This document provides an overview of antenatal care principles and practices. It defines antenatal care as the planned supervision of pregnant women to ensure a healthy pregnancy and delivery. The objectives are outlined as predicting and preventing problems to deliver a healthy baby from a healthy mother. Key components of care discussed include prepregnancy counseling, booking visits, routine examinations and tests, education, and individualized risk-based care. Warning signs, fetal growth benchmarks, and presentations are reviewed. The document also discusses models of antenatal care and classifications of drugs in pregnancy.
E. Atypical HUS (aHUS)
1. Epidemiology. aHUS is much less common than STEC-HUS.
2. Etiology
a. Drugs (e.g., oral contraceptives, cyclosporine, tacrolimus) or pregnancy may cause
aHUS.
b. Inherited aHUS occurs with both autosomal dominant and autosomal recessive
inheritance patterns, although not all patients have identifiable mutations. These
genetic mutations cause chronic, excessive activation of complement, which also
leads to platelet activation, endothelial cell damage, and systemic thrombotic
microangiopathy.
3. Clinical features. Clinical findings are similar to those of STEC-HUS. Diarrhea may also
be present, and severe proteinuria and hypertension are more consistently found. The
clinical course is generally more severe with multiorgan damage.
4. Management. Treatment is supportive. Inciting medications, if any, must be stopped
immediately.
5. Prognosis. Some patients have a chronic relapsing course (recurrent HUS). All patients
with aHUS have a higher risk of progression to ESRD than patients with STEC-HUS.
E. Atypical HUS (aHUS)
1. Epidemiology. aHUS is much less common than STEC-HUS.
2. Etiology
a. Drugs (e.g., oral contraceptives, cyclosporine, tacrolimus) or pregnancy may cause
aHUS.
b. Inherited aHUS occurs with both autosomal dominant and autosomal recessive
inheritance patterns, although not all patients have identifiable mutations. These
genetic mutations cause chronic, excessive activation of complement, which also
leads to platelet activation, endothelial cell damage, and systemic thrombotic
microangiopathy.
3. Clinical features. Clinical findings are similar to those of STEC-HUS. Diarrhea may also
be present, and severe proteinuria and hypertension are more consistently found. The
clinical course is generally more severe with multiorgan damage.
4. Management. Treatment is supportive. Inciting medications, if any, must be stopped
immediately.
5. Prognosis. Some patients have a chronic relapsing course (recurrent HUS). All patients
with aHUS have a higher risk of progression to ESRD than patients with STEC-HUS.
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.
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
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.
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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
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
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
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
1. THE PRINCIPLES OF
ANTENATAL CARE
(Including PA& Teratogenic
Drugs)
PROF. DR. IRAM CHAUDHRY
FCPS(OBS. & GYNAE) MHPE.
BAHAWALPUR.
2. Definition
‘A planned program of observation,
education, and medical management of
pregnant women directed toward making
pregnancy and delivery a safe and
satisfying experience.’ (American college
of O&G)
3. WHAT IS ANTENATAL CARE
Care of women during pregnancy
Or
“Periodic and regular supervision
including examination and advice of
a woman during pregnancy is called
Antenatal care”
4. Objectives
To ensure a normal pregnancy with
delivery of a healthy baby from a
healthy mother
5. Principles
To predict problems on the basis of history
and physical examination.
To prevent or reduce the severity of
problems by prophylactic measures
To detect and treat conditions having
harmful effects on the mother or fetus.
To provide education, information and
reassurance for mother and partner.
6. Current Approach
• Prepregnancy counselling
• Booking visit
• Routine antenatal visits
• Antenatal education classes
• Inpatient care
9. Antenatal care comprises -
1.Registration of pregnancy
2. History taking
3.Antenatal examinations
[general and obstetrical]
4. Laboratory investigations
5. Health education
11. History
1. Particulars of the patient
2. Chief complaints with duration
3. Past history
4. Obstetric history
5. Menstrual history
6. Family history
7. Drug History
8. History of immunization
9. Socio-economic history
10. Contraceptive history
11. History of allergy
12. Complete Examination
• Weight, height, BMI
• BP
• Full CVS and resp exam
• Breast check- inverted nipples
• Abdominal Examination:
• SFH: Palpable after 12 wks
• Fundus at umbilicus- 20 wks
Xiphisternum - 36 wks.
13. Investigations
Booking- blood tests:
• FBC
• Blood group and antibody screen
• Hep B & C, syphilis, rubella, HIV serology
• Triple test at some centers
• For at risk; sickle test, Hb electrophoresis
• Urine dip- protein and glucose
14. Genetic Risk
• Maternal age > 35yrs
• Afro-Caribbean- sickle cell
• Mediterranean or Asian- thalassemia
• Previous child with abnormality
• Inherited diseases- hemophilia
15. Screening Tests
10-12 weeks booking scan
Confirm IU preg, foetal HR
11-13 wks nuchal translucency
Together with age, estimates likelihood of
Downs (normally 1/500)
14-20 wks. serum screening for Downs
(triple test not used at PRH; CVS or
amniocentesis instead)
16. Screening Tests
anomaly scan: 18-20 wks. x
20-22 wks.
Accurate assessment of gestational age.
Multiple pregnancy detection.
Placental site localization
Detection of congenital abnormalities:
all 4 chambers of heart
17. • Timing variable but traditionally
- Every 4 wks until 28wks
- 2 wks until 36wks
- Weekly thereafter
• BP and urine checked at each visit
• Abd. presentation assessed from 32wks
after 36wks breech needs managing
fetal head engages at 36-38wks in
primigravida
Subsequent Visits
18. Subsequent Visits
• Patient complains & Identification of problem
• General examination
• Gestational Age
• Foetal movement
• SFH measurement
• Health education
• Prophylaxis & treatment of anemia
• Developing individualized birth plan
19. Subsequent Visits
• Blood tests:
- Rhesus neg women have titres
measured at 30 and 36wks. Anti-D given
at 28 and 34 wks?
20. 50% IUGR remain undetected
Clinical assessment
Fetal movements
Ultrasound Assessment, used in series
Biophysical profile
Limb and body movements, breathing, tone,
amniotic fluid vol, HR variability on CTG
Fetoplacental Blood Flow ( Doppler Studies)
Cordocentesis, for blood transfusions too
Assessment of fetal Growth and Wellbeing
21. Models of ANC
• Focused ANC- also called “new” or “WHO”
models
– Evidence based interventions and visit patterns
that benefited mothers and their fetus and were
cost effective as well
– 4 routine visits, with a few evidence based
diagnostic and intervention modalities.
– at 16,28,32 and 36 weeks
– Additional visits on individual basis
22.
23. Visit First Visit Second visit Third visit Fourth visit
Gestational
age
<16 weeks 28 weeks 32 weeks 36 weeks
Activities •Classification to
either the basic or
specialized
component
•Clinical exam
•Hgb test
•GestationalAge
determination
•Blood pressure
•Weight/Height
•Syphilis/STIs
•Urinalysis
•ABO/RH
•TT administration
•Iron
supplementation
•Document on
ANC
•Clinical exam for
anemia
•Gestational age;
FH; FHB exam
•Blood
pressure
•Weight-only
if underweight
at
initial visit
•Urinalysis- for
nullipara or
pr. pre-eclampsia
•Iron supplement
•Complete on
ANC
card
•Hgb test
•TT second dose
•Instructions for
birth planned
•Recommendations
for
lactation/contrace
ption
•Document on
ANC card
•Examine for breech
presentation
•Document on
ANC card
24. Elderly primi (30 yr. and above)
Short statured primi (140 cm and
below)
Mal presentations
APH, threatened abortion
Pre – eclampsia, eclampsia
Risk Approach
25. Risk Approach
• Anaemia
• Twins, hydramnios IUFD, Still
birth
• Elderly grand multiparas
• Prolonged pregnancy
• H/o past caesarean or instrumental delivery Treatment
for infertility
37. Fetal alcohol syndrome
is the most severe fetal alcohol spectrum
disorder. These are a group of birth defects that
can happen when a pregnant woman drinks
alcohol. Other fetal alcohol syndrome
disorders (FASDs) include:
•Partial fetal alcohol syndrome
•Alcohol-related birth defects
•Alcohol-related neurodevelopment disorder
•Neurobehavioral disorder associated with
prenatal alcohol exposure
Editor's Notes
Followed large randomized multicenter trials between the traditional and focused ANC programs that is identified as: