Is a condition seen in some cases of AIDS or immunosuppression, in which the immune system begins to recover, but then responds to a previously acquired opportunistic infection with an overwhelming inflammatory response that paradoxically makes the symptoms of infection worse.
Is a condition seen in some cases of AIDS or immunosuppression, in which the immune system begins to recover, but then responds to a previously acquired opportunistic infection with an overwhelming inflammatory response that paradoxically makes the symptoms of infection worse.
This ppt discusses pharmacological actions, toxic effects and clinical applications of corticosteroids. It also mentions precations to be taken while using steroids
This slide is based upon prokinetic agents with detailed descriptions of their dosage to be taken with their respective usage in conditions and effects to be careful. I hope you will get the best of your knowledge from the respective material.
Hello Guys,
This presentation consists of the updated guidelines under National tuberculosis elimination programme of India (MOHFW). The presentation includes case definitions and diagnostic algorithms for Pulmonary, Extrapulmonary and Drug resistant TB(MDR/ XDR TB) and the tratment protocols in pediatric cases.
Hope you find it useful.
an overall overview in corticosteroids and its application in oral and maxillofacial diagnostic medicine and pathology drawing to the conclusions of the limitations and drawbacks of these medicines. i have also included the precautions to be taken in dental therapeutic procedures fo
This ppt discusses pharmacological actions, toxic effects and clinical applications of corticosteroids. It also mentions precations to be taken while using steroids
This slide is based upon prokinetic agents with detailed descriptions of their dosage to be taken with their respective usage in conditions and effects to be careful. I hope you will get the best of your knowledge from the respective material.
Hello Guys,
This presentation consists of the updated guidelines under National tuberculosis elimination programme of India (MOHFW). The presentation includes case definitions and diagnostic algorithms for Pulmonary, Extrapulmonary and Drug resistant TB(MDR/ XDR TB) and the tratment protocols in pediatric cases.
Hope you find it useful.
an overall overview in corticosteroids and its application in oral and maxillofacial diagnostic medicine and pathology drawing to the conclusions of the limitations and drawbacks of these medicines. i have also included the precautions to be taken in dental therapeutic procedures fo
National Tb pragramme, Has been in operation since 1962
Inadequacies that led to RNTCP :
Treatment success rates were unacceptably low.
There is no unique diagnostic method.
No Treatment Protocol.
Only 30% is diagnosed, so death and default rates remained high.
In 1993 to overcome the drawbacks mentioned, the NTP was revitalized and RNTCP was formulated.
Implemented in a phased manner, by 2000 it covered the whole country.
Objectives:
Achievement of at least 85 percent cure rates of infectious cases of TB.
Augmentation of case finding activities through quality sputum microscopy to detect atleast 70 percent of estimated cases.
1. Intensified active case finding
2. Diagnostic Criteria Changes :
Changes in few definitions like Defaulters → Loss to follow up , Relapse Tb → Recurrent TB.
In Adults – CBNAAT/ True NAAT is done in all cases of TB ( earlier CBNAAT was performed only for high risk cases )
In Paediatric age group – Chest X-ray and TST to be done first.
3. Treatment Criteria Changes :
Regimens with injectable agents are no longer recommended. Currently, for any case of TB only All Oral regimens are initiated
For Drug Sensitive TB 2months of HRZE and 4 months of HRE
For INH resistant TB – RZE + Levofloxacin for 6 months
In All oral MDR Rx regimen : only continuous phase for 18 months
✓ BEDAQUILINE or DELAMANID × 6 months
✓ LEVOFLOXACIN , LINEZOLID , CLOFAZAMINE , CYCLOSERINE × 18 months
Isoniazid Preventive therapy is given for all contact.
Decentralized Tuberculosis unit and DMC (Designated microscopy
centre) and Peripheral Health Institute at the door steps of the patients.
SMEAR MICROSCOPY FOR ACID FAST BACILLI
RAPID DIAGNOSTIC MOLECULAR TESTING
RADIOGRAPHY where available
TUBERCULIN SKIN TEST
CULTURE
S.No CBNAAT TruNAAT
1 PCR based PCR based
2 Cartridge based Chip based
3 AC environment needed No need
4 Cartridge to be stored in cold atmosphere No need
5 Continuous power supply needed Battery operated
6 Less manual work Semi automatic (Technician oriented )
7 Detects MTB as well as Rif resistance simultaneously Need separate chips for MTB and Rif resistance detection
8 Cross contamination unlikely Cross contamination possible
9 TAT : 112 min TAT : 60 min for MTB
60 min for Rif resistance
10 Intermediate level labaratories Point of care level
MTB not Detected
MTB detected, High/medium/low/very low, rifampicin resistance detected
MTB detected, High/medium/low/very low , rifampicin resistance not detected
MTB detected, High/medium/low/very low , rifampicin resistance indeterminate, Repeat the test in new sample.
Invalid result (Retest in fresh specimen)
Error (Repeat the test in same sample)
Clinical evaluation Laboratory based evaluation
History and physical examination Random blood sugar (RBS)
Height HIV testing following counselling
Weight Complete blood count (Hb, TLC, DLC, platelet count)
Psychiatric evaluation if required Liver function tests(including serum proteins)
TSH levels
Urine examination –
Recent guidelines in the treatment of tuberculosisSHOEBULHAQUE1
The treatment of tuberculosis (TB) typically involves a combination of antimicrobial medications to effectively combat the bacteria causing the infection, primarily Mycobacterium tuberculosis. The standard treatment regimen for drug-susceptible TB usually consists of a combination of four first-line drugs: isoniazid, rifampicin, ethambutol, and pyrazinamide.
Nowadays, we are using some other regimens in multiple drug resistant tuberculosis.
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clinical standards for ds tb treatment 2022 (1).pptxPathKind Labs
To diagnose and treat drug susceptible pulmonary tuberculosis is of paramount importance in our efforts to eliminate tuberculosis. This describes seven clincal standards which should be practiced to obtain optimum results
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
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
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.
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
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
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.
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.
1. Newly recommended regimens
(under RNTCP 2016) for treatment
of
Pulmonary Tuberculosis
and
Recent advances in anti-tubercular
drugs
Dr KG Bandekar
Dept of Pharmacology
2. Sub topics
• Introduction
• Current drugs and regimes
• New Regimens
• Need for newer drugs
• New targets, drugs/molecules under research
3. Introduction
• Tuberculosis is chronic granulomatous disease.
• Causative agent - Mycobacterium tuberculosis
bacterium.
• M. tuberculosis is aerobic.
• In India – 2.3 million cases.
• TB – a notifiable disease in India.
• RNTCP(Revised National Tuberculosis Control
Programme) – launched to control and treat.
5. Drugs currently used
1st line drugs .docx
2nd line drugs.docx
1st line drugs – High efficacy and low toxicity
2nd line drugs – Either low efficacy or higher
toxicity or both – are reserved drugs.
6. ADRs 1st line drugs
• Non hepatotoxic drugs – E and S
• Safe drug in Renal failure – R ( as it is secreted
in bile) – No dose adjustment in RF
• Least toxic drug – R
7. ADRs 1st line drugs
• H is metabolised by acetylation. Slow
acetylators - peripheral neuritis; fast
acetylators - hepatotoxicity
• Hepatotoxicity due to R is uncommon unless
pre existing liver disease is present and
presents as ‘hyperbilirunemia without SGPT
elevation’.
• E – optic neuritis ( low visual acuity, red/ green
colour blindness – green more than red)
8. Rifabutin and rifapentine
• Supplementary 1st line drugs
• Rifabutin is less effective against M.
tuberculosis than ‘R’.
• Rifabutin is used in HIV patients who are on
protease inhibitors / NNRTIs – less enzyme
induction compared to ‘R’. (Rifapentine is not
used)
• No dose adjustment in liver disease
14. PAS
• Related to sulfonamides.
• Affects folate synthesis.
• Least active drug.
• Only delays resistance.
• Causes kidney, liver, thyroid dysfunction.
15. Kanamycin and amikacin
• Injectable aminoglycosides.
• Can be used in Multi Drug Resistant -MDR
cases
16. Linezolid
• Oxazolidinone gp synthetic antibiotic.
• Inhibition of protein synthesis –unique binding
site 23 S of 50 S.
• Use in TB – off label use.
17. Bedaquiline
• Newer approved drug.
• Inhibits mycobacterial ATP synthase.
• Long half life.
• Used in MDR-TB.
• Pregnancy is a contraindication.
• Causes QT prolongation.
18. Chemotherapy
• Objective – Cure - elimination of both, fast
and slowly multiplying bacilli (including
persisters)
• Effectiveness evaluation – elimination of bacilli
from patient’s sputum.
• Correct drugs, correct dose, and for correct
length of time.
19. Rational of combination anti
tubercular drugs
• To prevent resistance.
• Resistant mycobacterial population (in
normally susceptible) -1 bacillus in 106
• Normally lesion contains > 108 bacilli.
• Hence – resistant strain readily selected if only
single drug is used.
20. Rational of combination anti
tubercular drugs contd…
• Two independently acting drugs in
combination are more effective.
• Probability of bacillus resistant to both drugs
initially – 1 in 106 X 106 = 1012 .
23. Regimens
• Long course – classical regimen - 18 months
H + 1/2 bacteriostatic drug/s
Sterilisation mainly dependent on H
• Short course chemotherapy - 6-8 months
Rapid bacteriological conversion
Low failure rates
Lower incidences of drug resistance
Intensive phase (2/3 months)+ Continuation
phase (4 – 5 months)
24. DOTS - Directly Observed Treatment
Shot course Chemotherapy
• By WHO
• Strategy to ensure cure by providing the most
effective medicine and confirming that it is
taken.
25. Current Regimen
Cat Intensive phase Continuation
phase
Duration
(months)
Remark
Cat I
New patient
(2) HRZE daily (4) HR daily 6 Optional
(2) HRZE daily (4)HR 3/week 6 If DOTS
ensured
(2) HRZE
3/week
(4) HR 3/week 6 DOTS ensured
or No HIV inf
Cat II
Previously
treated
(2) HRZES daily
+ (1) HRZE daily
(5) HRE daily 8 Low/medium
risk of MDR-TB
Empirical
(standardised)
MDR-TB
regimen –
country specific
Empirical
(Standardised)
MDR-TB
regimen –
country specific
18-24 or
Sensitivity test
is avl
High risk MDR-
TB
26. Chemotherapy of TB in pregnancy
• Except S continue all 1st line drugs
• Breast feeding mothers – full course ( breast
feeding to be continued)
• Mothers receiving H and breastfed baby – Vit
B6 supplementation daily
27. Drug regimen recommended in
RNTCP(2016)
1. Daily dose regimen
2. MDR/RR-TB cases (without additional
resistance)
3. XDR-TB
4. H resistant TB
5. BDQ containing regimen
6. Shorter MDR-TB regimen(as per WHO 2016)
28. 1. Daily dose regimen
• 2 categories
a) New
b) Previously treated
Type of TB case Regimen in
Intensive phase
(IP)
Regimen in
Continuation
phase (CP)
New (2) HRZE (4) HRE
Previously
treated
(2) HRZES + (1)
HRZE
(5) HRE
30. Drug resistance
• Multi drug resistance (MDR) – Resistance to H
and R and may be to any 1st line drug/s.
• Extensively drug resistance (XDR) – Resistance
to H,R,FQ and either aminoglycoside or Cm or
both.
31. 2. MDR/RR-TB cases (without
additional resistance)
Type of TB case Regimen
during IP
Regimen
during CP
R resistant + (H
sensitive or
unknown)
(6-9) km Lfx
Eto Cs ZEH
(18) Lfx Eto cs
E H
MDR TB (6-9) km Lfx
Eto Cs Z E
(18) Lfx Eto Cs
E
32. 3. XDR-TB
Type of TB case Regimen in IP Regimen in CP
XDR (6-12) Inj Cm,
PAS , Mfx, high
dose H, Cfz Lzd,
Amx/Clv
(18) PAS , Mfx,
high dose H,
Cfz Lzd,
Amx/Clv
33. 4. H resistant TB
Type of TB case Regimen in IP Regimen in CP
R sensitive ad
H resistant
(3-6)km Lfx R E
Z
(6) Lfx R E Z
34. 5. BDQ containing regimen
• Eligibility for BDQ regimen – Either of -
a) MDR/Rifampicin TB + res to all FQs
b) MDR/Rifampicin TB + res to all 2nd line drugs
c) XDR TB
Dose and duration
1. 0-2 week – Tab BDQ 400 mg daily + optimised
background regimen (OBR)
2. 3-24 week – Tab BDQ 200 mg 3/week + OBR
3. 25 week – to end of treatment – Continue OBR
41. SQ109
• Stage 2 clinical trial
• Bacteriocidal
• Acts by inhibiting mmpl3.(Mmpl3, an inner
membrane protein, responsible for transport
of lipids to outer membrane to synthesise
mycolic acid)
43. INH derivative LL-3835
• Incorporation of lipophilic moieties (INH
hybrids)into framework of INH can increase
permeation into bacterial cell therby
increasing anti –TB action.
• LL-3835 – INH pyrrole hybrid-in stage 2 clinical
trial.
• (Few pyrrole compounds have been shown to
have in vitro anti tubercular activity)
44. Aptamers
• Bind targets with great affinity.
• No immunogenicity.
• Mtb-Apt1 and Mtb-Apt-6 – shoed in vitro
activity.
• Binds to ?polyphosphate kinase2(PPK2) as
target. {PPK2- role in synthesis of mycolic acid}
50. 4. Mycothiol ligase (MshC)
• Mycothiol – LMW thiol that protects Mtb from
toxicity of drugs.
• Genes encoded – MshA,B,C,D.
• MshC important amongst them.
• Inhibitor – Dequalinium chloride - prevents
growth of Mtb.
51. 5. HisG
• ATP phosphoribosyl transferase (HisG).
• Histidine biosynthesis.
• Inhibitors of HisG – cidal
52. 6. ATP synthase
• 3 subunits for enzyme a,b,c.
• Inhibitors of C subunit have shown growth
inhibition.
• Inhibitor – R207910 – 20000 times more
affinity than human ATP synthase.
53. 7. Deformylase (def and fmt) and
methionine aminopeptidase)
• mRNA translocation begins with incorporation
of formylated methionine at N terminus.
• This residue is removed in 2 steps –
deformylation by deformylase followed by
hydrolysis of methionine by methionine
aminopeptidase.
• Protein synthesis.
54. B. Targeting dormant Mtb
• Dormancy – Physiological state characterised
by cessation in proliferation in in vitro and in
vivo
• Persistence – Tolerance by subpopulation of
bacteria to cidal effects of drugs.
55. 8. Isocitrate lyase (Icl)
• Icl-1 and Icl-2
• Inhibitors – growth inhibition, loss of
virulence.
• Inhibitors also act against persistent bacteria
in population.
56. 9. Proteasome complex
• Inhibition of proteasome activity increases
susceptibility of Mtb to nitrogen
intermediates which are antimicrobial
molecules secreted by macrophages.
57. 10. L,D-traspeptidase
• Interferes peptidoglycan metabolism
11 . DosR(DevR)
Hypoxia is sensed and transduced via DosR
which activates ‘dormancy regulon’ leading to
physiological adaptation.
Inhibitors of DosR affects dorancy.
58. 12. CarD
• Interacts with beta subunit of RNA polymerase
and regulates stringent response.
• Inhibting CarD – limits ability of Mtb to initiate
stringent response and to enter into
dormancy.
64. Repurposing commonly used drugs
• Valproic acid and vorinostat – Trials in HIV + TB
• Metformin – against intracellular
m.tuberculosis - in vitro
• Thalidomide and its analogue – in TB
meningitis (as immunomodulators)
65. References
• KDT
• Park PSM text book (2017 edition)
• Katzung
• Novel targets in M.tuberculosis:search for new
drugs. Gyanu Lamichhane.
• M.AlMatar et al./Biomedicine& Pharmacotherapy
91(2017) 546- 558
• UDP-GlcNAc pathway : potential target for
inhibitor dicovery against M.tuberculosis. Chitra
Rani