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H/O RC > Hemostasis/Thrombosis > Flashcards

Hemostasis/Thrombosis Flashcards

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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

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A

anticoagulation only
thrombolysis only if severe

21
Q

Bethesda unit definition and high tire cutoff

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A

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

BU>5 is high titre

22
Q

Mgt bleeding with inhibitor

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A

FEIBA = PCC
factor replacement (if low titre)

23
Q

Hypofibrinogenemia DDx

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A

malignancy
asparaginase
DIC
liver failure

24
Q

thrombin actions

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A

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

25
Endogenous inhibitors of coagulation
TFPI antithrombin: inhibits Xa, thrombin, IXa, XIa protein C/S thrombomodulin heparan sulfate
26
Describe fibrinolytic system
tpa converts plasmingen to plasmin plasmin degrades fibrin inhibition by PAI-1, a2-antiplasin, TAFIa
27
Vitamin K dependent factors
II, VII, IX, X, C, S
28
false positive prolonged coags DDx
LA Deficiency XII, prekallikrein, HMWK underfilling tube (excess citrate) heparain contamination delayed processing polycythemia (less relative plasma) difficult draw (factors consumed)
29
Neonatal factor levels
all are low except: - fibrinogen (N) - VIII (N/high) - VWF (N/high)
30
Factor pharmacokinetics Hemo A vs B
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
VWF genetics, function
chromosome 12 adhesion: cell surface collagen to plt GP1b/IX aggregation: plt-plt binding FVIII chaperone Multimers cleaved by ADAMTS13
32
ABO relationship to VWF
O - lowest VWF AB - highest VWF
33
VWD inheritance
aut dom type 3 - aut rec type 2N - compound heterozygous
34
Acquired VWD conditions
WT hypothyroid SLE congenital cardiac defects
35
VWD subtype pathophys
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
VWD subtypes with: - Act:Ag >0.6 - decreased multimers - RIPA + - decreased VIII binding
- Act:Ag >0.6: 1, 2N - decreased multimers: 2A, 2B - RIPA (ristocetin induced plt aggregation) + : 2B - decreased VIII binding: 2N
37
APS non-criteria manifestations
- 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
CAPS criteria and mgt
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
Stroke RF
SCD heart disease acute systemic: infection, dehydration, IDA, prothrombotic, moyamoya
40
Stroke mgt - cardioembolic - dissection - neonatal
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
Describe primary hemostasis
1) adhesion: collagen-plt binding (GP1B-IX-V) 2) activation: granule release 3) aggregation: GPIIb-IIIa activation
42
plt granule contents and fxn
dense: ADP - amplifies plt activation alpha: VWF and fibrinogen - amplifies adhesion/aggregation
43
Draw the coagulation cascade
44
Hemophilia severity
Severe: <1% Mod: 1-5% Mild: 5-40%
45
When to check for an inhibitor
- monthly for first 50 exposure days - pre-op - bleeding episode not responsive to factor
46
Inhibitor formation risk
H-A 30% H-B 5% <1% after 50 exposure days
47
Factor XIII deficiency manifestations
umbilical stump bleeding ICH
48
Explain RIPA assay
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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