It is a composite graphical recording of cervical dilatation and descent of head against duration of labour in hours.
It also gives information about fetal and maternal condition that are all recorded on single sheet of paper.
This ppt is made by Mr. arkab khan pathan under guidance of Mrs. RAKHI GOAR. this ppt contain the detail and all the lecture notes of HEG.
THANK YOU.
Arkab khan
It is a composite graphical recording of cervical dilatation and descent of head against duration of labour in hours.
It also gives information about fetal and maternal condition that are all recorded on single sheet of paper.
This ppt is made by Mr. arkab khan pathan under guidance of Mrs. RAKHI GOAR. this ppt contain the detail and all the lecture notes of HEG.
THANK YOU.
Arkab khan
Cephalopelvic disproportion (CPD) is a pregnancy complication that may interferes with vaginal delivery; making it dangerous or impossible and requires caeserean section.
Puerperium is the period following childbirth during which the body tissues, specially the pelvic organs revert back approximately to the pre-pregnant state both anatomically and physiologically. puerperium begins as soon as the placenta is expelled and lasts for approximately 6 weeks when the uterus becomes regressed almost to the non-pregnant size.
Cord prolapse is a frightening and life-threatening event that occurs in labor. Rapid identification and immediate appropriate response may well save the life of a neonate. Therefore, clinicians should be knowledgeable in its recognition and management.
It explains the mechanism of normal labour to medical and para-medical staff.It also puts light on principle movements underlying mechanism of normal labour with pictures.Thank You Like an share it to the maximum.
Detailed description of drugs in obstetrics for the midwifery students and beginners. Easy reference in one powerpoint presentation. Key details of drugs are mentioned . All drugs discussed as per INC Nursing syllabus for BSc & MSc Students.
Cephalopelvic disproportion (CPD) is a pregnancy complication that may interferes with vaginal delivery; making it dangerous or impossible and requires caeserean section.
Puerperium is the period following childbirth during which the body tissues, specially the pelvic organs revert back approximately to the pre-pregnant state both anatomically and physiologically. puerperium begins as soon as the placenta is expelled and lasts for approximately 6 weeks when the uterus becomes regressed almost to the non-pregnant size.
Cord prolapse is a frightening and life-threatening event that occurs in labor. Rapid identification and immediate appropriate response may well save the life of a neonate. Therefore, clinicians should be knowledgeable in its recognition and management.
It explains the mechanism of normal labour to medical and para-medical staff.It also puts light on principle movements underlying mechanism of normal labour with pictures.Thank You Like an share it to the maximum.
Detailed description of drugs in obstetrics for the midwifery students and beginners. Easy reference in one powerpoint presentation. Key details of drugs are mentioned . All drugs discussed as per INC Nursing syllabus for BSc & MSc Students.
A brief introduction regarding oxytocics & tocolytics which are the indispensable drugs in obstetrics. It consists of illustrative images, classification of drugs with their dosage, uses & side-effects along with contraindications
complcations of third stage of labour, includes PPH, Inversion of uterus, retained placenta, placenta accreta, increta, percreta, amniotic fluid embolism
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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.
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.
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.
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.
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
- 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
3. OXYTOCIN
It is synthesised in the supra-optic and para
ventricular nuclei of the hypothalamus.
a half life of 3-4 minutes and duration of
action of approximately 20 minutes
Mode of action
receptor and voltage mediated calcium
channels
amniotic and prostaglandin decidual
production
5. INDICATIONS
THERAPEUTIC:
Pregnancy:
Early:
• to accelerate abortion.
• To stop bleeding following evacuation of the
uterus.
• Used as an adjunct of abortion along with
other abortifacient agents.
Late:
• To induce labour.
• To facilitate cervical ripening for effective
induction.
• Augmentation of labour.
• Uterine intertia.
6. INDICATIONS
Labour:
In active management of third stage of labour.
Following expulsion of placenta.
Pueperium:
To minimize the blood loss and to control the PPH.
DIAGNOSTIC:
Contraction stress test
Principles:
The test is based on the determination of
respitratory function of the feto placental unit
during induced contractions
7. CST
Candidates for CST:
Intra uterine growth restriction.
Postmaturity.
Hypretensive disorders of pregnancy.
Diabetes
Contraindications:
Compromised fetus.
Previous history of caesarean section.
Complications likely to produce preterm labour.
APH.
8. INTERPRETATION :CST
Positive: persistent late deceleration of FHR following
50 % or more uterine contrations.
Negative: no late deceleration or significant variable
deceleration.
Suspicious: inconsistent but definite decelerations do
not persist with more uterine contractions.
Unsatisfactory: poor quality of recording or adequate
uterine contraction is not achieved.
Hyperstimultaion:
Deceleration of FHR with uterine contraction lasting >
90 seconds or occurring more frequently than every 2
minutes.
9. OXYTOCIN STIMULATION TEST
Procedure
Inference
Contraindications of oxytocin:
Pregnancy:
Grand multipara.
Contracted pelvis.
History of caesarean or hysterotomy.
Malpresentation.
Labour:
All the contraindications in pregnancy.
Obstructed labour.
Inco-ordinate uterine action.
Fetal distress.
Any time:
Hypovolemic state.
Cardiac disease.
10. OXYTOCIN STIMULATION TEST
Methods of administration:
Controlled intravenous infusion
For induction in labour
Use in labour
Intramuscular
5-10 units after the birth of the baby
as an alternative to ergometrine
11. ADVERSE EFFECTS
MATERNAL
Uterine hyperstimulation
Uterine rupture
Water intoxication
Hypotension
Anti-diuresis
FETAL
Fetal distress, fetal hypoxia and fetal death
12. NURSE’S RESPONSIBILITIES
Assess
Intake output ratio.
Uterine contractions and FHR.
Blood pressure, pulse and respiration.
Administer
By IV infusion. Monitor drop rate.
Make crash cart available.
Evaluate
Length and duration of contractions.
Notify physician of contractions lasting over 1 minute or
absence of contrcations.
Teach
To report increased blood loss, abdominal cramps or
increased temperature.
13. ERGOT DERIVATIVES
Mode of action:
Ergometrine acts directly on the myometrium
Effectiveness
It is highly effective in hemostasis
Indications:
Therapeutic:
To stop the atonic uterine bleeding following delivery,
abortion or expulsion of hydatidiform mole.
Prophylactic:
Against excessive haemorrhage following delivery.
16. Onset of action
Routes Ergometrine Methergin
IV
IM
Oral
45-60sec
6-7mt
10 mt
5.min
7 min
10 min
17. ERGOT DERIVATIVES
Hazards:
Common side effects are nausea and vomiting.
Precipitate rise of blood pressure, myocardial
infarction, stroke and bronchospasm because of
vasoconstrictive effect.
Prolonged use may result in gangrene formation of
the toes.
Prolonged use in puerperium may interfere with
lactation.
18. ERGOT DERIVATIVES
Cautions:
Ergometrine should not be used during
pregnancy, first stage of labour, second
stage of labour, second stage prior to
crowning of the head and in breech delivery
prior to crowning
19. ERGOT DERIVATIVES
Nurse’s responsibilities:
Assess
Blood pressure, pulse and respiration.
Watch for signs of haemorrhage.
Administer
Orally or IM in deep muscle mass.
Have emergency cart readily available.
Evaluate
Therapeutic effect: decreased blood loss.
Teach
To report increased blood loss, abdominal cramps,
headache, sweating, nausea, vomiting or dyspnoea.
21. PROSTAGLANDINS
Use in obstetrics
Induction of abortion.
Termination of molar pregnancy.
Induction of labour.
Cervical ripening prior to the induction of abortion or
labour.
Acceleration of labour.
Management of atonic PPH.
Medical management of tubal ectopic pregnancy.
23. PROSTAGLANDINS
Advantages:
It has got a powerful oxytocic effect,
irrespective of period of pregnancy. As such
it can be used independently specially in the
induction of abortion with success.
In later months it can be used for
acceleration of labour.
It has got no anti diuretic effect.
24. PROSTAGLANDINS
Drawbacks:
It is costly.
Unpleasant side effects on systemic use are
nausea, vomiting, diarrhoea, pyrexia or
bronchospasm.
When used as abortifacient, extensive lacerations
may occur.
Tachysystole.
25. ANTI-HYPERTENSIVE THERAPY
1. Symp
athom
imetic
s
1. adrenergic
Receptor
blocking
agent
1. vasodilat
ors
1. calcium
channe
l
blocke
rs
1. ACEI
Inhibit
ors
Methyldo
pa
Reserpin
e
Labetalol
Propanalol
Hydralazine
Prazocin
Sodium
nitroprusside
Nifedipine
nicardia
Captopril
lisinopril
26. METHYLDOPA
Mechanism of action
-Drugs of first choice
-Central and peripheral anti-adrenergic action
-Effective and safe for both mother and fetus.
Contraindications
-hepatic disorders
-psychic patients
-CCF
Dose
-orally 250mg bid may be increased to 1 gm tid
depending upon the response.
-IV infusion 250-500mg
28. LABETALOL
Mechanism of action
Combined alpha and beta adrenergic blocking agents.
Contraindication
hepatic disorders.
Dose
orally: 100mg tid. May be increased upto 800 mg daily.
-IV infusion [hypertensive crisis] 1-2 mg/mt until desired
effect
Side effects
Experience is less compared to methyl dopa. efficacy
and safety with short term use. Appear equal to methyl
dopa.
29. PROPRANOLOL
Mechanism of action
Beta adrenergic receptor blocker
Contraindication
bronchial asthma.
renal insufficiency.
diabetes.
Cardiac failure
The drug is better avoided for long term therapy
during pregnancy.
Dose
orally: 80-120 mg in divided doses
30. PROPRANOLOL
Side effects
maternal:
severe hypotension
sodium retension
Bradycardia
Bronchospasm
CCF
hypoglycaemia.
fetal:
bradycardia and impaired fetal responses to hypoxia,
IUGR when began in I and II trimester.
-neonatal: hypoglycaemia
31. PRAZOCIN
Mechanism of action
-selective post synaptic blocker. Decrease plasma
renin activity.
-reduces cardiac preload and after load.
Contraindication
Low first dose, to avid hypotension and syncope.
Dose
Orally 1 mg bd may be increased upto 20 mg/day
Side effects
-hypotension
-nasal congestion
-fluid retension
32. HYDRALAZINE
Mechanism of action
Arteriolar vasodilator.
Contraindication
Because of the variable sodium retention, diuretics should
be used.
Dose
orally: 100mg/day in 4 divided doses.
-IV : 5mg bolus followed by 25g in 200 ml NS at a rate of
2.5 mg/hr to be doubled every 30 mts.
Side effects
-maternal: hypotension,tachycardia, arrhythmia,
palpitation, lupus like syndrome.
-fetal: reasonably safe.
-neonatal: thrombocytopenia
33. NIFEDIPINE
Mode of action:
Direct arteriolar vasodilation.
Dose:
Orally 5-10 mg TID.
Contraindications:
Simultaneous use of magnesium sulphate could
be hazardous due to synergic effect.
Side effects:
Flushing
Hypotension
Head ache
Tachycardia
Inhibition of labour.
34. SODIUM NITROPRUSSIDE
Mechanism of action:
Direct vasodilator.
Dose:
Orally 6.25 bid.
Side effects:
Maternal
Nausea
Vomiting
Fetal
Oligohydramnios
IUGR
Fetal and neonatal renal failure.
35. NITROGLYCERINE
Mechanism of action
Release mainly venous but also arteriolar smooth
muscles.
Dose:
Given as IV infusion 5µg/min. to be increased at
every 3-5 min. upto 100µg/min.
Side effects:
Tachycardia
Headache
Methaemoglobinaemia
36. DIURETICS
Diuretics are used in the following
conditions during pregnancy.
Pregnancy induced hypertension with
massive edema.
Eclampsia with pulmonary edema.
Severe anemia in pregnancy with heart
failure.
Prior to blood transfusions in severe
anemia.
As as adjunct to certain antihypertensive
drugs, such as hydralazine or dioxide
37. FUROSEMIDE
Mechanism of action
Acts o loop of the Henle by increasing excretion of
sodium and chloride.
Dose
40 mg tab, daily following breakfast for 5 days a
week. In acute conditions, parentrally 40-120 mg
daily.
Contraindications:
Hypersensitivity
39. HYDROCLOROTHIAZIDE
Mechanism of action:
Acts on distal tubule by increasing excretion of
water, sodium, chloride and potassium. It is used in
edema and hypertension.
Dose:
PO 25-100 mg/day.
Side effects:
Polyuria, glycosuria, frequency.
Nausea, vomiting, anorexia.
Rash, urticarial, fever.
Increased creatinine, decreased electrolytes.
41. BETAMIMETICS
Commonly used drugs:
Terbutaline
Ritodrine
Isoxurpine
Mechanism of action:
Activation of the intracellular enzymes [adenylate
cyclase, cAMP, protein kinase] reduces intracellular
free calcium [Ca++] and inhibits the activation of
MLCK
42. BETAMIMETICS
Dose:
Ritodrine is given by IV infusion, 50µg/min. and
increased by 50µg every 10 min. until contractions
cease. Maximum dose of 350µg/ min. may be given.
Infusion is continued for about 12 hours after
contraction cease.
Terbutaline has longer half life and has fewer side
effects. Subcutaneous injection of 0.25 mg every 3-4
hours is given.
Isoxurpine is given as IV drip 100 mg in 5D. Rate 0.2
µg/minute. To continue for at least 2 hours after
contraction ceases. Maintenance is by IM 10mg six
hourly for 24 hours, tab 10 mg 6-8 hourly.
44. BETAMIMETICS
Side effects
Hyperglycemia
ARDS
Hyperinsulinemia
Lactic academia
Hypokalemia
Even death
Neonatal:
Hypoglycaemia
Intraventricular haemorrhage
45. INDOMETHACIN
Mechanism of action:
Reduces synthesis of PGs thereby reduces intracellular
free Ca++, activation of MLCK and uterine contractions.
Dose:
Loading dose , 50 mg P.O. or .P.R. followed by 25mg
every 6 hrs for 48 hours.
Side effects:
Maternal
Heart burn
G.I. bleeding
Asthma
Thrombocytopenia
Renal injury.
46. CALCIUM CHANNEL BLOCKERS
Nifedipine
Nicardipine
Mechanism of action:
Nifedipine blocks the entry of calcium inside the cell.
Compared to β- mimetics, effects are less. It is
equally effective to MgSO4.
Dose:
Oral 10-20 mg every 6-8 hours.
48. MAGNESIUM SULPHATE
Mechanism of action:
inhibition to calcium ion
Contraindications:
Myasthenia gravis
Impaired renal function
Dose:
Loading dose: 4-6 gm I.V. over 20-30 min. followed
by an infusion of 1-2 gm/hr to continue tocolysis for
12 hours after contarctions have stopped.
50. OXYTOCIN ANTAGONISTS:
Atosiban
Mechanism of action:
It blocks myometrial oxytocin receptors.
Dose:
I.V.infusion 300µg/min. initial bolus may be needed.
Side effects:
Nausea
Vomiting
Chest pain
51. ANTICONVULSANTS
1. MAGNESIUM SULPHATE:
Mode of action:
It decreases the acetylcholine release from the
nerve endings.
Dose:
IM – loading dose: 4 gm IV [20% solution] over 3-5
min. to follow 10 gm deep IM, 5gm in each
buttocks. Maintenance dose : 5gm deep IM on
alternate buttocks every 4 hrs.
IV- loading dose: 4-6 gm IV over 15-20 min.
maintenance dose: 1-2 gm/hr. IV infusion.
52. MAGNESIUM SULPHATE
Side effects:
MgSO4 is relatively safe and is the drug of choice.
Muscular paresis[ diminished knee jerks],
respiratory failure. Renal function to be monitored.
Antidote:
Injection of calcium gluconate 10% 10 ml IV.
53. DIAZEPAM
mode of action:
central muscle relaxant and anticonvulsant.
Dose:
20-40 mg IV
Side effects:
Maternal:
Hypotension
Fetal
Respiratory depression
Hypotonia
Thermoregulatory problem
54. PHENYTOIN
Mode of action:
Centrally acting anticonvulsant
Dose:
10 mg/ kg IV at the rate not more than 50 mg/ min
followed 2 hrs later by 5 mg/kg. In epilepsy 300-
400 mg daily orally in divided doses.
Side effects:
Maternal
Hypotension
Cardiac arrhythmias
Phlebitis at injection site.
Fetal
Fetal hydantoin syndrome
55. ANTICOAGULANTS:HEPARIN
Mechanism of action:
It inhibits action of thrombin
Dose:
5000-10000 I.U. to be administered parenterally [SC or IV].
Low molecular weight heparin is 2500 IU
Side effects:
Maternal:
Haemorrhage
Urticarial
Thrombocytopenia
Osteopenia.
Fetal
It does not cross the placenta
56. WARFARIN
Mechanism of action:
Interferes with synthesis of vit K dependent factors.
Dose:
10 mg orally
Side effects:
Maternal
Haemorrhage
Fetal
Contradi’s syndrome [skeletal and facial anomalies]
Optic atropy
Microcephaly
Chondrodisplasia punctate.
57. ANALGESIA AND ANAESTHESIA IN
OBSTETRICS
1. SEDATIVES AND ANALGESICS
OPIOID ANALGESICS:
PETHIDINE
Mechanism of action:
Inhibits ascending pain pathways in CNS , increase
pain threshold and alters pain perception.
Indications:
Moderate to severe pain in labour, postoperative pain,
abruption placentae, pulmonary edema.
Dose:
Injectable preparations contains 50mg/ml can be
administered SC, IM,IV. Its dose is 50-100 mg IM
combined with promethazine.
58. PETHIDINE
Contraindications:
Should not be used IV within 2 hrs and IM
within 3 hrs of expected time of delivery of the
baby, for fear of birth asphyxia. It should not
be used in cases of preterm labour and when
respiratory reserve of the mother is reduced
60. FENTANYL
Mechanism of action:
Inhbits ascending pathways in CNS, increases pain
threshold and alters pain perception.
Indications:
Moderate to severe pain in labour, post operative
apin an dadjunct to general anaesthetic.
Dose:
0.05 to 0.1 mg IM q1-2 hrs prn. Available in
injectable form, 0.05 mg/ml.
62. PENTACOZIN
dose of 30-40 mg
Naloxone is an efficient and reliable antagonist.
Adverse effects
Neonate respiratory depression secondary tothe
medication crossing the placenta and affecting
the fetus.
Unsteady ambulation of the client.
Inhibition of the mother’s ability to cope with the
pain of labor.
63. TRANQUILIZERS
DIAZEPAM:Usual dose is 5-10 mg.
MIDAZOLAM:Dose of 0.05 mg/kg is given
intravenously
COMBINATION OF NARCOTICS AND
TRANQUILIZERS
BUTORPHANOL and NALBUPHINE
64. INHALATIONAL METHODS
Nitrous oxide and air
Premixed nitrous oxide and oxygen
Trichloroethylene
Methoxyflurane, isoflurane, enflurane
65. EPIDURAL AND SPINAL REGIONAL
ANALGESIA
Adverse effects
nausea and vomiting.
Inhibition of bowel and bladder elimination
sensations.
Bradycardia or tachycardia.
Hypotension.
Respiratory depression.
Allergic reaction and pruritus.
66. PUDENDAL BLOCK
It consists of a local anesthetic such as
lidocaine(Xylocaine) or bupivacaine (Marcaine)
being administered transvaginally into the space in
front of the pudendal nerve.
67. EPIDURAL ANAESTHESIA
Epidural block consists of a local anesthetic
bupivacaine (Marcaine) along with an
analgesic morphine (Duramorph) or fentanyl
(Sublimaze) injected into the epidural space at the
level of the fourth of fifth vertebrae.
Adverse effects
Maternal hypotension.
Fetal bradycardia.
Inability to feel the urge to void.
Loss of the bearing down reflex.
68. SPINAL BLOCK
Spinal block consists of a local anaesthetic injected
into the subarachnoid space into the spinal fluid at
the third, fourth, or fifth lumbar interspace, alone or
in combination with an analgesic such as fentanyl .
Adverse effects
Maternal hypotension.
Fetal bradycardia.
Loss of the bearing down reflex.
69. PARACERVICAL BLOCK
It consists of lidocaine (Xylocaine) being injected
into the cervical mucosa early in labor during the
first stage to block the pain of uterine contractions.
Adverse effects include fetal bradycardia. Improper
technique can result in serious toxicity.
70. GENERAL ANAESTHESIA
100% oxygen is administered by tight mask fit for
more than 3 minutes. Induction of anaesthesia is
done with the injection of thiopentone sodium 200-
250 mg as a 2.5 % solution IV.,followed by
refrigerated suxamethonium 100 mg. the patient is
intubated with cuffed ET tube. Anaesthesia is
maintained with 50% NO2 , 50% oxygen and a trace
of halothane. Relaxation is maintained with non-
depolarizing muscle relaxant [ vecuronium 4 mg or
atracurium 25 mg].
71. FETAL HAZARDS ON MATERNAL
MEDICATION DURING PREGNANCY
Mechanism of teratogenicity
Folic acid deficiency.
Epoxides or arena oxides
Environmental and genes
abnormalities.
Maternal disease and drugs
Homebox genes
72. Maternal-fetal drug transfer and the hazards:
before D 31:
Teratogen produces an all or none effect.
D31-d71:
It is the critical period for organ formation.
After D 71:
The development of other organs continues.
73. PLACENTAL TRANSFER OF DRUGS
The factors responsible for transfer are:
Molecular weight [molecular wght more than 1000
Da do not cross the placenta].
Concentration of free drug.
Lipid solubility.
Utero-placental blood flow.
Placental solubility.
74. GUIDELINES
If the benefit outweighs the potential risks, only then
can the particular drugs be used with prior
counselling.
Only, well tested and reputed drugs are to be
prescribed and that too using the minimum
therapeutic dosage for the shortest possible
duration.
75. CATEGORY DESCRIPTION EXAMPLE
A Adequate studies in pregnant woman have failed to show a risk to the fetus in
the first trimester of pregnancy; there is no evidence of risk in last trimester.
Thyroid hormone
B Animal studies have shown an adverse effect on the fetus. But, there are no
adequate studies on humans. Pregnancy risk is unknown.
Insulin
C Animal studies have shown an adverse effect on the fetus, but there are no
adequate studies on humans, or there are no adequate studies in animals or
humans. Pregnancy risk is unknown.
Docusate-sodium
D There is evidence of risk to the human fetus, but potential benefits of use in
pregnant woman may be acceptable despite potential risks.
Lithium acetate
X Studies in animals or humans show fetal abnormalities, or adverse reaction
reports indicate evidence of fetal risk. The risks involved clearly outweigh
potential benefits
isotretinoin
76. drug Teratogenic effect
Cytotoxic drugs
-Diethyl stilbestrol
-androgenic steroids
-lithium
-anticonvulsants
Phenytoin
Valproate
-aspirin
-paracetamol
multiple fetal malformations and abortion.
vaginal adenosis, cervical hoods, uterine hypoplasia of
the female offspring.
masculinization of the female offspring.
cardiovascular anomalies, neonatal goitre, hypotonia and
cyanosis.
benefits of treatment outweigh the risks to the fetus.
Polytherapy should be avoided.
Increase risk of neural tube defects, neonatal bleeding.
high doses in the last few weeks cause premature
closure of ductus arteriosus. Persistent pulmonary
hypertension and kernicterus in newborn.
amount too small to be harmful.
77. drug Tertogenic effect
antimalarials
-corticosteroids
-aminoglycosides
-chloramphenicol
-tetracycline
-quinolones
-long acting
sulphonamides
-nitrofurantoin
chloroquine, quinine- no evidence of fetal toxicity in therapeutic
doses; benefits outweighs the risk.
high doses[ >10 mg prednisolone daily] may produce fetal and
neonatal adrenal suppression.
Auditory or vestibular damage.
Gray baby syndrome [peripheral vascular collapse].
Dental discolouration [yellowish] and deformity.
Inhibition of bony growth- should be avoided.
Arthropathy in animal studies
Neonatal hemolysis, jaundice and kernicterus.
Hemolysis in newborn with G6 PD deficiency, if used at term
78. drugs Teratogenic effect
-metronidazole
-ACE inhibitors
-vitamin K[large dose]
-all live viral vaccines
-narcotics
-anaesthetic agents
-anticogulants
[warfarin]
-antidepressants
[imipramine]
-benzodiazapines
o No evidence of fetal or neonatal toxicity,
high doses regimens should not be used.
o IUGR, fetal and neonatal renal failure.
o Hyperbilirubinemia and kernicterus.
o Potentially dangerous to the fetus.
o Depression of CNS-apnoea, bradycardia
and hypothermia.
o Convulsion, bradycardia, acidosis,
hypoxia, and hypertonia.
o Fetal bleeding and anomalies.
o cardiovascular abnormalities.
o Growth restriction, CNS dysfunction.
79. MATERNAL DRUG INTAKE AND
BREASTFEEDING
Transfer of drugs through breast milk depends on
following factors:
Chemical properties
Molecular weight
Degree of protein binding
Ionic dissociation
Lipid solubility
Tissue pH.
Drug concentration.
Exposure time.
80. DRUGS IDENTIFIED AS HAVING EFFECT ON
LACTATION AND THE NEONATE
Bromide: Rash. Drowsiness, and poor feeding.
Iodides: Neonatal hypothyroidism
Chloramohenicol: Bone marrow toxicity
Oral pill: Suppression of lactation.
Bromocriptine: Suppression of lactation.
Ergot: Suppression of lactation.
Metronidazole: Anorexia, blood dyscrasias, irritability, weakness,
neurotoxic disorders.
Anticoagulants: Haemorrhagic tendency.
Isoniazid: Anti-DNA activity and hepatotoxicity.
Anti-thyroid drugs and radioactive iodine: Hypothyroidism and
goitre, agranulocytosis.
Diazepam, opiates, phenobarbitone: Sedation effect with poor
sucking reflex.