This document summarizes bleeding in neonates. Neonates are susceptible to bleeding due to immature coagulation systems and deficiency of coagulation factors. Bleeding may present as oozing from umbilical stumps or bruising. Etiologies include deficiency of vitamin K dependent coagulation factors, platelet problems, and vascular abnormalities. Diagnostic workup includes history, exam, PT, APTT, and factor assays. Treatment involves vitamin K, fresh frozen plasma, platelets, or specific factor replacements depending on the underlying cause.
Haemorrhagic and Haemolytic of Newborn DiseasesNaqib Bajuri
actually for haemorrhagic newborn diseases, mainly focus of vit K def...the other is for revision n more commonly occur in child n adults....for haemolytic newborn disease, mainly focus on Rh disease n ABO incompatibility.....the other when childhoods
Haemorrhagic and Haemolytic of Newborn DiseasesNaqib Bajuri
actually for haemorrhagic newborn diseases, mainly focus of vit K def...the other is for revision n more commonly occur in child n adults....for haemolytic newborn disease, mainly focus on Rh disease n ABO incompatibility.....the other when childhoods
Anemia and Preemies: Contemporary Approach to Diagnostics, Preventive Measure...MCH-org-ua
International conference «Actual approaches to the extremely preterm babies: International experience and Ukrainian realities» (Kyiv, Ukraine, March 5-6, 2013)
hemolytic disease of new born is an aquire alla immune hemolytic anemia characterize by production extravascular destruction of RBC within the spleen of new born baby resulting anemia, positive coomb,s test
Anemia and Preemies: Contemporary Approach to Diagnostics, Preventive Measure...MCH-org-ua
International conference «Actual approaches to the extremely preterm babies: International experience and Ukrainian realities» (Kyiv, Ukraine, March 5-6, 2013)
hemolytic disease of new born is an aquire alla immune hemolytic anemia characterize by production extravascular destruction of RBC within the spleen of new born baby resulting anemia, positive coomb,s test
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 .
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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.
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
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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!
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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
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.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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