Bronchiectasis is a chronic, irreversible dilation of the bronchi and bronchioles. Or •Bronchiectasis is characterized by permanent, abnormal dilation of one or more large bronchBronchiectasis.
Bronchiectasis is a chronic, irreversible dilation of the bronchi and bronchioles. Or •Bronchiectasis is characterized by permanent, abnormal dilation of one or more large bronchBronchiectasis.
Lung abscess is a type of liquefactive necrosis of the lung tissue and formation of cavities (more than 2 cm) containing necrotic debris or fluid caused by microbial infection.
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.
Bronchiectasis
A condition characterized by chronic permanent dilation & destruction of bronchi due to destructive changes in the elastic and muscular layers of bronchial walls.
The common thread in the pathogenesis of bronchiectasis consists of difficulty clearing secretions & recurrent infections with a “vicious circle” of infection and inflammation resulting in airway injury and remodelling.
PLEASE REFER TO REFERENCE TEXTBOOKS FOR CLARITY.
Hemiparesis is unilateral paresis, that is, weakness of the entire left or right side of the body (hemi- means "half"). Hemiplegia is, in its most severe form, complete paralysis of half of the body. Hemiparesis and hemiplegia can be caused by different medical conditions, including congenital causes, trauma, tumors, or stroke
Hypenension: Commonest cause of intracerebral haemorrhage.
Rupture of an intracranial aneurysm, angioma or A-V malformation: commonest cause of subarachnoid haemorrhage.
Haemorrhagic blood diseases: purpura, haemophilia.
Anticoagulants.
Trauma to the head: commonest of subdural haematoma.
II. Infective: ;
Encephalitis
Meningitis – Brain abscess.
III. Neoplastic: e.g. Meningioma.
IV. Demyelination: multiple sclerosis may present with hemiplegia.
V. Traumatic: e.g. Cerebral laceration and subdural haematoma.
VI. Hysterical: patient suffering from paralysis in the absence of organic lesion.
Lung abscess is a type of liquefactive necrosis of the lung tissue and formation of cavities (more than 2 cm) containing necrotic debris or fluid caused by microbial infection.
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.
Bronchiectasis
A condition characterized by chronic permanent dilation & destruction of bronchi due to destructive changes in the elastic and muscular layers of bronchial walls.
The common thread in the pathogenesis of bronchiectasis consists of difficulty clearing secretions & recurrent infections with a “vicious circle” of infection and inflammation resulting in airway injury and remodelling.
PLEASE REFER TO REFERENCE TEXTBOOKS FOR CLARITY.
Hemiparesis is unilateral paresis, that is, weakness of the entire left or right side of the body (hemi- means "half"). Hemiplegia is, in its most severe form, complete paralysis of half of the body. Hemiparesis and hemiplegia can be caused by different medical conditions, including congenital causes, trauma, tumors, or stroke
Hypenension: Commonest cause of intracerebral haemorrhage.
Rupture of an intracranial aneurysm, angioma or A-V malformation: commonest cause of subarachnoid haemorrhage.
Haemorrhagic blood diseases: purpura, haemophilia.
Anticoagulants.
Trauma to the head: commonest of subdural haematoma.
II. Infective: ;
Encephalitis
Meningitis – Brain abscess.
III. Neoplastic: e.g. Meningioma.
IV. Demyelination: multiple sclerosis may present with hemiplegia.
V. Traumatic: e.g. Cerebral laceration and subdural haematoma.
VI. Hysterical: patient suffering from paralysis in the absence of organic lesion.
Now a days TBM is super most disease in Indian children.
Tuberculous meningitis (TBM) is difficult to diagnose, and a high index of suspicion is needed to make an early diagnosis.
Neonatal problems
Neonatal jaundice
Pathophysiology and epidemiology
Visible at >85 μmol/L of bilirubin (BR). The BR is usually unconjugated, which is fat-soluble thus can enter tissue (and cross the blood-brain barrier), causing damage.
Common: affects 60% of term babies, and 80% of preterm.
Usually physiological: onset after the first 24h, with BR not exceeding 200 μmol/L. Due to liver immaturity and replacement of fetal Hb.
Early jaundice (onset <24h)
Causes:
Hemolytic disease: Rh incompatibility, ABO incompatibility (usually mild), G6PD deficiency, or spherocytosis. Make sure to ask about blood group and family history of hemolytic anaemia.
Congenital infection: Group B Strep, TORCH (Toxoplasmosis, Rubella, CMV, HSV).
this is presentation done for a morning session of dhaka medical college hospital, paediatrics department by dr. tasnuba atique and nur-e-jannat naima. the information was collected from various textbooks and arranged in an easy-to-read manner to conduct a presentation of 45 minutes.
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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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
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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
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.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
4. Pathogenesis
Tuberculous meningitis is always a secondary lesion
with primary usually in the lungs
Meningitis results from formation of a metastatic
caseous lesion in the cerebral cortex, meninges and
choroid plexus during the process of initial occult
lympho-hematogenous spread of primary infection.
5. Then Caseous foci form on the surface of brain (
Rich’s foci). They increase in the size and discharge
bacilli in CSF.
A thick , gelatinous exudate may infiltrate the
cortical or meningeal blood vessel , producing
inflammation, obstruction , or infarction .
Most commonly involved site is the brain stem
causing frequent involvement of 3rd , 6th and 7th
cranial nerves.
Basal cisterns are obstructed causing
communicating hydrocephalus. Accompanying
inflammation may cause cerebral edema.
6. Clinical Features:
In a classical case, onset is insidious but may be
fulminant in certain cases.
A more rapid progression of the disease may occur
in young infants in whom symptoms develop for only
several days before the onset of acute hydrocephalus
brain infarction , or seizures.
Classically , the onset is gradual (over several weeks).
The clinical manifestations may be divided into 3
stages and each stage last approximately 1 week.
7. Stage 1(Prodromal stage):
Lasts for 1-2 weeks
The child becomes listless or irritable ,loss interest in
the play ,has fever, anorexia,vomiting , constipation
and weight loss.
May complain of headaches and drowsiness.
No focal neurologic signs.
May be loss of or stagnation of the developmental
milestones.
8. Stage 2:
Onset is more abrupt.
Signs of meningeal irritation with increased CSF pressure.
Positive Kerning and Brudziniski signs with increased
tendon jerks and extensor plantar responses.
There may be generalized hypertonia.
Headache is cardinal symptom in older children with
constant Fever.
Vomiting and constipation may become severe.
Abducent nerve paralysis is common . Oculomotor lesion
causes internal squint . Facial palsy is also common.
May have disorientation , and speech and movement
disorders.
9. In the infants anterior fontanelle may be bulging and
sutures become separated with “crackpot” sign.
In older children papilledema develops. Head
circumference starts enlarging rapidly.
Choroid tubercles may be seen on fundoscopy.
Child is semiconscious and develops convulsions.
10. Stage 3:
Rapidly become comatose .
High grade irregular fever and convulsions.
There may be hemiplegia or paraplegia.
Extreme neck stiffness opisthotonus develops with the
decerebrate rigidity and pupil become dilated and
fixed.
Deterioration of vital signs especially hypertension.
Death may occur if treatment is started late during
this stage.
11. DIAGONSIS
1. Suspicion:
• A high index of clinical suspicion is important where
tuberculosis contact is positive.
• Tuberculin skin test is negative is 50% of the patients.
2. Blood:
• ESR is high
• Total and differential leukocyte count reveals normal count
with predominant lymphocytosis.
3. X-Rays Chest:
• Chest X-rays may be normal in 20-50% of the cases.
• Usually there is some evidence of tuberculosis in the lungs
, hilar adenopathy , and patch of pneumonia or miliary
tuberculosis
12. 4. LUMBER PUNCTURE (CSF examination):
• CSF pressure increased.
• Color is clear, hazy or straw colored.
• Cobweb is formed when left for over 12 hours.
• Protein is markedly raised( 400-5,000mg/dl) because of
hydrocephalus and spinal block.
• Glucose is decreased (below 40 mg/dl).
• Pleocytosis with predominant lymphocytes (10-
500/mm3).
• Smear and culture: Ziehl- Nelson stain may reveal
acid-fast bacilli .CSF culture confirms the diagnosis.
• Mycodot : Antigen detection by polymerase chain reaction.
13. 5. GASTRIC LAVAGE OR SPUTUM EXAMINATION for
tubercle bacilli.
6. LYMPH NODE BIOPSY in certain cases to confirm the
diagnosis.
7. FUNDOSCOPY (choroid tubercles , papilledema or optic
atrophy)
8. CT SCAN with contrast may help establish a diagnosis of
tuberculous meningitis. It also aids in evaluating the success of
therapy. There may be:
Brain stem meningitis (Brain Enhancement ).
Hydrocephalus,
Focal infarcts
Tuberculomas
(CT scan may be normal during the early stages of the TBM).
14. MANAGEMENT:
Specific Treatment:
Start treatment with 4 anti- tuberculous drugs and treatment should
be continued for 12 months.
1. Isoniazid (INH):
• It is the drug of first choice.
• It is rapidly absorbed and penetrates into the CSF.
• Isoniazid and rifampicin and highly bactericidal for
M.tuberculosis.
• Dose is 10-15 mg/kg/day.
• Main side effect are hepatotoxicity , peripheral
neuropathy ,optic neuritis, hypersensitivity and
fever. Neuritis is due to competitive inhibition of
pyridoxine.
• Transient elevation of amino-transferases may be seen
at 6-12 weeks, but therapy should continue.
15. 2. Rifampicin:
• It is also a first line drug, well absorbed and
penetrates CSF well.
• Dose is 10-20mg/kg/day one half an hour before
breakfast
• It causes orange discoloration of the urine and
tears , GIT disturbance and hepato-toxicity.
• Combined use of INH and rifampicin increases the
risk of hepatotoxicity , which can be decreases by
lowering the dose of INH (10 mg/kg/day)
16. 3. Pyrazinamide
• It is bactericidal in acid medium and enters CSF readily.
• It is used as a third drugs for 2-3 months initially
• Dose is 30 mg/kg/day.
• Main side effect are arthralgia ,arthritis ,hyper-uricemia
(gout)
4. Streptomycin:
• It is bactericidal for extracellular tubercle bacilli, but its
penetration into macrophages is poor.
• Its penetrance into CFS through inflamed meninges is
excellent but do not cross the un-inflamed meninges.
• Dose 20-40 mg/kg/day given 1/M for 2 months.
• Side effect are ototoxicity (vestibular or hearing loss)
nephrotoxicity and may cause hypersensitivity reactions.
17. 5. Ethambutol:
• It is not recommended below 6 years of age.
• Dose 15-25 mg/kg once daily.
• Side effects are Optic neuritis ,hypersensitivity and
GIT upsets.
18. GENERAL MEASURES:
1. Corticosteroids:
• Decrease mortality rate and long term neurologic
sequelae.
• Reduce vasculitis ,inflammation , and intracranial
pressure.
• Dose of prednisolone is 1-2mg/kg/day for 6-8 weeks.
• Help to reduce cerebral edema and prevents
formation of adhesions .
2. Careful record of vital signs
19. 3. Daily monitoring of complications:
Main complications are to be monitored
• Raised intracranial pressure
• Drugs toxicity, etc.
4. Phenobarbitone:
Dose 5 mg/kg/day to control convulsions.
5. Antipyretics:
Paracetamol(10—15mg/kg/dose 4-6 hourly) and fresh water
sponging to control temperature.
6. Pyridoxine:
1 mg/kg/day daily to prevent polyneuritis.
20. 7. Feeding :
NG tubes feeding according to requirement .
Ideally 100 calories /kg/day are given . Iron and
multivitamins can be added too.
8. Bed Sores :
Change posture every two hours.
9. Care of comatose Patient.
10. Care of bowel and bladder .
11. Screening:
Important to screen the family members for tuberculosis
and treat infected persons.
22. PROGNOSIS:
It depends upon two factors:
1. Age of patient
2. Stage of disease at which treatment started.
Without treatment it is fatal.
In stage1, 100% cure rate is expected.
Even with optimal therapy mortality ranges from 30-50%
and incidence of neurologic sequelae is 75-80%
especially in stage 3. There may be blindness, deafness
, paraplegia, mental retardation and diabetes insipidus.
Infants and young children have poor prognosis as
compared to older children