General/MCQs Flashcards

1
Q

Causes of oligohydramnios?

A

From head down:
1.Postdates
2. IUGR
3.Chromosomal anomalies
4. Duodenal atresia
5.Renal agenesis/dysgenesis
6.Polycystic kidneys
7.Urinary tract obstruction
8.PPROM
9.Fetal infection

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2
Q

List causes of Intrauterine demise?

A

There are maternal, placental and fetal causes.

Maternal:
- DM
- HTNsive disorders
- HbSS
- autoimmune diseases: SLE, thyroid disease, antiphospholipid antibody syndrome
- thrombophilias ( apa, prot c/s deficiency, factor v Leiden…)
- maternal infection (septicaemia, hypotension)

Placental:
- IUGR
- Placental infarction
- placental abruption
- feto-maternal haemorrhage (can occur with ECV)
- twin-to-twin transfusion syndrome

Foetal
- chromosomal abnormalities
- congenital abnormalities
- fetal viral and bacterial infections: TORCH, listeriosis, parvovirus
- immune haemolytic disease
- cord accidents (cord prolapse)
- fetal metabolic disorders

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3
Q

What are the causes of non-immune hydrops?

A
  • idiopathic (30%)
  • infections (parvovirus, syphilis, cmv, toxo, herpes simplex, leptospirosis, chagas disease)
  • anaemia (due to fetal infection, homozygous alpha thal)
  • chronic fetomaternal haemorrhage
  • twin to twin transfusion

** all are causes of intrauterine demise!!*

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4
Q

What are the side effects of tranexamic acid?

A

Nausea, vomiting, diarrhea, disturbance in colour vision

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5
Q

Which progesterone can virilize a female foetus?

A

Gestrinone

Patients should use barrier contraception

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6
Q

How does phaeochromoxytoma present in pregnancy?

A
  1. HTNsive crisis or paroxysmal HTN
    +/- 2. cerebral haemorrhage or 3. heart failure
  2. Circulatory collapse following delivery w/ palpitations, anxiety head ache, vomiting, glucose intolerance
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7
Q

What is the fetal loss rate associated with phaeochromocytoma?

A

15-50%

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8
Q

How is phaeo diagnosed?

A

Urinary vanil-lyl-mandelic acid

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9
Q

T/F. Phaeo causes preeclampsia?

A

FALSE

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10
Q

Which drugs may exacerbate myasthenia Gravis?

A
  • Lithium salts (inhibits excitatory neurotransmission)
  • magnesium salts (competitively inhibits ca)
  • propranolol beta blocker, can cause fatigue
  • aminoglycosides (genta/strepta/neomycin, amikagin..)
  • macrolides (clinda/erythromycin)
  • tetracycline
  • sulfonamides (bactrim), penicillin
  • fluroquinolones (ciproflox, levo/nor/ofloxacillin)
  • barbiturates
  • polymyxin b
  • procainamide
  • halothane
  • quinine
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11
Q

T/F. In pts with APA/antiphospholipid antibody syndrome ASA alone improves live birth rates?

A

False. ASA + heparin improves live birth rates

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12
Q

T/F. Thrombocytopenia is not a recognized complication of APA?

A

False

Increased thrombus formation uses up platelets

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13
Q

T/F. Acute hydramnios and broad ligament haematoma are causes of prerenal renal failure?

A

False. They cause postrenal renal failure by compressing and obstructing the ureters.

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14
Q

How does phenylketonuria affect the foetus?

A

Phenylpyruvate products cross the placenta and deposit in foetal brain tissue.

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15
Q

What kind of inheritance is assoc with phenylketonuria?

A

Autosomal recessive

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16
Q

Risk of foetus being affected if mother has phenylketonuria?

A

1 in 4 (25%), if partner is a carrier

If partners not a carrier. All children would be carriers

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17
Q

What is phenylketonuria?

A

An autosomal recessive condition that causes deficiency of phenylalanine hydroxylase

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18
Q

Treatment for PKU

A

Diet low in phenylalanine and tryptophan for 20days/ into adulthood.
Has a GOOD outcome.

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19
Q

Patient with a viable intrauterine pregnancy presents with mild abdominal pain and difficulty passing urine for the past 12 hrs. Vitals are stable and abd exam shows a distended lower abdomen.
Justify your next step.

A

Immediately catheterize and reassure. It is common for patients with a retroverted uterus to have acute urinary retention in the early weeks of gestation.

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20
Q

Patient presents with a heterotopic pregnancy at 10 weeks gestation. Live intrauterine gestation and ectopic w/o cardiac activity. Justify your next step?

A

Offer laparoscopic salpingectomy as it is a minimally invasive procedure. It will allow for removal of the ectopic pregnancy with minimal disturbance to the uterus. Thus allowing the intrauterine pregnancy to continue.

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21
Q

Next step for a patient with a spontaneous, viable 7 week, quadruplet pregnancy?

A

Extensive counselling about the risk of pregnancy to both mother and the fetuses.
- Counsel about selective fetal reduction.

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22
Q

What is Wernicke’s encephalopathy and what are the features?

A

Wernicke’s encephalopathy is a medical emergency that occurs due to thiamine deficiency.

  • presentation is gradual and episodic and can progress to being fatal BUT reversible.
  • permanent impairment is common and complete remission occurs in 29%.
  • Features:
    Confusion
    Drowsiness/memory problems
    Blurred vision
    Unsteadiness
    Opthalmoplegia
    Nystagmus
    Hyporeflexia or areflexia
    Finger to node ataxia
    Gait ataxia
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23
Q

What is the mortality rate of Wernickes encephalopathy? What happens if it progresses?

A

10-15%

Can progress to KORSAKOFF’s encephalopathy
— causes 1. Antegrade & retrograde amnesia, b.Confabulation

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24
Q

Treatment for Wernicke’s encephalopathy?

A

Vitamin B1/thiamine:
50mg po tds or
200mg IV od x 3/7 or
Pabrinex contains 250mg thiamine
— and also: riboflavin, pyridoxine, nicotinamide and vit C

25
Q

W.r.t carbohydrate metabolism which substrates are used for energy in the fetus and mother?

A

Glucose and amino acids for fetus

Ketone bodies, fatty acids and glycerol for mother

26
Q

As pregnancy progresses, how does the mother’s body compensate for the increased insulin resistance?

A

Hyperplasia of the islet cells of Langerhaans in the pancreas increases insulin production.

27
Q

What is serum ferritin, what is its role and how is the value interpreted?

A
  • it’s a stable glycoprotein that ACCURATELY reflects iron stores in the absence of inflammatory changes.
  • is an acute phase reactant = levels rise with active infection/inflammation.
  • It is the first lab test to become abnormal when iron stores decrease.
  • BEST test to determine iron deficiency anaemia in pregnancy
28
Q

How do ferritin levels change in pregnancy?

A

If adequate stores preconception, levels rise initially
- then progressively fall after 32 weeks to 50% prepregnancy level.
– due to haemodilution and mobilization of iron to fetus.

29
Q

What level of ferritin indicates deficiency? How do u treat?

A

Treat when levels fall below 30 microgram/L, as this indicates early iron depletion.

Levels <15microgram/L = iron depletion

Treat with oral iron supplements

30
Q

Incidence of UTI in pregnancy?

A

8%

31
Q

Risk of recurrent UTI in pregnancy?

A

4-5%

32
Q

What are the possible complications of UTI in pregnancy?

A

Maternal:
Chorioamnionitis
Endometritis
Preterm labour
Preterm delivery

Foetal:
FGR
Neurodevelopmental delay
Stillbirth
Preterm birth
Increased perinatal morbidity & mortality

33
Q

Why is the risk of UTI increased in pregnancy?

A

Due to the physiological changes of pregnancy which include:
- dextrorotation of uterus and possible compression of right ureter
- increased prostaglandins decreases ureteric peristaltic and causes ureteric dilation
- decreased bladder
- changes in bladder volume

34
Q

Features of phaeochromocytoma?

A
  • bilateral 10%
  • familial 10%
  • assoc with HTN in most cases
  • headache, palpitations, sweating, arrhythmia
  • tx: medical management preferred in pregnancy- alpha blockers first then beta blockers
35
Q

Who should be involved in managing a pregnant patient with a prolactinoma?

A
  • obstetrician
  • endocrinologist
  • ophthalmologist
36
Q

How should a pregnant patient with a microadenoma be managed?

A
  • By a multidisciplinary team made of the obstetrician, endocrinologist and ophthalmologist.
  • this pt has a <5% risk of acute symptomatic enlargement, hence meditation can be stopped (by endocrinologist).
  • pt should be advised of symptoms to look out for and return for review if any are noticed, namely;
    —-headache (caused by pressure on the dura) and visual disturbances (caused by compression of the optic nerve by tumour enlargement).
37
Q

How should a pregnant patient with an asymptomatic macroadenoma be managed?

A
  • By a multidisciplinary team made of the obstetrician, endocrinologist and ophthalmologist.
  • The risk of symptomatic exacerbation is 30-35%
  • the decision to continue bromocriptine should be individualized and made in conjunction with the endocrinologist.
  • these patients should have visual testing done every 3 months.
  • If she becomes symptomatic then she should be evaluated monthly.
  • Cabergoline is used in refractory cases.
38
Q

Effect of bromocriptine/cabergoline on the fetus? Any maternal risks?

A

Neither are known to be teratogenic.

Long term use is associated with a small increased risk of heart valve fibrosis.
— consider ECHO if she has a significant murmur.

39
Q

What is the treatment of severe TTTS presenting before 26 weeks gestation?

A

Fetoscopic Laser coagulation of placental vessels.

40
Q

What kind of study includes all the patients initalially recruited in the final analysis?

A

Intention to treat analysis

41
Q

How is the sample size of a study calculated?

A

Using the Power calculation.
- determined by the sample size and the difference between the magnitudes of difference between the outcomes.

42
Q

Treatment for DIC

A

FFP

43
Q

Choices of toxolytic for a patient with uterine inversion

A

Terbutaline 0.1 - 0.25mg iv
Nitroglycerin 0.25 - 0.5 mg iv
MgSO4 4-6g IV over 20min

44
Q

How is breast cancer diagnosed in clinic?

A

Triple assessment:
- clinical assessment
- mammography/ ultrasound
- FNAC/ core needle biopsy

*fine needle aspiration cytology

45
Q

Causes if pituitary insufficiency?

A

Four (4):
1. Autoimmune lymphocytic infiltration
2. Pituitary apoplexy/Sheehan’s syndrome
3. Tumour
4. Surgery

46
Q

What are the key points about Sheehan’s syndrome/pituitary apoplexy?

A
  • occurs after massive pph➡️ pituitary hypoperfusion, ischaemia and necrosis.
  • may present postpartum with failure to Lactate
  • onset may be insidious with average delay of 7 years for diagnosis
    ■may present as:
    ▪︎Loss of public hair (acth)
    ▪︎hypothyroidism (tsh)
    ▪︎vaginal atrophy (ldh,fsh, no oestrogen)
    ▪︎oligo/amenorrhea
    — some may conceive but they are usu. infertile
    —- in pregnancy give thyroxine 100-200mcg/day and steroids/prednisone 5mg am, 2.5mg pm and readjust doses postpartum.
47
Q

What percentage of women experience severe nausea and vomiting?

A

30%

48
Q

What is the PUQE score?

A

The Pregnancy Uniqe-Quantification of Emesis Score is used to CLASSIFY the SEVERITY of nausea and vomiting.

■Looks at 3 criteria (in the past 12 hrs):
▪︎ duration of nausea (past 12 hrs)
▪︎# of vomiting episodes (12hrs)
▪︎# of episodes of dry heaves (12 hrs)

■ Baded on total score the NVP is classified as mild, moderate or severe
▪︎Mild: score of 4-6
▪︎Moderate: score of 7-12
▪︎Severe: 13 and above

49
Q

T/F regarding Cushing syndrome: pituitary adenomas are more common than adrenal adenoma in pregnancy

A

False

Adrenal adenomas are more common.
- only produce excess cortisol (adenoma of Zona fasciculata only) so is more likely to be found in pregnancy as fertility is not impaired.

Go = Salt/mineralocorticoids
Find = Sweet/glucocorticoids
Rex =Sex/androgens

*zona glomerulosa
*zona fasciculata
*zona reticularis

50
Q

Preferred screening test for Cushings syndrome? Other diagnostic tests

A

24hr free urinary cortisol
- usu elevated 4 times normal

Others:
Dexa suppression test with 8mg dexa - identifies adrenal (adenoma production reduced 50%) vs ectopic (not suppressed).
U/S
MRI - primary pituitary disease/adenoma (Cushings disease) increases ACTH production (adrenal hyperplasia) and– thus elevates circulating cortisol (Cushings syndrome).
▪︎Increased ACTH = adrenal hyperplasia, Increases androgens = negative feedback on pituitary = decreased LH and FSH = oligo/anovulation = decreased fertility

51
Q

20 y.o, 30 wks, 15 day h/o productive cough and fever. BMI of 19 and GDM since 20 wks gestation. She has poor weight gain. What’s her diagnosis? Key points of the diagnosis?

A

Cystic fibrosis

  • up to 20% have GDM or preexisting DM
  • poor weight gain usually
  • 25% deliver prematurely
  • FEV1 <50% [or even 70%] essential prior to safely starting pregancy
52
Q

Complications of prolonged Heparin use?

A
  1. Heparin induced thrombocytopenia
  2. Osteopenia
  3. Haemorrhage
  4. Hypersensitivity
53
Q

What are the benefits of Unfractionated heparin?

A
  1. Has shorter half life than LMWF
  2. Completely reverses by protamine sulphate
  3. Required internal between UFH and regional analgesia is shorter than LMWH (4hrs vs 12hrs)
  4. Less concern about neuraxial haematomas
54
Q

Disadvantages of UFH?

A
  1. Increased risk of heparin induced thrombocytopenia
  2. Platelets should be monitored every 2-3hrs from day 4-14 or until heparin is stopped.
55
Q

Patient with rheumatoid arthritis. Which medication is safe for pregnancy?
Certolizumab, etanercept, infliximab, rituxomab?

A

Certolizumab is a pregnancy friendly anti-TNF drug.

Does not actively cross plaventa therefore doesn’t accumulate in foetus.
Safe in all trimesters.

56
Q

Pt with Rheumatoid arthritis. Which drug should be stopped prior to conception?

A

Rituximab

A monoclonal anybody that depletes B cells.

57
Q

In UK what percentage of deliveries are:
A. Via csection
B. Elective csection
C. Emergency csection

A

A. 25%-30%
B. 10%
C. 15%

58
Q

How long should a ctg trace be kept?

A

Indefinitely ideally if there is a concern that the baby could experience developmental delay. Store them electronically.

If no concerns about neonatal development, keep for 25 year