OBSTETRICS & GYNECOLOGY II 2.

04
ANEMIA, PULMONARY, AND THYROID DISORDERS
August 9, 2019 | Dr. Vidanes
Transcriber/s: 9A

OUTLINE  Greatest during the second trimester

 Anemia  Plasma volume virtually ceases late in pregnancy (3rd
 Iron Deficiency Anemia trimester) but Hb mass continue to increase (where
 Anemia from Acute Blood Loss the criteria for diagnosing anemia increases again)
 Anemia of Chronic Disease  Late in pregnancy, plasma expansion essentially
 Megaloblastic Anemia ceases, while hemoglobin mass continues to accrue
 Thalassemias  28-32 weeks AOG (peak of anemia)
 Pulmonary Disorders
 Bronchial Asthma FROM 2020 trans
 Pneumonia (Bacterial, Influenza) Expansion in the plasma volume is a maternal physiologic
 Tuberculosis process in pregnancy and is necessary as a preparation for
 Thyroid Disorders birth where a large amount of blood is lost during delivery.
 Hyperthyroidism
 Thyrotoxicosis
 Thyroid storm
 Hypothyroidism
LEGEND:
Past Trans Recordings

OBJECTIVES:
 Correctly diagnose anemia during pregnancy
 Formulate appropriate management plan for anemia
in pregnancy
 Correctly diagnose pulmonary disease in pregnancy
 Formulate the appropriate management plan for
pulmonary diseases in pregnancy
 Correctly diagnose thyroid disorders in pregnancy
 Formulate the appropriate management plan for Figure 1. Mean hemoglobin concentrations (black line) and
thyroid disorders in pregnancy 5th and 95th percentile (blue lines) of healthy pregnant
women taking iron supplements.
ANEMIA
 WHO estimates that global prevalence of anemia is
25% (1.62 billion people; confidence interval 1.50- FROM 2020 trans
1.74 billion). Approaching second trimester, it decreases but later on it
 Food and Nutrition Research Institute 2012 eventually increases. After delivery, the Hb will fluctuate
o Philippines (Maternal anemia is 43.9% and but if the woman is not experiencing any other loss, the Hb
among lactating mothers is 42.1%) will rise and eventually exceed non-pregnant levels in a few
 The frequency of anemia is dependent in multiple months - like a hypercompensation mechanism.
factors:
o Geography
o Ethnicity DEFINITION BASED IN TRIMESTERS
o Socioeconomic level Table 1. Definition of anemia based in trimesters
o Nutrition STAGE OF PREGNANCY ANEMIC IF EQUALS AND LESS
o Pre-existing iron status THAN (g/dL)
1st trimester: 0-12 weeks 11
o Pre-existing iron supplementation
2nd trimester: 13--28 weeks 10.5
3rd trimester: 29 weeks to term 11.0
PATHOPHYSIOLOGY OF PHYSIOLOGIC ANEMIA
Postpartum 12.0
 Modest fall in hemoglobin levels and hematocrit
MEMORIZE this table!!!
values during pregnancy is caused by a relatively
greater expansion of plasma volume compared with
the increase in red cell volume.

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 WHO DEFINITION BASED ON SEVERITY
Table 2. Severity of anemia according to WHO.
Category Anemia Severity Hb level (g/dL)
1 Mild 9.5-10.5
2 Moderate 8.0-9.4
3 Severe 6.9-7.9
4 Very severe < 6.9
Less economically advantaged regions have more incidence of
anemia compared to the more fortunate regions.
EFFECT OF ANEMIA ON PREGNANCY
 First trimester anemia
o Low birth weight infants
o Preterm births
o Small-for-gestational age infants
 Mid-trimester anemia
o Preterm births
 Third trimester anemia
o Lower mental development up to 2 years of
age
CAUSES OF ANEMIA DURING PREGNANCY
ACQUIRED
 Iron-deficiency anemia (most common)
 Anemia from acute blood loss
o IDA and Anemia from acute blood loss are
the major causes of Anemia during
pregnancy. Once these two are ruled out,
think of other causes of anemia (as listed
below)
 Anemia of inflammation or malignancy
 Megaloblastic anemia (common in the Philippines)
 Acquired hemolytic anemia
 Aplastic or hypoplastic anemia
HEREDITARY
 Thalassemia’s - SEAs have a higher incidence
o Sickle-cell hemoglobinopathies
o Other hemoglobinopathies
o Hereditary hemolytic anemia
IRON DEFICIENCY ANEMIA (IDA)
 MOST COMMON anemia in more than 90% of
pregnant cases
 Due to the increased diversion of iron to the growing
fetus, the placenta, and the increased maternal red
cell mass
 Shortage of iron stores, transport and functional iron,
resulting in reduced hemoglobin in addition to low
serum ferritin, low transferrin saturation and
increased protoporphyrin concentration
 IDA is often manifested by a drop in Hb level in the
midtrimester (2nd trimester)
 In SINGLETON gestation, the maternal need for iron
averages 1000 mg. (REMEMBER!!!)
 MULTIFETAL gestational requirements of iron are
considerably HIGHER than 1000 mg. (REMEMBER!!!)
SAMPLE QUESTION DURING CLASS:
13 weeks AOG, Hemoglobin: 10.5
WITH ANEMIA OR NONE?
FROM 2020 trans
 If pregnant woman is not able to reach the total
amount that is needed for pregnancy. Say she is only
taking 500mg, 300mg of that is always allocated for the
fetus (300mg is fixed). This is a protective mechanism
so that the fetus itself will not be anemic.
 The original 500mg allocation for the expansion of the
maternal Hb mass will only be 50% of the remaining
200mg, which would be less in comparison.
DIAGNOSIS OF IDA
Diagnosis of IDA is straightforward. If the Hb levels are below
the cut-off (refer to table 1), the first thing you should think of
is IDA. When you have a mother that is anemic, do peripheral
blood smears.
 RBC hypochromia and microcytosis
 The above mentioned are not as prominent in
pregnant women compared to non-pregnant women.
 Serum ferritin levels low
o If serum ferritin levels are low and you see
hypochromia and microcytosis in PBS, more
or less it is IDA.
 Bone marrow aspiration: No stainable bone marrow
iron
Figure 2. PBS showing RBC hypochromia and microcytosis,
although this image is not as prominent in pregnant women
compared to non pregnant women.
(REMEMBER this blood picture!!!!) Also note for CENTRAL
PALLOR ON PBS Evaluation
 Hemoglobin
 Hematocrit
 Red cell indices
 Peripheral blood smear
 Serum iron
 Serum ferritin (most important)
 Although serum ferritin levels normally decline during
pregnancy, levels < 10-15 mg/dL confirm IDA.
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 TREATMENT OF IDA
 Oral iron (ferrous sulfate, fumarate, or gluconate)
o at least 200 mg elemental iron daily
 If oral iron not tolerated
o (give iron in IV form) - ferrous sucrose
 Blood transfusion only if there is hypovolemia from
other blood loss or emergency operative procedure
on a severely anemic patient
 Do not do blood transfusion if the px is
asymptomatic!!

FROM 2020 trans FROM 2020 trans

Iron preparation can irritate the GI lining; the patient will When there is anemia from acute blood loss; blood
often complain of peptic ulcer-like symptoms. And if it transfusion is not indicated if:
causes the anemic patient to throw up, give parenteral  The HB is at least 7g/dL
preparation.  Mother is hemodynamically stable
 Mother is ambulatory
 Oral therapy for 3 months is enough, unless if there
Table 3. Commonly used iron preparations: is ongoing bleeding.
Preparation Iron % Fe Elemental
compound (mg) Fe (mg)
(mg/tab) ANEMIA OF CHRONIC DISEASE
Ferrous sulfate 325 20 65  Chronic renal failure
Ferrous sulfate, 200 30 60  Suppuration
dessicated
 Inflammatory bowel disease
Ferrous gluconate 325 12 36
Ferrous fumarate 325 33 106  SLE
*Ferrous sulfate is still the more popular choice since the more  Granulomatous infections
concentrated Ferrous fumarate may not be easily tolerated.  Malignancy
(NICE TO KNOW according to Doc)  Rheumatoid arthritis

FROM 2020 trans FROM LECTURE RECORDINGS

 Daily recommendation of elemental iron  Chronic Disease is usually characterized (and
supplementation for pregnant woman - 30-60 mg/day, differentiated from IDA) by: WEAKNESS, WEIGHT LOSS
400 mcg of folic acid - regardless of anemia status. AND PALLOR.
 4mg of folic acid is given if the patient has a history of  It is also the 2nd most common cause of anemia
previous pregnancy with the fetus having neural tube worldwide
defects, and therapy is started preferably prior the
pregnancy CHRONIC RENAL DISEASE
 It is also recommended that women of reproductive
 Common cause of anemia in chronic disease
age take at least 400 mcg supplementation of folic acid,
 May be accompanied by anemia
regardless of plans of becoming pregnant or not.
 Erythropoietin deficiency
 Those with acute pyelonephritis with sepsis may
ANEMIA FROM ACUTE BLOOD LOSS develop anemia BUT through acute RBC destruction.
 Early pregnancy o Erythropoietin production is normal
 Abortion
 Ectopic pregnancy
FROM LECTURE RECORDINGS
 Hydatidiform mole
REMEMBER: If it is chronic renal failure, it is accompanied
 Much more common postpartum from obstetrical
hemorrhage by anemia because of erythropoietin deficiency but if the
 After anemia has been corrected, oral therapy should patient is brought about by infection such as acute
be continued for 3 months to replenish iron stores. pyelonephritis with sepsis, there will also be anemia but the
erythropoietin is normal. It will only cause anemia because
of acute RBC destruction

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 TREATMENT PREVENTION
 Recombinant erythropoietin  Folate-rich diet
 usually considered if Hct is 0.20 or below o dark leafy vegetables
 May cause hypertension o asparagus
 In non-pregnant patients, risk of pure red cell aplasia o beans, peas, and lentils
and anti-erythropoietin antibodies o broccoli
o citrus fruits
MEGALOBLASTIC ANEMIA o animal liver (best source)
 Two types:  not raw animal liver
o Folic Acid Deficiency o egg yolk
o Vitamin B12 Deficiency  Folic acid supplementation
 Blood and bone marrow abnormalities from impaired o 400 μg/day
DNA synthesis o 4g/day (for previous infant with neural tube
o leads to large cells with arrested nuclear defects)
maturation
o cytoplasm appears normally VITAMIN B12 DEFICIENCY
 Cyanocobalamin deficiency (rare)
FOLIC ACID DEFICIENCY  Addisonian pernicious anemia
 During pregnancy, almost always due to folic acid o Extremely uncommon autoimmune disorder
deficiency usually in women >40 years of age infertility
 In women with poor diet of green leafy vegetables,  In pregnant women, usually after gastric resection
legumes, or animal protein  Other causes: Crohn’s disease, ileal resection,
 Exacerbated by anorexia and alcohol ingestion (not bacterial overgrowth in small bowel which occurs in
common in Filipinos) injudicious use of antibiotics
 can cause neural tube defects (cleft lip palate,
hydrocephalus, spina bifida) TREATMENT
 Women with total gastric resection require 1000 μg
DX OF FOLIC ACID DEFICIENCY Vitamin B12 IM monthly
 Earliest biochemical evidence: low plasma folic acid
concentrations
FROM LECTURE RECORDINGS
 Morphologic changes
REMEMBER: Take note of the causes of Vitamin B12
o Hypersegmented neutrophils
Deficiency. In pregnant women, it is caused by gastric
o Macrocytic erythrocytes
o Peripheral nucleated RBCs (late effect) resection ONLY with other causes such as Crohn’s Disease,
o Bone marrow aspiration shows Ileal resection and bacterial overgrowth in small bowel
megaloblastic erythropoiesis,
thrombocytopenia, and/or leukopenia
 The fetus and the placenta extract folate from the THALASSEMIAS
maternal circulation so effectively, the fetus will not  Common in Southeast Asians
be anemic despite of severe maternal anemia  The most common single-gene disorders worldwide
 Genetically determined hemoglobinopathies
FOLIC ACID REQUIREMENTS  Classified according to the globin chain that is
 Non-pregnant women: 50-100 μg/day deficient
 During pregnancy: 400 μg/day  Impaired production of one or more of normal globin
peptide chains
TREATMENT  May result in:
o ineffective erythropoiesis
 Folic acid supplementation (as little as 1g/day)
o hemolysis
 Iron supplementation
o anemia
 Nutritious diet
 2 Major Forms:
o Rich in iron: green leafy vegetables and
o Alpha thalassemia
legumes
o Beta thalassemia
 Quick response to treatment, 4-7 days after
 Normal Hemoglobin molecule-it has iron surrounded
treatment, reticulocyte count is increased,
by an alpha and a beta chain.
thrombocytopenia/ leukopenia corrected

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 HEMOGLOBIN H DISEASE (β4)
 Compound heterozygous state
 Only one functional α-globin gene per diploid genome
 Compatible with extrauterine life
 RBCs a mixture of Hb γ4, Hb β4, and Hb A
 Neonate appears well at birth
 Soon develops hemolytic anemia
 Most of Hb γ4 replaced by Hb H
 Anemia worsened during pregnancy
 They may need lifetime blood transfusions
Figure 3. Biochemical structure of hemoglobin

ALPHA-THALASSEMIA ALPHA-THALASSEMIA MINOR

 The problem in alpha thalassemia will depend on the  May present as iron deficiency anemia unless
genotype. promptly diagnosed
 Four α-globin genes (located in chromosome 16)  Minimal to moderate hypochromic microcytic anemia
o result to being more complicated than beta
 No associated clinical abnormalities and often goes
thalassemia
unrecognized
 Four genotypic and phenotypic types
 Hb γ4 present at birth but levels drop and not
 There are patients who experience recurrent hydrops replaced by Hb H
because the parents are silent carriers of the disease
 Hb in patients may be normal to slightly depressed
or have a mild form of thalassemia
 Tolerates pregnancy well
Table 4. Genotypes and phenotypes of Alpha Thalassemia
SILENT CARRIER
Syndromes
 Single gene deletion
 No clinical abnormality evident

BETA-THALASSEMIA
 Gene cluster on chromosome 11
 Supposedly less common than alpha thalassemia.
Some surveys say it is more common in the
Philippines. However, some say alpha-thalassemia is
still more common.
 Consequence of impaired β-globin chain production
or α-chain instability:
o Decreased β-chain production
HEMOGLOBIN BART DISEASE (Y4) o Excess α-chains precipitate causing cell
 Increased affinity for oxygen membrane damage
 Common cause of stillbirth in Southeast Asia  Major and minor subtypes
 Hydrops fetalis
BETA-THALASSEMIA MAJOR
 Cooley anemia
 also called homozygous β-thalassemia
 Neonate healthy at birth
 Hemoglobin F falls
 Eventually, infant becomes severely anemic with
failure to thrive
Figure 4. Hydrops Fetalis o May require blood transfusions
o Iron chelation with deferoxamine
 Fetal hydrops means that you have fluid in at least  Prior to chelation and transfusions, pregnancy was
two body cavities, typically fetal ascites and skin/scalp rare
edema
 Pregnancy recommended only if with normal
 In this example, fetal hydrops is characterized by the maternal cardiac function
bloated fetus and edematous placenta
 Prolonged hypertransfusion to maintain Hb at 10 g/dL
 Hydrops fetalis is not compatible with extrauterine is required during pregnancy
life; some may be successfully delivered alive but will
eventually die within minutes
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  Iron supplementation is not effective in patients with Table 5. Respiratory Changes in Pregnancy
β-thalassemia
INCREASED DECREASED
 Many patients with β-thalassemia are dependent on
serial blood transfusions, most of them are admitted Vital Capacity, 20% Expiratory 1300mL to
once or twice a month for blood transfusions. Inspiratory (Late Reserve Volume 1100mL
o This may lead to hemochromatosis which Capacity Pregnancy) (ERV)
may be fatal in some cases.
Tidal Volume 40% Residual Volume 1500mL to
1200mL
BETA-THALASSEMIA MINOR
(20%)
 Heterozygous trait
 Hb A2 (2α + 2β) > 3.5% Minute 30-40% Chest wall
 Hb F (2α + 2γ) > 2% Ventilation compliance
 Anemia is mild
CO2 Production 30% Functional
 RBCs hypochromic and microcytic, presenting similar
Residual
to IDA Capacity
 If serum ferritin level is normal, do hemoglobin
electrophoresis just to rule out thalassemia. pO2 100 to 105 pCO2 40 to 32
mmHg mmHG

BETA-THALASSEMIA MINOR IN PREGNANCY

 There is usually pregnancy-induced augmentation of BRONCHIAL ASTHMA
erythropoiesis  300 million (all ages)
 No specific therapy is required during pregnancy  Prevalence (global 1-18%) in the Ph 6.2%
 Prophylactic iron and folic acid  3-8% pregnant women
 Incidence of IUGR and oligohydramnios increased 2x  0.9% total obstetric admissions (POGS accredited
hospitals 2004-2015)
FROM 2020 trans  Chronic inflammatory airway syndrome
In anemia during pregnancy, the most common cause is still  Increased airway responsiveness
iron deficiency anemia. That’s why for pregnant patient,  Persistent subacute inflammation
basic prenatal labs include CBC to screen for women with  Major hereditary component: chromosome 5q
anemia. If the patient has anemia, work up the patient. Do o Cytokine gene clusters
peripheral blood smear and serum ferritin level. If it still not o B-adrenergic glucocorticoid receptor genes
diagnostic for either IDA or folic acid deficiency, start o T-cell antigen receptor gene
 Hallmarks (KNOW THIS)
screening for thalassemia.
o Reversible airways obstruction
o Bronchial smooth muscle contraction
o Vascular congestion
PULMONARY DISORDERS o Tenacious mucus
 Bronchial asthma o Mucosal edema
 Pneumonia  Increased responsiveness to
 Tuberculosis o Aspirin, cold air, exercise, irritants, viral
infection
 Airway inflammation caused by response to:
RESPIRATORY CHANGES DURING PREGNANCY
o Mast cells, eosinophils, lymphocytes,
 Tidal Volume - increased due to respiratory bronchial epithelium
stimulation by PROGESTERONE  Mediators:
 Chest wall Compliance - reduced by a third due to o Histamine, leukotrienes, prostaglandins,
expanding uterus and increased abdominal cytokines
pressure. (lecture recording)  IgE plays a central role in its pathophysiology

CLINICAL COURSE
 From mild wheezing (most common among pregnant
women) to severe bronchoconstriction
 Airway obstruction and decreased airflow

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 CLINICAL STAGES OF ASTHMA Table 6. Classification of Asthma Severity
(DOC: PLEASE REMEMBER THE VALUES!)

(DOC: Memorize this by heart so when given a case, you

know the diagnosis, severity, and management.)

EFFECTS OF ASTHMA ON PREGNANCY

 No predictable effect of pregnancy on asthma
 1/3 improved, 1/3 worsened, 1/3 unchanged

For the ⅓ that worsened, the chances of pre-eclampsia is very

high and requires immediate medical attention.
Figure 5. Clinical Stages of Asthma
 Early stages of asthma may be well tolerated by non- PREGNANCY OUTCOME
pregnant women; however, it may be dangerous for  Unless severe, outcomes are generally excellent
the pregnant woman and fetus  Spontaneous abortion may be slightly increased in
 Smaller FRC and increased effective shunt make her some.
more susceptible to hypoxia and hypoxemia  For those with severe cases, chances are increased
 From mild wheezing (most common among pregnant for:
women) to severe bronchoconstriction o Pre-eclampsia
o Preterm Labor
FROM 2020 trans (NOT MENTIONED IN THE CLASS; READ o IUGR
AT YOUR OWN RISK) o Perinatal Mortality
 Unless the disease is severe, pregnancy outcome is  Significantly increased morbidity is linked to more
usually good; however, spontaneous abortion is severe/ progressive disease, poor control, or both.
thought to be increased. Some but not all incidences of  Life-threatening Complications from status
pre-eclampsia, growth restriction, and preterm labor asthmaticus:
are only slightly increased, therefore we can surmise o Respiratory arrest
that the more severe the disease is, the worse the o Pneumothorax
pregnancy outcomes. o Pneumomediastinum
o Acute cor pulmonale
o Cardiac arrhythmia
 In the initial phase, hypoxia will be well augmented by Table 7. Maternal and Perinatal outcomes in pregnancies
hyperventilation which maintains arterial PO2 within Complicated by Asthma
normal range and causing decrease in PCO2. This will
lead to respiratory alkalosis. Due to severe obstruction,
ventilation becomes impaired. There will be respiratory
fatigue causing CO2 retention and eventually cause
respiratory failure if there is continuous obstruction.
 If you have asthma, you should always have short
acting beta agonists for acute attacks.
 Another way to diagnose asthma is by Forced
Expiratory Volume (FEV) where the patient is asked to
blow into a spirometer, which usually yields a result of
<1L in patients with asthma or those who have chronic
restrictive lung disease such as in chronic smokers

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 CLINICAL COURSE STEPWISE THERAPY OF CHRONIC ASTHMA DURING
 Perinatal outcomes generally good with reasonable PREGNANCY:
control of asthma Table 8. Chronic Asthma Therapy during Pregnancy
 Fetal response to chronic maternal hypoxemia
o Decreased umbilical blood flow SEVERITY THERAPY
o Increased systemic and pulmonary vascular
Mild Inhaled B-agonists as needed (for all categories)
resistance
Intermittent
o Decreased cardiac output
 Increased incidence of fetal growth restriction with Mild Low-dose inhaled corticosteroids (ICS) (every 3-4
asthma severity Persistent hours)
 Aside from fetal growth restriction, incidence of Alternative: Cromolyn, anti-leukotrienes (i.e.
pulmonary HPN is also high in fetuses of women with Zileuton, Zafrilukast, Montelukast), or
poor asthma control. Theophylline. These drugs are given orally or
inhalation for prevention
 When respiratory alkalosis occurs, fetal hypoxemia
develops before maternal oxygenation is Moderate Low-dose ICS and long-acting B-agonists (LABA)
compromised Persistent Alternative: low-dose ICS AND Theophylline/anti-
 Decreased uterine blood flow, maternal venous leukotriene
return
 Most commonly used asthma drugs are not Severe High-dose ICS, LABA, Oral corticosteroids (OCS)
considered teratogenic Persistent Alternative: high-dose ICS, Theophylline AND OCS

FROM 2020 trans

The fetus is able to adapt to maternal hypoxemia and will
then conserve the limited oxygen supply, such that there is
growth restriction that may be revealed by ultrasound and
biophysical profile as hypoactivity of the fetus

Due to lack of health education, most women, regardless of

their disease, tend to discontinue intake of their
medications when they get pregnant; such actions
exacerbate or increase unnecessarily the incidence of acute Figure 6. Treatment of Asthma
asthma attacks *Depending on the severity, a combination of drugs will be
used. see figure above. (PLEASE MEMORIZE THE FIGURE) no
CLINICAL EVALUATION need to memorize DAW the specific drug; just know the
PULMONARY FUNCTION TEST type of drug needed depending on severity:
 sequential measurement: FEV1 or PEFR are the best  Inhaled B-agonists
measure of severity o Albuterol* (most preferred)
o Terbutaline
o Isoetharine
o Epinephrine
o Metaprotenol
o Isoprotenol
 Inhaled Corticosteroids
MANAGEMENT OF CHRONIC ASTHMA o Budesonide* (preferred)
 Patient education (most important)  Long-acting B-agonist
o bring inhaler at all times o Salmeterol
o avoid allergens to prevent so that attacks
will be lessened MANAGEMENT IF ACUTE ASTHMA
 Avoidance of environmental precipitating factors  Similar to non-pregnant patient
 Assessment of pulmonary function and fetal well-  Lowered threshold for hospitalization
being  IV hydration help clear secretions
 Pharmacologic therapy if needed (must not be  Supplemental oxygen by mask (up to 10 L via face
teratogenic to avoid mortality and morbidity) mask)
 Continuous pulse oximetry
 Electronic fetal monitoring

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THERAPEUTIC AIMS:  Health- associated pneumonia (HCAP)
 pO2 > 60 mm Hg  Hospital- acquired pneumonia (HAP)
 O2 saturation ≥90- 95%
FIRST-LINE TREATMENT BACTERIAL PNEUMONIA
 Inhaled β-agonist  Etiologic agents
 Inhaled corticosteroids o Steptococcus pneumoniae (most common)
SEVERE ACUTE ASTHMA o Influenza A (common)
 Inhaled corticosteroids given early o Legionella
 Corticosteroid infusion o Chlamydophila pneumonia
 Oral prednisone o Haemophilus influenzae
 Magnesium sulfate for severe exacerbations o Mycoplasma pneumonia
PATIENTS MAY BE DISCHARGED IF (REMEMBER THIS)  Risk factors
 Initial therapy with β-agonist results in FEV1 or PEFR o Smoking
> 70% of baseline o Chronic bronchitis
ADMISSION IF o Asthma
 FEV1 or PEFR < 70% after 3 doses of β-agonist  Asthmatic patient is always at high
risk in acquiring pneumonia
LABOR AND DELIVERY o Binge drinking
o HIV infection
 Maintenance medications continued through
delivery
DIAGNOSIS
 Stress-dose corticosteroids given to any woman
given systemic steroid therapy within 4 weeks  Symptoms
o Hydrocortisone 100 mg IV q 8 hours and for o Cough
24 hours after delivery o Dyspnea
 May undergo normal delivery but inform patient that o Sputum production
she should be under epidural anesthesia o Pleuritic chest pain
o Some medications like pain reliever can (Mild upper respiratory symptoms and malaise usually
cause asthmatic attack precede these symptoms.)
 CAN USE:  Signs
o Oxytocin o Mild leukocytosis
o Prostaglandin E1 or E2 o Infiltrates on chest radiographs
o Non-histamine releasing narcotic  The two symptoms that differentiate it from an
o Epidural anesthesia ordinary upper respiratory tract infection are
o Conduction anesthesia dyspnea and pleuritic chest pain
 MUST NOT USE (will induce asthmatic attack):
o Prostaglandin F2α CRITERIA FOR SEVERE COMMUNITY ACQUIRED PNEUMONIA
o Ergotamine derivatives (methylergonovine  RR ≥ 30/min
used to make uterus contract after  PaO2/Fi02 ≤ 250
pregnancy)  Multilobular infiltrates
 Confusion/disorientation
FROM 2020 trans  Uremia
If stress-dose corticosteroids are not given, and instead, you  WBC <4000/ µL
use steroids to start with, the patient’s asthma may worsen.  Platelets < 100,000/ µL
 Core temperature of < 36˚C
o You should be alarmed when you encounter
PNEUMONIA (BACTERIAL, INFLUENZA) this, because you would expect that in a
 Leading cause of death in the US person with pneumonia the temperature
 4.2% of antepartum admissions for non-obstetrical would be high (feverish)
admissions  Hypotension requiring aggressive fluid resuscitation
 Pathogens are:
o Viruses 23% EMPIRICAL ANTIMICROBIAL TREATMENT FOR COMMUNITY
o Bacteria 11%
ACQUIRED PNEUMONIA (CAP)
o Both 3%
o Fungi or Protozoa 1%
FROM 2020 trans
PNEUMONIA CLASSIFICATION ● Nursing home-acquired pneumonia (NHAP)
Ventilator-assisted pneumonia (VAP).
 Community- acquired pneumonia (CAP)

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  Community- acquired pneumonia (CAP)
 Uncomplicated, otherwise healthy
o Macrolides: Clarithromycin or Azithromycin
or Erythromycin PLUS Oseltamivir for
suspected influenza infection
 Severe Pneumonia
o Respiratory fluoroquinolones: moxifloxacin,
gemifloxacin, or levofloxacin or Beta
lactams: amoxicillin/clavulanate,
ceftriaxone, cefotaxime, or cefuroxime plus
a macrolide PLUS Oseltamivir for suspected
influenza A infection
 Note: If CA-MRSA is suspected Vancomycin and
Linezolid is added
** Remember these treatments plans!!
Figure 7. Treatment Plan for CAP
PREGNANT WOMEN WITH PNEUMONIA
 Should hospitalize
o unlike non-pregnant women with
community acquired pneumonia,
they (pregnant women) are at
greater risk for morbidity and
mortality
 Antimicrobial treatment empirical
o 1st line usually a macrolide (azithromycin,
clarithromycin or erythromycin)
 Women with severe pneumonia
o Respiratory fluoroquinolone
o B-lactam + Macrolide
 Clinical improvement in 48-72 hours
 Lysis of fever in 2-4 days
 Resolution of radiographic abnormalities up to 6
weeks
o You should not rely on x-ray findings in
deciding whether you patient is improving or
not
 Minimum of 5 days therapy
You may notice once you rotate in the wards; there would be a
situation wherein, request for chest x-ray and result would
show infiltrates. After a few days, another chest x-ray was done
and result would show the presence of infiltrates though lesser
in number compared to the first one but patient was allowed
to go home. That is because even if patient is fully treated you
will still be able to see radiologic abnormalities up to 6 weeks.
If you see that there is clinical improvements (i.e. decreasing
WBC, lysis of fever, patient is breathing well) you don’t have to
be so concerned with the x-ray findings if you see that there is
a decrease in the number of infiltrates. So in most situations
this is what happens in a previously healthy woman, unless she
has an underlying chronic disease.
PREGNANCY OUTCOMES WITH PNEUMONIA
 Outcome will depend on the severity of
pneumonia
 Maternal and perinatal morbidity and
mortality still about 1%
 1/3 of cases with PROM and preterm delivery
PREVENTION
 Pneumococcal vaccine
o 60-70% protective vs 23 serotypes
o Currently not recommended by ACOG for
healthy pregnant women
o For immunocompromised, significant
smoking history, with diabetes, cardiac,
pulmonary or renal disease and asplenia
Table 9. Pneumoccocal Vaccine
INFLUENZA PNEUMONIA
 Influenza A and B (RNA viruses)
 Spread by Aerosolized droplets
 Onset 1-4 days after exposure
 Mostly self limited in healthy adults
 Difficult to distinguish from bacterial pneumonia
 Primary influenza Pneumonitis = Most Severe
 More commonly, secondary pneumonia develops
from bacterial superinfection with strep or staph
MANAGEMENT OF INFLUENZA PNEUMONIA
 Supportive Treatment
 Neuraminidase inhibitors within 2 days of symptoms
o Oral Oseltamivir 75mg 2x a day for 5 days
o Inhaled Zanamivir 10mg a day for 5 days
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 o Sensitive to patients without BCG
 Positive Skin Test - >5mm diameter
FROM LECTURE RECORDINGS  Chest radiograph
REMEMBER:  Interferon-Gamma- Release Assay (IGRAs) are used
 Beta Lactams + Macrolides = if Fluoroquinolones in patient who have BCG vaccination (Remember!)
doesn’t work on severe patients
 Beta Lactams + Macrolides + Oseltamivir = use IF TREATMENT OF TUBERCULOSIS: ACTIVE INFECTION
SEVERE WITH INFLUENZA  Four drug regimen (6 months)
 Uncomplicated pneumonia + influenza = Macrolides + o Bactericidal phase (first 2 months) -
Oseltamivir Isoniazid, Rifampicin, Ethambutol, and
 If UP w/o Influenza = Macrolides ONLY Pyrazinamide
 If Pneumonia is not severe = DO NOT give o Continuation Phase (4 months) - Isoniazid,
Fluoroquinolones RIfampicin
 Meningitis - Levofloxacin may be added
 HIV patients - Rifampicin or Rifabutin is
PREVENTION
contraindicated if certain protease inhibitor or non
 Influenza A vaccination nucleoside reverse transcriptase inhibitor are being
 Affords protection for ⅓ of infants for at least 6 administered.
months  Second line regiment: Aminoglycoside:
Streptomycin, Kanamycin, Amikacin, Capreomycin -
TUBERCULOSIS Contraindicated in pregnant patient due to ototoxic
 Inhalation of Mycobacterium tuberculosis to the fetus
 >90% of patients, infection is contained (dormant for
a long period of time) TREATMENT OF TUBERCULOSIS: LATENT INFECTION
 Affects immunocompromised patients  Isoniazid 300mg orally daily given 6 to 9 months (safe
Manifestations: in pregnancy)
 Cough with minimal sputum production
 Low-grade fever NEONATAL TUBERCULOSIS
 Hemoptysis  Tubercular bacillemia infecting placenta
 weight loss  Neonatal aspiration of infected secretions at delivery
EXTRAPULMONARY TB
 Manifestations:
 Lymphadenitis, pleural, genitourinary, skeletal, o Hepatosplenomegaly
meningeal, gastrointestinal, and miliary TB o Respiratory distress syndrome
o Fever
SIGNS OF TB o Lymphadenopathy
 Chest x-ray (presence of infiltration, cavitations, or  Neonatal infection unlikely if mother treated before
mediastinal lymphadenopathy) delivery or sputum is negative
 Acid-fast bacilli sputum smear (positive 2 of 3 culture  Isolation of newborn suspected of having active
individual) disease
 Breastfeeding not contraindicated
FROM LECTURE RECORDINGS
REMEMBER: THYROID DISORDERS
 AFB smear of 2 of 3 positive plus X-ray = PTB NORMAL TSH LEVELS PER TRIMESTER
 PPD plus CXR = PTB  First trimester- 0.60-3.40 miu/L
 Second trimester- 0.37- 3.60miu/L
 Third trimester- 0.38-4.04 miu/L
TB AND PREGNANCY
 Increase in: FREE T4 LEVELS PER TRIMESTER
o Preterm delivery
 First trimester- 0.8 1.2 ng/Ml
o Low-birthweight and growth-restricted
newborns  Second trimester- 0.6 1.0 ng/Ml
o Pre-eclampsia  Third trimester- 0.5- 0.8 ng/Ml
o Perinatal mortality
THYROID CHANGES DURING PREGNANCY
DIAGNOSIS  Increased production of thyroid hormones by 40-
 Intracutaneous Purified Protein Derivative (PPD) 100% during pregnancy
o 5 tuberculin units  Moderate thyroid gland enlargement
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 o caused by fetal exposure to maternally
HYPERTHYROIDISM administered thionamides
 2-7 in 1000 pregnancies  Non goitrous hypothyroidism
 Mild hyperthyroidism may be difficult to diagnose o transplacental passage of maternal TSH-
 Findings: receptor blocking antibodies
o Tachycardia  Fetal thyrotoxicosis
o Thyromegaly o after maternal thyroid gland ablation
o Exophthalmos
o Failure to gain weight
THYROID STORM/HEART FAILURE
 Laboratory findings (MEMORIZE)  VERY DREADED complication of hyperthyroidism
o Serum TSH decreased  Acute, life-threatening hypermetabolic state (rare)
o Serum free T4 (fT4) increased  Cardiomyopathy from effects of thyroxine more
o Rarely increased serum triiodothyronine common (pulmonary hypertension and heart failure)
(T3)- T3 toxicosis  High output failure will lead to dilated
cardiomyopathy then eventually maternal death
THYROTOXICOSIS  To know whether the patient is in thyroid storm or
 Overwhelming cause is Grave’s disease not, use the Burch-Wartofsky Point Scale
 Treatment (according to American Thyroid o Score of more than 45, highly suggestive of
Association) thyroid storm
o 1st trimester- PTU 50-150mg TID initial daily o Score of 25-44, suggestive of impending
dose (remember) storm
o 2nd trimester: Methimazole 10-20mg initial o Score of below 25, suggestive of unlikely
daily dose (remember) thyroid storm
 Parkland hospital: PTU throughout pregnancy (300-
450mg in 3 divided doses for pregnant women)
 Free T4 every 4-6 weeks
 Side effects of Therapy
o Transient leukopenia in 10%
o Agranulocytosis in 0.3-0.4%
o Hepatotoxicity in 0.1-0.2%
o Anti-neutrophilic cytoplasmic antibodies
develop in 20%
 Subtotal thyroidectomy in pregnant women seldom
done but if needed usually done in 2nd trimester
 Thyroid ablation with radioactive iodine (RIA)
contraindicated during pregnancy
 If treated with RIA, avoid pregnancy for 6 months, and
delay breastfeeding for 3 months Figure 8. Point Scale for the thyroid storm diagnosis

PREGNANCY OUTCOME IN PATIENTS WITH TREATMENT FOR THYROID STORM

HYPERTHYROIDISM
 Depends largely on metabolic control
 In untreated women or remain hyperthyroid despite
therapy:
o Pre-eclampsia
o Heart Failure
o Preterm delivery
o Growth restriction
o Stillbirth
o Infant with hearing loss

FETAL AND NEONATAL EFFECTS IN HYPERTHYROIDISM

 Goitrous thyrotoxicosis
o caused by placental transfer of thyroid
stimulating immunoglobulins
 Goitrous hypothyroidism Figure 9. Treatment plan for Thyroid Storm

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 ICU setting SUBCLINICAL HYPOTHYROIDISM
 Pharmacologic  5% incidence in reproductive age women
o PTU 1000mg orally then 200 mg q 6 hours  Women with TSH levels >10-15 mu/L at high risk of
o Iodide given 1 hour after initial PTU dose developing overt hypothyroidism in 5 years
 500-1000 mg sodium iodide q 8  Undiagnosed maternal hypothyroidism may impair
hours fetal neuropsychological development
 5 drops of supersaturated solution TREATMENT:
of potassium iodide (SSKI) q 8 hours  In subclinical hypothyroidism treat with
 10 drops of lugol’s solution q 8 Levothyroxine because of the risk to cause mental
hours retardation of fetus unlike in subclinical
o 2mg dexamethasone IV q 6 hours x 4 doses hyperthyroidism wherein treatment is not necessary.
o B-blocker to control tachycardia if needed (REMEMBER THIS)
 Summary treatment:
o 1st trimester: PTU PREGNANCY OUTCOME IN HYPOTHYROIDISM
o 2nd and 3rd: Methimazole  Tubercular bacillemia infecting placenta
 Preeclampsia
SUBCLINICAL HYPERTHYROIDISM
 Placental abruption
 Abnormally low serum TSH with normal thyroxine  Cardiac dysfunction
levels
 Low birth weight
 Long-term effects
 Stillbirths
o Osteoporosis
o Maternal Hashimoto thyroiditis is not
o Cardiovascular morbidity
typically associated with fetal thyroid
o Over thyrotoxicosis
dysfunction
o Thyroid failure
 Affects 1.7% of pregnant women FETAL AND NEONATAL EFFECTS IN HYPOTHYROIDISM
 No need to treat, just periodic surveillance
 Goitrous thyrotoxicosis
o caused by placental transfer of thyroid
HYPOTHYROIDISM
stimulating immunoglobulins
 2-12 per 1000 pregnancies  Goitrous hypothyroidism
 Scarier than hyperthyroidism because preeclampsia is o caused by fetal exposure to maternally
more common administered thionamides
 Manifestations:
o Fatigue FROM LECTURE RECORDINGS
o Constipation REMEMBER:
o Cold intolerance
 Clinical/ overt hypothyroidism: Abnormally ↑TSH
o Muscle cramps with↓T4
o Weight gain
 Subclinical hypothyroidism: Abnormally ↑TSH with
o Edema
Normal T4
o Dry skin
o Hair loss
o Prolonged relaxation of DTR IODINE AND PREGNANCY
 Iodine required for fetal neurologic development
OVERT HYPOTHYROIDISM soon after conception
 Opposite of overt hyperthyroidism o Severe deficiency associated with endemic
 Hashimoto thyroiditis most common cause in cretinism
pregnancy o endemic cretinism is a reflection of poor
o Glandular destruction from autoantibodies iodine intake
(anti-TPO antibodies)  Mild deficiency unlikely to cause intellectual
 Difficult to diagnose during pregnancy impairment
 Thyroid Testing o Iodized salt - apparently in the Philippines,
 Treatment: iodine intake is not sufficient
o Levothyroxine 1-2ug/kg/day (100ug/day)  Moderate deficiency has intermediate and variable
o Serum thyroxine level measured 4-6 week effects
intervals  Severe deficiency associated with endemic cretinism
o Thyroxine dose adjusted by 25-50ug
increments to reach normal TSH levels (0.5- PREGNANCY OUTCOME
2.5 mu/L)  Depends largely on metabolic control

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  In untreated women or remain hyperthyroid despite ------ END -------
therapy. May have the following:
o Preeclampsia
o Heart failure
o Preterm delivery
o Growth restriction
o Stillbirth
o Infant with hearing loss

POSTPARTUM THYROIDITIS
3. Transient autoimmune thyroiditis
4. 5-10% during 1st year postpartum
5. Up to 25% of women with type 1DM REFERENCES
6. Women with postpartum thyroiditis have 30% risk of 1. 2020 TRANS
developing permanent hypothyroidism 2. Recordings
3. Dr. Vidanes’ handout
FETAL AND NEONATAL EFFECTS: 4. Books
5. Nongoiterous-transplacental passage of maternal TRANSCRIBERS
TSH-receptor blocking antibodies. 1. TRANS GROUP: 9A
6. Fetal thyrotoxicosis 2. SUBTRANSHEAD: SA
a. after maternal thyroid gland ablation 3. EDITOR: CFCS
7. Recommended daily iodine intake during pregnancy 4. TRANS HEAD: AMDL
is 220ug/day
8. Iodine supplementation before pregnancy
PAST E (2014)
1. The following lung volumes are INCREASED during
FROM 2020 trans pregnancy, EXCEPT:
Diagnosed infrequently after delivery. Vague, nonspecific a. expiratory reserve volume
symptoms. Supposedly normal during pregnancy. After b. minute ventilation
pregnancy they seem listless, slow, not as smart (could be a c. tidal volume
sign of postpartum depression but rule out postpartum d. vital capacity
thyroiditis first) 2. A 26 y/o pregnant woman comes in for prenatal check-
up. She gives a history of asthma and on questioning reports
attacks occurring about 2-3 times a week with nocturnal
Table 10. Postpartum Thyroiditis
awakening 3-4 times a month. She complains of minor
Phase of limitation of normal daily activities. You classify her as
Postpartum having what kind of asthma?
Thyroiditis a. intermittent
b. mild persistent
Factor Thyrotoxicosis Hypothyroidism
c. moderate persistent
Onset 1-4 months 4-8 months d. severe persistent
3. The patient above would benefit from what kind of
Incidence 4 percent 2-5 percent pharmacologic therapy?
a. albuterol
Destruction-induced b. budesonide + isoproterenol
Mechanism Thyroid insufficiency
hormone release c. beclomethasone + salmeterol
d. budesonide + albuterol + terbutaline
Small, painless Goiter, fatigue,
4. A 35 y/o G4P3(3003) asthmatic comes to the emergency
Symptoms goiter; fatigue inability to
palpitations concentrate room on New Year's eve for acute exacerbation. She has
good compliance with her medications. She refuses hospital
B-blockers for Thyroxine for 6-12 admission. You agree to send her home if initial treatment
Treatment
symptoms months will result to O2 saturation of 95% and PO2 levels (in mmHg)
of at least:
⅓ permanently a. 60
Sequelae ⅔ become euthyroid
hypothyroid b. 70
c. 80
⅓ develop
d. 90
hypothyroidism

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5. The following medications should NOT be used in an c. 100
asthmatic patient during labor and delivery? d.95
a. methylergonovine 14. According to WHO, a hemoglobin level of 6.5 g/dL is
b. prostaglandin E1 what severity of anemia?
c. prostaglandin E2 a. moderate
d. oxytocin b. severe
6. A 42 y/o G1P0 comes to emergency room at 32 weeks’ c. very severe
age of gestation for 2 day history of cough, fever and d. extremely severe
pleuritic chest pain. On physical examination, temperature 15. Of the 1000 mg of iron that a pregnant woman requires,
is 38.8°C, respiratory rate of 25 per minute and rales on the how many percent is allotted to the fetus?
right mid-to-lower lung fields. Hemogram shows WBC of a. 30
19.3 and chest radiograph reveal dense infiltrates on both b. 40
lung fields. Which of the following is the most appropriate c. 50
treatment for this patient? d. 60
a. clarithromycin 16. Which of the following iron preparations provides the
b. co-amixoclav greatest percentage of elemental iron?
c. levofloxacin a. ferrous sulfate
d. oseltamivir b. ferrous gluconate
7. Pyridoxine is given to pregnant women taking isoniazid c. ferrous fumarate
for tuberculosis to: d. ferrous carbonate
a. prevent drug resistance 17. Pernicious anemia is due to lack of which of the
b. potentiate drug action following substance?
c. decrease hepatic toxicity a. Cyanocobalamin
d. increase gastrointestinal absorption b. Erythropoietin
8. Which of the following anti-tuberculosis drugs is c. Folic Acid
contraindicated for use during pregnancy? d. Iron
a. Ethambutol 18.The daily folic acid requirements (in ug) for a normal
b. Rifampicin pregnant woman with history of infants with neural tube
c. Pyrazinamide defects is:
d. Amikacin a. 400
For 9 and 10, match the following with the laboratory b. 800
findings c. 2500
4. a. clinical hyperthyroidism d. 4000
a. b. clinical hypothyroidism 19. A fetus with homozygous α-thalassemia will present as:
5. c. subclinical hyperthyroidism a. hypochromic microcytic anemia
6. d. subclinical hypothyroidism b. moderate anemia
c. severe anemia
9. High T4, low TSH d. hydrops
10. Normal T4, high TSH 20. A pregnant woman with thalassemia major requires
prolonged hyper-transfusions to maintain hemoglobin
11. A 29 y/o G1 comes to the emergency room with levels (in g/dL) not below:
symptoms of thyroid storm. Which of the following drugs a.9.5
should be administered first? b. 10
a. Dexamethasone c.10.5
b. Propylthiouracil d. 11
c. Sodium iodide
d. Thyroxine A-B-B-A-A/A-C-D-A-D/B-B-B-B-B/C-A-D-D-B
12.What is the recommended daily iodine intake (in ug) PAST E (2019)
during pregnancy? 1. 1. A 32 year old G3P2(2002) is being treated for iron-
a. 150 deficiency anemia but is having severe gastrointestinal
b.220 irritation with oral iron preparations. What is the
c.250 appropriate alternative therapy?
d.300 a. Deferoxamine
13. Anemia in an iron-supplemented pregnant woman in b. Iron sucrose
the 3rd trimester is defined as hemoglobin level (in mg/L) of c. Recombinant erythropoietin
below: d. Blood transfusion
a. 110
b. 105

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2. 2. A 39 year old G3P1(1011) came to the emergency room c.Folic acid deficiency
at 32 weeks age of gestation for diarrhea. Vital signs are as d.Beta-thalassemia
follows: HR: 96 beats/minute, RR: 24/ minute, temperature 10. A 27 year old primigravid came in for prenatal checkup.
of 38.9 C. On physical examination, you note a 5 x 4 cm You note mild pallor and order blood work-up which
anterior neck mass that moves on deglutition, with cold and showed mild hypochromic microcytic anemia, and HbA2 >
clammy extremities and grade I bipedal edema. What is the 3.5%. What is the
most appropriate first-line medication? most appropriate management?
a. Propylthiouracil a. Recombinant erythropoietin
b. Potassium iodide b. Serial blood transfusions
c. Propranolol c. Iron chelation
d. Dexamethasone d. Supplemental iron
3. 3. What is the advantage of methimazole use over other 11. A 27 year old G2P1(1001) came in prenatal checkup at
thyroid medications during pregnancy? 18 weeks age of gestation. You note a 3x3 cm anterior neck
a. Better gastrointestinal absorption mass that moves on deglutition. Laboratory tests show the
b. Lesser risk of hepatotoxicity following: TSH: 0.2mIU/L, fT4: 1.4 ng/mL. What is the most
c. Decreased risk of fetal anomalies appropriate diagnosis?
d. More convenient dosing schedule a. Subclinical hypothyroidism
5. 4. In a singleton pregnancy, how much of iron (in mg) is b. Subclinical hyperthyroidism
excreted and not utilized by the mother or the fetus? c. Clinical hyperthyroidism
a. 200 d. Clinical hypothyroidism
b. 250 12.During normal pregnancy, the following respiratory
c. 300 parameters are INCREASED except:
d. 350 a. Minute ventilation
7. 5. Anemia is diagnosed during pregnancy when hemoglobin b. Vital capacity
level (in mg/dL) falls below: c. Functional residual capacity
a. 9.5 d. Tidal volume
b. 10.0 13. After an acute episode of community-acquired
c. 10.5 pneumonia, radiologic findings are expected to resolve by
d. 11.0 how many weeks post-treatment?
6. A 28 year old primigravid came in for prenatal checkup at a. 2
8 weeks age of gestation. She reports fatigue, cold b. 4
intolerance, dry skin and constipation. Laboratory tests c. 6
reveal T4: 5.22 mIU/L and free T4: 0.21 ng/mL. What is the d. 8
most appropriate management? 14.An 18 year old primigravid came to the emergency room
a.Reassurance at 40 weeks age of gestation for labor pains. She was
b.Levothyroxine diagnosed with bronchial asthma last year with her last
c.Propylthiouracil attack one week ago. Physical examination shows normal
d.Methimazole lung findings and her cervix is noted to be 2cm dilated with
7. A woman with alpha-thalassemia gives birth to a neonate uterine contractions coming in every 8-10 minutes. All of
showing signs of severe hemolytic anemia. What is the most the following
probable phenotype? medications can be used, EXCEPT:
a. αα/αα a.Oxytocin
b. --/-- b.Dinoprostone
c. --/αα c.Misoprostol
d. αα/-- d.Methlyergometrine
8. 8. Which of the following ferrous compounds yields the 15. What is the recommended daily iodine intake (in
LEAST amount of elemental iron per gram? micrograms/mcg) during pregnancy?
a. Gluconate a. 160
b. Carbonate b. 180
c. Sulfate c. 200
d. Fumarate d. 220
9.A 21 year old G1 was diagnosed with anemia after
complaining of easy fatigability.Peripheral blood smear ANSWERS: B A B A B B C A C D C C C D D
shows macrocytic erythrocytosis. What is the most
probable cause
of the anemia?
a.Alpha-thalassemia
b.Iron deficiency

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APPENDIX

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