. Emboli to brain
    Cerebral infarction
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2
Q

AF ECG readings

A

Irregularly irregular rhythm · No P waves

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3
Q

valvular AF

A

moderate or severe mitral stenosis (LA –> LV)

presence of mechanical prosthetic heart valve

= WARFARIN

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4
Q

non-valvular AF

A

includes AF with other valvular heart lesions

= DOAC

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5
Q

SPAF
Anticoagulants - VKA

A
  • Reduce stroke risk by 64%, 26% death in AF pt
  • Mitral stenosis, mechanical heart valves
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6
Q

SPAF anticoagulants – DOAC preferred?

A
  • Reduce ischemic stroke by 19%, risk of hemorrhage by 50%
  • Recommended to all other AF pts
      ○ CHA2DS2-VASc score =/>2 (offered)
  ○ CHA2DS2-VASc score <2 (considered)
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7
Q

CHA2DS2 VA

A

CHF
HTN
Age =/> 75yo (2)
DM
stroke, TIA, thromboembolism (2)
vascular disease
age 65-74

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8
Q

CHADSVASC score 0 (M,F) need to tx?

A
  • No anticoag
  • No antiplt (aspirin, * clopidogrel not recom for SPAF)
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9
Q

CHADSVASC score 1 (M,F) meaning

A

Consider anticoag based on risk factors

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10
Q

CHADSVASC score =/>2

A

Offer, recommended warfarin/ NOAC

Discuss bleeding risk factors, tx options

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11
Q

favour warfarin (in general)

A
  • maintain INR within therapeutic range TTR 70%
  • SE of DOAC
  • mod-severe liver or renal impairment
  • sig DDI with DOAC
  • valvular AF, APS
  • GI alterations
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12
Q

favour DOAC

A
  • pt unable to monitor INR (venous access/ lab access)
  • reluctant to monitor VKA, narrow TI)
  • DDI
  • ease of dosing
  • safer (less major bleeds)
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13
Q

bleeding risk HASBLED

max 9

A

HTN > 160mmHg

Abnormal renal function SCr > 200umol/L OR Ab liver function AST, ALT >3X [1,1]

stroke (hx)

bleeding (hx / predispose)

labile INR (<6/10 in range)

elderly (>65yo)

Drug (antiplt, NSAID, alc >8unit/wk) [1,1pt]

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14
Q

HASBLED scores

A

0 = low risk
1-2 = mod risk
=/> 3 = high risk

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15
Q

what to do if there is high risk for bleeding

A
  • assess risk of stroke vs bleeding
  • cause of bleeding
  • identify & tx comor (HTN)

continue NOAC, dont stop unless CI

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16
Q

consel on need

A

1) stroke risk
2) SE of OAC – mitigate bleeding risk
3) compare DOAC or VKA

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17
Q

ABC pathway

A

A: avoid stroke, OAC

B: better sx control (rate BB, CCB> rhythm Na, K)

C: CVS and other comor risk factors

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18
Q

OAC dose for Afib

dabigatran

A

150mg BD

110mg BD (if =/>80yo/ use PGPi/ high risk of bleed)

no crcl dose adj unless CI <30ml/min

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19
Q

OAC dose for Afib

rivaroxaban

A

20mg OD

crcl 30-50ml/min : 15mg OD

CI: <15 ml/min

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20
Q

OAC dose for Afib

apixaban

A

5mg BD

2.5mg BD (any 2: age=/>80yo, weight =/<60kg, scr =/> 1.5mg/dL or 132mmol/L)

crcl 15-29: 2.5mg BD

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21
Q

OAC dose for Afib

edoxaban

A

60mg OD

30mg OD (if ANY 1: crcl 30-50ml/min, weight =/<60kg, concom verapamil, quinidine, dronedrone)

CI: crcl<15

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22
Q

interval for FU depends on

A

1mnth: initiate

4mnth: =/>75yo, frail, dabi

crcl/10 mnth: crcl =/< 60ml/min

immediate: hep, renal function (NSAID, infection, dehydration)

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23
Q

at each FU check for:

A

1) adherence (cognitive, minor bleeds)
2) thromboembolism
3) bleeding (cause??)
4) SE
5) co-medications (aspirin, NSAID)

  • blood sampling (hb, LFT, CrCL)
  • minimise bleeding risk factors (HTN, medication, INR)
  • optimal choice of DOAC?dose?
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24
Q

how much is metabolised by lvier

DRAW

A

VKA: INR (risk nephropathy, vas calcification)

15-29: consider benefit vs harm
D: 80% kidney 0% substrate, inhibitor, inducer
R: 66% liver metabolised
A: 75% liver
W: 99% liver

E: 50% liver metabolised

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25
why cockcroft gault
CKD-EPI, mdrd: determine staging of CKD
26
parameters for crcl by CG
gender actual BW (if morbid obese = IBW) age SCr
27
elderly considerations
1) dementia and compliance 2) frailty and falls (but benefit > risk) - edoxaban, apixaban
28
low BW choice
60-120kg lower BW = dose adj (apix, edoxaban)
29
high BW chocie
rivaroxaban (OD and wider indication range) apixaban (BD, easy to use in special pop)
30
DOAC DDI
CYP450 enzymes (apix 25%, 50% riva, edo) PGP substrate (apix, dabig, riva, edox) BCRP (apix, riva) OATP (riva)
31
potent PGPi (think of edoxaban)
verapamil, quinidine, dronedarone, amiodarone macrolides PO azoles: itra, keto, voric, posa ciclosporin
32
potent CYP3A4 inducer
rifampicin, CBMP, PT, PB st john wort
33
potent dual CYP3A4, PGP inhibitor
PO azole ritonavir clarithromycin
34
potent dual CY3A4, PGP inducer
valproic acid
35
liver impairment and DOAC
child pugh A child pugh B (caution, except edoxa/ riva: not recomm) child pugh C: DO NOT USE vka: INR 2-3
36
warfarin interindiv response
genetic (VKORC1, CYP2C9) environmental factors new factors
37
pgX FOR
1) existing clots (left V thrombus) 2) outpt commencement 3) complex DDI 4) questionable adherence
38
clotting factor t1/2 ranking
II > Protein S > X > IX> protein C > VII II: 42-72hrs protein S: 60hr
39
load warfarin because? - LMWH (sc)
hypercoagulable state 4-5d, due to low prot S,C long time to deplete vit K lvls long t1/2, many clotting factors involved esp if existing clot
40
what affects INR eg: indian higher mean daily dose (VKORC1)
PGx (esp if =/< 21mg/wk or =/>49mg/wk) chronic diseases, CHF, DM diet, compliance
41
PK DDI of warfarin
Absorption from gut Protein bind: NSAID use CYP450, CYP2C9 inhibition/ induction transporter enzymes
42
CYP2C9 inhibitors
preemptive dose adj (amiodarone, fluconazole, metronidazole)
43
CYP2C9 inducer
rifampicin (preemp adjust) CBMZP PB st john wort
44
antimicrobials effect on INR
disrupt gut bacteria, less menadione (vit K) incr INR
45
DDI with Abx
preemptive (SMX-TMP, cipro, metro) macrolides, amox/clav, doxy
46
monitor INR
3-5 days after start therapy 1-3d if unstable daily (admitted, unstable/ septic)
47
alcohol and INR
○ Binge: CYP450 enzyme inhibition INR blip incr ○ Chronic: CYP450 enzyme induced INR: decr
48
Incr physical activity
Incr warfarin meta INR decr
49
Smoking
CYP450 induction Incr warfarin meta INR decr
50
Liver impairment
Decr clotting factor synthesis Decr warfarin meta INR incr
51
Fluid retention
Absorp from oedematous gut vs liver congestion INR incr (liver, warfarin stay in body longer, more effect) INR decr (gut, dilute, less warfarin effect)
52
fever
Incr metabolism, clotting disorders, incr turnover of clotting factors Esp in sepsis INR incr
53
Thyroid disease
Hyperthyroidism incr clotting factor turnover INR incr
54
high vit K diet
leafy greens (kale, spinach etc) beef, prok canola oil green tea, chrysanthemum, herbal teal, soybean
55
DOAC coagulation assays deranged
PT aPTT ACT
56
DOAC bleeding management
mild bleed: continue (reconsider concmitant meds) mod: supp tx (fluid replacement, tx cause of bleed GIT) severe: prothrombin complex conc, reversal agents
57
reversal agents for DRAW
D: Idarucizumab 5g IV * Renally CL, can dialysis R, A: Andexanet alfa/ PCC W: PCC (prothrombin complex) * Fresh frozen plasma * Vit K (IV 5-10mg) * Overcorrection (high dose of vit K) assoc with delayed re-anticoagulation (up to 3wks)
58
unplanned invasive procedure
acute (in mins) - reversal of NOAC urgent (in hrs) - defer 12-24hr? hold off only if high bleeding risk expedited (days) - defer surgery if possible repeate coag panel after surgery
59
switching from NOAC --> VKA
Use NOAC like LMWH bridge (3-5d, along with VKA) INR > 2: stop NOAC, repeat INR 1day after INR <2: continue NOAC, repeat INR 1-3day
60
switching from VKA --> NOAC stop VKA wait til __ to start NOAC
-Based on t1/2 of clotting factors (by warfarin inhibition) - Low INR: withhold less days (2-3 days) □ INR =/<2: start NOAC (has shorter t1/2, no need load) * Unlike VTE - darbi, edoxa need LMWH □ If 2-2.5: KIV start current or next day □ If INR >3: hold warfarin, repeat INR 1-3day, decide based on INR
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