Hello people 🤓
Today’s thread is about
“Rheumatoid Arthritis”
Enjoy!🙃
.
Today’s thread is about
“Rheumatoid Arthritis”
Enjoy!🙃
.
Rheumatoid arthritis (RA) is a chronic systemic inflammatory disorder ☝🏼😲
Meaning that not only joints are affected but also other organs (like the skin, lungs, etc)
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(2nd & 3rd image are from: creakyjoints.org)
Meaning that not only joints are affected but also other organs (like the skin, lungs, etc)
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(2nd & 3rd image are from: creakyjoints.org)
Let’s start with anatomy shall we🥸
So you know that a joint is where 2 bones meet🙃
Each bone is covered by articular cartilage at the end which is 👉🏼A smooth connective tissue that helps bones glide over each other (with very little friction) to allow movement
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So you know that a joint is where 2 bones meet🙃
Each bone is covered by articular cartilage at the end which is 👉🏼A smooth connective tissue that helps bones glide over each other (with very little friction) to allow movement
.
The most common type of joint in the human body is the
‘Synovial joint’
It has an articular capsule which encloses the joint and it extends from the periosteum of the articulating bones🦴
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(Image is from: myhealth.alberta.ca)
‘Synovial joint’
It has an articular capsule which encloses the joint and it extends from the periosteum of the articulating bones🦴
.
(Image is from: myhealth.alberta.ca)
The outer layer is the fibrous layer it holds the articulating bones together
The inner layer is made of the synovial membrane, a highly vascularized layer of serous connective tissue👌🏼 It absorbs and secretes ’synovial fluid’ (a thick, viscid fluid)
+ Articular cartilage
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The inner layer is made of the synovial membrane, a highly vascularized layer of serous connective tissue👌🏼 It absorbs and secretes ’synovial fluid’ (a thick, viscid fluid)
+ Articular cartilage
.
So how does Rheumatoid arthritis happen , what is the pathogenesis? 🤔
Well unfortunately the exact pathogenesis is still not understood 🙁
Well unfortunately the exact pathogenesis is still not understood 🙁
But☝🏼😏
There’s a theory that says
a genetically susceptible individual(As in those who carry the HLA-DR1 and HLA-DR4) & are exposed to a certain external risk factor (like cigarette smoking, infection, or even trauma)
👉🏼 Trigger an ’autoimmune’ reaction and modifies antigen😱
There’s a theory that says
a genetically susceptible individual(As in those who carry the HLA-DR1 and HLA-DR4) & are exposed to a certain external risk factor (like cigarette smoking, infection, or even trauma)
👉🏼 Trigger an ’autoimmune’ reaction and modifies antigen😱
As in👇🏼
Type 2 collagen and vimentin (a type of protein) are converted from amino acid arginine into the amino acid citrulline
This process is called👉🏼Citrullination
(Image courtesy of: sciencedirect.com)
Type 2 collagen and vimentin (a type of protein) are converted from amino acid arginine into the amino acid citrulline
This process is called👉🏼Citrullination
(Image courtesy of: sciencedirect.com)
The (HLA-DR1 & HLA-DR4) genes 🧬 have a major influence on CD4 T-helper cells, How?🫣
When citrullination happens immune cells won't identify the changes that have happened due to the HLA-DR1 & HLA-DR4 genes🧬
So,
Antigens are transported to the lymph nodes by antigen-presenting cells where they're expressed to CD4 T-helper cells
(Image:mdpi.com)
So,
Antigens are transported to the lymph nodes by antigen-presenting cells where they're expressed to CD4 T-helper cells
(Image:mdpi.com)
This will stimulate B-cells
👉🏼 B-cells proliferate and differentiate into plasma cells👉🏼produce autoantibodies against the self-antigens
(Image courtesy of: intechopen.com)
👉🏼 B-cells proliferate and differentiate into plasma cells👉🏼produce autoantibodies against the self-antigens
(Image courtesy of: intechopen.com)
These T- helper cells and antigens go to into the joint, and since they're going to attack mode 🥷👊🏼 T-cells recruit inflammatory cells, like macrophages by cytokines secretion of interferon-gamma & IL-17
.
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When macrophages come to the area they also produce cytokines (TNF-a, IL-1, IL6)
They all mistakenly attack the synovium👉🏼causing an inflammatory response👉🏼 synovial hypertrophy👉🏼 and pannus formation (abnormal tissue)
(Image courtesy of: researchgate.net)
They all mistakenly attack the synovium👉🏼causing an inflammatory response👉🏼 synovial hypertrophy👉🏼 and pannus formation (abnormal tissue)
(Image courtesy of: researchgate.net)
But it doesn't stop here 😞
Due to the inflammation, abnormal tissue growth of proliferative granulation tissue, mononuclear inflammatory cells, & fibroblast-like mesenchymal cells 👉🏼 Pannus forms in the joint
Due to the inflammation, abnormal tissue growth of proliferative granulation tissue, mononuclear inflammatory cells, & fibroblast-like mesenchymal cells 👉🏼 Pannus forms in the joint
Pannus releases enzymes called lysosomes that damages cartilage, soft tissue and bone (causes bone erosions) ☹️
T-cells express RANKL (Receptor activator of NF-kappaB ligand)
RANKL is a type 2 membrane protein that are involved in Osteoclastogenesis
RANKL👉🏼binds to RANK induce osteoclast formation 👉🏼 bone destruction
RANKL is a type 2 membrane protein that are involved in Osteoclastogenesis
RANKL👉🏼binds to RANK induce osteoclast formation 👉🏼 bone destruction
The Antibodies involved are the
1. Rheumatoid Factor (RF)👉🏼 an IgM autoantibody against the Fc portion of IgG
The higher RF titers, the poorer the prognosis.😓
(Image courtesy of:practicalpainmanagement.com)
1. Rheumatoid Factor (RF)👉🏼 an IgM autoantibody against the Fc portion of IgG
The higher RF titers, the poorer the prognosis.😓
(Image courtesy of:practicalpainmanagement.com)
2. Anti–citrullinated protein antibody
👉🏼 targeted against citrullinated proteins👉🏼accumulate in the joint form immune complexes👉🏼Activate complement system👉🏼Cause inflammation 👉🏼Angiogenesis formation 😬🫢
👉🏼 targeted against citrullinated proteins👉🏼accumulate in the joint form immune complexes👉🏼Activate complement system👉🏼Cause inflammation 👉🏼Angiogenesis formation 😬🫢
Angiogenesis makes matters worse
It causes more inflammatory cells to reach the joint
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It causes more inflammatory cells to reach the joint
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Reaching the hallmark ✨ characteristic feature of rheumatoid arthritis
👉🏼constant symmetric polyarthritis (synovitis) affecting the hands and feet, and any joint with synovial membrane.
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👉🏼constant symmetric polyarthritis (synovitis) affecting the hands and feet, and any joint with synovial membrane.
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Once the inflammatory cells see that the space of the joint is tight they escape via blood vessels and go to👉🏼Extra-articular organs like the skin,heart,lungs,& eyes😱
Remember it’s a“systemic” infection
For example,Skin👉🏼formation of rheumatoid nodules
(nras.org.uk)
Remember it’s a“systemic” infection
For example,Skin👉🏼formation of rheumatoid nodules
(nras.org.uk)
Or in Blood vessels
👉🏼 Vasculitis and are prone to form atheromatous plaque
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👉🏼 Vasculitis and are prone to form atheromatous plaque
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Rheumatoid arthritis usually affects multiple Joints symmetrically
Like,Both hands ✋🏼🤚🏼 or both feet
Like,Both hands ✋🏼🤚🏼 or both feet
Usually, it starts affecting the smaller joints first like:
👉🏼Metacarpophalangeal joints (MCP) of the hand
Then
👉🏼proximal interphalangeal joints of the hand
Then
👉🏼The metatarsophalangeal joint of the feet
Remember, osteoarthritis is distal phalanges then carpometacarpal🙃
👉🏼Metacarpophalangeal joints (MCP) of the hand
Then
👉🏼proximal interphalangeal joints of the hand
Then
👉🏼The metatarsophalangeal joint of the feet
Remember, osteoarthritis is distal phalanges then carpometacarpal🙃
As it progresses it goes on to greater joints, like knees, elbows, and shoulders.
.
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Flares are symptoms that include joint pain, swelling, warmth and stiffness (especially in the morning) it remains more than 30 minutes ✋🏼😲🤚🏼
Overtime deformities of the hand start to appear 🤚🏼
Swan neck deformity
Ulnar deviation
Boutonnière deformity
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Swan neck deformity
Ulnar deviation
Boutonnière deformity
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Approach 🩺
Take history (especially asking if the joint stiffness persist>6weeks)
Physical Examination (like general examination and checking the range of joint movements, etc)
Rule out Differential Diagnosis;
(2nd image is from:creakyjoints.org)
Take history (especially asking if the joint stiffness persist>6weeks)
Physical Examination (like general examination and checking the range of joint movements, etc)
Rule out Differential Diagnosis;
(2nd image is from:creakyjoints.org)
Some of the Lab tests
👉🏼 Complete blood count (CBC)
👉🏼 Rheumatoid factor (RF) assay
👉🏼 Antinuclear antibody (ANA) assay
👉🏼 Anti−cyclic citrullinated peptide (anti-CCP)
👉🏼 Complete blood count (CBC)
👉🏼 Rheumatoid factor (RF) assay
👉🏼 Antinuclear antibody (ANA) assay
👉🏼 Anti−cyclic citrullinated peptide (anti-CCP)
Other investigations that is used is imaging like X-ray (commonly used), ultrasound, MRI
Here are the findings on an x-ray🧐
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Here are the findings on an x-ray🧐
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Treatment 💊
Disease-modifying anti-rheumatic drugs (DMARDs) like Methotrexate
👉🏼 they reduce inflammation and slow down the disease progression
Biologic DMARD like rituximab
👉🏼 They aim at a specific pathway of the immune system
Guidelines for management 👇🏼
Disease-modifying anti-rheumatic drugs (DMARDs) like Methotrexate
👉🏼 they reduce inflammation and slow down the disease progression
Biologic DMARD like rituximab
👉🏼 They aim at a specific pathway of the immune system
Guidelines for management 👇🏼
Just to clarify this is just textbook general information, management depends on case and treating physician
That’s it, this is end of my thread
I hope you got the most out of it, I know it’s a heavy topic but reviewing makes perfect
Thank you for reading it ☺️
.
I hope you got the most out of it, I know it’s a heavy topic but reviewing makes perfect
Thank you for reading it ☺️
.
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