Chapter 25 Endocrine Disorders in Pregnancy Flashcards

1
Q

diagnostic criteria for type 2 diabetes mellitus:

A

added hemoglobin A1c of >= 6.5

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2
Q

are there differences in pregnancy outcomes / glycemic control when pregestational diabetes is treated with subcutaneous insulin or insulin pump?

A

no

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3
Q

Lagner and colleagues found

A

glyburide and insulin equally efficacious in treatment of gestational diabetes mellitus (GDM) in all severity levels.

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4
Q

PTU may be rarely associated with

A

liver toxicity; therefore, liver function tests should be monitored during pregnancy

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5
Q

levothyroxine requirements have been seen to increase as early as 5th week of gestation. thyroid hormone important for cognitive development. it is recommended that levothyroxine be increased ___ upon a +pregnancy test

A

increase levothyroxine by 30% after a +pregnancy test

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6
Q

American Diabetic Association outlined 4 criteria for dx of type2 diabetes in nonpregnant :

A
  1. casual plasma glucose of >= 200 mg/dL
  2. fasting plasma glucose of >= 126mg/dl
  3. 2 hr glucose value of >= 200mg/dL on 75g, 2-h gTT
  4. hemoglobin a1c>= 6.5%
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7
Q

management of pregestational diabetes:

A

retinal and renal health; any meds being taken, esp antihypertensive or thyroid medications. assessment of patient’s risk of complications during pregnancy, including worsening of renal or ophthalmologic function.

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8
Q

gestational diabetes:

A

risk of fetal structural anomaly FOURFOLD to EIGHTFOLD higher.

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9
Q

the major congenital anomalies in DM preg pts occured in ___% for type1 DM and ___% for type2DM

A

4.8% for type1 diabetes and
4.3% for type2 diabetes
for congenital anomalies

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10
Q

Neural tube defects in insulin dependent diabetics increased ___, and congenital heart disease increased ___.

A

NT defects insulin dependent 4.2fold

congenital heart defect increased 3.4fold.

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11
Q

use of REGULAR insulin before each meal helps limit postprandial hyperglycemia.

A

true

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12
Q

to provide basal insulin levels between feedings, a longer-acting preparation is necessary such as isoprostane insulin (NPH) or insulin zinc (Lente)

A

true

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13
Q

dosing for DM

A

2/3 of total insulin in the morning, of which 2/3 are intermediate acting and 1/3 is regular insulin.

remaining 1/3 of the total insulin dose is given in the evening: 50% short acting insulin given prior to dinner, and 50% intermediate acting insulin given at bedtime.

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14
Q

elective c-s for suspected fetal macrosomia (US of greater than ____) would require 443 c/s to avoid one permanent brachial plexus injury

A

4500g.

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15
Q

preeclampsia is more common among women with diabetes, 2-3x more likely in women with pregestational diabetes.

A

true

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16
Q

renal function assessment should be performed EVERY TRIMESTER in women with evidence of pregestational diabetes

A

creatinine, blood urea nitrogen (bun), uric acid, 24 hr urine collection.

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17
Q

polyhydramnios

A

any single verticle pocket of amniotic fluid deeper than 8cm. or when sum of 4 pockets exceeds 24cm.

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18
Q

main clinical problems associated with hydramnios are

A

fetal malposition and preterm labor.

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19
Q

the nondiabetic fetus achieves pulmonary maturity at what gestational age?

A

34-35 weeks.

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20
Q

fetal lung maturity assay by presence of more than ……. in amniotic fluid from amniocentesis specimen

A

> 3% phosphatidyl glycerol

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21
Q

Gestational Diabetes definition:

A

glucose intolerance that begins or is first recognized during pregnancy.

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22
Q

risk factors for GDM:

A
  1. maternal age of 35 yrs or more
  2. BMI > 22kg/meter squared
  3. asian, latin
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23
Q

diagnosis of GDM:

A

screening with 50g glucose at 24-28 weeks.

24
Q

definitive diagnosis of gestational diabetes:

A

100g GTT; 2 or more values must be met or exceeded for diagnosis of GDM. overnight fasting.

25
Q

management of GDM:

A

glubyride: 2nd generation SULFONYLUREA. has been shown to cross placenta minimally .
Lagner and associates (2000) compared glyburide and insulin with GDM. showed equivalently excellent maternal glycemic control and perinatal outcomes.

26
Q

Metformin

A

frequently employed in pts with PCOS and type2 DM to improve insulin resistance and fertility.
-Metformin therapy has been demonstrated to improve success of ovulation induction and may reduce 1st trimester loss in women with PCOS.

27
Q

Dysregulation of local follicle regulatory systems by androgens and other factors impedes normal follicular growth, resulting in follicular arrest at the 4 to 8 mm diameter size [6]. A dominant follicle (ie, 18 to 25 mm in diameter) does not develop and, therefore, ovulation does not occur. Thus, the combination of elevated LH, hyperinsulinemia, ovarian androgen overproduction, and disruption of follicle growth produces the PCOS phenotype of oligoovulation and hyperandrogenism.

A

true

28
Q

metformin’s major effect is

A

DECREASE hepatic GLUCOSE production thus REDUCING the need for insulin secretion; it also decreases intestinal absorption of glucose and modestly improves insulin sensitivity. PRIMARILY used for type2 DM but also used for PCOS. Unlike sulfonylureas, it does not produce hypoglycemia in either normal subjects or patients with type 2 diabetes

29
Q

The most common side effects of metformin are gastrointestinal:

A

diarrhea, nausea or vomiting, flatulence, indigestion, and abdominal discomfort.

30
Q

dose of metformin:

A

500mg daily if ER, take at dinner time with meals.

31
Q

Although it might be preferable to treat only insulin-resistant women with PCOS, there is currently no readily available, reliable test to evaluate the presence of insulin resistance. Some clinicians do not test at all; others perform an oral glucose tolerance test to look for impaired glucose tolerance and check for elevated insulin levels.

A

true

32
Q

Maternal thyroid diseases.

A

estrogen dependent increase in thyroid-binding globulin. results in an increase in total thyroxine (TT4) and total triiodothyronine (TT3) levels throughout pregnancy.

33
Q

HCG has a stimulatory effect on the thyroid, such that

A

TSH can be NORMAL or DECREASED in 1st and early second trimester.

34
Q

Maternal TSH does NOT cross placenta

A

true

35
Q

maternal thyroid hormones and thyrotropin-releasing hormone (TRH) are transferred to the fetus throughout gestation.

A

true

36
Q

transplacental transfer of thyroid-stimulating immunoglobulin (TSI) may occur, causing fetal

A

thyrotoxicosis.

37
Q

other substances that may be transferred from maternal compartment to fetal compartment and affect fetal thyroid function are

A

iodine, radioactive isotope of iodine, propylthiouracil (PTU), and methimazole.

38
Q

HYPERTHYROIDISM results in increase of

A

low birth weight delivery

trend toward higher neonatal mortality.

39
Q

most common causes of thyrotoxicosis (85%)

A

is Graves disease.
other causes are acute thyroiditis, Hashimoto disease, hydatiform mole, choriocarcinoma, toxic nodular goiter, toxic adenoma.

40
Q

dx of hyperthyroidism

A

intolerance to heat, nerousness, irritability, emotional lability, increased perspiration, tachycardia and anxiety.

41
Q

lab difficult to eval because total serum thyroxin (T4) levels are normally elevated during pregnancy as a result of estrogen induced increases in thyroxine-binding globulin

A

true

42
Q

diagnostic lab:

A

low TSH, high free thyroxine T4

43
Q

methimazone thought to be associated with aplasia cutis in offspring. however, this causal relationship hasn’t been proved

A

true

44
Q

PTU crosses placenta more slowly than methimazole, and has become drug of choice during pregnancy.

A

PTU drug of choice in pregnancy. may be associated with liver toxicity, need to monitor liver function tests during pregnancy.

45
Q

Once hyperthyroid under control, important to keepPTU dose as low as possible, preferably <100mg daily. because

A

drug crosses placenta and blocks fetal thyroid function, possibly producing hypothyroidism in fetus.

46
Q

Hypothyroidism leading cause is

A

hashimoto’s thyroiditis - chronic autoimmune thyroiditis, characterized by painless inflammation and enlargement of thyroid gland.

47
Q

other causes of primary hypothyroidism, include iodine deficiency, thyroidectomy, ablative radioiodine therapy for hyperthyroidism

A

true

48
Q

2ndary causes of hypothyroidism:

A

sheehan’s syndrome.

49
Q

sheehan’s syndrome caused by

A

obstetric hemorrhage leading to pituitary ischemia, necrosis, and abnormalities in all pitituary hormones, lymphocytic hypophysitis, and hypophysectomy.

50
Q

signs and sx of hypothyroidism:

A

fatigue, cold intolerance, cramping, constipation, weight gain, hair loss, insomnia, mental slowness.

51
Q

def of hypothyroidism in labs:

A

high tSH, low free T4

52
Q

subclinical hypothyroidism

A

high TSH, freeT4normal.

53
Q

goal of therapy is normalization of TSH. TSH checked at

A

4-6 week increments and dose of levothyroxine adjusted by 25-50 increments.

54
Q

levothyroxine requirements have een seen to increase as early as 5th week. it is important for __ development and is recommended that doses of levothyroxine are increased 30% upon a + pregnancy test

A

levothyroxine requirements are important for cognitive development of the fetus, it is recommended an increased dose of 30%

55
Q

levels of vitamin D increase

A

2-3 fold.