Medical disorders in pregnancy

2. Asthma
Pulmonary embolism

3.  asthma is a common chronic inflammatory disease of
the airways characterized by variable and recurring
symptoms, reversible airflow
obstruction and bronchospasm.[2] Common symptoms
include wheezing, coughing , chest tightness, and shortness
of breath.[3]
 The MOST COMMON chronic disease in pregnancy.
(Affecting 3-12% of pregnant women)
 The inheritance risk of asthma for the fetus is around 6-30%
 Severity of asthma during pregnancy;
1/3 stable, 1/3 worsens, 1/3 improves.
 According to prospective study:
 Exacerbations of asthma are more likely to occur in women
with severe asthma than mild asthma.
 Most episodes occur around 24-36 weeks of pregnancy

4.  Due to prolonged maternal hypoxia in women with
symptomatic asthma, FGR (Fetal Growth Restriction) is
more common for them than in non-asthmatic women.
 Asthma does NOT seem to be a risk factor for pre-
eclampsia (though there is an increase in gestational
hypertension).
 Asthma does NOT usually affect labour and delivery (and
attacks are uncommon in labour).
 The risk of exacerbations does NOT increased by
postpartum. (Usually, those whose asthma deteriorated
during pregnancy will return to pre-pregnancy levels before
three month after birth).
 Maternal and fetal morbidity is DECREASED by adequate
management.

5.  regular medications should be continued throughout labor
 Parenteral steroid cover may be needed for those who are on regular
steroids
 bronchoconstrictors, such as ergometrine or prostaglandin F2α, should
be avoided.
 Adequate hydration is important in labor, and regional anesthesia
(selective epidural) favored over general, to decrease the risk of
bronchospasm, hyperventilation , provide adequate pain relief and to
reduce oxygen consumption and respiratory effort (all in which known to
aggravate the disease )

6. Many women with asthma are concerned
about the effect of drugs on the fetus, and
this can lead to inappropriate cessation of
treatment in early pregnancy.
 it is safer to take asthma drugs in pregnancy
than to leave asthma uncontrolled.

7.  Inhaled beta-sympathomimetics are safe, as is
theophylline, although its metabolism is altered and
drug levels need to be monitored.
 Long-acting B 2 agonists like salmetrerol do not cause
fetal malformation or FGR in prospective studies and
there is limited systemic absorption.
 Inhaled corticosteroids prevent asthma exacerbations
in pregnancy and have been shown to be safe with no
association with fetal malformations or perinatal
morbidity in large studies and reviews.
 Oral corticosteroid use in the first trimester has been
associated with an increased risk of fetal cleft lip or
palate in epidemiological studies, but the increase in
risk is small and not confirmed in other work.
 Data are scarce on the safety of the relatively newer
leukotriene antagonists, although no adverse
outcomes have been reported

8.  Pregnancy is a time to improve asthma care.
 ENCOURAGE smoking cessation.
 ENSURE patient education regarding condition
and adequate use of medications.
 ENSURE optional control and response to
therapy.
 MANAGE exacerbations aggressively and avoid
delays in treatment
 MANAGE acute attacks as in non-pregnant
women
 OFFER a multidisciplinary team approach

10.  Enhanced blood coagulability in pregnancy is due
to increased factors 2, 7, 8, 9 and 10.
 Vascular stasis is the strongest predisposing factor
with decreased pelvic and lower limbs blood flow.
 Mediating factor is frequently endothelial injury
from traumatic delivery or Cesarian Section

11.  Symptoms: Localized pain and sensitivity.
 Signs: Erythema, tenderness and swelling.
 Management: Conservative; Bed rest, local heat
NSAIDs

12.  Symptoms: Pain and sensitivity.
 Signs: Calf pain on foot dorsiflexion. (Homan Sign)
 Dx: Duplex Doppler
 Management: Full anti-coagulation with IV
heparin to increase aPTT by 1.5-2.5

13.  Symptoms: Chest Pain, dyspnea.
 Signs: Tachypnea, tachycardia.
 Most definitive Dx: Pulmonary Angiography
 Management: Full anti-coagulation with (IV,SQ)
heparin to increase aPTT by 1.5-2.5

14. Rheumatic Heart Disease
Congenital
Arrhythmias
Peripartum Cardiomyopathy

15.  Mitral stenosis is the most common lesion (90%)
 mechanical obstruction worsens as cardiac output increases
 Asymptomatic patients may develop symptoms of cardiac
decompensation or pulmonary edema as pregnancy
progresses.
 Atrial fibrillation is more common in patients with severe
mitral stenosis, and nearly all women who develop atrial
fibrillation during pregnancy experience congestive heart
failure.
 Tachycardia can result in decompensation (due to
inadequate diastolic filling)

16.  Rheumatic Heart Complications:
• Heart failure
• Subacute bacterial endocarditis
• Thromboembolic disease
• Fetal wastage

17.  Atrial or ventricular septal defects
 Primary pulmonary hypertension (Eisenmenger’s syndrome)
 Cyanotic heart disease (TOF, TOGV)
 Patients with corrected anatomical defects (e.g, TOF) or persistent (ASD,
VSD) can tolerate pregnancy. However, patients with primary pulmonary
hypertension or cyanotic heart disease with residual pulmonary
hypertension are in danger of undergoing decompensation during
pregnancy, which is associated with an increased risk for maternal
mortality during pregnancy or in the immediate postpartum period.
(overloading circulation → pulmonary congestion → heart failure →
hypotension with reversal of the left-right shunt → hypoxia → death)
 Significant pulmonary hypertension with Eisenmenger’s syndrome is a
contraindication to pregnancy.

18.  Supraventricular tachycardia (SVT) is the most
common, Usually benign, maybe secondary to
structural changes in heart since birth
 Atrial fibrillation and atrial flutter are more
serious and are usually associated with underlying
cardiac disease

19.  rare but occurs exclusively during pregnancy
 Patients have no underlying cardiac disease, and
symptoms of cardiac decompensation appear
during the last weeks of pregnancy or within
6 months postpartum.
 Pregnant women particularly at risk for
developing cardiomyopathy are those with a
history of preeclampsia or hypertension and
those who are poorly nourished.
 Dilational cardiomyopathy with decreased
ejection
fraction
 Mortality rate is at least 20%

20.  The New York Heart Association classification
 maternal and fetal risks for patients with class I
and II disease are small, whereas risks are greatly
increased with class III and IV disease or if there is
cyanosis.
 Type of lesion (stenotic vs regurgitant)
 Other patients at high risk include those with
significant pulmonary hypertension, a left
ventricular ejection fraction less than 40%, Marfan
syndrome, a mechanical valve, or a previous
history of a cardiac event or arrhythmia.

22.  All pregnant cardiac patients should be managed with the help
of a cardiologist (history, physical exam, ECG, ECHO). Frequent
antenatal visits and admissions may be needed for Class III and
IV patients.
 Avoidance of excessive weight gain and edema:
• Low Na+, left lateral decubitus position (to promote diuresis)
• If there is evidence of chronic left ventricular failure not
adequately treated with sodium restriction, a loop diuretic and
β blockers should be added.
• Aldosterone antagonists should be avoided because of their
potential antiandrogen effects on the fetus.

23.  Avoidance of strenuous activity (cardiac output
doesn’t meet metabolic demand)
 Avoidance of anemia (decrease in O2 carrying
capacity → increase in CO as compensation. If
mitral stenosis present → decrease in left
ventricular filling time → pulmonary congestion
and edema)
 Anticoagulation (Women with mechanical valves
require full anticoagulation with heparin in
pregnancy. Warfarin may be restarted post
partum)

24.  Cardiac patients should be delivered vaginally unless obstetric
indications for cesarean are present. They should be allowed to labor
in the lateral decubitus position with frequent assessment of vital
signs, urine output, and pulse oximetry. Adequate pain relief is
important.
 Pushing should be avoided during the second stage of labor
(↑intraabdominal pressure →↑venous return and CO → cardiac
decompensation)
 The second stage of labor can be assisted by performing an outlet
forceps delivery or by the use of a vacuum extractor.

25.  After delivery of the placenta, the uterus contracts, and about 500
mL of blood is added to the effective blood volume. Cardiac output
increases up to 80% above prelabor values in the first few hours
after a vaginal delivery and up to 50% after cesarean delivery. To
minimize the risk for overloading the circulation, careful attention
is paid to fluid balance and prevention of uterine atony.
Methergine should be avoided owing to its vasoconstrictor effects.
 Antibiotic prophylaxis is only recommended for high-risk patients
(e.g., prosthetic valves, unrepaired or incompletely repaired
congenital heart disease, congenital heart disease repaired with
prosthetic material, previous history of bacterial endocarditis and
valvulopathy in heart transplants) if bacteremia is suspected (such
as in the setting of chorioamnionitis).

26.  Acute cardiac decompensation with congestive heart failure should be
managed as a medical emergency. Medical management may include
administration of morphine sulfate, supplemental oxygen, and an
intravenous loop diuretic (e.g., furosemide) to reduce fluid retention and
preload. β Blockers should not be used in the setting of acute heart failure.
Vasodilators such as hydralazine, nitroglycerin, and rarely nitroprusside are
used to improve cardiac output by decreasing afterload. Some patients
may require inotropic support with dobutamine or dopamine. Angiotensin-
converting enzyme inhibitors are contraindicated in pregnancy. Calcium
channel blockers such as nifedipine may accelerate the progression of
congestive heart failure and should be avoided. Continuous pulse oximetry
can be very helpful in managing these patients. Monitoring with a
pulmonary artery catheter can provide a good index of left ventricular
function but is discouraged in those with pulmonary hypertension.

28.  What is seizure?
-is a sudden surge of electrical activity in the brain

29.  Epilepsy
 Eclampsia
 Encephalitis or meningitis
 Space-occupying lesions (e.g. tumour,
tuberculoma)
 Cerebral vascular accident
 Cerebral malaria or toxoplasmosis
 Thrombotic thrombocytopenic purpura
 Drug and alcohol withdrawal
 Toxic overdose
 Metabolic abnormalities (e.g. hypoglycaemia)

30.  Seizures unchanged. Up to 25% of these women
will experience deterioration of seizure control
during pregnancy, with 75% seeing no change. The
more severe the disorder, the more likely it will
worsen.
 Anticonvulsant metabolism increased. Seizure
medication clearance maybe enhanced by higher
hepatic microsomal activity, resulting in lower
blood levels.

31.  Pregnancy complications are minimal with
appropriate prenatal care and compliance with
anticonvulsant medications.

32. Congenital malformation rate is increased from 3% to
>10%. In addition, cerebral palsy, seizure disorders, and
mental retardation are increased in offspring of epileptic
women.
Maternal phenytoin use is associated with neonatal
deficiency of vitamin K-dependent clotting factors:
II, VII, IX, and X.

33. Ensure extra folic acid supplementation before conception and during
embryogenesis to minimize neural tube defects.
• Anomaly screening. Offer triple-marker screen (AFP, HCG,
Estriol)and second trimester sonography to identify neural tube
defects (NTDs) or other anomalies.
• Drug monotherapy. Use a single drug if possible, at the lowest
possible dose, to ensure freedom from seizures.
• Medication levels. Monitor anticonvulsant levels each trimester
and adjust dose as needed. Prevent seizures to minimize maternal and
fetal hypoxia.

34.  Pregnant women who is using phenytoin :
decrease Vit K dependent factor 2,7,9,10 … and
this will lead to hemorrhagic disease of newborn .
 We start folic acid for at least 3-4 months before
pregnancy (5 mg) to decrease the incidence of
NTDs anomalies.

36. UTI
Lower
Bladder Urethra
Upper
Ureter Kidney
Symptoms :
Lower : dysuria, frequency, urgency
Upper : flank pain, chills, rigor, fever
Most common cause is gram
negative bacteria (E.coli)

37.  This is the most common UTI in pregnancy
 Clinical Findings. No symptoms or signs are
present
 Significance. If not treated, 30% of cases will
develop acute pyelonephritis.
 Diagnosis. Made with a positive urine culture
showing >100 K CFU of single organism.
 Treatment. Single-agent, outpatient oral
antibiotics.

38.  This is UTI localized to the bladder without
systemic findings.
 Clinical findings. Urgency, frequency, and burning
are common.
 Significance. If not treated, 30% of cases will
develop acute pyelonephritis.
 Diagnosis. Made with a positive urine culture
showing >100 K CFU of a single organism.
 Treatment. Single agent, outpatient oral
antibiotics.

39.  This is UTI involving the upper urinary tract with systemic
findings. This is one of the most common serious medical
complications of pregnancy.
 Symptoms. Include shaking chills, anorexia, nausea,
vomiting, and flank pain.
 Signs. Include high fever, tachycardia, costovertebral angle
tenderness (R>L).
 Significance. Preterm labor and delivery can occur. Sever
cases are complicated by sepsis, anemia, and pulmonary
dysfunction, sometimes requiring ICU care, including
intubation.
 Diagnosis. Confirmed with positive urine culture showing
>100 K CFU of a single organism.
 Treatment. Hospital admission, generous IV hydration,
parenteral antibiotics e.g., ceftriaxone, and tocolysis as
needed.(7-14days)

40. Why mild hydronephrosis is more common on the
right kidney ?
Due to dextrorotation of the uterus to the right so it
makes compression on the right ureter between the
gravid uterus and iliopsoas muscle.

42.  60%-80% of pregnant women
 Complain is always during the first 8-12 weeks of
gestation
 Mild symptoms and dissappear during early second
trimester
 Underlying causes are not well understood
 Treatment : Symptomatic
- avoid large and late meals
- use extra pillow to elevate the head
when sleeping
- pyridoxine (vit B6)
- antiemetics (promethazine)

43.  Define:
- persistent nausea and vomiting in pregnancy that is
associated with ketosis and weight loss (>5% of
prepregnancy weight)
 Causes:
- psychological abnormalities, hormonal changes (high
Hcg and estradiol) , gastric dysrhythmias, hyperacuity
of the olfactory system, vestibular disorder, impaired
mitochondrial fatty acid oxidation.
 Incidence : 1%
 More frequent in first pregnancy, multiple pregnancy
and trophoblastic disease
 Recur with subsequent pregnancies

44.  History
-intractable vomiting
-inability to retain food and water
 Physical exam
- weight loss, dry and coated tongue , decrease skin
turgor
- absent abdominal pain and tenderness
 Lab work
- urine test > ketonuria
- blood test > electrolytes disturbance and acetone
> elevated amylase and lipase
 Treatment : Symptomatic
if failed outpatient management >> patients
admitted for IV fluid, electrolytes , glucose , vitamin
and medical therapy.
-Vitamin B 6 (pyridoxine), antihistamines, antiemetics
are used.
- acupressure and ginger
-if not respond to medical therapy may require
nasogastric feeding or parenteral nutrition.

45.  Also called heartburn
 In 70% of pregnant women
 Symptoms : substernal discomfort aggravated by meals and
recumbent position , hemetemesis, water brash
 Water brash : sudden filling of mouth with clear watery
material that has salty taste.
 Treatment : Symptomatic
-avoid large and late meals
-avoid recumbent position esp after meals
-use extra pillow to elevate the head when sleep
-antacids
-H2 blocker (cimetidine),proton pum inhibitor
(omeprazole)
* given 1-3hrs after meal and at bedtime.

46.  Pregnancy gives relative protection against the development of peptic
ulceration
 Pregnancy may improve an already present ulcer.
 The diagnosis of ulcer disease is mainly based on
- symptomatic improvement in response to conservative treatment.
- Endoscopy > for patients who do not respond to treatment, have more
severe gastrointestinal symptoms, or manifest gastrointestinal hemorrhage.
 Treatment :
- avoiding caffeine,alcohol,tobacco, and spicy foods
-administering antacids, proton pump inhibitors, or H 2-receptor
antagonists.
-Antibiotic therapy is indicated for patients with Helicobacter pylori
infection

47.  Also known as acid aspiration syndrome
 The pregnant patient in labor is at an increased risk for acid
aspiration because of delayed gastric emptying.
 Worse when associated with increased anxiety ,use of
sedatives, narcotics, anticholinergic agents ,increased
intraabdominal and intragastric pressure, making
regurgitation more likely.
Damage to the pulmonary tissue is greatest when:
-the pHof the aspirated fluid less than 2.5
-the volume is greater than 25 mL.
 Acute gastric aspiration is a cause of adult respiratory
distress syndrome (ARDS).

48.  Treatment :- supplemental oxygen, measures to
maintain the airway, and usual therapy for
treatment of acute respiratory failure.
 Preventive efforts
-decreasing the acid secretion by the stomach.
(women are usually not fed during labor)
-Liquid magnesium and aluminum antacids may
be given during labor to decrease the gastric
acidity
*If the patient is to undergo any surgical
procedure that requires general anesthesia, a “full
stomach” should be presumed and intubation
performed

49.  2 types: Crohn disease (regional enteritis) and ulcerative colitis.
 Patients with inflammatory bowel disease (IBD) are diagnosed
during their reproductive years
 Women with IBD have similar fertility rates to the general
population.
 Pregnancy does not usually alter the course of IBD.
 Women with IBD have higher rates of preterm delivery and low
birth weight infants.
 Predictors of poor outcome include: new-onset IBD, disease
activity and previous bowel resection.
 Patients with inflammatory bowel disease do well during
pregnancy, provided there are no acute exacerbations.
 If inflammatory bowel disease is active at the time of conception,
the spontaneous abortion rate is doubled.
 If surgery is required for complications of inflammatory bowel
disease, fetal survival is reduced.

50.  Supplementation > high-dose folic acid (5 mg
daily),supplemental vitamins D and B12 may also
be indicated.
 There is an increased rate of delivery by
Caesarean section in IBD.
 Treatment :
diarrhea –dietary restriction of lactose, fruits and
vegetables
-constipating agent (Pepto Bismol and
metamucil.
mild to moderate symptoms -sulfalazine

52.  Although the pathogenesis of this syndrome is unknown, some features
are present:
(1) cholestasis and pruritus in the second half of pregnancy without other
major liver dysfunction,
(2) a tendency to recurrence with each pregnancy,
(3) an association with oral contraceptives and multiple gestations(twins),
(4) a benign course in that there are no maternal hepatic squealy,
(5) an increased rate of meconium-stained amniotic fluid and fetal demise
 The main symptom is itching, without abdominal pain or a rash, which may
occur as early as 20 weeks of gestation. Jaundice is rarely observed.
 Most probably, genetic, geographic, or environmental factors are involved.
A mutation in the MDR3 gene may be associated with up to 15% of cases.

53.  Laboratory tests: show elevated levels of serum bile
acids(diagnostic findings). Serum levels of bilirubin and liver
enzymes are usually normal but may be mildly elevated.
 Treatment:
• Local measures such as cold baths, bicarbonate washes, or
phenol (0.5% to 1% in water-soluble creams) may be of
some help.
• Ursodeoxycholic acid is the treatment of choice. It
significantly prevent the pruritus and reduces serum levels
of bile acids, and bilirubin.
• Serial fetal observation is performed in the third trimester,
with delivery at term(<38wk) if testing remains reassuring.

54.  This is a serious complication that is peculiar to pregnancy.
The incidence is about 1 per 10,000 pregnancies. It most
commonly occurs in the third trimester of pregnancy or the
early postpartum period.
 The cause is unknown, it may in some instances result from
an inborn error of metabolism of fatty acid, possibly a
deficiency of long-chain 3-hydroxyl coenzyme A
dehydrogenase(LCHAD). It is associated with diffuse
microvesicular fatty infiltration of the liver resulting in
hepatic failure.
 Presentation is variable, with nausea and vomiting,
abdominal pain, jaundice, and increased irritability.
 - Extreme polydipsia or pseudo diabetes insipidus may be
present. Hypoglycemia is infrequently present.
 - Hypertension and proteinuria are present in about half of
patients, raising the issue of coexisting preeclampsia.
Invariably, patients suffer hepatic coma and renal failure.

55.  Laboratory : include:
 An increase in (PT) and (PTT)
 hyperbilirubinemia, hyperammonemia, hyperuricemia, and a
moderate elevation of the transaminase levels.
 Hematemesis and spontaneous bleeding become manifest as
disseminated intravascular coagulation (DIC) develops.
 Liver failure is indicated by elevated blood ammonia levels.
 Treatment:
• Termination of pregnancy and intensive supportive care are
indicated on diagnosis.
• Intensive supportive measures, such as administration of
intravenous fluids with 10% glucose to prevent dehydration and
severe hypoglycemia.
• For the coagulopathy of hepatic failure, vitamin K supplementation
is not effective, and fresh-frozen plasma should be given.
• With early recognition, immediate delivery, and advances in
critical care management, maternal mortality is about 7% to 18%,
and fetal mortality about 9% to 23%.
• * In those who survive, recovery is complete, with no signs of
chronic liver disease

56.  Viral hepatitis is the commonest cause of jaundice in
pregnancy worldwide.
 Acute viral hepatitis in the first trimester of pregnancy is
associated with a higher rate of spontaneous miscarriage.
 The clinical features of hepatitis are no different to the non-
pregnant patient, with the exception of hepatitis E infection
and herpes simplex hepatitis.
 Hepatitis E is more likely to lead to fulminant hepatic failure
in pregnancy, and is more common in primagravida and in
the third trimester. There is also a significant association
with obstetric complications, such as preterm delivery, fetal
growth restriction and stillbirth.
 In underdeveloped countries,20 percent of women infected
in the third trimester die of fulminant hepatitis. Herpes
simplex hepatitis is rare.

57.  While complications are common and associated perinatal
mortality high, antiviral agents like acyclovir have
dramatically improved outcomes.
 The incidence of hepatitis A in pregnancy is around 1 in
1000 and fetal transmission is extremely rare.
 Acute hepatitis B infection occurs in 1–2 per 1000
pregnancies and 1.5 per cent of pregnant women are
chronic carriers. There is no evidence that hepatitis B is any
more common in pregnancy.
 The prevalence of hepatitis C in pregnant women is
estimated at 1–2 per cent. Hepatitis C infection is also
associated with several adverse pregnancy outcomes, such
as preterm rupture of membranes and gestational diabetes,
as well as adverse neonatal outcomes, including low
birthweight and neonatal unit admission .

59.  Symptoms like heat intolerance, weight gain, fatigue and
palpitations resemble normal pregnancy.
 Free T4, Free T3 and TSH are assessed during pregnancy.
 In first trimester, TSH fall and fT4 rise. Later T4 falls.

60.  Found around 1% of pregnant woman
 Iodine deficiency as the commonest cause (Hashimoto
Thyroiditis in developed countries)
 Diagnosed by high TSH and the test are done on each
trimester*
 Maternal thyroxine level are very important for fetus in first
trimester.

61.  Most common is Graves’ Disease (2 per 1000 pregnancies).
Usually diagnosed before pregnancy.
 Diagnosed by decrease TSH and increase fT4.
 Treated with carbimazole or propylthiouracil (PTU)
 Radioactive iodine is CONTRAINDICATED
 Uncontrolled thyrotoxicosis is associated with increased risk
of miscarriage, preterm delivery and FGR.

62.  Life threatening event that arises in those with underlying
thyroid disease. (hyperthyroid)
 Can be fatal in 20-50% of untreated cases.
 Usually result of under treatment or infection.
 Diagnosis made on clinical grounds with laboratory
confirmation of hyperthyroid
 Treated with PTU and high dose corticosteroid while B-Blocker
are used to block the peripheral effect of thyroxine.

64.  Asymptomatic
 5-8% of all pregnancies (2% Non-preg)
 Urinary stasis, tract dilatation
 30% symptomatic UTI (Pyelonephritis)

65.  25% women are carriers
 1-2% will have Group B Strep infection
 1:1000 babies
 Pneumonia (early), Meninigitis (Late)

66.  Neissseria Gonorrhoea (1-6% pop)
 80% asymptomatic
 Pre-term labor, PPROM, Chorioamniionitis,
Endometritis
 opthalmia neonatorum (40%)
 Screening needed
 DOC :Cephtriaxone IM

67.  5-7% reproductive population
 Most are asymptomatic
 Pre-term labour, PPROM, Chorioamniionitis,
Endometritis
 Conjunctivitis (18-50%), Pneumonia (18%)
 Screening needed
 DOC :Azithromycin 1 gram

68.  T.Pallidum
 <1:1000 pregnant women
 Can infect trans placenta from 15th week
 Second stage by birth if not treated
 Screening
 Diagnostic tests – TPI, FTA-Abs
 DOC :High dose Penicillin

69.  1-2% all deliveries
 Clinical Diagnosis – fever, uterine tenderness,
Leucocytosis
 Histologic chorioamnionitis more common
 Polymicrobial
 Treatment – Antibiotics and delivery

71.  Toxoplasma Gondii (Protozoa)
 Cat faeces, raw/undercooked meats
 TORCH syndrome
 Chorioretinitis, Encephalitis, Neonatal Jaundice
 Serology = PCR
 DOC :Sulfonamides + Pyrimethamine

72.  Toxoplasmosis is a systemic parasitic disease
caused by the protozoan Toxoplasma gondii
occuring in 1 per 1000 pregnant women in the US
(the primary, i.e., the maternal infection).
 IgG antibodies to Toxoplasma are present in 15-
40% of women in reproductive age rendering
them immune for the future infections.
 Two types; maternal and fetal infections

73.  Risk factors for the disease include:
1. Ingesting undercooked meat or unpasteurized
goat’s milk
2. Drinking contaminated water
3. Exposure to feces from an infected cat
4. Tachyzoites from blood transfusion (rare)

74.  The clinical presentation of the disease varies,
mostly, the infections are subclinical and only
in 10% of maternal infections, it presents as a
mononucleosis like syndrome (i.e.,
lymphadenopathy including the tonsils and
the spleen, skin rash, headache and fever)

75.  Risk of transmission to the fetus at the first
trimester is 15%, which is the most severly
affecting the fetus. Whereas if it happens in the
second (25%), and the third trimester (65%),
usually does not produce congenital anomalies.
 About 15% of infants with congenital infections
are symptomatic at birth.

76.  It’s manifested by the
classical traid of :
 hydrocephalus
 intracranial calcifications
 chorioretinitis.
 Of the asymptomatic
infants, 25-50% exhibit
later squelae.

77.  detection of toxoplasmosis IgM antibodies in the
serum of the mother.
 Usually, detection of these antibodies is guided by
either routine screening or if the mother presents with
mononucleosis-like syndrome.
 For mothers that have a confirmed primary maternal
toxoplasmosis, amniocentesis for toxoplasmosis PCR
should be done at 18-20 gestational weeks to detect
fetal infection.

78.  Most infected infants have no apparent physical abnormalities at
birth, but without treatment, most of the infected infants develop
morbidity related to chorioretinitis, hydrocephalus or neurological
damage by the end of adolescence, thus, it necessitates treatment
of infected infants in the first year of life.
 DOC : Spiramycin is used for the treatment of maternal primary
infection.
 If fetal infection is identified, therapy with pyrimethamine and
sulfadiazine plus folinic acid should be given and has been shown
to reduce the severity of fetal damage.

79.  To avoid infection in the pregnant woman:
1. Avoid contact with cat litter or feces
2. Wear gloves while gardening
3. Avoid ingestion of undercooked meat or
unpasteurized goat’s milk
4. Drink filtered water

80. Autoimmune Disease in
Pregnancy
Idiopathic THROMBOCYTOPENIC PURPURA (ITP)
SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)
ANTIPHOSPHOLIPID SYNDROME
RHEUMATOID ARTHRITIS

81. THROMBOCYTOPENIA IN
PREGNANCY
● Defined as platelet count less than 150,000 per
microliter or platelet count below 116,000 per microliter
for pregnant patients.
● Encountered in 7-8% of all pregnancies.
● Clinical assessment is the most important factor for
the evaluation of pregnant patient with
thrombocytopenia.
● May history may include the following :
• 1) Current or previous bleeding problems
• 2) Family history of bleeding
• 3) Alcohol or substance abuse history
• 4) Past obstetrical history
• 5) Blood transfusion history

83. IDIOPATHIC THROMBOCYTOPENIC
PURPURA (ITP)
● ITP occurs when IgG antiplatelet antibodies
recognize membrane glycoproteins and coat the
platelets, which then are destroyed by the RES,
predominantly in the spleen.
● Antiplatelet antibodies may cross the placenta and
cause significant fetal thrombocytopenia (<50,000
per microliter), which could result in bleeding
complications in the neonate.

84. IDIOPATHIC THROMBOCYTOPENIC
PURPURA (ITP)
● DIAGNOSIS
● ITP is a diagnosis of exclusion. The following
may be noted :
• 1) Persistent thrombocytopenia
(<100,000 per microliter)
• 2) Increased number of
megakaryocytes in the bone marrow
• 3) Exclusion of systemic disorders or
medications/drugs
• 4) Absence of splenomegaly
• 5) 80% of cases are associated with
antiplatelet antibodies

85. IDIOPATHIC THROMBOCYTOPENIC
PURPURA (ITP)
● Clinical Manifestations
● The following may be noted :
• - Easy bruising
• - Petechiae
• - Epistaxis
• - Gingival bleeding
● Significant hemorrhage is rare, even when counts
fall to less than 20,000 per microliter

86. IDIOPATHIC THROMBOCYTOPENIC
PURPURA (ITP)
● Maternal treatment for ITP
1. Steroids (e.g prednisone)
2. Intravenous immunoglobulin (IVIG)
3. Anti-D immunoglobulin in Rh-Positive, non-
splenectomized women
4. Splenectomy (if fail to respond to medical therapy)
5. Platelet transfusion combined with high-dose steroids
and IVIG (in patients with life-threatening hemorrhage)
● Vaginal delivery should be facilitated and regional
anesthesia avoided if the platelet count is 80 10^9/L.
● Fetal blood sampling in labor and instrumental delivery
by ventouse are best avoided because of the risk of fetal
thrombocytopenia.
● A cord blood sample must be collected for platelet
counting, the neonatal platelet count occurs 2–5 days after
delivery.

87. SYSTEMIC LUPUS
ERYTHEMATOSUS (SLE)
● is a chronic autoimmune inflammatory disease.
● It is 10 times more common in women, particularly in
black and Asian populations, and the incidence is around 1
in 1000 women.
● It may cause disease in any system, but principally it
affects the joints (90 %), skin (80 %), lungs, nervous
system, kidneys and heart.
● SLE may be diagnosed prenatally or may be
suspected for the first time during pregnancy or
postpartum, usually as a result of complications.
● The diagnosis is suggested by the finding of a positive
assay for antinuclear antibodies

89. SYSTEMIC LUPUS
ERYTHEMATOSUS (SLE)
● SLE is characterized by periods of disease
activity, flares and remissions.
● Pregnancy increases the risk of flares,
but these also become more difficult to
diagnose accurately due to coincident
pregnancy symptoms.
● Flares are more common in the late second
and third trimesters, and are no more severe
than in non pregnancy.
● SLE is associated with significant risks of
miscarriage, fetal death, pre-eclampsia,
preterm delivery and FGR.

90. ANTIPHOSPHOLIPID SYNDROME
(APS)
● The term ‘antiphospholipid syndrome’ (APS) is used to
describe the association of anti-cardiolipin antibodies
(aCL) and/or lupus anticoagulant (LA) with the typical
clinical features of :
• - arterial or venous thrombosis,
• - early fetal loss
• - three or more miscarriages at less than 10 weeks,
• - or delivery before 34 weeks due to intrauterine
growth restriction or pre- eclampsia.
● APS may be primary or found in association with SLE.

91. ANTIPHOSPHOLIPID SYNDROME
(APS)
● Diagnosis based on clinical manifestations + antiphospholipid
antibodies
● Criteria for clinical manifestations :
1. Vascular thrombosis .
2. Unexplained pregnancy morbidity .
● Laboratory criteria :
• One or more should be positive on 2 or more occasions at
least 12 weeks apart :
1. Anticardiolipin
2. Lupus anticoagulant
3. Anti-123-glycoprotein 1
● Treatment:
● Low molecular weight heparin and low-dose aspirin are used
for treatment and prevention of recurrent miscarriage

92. RHEUMATOID ARTHRITIS
● Chronic inflammatory autoimmune disease affecting primarily
the synovial joints.
● It affects more women than men, and around 1 in 1000
pregnancies is affected.
● Most women with RA (75 % ) experience improvement during
pregnancy but only 16% enter complete remission from symptoms
.
●
● Unlike other connective tissue diseases, no adverse effect of
RA on pregnancy is reported, and there is no increase in
pregnancy loss rates.
● The main concern of RA patients is the safety of medication used
to control the disease.
● If paracetamol-based analgesics are insufficient,
corticosteroids are preferred to non-steroidal anti inflammatory
drugs, although the latter can be used up to 32 weeks if needed.
● Azothiaprine and hydroxychloroquine have been used in
pregnancy, with no increase in malformation rates reported and
no apparent adverse outcomes.

93.  Tala El Shami
 Tariq arar
 Firas abu hijleh
 Hisham alkhulaidi
 Laith nizar
 Hussain hejazi
 Ahmed hejazi
 Rabea abufoul
 Qais abu mekhlab
 Ibrahim al harethi
 Ahmed al enezi