A simplified guide to the most common diseases with fever & rash especially in pediatrics. The data have been trimmed as much as possible and focused on spot visual diagnosis of the disease.
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.
A simplified guide to the most common diseases with fever & rash especially in pediatrics. The data have been trimmed as much as possible and focused on spot visual diagnosis of the disease.
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.
1. Vesiculobullous lesions.pdf by dr jamalHawzhinFakher
It is ffycoycitcitxuxitxitxitditd5iditditfoyfogckgckgckgckgckgckgfkgckgcgkclgfhlchlflgdlgdkgfydoydlydlyflgflycyfyoxoyfoyxoyxgkxgkxglcoycoyfoyfoyfoyfoyfyodoyf
Skin, Soft Tissue, & Bone Infections Symposia - The CRUDEM FoundationThe CRUDEM Foundation
This is the Skin, Soft Tissue, & Bone Infections Symposia presented in Milot, Haiti at Hôpital Sacré Coeur in 2011. CRUDEM’s Education Committee (a subcommittee of the Board of Directors) sponsors one-week medical symposia on specific medical topics, i.e. diabetes, infectious disease. The classes are held at Hôpital Sacré Coeur and doctors and nurses come from all over Haiti to attend.
This is a presentation on cutaneous manifestations of tuberculosis. tuberculosis is a very important disease especially in the sub-Saharan region.
The pictures are not mine( from internet sites) and the study material majorly used was Fitzpatrick dermatology and extrapulmonary TB by Alper Senner. If anyone feels like some of the information is from their site and has been wrongly used do contact me via : lilacpreton12@gmail.com . This information is only for educational purposes.
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
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
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
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.
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
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
Antimicrobial stewardship to prevent antimicrobial resistanceGovindRankawat1
India is among the nations with the highest burden of bacterial infections.
India is one of the largest consumers of antibiotics worldwide.
India carries one of the largest burdens of drug‑resistant pathogens worldwide.
Highest burden of multidrug‑resistant tuberculosis,
Alarmingly high resistance among Gram‑negative and Gram‑positive bacteria even to newer antimicrobials such as carbapenems.
NDM‑1 ( New Delhi Metallo Beta lactamase 1, an enzyme which inactivates majority of Beta lactam antibiotics including carbapenems) was reported in 2008
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
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
DISSERTATION on NEW DRUG DISCOVERY AND DEVELOPMENT STAGES OF DRUG DISCOVERYNEHA GUPTA
The process of drug discovery and development is a complex and multi-step endeavor aimed at bringing new pharmaceutical drugs to market. It begins with identifying and validating a biological target, such as a protein, gene, or RNA, that is associated with a disease. This step involves understanding the target's role in the disease and confirming that modulating it can have therapeutic effects. The next stage, hit identification, employs high-throughput screening (HTS) and other methods to find compounds that interact with the target. Computational techniques may also be used to identify potential hits from large compound libraries.
Following hit identification, the hits are optimized to improve their efficacy, selectivity, and pharmacokinetic properties, resulting in lead compounds. These leads undergo further refinement to enhance their potency, reduce toxicity, and improve drug-like characteristics, creating drug candidates suitable for preclinical testing. In the preclinical development phase, drug candidates are tested in vitro (in cell cultures) and in vivo (in animal models) to evaluate their safety, efficacy, pharmacokinetics, and pharmacodynamics. Toxicology studies are conducted to assess potential risks.
Before clinical trials can begin, an Investigational New Drug (IND) application must be submitted to regulatory authorities. This application includes data from preclinical studies and plans for clinical trials. Clinical development involves human trials in three phases: Phase I tests the drug's safety and dosage in a small group of healthy volunteers, Phase II assesses the drug's efficacy and side effects in a larger group of patients with the target disease, and Phase III confirms the drug's efficacy and monitors adverse reactions in a large population, often compared to existing treatments.
After successful clinical trials, a New Drug Application (NDA) is submitted to regulatory authorities for approval, including all data from preclinical and clinical studies, as well as proposed labeling and manufacturing information. Regulatory authorities then review the NDA to ensure the drug is safe, effective, and of high quality, potentially requiring additional studies. Finally, after a drug is approved and marketed, it undergoes post-marketing surveillance, which includes continuous monitoring for long-term safety and effectiveness, pharmacovigilance, and reporting of any adverse effects.
DISSERTATION on NEW DRUG DISCOVERY AND DEVELOPMENT STAGES OF DRUG DISCOVERY
Approach to a child with fever and rash
1.
2. • This condition can be caused by drug reaction, infection or
an allergic reaction.
• Different agents can cause rash that look the same
• Often symptoms in addition to rash helps in making the
diagnosis.
• Most rashes caused by viruses do not harm child but some
are life threatening.
3. • 10% of all febrile children have dermatological problem.
• Morphology of skin lesion can contribute to diagnosis.
• In drug reactions we see more than one type of morphology at a
given point of time.
• At times lesion goes through stages, in such cases presenting
lesion along with relevant evidence from history on evolution
helps in diagnosis.
7. • WITH REGARD TO FEVER:
• Onset
• Duration
• Diurnal variation.
• Other symptoms.
• WITH REGARD TO RASH:
• Distribution of rash
• Morphology or pattern of rash.
• Evolution
• Prodrome, if any
8. • Grade of fever.
• Pattern of fever.
• Type of skin lesion.
• Distribution
• Site of first appearance.
• Evolution
• Tenderness
• Mucosal involvement
• Involvement of palms, soles.hair.nails.
• Other systems.
9. MACULE:
Circumscribed area of change in skin color without any
change in consistency.
<1cm diameter
PAPULES AND NODULES:
Solid lesion <0.5cm in diameter; major part of it
projecting above the skin is a papule.
Solid lesion >0.5cm but <1cm in diameter with major
part in the skin is a nodule.
10. PLAQUE:
Area of altered skin consistency, surface area of
which is greater than depth.
WHEAL:
Characteristic lesion in urticaria.
Pale or erythematous raised lesion which disappears
within 24-48hrs.
BLISTERS:
Circumscribed elevated, superficial fluid filled
cavity. If <0.5cm it is a vesicle; >0.5cm a bulla
11. PETECHIAE :
pin head sized macules of blood.
PURPURA:
large petechiae which do not blanch on pressure.
ECCHYMOSIS:
large extravasation of blood in the skin.
15. Eruptive (rash) phase: Rash appears on 4-6 day of fever.
MORPHOLOGY- Faint erythematous maculopapular rash.
DISTRIBUTION-
Starts behind the ears, involving the face & spreading
to trunk& then to legs and arms.
By the time it appears on feet ,it starts disappearing
from face in the same order.
Temperature normalises once rash starts fading.
Severity is proportionate extent & confluence of rash.
16.
17. PRODROME:
low grade fever
Malaise
sorethroat
Post auricular, sub-occipital lymph nodes :enlarged &
tender.
Rose spots on soft palate (forchheimer spots)before rash.
RASH
MORPHOLOGY
Discrete maculopapular rash variable in size and
confluence.
DISTRIBUTION
Starts on face & spreads rapidly over trunk.
Progression is fast. By 3rd day rash clears up without
significant desquamation.
18.
19. MEASLES (RUBEOLA) GERMAN MEASLES (RUBELLA)
Coryza &cough more severe. Coryza & cough mild
Confluent maculopapular rash with
slow progression and clearing.
Discrete maculopapular rash with
rapid progression and clearing.
Temperature rises abruptly with rash . Temperature don’t rise abruptly with
rash.
Lymphadenopathy not characteristic Retro-auricular, post . Cervical or
post.occipital lymphadenopathy is
characteristic.
Kopliks spots may be seen Forschheimers spots may be seen.
20. Rashes are seen in febrile phase and during convalscence.
FEBRILE PHASE:
During fever, whole body invariably covered with
bloachable erythematous flush.
Suffused & swollen face, injected eyes, reddened
ears,crimson malar area,swollen & purplish lips(measly
look).
Flush deepens with advancing disease.
In few patients, maculopapular exanthem erupt on top of
erythematous flush.
21. Hemorrhagic manifestations include petechiae and mucous
membrane bleed.
Early febrile phase shows positive torniquet test.
RECOVERY PHASE: (CONVALSCENCE)
Termination of illness is swift, marked by a distinctive
acral exanthem.
Bright red confluent petechial rash along lateral
margins of soles and palms.
In some areas there are small round areas of clear skin
giving it a name of annular petechial rash.(white isles in
sea of red).
22. • IT IS ALSO KNOWN AS TOURNIQUET TEST.
• Part of new WHO case definition of dengue.
• Marker of capillary fragility.
• Steps:
• Take patients BP.
• Inflate the cuff to a point midway between SBP & DBP and maintai
• Reduce and wait 2min.
• Count petechiae below antecubital fossa.
• A POSITIVE TEST IS 20 PETECHIAE PER 1 SQUARE INCH.
24. ROSEOLA INFANTUM(sixth disease) –
Herpes virus 6,7
rash with defervescence.
ERYTHEMA INFECTIOSUM(fifth disease):
Parvovirus p19
Slap cheek appearance.
Maculopapular rash on extensor aspect.
IMN:
Rash appears after giving ampicillin (20% children)
CHIKUNGUNYA:
Rashes are seen on the trunks & limbs; also on
face,palms & soles.
Petechiae occur alone or in association with rash.
28. • CHICKEN POX:
Moderate fever -- 2-3 days; maculopapular rash
MORPHOLOGY:
After appears which later turns into vesicles filled with
clear fluid which becomes cloudy & umblicated (dew drops
on rose petals)
Intensely pruritic.
DISTRIBUTION:
predominant on flexor surfaces.
• Palms& soles are seldom affected.
Pleomorphic.
29.
30. HERPES ZOSTER:
Uncommon in children. Reactivation of latent VZV.
MORPHOLOGY:
clustered vesicular rash on erythematous base.
DISTRIBUTION: 1 OR 2 dermatomes.
31.
32. • HAND FOOT MOUTH DISEASE.
• Caused by viruses of genus enterovirus.
• Rash is seen on palms and soles; less commonly on
flexors.
35. • HSP:
• Common vasculitic disorder of childhood.
• Non-thrombocytopenic palpable purpura.
• Rash over the extensor aspects of lower extremities and
buttocks.
• MENINGOCOCCEMIA:
• Rashes starts as scattering of small pin prick marks.(reddish or
brown).
• Later large patches of purple or red blotches or blood blisters.
• Will not blanch with pressure.
39. This sign is present when slight rubbing of the skin results
in exfoliation of the skin in its outermost layer.
Formation of new blisters in slght pressure (Direct Nikolsky)
Shearing of skin due to rubbing (Indirect Nikolsky )
40. • TOXIC EPIDERMAL NECROLYSIS:
• Immune complex mediated.
• Skin lesions begin as hot,tender,erythematous,morbilliform or
descrete macules that rapidly coalesce & become patches of
loose skin.