This document provides an overview of hypertension in pregnancy. It begins with classifications of hypertensive disorders in pregnancy and risk factors. The pathophysiology involves placental insufficiency causing endothelial dysfunction and an imbalance of vasoactive substances. Clinical manifestations involve multiple organ systems due to failure of autoregulation from high blood pressure. Management involves monitoring, prevention of complications, and delivery when indicated to resolve the condition.
Seizures during pregnancy can cause: Slowing of the fetal heart rate. Decreased oxygen to the fetus. Fetal injury, premature separation of the placenta from the uterus (placental abruption) or miscarriage due to trauma, such as a fall, during a seizure
Seizures during pregnancy can cause: Slowing of the fetal heart rate. Decreased oxygen to the fetus. Fetal injury, premature separation of the placenta from the uterus (placental abruption) or miscarriage due to trauma, such as a fall, during a seizure
Musculoskeletal system – movements of the lower limb technologiesKareem Magar
A teaching resource I created for an assessment for university. It lists all the main movements of the lower limb (hip joint, leg/knee and leg/foot), the muscles associated with each movement and any other relevant information. At the end is a table summarizing all the information in depth, including origin and insertion. Included within the presentation are pictures of every movement and muscle involved, as well as links to useful resources such as a 3D anatomy model.
A comprehensive overview of hypertensive disorders in pregnancy with its complications and management. Mainly focused on gestational hypertension, preeclampsia and eclampsia.
duct dependent heart lesions by Dr Parashuram Waddar 2021 ppt, for Pediatrics parasuramwaddar1
Duct dependent heart lesions by Dr Parasuram Waddar 2021.
Ductal anatomy and duct dependent circulation. Critical congenital heart disease, etiology, presentation, diagnosis and managment.
scenario
Incidence rate of CHD is 8-9/1000 live births, nearly 1.8- 2lacs children are born with CHD each year in India.
78.9- 81.4% Institutional deliveries.
20% of births in India occur at home, and the infant is likely to die before the critical, ductus-dependent CHD is diagnosed.
Fortunately, the rate of hospital deliveries have increased due to several incentivized schemes by the Govt of India.
Ductus-dependent CHD may still escape detection as babies are often discharged earlier.
Predischarge screening of newborns by pulse oximetry, which may pick up these CHDs, is often not practiced, especially in rural & semi-urban centers.
Lack of follow up care.
Delay in referral results in poor outcomes as co-morbidities may have already set in.
The risks of developing hypothermia and hypoglycemia during long, unsupervised transport further adds to the already serious condition of the infants with CHD.
Of these, nearly 60,000 to 90,000 suffer from critical CHD requiring early intervention.
Approximately 10% of present infant mortality in India may be accounted for by CHD alone.
Lack of awareness & delay in diagnosis is biggest obstacle.
Frontline health workers & primary caregivers are not sensitized to the problem of CHD.
PDA- Short circuit channel between the pulmonary artery and the aorta in the fetus, which bypasses the lungs to distribute oxygen received through the placenta from the mother’s blood.
It normally closes once the baby is born and the lungs inflate, separating the pulmonary and systemic circulations, thus converting parallel circulation into series.
Functional closure of the ductus arteriosus
occurs within 10-15 hours after birth in
healthy infants born at term.
This occurs by abrupt contraction of the medial
smooth muscular wall of the ductus arteriosus.
Multiple factors are responsible for the
closure of ductus arteriosus. Ex- Po2, GA,
PGE2 , etc.
Increase in the partial pressure of oxygen (PO2) from 25mmHg(in utero) to 50mmHg after lung expansion is the strongest stimulus.
Decrease in PGE2.
Anatomic closure completes by end 2-3 weeks.
Starting of ductus closure is the cause for deterioration in these lesions.
Definition of DDHL- These are critical congenital heart disease (cCHD), in which the permeability of the ductus arteriosus is mandatory in order to maintain systemic and pulmonary perfusion after birth.
These are most important d/d for newborns who are going to collapse in and around day3.
Critical congenital heart disease (cCHD) is the most common reason for acute cardiac failure in the neonatal period
Incidence- 25% of all CHDs, nearly 25% mortality in first year life.
The distribution of cCHD differs from the distribution of CHDs in general.
Left sided heart obstructions have the largest share w
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
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.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- 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
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Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
4. Introduction
Hypertensive disease in pregnancy is a major
cause of maternal and fetal morbidity and
mortality in the developing countries as well
as in the developed countries. It is one of the
most common causes of perinatal morbidity
and mortality, resulting in an estimated 35-
300 deaths per 1000 births/year worldwide,
depending on neonatal support capabilities of
the hospital delivering care. This mortality
rate is almost double that of normotensive
pregnancies.
5. Hypertensive disorders account for about 50,000
maternal death worldwide/year (Duley et al 1992) and
majority of these death occurs in the developing
countries.
In Tanzania about 15% of pregnant mothers die every
year due to PIH, and in MNH about 22% of maternal
death are caused by the PIH.
6. Prevalence
In the US: Preeclampsia is a complication
in approximately 12-22% of all
pregnancies.
In the general population prevalence is
about 6%, but this varies with the
geographical location, eg along the EA
cost the prevalence of PIH is higher
compared to highlands in the same
location. Duringcold season there is
peaking of the prevalence of PIH both in
coast areas of Africa and in mountain
areas of Latin America.
7. Classification of HDP.
Pt are considered to have hypertension if they have
either of the following
Systolic BP>140mmhg and DBP>90mmhg.Rise in
SBP>30mmhg and /rise in the DBP>15mmhg from
preconception or 1st trimester reading confirmed by
reading 6hrs apart
8. Gestational hypertension
Transient PIH if preeclampsia is present at the time of
delivery and BP is normal 12/52 after delivery.
Chronic PIH if BP persist 12/52 after delivery.
9. Preeclampsia- this is a syndrome xterised by HTN,Protinuria,
oedema,epigastic pain,visual disturbance and headache.
Eclampsia –the same as in preeclampsia but with the presence of fits.
10. Chronic hypertension
Essential
Sec to renal disease ,endocrine disease,
vascular abnormalities.
Chronic HTN with superimposed preeclampsia
11. Etiology and predisposing
factors
Age:PIH/ Preeclampsia usually occurs in women at both
extremes of reproductive age; however, the risk of
preeclampsia is greatest in women younger than 18
years and older than 35years.
12. Maternal risk factors for
preeclampsia
First pregnancy
New partner/paternity
History of preeclampsia
Family history of preeclampsia in a first-degree relative
13. Black race, Black women have higher
rates of preeclampsia complicating their
pregnancies compared to other racial
groups, mainly because they have a
greater prevalence of underlying chronic
hypertension. Among women aged 30-39
years, chronic hypertension is present in
22.3% of black people, 4.6% of white
people, and 6.2% of Mexican Americans.
Hispanic women generally have blood
pressure levels that are the same as or
lower than those of non-Hispanic white
women.
14. Medical risk factors for
preeclampsia
Chronic hypertension
Secondary causes of chronic hypertension
such as hypercortisolism,
hyperaldosteronism, pheochromocytoma,
or renal artery stenosis
Preexisting diabetes (type 1 or type 2),
especially with microvascular disease
Renal disease
Systemic lupus erythematosus
Obesity
Thrombophilia
16. Pathophysiology of
preeclampsia.
Although the exact pathophysiologic
mechanism is not clearly understood,
preeclampsia can be thought of as a
disorder of:
Endothelial dysfunction with vasospasm.
Rejection phenomenon(insufficient
production of blocking abs)
Imbalance between prostacyclin and
thromboxane A
Membrane fluidity.
Others like genetic predisposition
17. Rejection
phenomenon(insufficient
production of blocking abs)
The presence of the placenta is thought to be the
primary in the causation of PIH.During placenta
development the trophoblastic tissues invade both
myometrium and decidual cells in 2 ways:
Interstitial invasion - anchoring the placenta
18. Endovascular invasion- invades the maternal spiral
arteries and replaces the endothelium by
destroying the medial elastic tissues and muscular
tissues of the arterial wall. The arterial wall is
replaced by the fibrinoid material and form a
saclike structure. Fraction of spiral uterine
arterioles fails to dilate in the same way as in
normal pregnancy, thus decreasing the blood
supply to fetus (Khong et al, 1986). Electron
microscopic studies have shown characteristic
damage to endothelial cells that is somewhat
similar to that of vessels in transplanted but
rejected kidney. This observation has led to
suggestion that immunological mechanisms i.e.,
rejection of the fetus by maternal immune
system, may be operative in preeclampsia
(Kitzmiller and Benirschke, 1973).
19. PIH develops followings partial process of
placentation, the invaded arteries in the
1st phase is complete where as the 2nd
phase is partial and the myometrial
portion of the spiral arteries retain their
reactive musculoelastic walls.There is
development of acute atherosis in the
spiral arteries and this lesion is xterised
by fibrinoid necrosis of the arterial wall
and obliteration with corresponding area
of placental infarction.
20. Endothelial dysfunction
with vasospasm
Endothelin 1,2&3 are strong
vasoconstrictors released by endothelium
of blood vessels,kidney and CNS tissues.Its
fns is to cause vasoconstriction in the
control of placental blood vessel after
delivery and closure of the ductus
arteriousus in the new born.
Disruption of endothelial integrity caused
by the hypoxic condition created by the
placental insufficient would also be
associated with a general loss of
vasodilator capacity, which could account
for the enhanced pressor response to
angiotensin II and noradrenaline.
21. Imbalance between
prostacyclin and
thromboxane A
Prostacyclin is synthesized by the cell of endothelium
with the aid of cyclooxygense enzyme . Prostacyclin,
one of the prostaglandins, is a very potent vasodilatator
produced by the endothelium. Vessels of preeclamptic
women and umbilical veins of their fetuses produce far
less prostacyclin as compared with normal pregnancy
(Dadak et al., 1982).
22. Nitric oxide is another vasodilator produced by
endothelium (EDRF, endothelium-releasing factor)
which acts synergistically with prostacyclin (Moncada et
al., 1991). Nitric oxide production is also decreased
because of endothelial cell injury. Therefore it seems
clear that endothelial injury and decreased production
of vasodilatators play a major role in pathogenesis of
PIH
23. TA is generated by the platelets with the aid of
cyclooxygenase enzyme and is a strong vasoconstrictor.
Therefore imbalance btn PI&TA due to damage of
endothelium will favor vasoconstriction and platelets
aggregation hence worsen PIH.
24. MEMBRANE FLUIDITY
Changes in the cell membrane that affect the
functioning of receptors may also be
important in pregnancy induced hypertension
and pre-eclampsia. In studies using platelets
as models of vascular smooth muscle, the
density of binding sites for angiotensin II was
lower in women during a normal pregnancy
than in those who were not pregnant but was
unchanged in women with established
disease. A prospective study showed that
although primigravidas who remained
normotensive showed a very rapid fall in
binding site density during the first few weeks
of pregnancy, nulliparous women who
developed pregnancy induced hypertension
never showed such a fall. Membrane fluidity
is altered in established pregnancy induced
hypertension and pre-eclampsia
25. Pathogenesis of the disease
PIH is a mult-organ disease; therefore the
clinical presentation will involve several
organs as follows:
CNS
Brain tissues have a wide range of
autoregulation of BP and have a constant
cerebral perfusion at 55ml/min in the same
wide range (60-140 MAP).
When the BP rise and the autoregulation fails
then the endothelial tight junction open and
cause leakage of plasma and RBC to the
extravascular space (petechial h’ge or
intracranial h’ge
26. Pathology
Fibrinoid necrosis
Thrombosis of arteriole
Microinfarct and petechial h’ge
The brain stem and basal ganglia are
more affected compared to the other
parts of the brain.
Other parts include in the watershed area
–occipital and parietal areas where
anterior, middle and posterior meningeal
arteries meet.
Brain edema is common in prolonged
coma.
27. R/S
Pulmonary oedema which may be
cardiogenic or non-cardiogenic
It is very common after delivery either
due to over infusion of fluid in the
treatment of ARF or blood loss, or due to
delayed mobilization of intravascular fluid
to the intravascular compartment.
It may occur in the pt with underlying
heart disease, systolic dysfunction or in
aspiration of gastric content following
eclamptic fits and this may lead to
chemical pneumonitis or airways
obstruction from particulate matters.
28. CVS
Contracted intravascular compartment due to
generalized vasoconstriction and extravasations of fluid
to the extravascular compartment due to reduced
oncotic pressure (low albumin).
29. LIVER
HELLP syndrome
Subscapular h’ge
Elevated total bilirubin>1.2mg/dl
Decreased protein synthesis
33. ENDOCRINE
Estrogen increases production of rennin substrate,
rennin activity as well as AII
Plasma Aldosterone is also increased .
34. Clinical presentation &
diagnosis
History: Mild preeclampsia does not involve clinical
evidence of end-organ pathology, except for minimal
proteinuria. Severe preeclampsia is characterized by
end-organ damage due to systemic vasoconstriction.
Features of the history may include the following:
35. Headache
RUQ abdominal pain
Decreased urine output
Shortness of breath or dyspnea on
exertion
Hand and facial edema
Visual disturbances
Confusion and apprehension
Nausea and vomiting.
36. Physical: Findings at physical
examination may include
thefollowing Sustained systolic BP increases by 30 mm Hg, and diastolic
BP increases by 15 mm Hg, or absolute BP higher than 140
mm Hg/90 mm Hg.
Severe preeclampsia (sustained systolic BP >160 mm Hg or
diastolic BP >110 mm Hg with end-organ damage)
Tachycardia
Tachypnea
Pulmonary edema
Alteration of mental status
Hyperreflexia, clonus
Localizing neurologic deficits
Cerebrovascular accident
Generalized edema
Small fundal height for estimated gestational age
Intrauterine growth retardation
37. Management
Investigation
Laboratory
FBP may reveal the following:
Anemia due to the microangiopathic hemolytic
anemia and dilution of pregnancy
Thrombocytopenia (platelet count <100,000) due
to HELLP syndrome
The serum creatinine is elevated due to
decreased intravascular volume and a
decreased glomerular filtration rate (GFR).
Liver function test (LFT) results may reveal
the following:
38. Aspartate aminotransferase (SGOT) level higher than
72IU/L, total bilirubin levels higher than 1.2 mg/dL,
lactate dehydrogenase (LDH) levels higher than 600
IU/L
Elevated levels due to HELLP syndrome
The coagulation profile may reveal a normal
prothrombin time (PT) and a normal activated
partial thromboplastin time (aPTT), fibrin split
products, and fibrinogen levels
Rule out associated disseminated intravascular
coagulopathy (DIC).
Urinalysis may reveal the following findings:
Proteinuria
Positive human chorionic gonadotropin (HCG) result
39. Imaging Studies:
CT scan of the head
Obtain a head CT scan in patients with severe
preeclampsia and associated neurologic
deficits.
This is used to assess intracranial hemorrhage
or cerebrovascular accident.
MRI
Transabdominal sonogram
This is used to estimate gestational age.
It also is used to rule out abruptio placentae,
which can complicate severe preeclampsia.
40. TREATMENT
This will involve pharmacological and non
pharmacological mgn.
In case the pt has mild pre-eclampsia
Admit for bed rest
Assess the GA
Do Lab and Radiological investigation.
Administer steroid in the premature baby
and plan for delivery if BP is not
responding
41. In case the pt has severe
pre-eclampsia./eclampsia
The aim should be at:
Prevention of convulsion
Control of BP
Induce labor and deliver
Prevent more organ damage
Monitor i/o of fluid .
42. Pharmacological mgn
Magnesium sulphate is the drug of choice. It is given in
several regimens depending on the availability of the
equipment for monitoring serum magnesium level.
Prevention of convulsion
In MNH we use I/V regime of 4g given as a bolus then
maintance dose of 1g/hr. (98%are below the therapeutic
level)
Other center use I/M regime of 14g as a bolus given as 4g
i/v then 10g i/m in @ buttock then maintenance of 4g
i/v./hr
Loading dose of 6gi/v then maintenance dose of 2g/hr(50%
are below the therapeutic level) and the maintanence
dose of 3g i/v /hr non will be below the therapeutic level).
The therapeutic level of mg sulphate is 2-3.5mmo/l (4.8-
8.4mg/dl).
43. Magnesium toxicity
Serum mgso4 symptoms
4mmol/l loss of DTR
5-6mmol/l respiratory
paralysis
15mmol/l cadiac arrest
Action of mgso4: it cause vasodilatation of
blood vessel, block ca entry into neuron
and decrease amount of acetylcholine
released at neuromuscular junction.
45. Control of BP
Sympatholytic agent- Methyldopa
Ca chanel blockers- Nifedipine
Vasodilators - Hydralazine
Loop diuretics indicated only when there is sign of
pulmonary oedema
46. Prevention of
preeclampsia/eclampsia
Health education to the pregnant mothers
and the society about the danger sign.
Frequent ANC visit will be insuffient to
reduce the incidence of eclampsia, rather
drs and nurses should have life saving
skill available when the unforeseeable
preeclampsia occurs
Early referral of the pt
Equipped with anticonvulsant drug .
Use of ASA prophylactically in high risk
patient .
47. Reference
Williams textbook of obstetrics 20th edition
Current OBS & GYN internation edition
Dewhurt’s OBS &GYN for postgraduates6th edition
Maternity care in developing countries by Lawson
ACOG practice bulletin no 33, 2002
Online