This document provides an overview of meningitis in pediatrics. It discusses the demography and epidemiology, with the highest incidence being in neonates infected during birth. The most common causes vary by age. Clinical features include fever, irritability, and headache. Diagnosis involves lumbar puncture to examine CSF. Bacterial causes include pneumococcus, meningococcus, and H. influenzae. Treatment involves high dose IV antibiotics for 7-14 days. Complications can include seizures, cerebral edema, and death if not treated promptly. Prevention involves vaccination and antibiotic prophylaxis for contacts of cases.
This week, cerebrospinal meningitis is on the news. This disease, which is majorly prevalent during the dry season has been reported to be ravaging five states in the North-West region of Nigeria including- Zamfara, Sokoto, Kebbi, Katsina and Niger States.
This presentation focuses on Acute Bacterial Meningitis.
Viral and fungal cause is mentioned but focus is on bacterial meningitis in Pediatrics Patient.
Feel free to correct if there is any error.
Refer to other reference books for clarity.
Infections and salivary gland disease in pediatric age: how to manage - Slide...WAidid
The slideset by Professor Susanna Esposito aims at explaining how to manage the salivary gland infections in pediatric age, from pathogenesis, to transmission, treatments and vaccination coverage, that should be urgently increased in Italy as well as in EU Countries.
This week, cerebrospinal meningitis is on the news. This disease, which is majorly prevalent during the dry season has been reported to be ravaging five states in the North-West region of Nigeria including- Zamfara, Sokoto, Kebbi, Katsina and Niger States.
This presentation focuses on Acute Bacterial Meningitis.
Viral and fungal cause is mentioned but focus is on bacterial meningitis in Pediatrics Patient.
Feel free to correct if there is any error.
Refer to other reference books for clarity.
Infections and salivary gland disease in pediatric age: how to manage - Slide...WAidid
The slideset by Professor Susanna Esposito aims at explaining how to manage the salivary gland infections in pediatric age, from pathogenesis, to transmission, treatments and vaccination coverage, that should be urgently increased in Italy as well as in EU Countries.
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
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.
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.
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.
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
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.
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
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
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.
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.
2. outlines
Introduction
Demography and epidemology
Predisposing factors
Etiology and Epidemology
Causes of meninigitis
Bacterial meningitis
Methods of transmission
DX
S&S
Treatment
3. DEMOGRAPHY AND EPIDEMIOLOGY
The highest incidence is among neonates, who
are usually infected by bacteria found in the birth
canal at the time of parturition.
◦ Group B streptococci (Streptococcus agalactiae)
account for the majority of cases; other causes include
Listeria monocytogenes, E.coli, other Gram-negative
bacilli, and enterococci.
From age 1 to 23 months, the most common
organisms are Streptococcus pneumoniae and
Neisseria meningitidis
4. Predisposing factors
Mucosal invasion of the nasopharynx
Direct extension of bacteria across a skull
fracture in the area of the cribriform plate
Systemic bacteremia as with endocarditis or a
urinary tract infection or pneumonia
Asplenia, corticosteroid excess, and HIV
infection
5. Etiology and epidemiology of meningitis
con.
Lack of immunity ( IgM or igG anti capsular antibody ) to
specific pathogens with young age.
recent colonization with pathogenic bacteria .
Close contact with invasive disease ( respiratory tract
secration)
Crowding , poverty , black race , male .
Defect in complement (C5- C8 ) associated with
recurrent meningococcal infection .
6. Etiology of meningitis con…
Ventricular peritoneal shunts
CSF leake due fracture,paranasal sinus
pneumococcal
Head trauma
Neurosurgical procedures
Splenic dysfunction
Immuno suppress patients with t- cell defect(
AIDS,malignancy)
7. Meningitis
o The brain and spinal cord are covered by
connective tissue layers collectively called the
meninges which form the blood-brain
barrier(BBB).
1-the pia mater (closest to the CNS)
2-the arachnoid mater
3-the dura mater (farthest from the CNS).
The meninges contain cerebrospinal fluid (CSF).
Meningitis is an inflammation of the meninges, which,
if severe, may become encephalitis, an
inflammation of the brain.
8.
9. Central Nervous System Infections
Meningitis is the most common causes of
fever associated with signs and symptoms
of CNS disease in children.
Specific microbes depend on :
age, immune status, epidemiology of the
pathogen.
10. Causes of Meningitis
-Bacterial Infections
-Viral Infections
-Fungal Infections
(Cryptococcus neoformans
Coccidiodes immitus)
-Inflammatory diseases
(SLE)
Cancer
-Trauma to head or spine.
11. Viral cause of meninigitis
Non polio enterovirus
Mumps virus
Measles virus
Influenza virus
Herpes simplex virus
13. Meningococcal Meninigitis
Etiological Agent: Neisseria meningitidis
Clinical Features: sudden onset. Sudden high
fever,seisures,poor feeding,headache,nausea
and vomiting
Reservoir: Humans only. 5-15% healthy
carriers
Mode of transmission: direct contact with
patients oral or nasal secretions. Saliva.
Incubation period: 1-10 days. Usually 2-4 days
Infectious period: as long as meningococci are
present in oral secretions or until 24 hrs of
effective antibiotic therapy
14. Cause of Bacterial Meningitis with
age group
• Birth - 4 wks: GBS, E.coli
4 - 12 wks: GBS, E.coli,
Pneumococcus
Salmonella, Listeria, H. Influenza
3 mths - 3 yrs: Pneumococcus,
Meningococcus
H. Influenza
3 yrs+ adult: Pneumococcus,
Meningococcus
15. Mode of transmission
Respiratory secretion/ droplet
Person to person contact(kissing
,saliva,contaminated food,mucus)
18. DIAGNOSIS
1) Lumbar puncture
Between L3 & L4 or L4 & L5
Confirms DX of meningitis
CSF
Pressure …..usually elevated to 100-300 mmH2O ( Nl
=50-80 mmH2O )
Gross appearance……turbid (WBC >200-400 /mm3)
WBC count (Nl =less than 5 , lymphocyte > 75% or
monocytes )
Usually elevated to >1000/mm3 (100 – 10,000/mm3 or
more )
Neutrophil predominance ( 75- 95% )
In 20 % of cases WBC < 250/mm3
Absent pleocytosis …….sever overwhelming sepsis
with meningitis
Pleocytosis with lymphocyte predominance…….during
early stages
Elevated protein …usually 100-500 mg/dl (Nl = 20 - 45
mg/dl )
Reduced glucose….usually <40 mg/dl (or <50% of serum
glucose ) ( Nl =>50mg/dl or 75 %of serum glucose )
Gram stain : positive in 70-90 % of cases
Culture
19. Contraindications for LP
- Increased ICP
- Sever cardiopulmonary compromise
- Infection of the skin overlying the site of the LP
- Thrombocytopenia( < 20,000/mm3 ) : Relative c/I
Traumatic LP
- Affects CSF, WBC & protein concentration
- Does not affect G/S , culture & Glucose level
- Repeat LP after sometime
2) Latex particle agglutination
- Highly sensitive but less specific
3) Blood culture : Positive in 80 -90 % of cases
4) Countercurrent immuno electrophoresis (CIE)
-Rapid & very specific
20. Typical Cerebrospinal Fluid Findings in
Patients with Bacterial Meningitis
Cerebrospinal Fluid Parameter Typical Finding
Opening pressure 200-500 mm H2O
White blood cell count 1000-5000/mm3
Percentage of neutrophils ≥80%
Protein 100-500 mg/dL
Glucose ≤40 mg/dL
CSF-to-serum glucose ratio ≤0.4
Gram stain Positive in 60%-90%
Culture Positive in 70%-85%
Polymerase chain reaction Promising*
21. CSF
Collect 1 ml of csf in each of 3 vials
Tube 1 culture and gram stain
Tube 2 glucose,protein
Tube 3 cell count and differential
22. Meningitis: Clinical features
Newborn & Infants: non-specific
Fever
Irritability
Lethargy
Poor feeding
High pitched cry, bulging AF
Convulsions,
26. TREATMENT
A) Antibiotics
◦ Always use high dose ,parenteral (IV)
antibiotics.
◦ Initial (empirical )choice of therapy
Vancomycin 60 mg/kg/24 hr, given every 6
hr
OR
Ceftriaxone 100 mg /Kg /24 hr once per
day or
50 mg/Kg /dose every 12 hrs for 7 – 10
days
OR
27. Patient allergic to b-lactam antibiotics
-CAF 100 mg /Kg /24hr given every 6 hr
OR
- Patient can be desensitized to the
antibiotic
◦ If patient is immuno compromised
-Ceftazidime and aminoglycoside need to be
included because of risk of gram –ve bacterial
meningitis e.g. P.aeruginosa ,E .coli
28. Duration of antibiotic therapy
a) Generally total of 10 days
b) Specific ( based on etiologic agent ) in
uncomplicated cases
N .meningitidis…….5 -7 days
H .influenzae type b……….7 10 days
S .Pneumoniae………..10-14 days
CSF culture –ve………7- 10 days
Gram –ve bacilli……03 weeks or 2 weeks after
CSF sterilization
( usually after 2 – 10 days of treatment )
Neonates ……..03 weeks
** N.B. In complicated cases of meningitis ,give
antibiotics for 10-14 days
30. Corticosteroids
Rapid killing of bacteria releases toxic cell
products.
This precipitates cytokine mediated infl.
response- edema & neutrophilic response.
This will lead to additional neurologic injury
with worsening of CNS Sx:
- Dexamethasone- 0.15mg/kg/dose q6hr-
2days (benefit max if given 1-2 hr before
antibiotics)
-.
31. Supportive care
NPO
IV fluid: 800-1000ml/m2/24hr(1/2-2/3rd
of maintenance)- shock treated
aggressively.
Septic shock- dopamine
Signs of ↑ ICP
-ET intubation& hyperventiln
(PCO2~25mmHg)
- IV lasix (1mg/kg), mannitol (0.5-1g/kg)
Seizures- first Rx-diazepam iv,or
lorazepam
32. cont’d
- do serum glucose, calcium, & sodium
levels
- After initial Rx, phenytoin (loading dose
of 15-20mg/kg, maintenance 5mg/kg/d)
Neurologic ass’t: esp.1st 72 hrs
-PR, BP, RR, Level of consciousness,
pupils, motor, Cranial nerves, Sz,
Head circumference, Urine output.
- Lab.- Sp. Gravity of urine
34. Prevention
-Vaccination & antibiotic prophylaxis
- N.meningitidis- rifampin
10mg/kg/dose q12 hr for 2 days –for
all close contacts of patients with
meningococcal meningitis.
- HIB- rifampin 20mg/kg/day,once, 4
days for all household contacts
Washing Hands frequently
Not share eating utensil,plates