Pregestational or Overt Diabetes Gestational Diabetes

DM in PREGNANCY
-diabetes before pregnancy or diagnosed early in pregnancy -diagnosed during the second half of pregnancy
• Confirmed 6 weeks postpartum Diagnosis of GDM with 75-g OGTT
Fasting Plasma glucose: ≥ 126 mg/dL or Fasting: ≥ 92 mg/dL
HbA1c: ≥ 6.5% or 1-hr OGTT: ≥ 180 mg/dL
Screening and Diagnosis
2-hour OGTT: ≥ 200 mg/dL or 2-hr OGTT: ≥ 153 mg/dL
Random plasma glucose + ≥ 200 mg/dL + polydipsia, polyuria, *one or more of these values must be equaled or exceeded for the
hyperglycemia symptoms weight loss diagnosis
Profile Screening recommendation
High risk for • All pregnant women w/ any risk factors should be screened
GDM at first prenatal visit with an FBS, HbA1c or RBS
• Those with negative screening result should be screened
again at 24-28 weeks AOG using 2-hour 75g OGTT
Strong familial history of diabetes, prior large newborn, persistent glucosuria, No risk factors • screened at 24-28 weeks AOG using 2-hour 75g OGTT
Criteria / risk factors unexplained fetal losses. BMI ≥25 kg/m², prior GDM, high-risk ethnicity, hypertension, for GDM
cardiovascular disease, polycystic ovary syndrome (PCOS). • Risk factor: prior GDM, glucosuria, family history or 1st degree relative with
T2DM, PCOS, >25y.o, overwight/obesity, macrosomia in previous pregnancy or
current, polyhydramnios in current pregnancy
• If OGTT at 24-48 weeks is normal, the wouman should be retested at 32 weeks
or earlier if s/sx of hyperglycemia are present in both mother and fetus
(polyphagia, polyhydramnios, accelerated fetal growth)
• All filipino gravidas are considered “high risk” by race or ethnic group (Pacific Islanders)
• All should be screened for T2DM in the first prenatal visit (FBS, HbA1c or RBS)
• For filipino gravidas with no other risk factors aside from race and the initial test is normal: screening for GDM done at 24-28 weeks using a 2-hour 75g OGTT. Other risk factors
identified: screening should proceeed immediately to 2-hour 75g OGTT at first consult
• Spontaneous Abortion
o elevated miscarriage risk if
▪ HbA1c: >12%,
▪ preprandial glucose >120mg/dL
• Preterm delivery
• Malformations
o Double the rate in fetuses of nondiabetic mothers
o Congenital anomalies constitute almost half of perinatal deaths in
diabetic pregnancies • Fetal macrosomia
o Etiological mechanism: excess production of toxic superoxide o Primary effect attributed to gestational diabetes
radicals, altered cell signaling pathways, upregulation of some o Excessive shoulder and trunk fat commonly characterize the
genes and activation of programmed cell death macrosomic newborn
• Altered fetal growth o Difficult delivery associated with: Shoulder dystocia
Fetal Effects
o Fetal overgrowth / Macrosomia • Neonatal Hypoglycemia
▪ Maternal hyperglycemia prompts fetal o Hyperinsulinemia provoke severe neonatal hypoglycemia within minutes
hyperinsulinemia and stimulates excessive somatic of birth
growth o 35 – 45 mg/dL
▪ Except for the brain, most fetal organs are affected o Correlates with umbilical cord C-peptide levels
▪ Excessive fat deposition on the shoulders and trunk,
which predisposes to shoulder dystocia
▪ Rises significantly when mean blood glucose
concentrations chronically exceed 130 mg/dL
o Diminished growth
▪ From congenital malformation
• Unexplained fetal demise
o 3-4x higher in women with pregestational diabetes

2025 clerkship cutie | FDR, RPDL

 o Stillbirth from placental insufficiency occur with increased
frequency in women w/ overt diabetes and associated w/ severe
preeclampsia
• Hydramnios
o Elevated HbA1c values in the third trimester were more likely to
have hydramnios
• Hypoglycemia: ≤ 45 mg/dL
• Hypocalcemia: ≤ 8 mg/dL
• Cardiomyopathy
• Long term cognitive development
• Inheritance
o T1DM: either parent affected – 3-4%
o T2DM: both parents affected – 40%
• Preeclampsia
o Complication that most often forces preterm delivery in diabetic
women
o Low-dose aspirin prophylaxis is recommended in women at high
risk of preeclampsia
• Diabetic nephropathy
o Small microaneurysm – first and most common visible lesion
o Microalbuminuria : 30-300mg protein in 24 hour urine
o Macroalbuminuria: ≥300mg protein in 24hr urine
▪ Preterm delivery, preeclampsia, fetal-growth restriction
significantly higher
o Pregnancy does not appear to worsen diabetic nephropathy
• Diabetic retinopathy
• Maternal Obesity
o Background / nonproliferative nephropathy
o Maternal BMI is an independent and more substantial risk factor for fetal
▪ Hemorrhages that leak serous fluid that creates hard
Maternal Effects macrosomia than is glucose intolerance
exudate
o Highest fraction of LGA neonates was attributable to maternal obesity
o Preproliferative retinopathy
plus excessive gestational weight gain
▪ Retinal ischemia and infarction that appear as cotton
wool exudate
• Diabetic neuropathy
o Diabetic gastropathy
▪ Causes nausea, vomiting, nutritional problems and
difficult glucose control
▪ High risk of morbidity and poor perinatal outcome
▪ Treatment: metoclopramide and dopamine D2
receptor antagonist
• Diabetic ketoacidosis
• Infections
o Candida vulvovaginitis
o Bacterial urinary and respiratory tract infection
• Preconceptional care • Management Diet
o Optimal glycemic control before conception o Daily caloric intake: 30-35 kcal/Kg
▪ HbA1c: ≤6.5% o 1800 – 2500 kcal/day
▪ Preprandial glucose: 70-100 mg/dL o 40% carbohydrate, 20% protein, 40% fat
▪ 2-hr post prandial: 100-120 mg/dL o Carbohydrate distributed throughout the day in three small to moderate
Management
▪ Mean daily glu conc: ≤110 mg/dL sized meals and two to four snacks
o 400 ug/d folate orally daily o Diets higher in complex carbohydrate and dietary fiber reduced the risk
▪ Decrease risk neural tube defect of macrosomia and likelihood of insulin use in women with GDM
• First-trimester care • Pharmacologic method recommended if diet modification does not consistently
o Careful monitoring of glucose control maintain:

2025 clerkship cutie | FDR, RPDL

 ▪ Fasting: ≤ 95 mg/dL o FBS: ≤ 95 mg/dL
▪ 1-hr postprandial: ≤140 mg/dL o 2-hr post prandial: ≤120 mg/dL
▪ 2-hr postprandial: ≤ 120 mg/dL • Delivery
▪ HbA1c: ≤6% o POGS recommendation
o Screening for aneuploidy ▪ Well controlled DM on diet: not later than 40 weeks
o Gravida with overt diabetes best treated with insulin ▪ Poorly controlled DM, diet or insulin: as early as 37 weeks
o Oral hypoglycemic agents not currently recommended ▪ If with preeclampsia:
• Second trimester • with severe features: 34 weeks
o Alpha-fetoprotein determination at 16-20 weeks • without severe features: 37 weeks
o Sonographic examination at 18-20 weeks ▪ Vaginal delivery preferred
o Fetal echocardiography ▪ CS for fetuses >4500gms (ACOG) >4000gms (POGS)
▪ Congenital cardiac anomalies 5x greater • Glucose monitoring
• Third Trimester and Delivery o Glucose assessment 4x daily
o Fetal surveillance testing at 32-34 weeks gestation ▪ 1st check: performed during fasting
▪ Fetal movement counting, periodic fetal heart rate ▪ 2nd to 4th check: done 1 or 2 hours after each meal
monitoring, intermittent biophysical profile evaluation, • Breastfeeding
and contracting stress testing o Prevent neonatal hypoglycemia
o Perform fetal kick counts beginning early in 3rd trimester o Protect against overweight and obesity in childhood and adolescence
o 34 weeks: admission offered to all insulin-treated women ▪ Inconclusive data against overweight and T2DM protection in
o Delivery: offspring
▪ 39 weeks: good glycemic control and reassuring o Protective effect against persistent maternal hyperglycemia
antenatal testing o Lower FBS by 4-5 mg/dL
▪ Earlier delivery: poor glycemic control or significant o lowers incidence of T2DM after GDM pregnancy by 36-57%
comorbidities o longer median time from delivery to development of DM
▪ Vaginal delivery/labor induction: when fetus not • Third Trimester and Delivery
excessively large o Fetal surveillance testing at 32-34 weeks gestation
▪ CS delivery: avoid traumatic birth of a large fetus ▪ Fetal movement counting, periodic fetal heart rate
• Puerperium monitoring, intermittent biophysical profile evaluation, and
o No insulin for the first 24 hours or more postpartum contracting stress testing
o Perform fetal kick counts beginning early in 3rd trimester
o 34 weeks: admission offered to all insulin-treated women
• Overt DM WITHOUT other complications
o Copper IUD – contraceptive of choice
o Other methods acceptable IF cu-iud unavaible or unacceptable for patient
▪ Combined oral contraceptive (COC)
▪ Progesterone-only injectables (DMPA/NET-EN)
▪ Implants (LNG/ETG)
▪ Levonorgestrel IUD (LNG-IUD) • All of the following contraceptive methods are acceptable
• Overt DM WITH complication ▪ Copper IUD
o Copper IUD – contraceptive of choice ▪ Combined oral contraceptive (COC)
▪ Progesterone-only pills (POP) – next in line
▪ Progesterone-only injectables (DMPA/NET-EN)
Contraception o Other methods acceptable IF cu-iud unavaible or unacceptable for patient
▪ Implants (LNG/ETG)
▪ Implants (LNG/ETG)
▪ Levonorgestrel IUD (LNG-IUD) ▪ Levonorgestrel IUD (LNG-IUD
o Contraindicated: o As long as walang overt diabetes
▪ Combined oral contraceptive (COC) o Granted after screening, normal nay un blood sugar nila
▪ Progesterone-only injectables (DMPA/NET-EN)
• Overt DM WITH SEVERE Complications
o Copper IUD – contraceptive of choice
o Contraindicated:
▪ Combined oral contraceptive (COC)
▪ Progesterone-only injectables (DMPA/NET-EN)
• Insulin considered standard therapy
Insulin management o Does not cross the placenta
• Insulin therapy is added if:
2025 clerkship cutie | FDR, RPDL
 o Fasting levels persist above 95 mg/dL
o 1-hr postprandial persistently exceed 140 mg/dL
o 2-hr postprandial > 120 mg/dL
• Starting dose
o 0.7 to 1 U/kg/d in divided doses

• 50- to 75-percent likelihood that women with gestational diabetes will develop overt diabetes within 15 to 25 years (American Diabetes Association, 2019)

Postpartum evaluation

• Recurrent rate of GDM is 48%

o Primiparas – 40%
o Multipara – 73%
Recurrent GDM
• Prepregnancy loss of atleast 2 BMI units was associated with a lower subsequent risk of gestational diabetes in women who were overwight or obese in the first pregnancy
• Risk Factor:
o Maternal BMI, Insulin use, Fetal macrosomia, Excessive weight gain

2025 clerkship cutie | FDR, RPDL

 Hypertensive
Definition Criteria for diagnosis additional Management When to Deliver
disorder
Antihypertensive medications :
At least half of serious - Methyldopa: DOC
Hypertension present before hemorrhagic strokes - 1st line: methyldopa, calcium
Deliver at 38–39 weeks if
Chronic hypertension pregnancy or diagnosed before 20 ≥ 140/90 mmHg on 2 occasions at least 4 hours apart associated with preeclampsia channel blocker or beta blocker
no complications
weeks of gestation are in women with chronic - ACE-inhibitors and
hypertension angiotensin receptor blocker
NOT recommended
- Temporary condition that
usually resolves postpartum;
Frequent BP monitoring,
New-onset hypertension ≥ 20 return to normal by 12 weeks
potential antihypertensives if Delay delivery at 37–38
Gestational weeks of gestation without postpartum
≥ 140/90 mmHg on 2 occasions at least 4 hours apart BP ≥160/110 mmHg, close weeks if mild and stable;
Hypertension proteinuria or end-organ - Failure of BP to normalize
surveillance for signs of earlier if severe
dysfunction postpartum requires
preeclampsia
changing diagnosis to chronic
hypertension
- ≥ 140/90 mmHg BP on ≥ 20 weeks of gestation who
develop proteinuria
- ≥ 140/90 mmHg BP on ≥ 20 weeks of gestation without
w/ HPN only in early gestation who
proteinuria but with:
develop proteinuria ≥ 20 weeks of
Chronic hypertension 1) sudden exacerbation of HPN
gestation or
with superimposed 2) new onset signs/symptoms (inc liver enzyme, RUQ 34 weeks
women w/ proteinuria ≤ 20 weeks
preeclampsia pain, severe headache)
of gestation with systemic
3) ≤100,000 umol/L platelet
involvement
4) pulmonary edema
5) renal insufficiency
6) sudden and sustained increase in protein excretion
- new onset BP elevation ≥140/90 mmHg ≥ 20 weeks
AOG with proteinuria (≥300 mg/24h) or If BP ≥160/110:
protein:creatinine ratio ≥0.3 or urine dipstick reading ≥ GI findings: - first line treatment is IV
+1 - RUQ pain / tenderness d/t hydrazaline and labetalol.
- absence of proteinuria: liver inflammation - When IV access not available
New-onset hypertension and
1) impaired liver function (x2 elevation of liver - increased intrahepatic first line of treatment Oral
proteinuria or end-organ
Preeclampsia transaminase) (normal value: AST - , ALT- ) pressure and stretching of the Nifedipine 37 weeks if stable
dysfunction after 20 weeks of
2)persistent cerebral/visual symptom (headache, Glisson capsule - second line option: IV
gestation
blurring of vision) Cardiovascular finding: nicardipine
3) pulmonary edema - sudden worsening edema
4) renal insufficiency (crea 97 umol/L or 1.1 mg/dL or The only cure is termination of
doubling of crea in the absence of renal disease) pregnancy
5) thrombocytopenia (≤100,000 umol/L platelet)
Prompt delivery
w/ preeclampsia with any of the following: ≥34wks - stabilize mother irrespective of AOG if:
- ≥160/110 on 2 occasions at least 4 hours apart - deliver - uncontrolled severe
- impaired liver function (x2 elevation of liver ≤34wks - admit ICU hypertension
transaminase) (normal value: AST - , ALT- ) -MgSO4 seizure - pulmonary edema
Preeclampsia with - persistent cerebral/visual symptom (headache, The only cure is termination prophylaxis - renal failure
- antihypertensive
severe features blurring of vision) of pregnancy - abruption placenta
(if BP ≥160/110 or
- pulmonary edema
MAP ≥125)
- renal insufficiency (crea 97 umol/L or 1.1 mg/dL or If 33-34 weeks: deliver
-Sonologic
doubling of crea in the absence of renal disease) monitoring after 48 hours of initial
- thrombocytopenia (≤100,000 umol/L platelet) -daily NST steroid therapy

2025 clerkship cutie | FDR, RPDL

 If ≤ 23 weeks:
termination of
pregnancy
Emergency management with Deliver immediately
complications include MgSO4, stabilization, and after maternal
Onset of seizures with intracranial hemorrhage, delivery as soon as possible stabilization, regardless
Eclampsia preeclampsia not attributable to ≥140/90 mmHg with seizures aspiration pneumonia, and of gestational age.
other causes maternal death The only cure is termination of No delay possible;
pregnancy immediate delivery is
essential
Deliver immediately
Unique presentation of
regardless of gestational
preeclampsia
age.
HELLP syndrome Hemolysis
No delay possible;
Elevated Liver enzyme
immediate delivery is
Low platelet
essential

MgSO4 toxicity • Endothelial Cell Dysfunction: Activation and injury of endothelial

cells, resulting in vascular damage, vasospasm, and increased blood
pressure.
• Immunological Factors: Maladaptation between maternal and
placental tissues, potentially leading to reduced immune tolerance.
Pathophysiology Placenta
Antidote: Calcium Gluconate IV (10 mL of 10% solution) • Abnormal Trophoblastic Invasion: The failure of trophoblasts to
Etiology of • Placental implantation with abnormal trophoblastic invasion of properly invade and remodel uterine spiral arteries results in poor
preeclampsia uterine vessels placental perfusion.
o Possible cause of vasoconstriction
• Placental Ischemia: Reduced blood flow leads to hypoxia and
• Dysfunctional immunological tolerance between maternal, paternal
oxidative stress, causing the release of antiangiogenic factors that
(placental), and fetal tissues
trigger systemic endothelial dysfunction.
• Maternal maladaptation to cardiovascular or inflammatory changes Cardiovascular System
of normal pregnancy
• Genetic factors that include predisposing genes and epigenetic • Vasoconstriction: Endothelial dysfunction leads to increased
sensitivity to vasoconstrictors like angiotensin II, causing
influences.
hypertension.
• Increased Blood Pressure: This is the hallmark of hypertensive
disorders and results from systemic vasoconstriction and increased
vascular resistance.
• Heart: The increased workload can lead to left ventricular
hypertrophy and, in severe cases, heart failure.
Kidneys
• Endothelial Dysfunction: Damaged endothelium in renal vessels
reduces glomerular filtration, leading to decreased urine output
(oliguria) and fluid retention.
• Proteinuria: Increased vascular permeability allows protein to leak
• Veins are invaded only superficially and trophoblastic invasion may
into the urine, a key diagnostic criterion for preeclampsia.
be incomplete
o Decidual vessels but not myometrial vessels become • Renal Ischemia: Reduced blood flow to the kidneys exacerbates
lined with endovascular trophoblasts hypertension and can lead to acute kidney injury.
o Result: mean external diameter is only half that of
corresponding vessels in normal placentals Liver
Etiopathogenesis • Abnormal Trophoblastic Invasion: Incomplete invasion of the uterine
vessels by trophoblasts, leading to poor placental perfusion.

2025 clerkship cutie | FDR, RPDL

 • HELLP Syndrome: Characterized by Hemolysis (destruction of red Risk factor and
blood cells), Elevated Liver enzymes (indicating liver damage), and aspirin use
Low Platelets (thrombocytopenia). from ACOG
• Liver Enzyme Elevation: Hepatic ischemia and microvascular injury
lead to hepatocellular damage and increased liver enzymes (AST,
ALT).
• Subcapsular Hematoma: Severe cases may result in liver swelling
and rupture, which is life-threatening.
Central Nervous System (CNS)
• Cerebral Edema: Endothelial dysfunction leads to increased
permeability of the blood-brain barrier, causing fluid leakage and
cerebral edema.
• Eclampsia: Characterized by seizures due to severe cerebral edema,
Indications for
ischemia, and hemorrhage.
prompt or delayed
• Visual Disturbances: Caused by retinal vasospasm and edema, delivery
leading to symptoms like blurred vision or temporary blindness.
Lungs
• Pulmonary Edema: Increased vascular permeability and fluid
overload can lead to fluid accumulation in the lungs, causing
respiratory distress.
• Acute Respiratory Distress Syndrome (ARDS): In severe cases, this
may develop due to systemic inflammation and endothelial damage.
Hematologic System
• Thrombocytopenia: Decreased platelet count due to platelet
activation and consumption in microthrombi formation.
• Disseminated Intravascular Coagulation (DIC): Severe endothelial
damage can trigger widespread clotting, leading to bleeding and
clotting complications.
• Hemolysis: Increased serum lactate dehydrogenase decreased
haptoglobin levels. Result from microangiopathic hemolysis due to
endothelial damage and subsequent platelet aggregation and fibrin
deposition
Uterus and Fetus
• Uteroplacental Insufficiency: Poor blood flow to the placenta leads
to fetal growth restriction, preterm birth, or even fetal demise.
• Abruptio Placentae: The risk of placental abruption increases, which
can cause severe bleeding and fetal distress.

Hemoconcentration HALLMARK of eclampsia, Patients with eclampsia are less tolerant to blood loss

2025 clerkship cutie | FDR, RPDL

 Treatment /
infection Maternal effect Fetal / neonatal effect diagnosis Notes
management
Asymptomatic n 30% of px Sepsis, Pneumonia, Meningitis • Nucleic Acid Amplification Penicillin G Vaginal delivery with
Group B UTI, Amnionitis, Endometritis Test (NAAT) intrapartum antibiotics
Streptococcus Manifestation in newborn: fulminant pneumonia and severe
sepsis
• Most are asymptomatic (70%) • Neonatal conjunctivitis • Nucleic Acid Amplification • Azithromycin, 1 g Infection at delivery poses
• 30% symptomatic o Most common Test (NAAT) orally a higher risk to the
o Urethral syndrome • Neonatal pneumonia o Gold standard o Preferred, 1st line newborn than to the
o Urethritis o From perinatal transmission • Amoxicillin, 500 mg mother
o Greater vestibular (Bartholin) gland • 65% of newborn infections occur during delivery TID
infection o Alternative
• Uncommon manifestation treatment
Chlamydial
o endometritis
infection
o Salpingitis • Avoided in pregnancy
Chlamydia
o Reactive arthritis o Fluoroquinolone
trachomatis
o Reiter syndome o Doxycycline
• CONTRAINDICATED
o Erythromycin
estolate
o Because
hepatotoxic

• Primary syphilis • Non-immune hydrops, • Direct diagnosis of early • Parenteral penicillin > horizontal transmission
Bacterial infection

o characteristic chancre • Late congenital manifestation: stage disease G Benzathine - minute abrasions on
▪ solitary, painless lesion w/ raised, firm o Hutchinson teeth, o Dark-field preferred treatment the vaginal mucosa
border and red, smooth ulcerated base o Saddle nose, microscropy for all stages during provide entry, and
w/o significant pus o 8th nerve deafness • Nontreponemal testing pregnancy cervical eversion,
• Secondary: o VDRL • Treatment before 24 hyperemia, and friability
o Diffuse macular rash, plantar and palmar o RPR weeks raise this risk
circular lesions • Treponemal specific test o Nontreponemal
o Condylomata lata – perineum and perianus o Confirm presence of test repeated in: > vertical transmission
• Latent: T pallidum specific - 3rd trimester - spirochetes readily
o Asymptomatic, antibody - or no sooner cross the placenta is the
• Tertiary: o FTA-ABS that 8 weeks after most common route
o Gummas, Neurosyphilis, Cardiovascular o TP-PA treatment unless - neonate contact with
Syphilis reinfection spirochete from lesions at
syphilis
Treponema
o Rarely seen in reproductive-aged women • Traditionally suspected delivery or across the
pallidum - may be repeated placental membrane
o nontreponemal tests
are used first for at delivery
screening, and
results are then
confirmed by a
treponemal-specific
test
• Newer sequence
o Screening begins first
with a treponemal-
specific test

2025 clerkship cutie | FDR, RPDL

 • Mild illness • One of the most complete teratogens • Suspected cases Postexposure
o Incubation 12 to 23 days o Effects are worst during organogenesis o IgM (+) = passive
• 25-50% asymtomatic o Defects are rare after 20 weeks’ gestation indicative of immunization with
• Generalized maculopapular rash • Features of congenital rubella syndrome recent IVIG may be of
o Begins on the face -> trunk -> o Sensorineural deafness infection benefit if given
o Mental retardation within 5 days of
extremities • Protected women
exposure
o Heart disease – Patent Ductus Arteriosus o IgG (+) = hx of
o Cataract adequate
o “Blueberry muffin” skin rash vaccination /
past exposure
o If IgG (-) = give
Rubella
2 MMR
(German
immunizations
Measles)
▪ 3 months
apart
▪ 2nd shot: at
Viral infections

least a
month
before
pregnancy

• Feto-Maternal Effects Screening recommendation on 1st prenatal

o Mainly vertical transmission checkup
o Risk of transmission to fetus from infected mother is 90% without active and passive immunization of the HbsAg result Next step
newborn HbsAg (+) Full hepatitis profile
▪ ☤ If not given active/passive immunization and liver enzyme test
o Some infants still acquire Hep B despite full immunization (10%) especially if mother is extremely viremic HbsAg (-) but high Repeat screening as
Hepatitis B
▪ It’s not a 100% guarantee even if you give active or passive immunization to the baby after birth risk patient necessary
especially if the mother has a high viral load
• Breastfeeding is allowed if on antiviral therapy • Treatment
• Mode of delivery: o Tenofivir (TDF) 300 mg/day
o Vaginal preferred DOC
o NOT an absolute indication for CS delivery ▪ Tablet form

2025 clerkship cutie | FDR, RPDL

 • Most primary infections are asymptomatic • Congenital CMV Syndrome CMV polymerase • Limited to
• Mononucleosis like syndrome o Most common cause of sensorineural deafness in children chain reaction (PCR) symptomatic
o Fever o Infected newborns may show: testing of amnionic treatment in
o Pharyngitis ▪ Petechiae, Mulberry skin spots, meningoencephalitis, fluid is considered the immunocompetent
o Lymphadenopathy periventricular calcifications, hepatosplenomegaly, gold standard for the women
o Polyarthritis thrombocytopenia, and jaundice. diagnosis of fetal • No curative
• Immunocompromised women • Non-immune hydrops, symmetrical IUGR, microcephaly infection treatment
o Hepatitis, retinitis, pneumonitis, o Symmetrical IUGR – body and head are the same size
myocarditis, gastroenteritis,
meningoencephalitis
Cytomegalovirus • Major concern if mother becomes first
(CMV) infected while pregnant
o Highest risk of having a congenitally
infected fetus
o Women who are seronegative before
pregnancy and then acquire primary
CMV infection during pregnancy are at
highest risk of having a congenitally
infected fetus

A – periventricular calcifications, B – mulberry spots, C – Malaki tiyan ng bata, Malaki ang liver at spleen niyan

• 1- to 2- days • Highest risk • VZIG • Primary infection

Viral infections

o Flu like prodrome o If Maternal vesicles appear between 5 days before delivery and 2 o Non immune (varicella zoster)
• 3-7 days days postpartum pregnant px o Transmitted by
o Pruritic vascular lesions that crust o Vertical transmission: between 13 and 20 weeks AOG o w/n 4 days respiratory droplets
o Starts at the head progressing • Congenital Varicella Syndrome exposure or direct contact
towards the trunk o Chorioretinitis, microphthalmia, cerebral cortical atrophy, • Acyclovir
• Contagious from 1 day before the rash hydronephrosis, cicatricial skin lesions, growth restrictions and limb o treatment
onset until all lesions become crusted hypoplasia
o Any baby born with a deformity – suspect Varicella

Varicella Zoster
Virus (VZV)

2025 clerkship cutie | FDR, RPDL

 • Primary herpes • Primary herpes • PCR Acyclovir • Most common STD
o Mild to moderate symptoms o 70% of cases o More accurate - suppression initiated • Most common cause of
▪ Fever o Spontaneous abortion • Tzanck smear at 36 weeks’ gestation genital ulcer
▪ Malaise o Symmetrical IUGR o More common, cost for gravidas with • Transmission: intimate
▪ Adenopathy o Microcephaly effective recurrences during sexual/mucocutaneous
▪ Genital lesions o Cerebral calcification • HSV culture pregnancy lowers the contact
• Recurrent herps • Intrauterine HSV infection o 20% false neg number of HSV • Primary infection ->
o More localized symptoms o skin o Fluid from vesicle, outbreaks at term Latency stage ->
o Migration of HSV from dorsal root ganglia ▪ blisters, scarring ulcer reactivation
o CNS • ELISA • Vertical transmission
▪ Hydranencephaly, microcephaly, intracranial occur by three routes:
calcification • Mode of delivery o Peripartum
o Eyes o CS if presents with ▪ Most frequent route
Herpes Simplex ▪ Chorioretinitis, microphthalmia the ff: ▪ Invades uterus
Virus (HSV) ▪ Presence of genital following membrane
lesion rupture
▪ Prodromal ▪ Transmitted by
symtoms contact at delivery
▪ Intact bag of water o Postnatal
Sexually transmitted infection

o BOW ruptured ≥8-12 o Intrauterine

hours, CS has no
value and fetus is
exposed and most
likely infected

• HPV 16, 18 • Vertical transmission rate are minimal • Clinical diagnosis • Trichloroacetic or • Genital wart eradication
o Lower reproductive tract dysplasia o Lower reproductive tract dysplasia o If nakita mo yun bichloracetic acid during pregnancy is
• HPV 6, 11 • Juvenile-onset recurrent respiratory papillomatosis lesions usually unnecessary
o Mucocutaneous genital warts (JoRRP) • NOT used during unless they are
▪ Condyloma acuminata o Rare, benign neoplasm of larynx pregnancy symptomatic
▪ If lesion is big enough it may obstruct o Hoarseness and respiratory distress o Cryotherapy, • Therapy is directed
birth canal and increase risk of bleeding o Caused by HPV 6, 11 podophyllin toward debulking
during labor symptomatic warts yet
Human • Risk for infection minimizing treatment
Papillomavirus o Maternal genital HPV infection toxicty to the mother
(HPV) o Longer labor and fetus.

2025 clerkship cutie | FDR, RPDL

 • Prenatal HIV screening
o Opt-out approach (ACOG, POGS)
▪ HIV testing is routinely included in antenatal testing, but this testing may be declined
o Repeat screening during the third trimester, preferably before 36 weeks’ gestation, is considered for all pregnant women
o Retesting is recommended in areas where HIV rates exceed 1 case per 1000 pregnant women screened or for those with risk factors
▪ Incarceration
▪ Injection drug use
▪ Prostitution
▪ w/ known HIV-infected sexual partner
▪ new or multiple sexual partner
▪ diagnosis of another STI
• Vertical Transmission – viral burden and neonatal infection rates are directly related
o Placenta (15-20%)
▪ 20 percent of vertical transmission occurs before 36 weeks’ gestation
o Birth Canal (45-50%)
o Breastmilk (14-16% risk w/ proven maternal disease, 29% risk w/ acute maternal infection
• FACTORS THAT INCREASE MATERNAL TO CHILD TRANSMISSION (MTCT)
o Fast or high maternal viral titers
o T-cell tropism
o
Sexually transmitted infection

Sensitivity to the enhancement of infection by maternal serum

• FACTORS THAT INCREASE INTRAPARTAL TRANSMISSION
o Viral presence in the vagina
o Presence of genital ulcers
Human
o Birth canal injuries (lacerations)
Immunodeficiency
o Microtransfusion from placenta
Virus (HIV)
o Prolonged rupture of BOW
• Therapeutics
o ART
▪ Reduces risks of MTCT if HIV-1 RNA count ≤ 500 copies per mL
▪ Takes atleast a month to take effect
• Delivery Planning
o Give ART atleast 4 weeks before delivery
▪ Viral load <50 copies/mL
• Transmission is greatly reduced
o Scheduled CS delivery
▪ Recommended w/ viral load copies >1000 copies/mL
▪ At 38 weeks gestation
o Vaginal delivery
▪ Viral load ≤ 1000 copies/mL
o Labor is not induced
▪ Prevent perinatal HIV transmission
• Postpartum care
o Breastfeeding
▪ US: not recommended where formula is readily available
▪ POGS: NOT allowed
▪ WHO: allowed since MCTC is only 1%
▪ ART decreases breastfeeding risks
• Should not be discontinued

2025 clerkship cutie | FDR, RPDL

Other Endocrine disorders
Hyperthyroidism • Hyperthyroidism
o Markedly depressed TSH, elevated thyroxine (T4)
• T3-toxicosis
o Hyperthyroism caused by abnormally high serum
triiodothyronine (T3)
• Subclinical Hyperthyroidism
o Low TSH, N T4, N T3
o Not associated with adverse pregnancy outcomes
• Thyrotoxicosis
o Secondary to Grave’s
o during the course of pregnancy, hyperthyroid symptoms may
initially worsen because of chorionic gonadotropin stimulation,
but then subsequently diminish with decreases in receptor
antibody titers in the second half of pregnancy
o Treatment: thionamide drugs
▪ Propylthiouracil(PTU)
• More preferred
• Crosses the placenta less readily o Dexamethasone
• Partially inhibits conversion of T4 to T3 ▪ Blocks peripheral conversion of T4 to T3
▪ Methimazole
• Methimazole embryopathy • Hyperemesis Gravidarum and Gestational transient thyrotoxicosis
o Esophageal atresia o Many women with hyperemesis gravidarum have abnormally
o Aplasia cutis high serum thyroxine levels and low TSH levels dueto TSH-
▪ Contraindicated receptor stimulation from massive—but normal for pregnancy—
• Thyroid ablation concentrations of hCG.
o Direct impact on fetal thyoid o antithyroid drugs are not warranted
• Fetus/neonate exposed to excessive maternal thyroxine: ▪ ondansetron, metoclopramide, and vitamin B6
o Goitrous thyrotoxicosis (pyridoxine) can help control severe nausea and
▪ Placental transfer of thyroid stimulating vomiting.
immunoglobulins • Thyrotoxicosis and Gestational Trophoblastic Disease
o Goitrous hypothyroidism o abnormally high hCG levels lead to overstimulation of the TSH
▪ Fetal exposure to maternally administered receptor.
thionamide o With definitive treatment (curettage / hysterectomy), serum
o Nongoitrous hypothyroidism free-T4 levels usually normalize rapidly in parallel with the
▪ Transplacental passage of maternal TSH-receptor decline in hCG concentrations.
blocking antibodies Hypothyroidism • Hypothyroidism
o Fetal thyrotoxicosis o Abnormally high serum TSH, abnormally low thyroxine (T4)
▪ Maternal thyroid gland ablation, usually with 131l • Subclinical Hypothyroidism
radioiodine o High TSH, N T4, N T3
• Thyroid storm and heart failure • Overt Hypothyroidism
o Acute and life threatening o Hashimoto thyroiditis – most common cause
o thyroid storm is a hypermetabolic state and is rare in pregnancy. o Treatment
o Pulmonary hypertension and heart failure from cardiomyopathy ▪ Levothyroxine 1 to 2 μg/kg/day or approximately 100
caused by the profound myocardial effects of thyroxine is μg daily
common in pregnant women ▪ Dietary iodine requirements are increased during
o Management: pregnancy
• 150 μg per day in childbearing-aged
women
• increased to 250 μg during pregnancy and
breast feeding.
• Congenital hypothyroidism
o Most preventable cause of mental retardation

2025 clerkship cutie | FDR, RPDL

Post partum • Postpartum thyroid dysfunction with an onset within 12 months of
Thyroiditis chilfdbirth includes hyperthyroidism, hypothyroidism, or both.
• Clinical Manifestations
• Typically develops months afte rdeliveryandcauses vague and nonspecific
symptoms that often are thought to be stresses of motherhood
• Clinical phases:
o destruction-induced thyrotoxicosis
▪ symptoms from excessive release of hormone from
glandular disruption: onset is abrupt, and a small,
painless goiter is commonly found; fatigue and
palpitations are common
▪ usually lasts only a few months.
▪ thionamides are ineffective, and if symptoms are
severe, a β-blocker agent may be given.
o clinical hypothyroidism from thyroiditis
▪ occurs between 4 and 8 months postpartum.
Parathyroidism • Hyperparathyroidism in pregnancy
o Symptoms include hyperemesis, generalized weakness, renal
calculi, and psychiatric disorders.
o Pregnancy theoretically improves hyperparathyroidism because
of significant calcium shunting to the fetus and augmented renal
excretion
o Management
▪ Surgical removal of a symptomatic parathyroid
adenoma is preferable
▪ Medical management may be appropriate in
asymptomatic pregnant women with mild
hypercalcemia -> patients are carefully monitored in
the postpartum period for hypercalcemic crisis
▪ Dangerously elevated serum calcium
• Diuresis with IV normal saline
• Furosemide
• Hypoparathyroidism
o Most common cause of hypocalcemia
o Characterized by: facial muscle spasms, muscle cramps, and
paresthesias of the lips, tongue, fingers, and feet.
▪ May progress to tetany and seizures
o Maternal treatment:
▪ 1,25-dihydroxyvitaminD3(calcitriol),
dihydrotachysterol
▪ large vitamin D doses of 50,000 to 150,000 U/day
▪ calcium gluconate or calcium lactate
Prolactinoma • Adenoma symptoms and findings
o amenorrhea,
o galactorrhea
o hyperprolactinemia.
• Pregnant women with microadenomas should be monitored for headaches
and visual symptoms.
o Visual field testing during each trimester
o Symptomatic tumor enlargement should be treated immediately
with a dopamine antagonist such as bromocriptine or
cabergoline.

2025 clerkship cutie | FDR, RPDL