Patient medication adherence, Medication adherence, Causes of medication non-adherence, Problems linked with Medication Non-adherence, Factors affecting medication adherence, Patient related factors, Social and Economic factor, Disease related factor, Health care provider related factors, Therapy related factors, pharmacist role in the medication adherence, role of pharmacist in the medication adherence, monitoring of patient medication adherence, Direct method, Indirect method
Patient medication adherence, Medication adherence, Causes of medication non-adherence, Problems linked with Medication Non-adherence, Factors affecting medication adherence, Patient related factors, Social and Economic factor, Disease related factor, Health care provider related factors, Therapy related factors, pharmacist role in the medication adherence, role of pharmacist in the medication adherence, monitoring of patient medication adherence, Direct method, Indirect method
Basic principles of chemotherapy/ AMAs covers definition, history of AMAs development, principles of AMAs, problems associated with AMAs, failure of therapy with examples.
Essential drug concept and rational use of medicinesPravin Prasad
Many medical students are unheard of the Essential Medicine List. This has been mentioned in very small sections in various textbooks that are in use in Nepal. The discussion on this topic is a must among medical and nursing students, as well as anyone related to field of Medicine
Basic principles of chemotherapy/ AMAs covers definition, history of AMAs development, principles of AMAs, problems associated with AMAs, failure of therapy with examples.
Essential drug concept and rational use of medicinesPravin Prasad
Many medical students are unheard of the Essential Medicine List. This has been mentioned in very small sections in various textbooks that are in use in Nepal. The discussion on this topic is a must among medical and nursing students, as well as anyone related to field of Medicine
Sterilization (or sterilisation) referring to any process that eliminates (removes) or kills (deactivates) all forms of life and other biological agents (such as prions, as well as viruses which some do not consider to be alive but are biological pathogens nonetheless), including transmissible agents (such as fungi, bacteria, viruses, prions, spore forms, unicellular eukaryotic organisms such as Plasmodium, etc.) present in a specified region, such as a surface, a volume of fluid, medication, or in a compound such as biological culture media
The granulation of manure into fertilizer and soil amendment products is becoming a popular option for large-scale farms learning to deal with increasing amounts of manure.
This presentation looks at the various systems available for granulating manure, as well as the advantages and disadvantages each has to offer.
Ppt about pediatric pneumonia, the definition, causes, pathological background, presentation, radiological findings and management.
It's prepared by doctor Musab MohamedAlamin Abdalla Hamid, a Sudanese doctor graduated from Omdurman Islamic University Faculty of Medicine and health siences
The bacteria that cause tuberculosis (TB) can develop resistance to the antimicrobial drugs used to cure the disease. Multidrug-resistant TB (MDR-TB) is TB that does not respond to at least isoniazid and rifampicin, the 2 most powerful anti-TB drugs.
The 2 reasons why multidrug resistance continues to emerge and spread are mismanagement of TB treatment and person-to-person transmission. Most people with TB are cured by a strictly followed, 6-month drug regimen that is provided to patients with support and supervision. Inappropriate or incorrect use of antimicrobial drugs, or use of ineffective formulations of drugs (such as use of single drugs, poor quality medicines or bad storage conditions), and premature treatment interruption can cause drug resistance, which can then be transmitted, especially in crowded settings such as prisons and hospitals.
In some countries, it is becoming increasingly difficult to treat MDR-TB. Treatment options are limited and expensive, recommended medicines are not always available, and patients experience many adverse effects from the drugs. In some cases even more severe drug-resistant TB may develop. Extensively drug-resistant TB, XDR-TB, is a form of multidrug-resistant TB with additional resistance to more anti-TB drugs that therefore responds to even fewer available medicines. It has been reported in 117 countries worldwide.
Drug resistance can be detected using special laboratory tests which test the bacteria for sensitivity to the drugs or detect resistance patterns. These tests can be molecular in type (such as Xpert MTB/RIF) or else culture-based. Molecular techniques can provide results within hours and have been successfully implemented even in low resource settings.
New WHO recommendations aim to speed up detection and improve treatment outcomes for MDR-TB through use of a novel rapid diagnostic test and a shorter, cheaper treatment regimen. At less than US$ 1000 per patient, the new treatment regimen can be completed in 9–12 months. Not only is it less expensive than current regimens, but it is also expected to improve outcomes and potentially decrease deaths due to better adherence to treatment and reduced loss to follow-up.
Solutions to control drug-resistant TB are to:
cure the TB patient the first time around
provide access to diagnosis
ensure adequate infection control in facilities where patients are treated
ensure the appropriate use of recommended second-line drugs.
In 2015, an estimated 480 000 people worldwide developed MDR-TB, and an additional 100 000 people with rifampicin-resistant TB were also newly eligible for MDR-TB treatment. India, China, and the Russian Federation accounted for 45% of the 580 000 cases. It is estimated that about 9.5% of these cases were XDR-TB.
Pulmonary tuberculosis
The bacterium Mycobacterium tuberculosis causes tuberculosis (TB), a contagious, airborne infection that destroys body tissue. Pulmonary TB occurs when M. tuberculosis primarily attacks the lungs. However, it can spread from there to other organs.
New treatment regimen is mentioned here.
Newer diagnostic methods in tuberculosis detectionApollo Hospitals
One-third of the world's population has been infected with Mycobacterium tuberculosis, with new infections occurring in about 1% of the population each year. However 90–95% of infections remain asymptomatic. Thus early diagnosis of tuberculosis and drug resistance improves survival and helps to promote contact tracing, implementation of institutional cross-infection procedures, and other public-health actions. There have been many advances and modifications to the methodology for tuberculosis diagnosis some of which are very promising. But these advances have not kept pace with the explosion of tuberculosis or the outbreak of drug resistant tuberculosis. This review describes some of the newer advances in tuberculosis diagnostics and the challenges they face.
Role of pharmacist in Community pharmacy and public health practice in India:...Yamini Shah
The knowledge, skills and expertise of a pharmacist enable them to support the public health care by promoting healthy lifestyles, preventing long-term illness and by guiding patients to better manage their medicines. A community pharmacist strengthens the public health system in a broad perspective. To improve health, patient care and medication-related outcomes through education, clinical practice and research. To ensure the safety and efficacy of medications which are prescribed by medical practitioner.
CO–PROCESSED EXCIPIENTS FOR TABLETS.pdfYamini Shah
Purpose of the present review is to provide an in depth knowledge on recent developments in excipients preparation, technology and approaches involved in their formation and development. Excipients play an important role in dosage form development. In conventional formulation of dosage forms, each excipient is used to provide its required function/performance. Presently, excipient manufacturers have focused their attention on producing a multifunctional excipients with improvement in their performance and quality of dosage form. Manipulation in the functionality of excipient is provided by the co-processing of two or more existing excipients.
ANTI-VIRAL HERBAL PHYTOCONSTITUENTS OF TULSI (OCIMUM SANCTUM) AGAINST COVID-1...Yamini Shah
A novel corona virus originated from Wuhan, China in 2019. Millions of people were affected due to this virus outbreak and quarantined for almost 2 years resulting in great loss in millions of lives in the world. This also resulted in a great impact in economy and health sector globally. After the outbreak the development of cure against SARS-CoV-2 is in full motion, less efforts have been spent on the prevention of rapidly spreading respiratory infectious agents. At present there is no effective treatment that could mitigate SARS-CoV-2. Available clinical intervention for covid-19 is only limited to support. Due to dreadful situation caused by COVID-19, there is an immediate need to discover potent therapeutic agents and targeted deliveries which can inhibit COVID-19 entry, progression and spread in human beings. Comprehensive understanding on the life cycle of SARS-CoV-2viruses and their interaction with hosts is important in the fight against these viruses. Thus, there is an urgent need for effective treatment. Intensive research on synthetic, semi synthetic, herbal, ayurvedic, siddha and unani drugs is necessary for this cause. In this review we focus on literature investigated on herbal drugs which might help in inhibition of COVID-19 via inhibition of angiotensinogen converting enzyme (ACE) and RNA dependent RNA polymerase (RdRp) through computational studies using AutoDockVina followed by their formulation development.
Ultraviolet radiation (UVR) has been shown to cause skin disorders, including sunburn and symptoms such as erythema, ageing and formation of wrinkles, pigmentation or dyspigmentation, DNA damage and ultimately photocarcinogenesis on prolonged exposure. It has been reported that sunscreens have beneficial effects in reducing the incidence of skin disorders and protect the skin against exogenous and endogenous harmful agents by absorption, scattering and by blocking phenomena. Ultraviolet (UV) rays are classified into three wavelengths UV-A, UV-B and UV-C. The generation of reactive oxygen species (ROS), which can react with DNA, proteins, and fatty acids in the skin causes oxidative damage and impairment of antioxidant system in the human body is triggered by skin exposure to sunlight and other climatic circumstances. Such injuries disrupt the skin’s regulation pathways, causing photoaging and the development of skin cancer. Active ingredient of sunscreen agents are synthetic substances which are divided into organic and inorganic filters used in the market. Synthetic agents have shown some serious side effects. Therefore, to overcome this deleterious effects natural sunscreens were found by the researchers from nature. Natural products are efficacious as sunscreens and produce healing, softening, rejuvenating, and sunscreen effects. However, the use of sunscreen has faced many challenges, including inducing photoallergic dermatitis, environment pollution, and deficiency of vitamin D production. Therefore, consumers should efficiently apply suitable herbal formulations to improve sun protection as well as to avoid the side effects of synthetic sunscreens.
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
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.
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.
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.
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.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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.
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
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
- 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
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Anti tuberculous Drugs and Patient Counseling
1. Anti Tuberculous Drugs And
Patient Counseling
Dr. Yamini D. Shah
Associate Professor
L.M.College Of Pharmacy, Ahmedabad
email id: ydslmcp@gmail.com
2. TUBERCULOSIS ?
• Chronic granulomatous disease caused
by Mycobacterium tuberculosis.
• Tuberculosis typically attacks the lungs,
but can also affect other parts of the
body.
• It is spread through the air when people
who have an active TB infection cough,
sneeze, or otherwise transmit respiratory
fluids through the air.
3. TUBERCULOSIS AND GLOBAL CHALLENGES
Tuberculosis (TB) persists as a global public health problem of serious magnitude
requiring urgent attention. Current global efforts to control TB have three distinct but
overlapping dimensions: humanitarian, public health, and economic.
4. MAGNITUDE OF THE PROBLEM
Source: WHO Geneva; WHO Report 2013: Global Tuberculosis Control; Surveillance, Planning and
Financing
Global annual incidence = 9.1 million
India annual incidence = 1.9 million
India is 17th among
22 High Burden
Countries (in terms
of TB incidence rate)
8. ESTIMATED INCIDENCE OF TB IN
INDIA*
National 75
North Zone 95
East Zone 75**
West Zone 80
South Zone 75**
North
West East
South
** For programme monitoring
purpose estimated cases in East &
South zones have been kept at the
national level of 75 and this is
within the upper limit of CI or ARTI
in these zones
9. EVOLUTION OF TB CONTROL IN INDIA
1950s-60s Important TB research at TRC and NTI
1962 National TB Programme (NTP)
1992 Programme Review
only 30% of patients diagnosed;
of these, only 30% treated successfully
1993 RNTCP pilot began
1998 RNTCP scale-up
2001 450 million population covered
2004 >80% of country covered
2006 Entire country covered by RNTCP
10. SOCIALAND ECONOMIC BURDEN OF TB IN INDIA
Estimated burden per year
• Indirect costs to society $3 billion
• Direct costs to society $300 million
• Productive work days lost due to TB illness 100 million
• Productive work days lost due to TB deaths 1.3 billion
• School drop-outs due to parental TB 300,000
• Women rejected by families due to TB 100,000
TRC, Socio-economic impact of TB on patients and family in India, Int J Tub Lung Dis 1999 3: 869-877
11. PHYSIOLOGY & STRUCTURE
Gram +ve , aerobic acid fast bacilli.
Resistant to disinfectant ,detergent.
Capable of intracellular growth.
Human are the only natural reservoir.
TUBERCULOSIS DIAGNOSIS
Clinical (presenting symptomsTB)
Diagnostic Imaging(X-Rays)
Bacteriology (smears, cultures)
Pathology of biopsy specimens
Epidemiological Factors
12.
13.
14. Medical History
• HIV status
• Symptoms of disease
• History of TB exposure, infection, or disease
• Past TB treatment and Demographic risk factors for TB
• Other medical conditions that increase risk for TB disease
15. EVALUATION TEST FOR TB
Emerging Rapid Methods
Fast Plaque TB uses phage amplification technology.
ELISA(QuantiFERON–TB)
Enzyme-Linked immuno spot (ELISPOT). ELISPOT proved highly
useful to detect active tuberculosis in Adults and children.
Microscopic Observation Drug Susceptibility Assay. ( MODS )
A new method gained importance in several reviews.
Use a tissue culture plate based assay with use of Middle Brook
7HG. Needs a inverted light microscope.
Even the drug resistance can be tested with Rifampicin, and
Isoniazid.
16. Non Specific Tests: Tuberculin Test ( Mantoux Test )
Test to be interpreted in relation to clinical evaluation.
Even the induration of 5 mm to be considered positive when tested on HIV
patients. Lacks specificity.
Specimen Collection Procedure
Obtain 3 sputum specimens for smear examination and culture
Spot, first morning, spot. Follow infection control precautions during specimen
collection
Sputum Smear Examination
Always aim for three specimens at each exam
Always store at a cool temperature and away from sunlight to preserve the
quality of specimens. 3 respiratory specimens will detect 90% of smear-positive
cases
18. Chest Radiograph
Diagnosis of PTB solely on basis of
CXR not encouraged
May have unusual appearance in HIV-
positive persons
CXR is helpful in HIV+, smear -
negative patients
Cannot confirm diagnosis of TB Arrow points to cavity in
patient's right upper lobe.
19. SEROLOGY IN TUBERCULOSIS.
• Several serological methods were evaluated.
• But never gained the acceptance of the majority of the clinicians.
• Serological tests are low sensitivity.
• Many physicians depend on serology in extra pulmonary tuberculosis.
HIV/AIDS - TUBERCULOSIS
• Consider the HIV status
• Identify the severity of Tuberculosis.
• Early use of chest radiography.
• Maximal number of sputum smear examinations.
• Sputum concentration methods to be encouraged even by smaller laboratories.
• Explore the use of Florescent Microscopy.
• All smear negative specimens should be cultured.
20. EXTRA PULMONARY TUBERCULOSIS
• Optimal specimen collection a priority,
• Molecular Methods are growing need.
• Clinicians start drug regimes on empirical basis.
• Several serological tests for antibody determinations are evaluated.
PULMONARY TB
• Productive, prolonged cough (duration of 2-3 weeks)
• Chest pain and Hemoptysis (bloody sputum)
• Signs may vary based on HIV status
ATYPICAL MYCOBACTERIUM
• Needs different drug regimes, unlike typical Mycobacterium isolates.
• Now a gowning concern in the era of AIDS.
21. FUTURE PERCEPTIONS
• It is highly essential to explore and discover rapid, simple, and
accurate tuberculosis diagnostic tools.
• A massive investment, greater scientific interest, political
commitment a top priority,
• Man power development, Human resource utilization a greater
concern.
• Microscopy and Florescent Microscopy utilization should be
immediate concern, and strengthening of treatment initiation
protocols.
• Effective methods in diagnosing smear negative patients a growing
priority.
25. Mechanism of
action
The activated form of isoniazid - forms a covalent complex with an
inh-A (Acyl carrier protein -AcpM) and KasA, a ß-ketoacyl carrier
protein synthetase, which blocks mycolic acid synthesis and kills the
cell.
Absorption Rapid and complete; rate can be slowed with food. Peak Plasma Time:
1-2 hr
Distribution All body tissues and fluids including CSF; crosses placenta; enters
breast milk Protein Bound: 10-15%
Metabolism Hepatic ( fast, slow acetylators)
Elimination From 50 to 70 percent of a dose of isoniazid is excreted in the urine
within 24 hours
Half life Fast acetylators: 0.5 to 1.6 hours. Slow acetylators: 2 to 5 hours.
Adverse effects Peripheral neuritis
Hepatitis
Psychosis
Seizures
Anorexia
GIT discomfort
Fever
ISONIAZID
26. Mechanism of
action
Rifampin binds to the β subunit of bacterial DNA–dependent RNA
polymerase and thereby inhibits RNA synthesis. Resistance results
from any one of several possible point mutations in repoB, the gene for
the β subunit of RNA polymerase.
Absorption PO well absorbed; food may delay absorption
Peak plasma time: 2-4 hr
Distribution Highly lipophilic; crosses blood-brain barrier well, with or without
inflammation
Protein bound: 80%
Metabolism Metabolized by liver; undergoes enterohepatic recirculation
Elimination Feces (60-65%) and urine (~30%) as unchanged drug
Half life 3-4 hr (prolonged in hepatic impairment); in end-stage renal disease,
1.8-11 hr
Adverse effects Hepatotoxicity
GIT disturbances
Flu-like syndrome
CNS symptoms – drowsiness, ataxia, confusion, peripheral neuropathy
Hypersensitivity reactions
Staining of secretions
RIFAMPICIN
27. Mechanism of
action
Susceptible strains release pyrazinamidase, which converts PZA to
pyrazinoic acid (POA). POA decreases the pH below that which
retards the growth of M. tuberculosis and inhibiting the fatty acid
synthesis .
Absorption well absorbed
Distribution Protein binding: 50%.widely into body tissues and fluids including
liver, lung, and CSF. Relative diffusion from blood into CSF: adequate
with or without inflammation . CSF: blood level ratio: inflamed
meninges: 100%
Metabolism hepatic
Elimination urine (4% as unchanged drug)
Half life 9-10 hr
Adverse effects Malaise, Nausea, Vomiting , Anorexia, Arthralgia, Myalgia, Fever,
Rash, Itching, Acne, Photosensitivity, Gout, Dysuria, Porphyria,
Thrombocytopenia, Hepatotoxicity, Interstitial nephritis.
Pyrazinamide
28. Mechanism of
action
Ethambutol inhibits mycobacterial arabinosyl transferases. Arabinosyl
transferases are involved in the polymerization reaction of
arabinoglycan, an essential component of the mycobacterial cell wall.
Absorption Bioavailability: ~80%
Peak Plasma Time: 2-4 hr
Distribution Widely throughout body; concentrated in kidneys, lungs, saliva, and
red blood cells CSF: blood level ratio: 0% (normal meninges); 25%
(inflamed meninges) Protein binding: 20-30%
Metabolism Hepatic (20%) to inactive metabolite
Elimination ~50% urine; ~50% feces as unchanged drug.
Half life 2.5-3.6 hr; 7-15 hr (end-stage renal disease)
Adverse effects Acute gout or hyperuricemia, Abdominal pain, Anaphylaxis,
Confusion, disorientation, Fever, Headache, LFT abnormalities,
Malaise, Nausea
Optic neuritis; symptoms may include decreased acuity, color
blindness or visual defects (usually reversible with discontinuation)
Peripheral neuritis
Rash
Ethambutol
29. Mechanism of
action
Irreversibly inhibits bacterial protein synthesis. Protein synthesis is
inhibited in at least three ways:
1. Interference with the initiation complex of peptide formation.
2. Misreading of mRNA, which causes incorporation of incorrect
aminoacids into the peptide, resulting in a nonfunctional or
toxic protein.
3. Breakup of polysomes into nonfunctional monosomes.
Absorption well absorbed; not absorbed from gut
Distribution To extracellular fluid including serum, abscesses, ascitic, pericardial,
pleural, synovial, lymphatic, & peritoneal fluids; crosses placenta;
small amounts enter breast milk
Metabolism Protein Bound: 34%
Elimination urine (90% as unchanged drug); feces, saliva, sweat, & tears (<1%)
Half life newborns: 4-10 hr; adults: 2-4.7 hr, prolonged with renal impairment
Adverse effects Hypotension, Neurotoxicity, Drowsiness, Drug fever, Skin rash,
Nausea, Vomiting, Eosinophilia , Arthralgia, Tremor, Ototoxicity
(auditory, vestibular), Nephrotoxicity.
Streptomycin
30. Mechanism of
action
Aminosalicylic acid is a folate synthesis antagonist that is active
almost exclusively against mycobacterium tuberculosis.
It is structurally similar to p-amino benzoic acid(PABA) and the
sulfonamides.
Absorption T max is about 6 h
Distribution About 50% to 60% is protein bound.
Elimination 80% is excreted in the urine with at least 50% excreted in acetylated
form.
Half life The t 1/2 of free aminosalicylic acid is 26.4 min.
Adverse effects Nausea; vomiting; diarrhea; abdominal pain, Goiter with or without
myxedema., Hypersensitivity (eg, fever, skin eruptions, leukopenia,
thrombocytopenia, hemolytic anemia, jaundice, hepatitis,
encephalopathy, Loffler syndrome, vasculitis).
PARAAMINO SALICYLIC ACID
31. Mechanism of
action
Ethionamide, like pyrazinamide, is a nicotinic acid derivative related
to isoniazid. It is thought that ethionamide undergoes intracellular
modification and acts in a similar fashion to isoniazid.
Absorption Completely absorbed following oral administration. Bioavailability
approximately 100%.
Distribution Volume of distribution 93.5 L. Approximately 30% bound to proteins.
Metabolism Metabolism: Hepatic . Metabolized to the active metabolite sulfoxide,
and several inactive metabolites. The sulfoxide metabolite has been
demonstrated to have antimicrobial activity against Mycobacterium
tuberculosis.
Elimination Less than 1% of the oral dose is excreted as ethionamide in urine.
Half life 2 to 3 hours
Adverse effects Disorder of gastrointestinal tract (50%)
Postural hypotension
Dizziness
Drowsiness
Headache
Peripheral neuropathy
Psychosis
ETHIONAMIDE
32. Mechanism of
action
It inhibits the incorporation of D- alanine into peptidoglycan
pentapeptide by inhibiting alanine racemase, which converts L-alanine
to D- alanine, and D- alanyl-D –alanine ligase (finally inhibits
mycobacterial cell wall synthesis).
Cycloserine used exclusively to treat tuberculosis caused by
mycobacterium tuberculosis resistant to first line agents
Absorption Rapidly and almost completely absorbed (70 to 90%) from the
gastrointestinal tract following oral administration.
Distribution CSF concentration equal to that in plasma
Metabolism liver
Elimination urine
Half life with normal renal function is 10 hours, and is prolonged in patients with
impaired renal function.
Adverse effects Confusion
Dizziness
Headache
Seizure
Psychosis
CYCLOSERINE
33. Mechanism of
action
Bacteriostatic- inhibits cyclopropanaton of cell wall mycolic acids.
Half life 12 hrs
Adverse effects hepatitis, exfoliative dermatitis, SJS, bone marrow depression rarely
Common: Abdominal discomfort, loose motions, rashes, mild anemia,
anorexia.
THIOACETAZONE
Mechanism of
action
Bactericidal and believed to inhibit protein synthesis by binding to 30 S
ribosomal subunit.
Elimination urine
Adverse effects Agranulocytosis, Anorexia, Diarrhea, Dyspnea, Elevated BUN,
Enterocolitis, Headache, Incr salivation, Muscle cramps, Nausea,
Nephrotoxicity, Neurotoxicity, Ototoxicity, Pruritus.
KANAMYCIN
34. Mechanism of
action
Binds to 50S ribosomal subunit of susceptible microorganisms and
blocks dissociation of peptidyl t-RNA from ribosomes, causing RNA-
dependent protein synthesis to arrest; does not affect nucleic acid
synthesis
Absorption Rapidly absorbed
Bioavailability: 37%; variable effect with food
Peak plasma time: 2.3-4 hr
Distribution Extensively distributed into skin, lungs, sputum, tonsils, and cervix;
penetrates cerebrospinal fluid (CSF) poorly
Metabolism Metabolized in liver
Elimination Immediate release, ~70 hr; extended release, 59 hr
Half life Excretion: Feces (50% as unchanged drug), urine (5-12%)
Adverse effects Diarrhea ,Nausea ,Abdominal pain ,Loose stool ,Cramping ,Vaginitis
,Dyspepsia ,Flatulence ,Vomiting ,Malaise,Agitation, Allergic reaction,
Anemia, Anorexia, Candidiasis, Chest pain, Conjunctivitis, Constipation,
Dermatitis (fungal), Dizziness, Eczema
AZITHROMYCIN
35. Mechanism of
action
Semisynthetic macrolide antibiotic that reversibly binds to P site of 50S
ribosomal subunit of susceptible organisms and may inhibit RNA-
dependent protein synthesis by stimulating dissociation of peptidyl t-
RNA from ribosomes, thereby inhibiting bacterial growth
Absorption Highly stable in presence of gastric acid (unlike erythromycin); food
delays but does not affect extent of absorption
Distribution Distributed widely into most body tissues except central nervous system
(CNS)
Protein bound: 42-50%
Metabolism Partially metabolized by CYP3A4
Metabolites: 14-OH clarithromycin (active)
Elimination Approximates normal glomerular filtration rate (GFR)
Excretion: Urine (30-55%)
Half life Immediate release, 3-7 hr; active metabolite, 5-9 hr
Adverse effects Gastrointestinal effects, general, Abnormal taste, Diarrhea, Nausea,
Vomiting, Abdominal pain, Rash, Dyspepsia, Headache, Elevated
prothrombin time,Anaphylaxis, Anxiety, Clostridium difficile colitis,
Dizziness, Dyspnea, Elevated liver function tests
CLARITHROMYCIN
36. Mechanism of
action
Irreversibly binds to 30S subunit of bacterial ribosomes; blocks
recognition step in protein synthesis; causes growth inhibition. For
gram-negative bacterial coverage of infections resistant to gentamicin
and tobramycin
Absorption IM: May be delayed in bedridden patient
Distribution 0.25-0.4 L/kg, primarily into extracellular fluid (highly hydrophilic);
penetrates blood-brain barrier when meninges inflamed; crosses
placenta.
Elimination urine (94-98%)
Half life 2-3 hr
Adverse effects Neurotoxicity, Nephrotoxicity (if trough >10 mg/L), Ototoxicity,
Hypotension, Headache, Drug fever, Rash, Nausea, Vomiting,
Eosinophilia, Tremor, Arthralgia
AMIKACIN
37. Mechanism of
action
Inhibits DNA-dependent RNA polymerase
Absorption readily, 53%
Distribution body tissues including the lungs, liver, spleen, eyes, & kidneys
Vd: 9.32 L/kg
Protein Bound: 85%
Bioavailability: absolute: HIV: 20%
Metabolism hepatic CYP3A4 to active and inactive metabolites
Elimination Urine: 10% as unchanged drug, 53% as metabolites
Feces: 10% as unchanged drug, 30% as metabolites
Half life 45 hr (range: 16-69 hr)
Adverse effects Discoloration of urine, Neutropenia, Leukopenia, Rash ,
Thrombocytopenia, Abdominal pain, Diarrhea , Eructation , Headache,
Nausea/vomiting, Anorexia, Flatulence
RIFABUTIN
38. Mechanism of
action
They inhibit bacterial DNA synthesis by inhibiting bacterial
topoisomerase II (DNA Gyrase) and topoisomerase IV.
Inhibition of DNA Gyrase prevents the relaxation of supercoiled DNA
that is required for normal transcription and replication.
Inhibition of topoisomerase IV interferes with separation of replicated
chromosomal DNA into the daughter cells during cell division.
Absorption Rapidly absorbed orally- but food delays absorption,
Distribution High tissue penetration: lungs, sputum, muscle, prostate but low in CSF
Elimination Excreted primarily in urine, urinary and biliary concentrations are 10-50
times more than plasma
Half life 3-8hrs,
Adverse effects Nausea, vomiting,diarrhoea(most common). Headache, dizziness,
insomnia, skin rash, photosensitivity. Damage growing cartilage and
cause an arthropathy. Tendinitis, tendon rupture.
FLUOROQUINOLONES
39. Determining Drug Completion
1) Within 3 months for initial phase
2) Within 6 months for 4-month continuation phase
Consider therapy interrupted if target doses not met within
specified time period
Management of Initial Phase Treatment Interruptions
• If lapse > 14 days, start from beginning
• If lapse < 14 days, continue treatment to complete total doses
warranted (if can be completed within 3 months)
40. • If received > 80% continuation-phase doses and:
1) sputum AFB smear negative on initial presentation, further
therapy not necessary
2) sputum AFB smear positive on initial presentation, continue
to complete full course
• If received < 80% continuation-phase doses and:
1) lapse < 3 months duration, continue to complete full course
(as long as all doses can be completed within 6 months)
2) lapse was 3 months or greater, then start initial phase 4-drug
regimen from the beginning
41. COMMON ADVERSE REACTIONS TO DRUG TREATMENT
Caused by Adverse Reaction Signs and Symptoms
Ethambutol Eye damage Blurred or changed vision, Changed color vision
Rifamycins
• Rifabutin
• Rifapentine
• Rifampin
Thrombocytopenia
GIT intolerance
Drug interactions
Easy bruising
Slow blood clotting
Upset stomach
Interferes with certain medications, such as birth
control pills, birth control implants, and methadone
treatment
Isoniazid,
Pyrazinamide,
or
Rifampin
Hepatitis Abdominal pain, Abnormal liver function test
Fatigue
Lack of appetite
Nausea, Vomiting
Yellowish skin or eyes, Dark urine
Isoniazid Peripheral neuropathy Tingling sensation in hands and feet
Pyrazinamide GIT intolerance
Arthralgia
Arthritis
Upset stomach, vomiting, lack of appetite
Joint aches
Gout (rare)
Streptomycin Ear damage
Kidney damage
Balance problems
Hearing loss, Ringing in the ears
Abnormal kidney function test results
42. DRUG INTERACTIONS
Relatively few drug interactions substantially change concentrations of
antituberculosis drugs
Antituberculosis drugs sometimes change concentrations of other drugs
Rifamycins can decrease serum concentrations of many drugs, (e.g., most
of the HIV-1 protease inhibitors), to subtherapeutic levels
Isoniazid increases concentrations of some drugs (e.g., phenytoin) to
toxic levels
43. RELAPSE
A patient’s cultures become and remain negative while receiving
antituberculosis drugs, but at some point after completion of therapy:
patient develops culture-positive TB disease again, or
patient experiences clinical or radiographic deterioration consistent
with active TB disease
Most relapses occur within the first 12 months after completion of
therapy
Patients with cavitation on initial chest radiograph and a positive culture at
completion of 2 months of therapy are at increased risk of relapse with
standard 6-month regimens
Patients with relapse are at increased risk for acquired drug resistance,
especially if the therapy was not directly observed
44. TREATMENT FAILURE
Defined as positive cultures after 4 months of treatment in patients
for whom medication ingestion was ensured
Single new drug should never be added to a failing regimen; it may
lead to acquired resistance to the added drug
Add at least three new drugs (e.g., fluoroquinolone, ethionamide,
and an injectable drug: SM, amikacin, kanamycin, or capreomycin)
to the existing regimen being cognizant of the possibility of drug
resistance
45. DRUG RESISTANCE
Established only by drug-susceptibility testing
Treatment of TB caused by drug-resistant organisms should be done
in close consultation with an expert
Patients not on DOT in the past or who had irregular treatment are at
risk of drug resistance
Consider the following expanded regimen for drug resistance:
INH, RIF, PZA, EMB plus three additional agents based on
probability of in vitro susceptibility (e.g., fluoroquinolone,
ethionamide, or an injectable drug: SM, amikacin, kanamycin, or
capreomycin)
46. SPECIAL TREATMENT SITUATIONS HIV/AIDS
Treatment for HIV-positive patients same as for HIV-negative
patients, except
Once-weekly INH-rifapentine in continuation phase is
contraindicated in HIV-positive patients
Twice-weekly INH-RIF or INH-rifabutin should not be used
in patients with CD4+ T-lymphocyte counts less than 100/l
Every effort should be made to use a rifamycin-based regimen for
the entire course of therapy
47. SPECIAL TREATMENT SITUATIONS (CHILDREN)*
Thrice-weekly therapy not recommended
Recommended duration of treatment is 6 months (absence of factors
associated with increased risk of relapse)
Use DOT
Treat young children (<5 years old) with three (rather than four) drugs in
initial phase (i.e., INH, RIF, and PZA)
EMB not recommended unless increased likelihood of INH resistance or
diagnosis of adult-like TB**
* Defined as persons <15 years old
**Defined as upper-lobe infiltration and cavitation associated with sputum
production
48. TREATMENT SITUATIONS EXTRAPULMONARY TB
Similar treatment regimen for pulmonary TB*
6- to 9-month regimens that include INH and RIF are effective
Corticosteroids used as adjunctive therapy for patients with TB
meningitis and pericarditis
If PZA cannot be used in the initial phase, continuation phase must
be increased to 7 months
* Except for central nervous system (CNS) TB, including meningitis; length of
therapy is 9-12 months
49. TREATMENT SITUATIONS PREGNANCY - BREASTFEEDING
Untreated TB represents greater hazard to a woman and her child than
treatment of disease
Treatment of pregnant woman with suspected TB should be started if
probability of TB is moderate to high
Initial phase treatment regimen should consist of INH, RIF, and EMB
SM should not be substituted for EMB because of possible teratogenic
effects
PZA not generally recommended for pregnant women in the United States
50. TREATMENT SITUATIONS RENAL INSUFFICIENCY-
END-STAGE RENAL DISEASE
Renal insufficiency complicates management of TB because some
antituberculosis medications are cleared by the kidneys
Dosage should not be decreased because peak serum concentrations may be
too low; smaller doses may decrease drug efficacy
Dosing interval of antituberculosis drugs should be increased
Most drugs can be given 3 times weekly after hemodialysis; for some drugs,
dose must be adjusted
51. SPECIAL TREATMENT SITUATIONS HEPATIC DISEASE
Must consider regimens with fewer hepatotoxic agents for patients with
liver disease
Recommended regimens:
1) Treatment without PZA Initial phase (2 months): INH, RIF, and
EMB Continuation phase (7 months): INH and RIF
2) Treatment without INH Initial phase (2 months): RIF, PZA, and
EMB Continuation phase (4 months): RIF, EMB, and PZA
52. REFERENCES
1. Continuing education credit will be awarded through: CDC’s Public Health
Training Network (PHTN) http://phppo.cdc.gov/phtnonline
2. MMWR at http://www.cdc.gov/mmwr
3. CDC’s Morbidity and Mortality Weekly Report:http://www.cdc.gov/mmwr
4. American Thoracic Society:
http://www.thoracic.org/adobe/statements/treattb.pdf
5. Recent Advances in Multi-Drug-Resistant Tuberculosis and RNTCP
Gagandeep Singh Grover and Jaspreet TakkarIndian J Community Med. 2008
October; 33(4): 219–223.
6. DOTS-Plus Guidelines-Central TB Division, Directorate General of Health
Services, Ministry of Health & Family Welfare, Nirman Bhavan, New Delhi
– 110011