This document provides information on various illnesses that can occur or be exacerbated during pregnancy, including anemia, tuberculosis, asthma, diabetes, HIV/AIDS, hepatitis, and others. It focuses in depth on anemia, discussing normal blood values, causes of anemia during pregnancy including iron deficiency and megaloblastic anemias, effects of anemia on pregnancy, diagnosis, and treatment options. It also provides a brief overview of hemoglobinopathies like sickle cell anemia.
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1-Differentiate between the different causes of anemia
2. Discuss the investigations that may clarify the diagnosis
3. Recognize the predisposing factors and consequences of iron deficiency anemia and discuss how to manage it
4. Discuss the hereditary basis and clinical features of sickle cell anemia and thalassemia .
prepared by med_students0
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1-Differentiate between the different causes of anemia
2. Discuss the investigations that may clarify the diagnosis
3. Recognize the predisposing factors and consequences of iron deficiency anemia and discuss how to manage it
4. Discuss the hereditary basis and clinical features of sickle cell anemia and thalassemia .
prepared by med_students0
Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
Iron deficiency Anaemia is the most common nutritional deficiency in the world. This presentation to learn about Iron deficiency Anaemia. Here I discuss causes, clinical features, lab diagnosis and treatment of Iron deficiency Anaemia. I think it will help those who want to know about IDA.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
Iron deficiency Anaemia is the most common nutritional deficiency in the world. This presentation to learn about Iron deficiency Anaemia. Here I discuss causes, clinical features, lab diagnosis and treatment of Iron deficiency Anaemia. I think it will help those who want to know about IDA.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
The Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
4. Normal Blood Standards
A. Red blood corpuscles (RBCs):
1- Number:
•In females : 4.5-5 millions/mm
2- Haemoglobin (Hb%): In females : 12-14 gm/100 cc
(dl) blood.
During pregnancy: 10-12 gm/dl i.e. physiological
anaemia due to the increase in plasma volume more
than RBCs volume.
4
5. Normal Blood Standards…..
3- Haematocrit value:
•It is the volume of packed RBCs in 100 cc of blood.
In females: 42%.
4- Reticulocytes: 0-2%.
They are cells with remnants of the nucleus.
Reticulocytosis indicates over active bone marrow as
in haemolytic anaemia.
5
6. Normal Blood Standards …..
B. Leucocytes
1- Total leucocytic count: 4.000-10.000/mm3.
It increases during pregnancy to 9.500-10.500/mm3 and up
to 16.000/mm 3 during labour and the first week of
puerperium.
2- Differential leucocytic count:
• Basophils 0-1%.
•Eosinophils 3-5%.
•Monocytes 3-8%.
•Lymphocytes 20-30%.
• Neutrophils 60-70%.
6
7. Normal Blood Standards …
C. Platelets:
•200.000-400.000/mm3
D .Bleeding time: 2-4 minutes.
E. Coagulation time: 4-8 minutes.
7
8. Introduction
Iron deficiency anemia is common affecting all
population.
Pregnant mothers are at high risk b/c of increase
demand.
Prevalence of anemia is (35-75%),average being(56%).
Associated with preterm labor &LBW( 3x)
WHO estimate that anemia contribute approximately 20
% maternal deaths worldwide(1995 report)
8
9. Definition
Anemia is defined as hemoglobin concentration less
11 g/dL during pregnancy or the puerperium.(WHO)
CDC defined anemia is less than 11g/dl in the first
& third trimester , less 10.5g/dl for second trimester
pregnancy.
Level Hb is affected by sex, race, pregnancy &iron
supplement.
9
11. Normal blood values in non-pregnant and
pregnant state
Non-pregnant Second half pregnancy
Hemoglobin (Hb) 14.8 gm/100 mL 11–14 gm/100 mL
Red blood cells (RBC) 5 million/cu mm (mm3 ) 4–4.5 million/mm3
cked cell volume (PCV) (Hematocrit) 39–42 percent 32–36 percent
Mean corpuscular hemoglobin (MCH) 27–32 micromicron (picogram-pg) 26–31 pg
Mean corpuscular volume (MCV) 75–100 cubic micron (m3 ) 75–95 m3
Mean corpuscular hemoglobin
concentration (MCHC)
32–36 percent 30–35 percent
Serum iron) mL) 60–120 mg/100 mL Slightly lowered (65–75
mg/100 mL
Total iron binding capacity (TIBC) 300–350 mg/100 mL Increased (300– 400
mg/100
Saturation percentage (Ratio— Serum
iron: TIBC)
30% Less than 16%
Serum ferritin 20–30 mg/L (mean) 15 mg/L (mean)
11
12. Causes of anemia
I)Common causes :(85 %)
*Physiological anemia
*iron deficiency anemia ( IDA)
II) Uncommon causes:
*folic acid deficiency
*heamoglbinopaties
*sickle cell disease
*B-thalassemia minor
12
III) Rare causes:
• B-thalassemia major
• A-thalassemia
• vit B 12 deficiency
13. Functional Causes of anemia
1. Inadequate diet:
*iron,folate or vit B 12 deficiency.
2. Malabsorption syndrome:
* pregnancy/ GI-disease/ food /drugs
3. Blood loss:
* hemorrhage/helementic infestation.
4) Increase red cell destruction:
* heamolysis
13
14. Anaemia can be classified according to severity as
mild, moderate, severe and very severe
14
15. Effects of anemia on pregnancy
• Low hct level associated with LBW
• Preterm delivery
• WHO estimate shows 20% contribution to maternal
death ( 1995 report)
• Depending cause anemia will be associated with high
MMR/PMR e.g. sickle-cell anemia, adverse outcome
related to vascular complication of sickling rather than
level of Hb.
15
16. Iron-Deficiency Anemia
•It is the most common type of anaemia (95%).
Daily Requirements:
•Normal iron requirement is 10 mg/day of which 1mg
is absorbed.
•Requirement increases during pregnancy to 15mg/ day.
16
17. Mechanism of IDA
Aetiology
1- Inadequate intake of iron.
2- Defective absorption of iron e.g. achlorhydria.
3- Increased demand e.g. menstruation and pregnancy.
4- Chronic blood loss e.g. abnormal uterine bleeding
and piles.
17
19. Contii…
B. Signs:
Pallor which can be detected in the face, palm of the
hand, nail bed and mucus membranes of the mouth and
conjunctiva.
- Angular stomatitis and red glazed tongue.
- Nails are brittle, striated with loss of their luster.
- Spooning of the nails may occur in severe cases.
19
20. Contii…
Investigations:
1. RBCs , haemoglobin and haematocrit: below normal.
2. Serum iron concentration: below normal (n=125 m
g/dl).
3. Iron binding capacity :below normal (n=400 m g/dl).
4. Transferrin saturation: below normal (n= 30%).
5. Blood film: microcytic hypochromic anaemia
20
21. Contiii…
Treatment:
1. Diet: liver, meat, kidney, eggs and green vegetables are rich in iron.
2. Oral iron therapy: * one iron tablet/three time/day recommended
after meals.
* iron preparations with elemental iron.
#ferrous gluconate,325mg (37-39mg)
#ferrous sulfate, 325mg (60-65mg)
# ferrous fumerate,325mg( 107mg)
Side effects: nausea, vomiting and constipation.
. one tablet of ferrous sulfate daily provide prophylaxis, it contains
60mg of elemental iron (10% of it will be absorbed)
A) response of treatment is increase in Hb 1g/4wks or Hct by 3%/ 4
wks treatment if response is unsatisfactory look for other causes of
anemia.
21
22. Contii…
* ii) Parenteral therapy:
# indicated:
*non-compliant patient
* unable to take po medication( PUD)
*Severe anemia (requiring blood transfusion)
# Cases seen for the first time during the last 8–10
weeks with severe anemia.
22
23. Contii…
* intravenous therapy in pregnancy primarily deals with iron
sucrose.
*patient finishing course of treatment received a mean of
1000mg elemental iron.
* Hb increases an average of 1.6g/dl from the beginning of
to the end.
*ferritin level increase from 2.9ng/ml to 122.8ng/ml by the
end of therapy ( decrease only to mean 109.4ng/ml 2 weeks
later.
23
24. Contii…
iii) Erythropoietin(recombinant human) therapy:
*traditional approach for postpartum anemia has
been oral iron &transfusion both involves serious
disadvantage, other strategies is parental and
erithropiten therapy.
24
25. Co ntii…
iv) blood transfusion : rarely indicated,
* severe anemia (<5g/dl),preparing for delivery or
surgical intervention.
*poor response to available iron therapy
* congestive heart failure secondary to severe
anemia
*acute blood loss with hemodynamic instability
* anemia's following sickle cell/beta-thallasmeia
/ * one unit blood raise Hb/Hct (0.8-1g/ 3%/unit of
blood respectively.
* packed RBC is preferred to whole blood if there
is no associated hypovolumia.
25
26. Conti…
B) ante partum/postpartum treatment :
i) ante partum management
* high risk pregnancy/frequent visit
* iron therapy based on patient condition
* strong nutritional advice ( iron rich)
* prepare and plan for delivery
ii)intra-partum management:
* position / oxygen supplement
* control pain/ reduce anxiety
26
27. Contii…
* avoid fluid overload ( risk of CHF)
* shorten second stage of labor
*avoid excessive blood loss/ prevent PPH
* first 72 hrs after deliver risk CHF is very high due
to auto transfusion from closure of placenta bed,
follow up controlling IV-fluid is very important.
* determine Hb/Hct level after delivery and treat her
accordingly
27
28. Megaloblastic Anaemia
• These anemias are characterized by blood and bone-marrow
abnormalities from impaired DNA synthesis.
• It is caused by deficiency of folic acid and / or vitamin B12
Folic Acid Deficiency Anaemia: It is uncommon.
Daily Requirement:
• Normal folate requirement is 500 mg /day and a similar
amount is needed during pregnancy so that the daily
requirement during pregnancy is 1mg.
28
30. Contii…
Clinical Picture:
General symptoms of anaemia (see before).
GIT manifestations in the form of:
- dyspepsia,
- anorexia,
- nausea,
- vomiting,
- diarrhoea,
- beefy (red, glassed) tongue,
- hepatosplenomegaly.
30
31. Contii..
Investigations:
1. Blood film:
- Macrocytic hyper chromic RBCs.
- Hyper segmented neutrophilic nuclei (>5 lobes).
2. Serum folate level: is low measured by
radioimmunoassay.
3. Bone marrow: abnormal red cell precursors
(megaloblasts). 31
32. Treatment:
- Diet rich in folic acid as liver, kidney and meat.
- Folic acid 5-15 mg /day orally.
32
33. Vit. B 12 Deficiency Anaemia (Addisonian
Pernicious Anaemia):
•It is rare.
Daily Requirement: less than 1mg.
Aetiology:
•Inadequate intake (rare).
•Deficient intrinsic factor as in atrophic gastritis or
gastrectomy…… results in failure to absorb vitamin B12
•Malabsorption syndrome.
•Increased demand e.g. pregnancy.
33
34. Clinical Picture:
•General symptoms of anaemia.
•GIT manifestations: as folic acid deficiency.
•Nervous manifestations:
- Sub acute combined degeneration.
- Peripheral neuritis
34
35. Investigations:
• As folic acid deficiency + decreased serum vit. B12
Treatment:
• Vit. B12
• IM injection
N.B. Folic acid is never given alone for B12 deficiency
anaemia as it will increase the nervous manifestations.
35
36. Contii…
2. hemoglobinopathies: Sickle-Cell Hemoglobinopathies
Hb a tetrameric protein composed of two pairs of polypeptide
chains with heme group attached to each chain.
Normal adult Hb A1 comprises 95% of Hb, consists of two
alpha two beta chains, remaining 5% of Hb is HbA2( two
alpha two delta chains) and/or HbF( two alpha chain, two
gamma chains)
Hemoglobinopathies arises when there is change in structure
or defect to synthesize a specific polypeptide chain.
a) Sickle hemoglobin (Hemoglobin S) results from a single -
chain substitution of glutamic acid by valine because of an A
for T substitution at codon 6 of the -globin gene
36
37. Contii…
At low oxygen tension RBC containing Hb S assume sickle
shape.
Sludging in small vessels occurs resulting in microifarction of
the affected organ.
Sickle cell have life span of 10 days ( as compared to 120 days
of normal RBC) sickling is activated by dehydration, hypoxia
and acidosis.
1:12 African- American adults are heterozygous for Hb S has
sickle cell traits.
These individuals generally have 35-45% of HbS and are
asymptomatic, child of two sickle cell trait will have 50%
probability of inheriting triat and 25% having actual sickle cell
disease.
37
38. Conti…
If women has HbS, spouse tasted for, if both carrier
prenatal diagnosis ( <20 wks) using DNA analysis(PCR).
Painful vasooclusive episodes of multiple organs are the
clinical hallmark of sickle cell anemia.
Risk of spontaneous abortion, IUGR, IUFD, UTI, PIH in
addition to vasooclusve episodes multiple organs.
Antepartum folate prophylaxis, iron supplement is
contraindicated (risk of iron overload)
38
39. Contii…
Prophylactic exchange transfusion (controversial)
* replace sickle cell with fresh RBC improves vaso-
oclussive episodes).???
Avoid dehydration, hypoxia that triggers sickling.
Vaginal delivery is preferred, c/s reserved for obstetrics
indications.
Labor in LLP recumbent position /receive supplemental of
oxygen
Adequate hydration maintained/fluid over load must be
avoided.
conduction anesthesia recommended provide pain relief and
can be used for c/s.
39
40. Contii…
b) Hemoglobin SC diseases:
Hb C another beta chain variant in which lysine is substituted
for glutamic acid at six position.
Clinically significant disease occur in 1:833 african-americans
adults.
Women with both S and C Hb suffers less morbidities in
pregnancy.
Increase risk of spontaneous abortion,PIH.
Because patient with SC disease have mild symptoms, may not
be undiagnosed.
Crisis is following sequestration of large volume of RBC in
spleen accompanied by fall Hct.
Because of increased spleenic activity mild thrombocytopenia
occurs.
40
41. Contii…
c. Thalassemia:
Results from defect in rate of globulin chain synthesis, any
polypeptide chain can be affected.
Thalassemias are classified according to the globin chain that is deficient, and several
hundred syndromes have been identified.
The two major forms involve impaired production or instability either of -peptide
chains—causing -thalassemia or of -chains—causing –thalassemia
Heterozygous patients are asymptomatic, thalassmeia can be
detected by prenatal diagnosis.
Homozygous alpha thalassmeia results in the formation of
tetramers of beta chain known as Hb of brat. This pathology
results in hydrops fetalis.
41
43. Contii…
The umbilical vein diameter, velocity and blood
flow to the fetuses with Hb bratt were usually
higher than fetus from other cause of hydrops
fetalis.
Beta-thallameia is most common, patient with
heterozygous state asymptomatic.
Detected by increase of HbA2,in homozygous state
HbA1 suppressed, state is labeled as thalassmia
major.
Patient with this disorder dependent on
transfusion.
Marked hepatospleenomegaly, bone marrow
changes secondary to increased heamatopoiesis
Individuals dies of infective CV- complications 43
44. Contii…
Few patient who do become pregnant generally
develop severe anemia and CHF.
Prenatal care is dependent on blood transfusion similar
to sickle cell anemia.
Heterozygous beta-thalasemia has different expression.
Thallasemia minima have microcytosis, asymptomatic.
Thallasemia intermediate spleenomegaly, anemia, high
cardiac out put failure and may become dependent for
blood transfusion.
44
45. Aplastic Anemia
• Aplastic anemia describes a disorder of pluripotential bone marrow
stem cells that results in a reduction of all three hematopoietic cell
lines—red blood cells, white blood cells, and platelets. Pure red
cell aplasia, in which only the red cells are affected, rarely occurs.
• Anemia results from the failure of the marrow to replace senescent
red cells that are destroyed and leave the circulation, although the
cells that remain are of normal size and color.
46. • In most cases, aplastic anemia and pregnancy simultaneously occur
by chance.
• Management depends on gestational age, severity of disease, and
whether treatment has been given. Supportive care includes
continuous infection surveillance and prompt antimicrobial therapy.
Granulocyte transfusions are given only during infections. Red cell
transfusions are given to improve symptomatic anemia, and routinely
to maintain the hematocrit at approximately 20 volumes percent.
Platelet transfusions may be needed to control hemorrhage. Even
when thrombocytopenia is intense, the risk of severe hemorrhage
can be minimized by vaginal rather than cesarean delivery.
• Bone Marrow Transplantation
46
47. Prevention
•Routine screening for anaemia in adolescence,
nutritional education about foods rich in iron(meat,
liver, leafy green vegetables, legumes) and folate
(liver, egg yolk, yeast and leafy green vegetables) to
encourage consumption, early as well as regular
antenatal clinic attendances, iron, folate
supplementation in pregnancy and early treatment
of concomitant infections.
• In areas of high malaria endemicity, intermittent
prophylactic therapy with pyrimethamine
sulphodoxine for malaria should also be given at 16-
17 weeks and 4 weeks later.
•A third dose is given in HIV infection.
47
50. Introduction
•DM is the most common medical problem
complicating of pregnancy.
•Approximately 1% of all pregnant are diabetes.
•Majority is gestational diabetes mellitus (GDM).
51. Definition
♥ GDM is appearance of diabetes for the first time
during pregnancy and disappears postpartum..
♥ Pre-pregnancy diabetes is diagnosed prior to onset of
pregnancy.
•This can be type 1 or type 2.
Women can be separated into those who were known
to have diabetes before pregnancy—pregestational or
overt, and those diagnosed during pregnancy—
gestational.
52. Phases of Diabetes Mellitus
1. Potential diabetes: There is high risk of developing
diabetes e.g. if one or both parents is diabetic.
2. Prediabetes: The period preceding the development of
diabetes. It is a retrospective diagnosis.
3. Latent diabetes: Diabetes appears only under stress
conditions as pregnancy (gestational diabetes) or with
cortisone administration.
4. Chemical diabetes: An abnormal glucose tolerance test
without symptoms.
5. Clinical diabetes: An abnormal glucose tolerance test
with symptoms of diabetes. 52
53. Effect of Pregnancy on Diabetes
1. Pregnancy is diabetogenic due to increased
production of insulin antagonists as human placental
lactogen, placental insulinase, cortisol, oestrogens
and progesterone.
2. Insulin requirements: increases during pregnancy due
to increased production of insulin antagonists while it
decreases postpartum.
3. Reliance on urine for control of diabetes may lead to
insulin overdosage due to lowered renal threshold for
glucose. 53
54. Effect of Diabetes on Pregnancy
Maternal:
1. Pregnancy induced hypertension (30%).
2. Infections: as monilial vulvo-vaginitis, urinary
tract infections, puerperal sepsis and breast
infection.
3. Obstructed labour due to large sized baby.
4. Deficient lactation: is more common.
54
55. Effect of Diabetes on Pregnancy
Foetal:
1. Abortions.
2. Polyhydramnios (30%): due to large placenta and
foetal size.
3. Congenital anomalies(6%):This is about 4 times the
normal incidence(1.5%). Sacral dysgenesis is a
specific anomaly related to diabetes.
4. Macrosomia: i.e. foetal weight > 4 kg at term may
cause obstructed or traumatic delivery.
5. Preterm labour: with its complications mainly due to
polyhydramnios.
55
56. Effect of Diabetes on Pregnancy…
Fetal …..
6. Intrauterine foetal death (5%):especially in the last 4
weeks due to;
- ketosis,
- hypoglycaemia,
- pre-eclampsia,
- congenital anomalies,
- placental insufficiency.
56
57. Effect of Diabetes on Pregnancy…
Fetal………
7. Neonatal mortality and morbidity(5%): due to ;
• hypoglycaemia,
• respiratory distress syndrome,
•congenital anomalies,
• birth trauma,
•hyperbilirubinaemia due to immaturity of the foetal
liver
• hyperviscosity,
• hypocalcaemia and hypomagnesaemia which may
result from decreased parathyroid hormone.
57
58. Diagnosis
A. History:
•History of diabetes or symptoms suggesting it as loss
of weight, polydipsia (thirst), polyuria and polyphagia.
•History of frequent severe pruritis (recurrent monilial
infection).
•History of repeated abortions, intrauterine foetal
deaths or delivery of oversized babies.
58
59. Diagnosis …….
B. Investigations:
1. Positive urine test: during routine antenatal care.
2. Fasting and 2 hours postprandial venous plasma sugar.
59
Fasting 2h
postprandial
Result
<100mg/ dl <145mg/ dl Not diabetic
>145mg/ dl >200mg/ dl Diabetic
100-145 mg/d 145-200mg/ dl Border line
indicates glucose
tolerance test.
N.B. The whole blood glucose values are 15% lower.
60. Investigation ……
3. Glucose tolerance test (GTT):
• Prerequisites:
• Normal diet for 3 days before the test.
• No diuretics 10 days before.
• At least 10 hours fast.
• Test is done in the morning at rest.
60
61. 3. Glucose tolerance test (GTT)…..
(I) Oral glucose tolerance test:
• Giving 75 gm (100 gm by other authors) glucose in 250
ml water orally.
(II) Intravenous glucose tolerance test:
• Giving 25 gm rapid IV, has little practical value due to
bypassing the gut so there is no stimulus to gut hormone
production particularly glucagon.
61
62. Criteria for glucose tolerance test:
The maximum blood glucose values during
pregnancy:
• fasting 90 mg/ dl,
•one hour 165 mg/dl,
•2 hours 145 mg/dl,
•3 hours 125 mg/dl.
•If any 2 or more of these values are elevated, the
patient is considered to have an impaired glucose
tolerance test.
62
63. Indications of performing glucose tolerance test:
1. Positive urine test.
2. First degree family history of diabetes.
3. Gross obesity.
4. Previous Macrosomic babies.
5. Previous unexplained intrauterine or neonatal
deaths.
6. Previous 2 or more unexplained abortions.
7. Current or previous congenital anomalies.
8. Current or previous polyhydramnios.
63
64. Diagnosis …..
Investigation ……
4. Glycosylated haemoglobin (Hb A1):
•It is normally accounts for 5-6% of the total
haemoglobin mass.
•A value over 10% indicates poor diabetes control in
the previous 4-8 weeks.
•If this is detected early in pregnancy, there is a high
risk of congenital anomalies and in late pregnancy it
indicates increased incidence of macrosomia and
neonatal morbidity and mortality.
64
65. Differential Diagnosis of Glycosuria:
1. Lactosuria: may be present during pregnancy, labour
or puerperium. Lactose is differentiated by:
- Osazone test,
- it does not ferment yeast, and
- glucose oxidase test is negative.
2. Alimentary glycosuria:
- Usually occurs early in pregnancy due to rapid absorption of
glucose from the gut.
- No symptoms of diabetes.
- GTT is normal.
65
66. Differential Diagnosis of Glycosuria…..
3. Renal glycosuria:
- usually occurs in mid pregnancy due to lowered renal
threshold.
No symptoms of diabetes.
GTT is normal.
4. Reducing agents: as vitamin C, salicylates and
morphine.
5. Diabetes mellitus.
66
67. Management
A. Antenatal care:
1. Frequent antenatal visits: for maternal and foetal
follow up.
2. Control of diabetes:
I. Diet: is arranged to supply 1800 calories/ day with
restriction
of carbohydrates to 200 gm/ day, less fat and more
proteins and vitamines.
68. Management ….
II. Insulin therapy:
• Oral hypoglycaemics are contraindicated during
pregnancy, labour and early puerperium as they are
not adequate for controlling diabetes, have
hypoglycemia. teratogenic effects and may result in
neonatal
• Doses of insulin tend to increase in the first half of
pregnancy, then stabilise and finally rise in the last
quarter, to be decreased again postpartum.
68
69. • Twice daily ( before breakfast and before dinner)
injections of a combination of short and intermediate
acting insulins are usually sufficient to control most
patients otherwise a subcutaneous insulin pump is used.
• Monocomponent insulins which do not provoke
production of antibodies are preferable e.g. "Actrapid"
(short acting) and " Monotard“ (intermediate acting).
Management ….
70. .
The total first dose of insulin is calculated by;
•Starting with a low dose of 20 units combined insulin
then increase it according to the blood sugar level or,
according to the patient’s weight as follow:
• In the first trimester ............patient’s weight x 0.7
• In the second trimester.........patient’s weight x 0.8
• In the third trimester............patient’s weight x 0.9
Management ….
71. •If the total dose of insulin is less than 50 units/ day, it is
given in a single morning dose with the ratio:
•Short acting (regular or Actrapid)/Intermediate (NPH or
Monotard) = 0.5 In higher doses, 2/3 the dose is given
in the morning with the same ratio and 1/3 the dose is
given in the evening in a ratio 1:1.
71
Management ….
72. Blood sugar analysis is carried out 4 times daily to
regulate the doses as follow:
72
• The aim is to achieve normoglycaemic values as in
GTT.
73. 3- Hospitalization :if diabetics are not controlled as
outpatients or complications develop.
4- Evaluation of foetal well – being by:--
•ultrasound .................................................weekly,
•cardiotocography........................................ weekly,
•serial oestriol estimation ........... 3 times/ weekly,
•amniocentesis before delivery for detection of
phosphatidyl glycerol that indicates lung maturity. L/S
ratio is less reliable in diabetics. 73
Management ….
74. B. Delivery:
1. Timing: pregnancy is terminated at 37 completed
weeks to avoid intrauterine foetal death.
2. Mode of delivery: vaginal delivery is induced in
normal presentation, favorable cervix, average sized
baby and no foetal distress. Otherwise, caesarean
section is indicated.
74
Management ….
75. 3. Insulin therapy:
Day prior to delivery:
• Normal diet, - normal morning insulin, reduce evening
insulin by 25% or omit intermediate acting insulin.
Day of delivery:
5% glucose infusion in a rate of 125 ml/hour + short acting
insulin 1-2 units/hour.
Postpartum: Continue
5% glucose + insulin till oral feeding is established.
When oral feeding is allowed the pre-pregnancy dose of
insulin is given.
75
Management ….
76. 4. Neonatal care:
•The neonate is managed as a premature baby as it is
more liable for RDS.
•5% glucose may given IV at a rate of 0.24 gm / kg/
hour to guard against possible neonatal
hypoglycaemia. Pulsed IM glucose is not preferred
as they may sustain the output of insulin from the
foetal pancreas.
Management ….
77. C. Contraception:
•Mechanical and chemical methods or sterilization are
allowed but hormonal methods are diabetogenic and
IUDS may cause PID.
•Progestogen only contraception may be used if the
patient will accept the high possibility of menstrual
irregularity.
77
Management ….
78. Cardiac disease
•Introduction
•Changes in cardiovascular dynamics during
pregnancy.
•In normal pregnancy the haemodynamic profile
alters inorder to meet the increasing demands of
the growing fetoplacental unit.
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79. Introduction ----
•Normal, healthy pregnant women are able to adjust to
those physiological changes quite easily. In women with
coexisting heart disease, however the added workload can
precipitate complications.
•The three peak periods of cardiovascular stress are:
•28-32 wks of pregnancy
•During labour
•12-24hrs post partum are the most critical and life
threatening for women with heart disease.
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80. Types of heart disease
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•Heart disease can be can be broadly classified in
to:
•Congenital heart disease
•Acquired heart disease
•Congenital heart disease is the principal
cardiovascular problem complicating pregnancy in
the many countries.
81. Type of heart disease ----
1. Congenital heart disease
•The most common congenital heart disease found
in pregnancy are:
•Atrial septal defect(ASD)
•Ventricular septal defect(VSD)
•Patent ductus arteriosus(PDA)
•Pulmonary stenosis
•Aortic stenosis and tetralogy of fallot
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82. Type of heart disease ----
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CHD is also associated with increase fetal
complications like with the maternal functional
class and the degree of cyanosis.
These include:
•Fetal loss
•Intrauterine growth restriction(IUGR)
•Pre-term birth
•An increased risk of fetal CHD
83. Type of heart disease ----
2. Acquired heart disease
These include the following
•Rhematic heart disease
•Myocardinal and ischaemic heart disease
•Aortic dissection(acute)
•Endocarditis
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84. Type of heart disease ----
A. Rhematic heart disease
•RHD remains the most common cardiac problem
in the most part of worlds.
•It causes inflammation and scaring of the heart
valves and results in valve stenosis, plus or minus
regurgitation, valve stenosis is often diagnosed
because of :
•Sever breathlessness
•Tiredness for the first time during pregnancy
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85. Type of heart disease ----
•Management
•Most women with valvular heart disease can be
manged medically which aims to reduce the work
rate of the heart during pregnancy.
•This involves:
•Bed rest
•Oxygen therapy
•Use of cardiac drug e.g diuretic(reduces fluid load),
digoxin(reduces and regulates the heart rate)
•Heparin(reduces risk of thromboembolic disease)
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86. Type of heart disease ----
•Women with more severe sympotomatic disease
may require surgical interventions such as vave
replacement
•Antibiotic prophylaxis is recommended for all
women with valvular lesions during labour.
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87. Type of heart disease ----
B. Myocardinal and ischaemic heart disease
•Myocardial infarction is most likely to occur in the
third trimesters and peri partum period
•Risk factors includes:
•Increased maternal age
•Obesity
•Diabetes
•Pre-existing hypertension
•Smoking and Family history
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88. Type of heart disease ----
Symptom
•Abdominal or epigastric pain
•Vomiting
•Abnormal elevated cardiac enzymes
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89. Type of heart disease ----
C. Endocarditis
•Is an inflammation of the heart usually involving
the heart valve.
•It is one of the most serious complications of the
heart disease.
•Predisposing factors
•Women with valvular heart disease
•History of endocarditis
•Intravenous substance misusers
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90. Type of heart disease ----
Prevention
•Recognition of risk factors and use of strategies to
minimize bacteraemia
e.g. - Good dental hygiene
- Avoidance of drug misuse
- Early treatment of sepsis and administration
of antibiotic prophylaxis to these with high risk
cardiac conditions.
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91. Classification of cardiac disease
•Classification of cardiac disease based on exercise
tolerance is useful for describing the extent of the
immediate problem but has little predictive value.
•Class I: No limitation of physical activity. Ordinary
activity does not cause fatigue, palpitations,
dyspnea, or angina
•Class II: Slight limitation of physical activity.
Comfortable at rest. Ordinary physical activity
results in fatigue, palpitations, dyspnea, or
angina
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92. Classification of cardiac disease---
•Class III : marked limitation of physical activity.
Comfortable at rest. Less than ordinary physical
avtivity results in fatigue, palpitations, dyspnea, or
angina.
•Class IV: Inability to carry any physical activity
without discomfort. Symptoms of cardiac
insufficiency or angina may be present even at
rest, are intensified by activity.
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93. Recognition of cardiac compromise
•Many of the symptoms of normal pregnancy
resemble those of heart disease.
•These include:
•Fatigue, cardiac enlargement,
•Shortness of breath(dyspnea)
•Difficulty in breathing
•Palpitations
•Bounding/collapsing pulsing
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94. Recognition of cardiac compromise --
•Chest pain, IUGR , tendency of preterm delivery
and prematurity
•Development of peripheral oedema
•Distended jugular veins and progressive limitation
of physical activity.
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95. Diagnosis
•Full cardiovascular examination, history and
assessment of life style risk factors
•Blood test- full blood count, clotting studies and
cardiac enzymes
•Chest cardiograph
•E cardiogram to look at cardiac chambers, valve
and great valves
•Other imaging –CT chest scan or MRI
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96. Complications
1. Maternal
•Pulmonary edema due to arterial failure
•Tachycardia due to emotion or exertion and
sudden increased blood volume following labour
•Congestive cardiac failure
•Myocardial failure due to mechanical obstruction
•Pulmonary edema
•Pulmonary embolism
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97. Complications ----
•Active rheumatic carditis death occurs
following delivery
•Obstetric shock
•Sub acute bacterial endocarditis
•Rupture of the cerebral aneurysm
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98. Complications ----
Usual times of maternal death are:-
•During 28-32 wks of pregnancy
•During labour
•Immediately following delivery or early
puerperium
•End of first week of puerperium
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100. Management
Antenatal care
•Management requires a multidisciplinary
approach involving midwives, obstetricians,
cardiologists and anaesthetists
•More frequent ANC visit than healthy pregnant
women
•Visit to a joint clinic run by a cardiologist and
obstetrician are usually every 2wks until 30 wks’
gestation and weekly thereafter until birth.
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101. Management ----
•Evaluation of fetal well-bing include use of :
Ultrasound examination to confirm gestational
age and congenital abnormality
Assessment of fetal growth and amniotic fluid
volume both clinically and by ultrasound
Monitoring of fetal heart rate by CTG
Measurement of fetal and maternal placental
blood flow.
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102. Management ----
Physical and psychological care
•Advice with regard to modifying and adjusting
physical activity during pregnancy
•Dietary advice guidance should be given what
constitutes a well-balanced diet. Cholesterol,
sodium-rich foods and salt should be restricted.
Weight gain should be monitored.
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103. Management ----
•Prevention of infection:- infections often cause a
pyrexia and tachycardia, which will put an added
strain on the heart. In addition the infective
organism can cause further damage in women
with heart lesions by causing endocarditis.
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104. Management ----
•Intrapartum care:
•A coordinated team approach with good
communication between the midwife,
obstetrician, cardiologist, neonatologist,
anaesthetist, the woman and her family is
essential. women with heart disease may have
uncomplicated labours. Vaginal birth is preferred
unless there is an obstetric indication for
caesarean section.
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105. Management ----
•During labour
•The patient is confined to bed comfortable
•Oxygen should be kept by the side of the patient
and administered when required
•Patient should be sedated by IM by morphine 15g
or by peptidase 100mg
•Nutrition should be maintained by glucose drinks
•To check vital signs carefully if weak and fast pulse
is recorded _>100/minut, IV should be secured
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5
106. Management ----
•Forceps delivery or LSCS may be needed as the
combination of the mother. But LSCS the
anaesthesia should be given by expert anesthetist.
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107. Management ----
During puerperium:
•Closely observed for the 1st 24hrs
•Absolute bed rest in comfortable position
•Oxygen administration continuously to be given
•Pulse and RSR to be recorded frequently
•Prophylaxis antibiotic to be given to prevent
puerperal endocarditic
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108. Management ----
•Family planning oral pills and IUCD is
contraindicated for fear of infection
•Barrier method of contraceptive condom is best
to advised the mother
•If her heart is not well compensated the husband
is advised to do vasectomy.
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109. Respiratory disorders
Asthma
•Introduction
•Asthma, which may be the most common
potentially serious complication of pregnancy, is
characterized by chronic airway inflammation with
increased airway responsiveness to a variety of
stimuli, and airway obstruction that is partially or
completely reversible.[
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110. •It affects 2-12 % of pregnant women worldwide
with 5.8% of women hospitalized for asthma
during pregnancy. Prevalence is increasing mainly
due to environmental factors such as change in
indoor environment, smoking, family size, pollution
and diet
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111. •Effect of asthma on pregnancy
•Asthma, which may be the most common potentially
serious complication of pregnancy, is characterized by
chronic airway inflammation with increased airway
responsiveness to a variety of stimuli, and airway
obstruction that is partially or completely reversible.
•It affects 2-12 % of pregnant women worldwide with
5.8% of women hospitalized for asthma during
pregnancy. Prevalence is increasing mainly due to
environmental factors such as change in indoor
environment, smoking, family size, pollution and diet
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112. • Diagnosis
• The characteristic symptoms of asthma are:
• Chest tightness
• Dyspnea
• Wheezing and coughing
• Measuring peak expiratory flow (PEF) using a PEF meter is useful tool for
making a diagnosis and determining how well a person’s asthma is
controlled.
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113. Management
•The ultimate goal of asthma therapy is
maintaining adequate oxygenation of the fetus by
prevention of hypoxic episodes in the mother. The
effective management of asthma during
pregnancy relies on four integral components
outlined below.
•Objective Measures for Assessment and Monitoring
•Subjective measures of lung function by the patient and
physician provide an insensitive and inaccurate
assessment of airway hyperresponsiveness, airway
inflammation, and asthma severity.
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114. Avoid or Control Asthma Triggers
•Limiting adverse environmental exposures during
pregnancy is important for controlling asthma.
Irritants and allergens that provoke acute
symptoms also increase airway inflammation and
hyperresponsiveness. Avoiding or controlling such
triggers can reduce asthma symptoms, airway
hyperresponsiveness, and the need for medical
therapy.
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115. Patient Education
•Women should be made aware that controlling
asthma during pregnancy is especially important
for the well-being of the fetus. Education should
emphasize reduction of asthma triggers. The
patient should have a basic understanding of the
medical management during pregnancy.
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116. Pharmacologic Therapy
•The goal of asthma therapy is multiphasic:
•(1) Relieve bronchospasm,
•(2) protect the airways from irritant stimuli,
•(3) Prevent the pulmonary and inflammatory response to
an allergen exposure, and
• (4) Resolve the inflammatory process in the airways,
leading to improved pulmonary function with reduced
airway hyper responsiveness. The step care therapeutic
approach includes increasing the number and frequency
of medications with increasing asthma severity.
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117. Intrapartum care
•If an asthma attack does occur it should be
treated in the usual way. Women should continue
their usual asthma medications during labour and
it is important that they remain well hydrated.
Maternal and fetal condition should be monitored
closely such as:
•Respiratory function
•Pulse oximetry
•Oxygen therapy and
•Continuous fetal heart rate monitoring
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118. •NB. certain antihypertensive drug and use of
ergometrine or prostaglandinF2a for management
of PPH may cause bronchospasm and should be
avoided or use with caution.
•Oxytocin and prostaglandin E2 are safe to use for
induction of labour
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119. Postnatal care
•Breastfeeding should be encouraged, particularly
as it may protect infants from developing certain
allergic conditions.
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120. Pulmonary tuberculosis(TB)
•Tuberculosis (TB) is an air-born infectious disease
caused by the tubercule bacillus, Mycobacterium
tuberculosis. It is transmited through inhalation of
infected air-born droplets from a person with
infectious TB. It may also caused by consumption
of un boiled milk and dairy products.
•Pulmonary TB (PTB) = accounts for 80% of all TB
case
•Extra-Pulmonary TB (E PTB) = accounts 20%
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121. •Most cases occur in inner city areas where
additional social factors such as poverty,
homelessness, substance misuse, poor nutrition
and crowded living conditions contribute to the
transmission of the disease.
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122. • Diagnosis:
• The onset of primary TB is often insidious and the
symptoms are non-specific:
•Fatigue
•Malaise
•Loss of appetite
•Loss of weight
•These can be interpreted as usual symptoms
occurring in pregnancy leading to a delay in
diagnosis.
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123. The classic symptoms are:
• Persistent cough for more than two weeks
•Productive cough with or with out blood stained
sputum shortness of breath and chest pain
•Loss of wt, intermittent fever night sweats loss of
appetite fatigue and malaise
•Sputum and chest x-ray
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124. •Microscopic examination of sputum smears at
least 3 AFB are seen examined in two
consecutive days
•. Radiological examination: some individuals who
had TB previously that has been cured and there
for do not require treatment may have x ray
suggestive of active TB
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125. Management
•Standard anti-tuberculosis therapy is considered
safe in pregnancy. TB is treated in two phases.
•The first involves taking rifampicin, isoniazid,
pyrazinamide and ethambutol daily for 2
monthes.
• In the second (continuation) phase, rifampicin and isoniazid are taken for a
further 4 months.
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126. •Attention should also be placed on :
•Rest, Good nutrition and education with regard
to preventing the spread of the disease
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127. •Postnatal care
•After birth, babies born to mothers with infectious
TB should be protected from the disease by the
prophylactic use of isoniazid syrup(5mg/kg per day)
and pyridoxine(5-10mg/day) for 6 weeks and then
tuberculin tested. If negative, the neonatal Bacille
Calmette- Guerin(BCG) vaccination should be given
and drug therapy discontinued.
•The baby cannot be infected by the mother via the
breastmilk unless she has tuberculous mastitis.
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128. prevention of TB
•vaccination of children with BCG vaccine
•case finding continuous searching for new
patients
•case holding continuous treatment of known
cases
•health education about
•transmission of TB
•cover mouth when coughing
•spite in to a container with cover never spite in any
where
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129. •Prevention of malnutrition
•Avoid overcrowding
•all children under the age of 6 who have a family
member with pulmonary tuberculosis are properly
screened and receive either a full course of anti
TB treatment or preventive treatment by
Isonized drugs
•Isolation for pulmonary tuberculosis till patient
finished intensive phase of chemotherapy
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130. •concurrent disinfection hand washing and
good housekeeping practices
•pasteurize or boil milk before consumption
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Editor's Notes
The term anaemia refers to the reduction in the oxygen-carrying capacity of the blood due to fewer circulating red blood cells than normal or a reduction in the concentration of haemoglobin. The deficiency may occur as a result of a reduction in the production or an increased loss of erythrocytes.
The modest fall in Hgb levels during pregnancy is caused by a relatively greater expansion of plasma volume compared with the increase in red cell volume .
Anaemia is a reduction in the number of RBCs and haemoglobin content with a corresponding reduction in the oxygen carrying capacity of the blood.
The disproportion between the rates at which plasma and erythrocytes are added to the maternal circulation is greatest during the second trimester.
Late in pregnancy, plasma expansion essentially ceases, while hemoglobin mass continues to increase
The etiology of the more common anemias encountered in pregnancy are listed in Table 51-2. The specific cause of anemia is important when evaluating effects on pregnancy outcome. For example, maternal and perinatal outcomes are seldom affected by moderate iron-deficiency anemia, yet they are altered markedly in women with sickle-cell anemia.
Poor intake:
•Diet deficient in folates.
•Vomiting in pregnancy.
2Increased utilization:
•Demands of pregnancy.
•Rapid growth of fetal, placental and uterine
tissues.
Anaemia can be classified as physiological (eg pregnancy), according to the aetiology (Table
1) and red blood cell morphology (Table 2).
Classification based on red cell morphology classifies anaemia based on the size and shape
of the red blood cell,(normocytic MCV80-90fl, macrocytic MCV>100fl, microcytic
MCV<80fl), as well as .pigmentation (hypochromic, normochromic, hypochromic) (Table 2).
In a typical singleton gestation, the maternal need for iron averages close to 1000 mg. Of this, 300 mg is for the fetus and placenta; 500 mg for maternal hemoglobin mass expansion; and 200 mg that is shed normally through the gut, urine, and skin. The total amount of 1000 mg considerably exceeds the iron stores of most women and results in iron-deficiency anemia unless iron supplementation is given.
In a typical singleton gestation, the maternal need for iron averages close to 1000 mg. Of this, 300 mg is for the fetus and placenta; 500 mg for maternal hemoglobin mass expansion; and 200 mg that is shed normally through the gut, urine, and skin. The total amount of 1000 mg considerably exceeds the iron stores of most women and results in iron-deficiency anemia unless iron supplementation is given.
Serum ferritin levels normally decline during pregnancy . Levels less than 10 to 15 mg/L confirm iron-deficiency anemia
Serum ferritin levels, however, are lower than normal, and there is no stainable bone marrow iron. Iron-deficiency anemia during pregnancy is the consequence primarily of expansion of plasma volume without normal expansion of maternal hemoglobin mass.
Worse if:
(a) Multiple pregnancy.
(b) Grand multiparity.
(c) Fetal haemolysis (in Rh effect).
(d) Infection.
Serum ferritin indirectly reflect iron store.
Levels less than 10 to 15 mg/L confirm iron-deficiency anemia
Indications of parenteral therapy: — Contraindications of oral therapy as previously mentioned. — Patient is not cooperative to take oral iron. — Cases seen for the first time during the last 8–10 weeks with severe anemia.
Sickle hemoglobin (hemoglobin S) results from a single -chain substitution of glutamic acid by valine because of an A for T substitution at codon 6 of the -globin gene
. referred to as pernicious anemia of pregnancy
Folate deficiency:( <5ng/ml)
*water soluble vitamin, found in green vegitable,peanuts and liver.
*folate store in the liver is sufficient for 6wks, after 3 wks dietary deficiency serum folate falls, 2 wks later nutorphil hypersegementaion results, after 17 wks folate deficiency RBC folate drops in next week bone marrow megaloblastic develop.
* during pregnancy folate deficiency is common cause of megaloblatic anemia as vit B12 is rare.
The fetus and placenta extract folate from maternal circulation so effectively that the fetus is not anemic despite severe maternal anemia. There have been instances in which newborn hemoglobin levels were 18 g/dL or more whereas maternal values were as low as 3.6 g/dL (Pritchard and Scott, 1970).
Daily requirement for non-pregnant is 50 microgram during pregnancy raise to 3-4x.
Clinical megaloblastic rarely occurs before third TM, if the patient had risk develop mild anemia.
Serum folate/RBC folate best test to detect folate deficiency before megaloblastosis develops.
Most non –prescription prenatal vitamin have 0.8mg as compared to prescription requiring preparations (1mg of folic acid)but the amount is more than adequate to treat or prevent folate deficiency.
The earliest biochemical evidence is low plasma folic acid concentrations
Women with multiple gestation, frequent conception hemoglobinopaties,receiving anticonvulsants, requires 1mg folic acid supplement daily.
If women folate deficient reticulocyte count will be depressed, after three days treatment reticulocytosis usually occur.
Hct level may rise as much as 1%/ day after one week of folate replacement.
If patient do not develop reticuloctosis after one week folate replacement appropriate test for IDA should performed.
Reticulocytosis; nouna condition in which the number of reticulocytes in the blood increases unusually
Treatment
The treatment of pregnancy-induced megaloblastic anemia should include folic acid, a nutritious diet, and iron. As little as 1 mg of folic acid administered orally once daily produces a striking hematological response. By 4 to 7 days after the beginning of treatment, the reticulocyte count is increased, and leukopenia and thrombocytopenia are corrected.
In Addisonian pernicious anemia, a lack of intrinsic factor results in failure to absorb vitamin B12
During pregnancy, vitamin B12 levels are lower than nonpregnant values because of decreased levels of binding proteins that include haptocorrin (transcobalamins I and III) and transcobalamin II (Morkbak and colleagues, 2007). Women who have had a total gastrectomy require 1000 g of vitamin B12 intramuscularly at monthly intervals. Those with a partial gastrectomy usually do not need such therapy, but vitamin B12 levels during pregnancy should be measured (see Appendix).
. *single substitution of valine for glutamic acid at six position beta polypeptide causes significant change physical characteristics of this Hb. Sickle-cell diseases include sickle-cell anemia—Hgb SS; sickle cell-hemoglobin C disease—Hgb SC; sickle cell--thalassemia disease—either Hb S/Bº or Hb S/B+, and sickle-cell E disease—Hgb SE (Stuart and Nagel, 2004). All are also associated with increased rates of maternal and perinatal morbidity and mortality.
Chemistry a polymer comprising four monomer units.
Haemoglobinopathies are inherited disorders affecting haemoglobin structure (Sickle cell disorders) or synthesis (thalassemias).
They are usually seen in individuals from Africa, the Middle East, the Mediterranean, Asia and the Far East.
The haemoglobinopathies that cause anaemia in pregnancy are sickle cell disorders- HbSS, HbSC and HBS-thalassemia.
Haemoglobinopathies cause a chronic haemolytic anaemia. In sickle cell disorders, the abnormal haemoglobin S sickles in hypoxic states, predisposing the structurally damaged cells to early destruction hence affected persons are chronically anaemic.
Folate demands are increased and concurrent infections will worsen anaemia.
These genetically determined hemoglobinopathies are characterized by impaired production of one or more of the normal globin peptide chains. Abnormal synthesis rates may result in ineffective erythropoiesis, hemolysis, and varying degrees of anemia. Thalassemias are classified according to the globin chain that is deficient, and several hundred syndromes have been identified. The two major forms involve impaired production or instability either of -peptide chains—causing -thalassemia or of -chains—causing -thalassemia. The incidence of these traits during pregnancy for all races is 1 in 300 to 500 (Gehlbach and Morgenstern, 1988).
-Thalassemias
Because there are four -globin genes, the inheritance of -thalassemia is more complicated than for -thalassemia
Beta-Thalassemias
These are the consequences of impaired production of -globin chains or instability of chains
Range from minimal suppression to complete either alpha or beta thalassmia occur.
Heterozygous; having two or more different versions of a specific gene.
The deletion of all four -globin chain genes (––/––) characterizes homozygous –thalassemia
Because chains are contained in fetal hemoglobin, the fetus is affected. With none of the four genes expressed, there are no -globin chains, and instead, hemoglobin Bart (4) and hemoglobin H (4) are formed as abnormal tetramers (see Chap. 4, Fetal Hemoglobin).
Diagnosis of -thalassemia major is more difficult than detecting abnormal hemoglobins because of the large number of mutations.
With -thalassemia minor, hemoglobin A2, which is composed of two - and two -globin chains, is increased to more than 3.5 percent
There is no specific therapy for -thalassemia minor during pregnancy. Prophylactic iron and folic acid are given. Sheiner and associates (2004) reported that fetal-growth restriction and oligohydramnios were increased twofold in 261 affected women. Hemoglobin Bart has an appreciably increased affinity for oxygen, and hemoglobin Bart disease is a common cause of stillbirths in Southeast Asia.
Prenatal diagnosis of -thalassemia major is more difficult than detecting abnormal hemoglobins because of the large number of mutations. To diagnose a particular mutation, targeted mutation analysis is done that requires prior identification of the disease-causing mutation for that particular family (American College of Obstetricians and Gynecologists, 2007). Most of these are done using samples obtained by CVS
Diabetes is now classified based on the pathogenic processes involved (Powers, 2008). Absolute insulin deficiency characterizes type 1 diabetes, whereas defective insulin secretion or insulin resistance characterizes type 2 diabetes
Diagnostic criteria for Diabetes mellitus prior to pregnancy
Symptoms of Diabetes Mellitus plus:
Random plasma glucose concentration ≥200mg/dl .
Fasting plasma glucose ≥126 mg/dl.
Two –hour post load glucose level equal to or greater than 200 mg/dl during an oral glucose tolerance test (OGTT).
The test should be performed as described by the World Health Organization using a glucose load containing the equivalent of 75-g anhydrous glucose dissolved in water.
1. Impaired fasting glucose (IFG): fasting glucose of more than 110 but less than 126 mg/dl.
2. Impaired glucose tolerance (IGT): 2-hour value of the glucose tolerance test (GTT) of more than 140 but less than 200 mg/dl.
Diagnosis is made when any two values are met or exceeded but still others suggest only one abnormal value is enough.
Whole blood glucose values are lower than plasma levels due to glucose uptake by hemoglobin
In those who meet the following criteria
• Maternal age > 35 yrs.
• Previous Macrosomic infant ( ≥4000gm)
• Previous unexplained fetal death
• History of pregnancy with GDM
• Strong immediate family history of diabetes.
• Obesity ( > 90kg)
• Previous congenital abnormal fetus
• Glucosuria.
The recommended time of screening 1-hour challenge test is administered between 24 and 26 weeks of gestation.
Classically, screening has consisted of a blood glucose determination 1 hour after the ingestion of a 50-g glucose load.
If the blood glucose concentration exceeds 140 mg/dl, a 3-hour oral GTT has been recommended.
Main stay of management
• Exercise
• Diet
• Initiate insulin if fasting glucose level is above 95mg/dl or 2hrs postprandial is more than 120mg/dl.
There is no universal formula, and treatment must be individualized.
The desired dosage schedule should be one that resembles insulin production in the normal patient as closely as is technically possible.
The preferred regimen is multiple injections consisting of rapid-acting insulin before each meal and at bedtime, with the latter mixed with intermediate-acting insulin.
The recommended initial therapeutic approach should be dietary manipulation and prescribed exercise in an effort to maintain euglycemia and to prevent excessive fetal growth and initiate insulin if this is not achieved
FBS > 95mg/dl
One hour post prandial blood glucose concentration > 120 mg/dl on two or more occasions within a two wk. interval despite attempted dietary control.
In the 1st trimester, reduce insulin dose by 10-25% to avoid hypoglycemia.
A typical insulin dose is 0.7 units/kg in the 1st trimester, but this must be increased progressively with gestational age.
New cases need Hospitalization for the skill and education on insulin therapy.
A combination of short & intermediate acting insulin is necessary to maintain glucose levels in an acceptable range.
pregnant women
Careful monitoring of blood glucose
An ideal typical glucose monitoring involves capillary glucose checks on rising in the morning,1 or 2hr after breakfast, before& after lunch, before dinner & at bed time and after achieving good control it can be reduced to 3 days per week done randomly.
In resource poor settings FBG & 2hrs postprandial should be checked at least twice weekly.
FBS > 95mg/dl
Pre-meal glucose 70-95mg/dl
• PP glucose <130mg/dl at 1hr. or <120mg/dl at 2hrs.
• No significant hypoglycemia(Glucose <60mg/dl)during the hours of sleep.
An optimal time for delivery of most diabetic pregnancies is between 38 & 40 WKS.
Induction of labor at 38 WKs of gestation is recommended in patients with poor glucose control and macrocosmic and all insulin requiring diabetes should be induced at GA of 40 WKs if spontaneous labor has not occurred.
If A patient has maintained excellent glycemic control and all parameters of fetal surveillance have remained normal, with no obstetric problems dictating early delivery await the spontaneous onset of labor.
If early delivery is indicated before GA 38 WKs, lung maturity should be assessed by amniocentesis.
Cesarean section is indicated only upon obstetric indications.
1-Insulin infusion method
Withhold the morning insulin injection.
Begin & continue glucose infusion (5%DW) at 100ml/hr throughout labor.
Begin infusion of regular insulin at 0.5 unit/hr (5IU insulin in 1000ml of 5%%DW)
Begin Oxytocin as needed
Monitor maternal glucose levels hourly.
Adjust insulin infusion as follows.
Barrier methods are safe & without metabolic side effects.
Women with preexisting diabetes, who do not have serious vascular disease, may be prescribed either the lowest dose combination or progestin only contraceptive under medical supervisions.
Neither DMPA nor Norplant is recommended as 1st line methods of contraception in woman with diabetes.
• Permanent methods of contraception are ideal if family size is complete.