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Anna and louise > Rheumatology / immunology > Flashcards

Rheumatology / immunology Flashcards

1
Q

Described immunology changes in pregnancy

A

Shift away from cell-mediated immunity (T-helper 1 response) to humoral immunity (Th 2 response)

  • Cell-mediated = T-helper 1 + macrophages + cytotoxins / cytokines
  • Humoral = T-helper 2 + plasma cells + B cells –> antibodies and immunoglobulins

This probably occurs to protect the fetus from immunological attack by the mother
Changes are reversed postpartum

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2
Q

Effect of pregnancy on RA

A

70-80% improve during pregnancy
If improved in previous pregnancy, likely to improve in subsequent pregnancies
Improvement usually begins in first trimester

Most will relapse in the postpartum period (90% within first 4/12) - may be related to resurgence of T cell-mediated immunity. PP flare exacerbated by breastfeeding

Worsening symptoms may be due to withdrawal of disease-modifying anti-rheumatic drugs (DMARDs) in pregnancy

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3
Q

Effect of RA on pregnancy

A

Pregnancy outcomes if well-controlled RA are comparable to general population

Increased risk of SGA and PTB
Infants of women who have anti-Ro antibodies are at risk of neonatal lupus

Atlanto-axial subluxation is a rare complication of a GA
Very rarely, limited hip abduction is severe enough to impede vaginal delivery
Main concerns relate to medication safety during pregnancy and lactation

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4
Q

Pre-pregnancy counselling for RA

A

Avoid pregnancy during active RA
Avoid NSAIDs
- May affect blastocyst implantation and miscarriage (cause or association unclear)
Use contraception when taking teratogenic drugs
- Discontinue methotrexate, cyclophosphamide, chlorambucil, penicillamine, gold salts for >3/12 prior to conception

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5
Q

Drugs contraindicated in pregnancy

A 
Methotrexate
cyclophosphamide
chlorambucil
penicillamine
gold salts

Switch >3/12 prior

Leflunomide - stop >2y pre-pregnancy
Rutixamab - stop 6/12 pre

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6
Q

Corticosteroids in pregnancy

A

Safe
Preferable to NSAIDs
Give lowest possible dose
Increased risk of maternal HTN, PET, GDM, PTB and osteoporosis
Monitor BP and glucose levels regularly
Calcium and vitamin D supplements recommended

IV hydrocort in labour

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7
Q

Safe in pregnancy

A

Corticosteroids
Azathioprine (As fetal liver lacks enzyme to convert it)
Maybe NSAIDs (short courses in second trimester)
Sulfasalazine (given with folic acid 5mg)
Hydrochloroquine
Inflixamab (monoclonal antibody, stop in third trimester, crosses placenta but not teratogenic, no live vaccines for baby until >6/12, crosses breast milk but destroyed in fetal stomach)

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8
Q

Management of RA

A

Antenatal:

  • Screen for anti-Ro and anti-La
  • FBC (no benefit to monitoring ESR and RF)
  • Assess ROM at neck and hips

Aim for vaginal birth
Hydrocortisone 100mg IM q6h if taking >7.5mg prednisolone for >2/52 in pregnancy

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9
Q

Pathogenesis of SLE

A

Environmental triggers - UV light, viral infection
There is polyclonal B-cell activation, impaired T-cell regulation of the immune response and failure to remove immune complexes
Circulating non-organ-specific autoantibodies
Deposition of immune complexes causes vasculitis

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10
Q

Incidence of SLE

A

UK incidence 1 in 1000 women
Affects women > men (9:1)
Particularly during the childbearing years (15:1)

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11
Q

Bloods in SLE

A

FBC - normochromic normocytic anaemia, neutropenic, thrombocytopenia
Raised ESR
Normal CRP
Anti-nuclear antibody (ANA) - 96%
Anti-double-stranded DNA (anti-dsDNA) - 80% (more likely to have renal GN)
Anti-Sm antibodies (30-40%)
Anti-Ro (30%) / anti-La (20%)
Anti-phospholipid antibodies (aPLs) - 40%

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12
Q

Effect of pregnancy on SLE

A

Pregnancy and especially the puerperium increase the likelihood of flare from ~40% to 60%
Flare is more likely if disease has been active within 6/12 of conception

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13
Q

Effect of pregnancy on lupus nephritis

A

Risk of renal flare is 30%
Risk is much higher if the lupus nephritis is not in remission or only partial remission at conception (50-60%)
Delay pregnancy until >6/12 after flare

Pregnancy outcome is particularly affected by renal disease
Even quiescent renal disease a/w increased risk of fetal loss (up to 36%), PET (25-30%) and FGR - especially if proteinuria and HTN
Risk of preterm birth and LBW is ~30%

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14
Q

Effect of SLE on pregnancy

A 
Maternal risks:
VTE
PET (3x)
Maternal death (20x)
Risk of stroke 
Fetal risks:
Spontaneous miscarriage
Fetal death
Preterm delivery
FGR (1 in 4)
Neonatal lupus syndrome

In women in remission >6/12, without HTN, renal involvement, APS, risks are probably no higher than in the general population

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15
Q

Implication of anti-Ro and anti-La

A

Passively acquired autoimmunity
Autoantibodies cross the placenta –> immune damage to the fetus

Risk of transient neonatal cutaneous lupus is ~5%

Risk of congenital heart block is ~2%

Risk of neonatal lupus if previous child affected:

  • 16-18% with one affected child
  • 50% if two
  • Subsequent infants tend to be affected in the same way as their siblings

Taking hydroxychloroquine reduces risk

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16
Q

Presentation of cutaneous neonatal lupus

A

Cutaneous neonatal lupus is the most common
Usually manifests in the first 2/52 of life
Typical erythematous geographical skin lesions
- Usually on face or scalp
- Photosensitive - appearing after exposure to sun or other UV light
Rash disappears spontaneously within 4-6 months
Scarring is unusual
Advise avoiding sunlight and phototherapy

17
Q

Presentation and treatment of congenital heart block

A

Appears in utero
Permanent
15-20% mortality
In severe cases heart failure leads to hydrops fetalis and IUFD
Usually detected at 18-28/40 via fetal bradycardia, confirmed by detailed scanning showing atrioventricular dissociation with structurally normal heart
Maternal autoantibodies confirm neonatal lupus
Dexamethasone may reverse lesser degrees of heart block or prevent progression to complete heart block
Salbutamol to mother if bradycardia causing fetal heart failure

50-60% require pacemakers in early infancy

18
Q

Preconception counselling SLE

A

Assess disease - activity and organ involvement
Baseline proteinuria, renal function, and BP help guide prediction of risk to pregnancy
Outcome is improved if conception occurs during disease remission

Knowledge of antibody status (anti-Ro/La, aPLs, anti-dsDNA, complement C3 and C4)
- Help predict risk / neonatal implications

Review meds
Often on azathioprine and hydrochloroquine
- Both safe
Folic acid 5mg OD if on sulfasalazine

19
Q

Antenatal management of SLE

A

MDT
Low-dose aspirin from 12/40 if lupus nephritis, aPLs or vasculitis
Uterine artery Dopplers at 20-24/40 in at risk fetuses
Serial growth scans
Establish bloods baseline values with serial measurements with intervals depending on disease severity for:
- FBC, U&E, Cr, LFTs
- Anti-dsDNA and complement titres
- Quantify proteinuria

Hydroxychloroquine should be continue as stopping may precipitate flare
HTN management

20
Q

SLE disease flare antenatally

A

Features suggesting disease flare:

  • Symptoms - arthralgia, pleuritis pain, skin rash
  • Rising anti-dsDNA antibody titre
  • Red blood cells or cellular casts in urinary sediment
  • Fall in complement levels may help differentiate PET from active lupus - >25% fall in C3 or C4 suggests active SLE

Disease flare management:

  • Corticosteroids (first-line)
  • Azathioprine, NSAIDs, aspirin, or tacrolimus
21
Q

Features that suggest SLE flare over PET

A

Active disease within 6/12 conception, extreme fatigue, skin lesions, arthralgia, fever not due to infection

> 2x increase in PCR suggests worsening lupus nephritis or PET

PET

  • Elevated serum urate
  • Abnormal LFTs
  • Low placenta growth factor
  • Antithrombin deficiency

SLE

  • Leukopenia
  • Raised ds-DNA levels
  • Reduced complement levels (C3 or C4)
22
Q

What is Takayasu’s arteritis

A

Predominantly affects large arteries (including aorta and its major branches, pulmonary arteries)
Inflammation leads to fibrosis, stenosis and thrombosis
Aneurysms may also be a feature

Predominantly affects women (8:1) of childbearing age

Features: HTN, vascular bruit, fever, raised ESR/CRP

23
Q

Pregnancy implications of Takayasu’s arteritis

A

Increased risk of:
- PET
- FGR
There is an association between disease severity and adverse pregnancy outcome

Management in pregnancy
Corticosteroids = first-line
Azathioprine
BP control is important

24
Q

What is scleroderma?

A

Rare
More common in females (3:1), especially in childbearing year (15:1)
Autoimmune condition, causing fibrosis of skin +/- visceral organs and vasculopathy

Localised cutaneous form
Systemic sclerosis - Raynaud’s and organ involvement
CREST
- calcinosis, Raynauds, oesophageal involvement, sclerodactyly, telangiectasia

25
Q

Effect of pregnancy of sclerodermia

A

Localised cutaneous form - good prognosis
Early disease systemic sclerosis and/or renal involvement - risk of rapid overall deterioration and renal crisis
Raynaud’s - tends to improve
Risk of rapid overall deterioration and renal crisis - high risk of PP deterioration

26
Q

effect of scleroderma on pregnancy

A

Overall success rates: 70-80%
Increased risk of:
- Preterm delivery (25%)
- Miscarriage
- PET
- FGR
- Perinatal mortality
Venepuncture, venous access, BP measurement - may be difficult because of skin or blood vessel involvement
GA may be complicated by difficult intubation (partly from limited mouth opening)
Regional - may be difficult if skin involvement on back

27
Q

Management of scleroderma in pregnancy

A

Women with early diffuse disease should be advised to delay pregnancy until the disease has stabilised
Pre-pregnancy:
- Lung function tests
- ECHO
Women with multiple or severe organ involvement (pulmonary HTN, severe pulmonary fibrosis, renal involvement) should be advised against pregnancy

MDT
BP monitoring
Monitoring of fetal wellbeing
Steroid treatment for fetal lung maturity should be avoided - may precipitate a renal crisis
Benefits of ACE inhibitors in scleroderma renal crisis outweigh the risks to the fetus, and therefore use is justified if needed
Anaesthetic review`

28
Q

Why is sjogren’s syndrome important in pregnancy

A

70-80% have anti-Ro and anti-La

29
Q

Risks of type IV Ehlers Danlos

A

IV - Ecchymotic or vascular
High risk
Maternal mortality as high 25%
Increased risk of aortic and visceral rupture
Risk of uterine rupture, preterm delivery, skin fragility and poor healing

Avoidance of pregnancy or TOP recommended
C/s advised preterm (34/40) to reduce risk of uterine and aortic rupture of those with vascular EDS

Refer to geneticist pre-pregnancy for categorisation

30
Q

Risks of type III Ehlers-Danlos

A

Commonest form
May be a/w postural orthostatic tachycardia syndrome (but not a/w heart or aortic disease)
May have increased joint and back pain
Risk of preterm ROM, preterm cervical dilatation, precipitous labour, PPH, skin fragility and poor hearing
Prophylactic antibiotics in labour

Refer to geneticist pre-pregnancy for categorisation

31
Q

NSAIDs and pregnancy

A

Usually avoided, especially in the third trimester (discontinue by 32-34/40 if used at all)
May be used, especially short courses prior to 28/40 for control of arthritic pain if relative contraindication to steroids
May lead to oligohydramnios (via effect of fetal kidney, can lead to pulmonary hypoplasia) - Reversible after discontinuation
Premature closure of the ductus arteriosus (as they are prostaglandin synthetase inhibitors)

32
Q

Non-obstetric manifestations of APS

A 
DVT
Thrombocytopenia
Livedo reticularis skin disorder
Stroke
Superficial thrombophlebitis
PE
TIA
Haemolytic anaemia
Cognitive dysfunction
Renal disease or GIT disease, ocular disease, adrenal disease, osteonecrosis

Anna and louise (28 decks)

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