This document summarizes the classification, risk factors, pathophysiology, evaluation, and management of hypertensive disorders during pregnancy including gestational hypertension, preeclampsia, eclampsia, and HELLP syndrome. Delivery is the only cure for preeclampsia. Magnesium sulfate is the first-line treatment for eclampsia prevention and control of severe hypertension involves antihypertensive drugs.
Pregnancy-induced hypertension (PIH), also called toxemia or preeclampsia: This condition can cause serious problems for both the mother and the baby if left untreated. PIH develops after the 20th weeks of pregnancy. Along with high blood pressure, it causes protein in the urine, blood changes and other problems.
Pregnancy-induced hypertension (PIH), also called toxemia or preeclampsia: This condition can cause serious problems for both the mother and the baby if left untreated. PIH develops after the 20th weeks of pregnancy. Along with high blood pressure, it causes protein in the urine, blood changes and other problems.
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
A comprehensive overview of hypertensive disorders in pregnancy with its complications and management. Mainly focused on gestational hypertension, preeclampsia and eclampsia.
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
A comprehensive overview of hypertensive disorders in pregnancy with its complications and management. Mainly focused on gestational hypertension, preeclampsia and eclampsia.
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
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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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3. Gestationa Pre- Eclampsia
l HTN Eclampsia
Superimposed
Preeclampsia
SBP≥140
Proteinuria Generalized
or
seizures
DBP ≥ 90
Severe
Preeclampsia
≥ 0.3 g/ 24hr
> GA 20th wk before , during
>30 mg/dL
< PP 12th wk or after labor
(1+ on dipstick)
HELLP
syndrome
4. Preeclampsia
2~7% of healthy nulliparous; 0.8~5% of
multiparous women
The third leading cause of maternal mortality
(17%)
A major cause of neonatal morbidity and
mortality (intrauterine growth restriction,
abruptio placentae and the need for preterm
delivery) Preeclampsia
Deadly
Triad
Hemorrhage Infection
5. Severe preeclampsia
BP 160/110 mm Hg
Proteinuria 2.0 g/24 hours or 2+ dipstick
Increase severity /certainty
Serum creatinine >1.2 mg/dL unless known to be previously elevated
Platelets < 100,000/L
Microangiopathic hemolysis—increased LDH
Elevated serum transaminase levels—ALT or AST
Persistent headache or other cerebral or visual disturbance
Persistent epigastric pain
6. Superimposed
Chronic
Preeclampsia
HTN
SBP≥140
or Proteinuria
DBP ≥ 90
< GA 20th wk > 20th GA wk
> PP 12th wk
HTN + PTuria b4 20wk
↑proteinuria or
↑BP or
PLT < 100,000/L
7. Risk factors
Nulliparity
Age >35 years (superimposed) or teenager
Obesity
Multifetal gestation
Medical illness: Chronic hypertension, lupus
erythematosus, IDDM, APS, PT C/S deficiency, renal
disease
Genetic: Hx / FH of previous preeclampsia or eclampsia
Hydatidiform moles
Smoking, placenta previa
11. Evaluation of a new-onset HTN
Clinical findings:
headache, visual disturbance, epigastric pain, rapid
weight gain…
Measure BW QD
Analysis for proteinuria on admission and QOD
BP measurement Q4H
CRE, AST/ALT, CBC (for PLT). UA? LDH?
Coagulation profile?
Sonography: fetal size, amnionic fluid
William’s Obstertrics, 23ed
12. Management of HTN disorder
Dietary
Lifestyle
Place of care
Antihypertensive therapy
Corticosteroids
Mode of delivery
13. Management of HTN disorder
Dietary
Salt restriction is not recommended
Insufficient evidence to make recommendation
Lifestyle
Avoid vigorous exercise
Bed rest?
Place of care
Severe hypertension or preeclampsia
(BP>160/110)should be hospitalized
Laura Magee et al, 2008, JOGC
14. Management of HTN disorder
Antihypertensive therapy
For severe hypertension (BP>160/110)
BP goal: <160/110
Initial antihypertensive: labetalol, nifedipine
hydralazine.
MgSO 4 is not recommended as antihypertensive
(only transient decrease in 30 mins)
Continuous FHR monitoring is advised until BP is
stable.
Laura Magee et al, 2008, JOGC
15. Management of HTN disorder
Antihypertensive therapy
Non-severe hypertension (BP:140-159/90-109
mmHg)
BP goal: w/o cormorbid - 130-155/80-105
w/ cormorbid – 130-139/80-89
Drug of choice: methyldopa, labetalol, other beta-
blockers, CCB (nifedipine). (I-A)
ACEi and ARBs should not beused. (II-2E)
Atenolol and prazosin are not recommended.
Laura Magee et al, 2008, JOGC
16. Management of HTN disorder
Mode of delivery
Induction of labour
Vaginal delivery, unless C/S is indicated
Oxytocin at 3rd stage of labor, esp.
thrombocytopenia or coagulopathy
Ergometrine should not be given
Laura Magee et al, 2008, JOGC
17. Management of HTN disorder
Corticosteroids
To accelerate fetal pulmonary maturity
Pre-eclampsia & GA < 34 wks
Gestational HTN & GA < 34 wks, about to deliver
within next 7 days
Laura Magee et al, 2008, JOGC
18. Management of Pre-eclampsia
Delivery is the only cure
Timing of delivery
MgSO4
Plasma volume expansion
Laura Magee et al, 2008, JOGC
19. Management of Pre-eclampsia
Timing of delivery
GA < 34 wks: expectant management
GA: 34-36 wks, non-severe pre-eclampsia:
debated
GA > 37 wks: immediate delivery
Laura Magee et al, 2008, JOGC
21. Management of Pre-eclampsia
MgSO4
First-line Tx for eclampsia
Prophylaxis against eclampsia in severe-
preeclampsia
Phenytoin and BZD should not be used for
eclampsia prophylaxis, unless MgSO4 is
contraindicated or ineffective
Plasma volume expansion
Not recommended
Laura Magee et al, 2008, JOGC
22. Management for HELLP
syndrome
PLT count > 50x109 /L
Prophylactic transfusion of platelets is not
recommended
Consider ordering blood when PLT drop rapidly
PLT count < 20 x 109 /L.
Platelet transfusion prior to vaginal delivery or C/S)
Corticosteriods may be considered for PLT count
< 50x109 /L
Plasma exchange or plasmapheresis?
Laura Magee et al, 2008, JOGC
23. Postpartum treatment
BP follow-up
Peak postpartum, D3, D6
Antihypertensive therapy may be restart, BP
goal <160/110 mmHg
Acceptable in breastfeeding: Nifedipine, labetalol,
methyldopa, captopril, enalapril
NSAID should be avoid if hypertension is
difficult to control, or oliguria, CRE ↑, PLT↓
Thromboporphylaxis may be considered
Laura Magee et al, 2008, JOGC
Editor's Notes
most common within 24 hrs
Impaired remodelling of spiral a. Imcomplete trophoblast invasion The deeper myometrial arterioles do not lose their endothelial lining and musculoelastic tissue, and their mean external diameter is only half that of vessels in normal placentas release of placental debris that incites a systemic inflammatory response