Gestational diabetes (GDM) is glucose intolerance that begins or is first recognized during pregnancy. It can be caused by either pre-existing type 2 diabetes or a new onset of diabetes during pregnancy. The document discusses screening, diagnosis and management of both pre-existing diabetes and GDM during pregnancy. It aims to provide optimal glucose control to support fetal growth while avoiding risks of hyper- and hypoglycemia. Treatment involves medical nutrition therapy, glucose monitoring and may require insulin therapy in some cases. Close monitoring is needed throughout pregnancy and postpartum to support maternal and fetal health.
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.
When fetal head is delivered, but shoulders are stuck and cannot be delivered it is known as shoulder dystocia.
The anterior shoulder becomes trapped behind on the symphysis pubis, whilst the posterior shoulder may be in the hollow of the sacrum or high above the sacral promontory.
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.
When fetal head is delivered, but shoulders are stuck and cannot be delivered it is known as shoulder dystocia.
The anterior shoulder becomes trapped behind on the symphysis pubis, whilst the posterior shoulder may be in the hollow of the sacrum or high above the sacral promontory.
This talk was delivered for postgraduates and faculty of Dr. TMA Pai Hospital, Udupi on 07 March, 2017. This talk covered pathophysiology, screening, diagnosis, complications and management of diabetes mellitus in pregnancy.
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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
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.
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
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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. Gestational diabetes (GDM) is defined as any degree
of impaired glucose tolerance of with onset or first
recognition during pregnancy .
Many are denovo pregnancy induced
Some are type 2 ( 35-40%)
10% have antibodies
5. Difficult to distinguish pregestational Type 2 DM and denovo
GDM
Fasting hyperglycemia
blood glucose greater than 200 mg/dL on OGT
acanthosis nicgrans
HbA1C > 6%
a systolic BP > 110 mm Hg
BMI > 30 kg/m2
Fetal anomalies
Clues for Type 1
Lean
DKA during pregnancy
Severe hyperglycemia requiring large doses of insulin
6. Fuel metabolism in pregnancy
Goal is uninterrupted nutrient supply to fetus
The metabolic goals of pregnancy are
1) in early pregnancy to develop anabolic stores to meet
metabolic demands in late pregnancy
2) in late pregnancy to provide fuels for fetal growth and
energy needs.
7. Glucose metabolism in pregnancy
Early pregnancy
E2/PRL stimulates b cells –Insulin sensitivity same and
peripheral glucose utilisation – 10% fall in BG levels
Late pregnancy
Fetoplacental unit extracts glucose and aminoacids, fat is
used mainly for fuel metabolism
Insulin sensitivity decreases progressively upto 50-80%
during the third trimester
variety of hormones secreted by the placenta, especially
hPL and placental growth hormone variant, cortisol,
PRL,E2 and Prog
8. Glucose metabolism in pregnancy
Fetus
Fat
Glucose Aminoacids
Insulin Hyperins
ulinemia
FASTING
accelerated
starvation and
exaggerated ketosis
(maternal
hypoglycemia,
hypoinsulinemia,
hyperlipidemia, and
hyperketonemia)
FED
hyperglycemia,
hyperinsulinemia,
hyperlipidemia,
and reduced tissue
sensitivity to
insulin
9. RISK FACTORS
History of macrosomia:birth weght>4 Kg,h/o GDM previous
pregnancy
Race
Polycystic ovarian syndrome
Essential hypertension or pregnancy-related hypertension
history of spontaneous abortions and unexplained stillbirths
strong family history of diabetes (especially in first-degree
relatives)
obesity ( [BMI] > 30)
age older than 25 years
persistent glucosuria
10. “NO KNOWN RISK FACTORS IN 50% OF GDM”
ADA recommends selective screening for GDM, but
according to indian guidelines we follow universal
screening
11. Maternal complications
Worsening retinopathy – 10% new DR, 20% mild NPDR and
55% mod-severe NPDR progresses
Worsening proteinuria. GFR decline depends on
preconception creatinine and proteinuria
Hypertension and Cardiovascular disease
Neuropathy – No worsening (gastroparesis, nausea,
orthostatic dizziness can be worsened)
Infection
14. Diagnosis of GDM
The WHO 1999 criteria.
Introduced in 1999.
Glucose load is 75g.
GDM diagnosed if the plasma glucose is 140mg /dl or
above 2 hours after the glucose load.
In 2013 ,WHO dropped in own 1999 criteria and
accepted the IADPSG criteria.
15. IADPSG guidelines
Screening for GDM.
Performed at 24 to 28 weeks of gestation.
75g two hour OGTT is used.
GDM is diagnosed if any one value exceeds the
thresholds shown below.
fasting 1hr 2hr
Plasma glucose ≥92 ≥180 ≥153
(mg/dl)
16. Whom and when to screen? Indian
Scenario - The DIPSI Guidelines
75 gm GCT with single PG at 2 hrs –
≥ 140 mg/dL is GDM
≥ 120 mg/dL is DGGT
>200mg/dl is diabetes
Universal screening
First trimester, if negative at 24 – 28 weeks and then at 32 – 34
weeks
17. Why in India,separate guidelines for
screening?
Indian females-11 fold increased risk of GDM than
Caucasians.
Prevalence is 16.55%
Universal screening detects more number of GDM.
Single blood glucose measurement after
GCT,economically feasible,more patient compliance.
19. MANAGEMENT ISSUES
Patient education
Medical Nutrition therapy
Pharmacological therapy
Glycemic monitoring: SMBG and targets
Fetal monitoring: ultrasound
Planning on delivery
20. If FPG >120,start insulin
Others:Advise MNT,3 days of SMBG,fasting,and 3 one and
half hour post prandial blood glucose.
After MNT,1-2 weeks,start insulin if majority of fasting
ie,four-seven >90
Or majority of any one of PP >120
21. Medical nutrition therapy
Goals
Achieve normoglycemia
Prevent ketosis
Provide adequate weight gain
Contribute to fetal well-being
Nutritional plan
Calorie allotment
Calorie distribution
CH2O intake
22. Calorie allotment
30 kcal per kg current weight per day in pregnant women
who are BMI 22 to 25.
24 kcal per kg current weight per day in overweight
pregnant women (BMI 26 to 29).
12 to 15 kcal per kg current weight per day for morbidly
obese pregnant women (BMI >30).
40 kcal per kg current weight per day in pregnant women
who are less than BMI 22.
23. Postprandial blood glucose concentrations can be
blunted if the diet is carbohydrate restricted. Complex
carbohydrates, such as those in starches and
vegetables, are more nutrient dense and raise
postprandial blood glucose concentrations less than
simple sugars.
Carbohydrate intake is restricted to 33-40% of calories,
with the remainder divided between protein (about 20%)
and fat (about 40%).
With this calorie distribution, 75 to 80 percent of women
with GDM will achieve normoglycemia.
24. Calorie distribution
Variable opinion
Most programs suggest three meals and three snacks;
however, in overweight and obese women the snacks are
often eliminated
Breakfast — The breakfast meal should be small
(approximately 10%of total calories) to help maintain
postprandial euglycemia. Carbohydrate intake at
breakfast is also limited since insulin resistance is
greatest in the morning.
Lunch — 30% of total calories
Dinner — 30% of total calories
Snacks — Leftover calories (approximately 30% of total
calories) are distributed, as needed, as snacks.
25. Diabetes in Pregnancy: Physical Activity
Unless contraindicated, physical activity should be
included in a pregnant woman’s daily regimen
Regular moderate-intensity physical activity (eg, walking)
can help to reduce glucose levels in patients with GDM
Other appropriate forms of exercise during pregnancy
Cardiovascular training with weight-bearing, limited to the upper
body to avoid mechanical stress on the abdominal region
26. Monitoring BG
Atleast 4 times-self monitoring
Fasting and 3 one and half hour postprandial
After achieving target level,lab monitoring till 28 weeks
once in a month
28-32 weeks once in 2 weeks
>32 once a week
Other parameters to be monitored:fundus,micro
albuminuria
27. Glycemic targets
Mean plasma glucose of 105 mg/dl
Achieved by maintaining FPG at 90 & PP at 120
Mean plasma glucose should never go below 86
28. INSULIN THERAPY
Type of insulin used-always human insulin or analogues
In India,basal insulin is usually given as NPH.
Basal may be provided with long acting or intermediate acting
or continuos infusion
Insulin for post prandial control-short acting(regular or
analogue)
NPH-intermediate acting-category B
Detemir-long acting category B
Lispro,aspar ultra short acting-category B
Glargine-long acting-category C
29. INSULIN THERAPY
NPH is usually started at 4 units and then titrated
If morning PP is more,regular insulin in morning
If predinner is high,night dose of rapid insulin
Mixed split regimen-total insulin requirement-2/3 in
morning,1/3 night,of each dose 1/3 rapid and 2/3
intermediate acting.
30. Insulin
≈ 15% need insulin
Total dose varies. ≈ 0.7 to 2 units per kilogram (present pregnant
weight)
FBG high – Night NPH ≈ 0.2 units/kg
PPBG high – bolus ≈ 1.5 units/10 gm CH2O for breakfast and ≈ 1
unit /10 gm CH2O for lunch and dinner
If both pre and postprandial BG high or if the woman's
postprandial glucose levels can only be blunted if starvation
ketosis occurs - four injection/day regimen.
Total 0.7 unit/kg up to week 18
0.8 unit/kg for weeks 18 to 26
0.9 unit/kg for weeks 26 to 36
1. unit/kg for weeks 36 to term.
In a morbidly obese woman, the initial doses of insulin may need to
be increased to 1.5 to 2. units/kg to overcome the combined insulin
resistance of pregnancy and obesity.
31. Status of OHA in pregnancy
Metformin and the sulfonylurea glyburide are the 2 most commonly
prescribed oral antihyperglycemic agents during pregnancy
Due to efficacy and safety concerns, the ADA and DIPSI does not
recommend oral antihyperglycemic agents for gestational diabetes mellitus
(GDM) or preexisting T2DM
Medication Crosses
Placenta
Classification Notes
Metformin Yes Category B Metformin and glyburide may be
insufficient to maintain normoglycemia at
all times, particularly during postprandial
period
Glyburide Minimal
transfer
Some formulations
category B, others
category C
33. Management Intrapartum
Attention to labor pattern, as cephalopelvic disproportion may
indicate fetal macrosomia
If steroids or beta agonists used,increase insulin
Skip morning insulin on day of induction.
Usually no need of insulin while labour.
Hourly blood glucose monitoring during active labor, with
insulin drip if necessary
Notify pediatrics if patient has poorly controlled blood sugars
antepartum or intrapartum
34. Management Postpartum
For patients with pregestational diabetes, halve dose of
insulin and continue to check blood glucose in immediate
postpartum period
For GDM patients who required insulin therapy (GDMA2),
check fasting and postprandial blood sugars and treat with
insulin as necessary
For GDM patients who were diet controlled (GDMA1), no
further monitoring nor therapy is necessary immediately
postpartum
35. Metformin and glyburide are secreted into breast milk and are
therefore contraindicated during lactation
Breastfeeding plus insulin therapy may lead to severe
hypoglycemia1
Greatest risk is in women with T1DM
Preventive measures are: reduce basal insulin dosage and/or
carbohydrate intake prior to breastfeeding
For baby,start early breast feeding,CBG at 1 hour and 4 values in
first 24 hours,before each feed.<44 is considered hypoglycemia.
36. Management Postpartum
For all GDM patients, perform 75 gram 2-hour OGTT
at 6 week postpartum visit to rule out pregestational
diabetes
Most common recommendation is for primary care
physician to repeat
2-hour OGTT every three years
37. Who will progress to DM?
WC and BMI – stronset predictors
Autoantibodies
DM at earlier gestational age
Gestational requirement of insulin
Higher FBG
Higher BG on OGTT
Neonatal hypoglycemia
Recurrent GDM