Tuberculosis is a chronic infectious disease caused by the bacterium Mycobacterium tuberculosis. It typically affects the lungs but can also affect other parts of the body. It spreads through the air when people who are sick with TB disease of the lungs or throat cough, sneeze, speak, or sing. Diagnosis involves a combination of physical examination, chest X-ray, tuberculin skin test, blood tests, and microbiological examinations of body fluids and tissues. Treatment requires multiple antibiotics taken for a minimum of 6 months. Proper treatment is important to cure the individual and prevent further transmission.
More than 5.7 million new cases of TB (all forms, both pulmonary and extra-pulmonary) were reported to the World Health Organization (WHO) in 2013; 95% of cases were reported from developing countries
Latest figures from 20151 indicate an estimated 10.4 million people had TB, and 1.8 million people died (1.4 million HIV negative and 400 000 HIV positive).
Of further concern is that 480 000 cases of multidrug-resistant (MDR) TBa and a further 100 000 that were estimated to be rifampicin-resistant (RR) TB have occurred in the same period.
More than 5.7 million new cases of TB (all forms, both pulmonary and extra-pulmonary) were reported to the World Health Organization (WHO) in 2013; 95% of cases were reported from developing countries
Latest figures from 20151 indicate an estimated 10.4 million people had TB, and 1.8 million people died (1.4 million HIV negative and 400 000 HIV positive).
Of further concern is that 480 000 cases of multidrug-resistant (MDR) TBa and a further 100 000 that were estimated to be rifampicin-resistant (RR) TB have occurred in the same period.
Tuberculosis is a chronic, wasting, communicable disease, which made a huge comeback with the HIV pandemic, making it an opportunistic infection, and and an AID-defining infection. This presentation explores the different types of tuberculosis in terms of their locations (pulmonary and extra-pulmonary) as well as in terms of their drug susceptibility. It also addresses the approach to the management of each one of these.
Tuberculosis is an infectious disease. In this presentation shortly information has been extracted from text books of Medicine and Bangladesh National Guidelines of Tuberculosis (4th & 5th edition). here drugs, FDC and effects have been reviewed also.
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Pediatrics notes about "Tuberculosis". These notes were published in 2018.
You can download them also from
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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.
Tuberculosis is a chronic, wasting, communicable disease, which made a huge comeback with the HIV pandemic, making it an opportunistic infection, and and an AID-defining infection. This presentation explores the different types of tuberculosis in terms of their locations (pulmonary and extra-pulmonary) as well as in terms of their drug susceptibility. It also addresses the approach to the management of each one of these.
Tuberculosis is an infectious disease. In this presentation shortly information has been extracted from text books of Medicine and Bangladesh National Guidelines of Tuberculosis (4th & 5th edition). here drugs, FDC and effects have been reviewed also.
Visit...
Medishared.org
You can get..
--- Premium Layest Released Medical Books
--- MBBS & M.D Examination papers with Answer Keys
--- Important Exam Helping Documents
--- Detaile Explained MCQs
--- MCQs Online Testing
And Much more than your expectation from website.
Pediatrics notes about "Tuberculosis". These notes were published in 2018.
You can download them also from
- Telegram: https://t.me/pediatric_notes_2018
- Mediafire: http://www.mediafire.com/folder/u5u60m184t9z7/Pediatric_Notes_2018
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.
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.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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
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
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.
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
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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4. 4
ETIOLOGY
• M. tb complex (MTBC) includes other mycobacteria that
can cause TB: M. bovis, M. africanum, M. canettii, M.
microti
• M.Tuberculosis.
The tubercle bacilli are :
• An aerobic.
• Non-spore forming.
• Non-motile.
• Grow best at(37-41)ْc.
• Acid alcohol fast bacilli i,e.(is difficult to stained due to
high lipid contents of the cell wall and once stained they
resist decolorization with acid-alcohol).
• Ziehl-Neelsen staining methods for identification.
6. Global Problem
- WHO declared TB a global emergency 1993
- 9.6 million new cases/yr of which 37% are
unreported /undiagnosed.
- Leading cause of death worldwide,1.5 million
death/year.
- Co-infection with HIV in 12% of new cases
- Major problem with affordable therapy in some
countries
7. Tuberculosis
• 1882 – Robert Koch – “one seventh of all
human beings die of tuberculosis and… if one
considers only the productive middle-age
groups, tuberculosis carries away one-third
and often more of these…”
10. How Are TB Germs Spread?
• TB germs are passed through the air when a person
who is sick with TB disease coughs, sings, sneezes, or
laughs
• To become infected with TB germs, a person usually
needs to share air space with someone sick with TB
disease (e.g., live, work, or play together)
• The infectivity depends on the number of bacilli
present in droplets.
• These number is greatest in secretion from individual
with +ve culture sputum
12. Risk Factors for TB Infection
• Sharing air space with someone sick with TB
disease (e.g., live, work, or play together)
• Crowded living conditions
• Residency or travel in a country with a high
incidence of TB disease
• High risk occupations including laboratory and
health care jobs
13. Risk Factors for TB Disease
• Low socioeconomic status
• Homelessness
• Diseases, conditions or drugs that weaken the immune
system – Cancer – Transplantation – Malnutrition –
Diabetes – Alcoholism – HIV infection
• TB is the leading cause of death worldwide in HIV
infected individuals • 10% lifetime risk for developing
active TB among HIV uninfected
• Major surgical procedures may occasionally trigger
dissemination
14. How Are TB Germs NOT Spread?
• Through quick, casual contact, like passing
someone on the street
• By sharing utensils or food
• By sharing cigarettes or drinking containers
• By exchanging saliva or other body fluids
• By shaking hands
• Using public telephones
15. TB Infection vs. TB Disease
• There is a difference between TB “infection”
and TB “disease”
• TB infection: TB germs stay in your lungs, but
they do not multiply or make you sick
– You cannot pass TB germs to others
• TB disease: TB germs stay in your lungs or
move to other parts of your body, multiply,
and make you sick
– You can pass the TB germs to other people
16. Latent TB vs. Active TB
Latent TB (LTBI) (Goal = prevent future active disease)
= TB Infection
= No Disease
= NOT SICK
= NOT INFECTIOUS
Active TB (Goal = treat to cure, prevent transmission)
= TB Infection which has
progressed to TB Disease
= SICK (usually)
= INFECTIOUS if PULMONARY (usually)
= NOT INFECTIOUS if not PULMONARY (usually)
19. Primary Tuberculosis
- Primary complex = lesion + draining gland
- usually asymptomatic (75%)or have flu-like
symptoms along with fever and chest pain
• Around 3 weeks after infection, they become PPD+
(skin test)
• For most, the lesions eventually heal with fibrosis and
calcification
• Dormant lesions that still contain bugs may reactivate
to yield secondary TB
20. 20
Primary pulmonary tuberculosis:
• Usually asymptomatic.
• Non productive cough ,mild dyspnea ,Weakness or fatigue
,loss of appetite and difficulty gaining wt ,fever with night
sweats , anorexia with decreased activity.
• Diagnosis by +ve Mantoux test.
• Usually have a normal chest x-ray.
• Sometimes after 6 wks pt. develop Hypersenesitivity
manifestations which include:
1. Erythema nodosum.
2. phlyctenular keratoconjuctivitis.
3. fever & malaise.
4. pleural effusion.
• haemoptysis is rare .
21. Progressive Primary TB
• Some individuals (5-15%) don’t contain the primary
infection and develop a progressive disease that
resembles a necrotizing bacterial pneumonia
• This presents with fever, productive cough, and
chest pain
• Coughing aerosolizes secretions and distributes
them throughout the lung
• There are expanding areas of caseating necrosis
with irregular cavity formation along with erosion
of blood vessels resulting in hemoptysis
• Lesions will usually heal by fibrosis with adequate
treatment
• may have consolidation , cavitations and
lymphadenopathy in the chest -x ray
22. Post primary pulmonary tuberculoses
- Local spread – Pneumonia
- Haematogenous spread – Milliary
- Spread to bones and joints
- Spread to kidneys
- Reactivation
- Exogenous re-infection
23. • The lesions typically localize to the apex of the upper
lobes
• There is rapid tissue response (Th1) because of
previous sensitization
• Cavity formation is very likely
• Symptoms include low grade fever, night sweats, and
weight loss
• Without therapy, miliary TB may develop
24. Milliary Tuberculosis
- Uncontrolled haematogenous dissemination
- Progressive primary or reactivation
- Requires impaired immunity thus 50% in infants, elderly
and HIV+
- Clinical course variable; fumlinant to subacute
- Non specific presentation; failure to thrive ,night sweats,
pyrexia, ARDS
- Difficult to diagnose, 20% post mortem
- Hepatomegaly , ascites, deranged liver function
- Meningeal disease in 15 – 20%
25. • Multiorgan failure, septic shock, and
respiratory distress, followed by death, may
occur
34. Other Sites
- Lymph node
- Skin
- Meninges
- Renal tract
- Pericardial
-Hepatic and GI
-Bone
-Reproductive system
-Eye
35. Common Symptoms of TB Disease
• Cough (2-3 weeks or more)
• Coughing up blood
• Chest pains
• Fever
• Night sweats
• Feeling weak and tired
• Losing weight without trying
• Decreased or no appetite
• If you have TB outside the lungs, you may have
other symptoms
38. Diagnosis
Non-bacteriological
• screen HIV status
• Symptoms of disease
• History of TB exposure, infection, or disease
• Past TB treatment
• Demographic risk factors for TB
• Other medical conditions that increase risk for TB disease
(diabetes , immunosuppresion ,ESRD ,HIV , alcoholism
,silicosis )….
39.
40. 40
Investigations:
•Full Blood Count:
•Hb anemia.
•TWBC & Differential leukocytosis
lymphocytosis.
•ESR +++ >100 mm/hr.
•PBP Type of anemia.
•Chest x-ray severity of the disease. (usually
normal in primary T.B).
41. 41
*These chest X-rays show advanced pulmonary
tuberculosis. There are multiple light areas (opacities) of
varying size that run together (coalesce). Arrows indicate
the location of cavities within these light areas. The X-ray
on the left clearly shows that the opacities are located in
the upper area of the lungs toward the back. The
appearance is typical for chronic pulmonary tuberculosis.
43. 43
Mantoux test:
•An intradermal injection.
•Usually in the volar surface of the
forearm.
stabilized purified tuberculus
Antigen.(PPD).
•0.1ml volume slowly injected.
•Is the standard for screening high-risk
populations and for diagnosis in all ill
Pt. or contacts.
44.
45.
46.
47. 47
•10 mm induration reaction after 3 days
traditionally indicated infection.
• 5-10 mm induration indicates infection in a
high-risk populations(e.g , strong clinical
suspicion of TB , close contacts & HIV).
• 15 mm induration may be positive for low-
risk Pts.
48. 48
•Microscopic examination of sputum smears
•Sputum smear:
•defined as +ve < if at least 5 AFB are seen in 100 oil immersion fields of
the smear.
• sputum specimens must be collected and examined in 2-3 consecutive
days.
•Smear +ve pulm TB is confirmed when there are at least 2 AFB+ve
smear results or when one sputum specimen is +ve + radiographic
abnormalities consistent with active pulm TB.
sputum culture:
It is a complex and sophisticated tool which takes several weeks to
yeiled results (6 wks).
50. 50
TB suspect
Sputum examination
2 samples +ve or one positive
treat as + ve
2samples -ve
Give
antibiotics
No
improvment
Repeat sputum
At least 1+ve
2 -ve
Do other inv.
diagnostic
Treat as -ve
No TB
No TB
improved
51. 51
•Histo-pathological examination
Biopsies can play a role in the
confirmation of the diagnosis of extra
pulmonary TB , such as Tuberculus
lymphadenitis
Others
Automated test - Radiometric culture C14
PCR and other nucleic acid amplification
tests
Nucleic acid probes for various
mycobacteria
52.
53.
54. •
AIMS OF TREATMENT
1. To cure the Pt. of TB.
2. To prevent death from active TB.
3. To prevent complications.
4. To prevent relapse of TB.
5. To decrease transmission to others.
6. To prevent drug-resistance.
54
55. Notification
- TB is a notifiable disease
- Contact tracing
-Who was the source?
- Has the current patient been a source?
- Outcomes
- Not infected………….discharge
- Seroconversion but no clinical disease ……..chemo-
prophylaxis
- Active disease………..treatment
56. 56
*The requirements for adequate
chemotherapy are:
1. An appropriate combination of at least three to four drugs.
2. Prescribed in the correct dosage.
3. Taken regularly by the Pt.
4. For a sufficient period of time.
*The Pt. should be classified according to the following
criteria:
• Site of disease(pulm or extra-pulm).
• Severity of disease.
• bacteriological status(assessed by sputum microscopy).
• Hx of anti-TB treatment.
57. 57
Notes:
• Don’t start TB treatment until a firm diagnosis has
been made.
• Once diagnosis is made , and before beginning
treatment , every Pt. must be questioned carefully
as to whether or not they have ever taken anti- TB
drug before.
• Measuring baseline liver enzyme levels before the
initiation of isoniazid therapy is recommended only
in patients with a condition that puts them at risk
for hepatotoxicity, such as pregnancy or
postpartum status, human immunodeficiency virus
infection, alcoholism or chronic hepatitis.
58. 58
Antituberculus drugs:
*Rifampicin:
Is bacteriocidal ,excreted in bile but some times dose Not appear in
urine.
It found in form of tabs, capsules(300,150 mg)
Dosage:
10 mg/kg (<50kg ____ 450mg)
(>50kg ____ 600mg)
Adverse effect:
Hepatitis, hypersensetivity reactions, induction of Liver enzymes
Risk group of jaundice:
elderly women, alcoholic, pt with history of liver or Billiary disease.
59. 59
*Isoniazid:
Dose:
5mg/kg in chemotherapy
12mg/kg in miliary
Adverse effect:
Hepatits, hypersensetivity
*Pyrazinamide:
Given oraly, found in form of tabs 500mg, it execreted
By billiary system.
Dosage:
35mg/kg (<50kg ____ 1,5g)
(50-74 ___ 2g)
(>75kg ____ 2,5g)
Advese effect:
Arthralgia, hepatitis
.
60. 60
*Streptomycin:
Given in I.M inj, it excreted by glomerular filtration.
Dosage:
20mg/kg (<50kg _____ 750mg)
(>50kg _____ 1g)
(750mg given if pt >40years old)
Adverse effect:
Affect the 8th C.N, the vestibular effect is more than the
Auditary effect.
Pt presented with: unsteadiness of gait & nystagmus.
it’s ototoxic to fetus.
61. 61
*Ethambutol:
Given orally, excreted in the urine.
Dosage:
15mg/kg
Adverse effect:
Retrobulbar neuritis, pt presented with blurred vesion,
Disturbance of red.green vision.
(Best to be avoided in young children)
63. 63
DIRECTLY OBSERVED TREATMENT , SHORT
COURSE
•
Is in practice a public health programme , implemented
by the general health services , which when applied
widely and continuously can avert the suffering , death
and disability from TB.
•
It means that a TB Pt. who is eligible for short course treatment
has to be given his drugs under the direct supervision of a health
worker whenever taking a combination of medication which
include rifampicin.
64. 64
*Each of the standardised chemotherapeutic regimens for the smear +ve cases consist of 2
phses:
.1
The initial intensive phase:
• For 2 months new case.
• For 3 months re-treatment cases
*Aim: To reduce rapidly and if possible eliminate the actively multiplying mycobacteria
without allowing the development of acquired resistance to the applied drugs .
This is a vital stage of the treatment and it should be absolutely certain that the Pt.
completes it correctly.
2.The continuation phase:
•
2-3 drugs for 5 -6 months (Refina).
*Regimen
Pulmonary 6 , 8 moths
Extrapulm meningitis,miliary , bone/jont dis12 mo.
65. 65
Advantages of combinedtherapy:
-
INH is effective against rapidly metabolized bacilli.
-
pyrazinamide is effective in low PH & in prsistant
Bacilli (dormant).
-Rifampicicn is active against sporadically active bacilli.
There for combined therapy will attack the bacilli in all
Stages & will prevent the emergance of resistance to one
Drug.
66. • Follow-up of Treatment
1. History.
2. Examination.
3. Investigation
66
68. 68
Complications of TB
•Haemoptysis.
•Pleural effusion.
•Spontaneous pneumothorax.
•Bronchiactisis
•Fibrosis.
•According to the site e.g;
•TB spine paraplegia.
•Constrictive pericarditis.
•Death.
69. 69
Prevention
•BCG vaccination.
•Health education.
•Good ventilation & reduce crowding.
•Keep hospitalized Pt. in a separate ward for the 1st.
2wks of T.
•Good nutrition.
•Pasteurisation or sterilisation of milk.
•INH chemoprophylaxis (daily dose of 5 mg/kg for 6
mo) for high risk Pt.
70. Vaccines
–
BCG (the Calmette-Guérin bacillus), a live attenuated
vaccine derived from M. bovis, is the most established
TB vaccine. It is administered by intradermal injection
and is highly immunogenic. BCG appears to be
effective in preventing disseminated disease, including
tuberculous meningitis, in children, but its efficacy in
adults is inconsistent and new vaccines are urgently
needed. Current vaccination policies usually target
children and other high-risk individuals. BCG is very
safe with the occasional complication of local abscess
formation. It should not be administered to those who
are immunocompromised (e.g. by HIV) or pregnant.
71. HIV and TB
- Nearly 40 million HIV+ 70% in sub-Saharan Africa
- 23/24 countries with prevalence of >5%. are in
sub-Saharan Africa
- 12-13 million have HIV + TB
- Annual risk of clinical TB if HIV+ is about 10%
(compared to 10% lifetime risk if HIV-)
- Both diseases worsen each others outcome
- Presentations can be similar
(Weight loss, Lymphadenopathy, Fevers sweats)
72. Take home messages
- Primary tuberculosis is usually asymptomatic
- High degree of suspicion required to diagnose
pulmonary tuberculosis
- Radiology helpful but diagnosis ultimately rests on
cultured samples, Newer diagnostic methods are
being developed
- Mortality appreciable despite drug treatment
which is lengthy and requires skilled supervision
- Notification, contact tracing and follow up
essential
75. Sarcoidosis (Morbus Boeck)
• It is clinically well defined, systemic,
granulomatous disease of unknown origin.
•
Histology
•
Altered immune
response
75 75
76. Etiology and Pathogenesis
• Cause is unknown, although both genetic and
environmental factors suspected.
• Theory that disease develops in genetically
predetermined hosts who are exposed to
certain environmental agents that trigger an
exaggerated inflammatory immune response
leading to granuloma formation.
77. Etiology and Pathogenesis
• Hallmark is noncaseating granulomas, composed of a
central core of epithelioid histocytes and
multinucleated giant cells.
• Activated T cells and macrophages accumulate at site
of inflammation.
• Release chemoattractants and GF’s lead to cellular
proliferation and granuloma formation.
• Progressive granulomatous inflammation leads to
injury, dysfunction, and destruction of the affected
organs.
79. Clinical features
The peak incidence is in the third and fourth decade.
- Females are more affected than males
- The most common presentation is with respiratory symptoms
or abnormal X-ray (50%)
- Fatigue or weight loss (5%)
- Peripheral lymphadenopathy (5%)
- Fever (4%)
- Neurological presentations are rare
80. Clinical Presentation
• Onset of sarcoidosis in white patients is
usually asymptomatic.
• African Americans tend to present with an
earlier onset and a more aggressive and
severe clinical course.
• Chronic pulmonary sarcoidosis and the
disfiguring cutaneous lesions of lupus pernio
are also more common in African Americans.
81. Clinical Presentation
• Spontaneous remission in two-thirds of
patients within 2 years of presentation
• 10%-30% experience chronic disease causing
progressive organ damage
• Leads to death in 4% of patients, usually those
with pulmonary, cardiac, or CNS involvement
82. Systems affected by Sarcoidosis
Cardiac
30%
Palpitations, syncope, dizziness, chest pain,
arrhythmia, sudden death
Cutaneous
25%
Erythema nodosum, lupus pernio, plaques,
subcutaneous nodules, maculopapular eruption,
alopecia, hyper/hypopigmentation
Endocrine Hypo/hyperthyroidism, adrenal insufficiency
Exocrine Painless swelling of parotid gland, keratocon-
junctivis sicca
Hepatic
50-80%
Asymptomatic or abdominal pain, abnormal LFT’s,
hepatomegaly
Lymphatic Extrapulmonary lymphadenopathy, splenomegaly
Signs and symptoms
88. Clinical Presentation
• Most patients have the pulmonary
manifestations, most commonly presenting
with incidental findings on CXR.
• Interstitial disease
• Symptoms include dry cough, dyspnea, and
chest discomfort
• Unpredictable course
89. 4 Stages of Pulmonary Sarcoidosis
I Bilateral hilar lymphadenopathy
and paratracheal adenopathy
55-90%
remission
II Mediastinal adenopathy with
pulmonary parenchymal
involvements
40-70%
III Pulmonary parenchymal without
adenopathy
10-20%
IV Pulmonary fibrosis with
honeycombing
0-5%
92. Approach to Suspected Sarcoid
• History (occupational and environmental)
• PE (lungs, skin, eyes, liver, and heart)
• CXR, PFT’s and ECG
• CBC, ACE level, Calcium level
• HRCT CHEST
• BAL
• TBB: Biopsy for histological confirmation of
noncaseating granulomas and culture and/or special
staining to R/O fungal or TB (Tuberculin test:
negative)
• Ophthalmologic evaluation
97. Treatment
• Systemic corticosteroids for patients with
unresponsive ophthalmic manifestations,
cardiac, neurologic and progressive pulmonary
involvement.
• Systemic therapy for patients with
hypercalcemia.
98. Treatment
• Prednisone, 20 to 40 mg/d in divided doses or
alternate-day dosing is used for organ
involvement that is not life threatening.
• Higher dosage is used off-label for potentially
life threatening disease.
99. Treatment
Clinical improvement should be assessed after 3
months of corticosteroids.
Other immunosuppressive or anti inflammatory
if corticosteriods uncontrolling the disease or
there is side effects.
Long term adverse affects of therapy include
weight gain, mood swings, cataracts, GERD,
osteoporosis
100. Alternatives
Drug, dosage Use in sarcoidosis Comment
Methotrexate, 10-25
mg once weekly to
max of 1 g or 2 yrs
Chronic or worsening
disease, common second
line drug
Effect may take 6 mo,
Nausea, neutropenia,
and liver toxicity
Azathioprine
(Imuran), 50-200 mg
QD
Chronic or worsening
disease, advanced fibrotic
sarcoidosis
Nausea, neutropenia
Cyclophosphamide
(Cytoxan) 50-150 mg
QD or 500-2,000 mg
q 2wk IV
Refractory cases only Toxicity limits use,
Nausea, neutropenia
Requires intense
monitoring and F/U
Hydroxychloroquine
(Plaquenil), 200-400
mg QD
Cutaneous manifestations,
hypercalcemia, chronic
pulmonary fibrotic disease
Corneal deposits,
retinopathy. Ophtho
exam prior to treat-
ment and q 6 mo