This document provides information on rheumatoid arthritis (RA), including its presentation, pathogenesis, diagnostic criteria, management, and complications. Some key points:
- RA is a chronic inflammatory disease that primarily affects the joints in a symmetrical pattern. It has an unknown cause but is associated with certain genetic factors.
- Diagnosis is based on symptoms lasting over 6 weeks involving at least 3 joint areas. Serological markers and imaging can help with diagnosis. Untreated, it can lead to long-term joint damage and disability.
- Management involves early use of disease-modifying antirheumatic drugs (DMARDs) like methotrexate to reduce inflammation and prevent joint damage. Biologics may be
Dermatomyositis is a rare inflammatory myopathy with characteristic skin manifestations and muscular weakness.
Polymyositis is a similar disease without skin lesions.
Amyopathic dermatomyositis: typical cutaneous manifestation of DM without clinical and/or laboratory findings of muscle involvement for at least 6 months after the onset of skin rash.
Already the leading cause of disability in the US, shocking new information shows incidents of ischemic stroke increasing more than 50% in children from 5 to 14 years old since 1995. In younger patients (under 45 years old) there have been similar leaps among all types of stroke. Despite these increases many of victims go undiagnosed due the mindset that they are simply “too young for stroke”. This program improves our understanding, awareness, assessment, care and coordination to help EMS provide better outcomes for all victims of cerebrovascular accidents. In this session we explain the startling reasons behind these dramatic numbers, what EMS can do about them and the diagnostic approach that catches what others often miss in newborns, very young children and younger victims of stroke.
www.RESCUEDIGEST.com
www.ROMDUCK.com
Dermatomyositis is a rare inflammatory myopathy with characteristic skin manifestations and muscular weakness.
Polymyositis is a similar disease without skin lesions.
Amyopathic dermatomyositis: typical cutaneous manifestation of DM without clinical and/or laboratory findings of muscle involvement for at least 6 months after the onset of skin rash.
Already the leading cause of disability in the US, shocking new information shows incidents of ischemic stroke increasing more than 50% in children from 5 to 14 years old since 1995. In younger patients (under 45 years old) there have been similar leaps among all types of stroke. Despite these increases many of victims go undiagnosed due the mindset that they are simply “too young for stroke”. This program improves our understanding, awareness, assessment, care and coordination to help EMS provide better outcomes for all victims of cerebrovascular accidents. In this session we explain the startling reasons behind these dramatic numbers, what EMS can do about them and the diagnostic approach that catches what others often miss in newborns, very young children and younger victims of stroke.
www.RESCUEDIGEST.com
www.ROMDUCK.com
Rhematoid arthritis is systemic autoimmune inflammatory disorder of unknown etiology affecting multiple organ systems. These ppt includes comprehensive management of it.
Dr. Swamy Venuturupalli talks about Rheumatoid Arthritis, Early Diagnosis and Treatment at the James R. Klinenberg symposium on Rheumatic diseases in Pasadena, CA.
rheumatoid arthritis is a chronic, systemic, inflammatory autoimmune disorder that primarily affects the joints, but may also manifest with extraarticular features.
For information about the disease and learn more, you can obtain basic informations from the following file.
SLE is systemic autoimmune disease affecting mainly females in their reproductive age.
It has different presentations & autoantibodies that have to be followed by specialists in Rheumatology & Immunology.
It is wise to revise our Knowlege regularly to pickup the recent updates.
Sometimes it is difficult & even problem to deal with patient with refractory LN, so we are in need for expert perspectives as a guide to treat those cases.
Antiphospholid syndrome is a systemic autoimmune disorder affecting females more than males causing thrombosis &/or fetal losses.
GPs, internists, Rheumatologists & gynecologists must have how to diagnose & manage.
This is my advice for daily practice, so that all can manage patients with recurrent abortions &/or arterial or venous thrombosis.
thanks.
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
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
HOT NEW PRODUCT! BIG SALES FAST SHIPPING NOW FROM CHINA!! EU KU DB BK substit...GL Anaacs
Contact us if you are interested:
Email / Skype : kefaya1771@gmail.com
Threema: PXHY5PDH
New BATCH Ku !!! MUCH IN DEMAND FAST SALE EVERY BATCH HAPPY GOOD EFFECT BIG BATCH !
Contact me on Threema or skype to start big business!!
Hot-sale products:
NEW HOT EUTYLONE WHITE CRYSTAL!!
5cl-adba precursor (semi finished )
5cl-adba raw materials
ADBB precursor (semi finished )
ADBB raw materials
APVP powder
5fadb/4f-adb
Jwh018 / Jwh210
Eutylone crystal
Protonitazene (hydrochloride) CAS: 119276-01-6
Flubrotizolam CAS: 57801-95-3
Metonitazene CAS: 14680-51-4
Payment terms: Western Union,MoneyGram,Bitcoin or USDT.
Deliver Time: Usually 7-15days
Shipping method: FedEx, TNT, DHL,UPS etc.Our deliveries are 100% safe, fast, reliable and discreet.
Samples will be sent for your evaluation!If you are interested in, please contact me, let's talk details.
We specializes in exporting high quality Research chemical, medical intermediate, Pharmaceutical chemicals and so on. Products are exported to USA, Canada, France, Korea, Japan,Russia, Southeast Asia and other countries.
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
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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.
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
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
These 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
2. Prof. / Abd El-Azeim Al-Hefny
Prof. of Internal Medicine, Rheumatology & Immunology
Director of Rheumatology Unite
Ain Shams University
3. Chronic systemic inflammatory disease
Unknown etiology, association with HLA-
DR.
Starts at any age & peaks at30-50y.
It affects ~ 1-2% of the population in USA.
Female/male ratio ~ 3/1
4. Primarily affects the peripheral
joints in Symmetric pattern with
exacerbations and remissions .
It has variable extra-articular
features
5. In most cases, RA is a chronic
progressive disease that, if left
untreated, can cause joint damage
and disability with increased
morbidity & mortality.
6. Presentation of an antigen (e.g. bacteria, viruses) by APC"macrophage") activation of T
helper cells activation of B cells RF + IgG immune complexes in synovial fluid and
blood activation of complement and release of inflammatory mediators, proinflammatory
cytokines(TNF,ILK-1,ILK-6) chronic inflammation, granuloma formation and joint destruction.
7. Synovium in RA. Only modest synovial lining hyperplasia is present,
although sublining mononuclear cell infiltration, lymphoid
aggregates, and vascular proliferation are prominent
Normal synovium
Synovium in RA
12. 1. Morning stiffness > 1 hour*
2. Arthritis of 3 or more joint areas* (right & left
PIPJs, MCPJs, elbows, MTPJs, ankles, & knees)*
3. Hand arthritis (PIPJs, MCPJs, wrist)*
4. Symmetrical arthritis*
5. S.C. nodules (observed by physician)
6. Positive RF
7. Radiological findings in hand or wrist joints
(periarticular osteopenia, erosions)
* = present for at least 6 weeks.
At least 4 criteria should be present to
diagnose RA
16. Hand deformities
Chronic synovitis and tenosynovitis result in
characteristic joint deformities classic for chronic
rheumatoid arthritis.
Patients may have swan neck deformities, Boutonniere's
sign, ulnar deviation, cock-up toes, or hammer toes.
22. •20% of patients have SC rheumatoid nodules, most commonly situated over
bony prominences but also observed in the bursae and tendon sheaths. (firm,
non-tender, freely mobile)
•Nodules are occasionally seen in the lungs, the sclerae, and other tissues.
•Nodules correlate with the presence of RF ("seropositivity"), as do most
other extra-articular manifestations.
•all patients with rheumatoid nodules are seropositive for RF.
30. Target Population of the
Classification Criteria
Two requirements:
(1) Patient with at least one joint with definite
clinical synovitis (pain, tenderness &
swelling)
(2) Synovitis is not better explained by
“another disease”
Differential diagnoses differ in patients with different
presentations.
If unclear about the relevant differentials, an expert
rheumatologist should be consulted.
31. 2010 ACR/EULAR
Classification Criteria for RA
I- JOINT DISTRIBUTION (0-5)
1 large joint 0
2-10 large joints 1
1-3 small joints (large joints not counted) 2
4-10 small joints (large joints not counted) 3
>10 joints (at least one small joint) 5
II- SEROLOGY (0-3)
Negative RF AND negative ACPA 0
Low positive RF OR low positive ACPA 2
High positive RF OR high positive ACPA 3
III- SYMPTOM DURATION (0-1)
<6 weeks 0
≥6 weeks 1
IV- ACUTE PHASE REACTANTS (0-1)
Normal CRP AND normal ESR 0
Abnormal CRP OR abnormal ESR 1
What if the score is <6?
Patient might fulfil the
criteria…
Prospectively over time
(cumulatively)
Retrospectively if data
on all four domains have
been adequately
recorded in the past
“JOINT INVOLVEMENT”
- Any swollen or tender joint
(excluding DIP of hand and feet, 1st
MTP, 1st CMC)
“SEROLOGY”
Negative: ≤ULN (respective lab)
Low positive: >ULN but ≤3xULN
High positive: >3xULN
of “SYMPTOM DURATION”
Refers to the patient’s self-report on
the maximum duration of signs and
symptoms of any joint that is
clinically involved at the time of
assessment.
≥6/10 = definite RA
33. After 5 years of disease, approximately 30% of patients are
unable to work;
After 10 years, 50% have substantial functional disability.
Poor prognostic factors include:-
Persistent synovitis,
Increased clinical severity (more joints).
Early erosive disease (XR), poor functional status
Extra-articular findings .
Positive serum RF, CCP, acute-phase reactants (ESR,CRP)
Family history of RA,
Male sex, lower socioeconomic factors (level of education)
Advanced age.
35. RA is not a benign disease. With many complications
Deformities, Disability & handicap
Muscle weakness & wasting, C1-C2 subluxation (intubation)
Tenosynovitis, carpal tunnel syndrome, rupture of extensor
tendons, Baker's cyst (pseudo thrombophlebitis).
Secondary amyloidosis, focal GN, possible membranous
nephropathy
Osteoporosis
Rheumatoid vasculitis (2ry Vasculitis), PVD
Lymphatic obstruction , Lymphoproliferative disorder
Anemia: GI bleeding, anemia of chronic disease
Interstitial pulmonary disease, pulmonary nodules, …
Episcleritis and scleritis
2ry Sjögren's syndrome
Pericarditis, myocarditis, IHD & accelerated atherosclerosis
36. •The most common cause of
death (45%) in RA patients.
•Chung CP, Avalos I, Raggi P, Stein CM. Atherosclerosis and inflammation:
insights from rheumatoid arthritis. Clin Rheumatol. 2007;26(8):1228-1233.
Cardiovascular
disease
•The 2nd most common cause of
death
•Sites: Lung , Skin , Joints
Infection
•Lymphoma , lung cancer and
•non-melanoma skin cancer
Malignancies
38. RA is not a benign disease.
40% of patients with RA develop joint erosions on x-ray
within the first year and 75% do so within 2 years after
the onset of symptoms.
By MRI, joint damage can occur as early as 4 weeks after
onset of symptoms.
In one study, 45% of patients with RA developed joint
erosions within 4 months.
About 15% are classified as having serious illness,
which prognostically is equivalent to 3-vessel CAD.
39. The targets of treatment are to :
◦ Obtain remission or (if not possible) LDA
◦ Maintain remission
◦ Prevent flares & complications (deformities,
amyloidosis)
◦ Treat any complication if occurred
Early diagnosis & early referral to a
rheumatologist are essential for
proper management.
40. When?
• Early aggressive therapy (in the window of opportunity
ie. within the first 3 month of onset) ,
Why?
• To prevent the risk of bone erosions, joint destruction
& deformity (treat to target = t2t)
• Decreases the development of CVD & other co-
morbidities
• improves patient’s survival and quality of life.
41.
42. A) Synthetic DMARDs (mono or combin.):
MTX , Leflunomide , SSZ, HCQ , CS
C) Biologic DMARDs
1. TNF blockers
2. Targeting T cells
3. Selective B cell depletion
4. IL1 inhibitor
5. IL-6 inhibitor
D) Combination Therapy: MTX + Biologic
therapy
B) Bridge Stage Therapy
NSAIDs , CS
43. Drug Onset Dose Side effects
MTX One
month
7.5-25 mg/week, PO (on
an empty stomach) if >20
mg (SC or IM).
(Tab. 2.5 mg) (Vial 50 mg)
Add 1 mg folic acid daily
to guard against GI&
hematol. complications
GIT (Nausea,
vomiting).
Blood S/E: rare
Contraindicated in
renal or hepatic
disease.
Monitoring: CBC,
LFTs (AST or ALT)
monthly .
BUN & Na, K/6-12Mns.
SZZ 3-6 Mo 2-3 g PO, Enteric coated,
with meal.
Tab 500 mg
Monitoring: CBC , LFTs
/m for 3ms; then /3ms.
Allergic manifestation
GIT: (nausea &
vomiting).
HCQ 3-6 Mo 6.5mg/kg in 2doses
200-400 mg/d PO
Retinal examination
every 6 month - 1 year
Retinopathy is v. rare
and is reversible.
Nausea, rash
Skin hyperpigment.
44. Drug
Onset
of
action
Dose Side effects
Leflunomide One
month
100 mg loading 3 days?
Then 20 mg/d.
Most experts no longer
use a loading dose
because of increased side
effects esp. if combined
with MTX.
Falling of hair.
Diarrhea, nausea
Increase liver enzyme
but s. albumin and PT
are normal.
Monitoring: CBC .
LFTs and BP/m for
the first 6 months
and then 2ms.
Corticostero
ids.
Hours Not >7.5-10 mg/d.
+ calcium & vit. D.
HTN, DM
Osteoporosis.
DEXA/yr +/- Bisphos.
(Avara,
Apetoid,
Arthfree,
Vamid)
45. The most widely used combinations
include:
MTX, SSZ, and HCQ with or without
prednisolone
MTX plus leflunomide
46. - Leflunomide
-MTX
-SSZ
- HCQ 3-6 Months
DMARDs (1-6 Mo)
start Onset of
action
`
one month
- CS Hours
DMARDs has no analgesic effect
47. Symptoms modifying and not disease modifying drugs
(SMARDS) (i.e.) do not stop the progress of the
disease, so used during the bridge stage because
DMARDs has no analgesic effect.
NSAIDs
D M A R D s
START
Onset
of
action
48. A key mechanism is the interference with the
synthesis of pro-inflammatory prostaglandins by
inhibition of COX enzyme; isoform COX-2.
Traditional NSAIDs, however, also inhibit the COX-1
isoform, which may affect platelets and GI mucosa
leading to gastrointestinal mucosal injury.
COX-2 selective NSAIDs have a better GI safety, but
may induce CV complications with prolonged use??
Alternatively, reduction in gastrointestinal toxicity can
be obtained by co-administration of traditional
NSAIDs + PPI.
49. Taken in the morning (8-10 am) low dose < 10mg/d
gives a rapid relief of symptoms because:
it inhibits cytokines: (Anti-IL1, 2, Anti-TNFa) Anti-
COX, NSAIDs action, so they have actions equivalent
to DMARDs, NSAIDs & Anticytokines.
As well as inhibits lymphocyte proliferation and
antigen presentation.
GC were used only during the bridge stage but now,
are used in the combination therapy because it has a
(DMARD) effect
decrease side effects when used with Ca & Vit. D and
in a dose <10 mg/d (7.5mg) + Bisphosphonates
50. Adverse effects:
Osteoporosis, hypertension, hyperglycemia, fluid
retention and premature atherosclerosis.
Calcium and vitamin D supplements should be added if
use of glucocorticoids is planned for more than 3 months
Ask for DEXA during follow up + Bisphosphonates.
Intra-articular GC are not associated with significant
systemic adverse effects, and are used to control
inflammation in mono- or oligoarthritis.
55. Increased risk of bacterial infection
Screening for latent TB ( chest X ray &tuberculin)
CHF grades III & IV (Anti –TNF is contraindicated)
Optic neuritis and demylenating diseases (Anti –
TNF is contraindicated).
Significant coronary artery disease
Skin malignancy
COPD
Viral infection HCV or HBV (viral replication)
56. Avoid Vaccination with live vaccine (German
measles or oral polio or rabies )
Temporarily suspended in patients underlying
surgery > one week before & after surgery.
57. D) Combination Therapy
MTX + Biologic therapy
Combination between MTX and biologic therapy
provides greater benefit in improving signs &
symptoms
Preventing radiographic deterioration and
improving physical function in comparison to
monotherapy
No combination of biologic therapy because of
higher rate of adverse effects & lack of any
additive effect .
Don’t shift to another biologic except after at
least 3 month.
58. Surgical treatment
◦ Synovectomy (partial or total)
◦ Correction of deformities
◦ Arthroplasty
◦ Arthrodesis
Rehabilitation
How to select dugs for every patient??????
63. 1. Objective arthritis:
◦ Swelling, effusion
◦ Limitation of movement
◦ Tenderness
◦ Pain on motion
◦ Joint warmth
2. Continuous arthritis > 6 W,
in a child < 16yrs;
of unknown etiology.
3. Exclusion of other chronic arthritis (≈100)
4. No specific test to establish the diagnosis
IT IS A DIAGNOSIS OF EXCLUSION.
65. Woo P (2006) Systemic juvenile idiopathic arthritis:
Nat Clin Pract Rheumatol 2: 28–34 doi:10.1038/ncprheum0084
Arthritis with, or preceded by,
daily fevers of at least 2 weeks'
duration, quotidian fever for at
least 3 days, and the presence
of at least 1 of:
(i) evanescent, non-fixed,
erythematous rash;
(ii) generalized LNopathy;
(iii) hepatosplenomegaly.
(iv) Serositis .
Pale pink, blanching,
transient (minutes-hrs),
nonpruritic small rash
Found on the trunk &
extremities
Worsen with fever.
Systemic-onset JIA
Typical pale-pink, macular rash
66. Woo P (2006) Systemic juvenile idiopathic arthritis: diagnosis, management, and outcome
Nat Clin Pract Rheumatol 2: 28–34 doi:10.1038/ncprheum0084
Typical quotidian fever of systemic juvenile idiopathic arthritis, which is resistant
to high-dose oral prednisone (>1mg/kg)
Daily recurrent fevers of at least 2 weeks' duration, for at
least 3 days/w (rises > 39C & returns to < 37 between fever
spikes).
67. UVEITISERAsJIApoJIAoJIA
Topical
steroid
Sulfasalazine
(Male+periph.j)
NSAIDs/steroid
(fever, serositis)
MTXNSAIDs
MTXAnti-TNFIL-1 , IVIG,Sulfa/lefluoIA
steroid
InfliximabIL-6 antagonistAnti-TNFAs poJIA
TTT of ps-JIA:
It can be presented as oligo-, poly-, or ERA; so it
should be treated as the parallel JIA subset.
Indeed, there are strong indications that patients should
be treated aggressively as early as possible with MTX
(10mg/m2/w + folic acid) & if not controlled the use of
biologics should be considered for best outcome.
68. NSAIDs (eg, ibuprofen, 800 mg 3-4 times daily) or
naproxen (500 mg twice daily)
Corticosteroids, prednisone dose is 0.5 -1mg/kg /day.
Pulse methylprednisolone IVI (0.5-1g/d for 3d) for life-
threatening disease
Hydroxychloroquine, & methotrexate and biologic
agents (anti-TNF, IL-1a, & rituximab) in refractory cases.