UW Antiphospholipid + SLE 02-17 (1) Flashcards
UW. Antiphospholipid. table. clinical. vascular thrombosis?
Arterial or venous
UW. Antiphospholipid. table. clinical. pregnancy morbidity? 3
> = 3 consecutive, unexplained fetal losses before 10th week
> = 1 unexplained fetal losses after 10 week
> =1 premature births of normal neonates before 35th week due to preeclampsia, eclampsia, or placental insufficienty
UW. Antiphospholipid. table. clinical. pregnancy morbidity.
…
> = 1 unexplained fetal losses after 10 week
> =1 premature births of normal neonates before 35th week due to preeclampsia, eclampsia, or placental insufficienty
> = 3 consecutive, unexplained fetal losses before 10th week
UW. Antiphospholipid. table. clinical. pregnancy morbidity.
> = 3 consecutive, unexplained fetal losses before 10th week
…
> =1 premature births of normal neonates before 35th week due to preeclampsia, eclampsia, or placental insufficienty
> = 1 unexplained fetal losses after 10 week
UW. Antiphospholipid. table. clinical. pregnancy morbidity.
> = 3 consecutive, unexplained fetal losses before 10th week
> = 1 unexplained fetal losses after 10 week
…
> =1 premature births of normal neonates before 35th week due to preeclampsia, eclampsia, or placental insufficiency
UW. Antiphospholipid. table. Labs?3
lupus anticoagulant
anticardiolipin antibody
anti-beta2 glycoprotein antibody I
UW. Antiphospholipid. table. criterion?2
1 clinical + 1 lab. criterion must be met
UW. antiphospholipid.
APS is an autoimmune disorder caused by antiphospholipid antibodies (eg, lupus anticoagulant, anticardiolipin antibody) that create a hypercoagulable state leading to venous and/or arterial thrombosis (eg, transient ischemic attack).
During pregnancy, APS can cause placental vessel thrombosis, which may result in Recurrent pregnancy loss or in other pregnancy complications (eg, preeclampsia, placental insufficiency).
UW. antiphospholipid. Due to the high risk of venous and/or arterial thrombosis, patients require …….
require chronic anticoagulation.
UW. antiphospholipid. antogoagulation in pregnant?
pregnant patients receive low molecular weight heparin.
UW. antiphospholipid. anticoagulation in non-pregnant?
Nonpregnant patients are anticoagulated with warfarin
UW. etiologies for recurrent pregnancy loss.
There are multiple etiologies for RPL, including
structural (eg, uterine anomaly),
genetic (eg, aneuploidy), a
nd endocrine (eg, diabetes mellitus) causes.
However, in this young woman (UW case) who has also had a prior episode of sudden weakness and slurred speech (suggesting a transient ischemic attack), the most likely etiology of her RPL is antiphospholipid antibody syndrome (APS).
UW. Antiphospholipid-antibody syndrome (APS) is ……..? CP?
A prothrombotic autoimmune disorder that can present with recurrent pregnancy losses, arterial or venous thrombosis, and mild thrombocytopenia.
UW. Antiphospholipid-antibody require what?
APS require anticoagulation (eg, low-molecular-weight heparin in pregnant patients) to decrease the risk of complications.
UW. reccurent loss + Submucosal and intracavitary uterine fibroids. how is caused?
Submucosal and intracavitary uterine fibroids may cause RPL due to interference with implantation.
UW. recurrent + Subserosal fibroids???
Subserosal fibroids are located outside the uterine cavity and therefore typically DO NOT interfere with implantation or cause miscarriage.
only submucosal and intracavitary
UW case. 35yo + gravida 4 para 1 aborta 2. previous losses in early first trimester. now menses 7 weeks ago. 6 months ago had episode of slurred speech and sudden right arm weakness, that resolved after 2 days. Now UG empty uterus, hCG 23, closed cervix, no bleeding, uterus slightly enlarged, irregular shaped, ug - 2c, subserosal fibroid. BMI 32.
Cause of patients miscarriage?
Hypercoagulable state
UW. Antiphospholipid-antibody syndrome (APS). Antiphospholipid antibodies disrupt the function of …. and cause…..???
disrupt the function of platelets and vascular endothelial cells to create a hypercoagulable state.
UW. Antiphospholipid-antibody syndrome (APS).
The initial presentation of APS is often an unprovoked arterial or venous thrombosis (eg, stroke, deep venous thrombosis).
What additional presentation in pregnancy?
In pregnant patients with APS, persistent thrombosis of placental vessels causes pregnancy complications or recurrent pregnancy losses, as in this patient
UW. Antiphospholipid-antibody syndrome (APS).
typical thrombotic CP + no labs done yet to confirm. Next step in Mx?
Although additional antibody testing is needed to confirm the diagnosis of APS in this patient, the best next step is to initiate anticoagulation to decrease her risk of thrombosis and pregnancy complications.
In pregnant patients = low-molecular-weight heparin
UW. Antiphospholipid-antibody syndrome (APS).
APS antibodies (3 were mentioned) can cross react with what???????
These antibodies can cross-react with a VDRL test to produce a false-positive result.
In case was positive VDRL.
UW. Antiphospholipid-antibody syndrome (APS). APS antibodies (3 were mentioned) can interfere with what blood components?????
they can also interfere with coagulation test reagents, resulting in an artificially prolonged activated PTT. Mild thrombocytopenia (immune mediated) is typical.
UW. Antiphospholipid-antibody syndrome (APS). what CBC finding is typical?
Mild thrombocytopenia (immune mediated) is typical.
UW. Case: 25y/o. prior 2 pregnancies ended in first-trimester spontaneous abortions. Now 6 weeks gestation. Labs.: plt 98k; ADTL 46s; PT 10s; VDRL - positive; FTA-ABS - negative. UG - 6 weeks fetus. Best next step Mx?
LMWH.
Despite need to do antifosfolipid antibodies to confirm, but give anticoagulation to decr. risk for thrombosis and pregnancy complications. Bet atsakymuose buvo tik medikamentai, varianto kad daryti labs tai nebuvo.
UW. antifosfolipid. in case was VDRL - positive; FTA-ABS - negative. why not syphilis?
Syphilis, which is classically diagnosed when a screening test (eg, VDRL, a nontreponemal test) and a subsequent confirmatory test (eg, fluorescent treponemal antibody absorption [FTA-ABS], a treponemal test) are both positive.
This patient’s VDRL is likely a false-positive given her APS, and confirmatory testing with FTA-ABS (more specific than nontreponemal testing) is negative, making syphilis unlikely
UW. Antiphospholipid-antibody syndrome (APS). you give LMWH in pregnancy. What to do after pregnancy?
After delivery, this patient may be transitioned to warfarin.
UW. Antiphospholipid-antibody syndrome (APS) Vs SLE? CP
SLE - cause spontaneous abortion and thrombocytopenia, patients typically have additional renal and rheumatic disease (eg, lupus nephritis, arthritis). !!!!!!!!
UW. SLE Tx? (in comparison to antiphospholipid)
Corticosteroids (eg, prednisone) can be used to treat systemic lupus erythematosus.
UW. Antiphospholipid-antibody syndrome (APS) Vs SLE.
SLE is often associated with APS due to shared antibodies (eg, lupus anticoagulant).
.
UW. What lab abnormal in SLE which is normal in antiphospholipid?
Abnormal urinalysis due to lupus nephritis
UW. Corticosteroids are not used to treat APS.
only SLE
.
UW. SLE nephritis in pregnancy. CP?4
edema
malar rash
arthritis
hematuria
UW. SLE nephritis in pregnancy. labs? 4
nephritic range proteinuria
urinalysis with RBC and WBC casts
decr. complement levels
incr. AN titers
UW. SLE nephritis in pregnancy. Dx?
renal biopsy
UW. SLE nephritis in pregnancy. Obstetric complications? 5
preterm birth
C/s
preeclampsia
fetal growth restriction
fetal demise
23yo + primigravid + comes to EM due to decreased fetal movement for the past few days, regular, nonpainful uterine contractions but no vaginal bleeding or leakage of fluid. Estimated to be at 38 weeks. She has no known medical conditions but has had fatigue and joint stiffness for the past month. Temp 37,2, BP 128/86, pulse 94/min. Fundal height is 37 cm. Has an erythematous, confluent facial rash. The neck is supple. Cardiopulmonary examination is normal. The uterus is nontender. Fetal heart rate tracing is shown in the following exhibit [fetal bradycardia]. Most likely cause of this patient’s fetal heart rate tracing?
FETAL AV BLOCK
UW. Patients with SLE have an increased risk of obstetric complications, which can be maternal (eg, preeclampsia) or fetal (eg, neonatal lupus, intrauterine fetal demise).
.
UW. SLE. Neonatal lupus occurs due to passive placental transfer of maternal ……. 2??
anti-SSA (Ro) and anti-SSB (La) antibodies (which commonly occur in Sjogren but are also seen in ~30% of patients with SLE).
UW. SLE. Neonatal lupus. Primary findings? Cp 2
Fetal findings are primarily cardiac and cutaneous (eg, scalp or periorbital rash).
UW. SLE. Neonatal lupus. Most serious complication? when develops - weeks?
The most serious complication is fetal atrioventricular (AV) block, which develops at 18 to 24 weeks gestation.
UW. SLE. Neonatal lupus. mechanism of fetal AV block?
maternal autoantibodies binding to fetal cardiac cells and causing irreversible injury to the AV node
UW. SLE. Neonatal lupus. HR in fetal AV block?
Without normal AV conduction, the ventricular heart rate (eg, 50-80/min) determines the baseline fetal heart rate.
On fetal heart rate tracing, this appears as persistent fetal bradycardia (ie, <110/min).
UW. SLE. Neonatal lupus. With prolonged complete heart block what may manifest? 2
cardiomyopathy and hydrops fetalis may develop.
UW. SLE. Neonatal lupus. What is required if decreased fetal movements?
Therefore, this patient with decreased fetal movement requires additional testing (eg, biophysical profile, fetal growth ultrasound) and possible delivery.
UW. SLE + neonatal lupus. Congenital hypothyroidism. CP, when?
lethargy and bradycardia days to weeks after delivery.
Fetuses in utero are typically unaffected because some maternal thyroid hormone crosses the placenta
UW. SLE + neonatal lupus. cia prie sitos temos.
neonatal sleep. is related to brady?
NO!!! bradycardia is always abnormal.
Sleep - maybe a bit decr. frequency of accelerations, but HR normal.
UW. SLE + neonatal lupus.cia prie sitos temos.
incorrect gestational age. is related to brady?
NO!!! bradycardia (ie <110 is always abnormal)
fetuses at <32 weeks gestation have lower-amplitude accelerations and less variability
UW. SLE + neonatal lupus.cia prie sitos temos.
Intraamniotic infection, CP?
FETAL TACHY (not brady) + fever + uterine tender.
UW case. 26y/o + 34 weeks gestation + in EM due to decreased fetal movement for the past day. No prenatal care.
First 2 pregnancies ended in miscarriages at 8 weeks gestation. Now new pregnancy with new partner. BP 134/88, HR 98, temp. 37.5 C. Fundal height is 30 cm. UG reveals a singleton fetus with normal anatomy but no cardiac activity. Biparietal diameter and head circumference measure at 34 weeks gestation, and femur length and abdominal circumference measure at 30 and 28 weeks, respectively. The placenta is anterior, and the amniotic fluid index is 4 cm (normal: 5-24). Complete blood count is normal and maternal blood type is O positive.
Cause of fetal demise?
UTEROPLACENTAL ARTERY THROMBOSIS
multiple abortions = suspect antiphospholipid
UW. in antiphospholipid, what arteries affected?
uteroplacental arteries (ie, spiral arteries), which perfuse the placenta
UW. Intrauterine fetal demise, or stillbirth. Cause groups? 3
The underlying cause may be fetal, placental, or maternal.
UW. Intrauterine fetal demise, or stillbirth. Evaluation in case of it?
evaluation includes fetal studies (eg, autopsy, karyotyping), gross and microscopic examination of the placenta, and maternal testing guided by patient history.
UW. Intrauterine fetal demise, or stillbirth + antiphospholipid.
Uteroplacental artery thrombosis in the FIRST trimester typically results in pregnancy loss because …..???
the developing placental trophoblasts are highly sensitive to decreased perfusion
UW. Intrauterine fetal demise, or stillbirth + antiphospholipid.
The effects of thrombosis in the THIRD trimester are more insidious:???
Placental perfusion gradually decreases to the point of uteroplacental insufficiency, impaired fetal oxygenation/nutrient supply, and fetal growth restriction (eg, fundal height 30 cm at 34 weeks).
UW. Intrauterine fetal demise, or stillbirth + antiphospholipid. how develops uteroplacental insufficiency and fetal adoption?
Develops gradually, the fetus can initially adapt by redistributing blood flow to vital organs (eg, brain, heart) at the expense of the abdominal viscera, which causes an asymmetric or head-sparing pattern of growth restriction (eg, normal head measurement but lagging abdominal circumference).
Once the oxygen and nutrient supply decreases below the threshold for maintaining the vital fetal organs, stillbirth occurs.
UW. Intrauterine fetal demise, or stillbirth. antiphospholipid vs Chromosomal aneuploidies (eg, trisomy 13, trisomy 18).
Commonly diagnosed in stillborn infants and associated with fetal growth restriction. However, the growth restriction pattern is usually symmetric, and additional fetal anomalies (eg, microcephaly, cardiac defects) are typically present.
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