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SPAF Flashcards

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
Q

why cockcroft gault

A

CKD-EPI, mdrd: determine staging of CKD

26
Q

parameters for crcl by CG

A

gender
actual BW (if morbid obese = IBW)
age
SCr

27
Q

elderly considerations

A

1) dementia and compliance

2) frailty and falls (but benefit > risk)
- edoxaban, apixaban

28
Q

low BW choice

A

60-120kg

lower BW = dose adj (apix, edoxaban)

29
Q

high BW chocie

A

rivaroxaban (OD and wider indication range)

apixaban (BD, easy to use in special pop)

30
Q

DOAC DDI

A

CYP450 enzymes (apix 25%, 50% riva, edo)

PGP substrate (apix, dabig, riva, edox)

BCRP (apix, riva)

OATP (riva)

31
Q

potent PGPi

(think of edoxaban)

A

verapamil, quinidine, dronedarone, amiodarone

macrolides

PO azoles: itra, keto, voric, posa

ciclosporin

32
Q

potent CYP3A4 inducer

A

rifampicin, CBMP, PT, PB
st john wort

33
Q

potent dual CYP3A4, PGP inhibitor

A

PO azole
ritonavir
clarithromycin

34
Q

potent dual CY3A4, PGP inducer

A

valproic acid

35
Q

liver impairment and DOAC

A

child pugh A

child pugh B (caution, except edoxa/ riva: not recomm)

child pugh C: DO NOT USE

vka: INR 2-3

36
Q

warfarin interindiv response

A

genetic (VKORC1, CYP2C9)
environmental factors
new factors

37
Q

pgX FOR

A

1) existing clots (left V thrombus)

2) outpt commencement

3) complex DDI

4) questionable adherence

38
Q

clotting factor t1/2 ranking

A

II > Protein S > X > IX> protein C > VII

II: 42-72hrs
protein S: 60hr

39
Q

load warfarin because?

  • LMWH (sc)
A

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
Q

what affects INR

eg: indian higher mean daily dose (VKORC1)

A

PGx (esp if =/< 21mg/wk or =/>49mg/wk)

chronic diseases, CHF, DM

diet, compliance

41
Q

PK DDI of warfarin

A

Absorption from gut
Protein bind: NSAID use
CYP450, CYP2C9 inhibition/ induction
transporter enzymes

42
Q

CYP2C9 inhibitors

A

preemptive dose adj
(amiodarone, fluconazole, metronidazole)

43
Q

CYP2C9 inducer

A

rifampicin (preemp adjust)

CBMZP
PB
st john wort

44
Q

antimicrobials effect on INR

A

disrupt gut bacteria, less menadione (vit K)
incr INR

45
Q

DDI with Abx

A

preemptive (SMX-TMP, cipro, metro)

macrolides, amox/clav, doxy

46
Q

monitor INR

A

3-5 days after start therapy

1-3d if unstable

daily (admitted, unstable/ septic)

47
Q

alcohol and INR

A

○ Binge: CYP450 enzyme inhibition

INR blip incr

○ Chronic: CYP450 enzyme induced

INR: decr

48
Q

Incr physical activity

A

Incr warfarin meta

INR decr

49
Q

Smoking

A

CYP450 induction
Incr warfarin meta

INR decr

50
Q

Liver impairment

A

Decr clotting factor synthesis
Decr warfarin meta

INR incr

51
Q

Fluid retention

A

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
Q

fever

A

Incr metabolism, clotting disorders, incr turnover of clotting factors

Esp in sepsis

INR incr

53
Q

Thyroid disease

A

Hyperthyroidism incr clotting factor turnover

INR incr

54
Q

high vit K diet

A

leafy greens (kale, spinach etc)
beef, prok
canola oil

green tea, chrysanthemum, herbal teal, soybean

55
Q

DOAC coagulation assays deranged

56
Q

DOAC bleeding management

A

mild bleed: continue (reconsider concmitant meds)

mod: supp tx (fluid replacement, tx cause of bleed GIT)

severe: prothrombin complex conc, reversal agents

57
Q

reversal agents for DRAW

A

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
Q

unplanned invasive procedure

A

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
Q

switching from NOAC –> VKA

A

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
Q

switching from VKA –> NOAC

stop VKA wait til __ to start NOAC

A

-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

PR3154 (11 decks)

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