Rheumatoid Arthritis or RA is a medical condition of the joints - an autoimmune and inflammatory disease. This means that your own body attacks itself

What is an empath? What type of empath are you? How empaths are different from highly sensitive people (HSP). How characteristics of an empath can cause fatigue, digestive issues, low back pain, poor sleep, panic and more...

This contains a complete set of Rheumatology (part 1) flashcards. They are handmade by me, and suited to medical students or others training in a healthcare profession (eg. nursing, paramedics, PA etc). What's included?  These are a set of digital notes that you can download and recreate a set of 13 flashcards with. This set is focused on rheumatology, covering rheumatoid arthritis, AICTDs, septic arthritis, gout and fibromyalgia: 1. rheumatology overview 2. examination & GALS assessment 3. rheumatoid arthritis (overview) 4. rheumatoid arthritis (investigations & management) 5. autoimmune connective tissue disorders (AICTDs): overview & Sjögren's syndrome 6. AICTDs: SLE (overview) 7. AICTDs: SLE, Raynaud's and APLS 8. AICTDs: scleroderma & myositis 9. myositis (cont.) & septic arthritis 10. crystal arthropathies (overview) 11. gout (causes, RFs, tophi, diagnosis) 12. gout (management) & CPPD (overview) 13. fibromyalgia (overview) This is a digital download pack in PDF form. If you are printing the cards, for best quality I recommend using thick white paper or card and laminating for protection. Questions? -unfortunately due to the nature of this product, refunds are not accepted, but if you are unhappy please do not hesitate to contact me or Etsy -all the content of the notes is my own work, collating information from relevant lectures, textbooks and online resources (you can follow me at @medic.flashcards for more flashcards inspo and medical school content!) -any mistakes in the notes are my own  -if you have any questions, please feel free to email me  Contact me:  -my Instagram account is @medic.flashcards  -email me at j.flashcards [!at] gmail.com I really hope you find these notes helpful for your revision! I welcome any feedback you have for me.

Here’s everything you need to know about the early symptoms of lupus and lupus rash, as well as later symptoms you might experience from lupus complications.

Lupus is a systemic autoimmune disease that attacks the skin, muscles and more. While symptoms typically show up between ages 16-55, late-onset lupus can occur after age 50.

Part of living with RA is the rheumatoid arthritis flare up. In this post, RA patient Kate the (Almost) Great shares the beginner's guide to a flare.

Psoriasis is a chronic autoimmune disease that causes skin cells to multiply faster than normal resulting in red patches with white scales.

Immune-Mediated Necrotizing Myopathy (IMNM) (Necrotizing Autoimmune Myopathy), a form of idiopathic inflammatory myopathy characterized clinically by severe acute or subacute proximal muscle weakness, extremely elevated CK levels, and necrosis found on muscle biopsy.

Pain and depression are associated with both physical and mental fatigue independently of comorbidities and medications in primary Sjögren’s syndrome. On behalf of the UK primary Sjögren’s Syndrome Registry Objectives  To report on fatigue in patients from the United Kingdom primary Sjögren’s syndrome (pSS) registry identifying factors associated with fatigue and robust to assignable causes such as comorbidities and medications associated with drowsiness. Methods From our cohort (n = 608), we identified those with comorbidities associated with fatigue, and those taking medications associated with drowsiness. We constructed dummy variables, permitting the contribution of these potentially assignable causes of fatigue to be assessed. Using multiple regression analysis, we modelled the relationship between Profile of Fatigue and Discomfort physical and mental fatigue scores and potentially related variables. Results Pain, depression and daytime sleepiness scores were closely associated with both physical and mental fatigue (all p ≤ 0.0001). In addition, dryness was strongly associated with physical fatigue (p ≤ 0.0001). These effects were observed even after adjustment for comorbidities associated with fatigue or medications associated with drowsiness. Conclusions  These findings support further research and clinical interventions targeting pain, dryness, depression and sleep to improve fatigue in patients with pSS. This finding is robust to both the effect of other comorbidities associated with fatigue and medications associated with drowsiness. Introduction Primary Sjögren’s syndrome Recommendations Our data confirm the importance of fatigue symptoms— both mental and physical—to patients with pSS and permit identification of factors contributing to fatigue including other comorbidities and medications associated with drowsiness. Given the wide variety of potential factors contributing to fatigue, we support the view that a multidisciplinary approach is essential for the clinical management of fatigue in pSS.32 We observe that many patients with pSS are taking multiple medications and we recommend a medication review be undertaken to identify drowsy medications which could be contributing to fatigue. If these medications are discontinued, then a review should be arranged and if the fatigue does not improve, then treatment of comorbidities should be considered. However, as pain is a major contributor of both mental and physical fatigue, the contribution of some pain-modifying medications may be beneficial, despite their association with drowsiness. Patients with pSS should be tested for common comorbidities which can contribute to fatigue, including anaemia or hypothyroidism and offered appropriate treatments. We recommend screening for depression and anxiety and offering patients appropriate interventions to address these symptoms. Non-pharmacological interventions (such as talking therapies) may reduce the need for antidepressants and anti-anxiolytics, many of which are associated with drowsiness. We recommend that patients undergo a more detailed sleep assessment in order to screen for a primary sleep disorder. Patients identified with conditions such as obstructive sleep apnoea should be offered assignable causes such as Continuous Positive Airway Pressure (CPAP) treatment. Interventions such as cognitive behavioural therapy for insomnia (CBT-I) are a first-line treatment for insomnia associated with other medical conditions and may prove beneficial to patients with pSS. Patients with pSS should be offered appropriate pain management interventions. If pain is associated with poor sleep, then CBT-I with a pain adjunct has been suggested as a feasible treatment. Finally, in the absence of good evidence to support effective drug treatments, fatigue interventions in pSS might focus on a multidisciplinary approach incorporating activity management, graded exercise/ activity and CBT. See full report of this study. FIND OUT MORE ABOUT SJOGREN'S SYNDROME HERE: List of Sjogren's Syndrome Symptoms Increased prevalence of Sjogren's syndrome in high level chromium soils Study suggests future way to treat chronic eye problems and lymphoma in Sjogren's Syndrome. How Sjogren's is diagnosed Dry eye found in over 85% of Sjogren’s patients

Part of living with RA is the rheumatoid arthritis flare up. In this post, RA patient Kate the (Almost) Great shares the beginner's guide to a flare.

CREST syndrome is type of scleroderma is believed to be an autoimmune disorder. Mostly in lower arms and legs, below the elbows and knees, and sometimes affect the face and neck. Limited scleroderma…

What is an empath? What type of empath are you? How empaths are different from highly sensitive people (HSP). How characteristics of an empath can cause fatigue, digestive issues, low back pain, poor sleep, panic and more...

63% of people with lupus have an allergic disorder, often linked to production if IgE. Foods, medications, and the environment can be triggers for allergies

NCBJ POLATOM Radioisotope Centre has just introduced a new product to the nuclear medicine preparations market. Techimmuna will help to diagnose various cases of inflammation, in particular rheumatoid arthritis.

The concept of psoriatic arthritis (PsA) has evolved from that of a relatively obscure mild joint disease to that of a severe inflammatory arthritis involving bones, joints, and the surrounding tissue.

Polymyositis (PM) is a rare, chronic, systemic autoimmune muscle disease that affects the skeletal muscles, those involved with voluntary movement, causing muscle weakness. It can affect many different organs of the body including the muscles, lungs, and heart and it can cause muscle pain.

Raynaud Syndrome - Learn about the causes, symptoms, diagnosis & treatment from the Merck Manuals - Medical Consumer Version.

Part of living with RA is the rheumatoid arthritis flare up. In this post, RA patient Kate the (Almost) Great shares the beginner's guide to a flare.

Part of living with RA is the rheumatoid arthritis flare up. In this post, RA patient Kate the (Almost) Great shares the beginner's guide to a flare.

systemic lupus erythematosus (aka lupus or SLE)Overview Demographics • In terms of its demographics, it is at least 10 times more common in women than in men and it’s 4 times more common in blacks than in whites: in the US, it affects 1/1,000 in white women vs 1/250 black women. Environmental Triggers • Key environmental triggers include estrogen and UV light. Pathology • Most of the pathology in SLE is due to class 3 hypersensitivity reactions, wherein an array of different antibodies can attack various cellular components to generate pathologic pro-inflammatory immune complexes. Cells Under Attack • Cells under attack include: - Nucleic antigens and binding proteins (think: antinuclear antibodies (ANA) - Phospholipids (think: antiphospholipid antibody syndrome – a hypercoagulable, prothrombotic state) - Hematologic/immunologic cells (think: platelets, causing thrombocytopenia or erythrocytes, causing chronic anemia). • Knowing that many different autoantibodies can exist in SLE helps us understand the heterogeneity of its clinical manifestations.Clinical Manifestations Mucocutaneous Manifestations Acute skin manifestations include: • Malar rash, which is an erythematous butterfly rash that spares the nasolabial folds (note that we can use this sparing to help distinguish it from the rash of dermatomyositis). • Photosensitive rash, which is a sunlight triggered flat, maculopapular erythematous rash: NSAIDS and thiazide diuretics are a trigger for this rash in patients with SLE.Chronic skin manifestations include (for example): • Alopecia, which is a common finding, and manifests with hair thinning or patchy hair loss that may be related to a medication OR may improve with medication administration and disease reduction. • Chilblain lupus: a painful, violaceous frostbite-appearing rash that occurs in cold-exposed areas. • Discoid rash: a chronic, coin-shaped (hence: discoid), scarring form of rash with prominent central depigmentation – it occurs in sun-exposed skin surfaces. • Lupus tumidus: a photosensitive, erythematous, non-scarring urticarial form of rash. • Lupus profundus (aka panniculitis): a painful, nodular, subcutaneous inflammatory. • Painless oral and nasal uclers. • Seborrheic dermatitis: scaly, erythematous plaques in the face, including the eyebrows, nose, and nasolabial folds.Arthritis • Next for arthritis, make note of Jaccoud arthropathy, which is tendon laxity that produces reversible deformities, such as swan-neck deformity (which we addressed in rheumatoid arthritis). A key distinguishing feature from RA is that the deformity is reversible.Cardiopulmonary and Vascular manifestations • First, serositis (serous membrane inflammation), which can manifest with: - Pleuritis (in the lungs): presents with pleuritic pain or pleural effusion. - Pericarditis (in heart): presents with pericardial pain or effusion. - Note that peritonitis is another form of serositis that can occur but is less common. • From a strict pulmonary standpoint, include pneumonitis, alveolar hemorrhage, and pulmonary arterial hypertension. • From a strict cardiac standpoint, include mitral or aortic valvular thickening with or without Libman-Sacks endocarditis (these are non-bacterial valvular vegetations – we distinguish them from infectious endocarditis). • From a vascular standpoint, include atherosclerosis, which can cause thromboembolic events, and, most commonly, Raynaud’s phenomenon (a vasospastic phenomenon of the digits).Renal • Renal disease, called lupus nephritis, can manifest with polyuria and nocturia, abnormal appearing urine (bloody or foamy), lower extremity edema, and hypertension. • We divide lupus nephritis into 6 classes, which range from minimal disease restricted to immune deposition in the mesangium, called Class I: minimal mesangial lupus nephritis, all the way to severe disease, requiring renal transplantion, called Class 6: advanced sclerosing lupus nephritis, manifesting with sclerosis of greater than 90% of the glomeruli. • For reference the disease classification is as follows: - Class I: Minimal Mesangial Lupus Nephritis Normal glomeruli; mesangial immune deposits; normal renal function; no treatment required. - Class II: Mesangial Proliferative Lupus Nephritis Mesangial hypercellularity; minimal renal impairment; Treatment involves angiotensin-converting-enzyme inhibitor (ACE inhibitor) when proteinuria is greater than 0.5 g/day. - Class III: Focal Proliferative Lupus Nephritis - Segmental lesions in less than half of the glomeruli; hypercellularity and immune complex deposition in the mesangium and extending into the subendothelial space and mesangium; renal failure is present with systemic manifestations of hypertension and lower extremity edema; immunosuppressive treatment is required. - Class IV: Diffuse Proliferative Lupus Nephritis When Class 3 disease extends to greater than 50% of glomeruli it becomes Class 4 disease. As well, there are additional pathologic findings, including cellular glomerular crescent formation, a key finding of severe inflammatory glomerulonephritis. Immune suppression is required. - Class V: Membranous Lupus Nephritis This is a distinct, less common, form of lupus nephritis that involves subepithelial immune deposition with resultant thickening of capillary loops and can occur in isolation or concomitantly with Class 3 or 4 disease. It notably manifests with severe proteinuria but a lack of anti-dsDNA antibodies. - Class VI: Advanced Sclerosing Lupus Nephritis Greater than 90% of the glomeruli are already sclerotic with no ongoing active disease, so renal transplant is necessary and there is no role for immune suppression at this point.Neuropsychiatric • Notable CNS manifestations include seizures and headaches and demyelination, albeit rare, a longitudinally extensive myelopathy (spinal cord demyelination) which we typically associate with neuromyelitis optica (NMO). • Importantly, include psychosis via a small-vessel vasculopathy (small-vessel thrombosis) rather than inflammatory vasculitis (which we might expect). • Albeit less dramatic, arguably the most common neuropsychatric manifestation is fatigue. • Notable PNS manifestations include various neuropathies.Hematologic/Immunologic • Hematologic/Immunologic disorders include hemolytic anemia, leukopenia (or lymphopenia), and thrombocytopenia. • Essentially a reduction in blood and immunologic components.Lupus Autoantibodies ANA (antinuclear antibody test) • ANA (antinuclear antibody test) is a highly sensitive but non-specific test: a negative test can help exclude the diagnosis of SLE but a positive test is fairly unhelpful. - To help with its specificity of the test, we consider the degree of dilution at which the ANA is still positive, called the ANA titer; this reflects the degree of positivity (and thus specificity) of the test. - Antibody positivity at a dilution of 1:40 is common in the general population (est. 30% of the normal population) whereas positivity at a dilution of 1:320 is rare (est. 3% of the normal population). Anti-dsDNA (double-stranded DNA) and Anti-Sm (Smith) • Both anti-dsDNA (double-stranded DNA) and anti-Sm (Smith) autoantibodies are highly specific for SLE. • Importantly, anti-dsDNA levels correlate with disease activity whereas anti-Sm levels do not. Anti-histone antibodies • Histone autoantibodies are commonly associated with drug-induced lupus. • Although they are 90% sensitive for drug-induced lupus, up to 70% of SLE patients can also be positive for anti-histone antibodies, so we don’t use them to distinguish drug-induced lupus from systemic lupus erythematosus. • Common clinical manifestations of drug-induced lupus are cutaneous manifestations along with arthralgias, myalgias, and fever. Internal organ involvement (other than serositis) or neuropsychiatric manifestations are rare. • Common drug-induced lupus triggers: - Hydralazine, Isoniazid, Minocycline, Procainamide, Tumor necrosis factor alpha inhibitors (anti-TNF agents) • Many other drugs have also been shown to cause drug-induced lupus, including: - Chlorpromazine, Diltiazem, Methyldopa, and Quinidine. Antiphospholipid antibodies • Antiphospholipid antibodies (antibodies directed at phospholipids or their binding plasma proteins) are present in roughly half of SLE patients and are an important marker of thromboembolism risk, including arterial thromboembolism, deep venous thrombosis, and they are an important cause of fetal loss (late-term miscarriages).Additional lab tests • Before we address antiphospholipid antibody syndrome and antiphospholipid antibodies, themselves, in more detail, note that additional helpful lab laboratory tests to diagnose lupus include low complement levels and the findings of a positive direct Coombs test without evidence of hemolytic anemia.Pathogenesis of immune complex-mediated hypersensitivity: • Immune complexes become deposited on the vessel wall (or, in some cases, in the tissues). • As a result, complement and neutrophil activation occurs, leading to the release of pro-inflammatory cytokines, enzymes, and reactive oxygen species. • Increased vessel permeability allows the inflammatory molecules to cause additional tissue damage outside of the vessel.

SLE is an inflammatory disease of autoimmune nature involving the connective tissue of several organs systems and associated with a variable course

Sugar and sweet treats will increase a person's autoimmune symptoms and studies now prove it. Here are 3 strategies to help yourself today.

11+ nursing health assessment mnemonics & tips to help you through your nursing assessment and physical examinations and data gathering.

In this post, arthritis patient and long-time infusion patient Kate the (Almost) Great shares her "beginner's guide" for getting an infusion for arthritis.

Part of living with RA is the rheumatoid arthritis flare up. In this post, RA patient Kate the (Almost) Great shares the beginner's guide to a flare.

Dermatomyositis is a rare, autoimmune muscle disease that involves the skeletal muscles, those involved with movement, along with skin rashes such as the classic heliotrope rash. Find Dermatomyositis causes, symptoms, treatments and more.

Learn more about scleroderma and systemic sclerosis, an autoimmune disease that affects the skin and internal organs.

WebMD explains disorders that happen when your immune system, which is supposed to protect you, mistakenly attacks healthy parts of your body and what kind of treatments may be used.

WebMD's slideshow helps you understand the symptoms of lupus, an autoimmune disorder that can affect the skin, joints, and organs.

"That's what happens when your body decides to wage war on itself."

ContentsIntroductionFeatures of inflammatory arthritisRheumatoid ArthritisEpidemiology and AetiologyClinical featuresSystemic SignsEye Changes in Rheumatoid arthritisPulmonary changes in RAPresentationsPathologySystemic pathologyInvestigationsNormal initial investigationsDifferentialsManagementSymptomatic reliefSteroidsDMARD’s – Disease modifying anti-rheumatic drugsManaging other risk factorsGeneral PrognosisFlashcardReferencesRelated Articles Introduction RA is a type of inflammatory arthritis. Other examples include seronegative spondyarthritides, reactive arthritis, lyme arthritis, crystal arthritis and postviral arthritis. Features of inflammatory […]

What is Giant Cell Arteritis? Giant Cell Arteritis (GCA), also known as Temporal Arteritis, is an autoimmune condition that causes inflammation in both large and medium sized blood vessels, a... Read More