Gestational diabetes/HTN pregnancy Flashcards

1
Q

Gestational Diabetes Mellitus (GDM)

General

A

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

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2
Q

GDM

Classification & Etiology

A

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

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3
Q

GDM

RF

A

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

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4
Q

GDM

Clin man

A

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

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5
Q

GDM

Dx and labs

A

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

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6
Q

Normal or Abnormal?

A

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

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7
Q

GDM

Glucose goals and lifestyle mods

A

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)

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8
Q

GDM

Pharm Tx
Dosing per trimester

A

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

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9
Q

Checking the baby post GDM

A

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

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10
Q

GDM

Complications

A

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

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11
Q

GDM

Shoulder Dystocia

A

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

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12
Q

GDM

Prognosis

A

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

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13
Q

Hypertensive Pregnancy Disorders

A

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

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14
Q

HTN pregnancy

RF

A

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

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15
Q

Chronic hypertension

General

A

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

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16
Q

Gestational hypertension

General

A

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

17
Q

preeclampsia

General

A

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

18
Q

preeclampsia

Patho

A

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

19
Q
A

TRIAD

Protein in the urine is a marker of glomerular damage

20
Q

preeclampsia

Clin Man

A

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

21
Q

HELLP syndorme

general

A

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

22
Q

eclampsia

General

A

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

23
Q

Preeclampsia & Eclampsia

Complications

A

Intracranial hemorrhage (stroke)
Pulmonary edema
Renal failure
Coagulopathy
Hemolysis
Liver injury
Thrombocytopenia
IUGR
Oligohydramnios
Placental abruption
Nonreassuring fetal status

24
Q

HTN pregnancy

Dx

A

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

25
Q

Preeclampsia

Dx without proteinuria (5)

A

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

26
Q

HELLP syndrome

Dx

A

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)

27
Q

Eclampsia

Dx

A

Generalized tonic–clonicseizures

From intrapartum up to 72 hours postpartum

Secondary to untreated and/or undertreated preeclampsia

28
Q

HTN pregnancy

Prevention and definitive Tx

A

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)

29
Q

HTN pregnancy

First-line therapies for BP control:

A

Labetalol
Hydralazine
Nifedipine

30
Q

HTN pregnancy

Teratogenic BP medications:

A

ACE
ARB
Mineralocorticoid receptor antagonists - Potassium-sparing diuretics

Teratogenic BP medication are NOT used in pregnancy

31
Q

HTN pregnancy

Time of delivery

A

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

32
Q

HTN pregnancy

Magnesium seizure prophylaxis

A

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