Polycythemia in newborns is defined as an increased total red blood cell mass with a hematocrit greater than 65%. This can lead to hyperviscosity or increased blood viscosity. Polycythemia occurs in 1-5% of term newborns, often due to placental transfusion or insufficiency. Symptoms include poor feeding, lethargy, and hypotension due to regional hypoxia from hyperviscosity. Treatment involves partial exchange transfusion for symptomatic infants or increased fluids and monitoring for asymptomatic infants with hematocrits between 70-65%. The prognosis is generally good but partial exchange transfusion may increase risks of gastrointestinal disorders.
overview of anatomy and physiology of the thyroid gland,fetal period and pregnancy physiological changes ....then overview of congenital hypothyroidism plus management
overview of anatomy and physiology of the thyroid gland,fetal period and pregnancy physiological changes ....then overview of congenital hypothyroidism plus management
childhood hypertension is unique presentation by Dr. Hemraj Soni,
very compressive, complied,upgraded, presentation......will definative helpfull for paediatrician n resident doctor............
childhood hypertension is unique presentation by Dr. Hemraj Soni,
very compressive, complied,upgraded, presentation......will definative helpfull for paediatrician n resident doctor............
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
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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
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.
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
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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
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
2. Definition
Polycythemia ( polyglobulia)
is increased total RBC mass
Central venous hematocrit > 65%
the hemoglobin is greater than 22 mg/dL
Hct initially rises after birth due to placental transfer
of blood and decrease to baseline at 24 hrs
Hyperviscosity is increased viscosity of the blood
more than 2 SD of mean resulting from
increased numbers of RBCs
3. Blood viscosity is ratio of shear stress to shear
rate and is dependent on pressure gradient along
the vessel,radius,length of vessel and velocity of
flow of blood.
Viscosity is directly prop to Hct and plasma
viscosity whereas inversely proportional to
deformability of RBCs
Relation between Hct and viscosity is linear till
Hct is 60 % after that viscosity increases
exponentially
5. Incidence
1-5% of term newborns
It is increased in IUGR, SGA and post term
Half of these are symptomatic
Hyperviscosity occurs in 25% of infants with
hematocrit 60-64%
Hyperviscosity without polycythmia occurs in 1%
(nonpolycythemic hyperviscosity)
6. Pathophysiology
Clinical signs result from regional effects of
hyperviscosity and from the formation of
microthrombi
Tissue hypoxia
Acidosis
Hypoglycemia
Organs affected – CNS, kidneys, adrenals,
cardiopulmonary system, GI tract
8. Causes
Placental red cell transfusion --
-- Delayed cord clamping – at 1 min blood
volume of baby is 80 ml / kg.
-- At 2 min – blood vol of infant is 90 ml/kg
-- In newborn with polycythemia blood
volume
is inversly proportional to birth weight.
9. Causes
Placental red cell transfusion --
--Holding baby below the mother at delivery
-- Maternal to fetal transfusion – diagnosed with
K-B test
--Twin to twin trasfusion
--forceful uterine contraction before cord
clamping
10. Causes
Placental insufficiency
--Increased fetal erytropoesis d/t chronic
hypoxia
--SGA and IUGR
--Maternal hypertension like preeclampsia
--Post term
--Mothers with chronic hypoxia
(heart dis ,pulmonary dis)
--Pregnancy at hihg altitude ,maternal smoking
11. Other conditions
Diabetic mother – raised erythropoiesis
LGA
CAH,
patau syndrome,
edward syndrome ,
downs syndrome (PED)
Maternal use of propranolol
sepsis
16. SCREENING
Not routinly done in all term babies
high-risk neonates screened at 2 hours of age
If Hematocrit value >65% at 2 hours of age
repeat screening at 12 and 24 hours.
17. SCREENIG IS DONE IN ALL SYMPTOMATIC
CASES
If HCT more than 65%
Then again at 12 & 24 hrs
High risk infants
Screened at 2 hrs of life
18. Diagnosis
Central venous hematocrit > 65%
ALWAYS draw a central venous sample if the
capillary hematocrit is > 65%
Warmed capillary hematrocrit > 65% only suggestive
of polycythemia
BLOOD VISCOSITY – may be measured where
facility available
19. Management
Asymptomatic infants
HCT 60 -70 % increase fluid intake and repeat
HCT after 4 to 6 hr
central venous hematocrit >70%
(consider partial exchange transfusion)
20. Management
Symptomatic infants
with peripheral HCT > 65%
Partial exchange transfusion is advisable.
For exchange can use normal saline, 5% albumin, or
FFP
Volume exchanged =
(Weight (kg) x blood volume) x (observed hct -
desired hct)
/observed hct
Blood volume is 80-90 ml/kg in term and 90-100 ml/kg
in pre term
In exchange blood from umbilical vein and normal saline
infused in peripheral vein
22. AIIMS PROTOCOL
SYMTOMATIC – Partial exchange
transfusion(PET)
ASYMTOMATIC-
1. Hct >75% - transfusion
2. Hct 75 – 70 % - extra fluid alliquote @20 mkd
3. Hct <70 % - monitor Hct
The Cochrane review – with exchange
transfusion there
is no difference in morbidity of patient
23. Other labs to check
Serum glucose
Hypoglycemia is common with polycythemia
Serum bilirubin
Increased bili due to increased RBC turnover
Serum sodium, BUN, urine specific gravity
Usually high if baby is deyhdrated
Blood gas to rule-out inadequate oxygenation
as cause of symptoms
Platelets, as thyrombocytopenia can be present
Serum calcium b/c hypocalcemia can be seen
24. Prognosis
Increased risk of GI disorders and NEC with
partial exchange transfusion (PET)
PET is controversial!
Infants with asymptomatic polycythemia have an
increased risk for neurologic sequelae.