This document discusses the causes, presentation, diagnosis, and treatment of bleeding in neonates. Bleeding may occur due to immaturity of the hemostatic system or deficiencies in coagulation factors. Clinical presentations include oozing from the umbilical stump or bruising. Evaluation involves a detailed history and examination followed by laboratory tests like a PT, APTT, and specific factor assays. Treatment depends on the underlying etiology but may include vitamin K, fresh frozen plasma, platelets, or clotting factor concentrates. Conditions discussed in more detail include vitamin K deficiency, hemophilia, thrombocytopenia, and immune thrombocytopenia.
Anemia can be seen in the emergency department both as a primary pathological process or secondary to both medical and surgical diseases. Moreover, acute anemia can occur in children who have been otherwise healthy, who have systemic disease, or who have known hematologic disorders. Anemia may indicate a disorder with a single hematopoietic cell line (eg, red blood cells) or may be associated with changes in multiple cell lines indicative of bone marrow involvement, immunologic disease, peripheral destruction of erythrocytes, or sequestration of cells. Independent of the etiology, prompt diagnosis is predicated on understanding the classifications of anemia, the associated presenting symptoms, and the proper ordering and interpretation of laboratory studies. This article will discuss the evaluation, proper classification, differential diagnosis, and initial management of acute anemia using cases representative of those that might be seen in the pediatric emergency department.
pediatrics emergency, hypoglycemia of infancy.
Glucose level can drop if:
There is too much insulin in the blood (hyperinsulinism). Insulin is a hormone that pulls glucose from the blood.
The baby is not producing enough glucose.
The baby's body is using more glucose than is being produced.
The baby is not able to feed enough to keep glucose level up.
simlpe approach to anemia in children , how to diagnose anemia in kids ,types of anemias ,causes of anemia , iron deficeincy anemia, hemolytic anemias , laboratory tests in anemia ,
Anemia can be seen in the emergency department both as a primary pathological process or secondary to both medical and surgical diseases. Moreover, acute anemia can occur in children who have been otherwise healthy, who have systemic disease, or who have known hematologic disorders. Anemia may indicate a disorder with a single hematopoietic cell line (eg, red blood cells) or may be associated with changes in multiple cell lines indicative of bone marrow involvement, immunologic disease, peripheral destruction of erythrocytes, or sequestration of cells. Independent of the etiology, prompt diagnosis is predicated on understanding the classifications of anemia, the associated presenting symptoms, and the proper ordering and interpretation of laboratory studies. This article will discuss the evaluation, proper classification, differential diagnosis, and initial management of acute anemia using cases representative of those that might be seen in the pediatric emergency department.
pediatrics emergency, hypoglycemia of infancy.
Glucose level can drop if:
There is too much insulin in the blood (hyperinsulinism). Insulin is a hormone that pulls glucose from the blood.
The baby is not producing enough glucose.
The baby's body is using more glucose than is being produced.
The baby is not able to feed enough to keep glucose level up.
simlpe approach to anemia in children , how to diagnose anemia in kids ,types of anemias ,causes of anemia , iron deficeincy anemia, hemolytic anemias , laboratory tests in anemia ,
Interactive talk on common hematological and oncological emergencies - which if not noticed early can lead to irreversible complications and death .
Intended to be used for educational purposes for the fertile minds in medicine .
Rthajjwjkslllmsnhgsghjklsmsnhhsgjkskmnsnsbjjngghjkmnbvcfgggfffjkkkkkkklllkhgggvhnnmkjhttfd hmmmmmm bnkmmkkllllllll bnklkgffbnmkklkllojnbnmmlkkllkjjj mmmmkkklklkhghjkchjjkkkhggnlkmmnnkkkkllllllmmmmmkmkkllllllkkkmml ok thanks for your support rahyo ne kaha se ho tum log nahi ho payega kya hua hai kya tum hamesha uibbnnhhjjkkkkkkh bnkmmkkllllllll bnklkgffbnmkklkllojnbnmmlkkllkjjj mmmmkkklklkhghjkchjjkkkhggnlkmmnnkkkkllllllmmmmmkmkkllllllkkkmml bnkmmkkllllllll bnklkgffbnmkklkllojnbnmmlkkllkjjj mmmmkkklklkhghjkchjjkkkhggnlkmmnnkkkkllllllmmmmmkmkkllllllkkkmml ok to go if u ivvjlkmmnnnbhgghjj hmmmmmm bnkmmkkllllllll bnklkgffbnmkklkllojnbnmmlkkllkjjj you are my favourite friend of stool t shirt 🎽 you too thhuhhjkkkl fghjkllkkjffghjjj I understand my problem is on CPAP pt in the best of the best bhai 😀 to you and all the ay 🤣🤣 and all the best for exam today and all the best for exam 👍 and the tuu fghjkllkkjffghjjj kkllljjhhkkkkg ûyuuiiufhjkkhgjkkkjhhgg
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- 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
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the 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 lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
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. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
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!
2. Introduction
•
Neonates are susceptible to bleeding for
various reasons
Immaturity of the haemostatic system
because of quantitative and qualitative
deficiency of coagulation factors
Maternal disease and drugs
Birth trauma
Other conditions - sepsis and asphyxia
3. Clinical presentation
•
Bleeding in neonates may present with
Oozing from the umbilical stump
Cephalhaematoma
Bruising , Petechiae
Bleeding from peripheral venipuncture or
procedure sites
Bleeding following circumcision
Intracranial haemorrhage
Bleeding from mucous membranes
Unexplained anemia and hypotension
4. Etiology
A.Deficiency of clotting factors:
1.Transitory deficienciesDeficiency of vitamin K dependent
C.F- II, VII, IX, X.
Deficiency of anticoagulant proteins
C & S.
5. Causes:
a. Total parenteral nutrition or antibiotics
b. Lack of administration of vitamin K .
c. Drug intake in pregnancy
eg.i. Phenytoin, Phenobarbital, Salicylates .
(Interferes with the synthesis of vit. K
dependent c.f. )
ii. Calmodulin compounds
6. • The incidence among babies born to mothers
on these drugs have varied between 6-12%*.
In a recent series on children born to mothers
on anticonvulsants, abnormal PT was
documented in 14 out of 105 babies (13%)
, no overt bleeding was observed*.
7. 2. Disturbances of clotting
- Related to DIC due to
infection, shock, anoxia, NEC, renal vein
thrombosis, use of IV canula.
3. Inherited abnormalities of C.F.
a. X-Linked recessive diseasesi. Hemophilia-A : Factor VIII deficiency.
ii. Hemophilia-B : Factor IX deficiency.
8. b. Autosomal dominant diseases:
i. Von Willebrand disease – Deficiency of
VWF which is a carrier of factor VIII & as a
platelet aggregation agent.
c. Autosomal recessive diseases:
i. Severe factor VII & factor XIII deficiency –
intracranial hemorrhage in neonates
ii. Factor XI deficiency –
unpredictable bleeding during
surgery/trauma.
9. iii. VWD Type III
B. Platelet problems:
1. Qualitative disorders:
- Glanzman’s thrombasthenia.
- Bernard-Soulier syndrome
- Platelet type VWD
10. 2. Quantitive disorders:
- Immune thrombocytopenia
- Matrnal Preeclampsia, HELLP syndrome
or severe uteroplacental insuffuciency.
- DIC due to infection or asphyxia.
- Inherited marrow failure syndromes :
Fanconi anemia & congenital
amegakaryocytic thrombocytopenia
13. Diagnostic workup
• HISTORY: A detailed history and examination
essential in the assessment of bleeding neonate
History includes
• Maternal diseases as ITP, preeclampsia .
• Maternal exposure to drugs as
aspirin, anticonvulsants, rifampicin and isoniazid
• Family history of bleeding disorders
• Previous affected sibling
14. B. Examination:
First diagnose whether the infant is Sick or Well
1. Sick infant:
- DIC
- Bacterial/ viral infections.
2. Well infant:
- Vit K deficiency
- Isolated C.F. deficiencies
- Immune thrombocytopenia
- Maternal blood in infant’s GIT.
15. 3. Patchiae, ecchymosis, mucosal
bleeding: Platelet problem
4. Large bruises: DIC, C.F
deficiencies, liver diseases
5. Enlarged spleen : Possible congenital
infections or erythroblastosis.
6. Jaundice : Sepsis, liver
diseases, resorption of large hematoma.
16. C. Laboratory tests:
1. Apt test :
- To rule out maternal blood in infant’s
GIT
- Done in otherwise well infant with
only GI bleeding.
2. PBS :
- DIC- fragmented RBCs
- Congenital macrothrombocytopenias –
large platelets.
17. 3. PT
4. APTT
5. D-Dimer assays: Measure fibrin
degradation products in DIC & Liver
diseases causing defective clearing of
fibrin split products.
6. Specific factor assays & Von
Willebrand assay: For patients with +
ve family h/o.
18. Laboratory findings
Laboratory Studies
Other useful tests
DIC
Platelets PT
Likely Diagnosis
Fibrinogen, FDP, Sepsis
screen
Platelet consumption
(NEC, Renal vein thrombosis,
marrow infiltration, Sepsis)
LFT, Albumin
APTT
SICK INFANTS
N
N
Liver disease
N
N
N
N
Compromised vascular integrity
(hypoxia, prematurity, acidosis)
19. Laboratory Studies
Platelets PT
Likely Diagnosis
Other useful tests
Immune thrombocytopenia
Bone marrow hypoplasia
Maternal platelet count,
Platelet antigen typing,
Bone marrow, Fibrinogen,
FDP, Factor VII & IX assays
APTT
HEALTHY INFANTS
N
N
N
N
N
Vitamin K Deficiency
N
Heriditory C.F. deficiencies
N
Bleeding d/t local factors,
Plt function anomalies,
Factor XIII deficiency(rare)
N
Platelet aggregometry
Urea clot solubility
20. Treatment Of Bleeding
A. Inj Vitamin K1 (Aquaminophyton)
- 1 mg IV or IM if not given at birth.
- Infants on TPN
- Infants on Antibiotics > 2 weeks: at
least 0.5mg Vit K weekly.
- Preferred rather than FFP for prolonged
PT & PTT, FFP should be reserved for
emergencies.
21. B. FFP:
- 10ml/kg IV for active bleeding
- Repeated 8-12 hrly as needed.
- Replaces C.F. immediately.
C. Platelets:
- 1 Unit of platelet raises count by
50,000-100,000/mm3 in a 3kg
newborn.
- Platelet count slowly decreases if stores
3-5 days.
22. D. Fresh whole blood:
- 10ml/kg
- Can be repeated after 6-8 hrs as needed.
E. Clotting factor concetrates
- Severe VWD :
- VWF containing plasma derived factor VIII
concetrate.
- Known deficiency of factor VIII or IX :
Recombinent DNA derived factor VIII and
IX concetrate
23. F. Disorders due to problems other than hemostatic
proteins :
- Rule out the underlying possibilities
- eg. Infection, Liver rupture, catheter, NEC.
G. T/t of specific disorders :
1. DIC :
- Treat the underlying cause i.e. sepsis, NEC
- Make sure that Vit K1 has been given.
24. - Platelets/ FFP to keep platelet counts > 50,000/ml
and to stop bleeding.
- If bleeding persists,
i. Exchange transfusion with fresh whole blood
/Packed RBC/Platelets/FFP
ii. Continuous transfusion with platelets, packed
RBCs or FFP as needed.
iii. For hypofibrinogenemia : Cryoprecipitate
(10ml/kg)
25. VKDB
•
•
•
•
Early , Classic, and Late forms
Early VKDB – in first day
Severe bleeding – GI and ICH
Cause – Maternal drug intake
Phenytoin, phenobarb,
ATT, warfarin
26. VKDB
Classical form: 2-7 days of age
• 0.25-1.7% of all babies
• Cause – not received prophylaxis
on breast feeds, sterile gut, lack of
placental transfer
Late form : 2-8 weeks of age
• Boys > girls, 5-10/1 lac
• Well , breastfed, term baby
• Liver disease
• Malabsorption
27. Management of VKDB
• Prolonged PT , APTT (if severe)
• Normal platelets and fibrinogen
• Factor assays of vit K dependent
factors
• Treatment – 1mg iv or sc
• FFP in severe cases
28. Prophylaxis of VKDB
• Early VKDB- single IM inj of vit K at
birth and oral Vit K to mother for
last 4 weeks
• Classical and Late forms –
IM Vit K at birth
oral Vit K at 0 , 4 days and 4 weeks
In preterms – Weekly iv Vit K
29. Hemophilia in the Newborn
• Factor VIII or XI deficiency
– A good family history goes a long way
30. Hemophilia A
Most common inherited clotting factor def
X linked recessive, 1 in 4000 males
1/3rd of cases present in newborn period
ICH(25%), cephalhematoma(10-15%)
Post circumcision bleed is characteristic
Family history – absent in 30%
Inv – prolonged APTT, normal PT, normal
platelets.
• Factor VIIIc assay level <2% severe, 2-10%
moderate, >10% mild
•
•
•
•
•
•
•
31. Hemophilia B
•
•
•
•
•
•
XLR
Deficiency of Factor IX
Less common than the classical form
Prolonged APTT and low Factor IX
Rx- 100u/k iv OD , to raise levels to 100%
Avoid lumbar punctures, IM injections
32. Thrombocytopenia
•
•
•
•
•
Less than 150,000/uL
Incidence in newborns: 1-5%
Incidence in NICU – 15-30%
In VLBW and preterms – 50%
Causes of thrombocytopenia in newborn:
Neonatal megakaryocytes are smaller
Inadequate production of thrombopoietin
33. Causes of thrombocytopenia
• Immune-mediated
• Associated with infection - Bacterial or Nonbacterial
• Drug-Related
• Increased peripheral consumption of platelets –
Disseminated Intravascular Coagulation,
Necrotizing enterocolitis, hypersplenism
• Genetic and Congenital Anomalies
• Miscellaneous – asphyxia, IUGR, PIH, GDM
36. Immune Thrombocytopenia
• Neonatal allo-immune thrombocytopenia
(NAIT)
• Incidental thrombocytopenia of
pregnancy or Gestational
thrombocytopenia
• Autoimmune thrombocytopenic purpura
37. Neonatal allo-immune
thrombocytopenia (NAIT )
•
•
•
•
•
•
Incompatibility between mother and baby
Similar to Rh disease
Antibodies against HPA – 1 (most common)
In utero bleed can occur
Manifests with first pregnancy in 50%
Postnatal : petechiae, purpura
ICH in 10% with sequelae
38. NAIT
• Management – fetal blood sampling and
platelet transfusion or maternal IVIG
• If previous sibling had a significant bleed
• Caesarian section
• In newborn – maternal platelets or HPA
compatible platelets
• IVIG 1gm/k for 2 days or 0.5g/k for 4 days