PREGESTATIONAL CONDITIONS

CARDIAC CONDITIONS

INCIDENCE: 1% or 1 in every 100 pregnancies. Over 75% of heart disease in pregnancy is valvular, often Rheumatic Fever or RHD.

Effects of pregnancy on heart disease:

1. Increased blood volume and cardiac output Cardiac output and blood volume increase about 50% more during

pregnancy (increase workload to the heart) During labor and delivery, cardiac workload increases even more

(every time the uterus contracts about 1 or 2 units of blood are autotransfused from utero-placental to maternal circulation. When contraction stops, this volume returns to uteroplacental and the heart may not be able to compensate with such rapid shifting.

After delivery, the uteroplacental blood returns to maternal circulation increasing once again blood volume.

A woman who receives epidural or spinal anesthesia, her blood vessels dilate and blood pressure decreases that results to decreased venous return which prompts the heart to compensate to meet body’s needs by pumping harder

Excessive blood loss during second stage of labor.2. Systemic vascular resistance drops by 25% during pregnancy lowering blood

pressure.3. Gravid uterus can dramatically affect venous return in some positions

compressing IVC and can lead to hypotension.

FUNCTIONAL CLASSIFICATIONS OF HEART DISEASE:

CLASS I/ uncompromised– Patient is asymptomatic with no limitation of physical activity, no angina pain or discomfort with ordinary activity. Perinatal mortality is 5%

CLASS II/ slightly compromised – patient with slight limitation of physical activity, ordinary activities cause dyspnea, fatigue, chest pain and palpitations. Perinatal mortality is 10-15%

CLASS III/markedly compromised – with marked limitation because ordinary activities cause excessive fatigue, palpitations, chest pain, and dyspnea, only comfortable at rest. Perinatal mortality is 35%.

CLASS IV/severely compromised – experienced symptoms even at rest, unable to perform any activity without discomfort, perinatal mortality is more than 50%. Condition should be corrected by surgery. Abortion could be considered if gestation is less than 14 weeks and cannot be corrected by surgery and also sterilization.

SIGNS AND SYMPTOMS:

1. Difficulty of breathing like dyspnea and orthopnea2. Palpitations lasting several minutes associated with lightheadedness3. Arrhythmias/ dysrhythmias 4. Chest pain5. Hemoptysis6. Syncope with exertion7. Cyanosis8. Clubbing of fingers9. Neck vein distention10.Systolic and diastolic murmurs

MANAGEMENT:

Prenatal Care:

1. Assessment – management depends on the functional capacity of the heart determined before the 3rd month pregnancy and at 7-8th months.

Diagnostic tests ECG/EKG – electrocardiogram records the electrical activity of the

heart and shows abnormal rhythms and detects heart muscle damage Echocardiography/ heart ultrasound – evaluates heart structures

and functions of heart by using sound waves recorded on electronic sensor that produce a moving picture of heart and heart valaves.

2. Promotion of rest – 8-10 hours of sleep at night and frequent rest periods during the day, lie down for 30 minutes after each meal, allowed only light works; consider housework assistance such as cleaning, laundry and marketing, severely affected patients may need to be confined in the hospital as early as mid-second trimester to ensure rest and management.

3. Diet High in iron, protein, minerals and vitamins Limit sodium intake after 8-12 weeks to avoid fluid retention Weight gain of no more than 24 lb to prevent further increase of

cardiac workload4. Avoid high altitudes, smoking, unpressurized planes, and alcoholic intake5. Prevent infection

Avoid people with infection Early treatment of infection

6. Instruct on danger signs of heart failure Cough with rales Increasing dyspnea, rales and edema

7. Medications Iron supplements Digoxin, quinidine, procainamide, adenosine, and verapamil and

betablockers like propranolol to prevent arrhythmias Cardiac glycosides/digitalis therapy to increase efficiency of heart’s

pumping function, coronary artery perfusion, stroke volume, and ventricular fillingNursing implications:1. Monitor for toxicity – signs and symptoms are halo around lights,

anorexia and diarrhea, bradycardia and PVC’s2. Monitor K levels for hypokalemia (normal=4-5.4 mEq/L) can

precipitate arrhythmias3. Provide potassium supplements to prevent digitalis toxicity and

hypokalemia

Nitroglycerine to relieve chest pain by peripheral and coronary vasodilation and decreases myocardial oxygen demandNursing implications:1. Take it 5 minutes before effort every 5 minutes for 15 minutes upto

3 tablets, if not relieved, seek consultation2. Store at dark, covered bottle and replace after 3 months of

opening, protect from sunlight3. Side effects include hypotension so take while sitting, flushing,

burning and stinging sensation on tongue (oral/sublingual), if patch, put on non hairy and clear area on the chest

4. Wear medic alert and carry medication at all times5. Notify physician if with severe headache, weakness, blurry vision,

irregular heartbeat and dry mouth Antibiotics as ordered Diuretics Heparin is safest anticoagulant for pregnant women, do not use

warfarin.Nursing implications:1. Avoid aspirin, acetaminophen, steroids, dark greens2. Monitor PT 3. Observe for signs of spontaneous bleeding4. Heparin is discontinued at least 12 hours before labor induction and

resumed 6-12 hours after delivery8. CPR and BLS and cardioversion if with cardiac arrest

Intrapartal Care:

1. Vaginal delivery is preferred because CS increases risk for hemorrhage and infection however contraindicated if patient is with aneurysm and coarctation of aorta

2. Early hospitalization3. Monitor FHR and V/S continuously

Every 15 minutes on 1st stage and more frequently during the 2nd stage. Report tachycardia and RR of more than 24 bpm

Invasive hemodynamic monitoring like arterial line, central line, and pulmonary catheterization may be needed for severe cases

4. Woman in labor is positioned in semi-fowler’s or left lateral recumbent not in lithotomy position

5. Pushing is contraindicated, epidural anesthesia is given for painless pushless deliver, forceps may be used for easier expulsion. Spinal anesthesia is contraindicated.

6. On the 4th stage: If legs were elevated during labor, lower legs promptly to reduce

drainage of peripherally pooled blood into systemic circulation Ergot products are contraindicated because of their vasopressor

effects, oxytocin is given after placental delivery Monitor for shock and cardiac failure

Postpartum Care:

1. Promote rest.2. Confinement until cardiac status is stable3. Early but gradual ambulation4. Medications as ordered

Antibiotics Stool softeners Sedatives to promote rest

5. Breast feeding is allowed in Class I and II if there is no sign of cardiac decompensation during pregnancy, labor and delivery

DIABETES MELLITUS

- A hereditary endocrine disorder characterized by inadequate insulin production that results to impaired glucose absorption and metabolism resulting to hyperglycemia

SIGNS AND SYMPTOMS:

1. Hyperglycemia2. Glycosuria3. Polyuria4. Polydipsia

5. Weight loss6. Ketoacidosis due to breakdown of fats and proteins

EFFECTS OF PREGNANCY ON GLUCOSE CONTROL -pregnancy is known to be a diabetogenic state due to effects of placental hormones especially HPL which increases cells’ resistance to insulin

COMPLICATIONS:

1. Mother Increased tendency to preeclampsia and eclampsia, UTI and yeast

infection like candidiasis Higher incidence of dystocia due to large infant Large infants result to over distention of uterus increasing risk for

atony and hemorrhage Maternal death Diabetic retinopathy Diabetic nephropathy

2. Fetus/ infant With chronic hyperglycemia, placental insufficiency due to vascular

changes causing IUGR 1st trimester – spontaneous abortion and fetal anomalies 3rd trimester – intrauterine demise Hydramnios Prematurity Hyperbilirubinemia Hypocalcemia Predisposition to obesity and DM later in life Birth defects like heart, vessels, brain, spine, urinary and digestive

anomalies Macrosomia – maternal glucose stimulates fetal pancreas to produce

high insulin and converts this glucose to fats Stillbirth Hypoglycemia Respiratory distress – for too much insulin or glucose delays lung

maturity

INCIDENCE:

- Diabetes is most common endocrine disorder affecting pregnancy complicating about 4%

- Gestational diabetes – 88%, Type II -8%, Type I -4%

TYPES:

1. Type I-autodestruction of pancreatic cells by antibodies, insulin dependent for life

2. Type II – gradual onset, there is production of insulin but the cells developed resistance to it

3. Specific types – influenced by other conditions such as pancreatitis, infection and genetic defects

4. Gestational diabetes – develops only during pregnancy5. Pre-gestational diabetes – woman already have DM before conception

ASSESSMENT:

Risk Factors

1. Family history of type II2. Glycosuria3. Obesity – BMI is greater than 25 kg/m2 and waist to hip ration of >14. History of gestational diabetes with previous pregnancy5. With history of LGA delivery (more than 9 lbs or 4000 g)6. Previous impaired fasting glucose with fasting plasma glucose of 110-125

mg/dL7. Previous impaired glucose tolerance test with OGTT 2 hour glucose value of

140-199 mg/dL

Screening

1. 50 g Oral Glucose Tolerance Test (OGTT) between 24-28 weeks AOG irregardless of time of day and meals taken by mother. If plasma glucose value is >140 mg?dL after 1 hour, 100 g 3 hour OGTT is performed for further confirmation

2. FBS – done on an empty stomach 8 hours prior test, water can be given. 3. OGTT – FBS is taken first. Patient is given 75 g glucose dissolved in water.

Blood sample is taken and measured at 1, 2 and 3 hours after taking it. 4. GD is confirmed if 2 results from a 100 g OGTT indicate elevation. Normal

values are: Fasting plasma glucose – 95 mg/dL 1 hour plasma glucose - 180 mg/dL 2 hour plasma glucose - 155 mg/dL 3 hour plasma glucose – 140 mg/dL If one hour value is high, it represents decreased insulin capacity.

Limiting simple sugar in the diet is for lifetime An elevated 3 hour value represents decreased insulin receptors

MANAGEMENT:

Prenatal:

1. Pregnancy planning – a diabetic woman should have a stable disease state before conception and must be evidenced by:

Normal fasting blood glucose levels Normal glycosylated hemoglobin levels of 7 – 10% (reflects the

average measurement of the glucose levels over past 100-120 days)

2. Prenatal clinic visits: every 2 weeks upto 36 weeks AOG then weekly3. Diabetic diet

Caloric intake should be enough to meet pregnancy needs (1,800-2,400 cal/day)

20-25% caloric intake should come from protein rich foods 40-50% from CHO 30-40% from polyunsaturated fats Weight gain should be about 24 lbs Instruct to: reduce saturated fats and cholesterol and concentrated

sugars, increase dietary fiber, avoid feasting and fasting Have woman become familiar with food exchange list and caloric

values of foods4. Exercise – before, instruct mother to eat complex CHO to prevent

hypoglycemia5. Insulin therapy

-GD usually responds well to diet and exercise therapy however if blood glucose cannot be controlled or maintained, insulin therapy may be needed-Humulin is safest to use for pregnant women-schedule is twice a day, before breakfast and 30 minutes before dinner. Often, a fast and intermediate acting insulin are combined.-hypoglycemia could occur during the peak time of action

Short acting/regular Insulin – onset occurs 1 hour with peak action in 2 – 4 hours

Intermediate/ Lente – onset is 2-4 hours with peak at 8-12 hours Long acting/ Ultralente – onset is 4-8 hours with peak of 16-18

hours- instruct on signs of hypoglycemia caused by excessive insulin, exercise and insufficient dietary intake:

Pallor, weakness, numbness, headache, perspiration, confusion, irritability, blurred vision, hunger, convulsion, coma

Instruct CHO foods that can correct it like fruit juices, cola, sugar candy

6. Self monitoring of blood glucose (SMBG) Type I patients are recommended to test at least 3x a day.

Deserved values are:

1. Before meal –95 mg/dL2. One hour after - <140 mg/dL3. Two hour after - <120 mg/dL

She can decrease testing to 3x a week if she has good understanding on diet and glucose values are of desired range

7. Fetal well being monitoring8. Continuous evaluation of diabetic complications

Intrapartal Care:

1. Plan for delivery at 36-40 weeks, when the fetus is matured enough and not too large to cause cephalopelvic disproportion

2. Regular amniocentesis – L/S ration for the infants of diabetic mother is 3.5:1

3. Hospitalization and labor induction4. Regular insulin is given on the day of delivery, not long acting insulin

because insulin requirement is lowered immediately after delivery5. CS if infant is too large for vaginal delivery and that the cervix is not ripe

and the baby is in distress

Postpartum Care:

1. Inform woman that GD may recur in next pregnancy2. Women who developed GD have higher risk to develop DM later in life3. Newborn care:

Keep warm Observe respiration capacity Observe signs of hypoglycemia like shrill cry and weakness, give

glucose water Observe signs of hypocalcemia like tetany and tremors, give

calcium gluconate Observe for congenital anomalies like esophageal atresia and

neural tube defect4. IUD and oral pills are contraindicated as contraceptives. Norplant

(progestin implant system) and minipills (progestin only) may be used safely.

ANEMIAS OF PREGNANCY

- Is a condition of few RBC or a lowered ability of the RBC. In pregnancy, it is defined as hemoglobin level less than 11 g/dL in the 1st and 3rd trimester and 10.5 g/dL in the 2nd.

TYPES:

1. Iron Deficiency Anemia (IDA) –

2. Vitamin B12 deficiency3. Anemia due to Blood loss4. Folate Deficiency Anemia

RISK FACTORS:

1. Poor nutrition2. Excess alcohol consumption3. Medical history of any disorder that reduces absorption of nutrients4. Use of anticonvulsant drugs5. History of use of oral contraceptives6. G6PD deficiency common in Mediterranean, African Americans and Jewish;

Sickle cell disease common in African Americans, Italians and middle eastern and east Indians.

COMPLICATIONS:

1. Premature labor2. IUGR3. Complicated Blood Loss4. Increased susceptibility to infection

IRON DEFICIENCY ANEMIA

-Is the most common type during pregnancy. However, the newborn is not affected for the iron supply to the fetus is same with that of the non-anemic mother.

Predisposing Factors:

1. Poor diet/nutrition2. Heavy menses3. Pregnancies at close intervals or successive pregnancies

Signs and symptoms:

1. Easy fatigability2. Sensitivity to cold3. Proneness to infection4. Dizziness5. Laboratory Findings like in CBC

Effects on Pregnancy:

1. Decreased resistance to infection2. Prematurity and low birth weight infants3. Predispose to heavy bleeding during labor and delivery4. High digestive discomfort of pregnancy

Management:

1. Oral iron supplementation 200 mg of elemental iron daily Ferrous sulfate is the most absorbable, ferrous fumarate and

ferrous gluconate Side effects of these drugs are tarry stools, constipation and

gastrointestinal discomfort Never take with milk and calcium supplements Take with citrus juice to enhance absorption If given in liquid form, use straw or rinse mouth after If given parenterally, Z-track is used and do not massage Oral iron is continued upto 3 months after anemia is corrected to

build mother’s iron reserves2. Increase intake of vitamin C3. Increase intake of iron rich foods: lean meat, liver, dark green leafy

vegetables. Good food sources of iron include the following: Meats – beef, pork, lamb, liver, and other organ meats Poultry – chicken, duck, turkey, liver (especially dark meat) Fish – shellfish including clams, mussels, oysters, sardines and

anchovies Leafy greens of the cabbage family, such as broccoli, kale, turnip

greens and collards Legumes such as lima beans and green peas Yeast – leavened whole-wheat bread and rolls Iron – enriched white bread, pasta, rice, and cereals

ANEMIA FROM ACUTE BLOOD LOSS

Anemia from acute blood loss is due to bleeding disorders of pregnancy. These include: ectopic pregnancy, abortion, placenta previa, h-mole, and placenta previa and abruption placenta.

MANAGEMENT

1. If the hemoglobin level is more than 7m g/dl, iron replacement therapy until three months after anemia has been corrected.

2. For massive hemorrhage: blood transfusion of the whole blood. Packed red blood cells and plasma expanders to restore normal blood volume.

MEGALOBLASTIC ANEMIA

Megaloblastic anemia is a group of hematologic diseases caused by impaired DNA synthesis resulting in blood and bone marrow abnormalities.

TYPES OF MEGALOBLASTIC ANEMIA

1. Folic Acid Deficiency/Pernicious Anemia

2. Vitamin B12 Deficiency/Addison Pernicious Anemia

FOLIC ACID DEFICIENCY: Folic acid is necessary for the normal formation and nutrition of red blood cells. Deficiency in folic acid leads to the formation of large and immature blood cells that have shorter life span than normal red blood cells.

Effects on Pregnancy: Abruptio Placenta, Abortion, Neural Tube defects

Predisposing factors:

- long term use of pills- poor nutrition- multiple pregnancies- successive pregnancies

signs and symptoms

- nausea- vomiting- anorexia

Management:

1. treatment: Folic acid supplement 1 mg/day accompanied by iron2. prevention by vitamin of 400 mcg of folic acid daily and intake of: leafy,

dark green veggies, dried beans and peas, citrus fruits and juices/berries, fortified breakfast cereals, enriched grain products

VITAMIN B12 DEFICIENCY: Addison Pernicious Anemia is rare, there is autoimmune disorder caused by failure to absorb Vitamin B12 due to lack of intrinsic factor.

Causes:

- total gastrectomy (treated with lifetime monthly administration of 1000 mcg cyanocobalamine IM)

- Crohn’s Disease- Ilial resection- Bacterial overgrowth in large intestine

HEMOLYTIC DISORDERS IN PREGNANCY

-hemolytic disease of the newborn is caused either by Rh incompatibility or ABO incompatibility. The mother produces antibodies that destroy RBC of the fetus which results to fetal death and hyperbilirubinemia.

INCIDENCE:

-10% of women are at risk for Rh isoimmunization-neonatal morbidity is 1:1000

ABO INCOMPATIBILITY

-every person has a blood type either A,B, O or AB. These are found as proteins in RBC and body fluids

-ABO incompatibility in pregnancy occurs when maternal blood type is O and fetus is:

Type A – most common Type B- most serious Type AB- rare

-the mother gas antibodies against blood type A and B even before pregnancy and circulate in the maternal system so if she conceives a fetus with A or B blood and the fetal blood happens to enter maternal circulation or the other way around, the antibodies attack fetal blood

-it is uncommon for maternal blood to enter the fetal circulation because the antibodies are large IgM that cannot enter the placental barrier. Only during delivery or trauma to the uterine wall can it occur causing hemolytic disease in newborns.

RH INCOMPATIBILITY

Rh factor – a distinct protein antigen genetically determined that is found on the covering of RBC. If this is present in the cells, the person is Rh positive, if not, Rh negative. Presence of this antigen in blood makes it incompatible for blood that does not have it. The Rh is considered as a n antigen/foreign by the Rh negative blood prompting the person who is Rh negative to produce antibodies to destroy this antigen.

-about 85% are Rh positive and 15% are Rh negative

-the Rh positive gene is stronger/ more dominant that the Rh negative gene, even if combined with an Rh negative gene, the Rh positive gene prevails;

Both parents are Rh + = fetus is Rh + If one parent has Rh+ = fetus is Rh + If both are Rh – = fetus Rh –

Rh sensitization or isoimmunization – exposure of Rh negative blood to an Rh positive blood that results to production of antibodies against Rh antigens. It can occur by:

Sensitization from a previous pregnancy which occurs if a woman who is Rh negative conceives an Rh positive fetus. The fetal blood entered maternal circulation during delivery of placenta.

Inadequate response to prophylaxis Incompatible blood transfusion

- 0.5 mL of fetal Rh positive blood that enters maternal circulation of Rh negative blood can stimulate massive production of antibodies which is detrimental to a future conception of Rh positive fetus.

-these antibodies do not disappear in maternal blood stream once present. If fetus is Rh positive, the antibodies will attack the fetal blood causing erythroblastosis fetalis during pregnancy or hemolytic disease in newborns (HDN).

Effects of Erythroblastocis Fetalis:

anemia splenomegaly hepatomegaly hyperbilirubinemia hydrops fetalis stillbirth

Prenatal Screening

History: if woman is Rh negative, nurse must elicit careful history of past pregnancies, blood transfusion and abortion, invasive diagnostic procedure during pregnancy such as amniocentesis, intrauterine percutaneous unbilical blood sampling or chorionic blood sampling.Screening tests: Blood typing and Rh factor determination, if mother is Rh negative, father’s Rh should also be determined. If father is Rh positive:

Antibody titer test by Coomb’s test is done to find out if mother is sensitized

Direct Coomb’s test to determine presence of antibodies in fetal cord blood

If the antibody titer is negative, mother is given Rh immune globulin IM or anti Rho(D) gamma globulin (RhoGAM) at 28 weeks and within 72 hours after delivery to prevent maternal blood production of antibodies.

RhoGAM should be given to all Rh (-) women who delivered Rh (+) fetus, had ectopic pregnancies, stillbirth and abortion, had

received ABO compatible Rh positive blood, had an invasive procedure like amniocentesis

Signs and symptoms

-Mother is asymptomatic unless baby dies in utero and not born right away, cessation of pregnancy signs and symptoms, no fetal movements, not affected by erythroblastocis fetalis

MANAGEMENT:

Fetal surveillance: This is instituted if mother titer is positive. When the titer rises to 1:16 or more:

Amniocentesis every 2 weeks beginning 26 weeks gestation for examination of bilirubin level

Percutaneous umbilical blood sampling may be done if severe hemolysis is detected in amniocentesis, can be started at 18-20 weeks gestation

Ultrasound to assess complications such as hydrops fetalis, polyhydramnios, and enlargement of the heart

Intrauterine blood fetal transfusion:

to directly improve fetal tissue oxygenation prevents/reverses hydrops fetalis

-can be given at 10-day to 2 weeks intervals generally until 34-36 weeks gestation, when fetus is mature enough to be delivered

Labor and delivery: the goal is to minimize opportunity for maternal-fetal bleeds

do not remove placenta manually clamp cord immediately after birth ensure that a blood sample is drawn from the mother for blood test shortly

after birth to test for presence and quantity of fetal blood that entered maternal circulation.

Postpartum Care: the goal are to prevent sensitization in the unsensitized mother and to quickly diagnose and treat hemolytic disease in the newborn.

Immunize mother with RhoGAM within 72 hours after delivery if coomb’s test is negative

If blood test after delivery shows large quantity of fetal blood in maternal circulation, repeated doses of Rh immune globulin are necessary. Additional 300 mcg is given for every 30 mL of Rh positive blood or for every 15 mL fetal RBC in maternal circulation. These additional doses may be given at one time using multiple injection sites or at 12 hour intervals.

If Coomb’s test is positive for both mother and fetus, RhoGAM is no longer given because antibodies are already present but the newborn should be monitored for signs of hemolysis and treated promptly.

Management of hemolysis in newborns:

1. Suspension of BF in the first 24 hours to prevent pregnanediol in interfering the conjugation of indirect to direct bilirubin

2. Photothrapy speeds up maturation of liver to enable conjugation of indirect to direct bilirubin more efficiently

Close eyes and cover with dressing Expect stool to be loose and bright green in color and urine to be dark in

color because of urobilinogen level Assess for DHN. Monitor I and O, skin turgor Offer glucose water every 2 hours Maintain body temp between 36-37 degree Celsius Infant should be removed from isolette during feedings Exposure to early morning sunlight

3. Exchange transfusion Beneficial effects include removal of 85%s of sensitized RBC, bilirubin

from fetal circulation and prevents congestive heart failure Indicated when bilirubin level is 5 mg per 100mL at birth, 10 mg per 100

mL at 8 hours, 12 mg per 100 mL at 16 hours, 15 mg per 100 mL at 24 hours; bilirubin is rising more than 0.5 mg/hr in Rh incompatibility and 1 mg/hr in ABO incompatibility

The type of blood used for transfusion is O Rh negative blood even if the infant is Rh positive.

It involves alternately withdrawing minute amounts of infant’s blood (20 mL) and then replacing it with donor’s blood. Umbilical catheter is used to perform the exchange double the amount withdrawn.

Infusion of albumin several hours before the procedure increases the number of bilirubin binding sites and makes procedure more effective.

Calcium gluconate is administered after each 100 mL of blood to prevent the ACD (acid-citrate-destrose) component of stored blood from lowering calcium levels of infant.

If blood is heparinized, protamine sulfate is administered after transfusion to restore clotting ability.

Monitor HR,RR and BT during transfusion; umbilical bleeding and vital signs every 15 minutes during the first hour and then every 30 minutes for three hours more. Bilirubin level is monitored for 3 days after procedure.

HYPERTHYROIDISM AND HYPOTHYROIDISM

Hyperthyroidism

Hyperthyroidism in pregnancy is usually caused by Graves’ disease - Graves’ disease is an autoimmune disorder, which means the body’s immune system makes antibodies that act against its own healthy cells and tissues. In Graves’ disease, the immune system makes an antibody called thyroid stimulating immunoglobulin, sometimes called TSH receptor antibody, which mimics TSH and causes the thyroid to make too much thyroid hormone.

occurs in about one of every 500 pregnancies Rarely, hyperthyroidism in pregnancy is caused by hyperemesis gravidarum

—severe nausea and vomiting that can lead to weight loss and dehydration. This extreme nausea and vomiting is believed to be triggered by high levels of hCG, which can also lead to temporary hyperthyroidism that usually resolves by the second half of pregnancy.

Uncontrolled hyperthyroidism during pregnancy can lead to:

congestive heart failure preeclampsia—a dangerous rise in blood pressure in late pregnancy thyroid storm—a sudden, severe worsening of symptoms miscarriage premature birth low birthweight

Hyperthyroidism in a newborn can result in rapid heart rate that can lead to heart failure, poor weight gain, irritability, and sometimes an enlarged thyroid that can press against the windpipe and interfere with breathing. Women with Graves’ disease and their newborns should be closely monitored by their health care team.

Diagnosis: Hyperthyroidism is diagnosed through a careful review of symptoms, as well as blood tests to measure TSH, T4, and T3 levels.

Signs and symptoms: some are common features in normal pregnancies, including increased heart rate, heat intolerance, and fatigue.

Other symptoms more indicative of hyperthyroidism:

Rapid and irregular heartbeat a fine tremor unexplained weight loss or failure to have normal pregnancy weight gain severe nausea and vomiting associated with hyperemesis gravidarum.

Management:

Mild hyperthyroidism in which TSH is low but free T4 is normal does not require treatment.

More severe hyperthyroidism is treated with propylthiouracil or sometimes methimazole (Tapazole), drugs that interfere with thyroid hormone production.

Antithyroid drugs cross the placenta in small amounts and can decrease fetal thyroid hormone production, so the lowest possible dose should be used to avoid hypothyroidism in the baby.

Rarely, surgery to remove all or part of the thyroid gland is considered for women who cannot tolerate propylthiouracil or methimazole.

Radioactive iodine treatment is not an option for pregnant women because it can damage the fetal thyroid gland.

Hypothyroidism

Hypothyroidism in pregnancy is usually caused by Hashimoto’s disease – Hashimoto’s disease is an autoimmune disorder. In Hashimoto’s disease, the immune system makes antibodies that attack cells in the thyroid and interfere with their ability to produce thyroid hormones. White blood cells also invade the thyroid and decrease thyroid hormone production.

Occurs in one to three of every 1,000 pregnancies Hypothyroidism in pregnancy can also result from existing hypothyroidism

that is inadequately treated or from prior destruction or removal of the thyroid as a treatment for hyperthyroidism

Effects to the mother and baby:

congestive heart failure preeclampsia anemia—a disorder in which the blood does not carry enough oxygen to the

body’s tissues miscarriage low birthweight stillbirth

Because thyroid hormones are crucial to fetal brain and nervous system development, uncontrolled hypothyroidism—especially during the first trimester—can lead to cognitive and developmental disabilities in the baby.

Diagnosis: a careful review of symptoms and measurement of TSH and T4 levels.

Signs and symptoms: extreme fatigue, cold intolerance, muscle cramps, constipation, and problems with memory or concentration. High levels of TSH and low levels of free T4 generally indicate hypothyroidism. Because of normal pregnancy-related changes in thyroid function, test results must be interpreted with caution.

Management:

synthetic thyroxine, which is identical to the T4 made by the thyroid gland Women with pre-existing hypothyroidism will need to increase their

prepregnancy dose of thyroxine to maintain normal thyroid function Thyroid function should be checked every 6 to 8 weeks during pregnancy.

Synthetic thyroxine is safe for the fetus and necessary for its well-being if the mother has hypothyroidism.

HIV/AIDS IN PREGNANCY

virus is contracted through sexual intercourse, exposure to infected blood and by vertical transmission across the placenta to the fetus at birth or by breast milk to the newborn

caused by a retrovirus that infects and disables T-lymphocytesRisk Factors:

a. multiple sexual partnersb. bisexual partnersc. IV drug used. Blood transfusions (rare)

Diagnostic Procedures:

a. CD4 cell count – determines how many T4 cell are present and functioning

b. ELISAc. Western blot

Maternal Risks:

more prone to other STI’s, toxoplasmosis and cytomegalovirus neurologic involvement tuberculosis

Fetal/Neonatal Risks:

low birth weight preterm birth

Management: Zidovudine (ZVD)

SUBSTANCE ABUSE IN PREGNANCY

- Substance abuse occurs when a person experiences difficulties with work, family, social relations and health as a result of alcohol or drug use.

Cocaine -increases the likelihood of a birth defect and may also leave the child dependent on the substance, experiencing withdrawal symptoms such as muscle spasms, sleeplessness and feedi

Maternal Risks

1. Spontaneous first trimester abortion 2. Abruption placenta

Fetal/Neonatal Risks

1. Intrauterine Growth Restriction (IUGR) 2. Preterm birth 3. stillbirth

Nicotine Maternal Risks

1. Spontaneous abortion2. placental abruption

Fetal/Neonatal Risks

1. low-birthweight infant 2. Cleft lip and palate 3. Sudden Infant Death Syndrome (SIDS)

Marijuana

- increases the amount of carbon dioxide and carbon monoxide present in the blood of a pregnant woman, lowering the amount of oxygen supplied to the baby, and increasing the baby's risk of developmental and behavioral problems.

Heroin

-leads to premature birth and low-birth weight, but can cause more serious problems such as hypoglycemia (low blood sugar), intracranial hemorrhages (brain bleeding) and withdrawal symptoms.

Hallucinogens

-such as LSD and PCP, has the potential to cause brain damage to the baby or cause the baby to develop poor muscle control and, when used frequently, hallucinogens can cause the baby to suffer withdrawal symptoms.

Methamphetamine

-cause an increase in the baby's heart rate similar to that which the mother experiences, can reduce the level of oxygen supplied to the baby, can increase the chance of premature labor and low-birth weight, and cause the baby to suffer withdrawal symptoms.

Alcohol-can lead to premature birth, low birth weight, a variety of physical and mental defects, and a number of fetal alcohol syndrome disorders (FAS) - is a term to identify the conditions found occurring among infants exposed to alcohol prior to birth: problems with eating, sleeping, hearing, eyesight, low-birth weight and underdevelopment.

Maternal Risks

1. Maternal malnutrition2. Bone marrow suppression

3. Increased incidence of infection 4. Liver disease 5. Withdrawal seizures in the intrapartal period 6. Delirium tremens in the postpartal period

Fetal/Neonatal Risks

1. Congenital defects 2. Withdrawal syndrome in the newborn3. Fetal alcohol syndrome