This document discusses hypertensive disorders of pregnancy, including preeclampsia and eclampsia. It defines the conditions and classifications, describes risk factors and potential complications, and outlines diagnostic criteria and management approaches. Preeclampsia is a leading cause of maternal mortality characterized by new hypertension and proteinuria after 20 weeks of gestation. It can range from mild to severe depending on symptoms, and severe preeclampsia is treated with aggressive delivery and antihypertensive medications. Eclampsia involves seizures in preeclampsia patients and is managed with magnesium sulfate. Overall, delivery is the only cure for preeclampsia and management aims to carefully control blood pressure and monitor for maternal-fetal complications.
A comprehensive guide to the management of hyperglycaemia in pregnancy aimed at the primary care physician and based on latest evidenced based criteria. Includes information from latest studies such as HAPO study and ACHOIS, and involves guidelines from the IADPSG, ADA, WHO and Malaysia.
Pregnancy-induced-hypertension is hypertension that occurs after 20 weeks of gestation in women with previously normal blood pressure. Pregnancy-induced hypertension (PIH) complicates 6-10% of pregnancies. It is defined as systolic blood pressure (SBP) >140 mmHg and diastolic blood pressure (DBP) >90 mmHg. It is classified as mild (SBP 140-149 and DBP 90-99 mmHg), moderate (SBP 150-159 and DBP 100-109 mmHg) and severe (SBP ≥ 160 and DBP ≥ 110 mmHg).
Gestetional hypertension, Preeclampsia and Eclampsiasunil kumar daha
Please find the power point on Gestetional hypertension, Preeclampsia and Eclampsia . I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
These lecture slides, by Dr Sidra Arshad, offer a quick overview of 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 leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
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. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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
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2. Introduction
• The hypertensive disorders of pregnancy are
major contributors to maternal and perinatal
morbidity and mortality.
• The Centers for Disease Control and
Prevention (CDC) have reported that
preeclampsia/eclampsia is the third leading
causeof maternal mortality in the United
States, primarily due to CNS hemorrhage.
3. Incidence
• The combined incidence of
hypertensive disorders in pregnancy
varies depending on the population
being studied and on the criteria used
but is reported to range from 12% to
22%, whereas the
preeclampsia/eclampsia syndrome
occurs in about 5% to 8% of
pregnancies.
4. Classification and Definitions
• Preeclampsia or eclampsia
(hypertension and proteinuria unique to
pregnancy)
• Chronic hypertension
• Chronic hypertension with
superimposed preeclampsia
• Gestational or transient hypertension
5. CHRONIC HYPERTENSION
• known hypertension before pregnancy,
development of hypertension before20
weeks’ gestation, or, in cases in which
hypertension is first noted during
pregnancy, persistence of elevated
blood pressures greater than 12 weeks’
postpartum.
6. • It is important to review the
antihypertensive medications being taken
and to discontinue any that are potentially
teratogenic.
• Methyldopa is considered to be the safest
antihypertensive medication in pregnancy,
and calcium channel blockers and
labetalol are also considered to be safe.
• β-Blockers should be used with caution
because they may cause fetal growth
restriction and may affect the
interpretation of the NST.
7. CHRONIC HYPERTENSION WITH
SUPERIMPOSED PREECLAMPSIA
• The diagnosis of superimposed
preeclampsia should be reserved for
those women with chronic
hypertension who develop new-onset
proteinuria (≥0.3 g in a 24-hour
collection) after the 20th week of
gestation.
8. GESTATIONAL
HYPERTENSION
• The diagnosis of gestational hypertension is
made if hypertension without proteinuria first
appears after 20 weeks’ gestation or within
48 to 72 hours after delivery and resolves by
12 weeks postpartum.
• A significant percentage of women with
apparent gestational hypertension go on to
develop proteinuria and the full preeclampsia
syndrome at a later stage in pregnancy.
• The diagnosis of gestational hypertension
can only be made in retrospect.
9. Preeclampsia
• a syndrome unique to pregnancy,characterized
by the new onset of hypertension and proteinuria
in the latter half of gestation.
• The following two criteria are essential for the
diagnosis of preeclampsia:
(1) the development of hypertension(systolic
blood pressure ≥ 140 mm Hg or diastolic blood
pressure ≥ 90 mm Hg), in a woman whose blood
pressures were previously normal, after the 20th
week of pregnancy
(2) the development of new-onset proteinuria
after the 20th week of gestation. Proteinuria is
10. preeclampsia is often preceded by, or
associated with, the development of
generalized edema. Dependent edema
(edema of the lower extremities) is very
common in normal pregnancies.
Hand and facial edema are more likely to be
associated with preeclampsia, but if
unaccompanied by hypertension and
proteinuria, they are not diagnostic of the
preeclampsia syndrome.
11. **predisposing risk factors:
• Primigravida but it also occurs in
multiparas.
• Extremes of age.
• diabetes mellitus, chronic
hypertension.
• Multiple gestation , polyhydrominous .
• Previous hx. Of PET .
• Hydrops fetalis .
• *** When it arises in the early second
trimester (14 to 20 weeks), a
12. ***ETIOLOGY :
Preeclampsia is called a “disease of
theories,” because genetic,
immunologic, vascular, hormonal,
nutritional,and behavioral factors have
all been proposed as causes.
No single, definitive “cause” has been
identified, and the origins of the disease
are considered to be multifactorial.
• The net effect of these processes would
be widespread vasoconstriction leading
to hypoxic and ischemic damage in
different vascular beds.
13.
14. ***Preeclampsia is divided into mild and
severe forms, depending on:
• the severity of the hypertension.
• the amount of proteinuria.
• and the degree to which other organ
systems are affected.
15. Criteria for Severe
Preeclampsia
• Severe hypertension (systolic blood pressure ≥160
mm Hg, or diastolic blood pressure ≥ 110 mm Hg)at
rest, on two occasions at least 6 hr apart
• Heavy proteinuria (at least 5 g in a 24-hr collection or
a qualitative value of 3+ in urine samples collected 4
hr apart)
• Oliguria (<500 mL in 24 hr)
• Cerebral or visual disturbances
• Pulmonary edema or cyanosis
• Epigastric or right upper quadrant pain
• Impaired liver function (elevated liver enzymes)
• Thrombocytopenia
• Fetal growth restriction
16. HELLP syndrome
• This syndrome occurs in preeclamptic
women with evidence of hemolysis,
elevated liver enzymes, and low platelets
(thrombocytopenia).
17. Complications of
preeclampsia
***Maternal complications:
• Multiorgan system dysfunction including
renal failure, hepatic Failure
• central nervous system (CNS)
hemorrhage ,stroke.
• pulmonary edema
• placental abruption
• disseminated intravascular coagulation
(DIC).
*** Fetal and neonatal complications:
• growth restriction.
• prematurity, and perinatal death.
19. ***By Hx.:
• should focus on whether there is any
past history of elevated blood
pressures or renal disease, either
before pregnancy or during previous
pregnancies.
• The patient should be carefully
questioned regarding symptoms of
severe preeclampsia or its
complications, including headache,
visual changes, nausea, vomiting,
abdominal or epigastric pain, and
20. *** by PE:
• Assessment of blood pressure, weight gain,
edema, fundal height, and reflexes.
• a qualitative assessment of urinary protein
excretion with a dipstick.
• In addition, findings consistent with severe
preeclampsia such as
• epigastric or right upper quadrant
tenderness, uterine
tenderness, petechiae due to low platelets, and
signs of
pulmonary edema should be sought.
• If there is severe headache or visual
symptoms, an ophthalmic examination may
be indicated.
21. *** Initial Laboratory Evaluation :
Complete blood count, platelet count, lactate
dehydrogenase: If abnormal, order d-dimers,
Coagulation panel, and smear
• Renal studies: Serum blood urea nitrogen,
creatinine, and uric acid; urinalysis; 24-hr
urine for protein and creatinine
• Liver function tests: serum aspartate
aminotransferase,alanine aminotransferase,
and bilirubin.
*** A careful fetal evaluation is also
22. • Delivery is the only
definitive cure for
preeclampsia.
23. • hospitalize patients with a presumed
diagnosis of preeclampsia to determine
the disease’s severity and maternal and
fetal stability.
• if mild and if there is no evidence of fetal
compromise,management consists of rest
and observation ,watching for possible
progression to severe preeclampsia. No
antiHTN or MgSO4 are used.
• Delivery if <36 wk with IV oxytocin to
induce labour C/S only for obstetrical
indication.
• MgSO4 for seizure prophylaxis (4 g load
and 2 g/hr maintenance) during labor and
delivery and continued for 12-24 hrs
24. ***If Severe :
• Aggressive prompt delivery is
indicated for any GA with evidence of
maternal or fetal risk:
- Give IV MgSO4 , loading dose 5-gm ,
then maintenance infusion of 2 g/h
- IV hydralazine and/or lebetelol
- vaginal delivery with IV oxytocin if
mother & fetus are stable
25. • The goal of antihypertensive therapy in
severe preeclampsia is to lower blood
pressure carefully to prevent CNS
hemorrhage.
• In general the blood pressure should not be
lowered to “normal levels” or less than
130/80 mm Hg. Caution must always be
exercised to not lower the arterial pressure
too much or too rapidly because either may
result in decreased uteroplacental blood flow
and fetal distress, which may necessitate
26. • Oral nifedipine has been used
successfully, but should be used
cautiously to avoid hypotension,
particularly when used in conjunction
with magnesium sulfate.
27. Eclampsia
• Is the presence of tonic-clonic seizures in a
woman with preeclampsia that cannot be
attributed to other causes.
• Eclamptic seizures can also occur before the
development of classic signs of preeclampsia.
• use of magnesium sulfate intrapartum and
postpartum for seizure prophylaxis in women
with preeclampsia.
• In a recent review of this subject, 38% to 53% of
eclamptic seizures occurred before labor, 18% to
36% occurred during labor, and 11% to 44%
occurred after delivery (usually within the first
28. ***Management of eclamsia:
• Protect mother airway & tongue
• Give IV MgSO4 5g to stop seizure, then
maintenance 2 g/h
• Aggressive prompt delivery at any GA after
stabalize the mother & the fetus