Gilbert’s syndrome is a common and harmless condition where people experience occasional episodes of jaundice (yellowing of the skin and whites of the eyes).
Gilbert’s syndrome is caused by a build-up of a yellow pigment,
called bilirubin, in the blood. Bilirubin is found naturally in the
blood and is formed when red blood cells break down. The body usually
removes bilirubin, but in Gilbert’s syndrome this process does not work
properly.
If you have Gilbert’s syndrome, during an episode of jaundice you may have symptoms such as:
-- stomach cramps
-- feeling very tired (fatigue)
-- problems concentrating and thinking clearly (brain fog)
-- a general sense of feeling unwell
However, around one in three people with Gilbert’s syndrome
experience no noticeable symptoms and the condition is only detected
during testing for other, unrelated conditions.
People with Gilbert’s syndrome often find that there are certain ‘triggers’ that can bring on jaundice, such as:
-- being dehydrated
-- going without food for long periods of time (fasting)
-- being ill with an unrelated infection
-- stress
-- in women, having their monthly period
The jaundice and any associated symptoms will pass without the need for treatment.
People with Gilbert’s syndrome are often concerned about
having jaundice because jaundice can often be a sign of an underlying
liver problem, such as cirrhosis (scarring of the liver) or hepatitis C.
However, it is important to stress that Gilbert’s syndrome is
harmless and has nothing to do with liver problems. People with
Gilbert’s syndrome are no more likely to develop liver disease than the
population at large.
AR inherited disorder of impaired copper excretion characterized by excessive deposition of copper in many tissues and organs, principally the liver, brain, and eye. • Discovered by Samuel Alexander kinnier Wilson. Liver fails to excrete sufficient Cu via the bile, and the ability to incorporate Cu into CP is diminished Due to loss of function mutations of the ATP7B gene on chromosome 13, which encodes a copper-transporting ATPase (ATP7B). Most common presentations are with liver disease or neuro- psychiatric disturbances. Kayser–Fleischer ring is the clinical hallmark of WD. caused by deposition of copper in Desçemet’s membrane of cornea. Penicillamine is the of choice.
Gilbert’s syndrome is a common and harmless condition where people experience occasional episodes of jaundice (yellowing of the skin and whites of the eyes).
Gilbert’s syndrome is caused by a build-up of a yellow pigment,
called bilirubin, in the blood. Bilirubin is found naturally in the
blood and is formed when red blood cells break down. The body usually
removes bilirubin, but in Gilbert’s syndrome this process does not work
properly.
If you have Gilbert’s syndrome, during an episode of jaundice you may have symptoms such as:
-- stomach cramps
-- feeling very tired (fatigue)
-- problems concentrating and thinking clearly (brain fog)
-- a general sense of feeling unwell
However, around one in three people with Gilbert’s syndrome
experience no noticeable symptoms and the condition is only detected
during testing for other, unrelated conditions.
People with Gilbert’s syndrome often find that there are certain ‘triggers’ that can bring on jaundice, such as:
-- being dehydrated
-- going without food for long periods of time (fasting)
-- being ill with an unrelated infection
-- stress
-- in women, having their monthly period
The jaundice and any associated symptoms will pass without the need for treatment.
People with Gilbert’s syndrome are often concerned about
having jaundice because jaundice can often be a sign of an underlying
liver problem, such as cirrhosis (scarring of the liver) or hepatitis C.
However, it is important to stress that Gilbert’s syndrome is
harmless and has nothing to do with liver problems. People with
Gilbert’s syndrome are no more likely to develop liver disease than the
population at large.
AR inherited disorder of impaired copper excretion characterized by excessive deposition of copper in many tissues and organs, principally the liver, brain, and eye. • Discovered by Samuel Alexander kinnier Wilson. Liver fails to excrete sufficient Cu via the bile, and the ability to incorporate Cu into CP is diminished Due to loss of function mutations of the ATP7B gene on chromosome 13, which encodes a copper-transporting ATPase (ATP7B). Most common presentations are with liver disease or neuro- psychiatric disturbances. Kayser–Fleischer ring is the clinical hallmark of WD. caused by deposition of copper in Desçemet’s membrane of cornea. Penicillamine is the of choice.
Encephalitis is a rare yet serious disease that can be life-threatening.
Encephalitis is an inflammation of the brain tissue.
The most common cause is viral infections.
In rare cases it can be caused by bacteria or even fungi.
Encephalitis is an inflammation of the brain tissue.
Primary encephalitis- It occurs when a virus directly infects the brain and spinal cord.
Secondary encephalitis- It occurs when an infection starts elsewhere in the body and then travels to your brain.
Older adults
Children under the age of 1 year
People with weak immune systems
Primary (infectious) encephalitis
Common viruses, including HSV (herpes simplex virus) and EBV (Epstein-Barr virus)
Childhood viruses, including measles and mumps
Arboviruses (spread by mosquitoes, ticks, and other insects), including Japanese encephalitis, West Nile encephalitis, and tick-borne encephalitis
Secondary encephalitis: could be caused by a complication of a viral infection.
Guillain barre syndrome - its clinical picture, presentation, investigations and treatment - management. Also images to further improve your understanding
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
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.
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
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!
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.
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.
6. What is AFP?
a clinical syndrome characterized by
Rapid onset of weakness including
(less frequently) weakness of the
muscles of respiration & swallowing
Progressing to maximum severity
within several days to weeks
7. Sudden onset of weakness or paralysis
over a period of 15 days in a patient aged
less than 15 years age
Flaccid paralysis evolving over hours or a few
days
suggests involvement of the lower motor
neuron complex
DEFINITION
8. Anterior horn cells AHC (spinal cord)
acute poliomyelitis
acute transverse myelitis
Peripheral Nerves
roots: GBS (post-infectious)
toxins: Diphteria, porphyria
N-M junction:
botulinum toxin , tick toxin
Metabolic: Periodic paralysis
Muscular: myositis (rare)
A lesion compressing the spinal cord must be ruled out
Syndromes Presenting as AFP (DD)
9.
10. Most common
Poliomyelitis
Guillain-Barre Syndrome
Transverse myelitis
Acute Flaccid Paralysis(AFP)
Differential diagnosis
11. AFP in <15yrs age child is
notify-able disease to WHO
Polio surveillance officers—all
districts
13. Poliomyelitis
Polio= gray matter
Myelitis= inflammation of the spinal cord
Most affects children < the age of 5
Global eradication in near future
Etiology
Enterovirus (RNA)
Three serotypes: 1, 2, 3
14. Clinical Classification of Poliomyelitis
Asymptomatic infection (Inapparent) (90- 95%)
Abortive poliomyelitis (5%)
Non- paralytic poliomyelitis (aseptic meningitis) (1- 4%)
Paralytic poliomyelitis (0.1-1%)
Spinal form
Bulbar form
Bulbospinal form
Encephalitic form
Poliovirus infections may follow one of several courses
15. Paralytic poliomyelitis
Prodromal period
Preparalytic period
Paralytic period
Convalescent period
Sequela period
Commonly known as Polio
Only 1/1,000 to 1/100 (0.1% to 1%) infected
individuals develop paralytic disease
16. Preparalytic period
High fever
Cutaneous hyperesthesia or paresthesia in the
extremities
Muscular pain is common
Muscles are tender even to gentle palpation
Severe headache & vomiting
Lethargy
Signs of meningeal irritation
(neck stiffness, Kerning & Brudzinski signs positive)
Paralytic poliomyelitis
17. Weakness of one or more muscle groups (spinal or
cranial)
Loose & Floppy Limbs, hypotonia-- Flaccid paralysis
Asymmetric paralysis
Paralysis is complete – fever normalizes
Weakness persists
Respiratory & vasomotor changes
Bladder & bowel dysfunction
Tendon reflexes are absent with paralysis.
Sensory defects do not occur in poliomyelitis
Paralytic poliomyelitis
Paralytic period
18. Spinal type: most common
Paralysis of extremities (muscle groups )
leg > arm
proximal > distal
Asymmetric paralysis
Paralysis of diaphragmatic & intercostal
muscles affects respiratory movement
Paralysis of abdominal muscle -- stubborn
constipation
Paralytic poliomyelitis
19. Sequela
Poliomyelitis may lead to severe asymmetrical
persistent paralysis
muscular atrophies
deformities of limbs
Paralytic poliomyelitis
20. Diagnosis
WHO recommends diagnosis of poliomyelitis be
confirmed by isolation and identification of poliovirus in
the stool, with specific identification of wild-type and
vaccine type strains
Polioviruses may be isolated from 80 to 90% of acutely
ill patients
whereas less than 20% may yield virus within 3-4 wk
after onset of paralysis
Identification of poliovirus in stool
21. Stool examination
Two samples 24 hr apart
Within 14 days of onset of paralysis
8-10 grams or thumb size
Collected in a clean wide mouth bottle –
(plastic or glass) with screw cap
Sample stored below 8°C
No dessication or leakage till received
at WHO Accredited Lab
Collection of sample
22. Laboratory Findings
Cerebrospinal fluid
aseptic menigitis
pleocytosis: 50~500×109
/L
protein: normal or slightly increase
glucose and chloride; normal
albuminocytologic dissociation
Serological Tests
Neutralizing antibodies (IgG)
Antibodies to C antigen (IgM)
Anti-D antibodies
23. Management
Isolation
Rest in bed
Neutral positioning of the limbs
Good nursing
No I.M Injection or surgery
Relief of pain and spasm of muscles
Physiotherapy
Treatment symptomatic and supportive
24. Prevention
control of source of infection:
isolation: 40 days after the onset of illness
protection of susceptible population-
vaccination :
attenuated live vaccine by
Oral -- OPV
killed virus vaccine
Injectable -- IPV
26. Guillain-Barre Syndrome
(GBS)
Post-infectious
acute, rapidly progressing
ascending
potentially fatal form of polyneuritis
involving mainly motor but sometimes also
sensory and autonomic nerves
also known as: Acute inflammatory demyelinating
polyneuropathy (AIDP)
27.
28.
29.
30.
31. Transverse Mylitis
A neurological condition
in which the spinal cord is
inflamed.
The inflammation damages nerve fibers,
and causes them to lose their myelin
coating leading to decreased electrical
conductivity in the central nervous system.
32. 2nd most common cause of symmetric AFP
Segmental dysfunction of spinal cord
without evidence of spinal cord
compression
Cause is either:
a direct viral infection
or
an autoimmune disease
Transverse Mylitis
33. Transverse Mylitis
Paralysis usually affect only Lower Limbs
(Paraplegia)
Rare above C-5→quadriplegia
Initially flaccid but gradual change to
spasticity over few weeks
Sensory loss (with sensory level on the
trunk) and
Autonomic disturbance (urinary retention
and stool incontinence) usually present
37. Botulism
It’s a toxic neuromuscular blockade
caused by Clostridium botulinum
(anaerobic gram positive)
According to the type of infection, there
are 3 types
Infant B. due to exposure to soil , honey
Food-borne B. due to ingestion improperly
home preserved foods containing the toxins
Wound B. due to wound contamination with
the organism
38. All three types of botulism result in
symmetric
descending
Flaccid paralysis of motor and
autonomic nerves
always beginning with cranial nerves
These symptoms preceded by
constipation (infant botulism)
If untreated - paralysis of respiratory →
death
Botulism
40. Pseudoparalysis
Not a true paralysis
May follow
Unrecognized trauma
Fracture
Sprain
Toxic synovitis of hip or knee
Acute osteomylitis
Careful exam show focal tenderness
Usually painful limping gait
Neurological exam → normal
42. Trauma to the back
Spinal epidural abscess
Vascular anomalies of the cord
Spinal cord tumors
Clinically difficult to differentiate from
Transverse Mylitis
CT scan/ MRI spine:
Sensitive
Can show nature of obstruction
Acute spinal cord compression
43. Prognosis & complications of AFP
According to cause
Poliomyelitis
Respiratory
death
Limb atrophy
GBS
Respiratory
autonomic crises
residual weakness
death
Acute transverse myelitis
Residual deficits --bowel and bladder
dysfunction & weakness - lower Limbs