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MBBS VI: O&G > Maternal medicine > Flashcards

Maternal medicine Flashcards

1
Q

What is the maternal respiratory changes in pregnancy?

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2
Q

What is the maternal cardiovascular changes in pregnancy?

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3
Q

What is the maternal GI changes in pregnancy?

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4
Q

What is the maternal urological changes in pregnancy?

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5
Q

What is the maternal haematological changes in pregnancy?

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6
Q

What is the maternal endocrine system changes in pregnancy?

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7
Q

When do pregnant ladies get affected by hyperemesis gravidarum (nausea and vomiting)?
What are the general features?
What Ix done?
What complications?
What Mx?

A

Nausea and vomiting common in 1st trimester and occurs till 12 weeks of gestation. Affects 70% of pregnant women.
Excessive or intactable vomiting to the extent of dehydration, electrolyte imbalance, acid base imbalance, weight loss for 5%, ketosis or acetonuria.
Related to the production of hCG which stimulates the chemoreceptors in hypothalamus and higher risk in: multiple pregnancy, gestational trophoblastic disease, hyperthyroidism, UTI

Dx: CBC, RFT, LFT, TFT (70% have suppressed TSH or elevated fT4), MSU (rule out UTI), pelvic USG (rule out multiple pregnancy and GTD)

Complications: hypoNa and hypoK, Mallory Weiss tear, wernickes encephalopathy

Mx:
Dietary modifications (decrease protein and fat, increase carbs): small frequent meals with fluid in between. Avoid greasy and highly spiced foods. Vit B1 (thiamine) for Wernickes encephalopathy. Avoid iron supplements to prevent GI disturbances

Monitor patient: IO chart, daily body weight monitoring, BP and pulse monitoring, urine ketones
IV and fluid replacement (hypoNa,hypoK)
Antiemetics: metoclopramide, dimenhydrinate (H1 receptor antagonist)

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8
Q

What is the pathophysio of heart burn in pregnancy?
What is treatment?
What is prevention?

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9
Q

What is the pathophysio of constipation in pregnancy?
What is treatment?
What is prevention?

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10
Q

What is the pathophysio of urinary frequency in pregnancy?
What is treatment?
What is prevention?

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11
Q

What is the pathophysio of backache in pregnancy?
What is prevention?

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12
Q

What is the pathophysio of leg cramps in pregnancy?
What is treatment?
What is prevention?

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13
Q

What is the pathophysio of varicosities in pregnancy?
What is prevention?

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14
Q

What is the pathophysio of fainting and dizziness in pregnancy?
What is prevention?

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15
Q

What is the pathophysio of carpal tunnel syndrome in pregnancy?
What is prevention?

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16
Q

What is the pathophysio of pruritis in pregnancy? When does it happen?
What is management?

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17
Q

What are the different types of hypertension in pregnancy?

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18
Q

Define hypertension and proteinuria in pregnancy

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19
Q

What is the etiology of hypertension in pregnancy?

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20
Q

What is the development of the placenta and blood supply in normal pregnancy?

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21
Q

What is the pathophysio of hypertension in pregnancy (placental and systemic endothelial dysfunction)?

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21
Q

What are the SS of hypertension in pregnancy?

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22
Q

What is the workup for proteinuria in pregnancy?

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23
Q

What are the biochemical tests done for suspected hypertension in pregnancy?
What would the expected results be?

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24
Q

What is the medical treatment for chronic hypertension in pregnancy?
Why is traditional antihypertensives not used?

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25
Q

What is radiological tests for hypertension in pregnancy to assess fetus?

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26
Q

What is the medical management of gestational hypertension?

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27
Q

What needs to be monitored in preeclampsia?

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28
Q

What is the general management of eclampsia?

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29
Q

What is definitive management of eclampsia?

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Induction of labour/C-section: decision made by senior staff after the convulsions have been controlled taking into consideration the parity, maturity, presentation, engagement and the size of the fetus and pelvis. Labor should be closely monitored with adequate analgesia and 2nd stage shortened by instrumental delivery. Syntocinon infusion instead of syntometrine should be used to prevent primary post partum hemorrhage.
Steroids: betamethasone is steroid of choice to promote fetal lung maturity if gestation age <34 weeks. Accounts for 65% reduction of respiratory distress syndrome. Dexamethasone is associated with lower incidence of neonatal intracranial hemorrhage but is associated with higher NICU admission rate

Anticonvulsants
* MgSo4: IV infusion continued for 24 hours after the last convulsion or 24 hours after delivery in the case of prophylaxis.
If convulsions recur more than 20 mins after initial IV infusion than 2gm of MgSO4 slow IV injection over 5-10 mins should be given –> or other anticonvulsants such as diazepam or thiopentone
* Method of admin: infusion pump –> loading dose of 4gm of MgSO4 solution in 100ml NS given over 20 min IV
* Toxicity includes areflexia, respiratory depression, altered cardiac conduction and cardiac arrest
* Knee reflex, RR and urine output must be checked q1h and MgSO4 should be withheld when 1 of the following is present: absence of knee reflex, respiratory rate <16/min, urine output <30ml/hour

Antihypertensives
* Indicated in patients with BP >160/100mHg or mean arterial pressure >125mmHg
* Medications given to maintain diastolic pressure <100mmHg
* IV labetolol or hydralazine are choices

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30
Q

What are maternal and fectal factors for complications of preeclampsia and eclampsia?

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31
Q

What are the indications for prophylactic medication for preventing pre-eclampsia?
Contraindiations or precautions?
What further rtresting should be if early onset preeclampsia?

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32
Q

What is done for prevention of eclampsia?

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33
Q

What are the 2 types of hyperglycemia in pregnancy?
How are they defined?

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34
Q

What are the RF of gestational DM?

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35
Q

What is the pathogenesis of gestational DM?

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36
Q

What are the maternal complications of GDM?

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37
Q

What are fetal complications of GDM?

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38
Q

How may neonatal morbidity be increased in GDM?

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39
Q

What is the timing for screening of GDM?

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Early OGTT done between booking visit and 16 weeks. Indicated in patients with classical and locally identified risk factors for GDM
* Advanced maternal age (AMA) >35 years old
* Maternal obesity
* Maternal glycosuria
* Family history of DM
* Previous big babies (macroosmia)
* Previous unexplained stillbirth or abnormal babies

Routine OGTT done between 28-32 weeks
* All low risk antenatal patients booked before 32 weeks should be screened between 28-32 weeks of gestation
* Patients booked after 32 weeks should have a routine OGTT arranged as early as possible unless delivery is imminent
* Patients with negative result for early OGTT should still have a repeat OGTT performed between 28-32 weeks of gestation
* Patient presented or diagnosed with fetal structural anomalies not related to known chromosomal abnormaliteis should have GDM excluded by OGTT if not yet performed

75g OGTT
DM: fasting (>7mmol/L), 2 hours glucose level (>11.1)
GDM: fasting (5.1-6.9mmol/L, 1hr glucose level (10mmol/L), 2 hour glucose level (8.5-11mmol/L)

Glycated haemoglobin: HbA1c correlates with blood glucose concentration over the prior 2-3 months
Fructosamine: correlates with blood glucose concentration over the prior 2-3 w3eeks. Reflects glycemic control over a shorter period of time compared with HbA1c

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40
Q

What are the follow up clinics for GDM?

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41
Q

What are the obstretic issues with GDM?

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42
Q

What is the postpartum care for GDM?

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43
Q

What is medical treatment for GDM?

A

Oral hypoglycemic agents: metformin and glyburide (glibenclamide)

44
Q

What is the pathogenesis of SLE?

A
45
Q

What is the ddx for SLE?

A
  • RA
  • Systemic sclerosis: coexistence of Raynaud phenomenon and GERD are typically observed in systemic sclerosis. Expresses anti-Scl-70
  • Sjogrens syndrome: presents with objective signs of keratoconjunctivitis sicca and xerostemia. Expresses anti-Ro/SSA and Anti-La/SSB
  • Bechets disease: oral aphthae are present in almost all patients with Bechets syndrome. Other overlapping features include inflammatory eye disease, neurological disease, vascular disease and arthritis
  • Dermatomyositis and polymyositis: have more overt proximal muscle weakness. Patients with dermatomyositis have characteristic skin findings including Gottrons papules, heliotrope eruptinon and photodistributed poikiloderma
  • Mixed connective tissue disease (MTCD): overlapping feaetures of SLE, systemic sclerosis and polymyositis. Expresses anti U1 ribonucleic acid (anti-U1 RNP)
  • Overlap syndrome: distinct entity where patient is diagnosed to have 2 well defined rheumatological syndrome most commonly RA and SLE
  • Undifferentiated connective tissue disease (UCTD)
46
Q

What is the skin and mucous membrane involvement of SLE?

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47
Q

What is the respiratory, cardiac, vascular, GI, UG, MSS, CNS involvement of SLE?

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48
Q

What is the haematological, ophthalmological involvement and constitutional symptoms of SLE?

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49
Q

What is the SLICC diagnostic criteria for SLE?

A

4 out of 17 criteria including at least 1 clinical criterion and 1 immunological criterion or
Biopsy proven lupus nephritis with +ve ANA or anti-dsDNA

Clinical criteria
* Acute cutaneous lupus: malar rash, photosensitive lupus rash, maculopapular lupus rash. Subacute cutaneous lupus: non indurated psoriaform, annular polycyclic lesion (more common): resolve without scarring
* Chronic cutaneous lupus: discoic rash (localized above neck, generalized), hypertrophic (verrucous) lupus, lupus panniculitis, lupus erythematomsus tumidus
* Non scarring alopecia: diffuse thinning or hair fragility with visible broken hairs
* Oral or nasal ulcers
* Joint disease: tenderness in >2 joints and >30 mins of morning stiffness
* Serositis: typical pleurisy >1 day, pleural effusion. Pericardial effusion, pericardial rub, pericariditis by ECG (in absence of other causes such as infection, uremia and Dressler syndrome)
* Renal: urine protein to creatinine ratio or 24 hour urine protien representing 500mg protein/24 hours, RBC casts
* Neurologic: seizure, psychosis, myelitis, peripheral or cranial neuropathy, mononeuritis multiplex
* Haemolytic anemia
* Leukopenia or lymphopenia
* Thrombocytopenia

Immunologic criteria
* ANA
* Anti-ds DNA
* Anti-Sm
* Antiphospholipid (lupus anticoagulant, anti B2 glycoprotein I, anticardiolipin antibody)
* Low complement: low C3, C4, CH50
* Direct Coombs test: posible in the absence of haemolytic anemia

50
Q

What are the biochemical tests and expected results for SLE?

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50
Q

What are the antibody tests for SLE?

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51
Q

For SLE what is the renal prebiopsy evaluation?
What are absolute contraindications? Relative contraindications?
Most common complications?

A
52
Q

What is the classification of lupus nephritis, what is its clinical presentation?

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53
Q

What are the radiological Ix that may be done in SLE?

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54
Q

What is the pregnancy planning for SLE?
Can contraception be used?
How does pregnancy affect SLE?
How does SLE affect pregnancy?

A
55
Q

What is the medical treatment of SLE?

A

Antimalarial drugs: hydroxyzhloroquine is indicated in all patients (reduces flare rate, organ damage and mortality. AE: GI disturbance most common, hyperpigmentation, myopathy, corneal deposition, Bulls eye maculopathy
NSAIDs: indication for serotiis, arthralgia and myalgia
Immunosuppressants
* Corticosteroids: oral (prednisolone), IV (methylprednisolone)
* Azathioprine indicated in lupus nephritis, diseases refractory to hydroxychloroquine
* Mycophenolate mofetil indicated for lupus nephritis (preferred over cyclophosphamide), diseases refractory to HCQ. AE: diarrhea, anemia, leukopenia.
* Cyclophosphamide indicated for lupus nephritis, CNS diseases. AE: gonadal toxicity (male: oligospermia, female: infertility). teratogenicity (dont use in pregnancy), hemorrhagic cystitis, bladder cancer. Secondary malignnacy: leukemia, lymphoma. Myelosuppression: neutropenia/ leukopenia/thrombocytopenia.
* Cyclosporin A indicated for lupus nephritis. AE: nephrotoxicity, tremor, gum hyperplasia.
* Methotrexate indicated for arthritis, skin diseases. AE: interstitial pneumonitis, liver cirrhosis, myelosuppression (pancytopenia)
* Belimumab, rituximab indicated in refractory SLE. AE: B cell depletion, reactivation of HBV/ TBV, progressive multifocal leukoencephalopathy

56
Q

What is the clinical and biochemical features of SLE?
What are poor prognostic factors?

A
57
Q

  1. What is the clinical dx and which is most likely etiological dx?
  2. In addition to those that had been done already, what are the most relevant investigations, and what are the expected findings?
  3. What drugs are commonly used as specific treatment of this condition?
  4. Apart from the underlying condition, what associated complications require attention (i.e. monitoring, prevention and treatment)?
A
  1. Acute nephritic syndrome secondary to lupus nephritis
  2. Protein to creatinine ratio by 24 hour urine sample. Creatinine clearance by 24 hour urine sample (show impaired renal function), blood test: anti dsDNA, decreased C3/C4, increased CRP (suggestive of concomitant infection). USG kidneys (confirm kidneys not shrunken before doing biopsy), renal biopsy (normal clotting profile done before)
  3. Corticosteroids, cyclophosphamide, azathioprine/mycophenolate mofetil (maintenance therapy following cyclophosphamide)
  4. Hypertension, hyperlipidemia, complications of treatment (leukopenia, infection, alopecia (cyclophosphamide), amenorrhea (cyclophosphamide)
58
Q

Q1: What are the possible causes of fever in this patient?
Q2: What are the possible causes of this patient’s chest pain?
Q3: What further investigations would you undertake for this patient?
Q4: How should this patient be treated if her problem was secondary to her relapse alone?
Q5: What is the likely cause of this patient’s right hip pain?
Q6: How would you control this patient’s right hip pain?

A
  1. Relapse of underlying SLE: infection due to immunocompromised state –> SLE itself is immunocompromising
  2. Serositis (pleura/pericardium/peritoneum), pulmonary embolism +/-infarciton: can gice rise to pleuritic chest pain
  3. Delineate underlying infection: CXR, blood cultures, sputum and urine smears and culture. Delineate possible SLE relapse: ANA, anti dsDNA, serum C3 and C4, Commbs test. Delineate possible renal involvement during relapse: urine microscopy, 24 hour urinary protien and creatinine estimation, renal biopsy
  4. Increase dosage of immunosuppressant. Azathioprine substituted to a more potent agent such as cyclosphosphamide, cyclosporin A or mycophenolic acid
  5. Bone necrosis of right femoral head due to steroid usage
  6. NSAID, steroid dosage adjustment PT, referral to orthopedic surgeon
59
Q

What are the APL antibodies involved?

A

o Anticardiolipin antibodies (aCL) IgG or IgM ELISA
o Anti-β2-glycoprotein-I antibodies IgG or IgM ELISA
o Lupus anticoagulant (LA) test

60
Q

What are the clinical manifestations of antiphospholipid syndrome?

A
61
Q

What is the diagnostic criteria (clinical and lab criteria) for antiphospholipid syndrome?

A
62
Q

What are the biochemical tests for antiphospholipid syndrome and how are they done?

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63
Q

What is general treatment principles of antiphospholipid syndrome?

A
64
Q

Define placental abruption

A

 Also known as abruptio placentae
 Refers to partial or complete premature placental detachment after 20 weeks of gestation and prior to delivery of the fetus
* Diagnosis is typically reserved for pregnancy over 20 weeks of gestation

65
Q

What is the classification of placental abruption?

A
66
Q

What are maternal and fetal risk factors for placental abruption?

A
67
Q

What is the pathophysio of placental abruption?

A
68
Q

What is SS of placental abruption?
What are the complications?

A
69
Q

What is the dx and Ix done for placental abruption?

A
70
Q

What is the treatment principles of placental abruption?

A
71
Q

What is placenta previa?
When is it suspected?

A
72
Q

What is the classification of placenta previa?

A
73
Q

What are the maternal and fetal risk factors of placenta previa?

A
74
Q

What is the pathogenesis of placenta previa?
What is the pathophysio of bleeding?

A
75
Q

What is the clinical manifestation of placenta previa?
What are the associated conditions?

A
76
Q

What PE and ix done in suspected placenta previa?

A
77
Q

What is the general principles of management of placenta previa?

A
78
Q

What is the management of asymptomatic vs symptomatic placenta previa?

A
79
Q

What is velamentous umbilical cord insertion, vasa previa?

A
80
Q

What is the clinical presentation of velamentous cord insertion vs vasa previa?

A
81
Q

What is the radiological Ix done for velamentous cord insertion vs vasa previa?
What would be seen?

A
82
Q

What is the treatment of velamentous insertion of cord vs vasa previa?

A
83
Q

What are the causes of oligohydramnios (less amniotic fluid than expected)?

A
84
Q

What are the causes of polyhydramnios (more amniotic fluid than expected)?

A
85
Q

What are the features of amniotic fluid?
Production and removal of amniotic fluid?

A
86
Q

What are the fetal complications of oligohydramnios?

A

P - Pulmonary Hypoplasia
O - Oligohydramnios
T - Twisted skin (wrinkly skin)
T - Twisted face (Potter facies)
E - Extremities defect
R - Renal a genesis (bilateral)

87
Q

What are the risks of polyhydramnios?

A
88
Q

What is PE and radiological Ix done for suspected oligohydramnios/polyhydramnios?

A
89
Q

What is the treatment of oligohydramnios?

A
90
Q

What is the management of polyhydramnios?

A
91
Q

What are the RF for preterm premature rupture of membrane (PPROM)?

A
92
Q

What is the ddx for PPROM?

A

 Urinary incontinence
 Vaginal discharge
* Related to infection
 Perspiration

93
Q

What is the clinical manifestation of PPROM?
What is the clinical course?

A
94
Q

What PE and reults for PPROM?

A
95
Q

What biochemical tests done for PPROM?

A
96
Q

What radiological exam and general management of PPROM?

A
97
Q

Management of PPROM with evidence of intrauterine infection?

A

 Delivery under antibiotic coverage irrespective of gestation if there is
* Antibiotics that cross placenta barrier should be chosen
* Dosage should be large enough to maintain a therapeutic level in fetus
* Parenteral route should be chosen initially to achieve a therapeutic level quickly

98
Q

Management of PPROM with no evidence of intrauterine infection + gestation <34 weeks?

A
99
Q

Management of PPROM with no evidence of intrauterine infection + gestation >34 weeks?

A
100
Q

What is the effect of pregnancy on prolactinomas?
How is micro and macroadenomas managed?
What is a worrying symptom?

A

Pituitary gland undergoes global hyperplasia during pregnancy. The increase in size is accompanied by a concomitant increase in size and population of lactotroph cells and a progressive increase in serum prolactin. The placental estrogen surge during pregnancy has been shown to induce the mitotic activity of lactotrophic cells.
* Tumor cells in patients with prolactinomas express estrogen receptors –> possible tumor enlargement during pregnancy.

  • Small macroadenoma stop DA therapy once pregnancy is confirrmed. If symptomatic –> return for FU. Visual perimetry routinely done.
  • If substantial tumor growth shown in MRI, immediate reinstitution of DA therapy is appropriate
  • Large macroadenomas must be definitively treated before conception by either aggresive DA therapy or surgical evacuation of the bulk of the tumor.
  • If tumors are DA sensitive, patients should be maintained on DA therapy throughout pregnancy and informed that these drugs inhibit lactation.

Worrying symptom is headache/visual field loss

101
Q

If uncertain about PROM what test can be done?
What is the Mx if positive test?

A

Actim test to confirm low suspicion of PROM.
If small amount of amniotic fluid leakage it can be high water leak that seals off afterwards. Can go home. However requires antibiotic prophylaxis oral erthromycin + IV ampicillin followed by oral amoxicillin to avoid chorioamniotis regardless of GBS result.

MBBS VI: O&G (109 decks)

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