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H/O RC > Hemostasis/Thrombosis > Flashcards

Hemostasis/Thrombosis Flashcards

1
Q

Virchow’s Triad

A

vascular trauma: trauma, sx, line, inf

Hypercoagulability: hereditary thrombophilia, malig, preg, infl, estrogen, dehydration

Reduced blood flow: immobility, prolonged travel, obesity, preg, congenital anomalies, Fontan, catheter

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2
Q

List the inherited thrombophilias (including anatomic)

A

FVL
Prothrombin gene mutation
Protein C/S deficiency
Antithrombin deficiency

PCV, PNH, hemoglobinopathies, SCD

Anatomic:
- IVC atresia
- May Thurner Syndrome: narrowed L iliac vein 2o compression from R iliac artery against lumbar spine
- Thoracic Outlet Syndrome: extra rib or muscle group compressing veins

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3
Q

FVL inheritance, mechanism, risk

A

aut dom

G1691A mutation
APC resistance - Protein C can’t inactivate FVa

5% lifetime risk
4x general population
low recurrence risk

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4
Q

Prothrombin gene mutation inheritance, mechanism, risk

A

aut dom

G20210A GOF mutation

3-4x general population
low recurrence risk

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5
Q

Protein C/S deficiency inheritance, mechanism, risk

A

aut dom

no inactivation of Va and VIIIa

severe congenital: 100%
PC: 7x general population
PS: 5x general population
high recurrence risk

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6
Q

Antithrombin deficiency inheritance, mechanism, risk

A

aut dom

quant or qual deficiency in antihrombin –> increased thrombin

8x general population
1% annual risk
high recurrence risk

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7
Q

Acquired thrombophilia states

A

Acquired Protein C/S deficiency
APS
pregnancy
Cancer
inflammation - acute phase reactants FVIII, VWF, TF
CVL
cardiac disease
trauma/surgery
Obesity
immobilization - stasis
nephrotic syndrome - loss of antithrombin in urine
liver failure - decreased synthesis of protein C/S
medications (OCP, asparaginase)

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8
Q

Thrombophilia workup

A

Hx, P/E, FHX

CBC
INR, PTT, fibrinogen
Protein C and S Ag and activity
FVL and prothrombin genetics
Antithrombin (chromogenic)
APS: LA, anti-cardiolipin, anti-beta2 glycoprotein
FVIII, VWF

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9
Q

Thrombophilia workup indications

A

unprovoked or recurrent VTE
VTE and SLE
VTE and strong FHx

purpura fulminans

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10
Q

VTE compression US findings

A

failure to compress vein
loss of phasic flow on Valsalva
absent flow (fully occlusive)

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11
Q

Kids-DOTT trial results

A

6w for acute provoked and resolved clot (not malignancy or PE)
Otherwise 3mo

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12
Q

Thrombolysis indications and contraindications

A

life/limb threatening arterial clot/DVT
- bilateral RVT, occlusive IVC, large iliofemoral
PE w hypotension or RH strain

bleeding risk, surgery <10d (NSx<60d), intracranial malig, seizure <48h, sepsis

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13
Q

What is warfarin induced skin necrosis etiology and prevention

A

transient hypercoagulability 2o reduction in Protein C/S (shortest half lives of K-dept factors) -> microvascular thromboses and tissue infarct

  • need 5d UFH bridge at start of warfarin
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14
Q

HIT etiology, presentation, tx

A

autoAb against heparain:plt factor 4 compelx -> plt activation

thrombosis

Tx: stop heparin, start another anticoagulation; avoid plt transfusion
- 2nd line IVIG, PLEX

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15
Q

APS criteria

A

thrombosis or pregnancy related morbidity
and
1+ LA/cardiolipin/beta2 glycoprotein

on 2 checks 12+ w apart

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16
Q

Lupus anticoagulant dx

A

mixing study - no PTT correction

RVVT: venom directly activates Xa, but excess phospholipid will overwhelm LA and create clot

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17
Q

1o Thromboprophylaxis indications

A

APS with SLE
homozygous protein C/S deficiency

dilated cardiomyopathy (warfarin)
primary pHTN (warfarin)
neonate with CVAD or UAC (UFH)
neonate cardiac cath (UFH)
long term home TPN (warfarin)
hemodialysis via arteriovenous fistula or CVAD (warfarin or LMWH)
KD moderate/giant aneurysm (warfarin/ASA)

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18
Q

post thrombotic syndrome s/s, epi, RF

A

venous insufficiency - pain/heaviness, paresthesia, cramping, pruritis, dilated veins, swelling, redness, edema

25% post extremity DVT

RF: young, obese, large clot, untreated/partially treated, delayed tx, elevated D-D or FVIII

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19
Q

RVT presentation and tx

A

palpable flank mass (45% neonates), hematuria, thrombocytopenia, kidney dysfunction, anuria

unilat: anticoagulate
bilat: thrombolysis -> anticoagulation

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20
Q

Intracardiac thrombus mgt

A

anticoagulation only
thrombolysis only if severe

21
Q

Bethesda unit definition and high tire cutoff

A

inhibitor that will decrease FVIII activity by 50% (after 2h at 37C)

BU>5 is high titre

22
Q

Mgt bleeding with inhibitor

A

FEIBA = PCC
factor replacement (if low titre)

23
Q

Hypofibrinogenemia DDx

A

malignancy
asparaginase
DIC
liver failure

24
Q

thrombin actions

A

crosslinks fibrinogen to fibrin
activates V, VIII, XI, XIII
TAFI activation
plt activation
w thrombomodulin, activates PC

25
Q

Endogenous inhibitors of coagulation

A

TFPI
antithrombin: inhibits Xa, thrombin, IXa, XIa
protein C/S
thrombomodulin
heparan sulfate

26
Q

Describe fibrinolytic system

A

tpa converts plasmingen to plasmin
plasmin degrades fibrin

inhibition by PAI-1, a2-antiplasin, TAFIa

27
Q

Vitamin K dependent factors

A

II, VII, IX, X, C, S

28
Q

false positive prolonged coags DDx

A

LA
Deficiency XII, prekallikrein, HMWK
underfilling tube (excess citrate)
heparain contamination
delayed processing
polycythemia (less relative plasma)
difficult draw (factors consumed)

29
Q

Neonatal factor levels

A

all are low except:
- fibrinogen (N)
- VIII (N/high)
- VWF (N/high)

30
Q

Factor pharmacokinetics Hemo A vs B

A

A: 1U/kg raises by 2%; dose 50 U/kg; half life 8-12h
B: 1U/kg raises by 1%; dose 100 U/kg; half life 18-24h

31
Q

VWF genetics, function

A

chromosome 12

adhesion: cell surface collagen to plt GP1b/IX
aggregation: plt-plt binding
FVIII chaperone

Multimers cleaved by ADAMTS13

32
Q

ABO relationship to VWF

A

O - lowest VWF
AB - highest VWF

33
Q

VWD inheritance

A

aut dom

type 3 - aut rec
type 2N - compound heterozygous

34
Q

Acquired VWD conditions

A

WT
hypothyroid
SLE
congenital cardiac defects

35
Q

VWD subtype pathophys

A

1: quantitative

2A: loss of plt binding (reduced multimers)
2B: increased plt binding (GOF)
2M: reduced GPIb plt binding (but normal multimer distribution)
2N: no VIII binding

3: absent

36
Q

VWD subtypes with:
- Act:Ag >0.6
- decreased multimers
- RIPA +
- decreased VIII binding

A
  • Act:Ag >0.6: 1, 2N
  • decreased multimers: 2A, 2B
  • RIPA (ristocetin induced plt aggregation) + : 2B
  • decreased VIII binding: 2N
37
Q

APS non-criteria manifestations

A
  • livedo reticularis (unbroken circles), livedo racemosa (broken circles), Raynauds
  • heme: thrombocytopenia, AIHA
  • neuro: migraine, chorea, transverse myelitis, cognitive defects
  • cardiac: valvular, MI
  • pulm: pHTN, interstitial fibrosis
38
Q

CAPS criteria and mgt

A

3+ organs/tissues
development <1w
histo intravascular thrombosis
APL on 2 occasions 6w apart

4/4 definite
1+2+3/4 is probable

triple therapy: anticoag (heparin) + steroid (pulse MP) + PLEX or IVIG

39
Q

Stroke RF

A

SCD
heart disease
acute systemic: infection, dehydration, IDA, prothrombotic, moyamoya

40
Q

Stroke mgt
- cardioembolic
- dissection
- neonatal

A

Neuroprotection: normal temp, BG, volemia, BP; treat seizures

Cardioembolic: LMWH/Warfarin x3mo
Dissection: LMWH/Warfarin x 3 mo –> ASA x2+y

Neonatal: only tx cardioembolic: anticoag x3-6mo –> ASA if cardiac lesion unrepaired

4% risk of symptomatic ICH

41
Q

Describe primary hemostasis

A

1) adhesion: collagen-plt binding (GP1B-IX-V)
2) activation: granule release
3) aggregation: GPIIb-IIIa activation

42
Q

plt granule contents and fxn

A

dense: ADP - amplifies plt activation
alpha: VWF and fibrinogen - amplifies adhesion/aggregation

43
Q

Draw the coagulation cascade

A
44
Q

Hemophilia severity

A

Severe: <1%
Mod: 1-5%
Mild: 5-40%

45
Q

When to check for an inhibitor

A
  • monthly for first 50 exposure days
  • pre-op
  • bleeding episode not responsive to factor
46
Q

Inhibitor formation risk

A

H-A 30%
H-B 5%
<1% after 50 exposure days

47
Q

Factor XIII deficiency manifestations

A

umbilical stump bleeding
ICH

48
Q

Explain RIPA assay

A

ristocetin inducted platelet agglutination
- positive in VWD Type 2B

high dose ristocetin stimulated binding but low dose will only cause binding in setting of GOF mutation

H/O RC (31 decks)

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