Gestational diabetes/HTN pregnancy Flashcards
Gestational Diabetes Mellitus (GDM)
General
Any degree of glucose intolerance with onset or first recognition during the second or third trimester of pregnancy
Epidemiology
Affects 2-10% of pregnancies in the United States
Ethnic and geographic prevalences mirror those ofdiabetes mellitus type II
African American, Hispanic American, Native American, Pacific Islander, and South or East Asian women
↑ risk (35-60%) of developing diabetes mellitus type II over 10-20 years after pregnancy
GDM
Classification & Etiology
Classified as:
Diet-controlled GDM (A1GDM)
Gestational diabetes managed without medication and responsive to nutritional therapy
Medication-controlled GDM (A2GDM)
Gestational diabetes managed with medication to achieve adequate glycemic control
Etiology
Unclear, but not autoimmune
↑insulinsecretion,but not sufficient to maintain normalglucoselevels
↓insulinsensitivity secondary to placental hormonal release (human placental lactogen) → hyperglycemia, particularly after meals
GDM
RF
Gestational diabetes in previouspregnancy
Hemoglobin A1C≥ 5.7% or elevated fastingglucoselevel prior topregnancy
Increased body weight (≥ 110% of ideal body weight or BMI > 30 during gestation)
Gaining excessive weight during 1st half of gestation
First-degree relative with DM
Previous children ≥ 4kg (8.8 lbs.) at birth(macrosomia)
Abnormal lipid studies (low HDL, triglycerides > 250 mg/dL)
Polycystic ovary syndrome (PCOS)
Any marker of insulin resistance (acanthosis nigricans)
Multiple (twin, triplet) gestation
GDM
Clin man
Because of universal screening in the United States, most cases are diagnosed before symptoms arise
Symptoms similar to those of diabetes mellitus type II
Nonspecific symptoms due to hyperglycemia:
Fatigue
Malaise
Anorexia
Headache
Blurred vision
Muscle cramps
Dehydration
Increased thirst
GDM
Dx and labs
Oralglucose-tolerance test is recommended during the 24th-28th week ofpregnancy
Recommended screening method has 2 steps
Step 1:
50-g, 1-hour oral glucose load and a single measurement of the glucose level at 1 hour
Abnormal result:
1-hour glucose level is > 130-140 mg/dL → proceed to Step 2
Results > 200 mg/dL → diagnostic for GDM
Step 2:
100-g, 3-hour oral glucose load and 3 measurements of the glucose level at 1 hour, 2 hours, and 3 hours
Abnormal results are:
Fasting > 95 mg/dL
1-hourglucose: ≥ 180 mg/dL
2-hourglucose: ≥ 155 mg/dL
3-hour glucose: ≥ 140 mg/dL
Two or more abnormal results establishes the diagnosis of GDM
Normal or Abnormal?
Normal Values:
Fasting: < 95; 1-hour: < 180; 2-hour: < 155; 3-hour: < 140
Patient #1
Fasting: 91; 1-hour: 187; 2-hour: 142; 3-hour: 120
Normal
Patient #2
Fasting: 82; 1-hour: 185; 2-hour: 152; 3-hour: 144
Abnormal
Patient #3
Fasting: 102 — Do we proceed with the 2-step glucose testing?
Yes
GDM
Glucose goals and lifestyle mods
Blood glucose goals
Fasting glucose < 95 mg/dL
1-hour postprandial < 140 mg/dL
2-hours postprandial < 120 mg/dL
Nonpharmacologic Tx – 1st approach
Diet modification
Nutritional counseling by a registered dietitian (ADA recommendation)
Personalized plan based on patient’s BMI (calorie allotment and distribution, carbohydrate intake)
Exercise
Minimum of 150 minutes weekly or 30 minutes of moderate-intensity aerobic exercise 5 times weekly
Frequent glucose monitoring (minimum 4x/day)
GDM
Pharm Tx
Dosing per trimester
If glycemic control is not adequate (elevated glucose for 1-2 weeks) despite adherence to diet and exercise → Pharmacologic Tx
Insulin – DOES NOT CROSS the PLACENTA
ADA recommended first-line treatment
Daily dosing requirements:
1st trimester 0.7 units/kg/day
2nd trimester 0.8 units/kg/day
3rd trimester 0.9-1.0 units/kg/day
Dosing:
Half the daily dose as basal insulin at bedtime
Half the daily dose as rapid-acting or regular insulin divided between meals
Oral hypoglycemic agents (metformin and glyburide) are increasingly being used for GDM despite the lack of FDA approval
Checking the baby post GDM
Regularultrasound starting at 18-20 weeks to evaluate fetal development
Antepartum fetal surveillance at 32 weeks
Kick counts
Healthy baby usually kicks, flutters, or rollsat least 10 times per hour
Nonstress tests (NSTs)
Baby’s heart rate is monitored to see how it responds to the baby’s movements
Consider inducing delivery atweek 39–40, ifglycemic controlis poor or if complications occur
GDM
Complications
Risk of complications is proportional to the level of hyperglycemia:
Miscarriage
Fetal deformities
Large-for-gestational-age fetus
Macrosomia
Weighs more than 8 pounds, 13 ounces
Risk factor for shoulder dystocia
Hypoglycemia in the infant
Preeclampsia
Development of DM type II
GDM
Shoulder Dystocia
Obstetrical emergency during childbirth
After vaginal delivery of the head, the baby’s anterior shoulder gets caught above the mother’s pubic bone
Complications:
Mother
Vaginal or perineal tears, postpartum bleeding, or uterine rupture
Baby
Brachial plexus injury or clavicle fracture
GDM
Prognosis
GDM resolves after pregnancy (most cases)
Screen for diabetes mellitus type II at 4-12 weeks post-partum
75-g, 2-hour glucose tolerance test
Abnormal results:
Fasting glucose: ≥ 100 mg/dL
2-hour glucose: ≥ 140 mg/dL
Repeat every 1-3 years
Hypertensive Pregnancy Disorders
Hypertension is defined as a BP > 140/90mmHg
Hypertensive disorders complicate 5%–10% of pregnancies
Includes:
Chronichypertension
Gestationalhypertension
Preeclampsia → eclampsia
HELLP syndrome: hemolysis, elevatedliverenzymes, and low platelet count
HTN pregnancy
RF
Moderate-risk factors:
Nulliparity
> 10 years between pregnancies
BMI> 30
African American race
Family historyof preeclampsia in 1st-degree relative
Advanced maternal age (≥ 35 years at time of delivery)
High-risk factors:
History of preeclampsia
History of chronichypertension
Diabetes
Renal disease
Autoimmune disease
Multiple gestation
Chronic hypertension
General
Asymptomatic
Systolic BP ≥ 140mmHg and/or diastolic BP ≥ 90mmHg
Begins before the 20th week of gestation, but often pre-existingthe pregnancy
Noproteinuria
No end-organ damage
Gestational hypertension
General
Asymptomatic
Systolic BP ≥ 140mmHg and/or diastolic BP ≥ 90mmHg
Begins after the 20th week of gestation
No history of pre-existinghypertension
Noproteinuria
No end-organ damage
preeclampsia
General
Occurs between 20 weeks of gestation and up to 6 weeks postpartum
Mild preeclampsia
Systolic BP ≥ 140mmHg, but < 160mmHg; and/or
Diastolic BP ≥ 90mmHg, but < 110mmHg
Proteinuria
Severe preeclampsia
Systolic BP ≥ 160mmHg; and/or
Diastolic BP ≥ 110mmHg
Proteinuria
End-organ damage
Mild preeclampsia BP readings, but the presence of proteinuria and end-organ damage = Severe preeclampsia
preeclampsia
Patho
Exact cause is unclear
Key feature – abnormal placental development
Normally, spiral arteries dilate to 5-10x normal size and develop into uteroplacental arteries; preeclampsia, spiral arteries are narrow and become fibrous → less blood supply → IUGR, fetal death
Pro-inflammatory proteins from the hypoperfused placenta enter maternal circulation → endothelial cells that line maternal blood vessels to become dysfunctional (vasoconstriction)
IUGR = Intrauterine growth restriction
TRIAD
Protein in the urine is a marker of glomerular damage
preeclampsia
Clin Man
Cerebral symptoms
Severeheadache
Altered mental status
Visual symptoms- reduced blood flow to the retina
Scotomata
Small area of the visual field has slightly worse visual acuity
Photophobia
Blurred vision
Temporaryblindness
Pulmonary edema
Dyspnea
Renal impairment withperipheral edema
Oliguria
Proteinuria
Hepatic impairment with RUQpain
HELLP syndorme
general
HELLP syndrome
Severe manifestation of preeclampsia
Endothelial injury → formation of tiny thrombi in the microvasculature and increased vascular permeability
Preeclampsia symptoms plus:
Hemolysis
Pallor
ElevatedLiverenzymes
RUQpain
Nausea andvomiting
LowPlatelets
May cause hepatichematomathat ruptures → hemoperitoneum
Serum aspartate aminotransferase (AST) and bilirubin are needed to evaluate liver function when making the diagnosis of HELLP syndrome
eclampsia
General
Preeclampsia with the presence ofseizures
Tonic-clonic seizures
Tonic phase
Abrupt LOC; stiffness of the extremities, chest, and back; potential for cyanosis
Clonic phase
Involuntary muscle twitching/jerking
Fetal seizure response
Bradycardia → tachycardia with heart rate variability; maternal stabilization → fetal stabilization
Positive ankle clonus
Rapid, muscular contraction and relaxation
Altered mental status
Preeclampsia & Eclampsia
Complications
Intracranial hemorrhage (stroke)
Pulmonary edema
Renal failure
Coagulopathy
Hemolysis
Liver injury
Thrombocytopenia
IUGR
Oligohydramnios
Placental abruption
Nonreassuring fetal status
HTN pregnancy
Dx
BP measurements on 2 separate occasions (at least 4 hours apart):
Systolic BP ≥ 140mmHg and/or
Diastolic BP ≥ 90mmHg
Urinalysis
Proteinuria criteria:
24-hoururinecollection ≥ 300 mg protein OR
Single voidedurineprotein/creatinine ratio ≥ 0.3
Dipstick reading of ≥ 2+ (use only if other quantitative methods not available)
DoNOTneed to wait 4 hours to confirm the diagnosis of severe preeclampsia prior to starting therapy
Preeclampsia
Dx without proteinuria (5)
Presenting withoutproteinuriamust meet 1 of the following criteria:
Thrombocytopenia (platelets< 100,000)
Renal insufficiency (baseline creatinine is doubled or serum creatinine > 1.1 mg/dL)
Pulmonary edema
Impairedliverfunction (AST/ALT> 2 times the upperlimitof normal)
New-onset headache that is unresponsive to medications and has no alternative cause
HELLP syndrome
Dx
Hemolysis
Anemia
LDH > 600 IU/L (> 2x upper limit of normal)
↑Bilirubin
Schistocytes on blood smear
↑ Liverenzymes (ASTand/orAST> 2x upperlimitof normal)
↓ Platelet count (< 100,000/mm3)
Eclampsia
Dx
Generalized tonic–clonicseizures
From intrapartum up to 72 hours postpartum
Secondary to untreated and/or undertreated preeclampsia
HTN pregnancy
Prevention and definitive Tx
Prevention
Used when 1 high-risk factor or ≥ 2 moderate-risk factors are present
Prophylaxis with 81 mg aspirin between 12 and 28 weeks and continued until delivery
Management
Definitive treatment of gestationalhypertension, preeclampsia, eclampsia, and HELLP is delivery
Abnormal findings that often require early delivery:
IUGR
Placental abruption, poor placental/umbilical blood flow
Nonreactive stress test
Abnormal amniotic fluid index (oligohydramnios)
HTN pregnancy
First-line therapies for BP control:
Labetalol
Hydralazine
Nifedipine
HTN pregnancy
Teratogenic BP medications:
ACE
ARB
Mineralocorticoid receptor antagonists - Potassium-sparing diuretics
Teratogenic BP medication are NOT used in pregnancy
HTN pregnancy
Time of delivery
Timing is dictated by BP control and disease severity
Delivery by induction of labor or cesarean section
Chronichypertension:
37‒40 weeks gestational age
Gestationalhypertensionand preeclampsia without severe features:
37 weeks gestational age
Preeclampsia with severe features and HELLP syndrome:
At the time of diagnosis if ≥ 34 weeks gestational age
Based on clinicaljudgmentif < 34 weeks gestational age
Eclampsia:
At the time of diagnosis, regardless ofgestational age
If preterm delivery is anticipated, a course ofcorticosteroidsis indicated to promote fetal lung maturity
HTN pregnancy
Magnesium seizure prophylaxis
Indications: Preeclampsia with severe features, HELLP syndrome, and Eclampsia
Magnesium sulfate loading dose of 4 g IV over 20 minutes, followed by at a constant IV infusion of 1–3 g/hour
Dose is adjusted based on the patient’s reflexes
Mechanism of action:
Triggers cerebral vasodilation, thus reducing ischemia generated by cerebral vasospasm during an eclamptic event
Acts competitively in blocking the entry of calcium into synaptic endings, thereby altering neuromuscular transmission
Monitor for magnesium toxicity or renal failure
Toxicity = loss of patellar reflexes,tachypneadue torespiratory muscle weakness
