This document summarizes hypertensive disorders of pregnancy. It defines hypertension and proteinuria in pregnancy and classifies hypertensive disorders into four categories: gestational hypertension, preeclampsia, pre-existing chronic hypertension, and chronic hypertension superimposed by preeclampsia. It discusses the definition, risk factors, maternal and fetal effects, complications, and management including antihypertensive treatment, magnesium sulfate for seizures, induction or C-section for delivery, and postpartum care. The goal of management is to minimize risks to the mother and fetus until delivery is safest for the baby.
A comprehensive overview of hypertensive disorders in pregnancy with its complications and management. Mainly focused on gestational hypertension, preeclampsia and eclampsia.
A comprehensive overview of hypertensive disorders in pregnancy with its complications and management. Mainly focused on gestational hypertension, preeclampsia and eclampsia.
diabetes is very common disorder in all age group i.e from infancy to secondary childhood age so intake of good healthy diet is very important for the production of insulin which is needed for body for regular activities
diabetes is very common disorder in all age group i.e from infancy to secondary childhood age so intake of good healthy diet is very important for the production of insulin which is needed for body for regular activities
Pre-gestational hypertension, pregnancy induced hypertension and pre-eclampsia
Go over the different forms of hypertension in pregnancy, pathophysiology and treatment
A blood glucose test measures the amount of a type of sugar, called glucose, in your blood. Glucose comes from carbohydrate, Protein and Lipid. It is the main source of energy used by the body. Insulin is a hormone that helps your body's cells use the glucose. Insulin is produced in the pancreas and released into the blood when the amount of glucose in the blood rises.
Blood Sugar (Glucose) Measurement, Monitoring and Data Analysis: A Review on ...Md Kafiul Islam
The presentation reviews the recent development in non-invasive blood sugar measurement and monitoring techniques, their pros and cons, comparative analysis and the key challenges in implementing such technique in continuous and regular health monitoring for wearable biomedical device technology
Discover the critical insights you need to understand and combat pre-eclampsia in this engaging presentation. My expertly curated slides offer a comprehensive overview of this pregnancy-related condition, covering its causes, symptoms, risk factors, diagnosis, treatment options, and preventative measures. Don't miss this opportunity to gain a deeper understanding of pre-eclampsia and protect the health of expectant mothers and their babies.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
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Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Best Ayurvedic medicine for Gas and IndigestionSwastikAyurveda
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
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
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
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
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ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
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
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
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Top 10 Best Ayurvedic Kidney Stone Syrups in India
Hypertensive Disorder of Pregnancy
1. Africa international university
faculty of medicine and health sciences
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Hypertensive
Disorder of
Pregnancy
Presented by:
Dr. Elwaleed Mudather
Gyae. & obs
2. Hypertensive disorders of
pregnancy
www.doctor.sd
o Hypertensive disorders in pregnancy are a
major cause of maternal and fetal mortality
- In the developing countries the maternal
mortality is about 70-120 per 100.000
maternities
- in UK it is about 0.9 per 100.000 maternities
accounting for about 16% of all maternal death
- The over all perinatal mortality is around 35 per
1000 total birth but may reach 160 per 1000
total birth is severe disease
3. www.doctor.sd
o Definition of hypertension:-
-BP should be measured in the sitting position .
- The sphygmomanometer at the level of the
heart .
- Using a cuff wide enough to cover 80% of arm
- Hypertension is defined as:-
o BP 140 over 90 mmHg or more measured in
two consecutive occasions 4 hours or more
apart
Increase of 30 mmHg systolic or 15 mmHg DBP.
From the pre pregnancy BP
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Definition of proteinuria
o 300 mg or more total protein excretion in
24hours urine collection.
Classification
- Based on these definitions hypertensive
disorders of pregnancy can be classified in to
5. 1) GESTATIONAL HYPERTENSION
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Onset of Hypertension without proteinuria
arising for the first time after 20 week of
gestation with resolution to baseline by 12
week postpartum .
6. 2) pre-eclampsia
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Hypertension of at least 140 over 90 mmHg
recorded on two separate occasions at least 4
hours apart & in the presence of at least
300mg of protein in 24 hours collection of
urine arising de novo after the 20th week of
gestation in a previously normotensive women
& resolving completely by the 6th postpartum
week
7. 3)Pre existing Chronic hypertension with or
without renal disease:-
www.doctor.sd
hypertension. diagnosed before pregnancy or in the first
20th week of pregnancy.
Can be ;-
o 1- Essential hypertension or
o 2-Secondary hypertension.
o --glomerulonephritis.
o --renal artery stenosis.
o --diabetic nephropathy.
o --Polycystic kidneys.
o --SLE.
o --conns syndrome
--Coarctation of the aorta. -
8. 4) Chronic hypertension superimposed by pre-
eclampsia
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proteinuria ,or other symptoms &signs of pre-
eclampsia developing for the first time in
pregnancy in a women with a chronic
hypertension.
9. GESTATIONAL HYPERTENSION
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1-more in multi than primigravida
2- frequency and severity increases with
maternal age.
3- often recurs and familial
4- those women have a high incidence of
hypertension later in life.
.
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pre- eclampsia
- It is a multi system disease specific to
pregnancy in human.
- Affecting 10-
15% of PG and 5 –
7% of multigravida .
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o Risks factors includes:-
- 1-More common at the extremes of age
- 2-More common in PG
- 3-More common in the short and obese women
- 4-Is familial and may recur
- 5-More common in cases with excessive
amount of chorinic tissue such as:-
---hydatidiform mole 70% of cases
- ---multiple pregnancy 25% of cases
- ---hydrops fetalis
- ---poorly controlled diabetes
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- 6--more common in patient with pre existing
chronic renal disease and previous PE.
- 7-Is not associated with increase incidence of
hypertension in later life.
- Clinical feature:-
PE is characterized by lack of symptoms until an
advanced stage reached. Patient may report.
Swelling of feet and ankle, difficulty in putting
on her shoes, tightness of rings and tightness
and puffiness of the face.
Sign includes hypertension and non dependent
oedema. urine may show proteinuria
13. Aetiology of pre-eclampsia:-
www.doctor.sd
- Cause is unknown
- Genetic factors together with an abnormal
immunological reaction to the first pregnancy
have been postulated this leads to defective
trophoblast invasion of the spiral arteries and as a
result the spiral arteries remain muscular, un
dilated and respond to presser agent such as
angiogenesis2. placental blood flow is therefore
reduced & this results in release of factors in the
maternal circulation that targeted the vascular
endothelium which result in wide vascular
endothelial dysfunction
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with the development of hypertension, altered
vascular reactivity, Activation of the
coagulation cascade and multi system
damage.
- generalized maternal endothelial damage
affects every system in the body with the
following effects.
15. www.doctor.sd
- Maternal effects
- Cardio vascular and pulmonary effect:-
* hypertension
* Peripheral oedema due to leaking endothelium
*Cardiac failure due to the high systemic vascular
resistance
*Pulmonary oedema may arise due to an imbalance
between a reduced colloid osmotic pressure, and the
pulmonary capillary wedge pressure
- *Acute adult respiratory distress syndrome also can
occur.
16. www.doctor.sd
The kidneys:-
- glomerular endothelial cells swell- block the
capillaries.
- Impaired renal function may result in a rise in
plasma urate (an early feature), urea, and
creatinine.
- Proteinuria develops.
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o The liver:_
- Hepato-celluar damage can occur due to fibrin
deposits in the sinusoids.
- In some cases jaundice and severe liver
damage can follow.
- The potentially dangerous HELLP syndrome
(haemolysis, elevated liver enzyme and low
platelets) must be considered in severe cases.
- Subcapsular haemorrhage and even liver
rupture my occur
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o Coagulation:-
- Increasingly generalized endothelial damage
commonly causes slight intravascular
coagulation.
- Disseminated intravascular coagulation (DIC) is
rare but serious
Central nervous system:-
- Sudden elevation of BP can causes arterial damage and
loss of vascular auto regulation which may leads to
cerebral oedma, haemorrhages and infacts
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- Cerebral haemorrhage & pulmonary oedema
are the commonest causes of maternal death
from eclampsia.
o Placenta:-
- Hypertension is associated with constriction of
uterine blood vessel. Pathological change in
spiral arteries and fibrin deposition, infacts and
other pathological change.
21. www.doctor.sd
- --- following prolonged hypoxia
- --- fluid over load
- Cardiac failure
- CVA and other haemorrhages
due to fibrinoid necrosis and rupture of wall of
small vessels.
- HELLP syndrome
o Renal failure due to :
---ischaemia
--- tubular necrosis
--- cortical necrosis
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o DIC.
o blindness
o Micro angiopathic haemolytic anaemia acute
or sub acute haemolysis with the appearance
of fragmented RBCs and reticuloytes in the
prephral blood smear associated with
thrombocytopenia haemoglobinaemia and
hemoglobinuria
23. Management of pre-eclapsia:-
www.doctor.sd
o The aim of management is:-
o To minimize the hazards both to the mother
and to the fetus until such a time as the fetus
stand a better chance of survival outside the
uterus than inside, or until further prolongation
of pregnancy creates a threats to the mother
life or health
24. Antenatal manangement
www.doctor.sd
- Initial assessment
- all patient found to have hypertension
should be admitted to hospital or obstetric day
unit for full initial assessment and plan of
management should be formulated according
to the severity of disease and the duration of
pregnancy.
25. www.doctor.sd
- Classification according to severity:
- hypertensive disorders can be classified
according to severity to
1.mild:-
DBP 90 and more but less than 110 mmHg
No significant proteinuria
Normal fetal growth
2. sever:-
- DBP 110 mmHg and more or
- DBP 90 and more with significant proteinuria or
fetal growth restriction.
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- 3- imminent eclampsia:-
- -DBP 90 or more with symptoms such as
- Severe persisting headache usually frontal but
may be occipital.
- Visual disturbance (flash of light diplopia)
- -upper abdominal pain, nausea, vomiting (due
to oedema of gastric mucosa, subcapsular Hge
and stretching of liver capsule ).
- Oliguria (urine less than 30 ml per hour)
- Hyperflexia or clonus
-
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- 4- eclampsia:-
- -DBP 90 and more +convulsion (grand
mal epileptiform convulsion).
Eclampsia
- In majority of cases it occur
antepartum usually in the last quarter
of pregnancy.
- In few case it occurs intrapartum or
postpartum
- Haemorrhagic complication are
common.
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neurological complications may include coma focal
motor deficits and cortical blindness.
Differential Diagnosis:-
o Cerebral malaria
o CVA
o Amniotic fluid embolism
o Water intoxication
o Meningitis
Pathology of Eclampsia:-
Is thought to involve cerebral vasospasm leading to
ischaemia, disruption of the blood brain barrier
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1) Mild hypertension without IUGR or
impairment of fetal well being:-
- In general implies minimal or no added risk to
the mother or fetus.
- No immediate indication for antihypertensive
or other treatment.
- Out patient surveillance on weekly ANC visits
with assessment of symptoms. Weight, BP,
fetal size & movement. Amniotic fluid volume,
Urine for protein CTG, scan for growth at 28-
34wks
30. www.doctor.sd
- Rest at home but it benefits have never been
clearly defined.
- Sedation is not necessary.
- If labour has not commenced at term induction
may be advocated largely on empirical ground.
2) severe PIH:-
o Admission to hospital
o BP and other vital sign 6 hourly
o Urine for protein daily
31. www.doctor.sd
- Fetal movement (kick chart)
- Clinical examination includes fundal height and
amount of liquor.
- Weekly renal and liver function test as well as
platelets count, coagulation status and protein
excretion. Elevated urate levels and falling
platelets reflect worsening of the clinical
condition.
- Fetal size and liquor volume are assessed by
ultra sound.
32. www.doctor.sd
- CTG is repeated at intervals determined by
clinical status and can be enforced by a
biophysical profile
- Doppler ultra sound :- absent or reversed flow
in the umbilical artery during diastoly is
associated with high perinatal mortality.
- Antihypertensive:-
- Is to protect the mother from the risk of
cerebral haemorrhage,
- left Ventricular failure, renal failure, DIC and
convulsion.
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- Is indicated when the mean arterial BP
exceed the threshold for vessel
injury(140mmHg)
- The drugs have no effect on the progress of
the disease.
Therapeutic options include the following.
1. Methyldopa
- central alpha stimulants
- Dose up to 2gm/day
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- Side effect include
sedation ,headache, nightmares depression,
dizziness, haemolytic anaemia positive
coombs test.
- 2- calcium channel blockers e.g. Nifedipine
- 3- vasodilators e.g hydrallazine
- 4- labetolol (100—200mg)
- has both Beta and alfa adrenoceptor
blocking action
35. www.doctor.sd
- Termination of pregnancy:-
- The definitive treatment of severe PIH is
delivery of the fetus.
- In most cases labour should be induced at
completed 37wks
- Elective C/S may be considered in patient less
than 34wks and when there is some additional
obstetric indication.
36. www.doctor.sd
- Management of imminent eclampsia and Eclampsia:-
- Left lateral position, secure air way, oxygen.
- Control of fits with anticonvulsants :
- 1- diazpam dose
10mg I.V in 4min. Followed by 40mg in 500cc
of 5%Dext.water 2-4ml/hour. Safe-
immediate action, but it has short action& can
sedate the fetus & the patient
- Magnezium sulphate: is the drug of first choice it is
- - Anti convulsant ,Antihypertensive and
tocolytic with prolong .action
37. www.doctor.sd
- Therapeutic dose is close to toxic dose.
- Dose ;--
intravenous;-
loading dose 4gm in 100ml over 15 -20 min.
Maintenance dose 1 - 1.5gm hourly for 24 hours
from the last fit.
intramuscular;-
loading dose10 gm as 50% sol. 5gm in each
buttock. maintenance 5gm as 50% sol. 4houly
- Monitoring by reflexes, respiratory rate (>16/min)
. urinary out put ( >30ml/ hour) and blood level.
- Toxic effect include
hypotension and respiratory failure.
- Antidote is Calcium. gluconate.
- 3- phenytoin
- 4- thiopentone
38. www.doctor.sd
o Control of hypertension:-
1- hydralazine : 5mg intravenous repeated every 20 min
to a maximum cumulative dose 20 mg.
2- labetolol :- 40mh I.V escalated to 40, 80 every 10
min to cumulative dose of 300mg
3- diazoxide (300mg).
- Maintenance of fluid, electrolytes and acid- base
balance by monitoring CVP, urea electrolytes and
blood gases
- Monitoring of Hb, platelets count, transaminases and
coagulation profiles
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o Delivery of fetus:-
o The definitive treatment of eclampsia is delivery
o Attempts to prolong pregnancy in order to improve
maturity are unlikely to be of value.
o However it is in appropriate to deliver an unstable
mother even if there is fetal distress.
o Once seizures are controlled, severe hypertension
treated and hypoxia corrected delivery can be
expedited
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o Vaginal delivery should be considered but caesarean
section is likely to be required in PG remote from
term with an unfavorable cervix.
o After delivery high dependency cares should be
continued for a minimum of 24 hours
o Treatment of complication.
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Prophylaxis :-
o Regular and efficient ANC is the best weapon in
prevention early detection and reduction of the
hazards of Pre-eclampsia
o Reduction of sodium is of no benefit