This document discusses hypertensive disorders of pregnancy, which complicate 5-10% of pregnancies. It defines various types of hypertensive disorders including gestational hypertension, chronic hypertension, preeclampsia, eclampsia, and preeclampsia superimposed on chronic hypertension. It outlines diagnostic criteria and management guidelines for each disorder. Key points covered include definitions, risk factors, complications, treatment and delivery timing based on gestational age. The goal of management is to ensure the safety of the mother and fetus.
A comprehensive overview of hypertensive disorders in pregnancy with its complications and management. Mainly focused on gestational hypertension, preeclampsia and eclampsia.
loss of biodiversity is the most important in biodiversity and conservation.it is useful to reduce the activities which are responsible for extinction and endangering of living organisms.
Pregnancy induced hypertension introduction
Classification of pregnancy induced hypertension
Preeclampsia -
Definition
Criteria for diagnosis of preeclampsia,
Epidemiology of preeclampsia,
Risk factors of preeclampsia,
Pathogenesis of preeclampsia,
Pathophysiology of preeclampsia,
Course of preeclampsia,
Complications of preeclampsia,
What is HELLP ?
Management of preeclampsia at home, at hospital, during labour, during puerperium,
Management of acute fulminant preeclampsia
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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
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 Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
HOT NEW PRODUCT! BIG SALES FAST SHIPPING NOW FROM CHINA!! EU KU DB BK substit...GL Anaacs
Contact us if you are interested:
Email / Skype : kefaya1771@gmail.com
Threema: PXHY5PDH
New BATCH Ku !!! MUCH IN DEMAND FAST SALE EVERY BATCH HAPPY GOOD EFFECT BIG BATCH !
Contact me on Threema or skype to start big business!!
Hot-sale products:
NEW HOT EUTYLONE WHITE CRYSTAL!!
5cl-adba precursor (semi finished )
5cl-adba raw materials
ADBB precursor (semi finished )
ADBB raw materials
APVP powder
5fadb/4f-adb
Jwh018 / Jwh210
Eutylone crystal
Protonitazene (hydrochloride) CAS: 119276-01-6
Flubrotizolam CAS: 57801-95-3
Metonitazene CAS: 14680-51-4
Payment terms: Western Union,MoneyGram,Bitcoin or USDT.
Deliver Time: Usually 7-15days
Shipping method: FedEx, TNT, DHL,UPS etc.Our deliveries are 100% safe, fast, reliable and discreet.
Samples will be sent for your evaluation!If you are interested in, please contact me, let's talk details.
We specializes in exporting high quality Research chemical, medical intermediate, Pharmaceutical chemicals and so on. Products are exported to USA, Canada, France, Korea, Japan,Russia, Southeast Asia and other countries.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
8. Swelling of the hands and the face or
leg edema after an overnight rest
9. 1. Gestational Hypertension
2. Chronic Hypertension
3. Pre-eclampsia
a. Mild/nonsevere
b. Severe
4. Eclampsia
5. Preeclampsia syndrome superimposed on
chronic hypertension
10. •
•
•
•
•
BP > 140 / 90 mm Hg for first time during pregnancy
No proteinuria
BP returns to normal before 12 weeks postpartum
Final diagnosis made only postpartum
(+) epigastric discomfort or thrombocytopenia
11. • BP > 140/90 mm Hg prepregnancy or diagnosed before 20
weeks' gestation not attributable to gestational trophoblastic
disease
Or
• Hypertension first diagnosed after 20 weeks' gestation and
persistent after 12 weeks postpartum
12. •
BP > 140 / 90 mm Hg for first time
during pregnancy
•
BP > 140/90 mm Hg prepregnancy
or diagnosed before 20 weeks
gestation
•
BP returns to normal before 12
weeks postpartum
•
Hypertension first diagnosed after
20 weeks' gestation and persistent
after 12 weeks postpartum
13.
14. • BP > 140/90 mm Hg after 20 weeks' gestation
• Proteinuria > 300 mg/24 hours or
> 1+ dipstick
24. 1. Placental implantation with abnormal trophoblastic invasion
of uterine vessels
2. Immunological maladaptive tolerance between maternal,
paternal (placental), and fetal tissues
3. Maternal maladaptation to cardiovascular or inflammatory
changes of normal pregnancy
4. Genetic factors including inherited predisposing genes as
well as epigenetic influences.
25.
26.
27.
28.
29.
30. 1. Termination of pregnancy with the least possible trauma to
mother and fetus
2. Birth of an infant who subsequently thrives
3. Complete restoration of health to the mother
31. 1. Weight
2. Proteinuria on admittance and at least every 2 days
thereafter
3. Blood pressure readings
4. Measurements of plasma or serum creatinine and liver
transaminase levels, and hemogram to include platelet
quantification.
5. Evaluation of fetal size and well-being and amnionic fluid
volume
35. • BP <140/100 mmHg
• Proteinuria < 1,000mg 24hr or <2+ on dipstick
• Platelet count > 120,000/mm
• Normal fetal growth and testing
• No indication for delivery
36. • Gestational age > 40 weeks
• Gestational age > 37 weeks if there is
• Bishop score > 5
• Fetal weight <10th percentile
• Non-reactive non-stress test
37. • Gestational age 34 weeks and above with the presence of
•
•
•
•
•
Labor
Rupture of membranes
Vaginal bleeding
Abnormal biophysical profile
Criteria for severe preeclampsia
• Expectant management should be considered for women
remote from term who have mild preeclampsia
38. • BP at each visit – at least once weekly
• Platelet count and liver enzymes at regular intervals
• NST at regular intervals
• Fetal growth every 2 to 3 weeks
39. • Anticonvulsants are not recommended
• Anti-Hypertension meds only for increase in BP from baseline
• Low dose aspirin and high dose calcium are not
recommended
57. Labetalol
Hydralazine
Nifedipine
IV Nicardipine
10 to 20mg IV, then 20-80mg q20-30 minutes
5mg IV or IM, then 5 to 10 every 20 to 40 minutes
10 to 30mg PO, q45 minutes
Start at 0.1mg/mL with maximum of 10mg/hr
Atenolol, ACEi, ARBs and diuretics should be avoided
58. • Indicated for lung maturity
• Between 24-34 weeks
• Betamethasone 12mg IM every 24 hours for 2 doses
• Dexamethasone 6mg IM every 12 hours for 4 doses
59.
60. • Control of seizure
• Correction of hypoxia and acidosis
• Control of blood pressure
• Delivery after control of seizure
61.
62.
63. • Low dose aspirin (65-85mg) at bedtime everyday for
12 weeks until birth
• ACEi and ARB are contraindicated
• Anti-hypertensive therapy
• Methyldopa 250-500mgPO BID-QID (max 2 g/day)
• Labetalol 1000499mg PO BID0ID (max 1200mg/day)
• Nifedipine 10-20mg PO BID-TID max, 120-180mg/day
One member of the deadly triad, along with hemorrhage and infection, that contribute greatly to maternal morbidity and mortality rates
In the local data, 32.1% of maternal mortality belong to the hypertension group
The diagnosis of hypertension should be based on office or in-hospital bp measurement and is based on the average of at atleas 2 measurements, taken using the same arm.
The diagnosis of hypertension should be based on office or in-hospital bp measurement and is based on the average of at atleas 2 measurements, taken using the same arm.
Proteinuria is defined as the resence of 0.3g or 300mg or more of prtein in a 24-hour urine specimen, which usually correlates with a +1 (30mg/dl) or freater, but should be confirmed with a random urine dipstick evaluation or and a 24-hour or timed collection.It may also be defined as greater than 30mg/mmol urinary creatinine in a spot urine sample
No longer a criterion for the diagnosis of hypertension in pregnancy
Headaches or visual disturbances such as scotomata can be premonitory symptoms of eclampsia. Epigastric or right upper quadrant pain frequently accompanies hepatocellular necrosis, ischemia, and edema that stretch Glisson capsule. This characteristic pain is frequently accompanied by elevated serum hepatic transaminase levels. Thrombocytopenia is also characteristic of worsening preeclampsia. It probably is caused by platelet activation and aggregation as well as microangiopathic hemolysis induced by severe vasospasm. Other factors indicative of severe preeclampsia include renal or cardiac involvement as well as obvious fetal-growth restriction, which attest to its duration.
A sudden increase in proteinuria or blood pressure or platelet count < 100,000/uL in women with hypertension and proteinuria before 20 weeks' gestation
Observations that abnormal interfaces between maternal, paternal, and fetal tissues may cause preeclampsia have led to hypotheses that the syndrome is a two-stage disorder.
Main pathophysiology of eclampsia is vasospasm in various organs, which is responsible for its symptomatology, however the cause of the vasospasm is unkown.
Schematic outlines the theory that the preeclampsia syndrome is a "two-stage disorder." Stage 1 is preclinical and characterized by faulty trophoblastic vascular remodeling of uterine arteries that causes placental hypoxia.Stage 2 is caused by release of placental factors into the maternal circulation causing systemic inflammatory response and endothelial activation.
Instead of being simply "one disease," preeclampsia appears to be a culmination of factors that likely involve a number of maternal, placental, and fetal factors. Those currently considered important include:
Normal third-trimester placental implantation shows proliferation of extravilloustrophoblasts from an anchoring villus. These trophoblasts invade the decidua and extend into the walls of the spiral arteriole to replace the endothelium and muscular wall. This remodeling creates a dilated low-resistance vessel. Placenta in preeclamptic or fetal-growth restricted pregnancy shows defective implantation. This is characterized by incomplete invasion of the spiral arteriolar wall by extravilloustrophoblasts and results in a small-caliber vessel with high resistance.Abnormally narrow spiral arteriolar lumen impairs placental blood flow. Diminished perfusion and a hypoxic environment eventually lead to release of placental debris that incites a systemic inflammatory response
NK cells are abundant in the non-pregnant endometrium (left panel) in the secretory phase of the menstrual cycle. In early pregnancy (right panel), interactions between fetal extravilloustrophoblast cells (EVT) and NK cells in the decidua contribute to the remodeling of the spiral arteries to allow increased blood supply to the fetus. Fetal trophoblast cells secrete soluble HLA-G (sG), which can be endocytosed by KIR2DL4 into endosomes. Endosomal signaling then results in a sustained proinflammatory/proangiogenic secretory response that may promote the vascular changes seen in early pregnancy.
Inflammatory changes are thought to be a continuation of the stage 1 changes caused by defective placentationDisruption of the endothelium results in a narrowed lumen because of accumulation of plasma proteins and foamy macrophages beneath the endothelium.
In many women with preeclampsia, especially those at or near term, all three objectives are served equally well by induction of labor. One of the most important clinical questions for successful management is precise knowledge of fetal age.
In many women with preeclampsia, especially those at or near term, all three objectives are served equally well by induction of labor.One of the most important clinical questions for successful management is precise knowledge of fetal age.
A systematic evaluation is instituted to include the following:Detailed examination followed by daily scrutiny for clinical findings such as headache, visual disturbances, epigastric pain, and rapid weight gain Weight determined daily Analysis for proteinuria on admittance and at least every 2 days thereafter Blood pressure readings in the sitting position with an appropriate-size cuff every 4 hours, except between 2400 and 0600 unless previous readings had become elevated Measurements of plasma or serum creatinine and liver transaminase levels, and hemogram to include platelet quantification. The frequency of testing is determined by the severity of hypertension. Some recommend measurement of serum uric acid and lactic acid dehydrogenase levels as well as coagulation studies, but studies have called into question the value of these tests (Conde-Agudelo, 2009; Cnossen, 2006; Thangaratinam, 2006, and all their colleagues). Evaluation of fetal size and well-being and amnionic fluid volume either clinically or using sonography.Goals of such management include early identification of worsening preeclampsia and development of a management scheme that includes a plan for timely delivery. If any of these observations lead to a diagnosis of severe preeclampsia as previously defined by the criteria in Table 34-2, further management is subsequently described.Reduced physical activity throughout much of the day is likely beneficial. Absolute bed rest is not necessary. Ample protein and calories should be included in the diet, and sodium and fluid intake should not be limited or forced. Further management depends on: (1) severity of preeclampsia, (2) gestational age, and (3) condition of the cervix.Fortunately, many cases are sufficiently mild and near enough to term that they can be managed conservatively until labor commences spontaneously or until the cervix becomes favorable for labor induction. Complete abatement of all signs and symptoms, however, is uncommon until after delivery. Almost certainly, the underlying disease persists until after delivery!
After the initial evaluation, a decision must be made to either manage the patient as an outpatient or an inpatient.
Most women with mild to moderate hypertension are managed at home. Outpatient management may continue as long as the disease does not worsen and if fetal jeopardy is not suspected. Sedentary activity throughout the greater part of the day is recommended. These women are instructed in detail to report symptoms
Hospitalization is recommended for patients with > 40 weeks AOGOr > 37 AOG if Bishop score > 5Fetal weight <10th percentileNon-reactive non-stress test
And for 34 weeks above, the presence of labor, rupture of membranes, vaginal bleeding, abnormal biophysical profile or those who fit the criteria for severe preeclampsia
As an out patient, the patient must be seen at least once weekly with recording the BP.Platelet count and liver enzymes, NST should be done at regular intervals and fetal growth must be recorded every 2 to 3 weeks.
The CPG does not recommended starting of anticonvulsants, aspirin or calcium and anti-hypertensives should be used sparingly and only in cases of increased BP from baseline.
International data shows that 5-6% of pregnant patients are hypertensive and 5-10% from those have severe preeclampsia.And hypertension is the 2nd most common cause of maternal death both in the US and in the Philippines.
Initial management includes stabilization of the mother’s condition, confirmation of gestational age and assessment of fetal well being
The physician must decide between delivery and expectant management. Studies were presented in Williams leading to a recommendation of Delivery for patients with > 34 weeks AOGHowever, there are exceptions
These are the circumstances in which expectant management of severe preeclampsia with < 34 weeks are acceptableProteinuriaIUGR with good fetal testingBlood pressure
Here are some indications for delivery with early-onset severe preeclampsia
Another decision that the physician must made is to deliver or to terminate the pregnancyIn a study by Bombrys in Williams included 200 women with severe preeclampsia and revealed no infant survivors in those presenting before 23 weeks AOG, leading to this recommendation by the authors.For women with pregnancies at 24 to 26 weeks, perinatal survival approached 60 percent, and it averaged almost 90 percent for those at 26 weeks.Maternal complications were common, and there were no infant survivors in those presenting before 23 weeks. Thus, the authors recommended pregnancy termination for these women. For those at 23 weeks, the perinatal survival rate was 18 percent, but long-term perinatal morbidity is yet unknown.
Drug of choice for the prevention of convulsionsUsed in the context of moderate to severe preeclampsia once delivery decision is made and in the immediate postpartum period
Recurrent seizures should be treated wit either a further bolus of 2g MgSO3 or an increased in the infusion rate to 1.5g or 2g/hour.
CNS depression are assessed by examining for patellar reflexesTreatment with calcium gluconate or calcium chloride, 1 g intravenously, along with withholding further magnesium sulfate, usually reverses mild to moderate respiratory depression.Because magnesium is cleared almost exclusively by renal excretion, the dosages described will become excessive if glomerular filtration is decreased substantively
Fluid restriction is advisable since pulmonary edema is a significant cause of maternal death
To assess the fetus, CTG should be done as it is the mainstay of fetal monitoring.
Atenolol causes increase in fetal growth restriction.ACE and ARB with unacceptable fetal adverse effects.Diuretics relative contraindication reserved for pulmonary edema.Anti-hypertensive drugs should be given 24 hours postpartum
Premature separation of a normally implanted placenta which compromises circulation to the fetus