an overview of Lupus for journalist
Lupus has a wide spectrum of manifestation. Some mild but in most cases it has a high impact of life and quality of life
Rhematoid arthritis is systemic autoimmune inflammatory disorder of unknown etiology affecting multiple organ systems. These ppt includes comprehensive management of it.
Acute rheumatic fever-definition,pathophysiology,clinical presentation and ma...onlinefreelancer1
A detailed approach to ACUTE RHEUMATIC FEVER,based on Harrison Principles of internal medicine and Braunwald Textbook of Cardiology.Useful for post graduate seminars.
A presentation on systemic sclerosis by Dr. Ashik Arefin.
Clinical aspects of systemic sclerosis. Basics of systemic sclerosis.
Treatment of systemic sclerosis
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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.
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
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.
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.
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 Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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
- 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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2. INTRODUCTION
Rheumatoid arthritis (RA) : the most common inflammatory arthritis, affecting from 0.5% to 1% of
the general population worldwide.
RA, a systemic disease, may also lead to a variety of extraarticular manifestations, including
fatigue,subcutaneous nodules, lung involvement, pericarditis, peripheral neuropathy, vasculitis, and
hematologic abnormalities
Early diagnosis of RA is pivotal to prevent damage and complications
3. CLINICAL FEATURES
The incidence of RA increases between 25 and 55 years of age, after which it plateaus until the
age of 75 and then decreases
C/O early morning joint stiffness lasting more than 1 h that eases with physical activity.
Small joints of hand and feet are the earliest involved joints
The initial pattern of joint involvement may be monoarticular, oligoarticular (≤4 joints), or
polyarticular (>5 joints), usually in a symmetric distribution.
the wrists, metacarpophalangeal (MCP), and proximal interphalangeal (PIP) joints are the most
frequently involved joints
DIP also can be involved , but is usually a manifestation of coexistant osteoarthritis
Flexor tendon tenosynovitis is a frequent hallmark of RA and leads to decreased range of motion,
reduced grip strength, and “trigger” fingers.
4. Ulnar deviation results from subluxation of the MCP
joints,
Hyperextension of the PIP joint with flexion of the
DIP joint (“swan-neck deformity”)
flexion of the PIP joint with hyperextension of the DIP
joint (“boutonnière deformity”)
Subluxation of the first MCP joint with
hyperextension of the first interphalangeal (IP) joint
(“Z-line deformity”)
5. Inflammation about the ulnar styloid and
tenosynovitis of the extensor carpi ulnaris
may cause subluxation of the distal ulna,
resulting in a “piano-key movement” of
the ulnar styloid.
6. MTP joint involt is an early feature of RA , but chronic inflammation of ankle and midtarsal areas
come later and may lead to pes planovalgus (flat feet )
Atlantoaxial involvement of the cervical spine may cause compressive myelopathy and
neurologic dysfunction.
RA rarely affects the thoracic and lumbar spine.
Extraarticular manifestations may develop during the clinical course of RA in up to 40% of
patients, even prior to the onset of arthritis
Subcutaneous nodules, secondary Sjögren’s syndrome, interstitial lung disease (ILD),
pulmonary nodules, and anemia are among the most frequently observed extraarticular
manifestations.
7. CONSTITUTIONAL SIGNS AND SYMPTOMS
include weight loss, fever, fatigue, malaise, depression, and in the most severe cases,
cachexia
the presence of a fever of >38.3°C (101°F) at any time during the clinical course should
raise suspicion of systemic vasculitis or infection.
8. NODULES
Subcutaneous nodules have been reported to occur in 30–40% of patients and more commonly in
those with the highest levels of disease activity
When palpated, the nodules are generally firm; nontender; and adherent to periosteum, tendons, or
bursae; developing in areas of the skeleton subject to repeated trauma or irritation such as the
forearm, sacral prominences, and Achilles tendon
may also occur in the lungs, pleura, pericardium, and peritoneum
Are usually benign
9.
10. PULMONARY INVOLVEMENT
Pleuritis, the most common pulmonary manifestation of RA, may produce pleuritic chest pain
and dyspnea, as well as a pleural friction rub and effusion
Pleural effusions : exudative with increased numbers of monocytes and neutrophils
ILD may also occur and can be a/w cigarette smoking
Recent studies have shown the overall prevalence of ILD in RA to be as high as 12%
Usual interstitial pneumonia (UIP) and non-specific interstitial pneumonia (NSIP) are the
main histological and radiologic patterns of ILD
PFT : restrictive pattern with reduced DLCO
Caplan’s syndrome is a rare subset of pulmonary nodulosis characterized by the development of
nodules and pneumoconiosis following silica exposure
11. CARDIAC INVOLVEMENT
The most frequent site of cardiac involvement in RA is the pericardium
But clinical manifestations of pericarditis occur in <10% of patients with RA
Cardiomyopathy, may result from necrotizing or granulomatous myocarditis, coronary artery
disease, or diastolic dysfunction.
This also may be subclinical and only identified by echo or cardiac MRI
Rarely, the heart muscle may contain rheumatoid nodules or be infiltrated with amyloid.
Mitral regurgitation is the most common valvular abnormality in RA
12. HAEMATOLOGIC
A normochromic, normocytic anemia often develops in patients with RA and is the most common
hematologic abnormality
ESR, CRP and platelet levels may be elevated
Felty’s syndrome is defined by the clinical triad of neutropenia, splenomegaly, and nodular RA
and is seen in <1% of patients
Occurs in late stages of RA
T cell large granular lymphocyte leukemia (T-LGL) may have a similar clinical presentation and
often occurs in association with RA., but it presents early
The most common histopathologic type of lymphoma is a diffuse large B cell lymphoma (DLBCL)
The risk of developing lymphoma increases if the patient has high levels of disease activity or Felty’s
syndrome.
13. SECONDARY SJÖGREN’S SYNDROME
is defined by the presence of either keratoconjunctivitis sicca (dry eyes) or xerostomia (dry mouth) in
association with another connective tissue disease, such as RA.
Approximately 10% of patients with RA have secondary Sjögren’s syndrome.
RHEUMATOID VASCULITIS
typically occurs in patients with long-standing disease, a positive test for serum RF or anti-CCP
antibodies, and hypocomplementemia
The cutaneous signs vary and include petechiae, purpura, digital infarcts, gangrene, livedo reticularis,
and in severe cases large, painful lower extremity ulcerations.
Vasculitic ulcers may be treated successfully with immunosuppressive agents
Sensorimotor polyneuropathies, such as mononeuritis multiplex, may occur in association with
systemic rheumatoid vasculitis.
14. ASSOCIATED CONDITIONS
CARDIOVASCULAR DISEASE
The most common cause of death in patients with RA is cardiovascular disease.
Incidence of CAD and carotid atherosclerosis is higher in RA pts
CCF occurs at 2 fold higher rate than in general population
OSTEOPOROSIS
Osteoporosis is more common in patients with RA than an age- and sex-matched population, with
prevalence rates of 20–30%.
Inflammation spill over to bone osteoclast activation generalized bone loss
Hip fractures are more likely to occur in patients with RA
15. HYPOANDROGENISM
Men and postmenopausal women with RA have lower mean serum testosterone, luteinizing
hormone (LH), and dehydroepiandrosterone (DHEA) levels than control populations.
Patients receiving chronic glucocorticoid therapy may develop hypoandrogenism owing to inhibition
of LH and follicle-stimulating hormone (FSH) secretion from the pituitary gland.
Men with hypoandrogenism should be considered for androgen replacement therapy, since they are
prone to osteoporosis
16.
17. EPIDEMIOLOGY
RA affects ~0.5–1% of the adult population worldwide.
Incidence has decreased due to proper treatment , but prevalence remains the same
RA occurs more commonly in females than in males, with a 2–3:1 ratio
Studies hypothesize that estrogen can stimulate production of tumor necrosis factor α (TNF-α), a
major cytokine in the pathogenesis of RA.
18. GENETIC CONSIDERATIONS
first-degree relative of a patient : risk of RA is 2–10 times greater than in the general population
Risk is a/w allelic variation in the HLA-DRB1 gene, which encodes the MHC II β-chain molecule
Carriership of the SE alleles ( shared epitope) is associated with production of anti-CCP antibodies
and worse disease outcomes.
non-MHC genes contributing to the risk of RA gene encoding protein tyrosine phosphatase non-
receptor 22 (PTPN22)
Others PAD14, APOM
19. ENVIRONMENTAL FACTORS
Most important : cigarette smoking ( relative risk of getting RA 1.5-3.5)
Women who smoke (2.5)
Risk from smoking related to RF and antiCCP antibody positive disease
Periodontitis due to Porphyromonas gingivalis may predispose to RA (citrullination of
arginine by peptidyl arginine deiminase (PAD) leads to anti CCP antibody production
20. PATHOPHYSIOLOGY
RA is characterised by infiltration of the synovial membrane with lymphocytes, plasma cells,
dendritic cells and macrophages.
In Lymphoid follicles in synovial membrane , T- and B-cell interactions occur cytokine release
activate B cells to produce autoantibodies (RF and ACPA)
Synovial macrophages : activated by TNF and interferon gamma (IFN-γ)
Macrophages pro-inflammatory cytokines, including TNF, IL-1 and IL-6
Synovial fibroblasts proliferate, causing synovial hypertrophy and producing matrix
metalloproteinases and the proteinase ADAMTS-5, which degrade soft tissues and cartilage
Prostaglandins and Nitric Oxide in inflamed synovium vasodilatation pain and swelling
Systemic release of IL-6 triggers production of acute phase proteins by the liver.
21. At the joint margin, the inflamed synovium (pannus) directly invades bone and cartilage to cause
joint erosions.
Bone erosion is due to osteoclast activation by RANKL
Angiogenesis highly vascular synovium proinflammatory cytokines recruit more
leukocytes more inflammation
Later, fibrous or bony ankylosis may occur
Muscles adjacent to inflamed joints atrophy and may be infiltrated with lymphocytes
progressive biomechanical dysfunction and may further amplify destruction
22.
23. DIAGNOSIS
Based on signs, symptoms
of chronic arthritis + lab and
radiographic evidence
ACR- EULAR score >= 6 :
definite RA
24. LAB FEATURES
Raised ESR,CRP
Serum IgM RF : 75–80% of patients with RA;
Anti CCP antibody : diagnostic specificity 95%, has significance for worse prognosis
SYNOVIAL FLUID ANALYSIS
WBC: 5000 and 50,000 /μL (<2000 WBC/μL in osteoarthritis)
Predominant cell : Neutrophil
Can confirm inflammation and exclude infection, crystal induced arthritis
25. JOINT IMAGING
Useful for diagnosis and for tracking progression of joint damage
Plain X Ray : most widely used – shows joint space narrowing
“Periarticular osteopenia”
other findings on X ray : soft tissue swelling, symmetric joint space loss, and subchondral
erosions, most frequently in the wrists and hands (MCPs and PIPs) and the feet (MTPs).
MRI and USG can detect synovitis, tenosynovitis, and effusions and has greater sensitivity for
identifying bony abnormalities.
Power color doppler is an USG based investigation which ca detect erosions
26. CLINICAL COURSE
The natural history of RA is complex and affected by a number of factors including age of onset,
gender, genotype and comorbid conditions
10% of patients with inflammatory arthritis fulfilling ACR classification criteria for RA will
undergo a spontaneous remission within 6 months
But majority show a pattern of persistent and progressive disease activity that waxes and wanes in
intensity over time
More than one-half of patients with RA are unable to work 10 years after the onset of their disease
The overall mortality rate in RA is two times greater than the general population, with ischemic
heart disease being the most common cause of death followed by infection
Median life expectancy is shortened by an average of 7 years for men and 3 years for women
compared to control populations
27. TREATMENT
The treatment goal is to suppress inflammation, control symptoms and prevent joint damage.
This involves a combination of pharmacological and non-pharmacological therapies
Various disease activity scores are employed : Disease Activity Score (DAS), Simplified Disease
Activity Index (SDAI), the Clinical Disease Activity Index (CDAI), and the Routine Assessment of
Patient Index Data 3 (RAPID3)
The medications used for the treatment of RA may be divided into broad categories
• Nonsteroidal anti-inflammatory drugs (NSAIDs)
• Glucocorticoids (prednisone and methylprednisolone)
• Conventional DMARDs
• Biologic DMARDs
28.
29. GLUCOCORTICOIDS
They may be administered in low to moderate doses to achieve rapid disease control before the
onset of fully effective DMARD therapy, which often takes several weeks or even months.
1- to 2-week burst of glucocorticoids may be prescribed for the management of acute disease flares
Chronic administration of low doses (5–10 mg/d) of prednisone control disease activity in
patients with an inadequate response to DMARD therapy.
High-dose : for severe extraarticular manifestations of RA, such as ILD
intraarticular injection of triamcinolone acetonide : limited no of affected joints
Bisphosphonates to prevent osteoporosis
30. CONVENTIONAL DMARDS
DMARDs are so named because of their ability to slow or prevent structural progression of RA.
Include : hydroxychloroquine, sulfasalazine, methotrexate, and leflunomide
Has delayed onset of action of ~6–12 weeks
Methotrexate is the pioneer and can stimulate adenosine release from cells, producing an anti-
inflammatory effect
Leflunomide, an inhibitor of pyrimidine synthesis : efficacy similar to methotrexate
Hydroxychloroquine has not been shown to delay radiographic progression of disease and thus is
not considered to be a true DMARD
Sulfasalazine can reduce radiographic progression of disease
31. BIOLOGIC DMARDS
They are protein therapeutics which target cytokines and cell-surface molecules.
TNF inhibitors :
• first approved biologicals
• include Infliximab ,Adalimumab ,Golimumab , Certolizumab and Etanercept
• Anti-TNF agents avoid in active infection or a history of hypersensitivity
• contraindicated in patients with chronic hepatitis B infection or class III/IV congestive heart
failure
• Screen for TB before starting the drug
• Never combine with anakinra severe infections
Anakinra, an IL-1 receptor antagonist: came later , rarely used now
Abatacept, rituximab, and tocilizumab are the newest members of this class