Rheumatology
Inflammatory Arthritis
Septic arthritis
Management and Tx:
- knee examination
- Hx
- hematology = FBC, ESR, CRP
- blood culture = bacterial type and drug sensitivities
- arthrocentesis = culture for bacterial type and drug sensitivities
- Abx = for specific bacteria
Notes:
- septic arthritis can be from trauma to the joints, especially the knees
- Bacterial agents for septic arthritis are usually age dependent:
--> children = Hemophilus Influenzae
--> teenagers = Neisseria Gonorrhea
--> adults = staphylococcus Aureus
Rheumatic Factor negative *PAIR Arthritis
HLA - PAIR of HULA BEE 27 BOMBERS
*Reactive Arthritis
- MOST COMMON after a GU bacterial infection
--> chlamydia trachomatus - LESS COMMON after a GI bacterial infection
--> campylobacter, salmonella
Reactive ARTHRITEEE:
"can't see, cant pee, cant bend my knee"
--> conjunctivitis
--> dysuria
--> knee arthritis or polyarthritis
"can't move my sacroili"
--> sacroiliitis in 20% of patients
AS = *Ankylosing Spondylitis
- 6 A's of AS
Notes:
- aortic incompetence is the biggest factor with AS
--> aortic regurgitation
AS Case
Notes:
- recall for Ankylosing Spondylitis -->think of 6 A's
--> especially aortic problems - also think of the rule of 2s
--> 0.2% of general population
--> 2% have HLA-B27 positive
Clinical Case
Large Vessel Arteritis
- 2 sets, both affect women
- Takayasu in young Asian women
- Polymyalgia / Giant Cell arteritis in older women
*Giant Cell Arteritis = GCA
Takayasu Arteritis
- young Asian women < 40
- IYA ATTACKA ya AORTA!!
Notes:
- note that PMR and GCA are from CD4 lymphocytes and macrophages that can turn into giant cells
- the main mediator for the inflammation is IL-6
- ESR is elevated fro the disease, but IL 6 actually gives the best factor of how severe the disease is
Clinical Cases
Clinical Case
Clinical Case
Notes:
- note that
PMR = *Polymyalgia Rheumatica
Notes:
- main difference between Takayasu arteritis and Giant Cell Arteritis /PMR = polymyalgia rheumatica
- Takayasu is in younger Asian females
--> GCA is in older people, ALL over 50 - Takayasu affects the aorta and its branches
--> GCA the temporal artery
IYA ATTACKA ya AORTA!!
- Takayasu affects the aorta and its branches
*Rheumatic Fever
- Rheumitral PYTHON
- from group A strep = strep pyogenes
- cross reactivity with IgM antibodies to the strep
- occurs 1-8 months after the strep throat
JONES Criteria
- Joint migratory arthritis
- O = heart carditis
- N = nodules under the skin
- E = erythematus marginalis
- S = sydenham chorea (soecifically in kids)
"Rheumitral Python"
--> RHD / MV regurge / Pyogenes / Rheumatoid M Pyogenes
- "RHD" = Rheumatic Heart Disease
- "Rheumitral" = MV Regurge, then chronic stenosis
- "Rheumatoid M Pyogenes " = IgM antibodies to Pyogenes
--> gives RHD and RH Fever , then chronic stenosis
--> can happen decades after exposure even?
"PYOGENES = PYO for PYOGENIC / G for JONES"
"PYO for PYOGENIC" = Pyogenic means PUS
--> "PIC your honey-crusted PUS"
--> "PIC" = Pharyngitis / Impetigo / Cellulitis
--> "honey-crusted PUS" = yellow lesions on skin
"G for JONES" = JONES major criteria for acute RH Fever means PUS
--> need 2 JONES major
--> OR 1 JONES major + 2 minor
Erythematus marginalis
sydenham chorea
--> specifically in kids
-->
Pathophys of Rheumitral disease
Giant Cell Arteritis F Factors
- similar to GB stones
--> think GIANT = Fat and forty females of GB
--> GCA is Women in fifties
- female
- fifty
- face pain = jaw claudication, vision loss
--> opthalamic artery occlusion - fifty ESR level
- four = HLADR4
- flu and fever from PMR
- firm temporal artery
*RA vs OA
*RA = Rheumatoid Arthritis
- "RheuMMatic Fc Factor = makes a PAIR of globulins" --> IgM targets the Fc site of IgG
--> RA actually due to antibodies against your own antibodies - IgM and Fc of IgG make antibody complexes
--> these specifically collect in the synnovial joint and fluid and acitvate the compliment there
--> chronic inflammation always
--> reason why you use anti-TNF-Alpha drugs
*OA= OsteoArthritis
Clinical Cases
Clinical Case
Notes:
- note that
Clinical Case
OA = Osteoarthritis
Clinical Case:
Notes:
- note that hyaline cartilage is made primarily of collagen type 2 cells and proteoglycans
--> hyaline cartilage is usually pink on histology - in OA,holes in the articular cartilage (made of hyaline cartilage) are degraded and pieces of this tissue end up in the synnovium of the joint
--> this is normal tissue and does not create inflammation, as seen in the case above
OA Clinical Case #2
Clinical Case:
Notes:
- risks for OA can be broken down into either 5 modifiable risks and 5 nonmodifiable risks
--> for OA --> look at your 2 hands = 5 nonmod risks and 5 mod risks - of the 5 nonmod risks, age is the largest, then being female (this kicks in only after 55), the family history, then abnormal joint alignement (scoliosis,etc), then joint trauma
- note that the difference between men and women is that women are more likely to get OA and they get it mostly in their knees
- men are less likely to get OA than women, and men often get it in their hips, rather than their knees
--> think it is more common for men to get their hips replaced and more common for women to get their knees replaced - note that in the modifiable risks, sedentary lifestyle and obesity are actually the number 1 and 2 risks over joint loading from overuse or work
--> this is surprising because we normally think of OA as coming from overuse of the joint, better to tell patients they can lower their risk most by being active and losing weight
*Gout
- urate crystals collect in the joints
--> unilateral - uric acid from xanthine oxidase from the IMP GMP AMP pruine sythesis / recycle pathway
- note that acutely XO inhibitors (allopurinol and febuxostat) are contraindicated in GOUT --> they can actually exacerbate arthritis
- used regular NSAID (indomethacin) and steroids
Urate crystal from synnovial fluid aspirate
*Sjoren Syndrome
- autoimmune athritic disease with antibodies against the exocrine glands of parotid sailvary glands and lacrimal glands of the eyes
- O in Sjoren gives the 2 eyes and mouth and the Ro antibody against the ribonucucleoprotein
*Home
*Mixed Rheumatoid Connective Tissue Diseases
- "Severely Punished Due to Severed RNP (Ribo nuclear Protein)"
*PMS = Polymiositis and DMS = Dermatomyositis
- PMS = progressive proximal muscle weakness
--> almost ALWAYS involves the bilateral shoulder
--> Polymio = PMS is the differential for PMR exept that PMR has bilateral shoulder PAIN, and not weakness for polymiositis - DMS = added skin problems
--> macular rash (BUT differnt from SLE since it includes the nasolabial folds)
--> classic heliotrope rash = perioccular edema and rash - Gottron papules = look very similar to gout tophi
- note that both PMS and DMS may be secondary paraneoplastic syndromes
--> need to rule this out
--> "POLy myositis" = pancreas, ovary + Lung cancers
need to be ruled out if PMS / DMS is a paraneoplastic syndrome
*SLE = Systemic Lupus Erythema
- 2 diseases wrapped in One
--> SLE causes "RASH OR PAIN" and aslo "RIP by PUMP"
--> either strict systemic disease = SLE or is drug induced = DILE
*DILE = Drug Induced Lupus erythamatous
- 3 drugs cause DILE
- isoniazid = main one from TB treatment
- also procainamide local anesthetic and hydralazine = nitrate cGMP for artioles>veins
- Drug induced SLE is unique from SLE "RASH OR PAIN"
- Drug induced SLE "has NO RASH and instead has OR HIP PAIN"
--> DILE has OR PAIN symptoms still
--> caused by HIP drugs = hydralazine, Isoniazid and Procainamide - think "TB sweats when you SLEEP and treating it gives you OR HIP PAIN when you SLE - eep"
--> isoniazid for TB can cause Drug induced SLE
*Systemic Sclerosis / Scleroderma
- 2 major types
- Diffuse Scleroderma
--> lots of skin involvement
--> very rapid progression and involvement of other tissues - Limited Scleroderma = CREST Syndrome
- note whenever you see Renaud's phenomenon and any autoimmunity problems or skin problems, think of CREST syndrome
- sclerosis can manifest in many ways
--> ex; PAH and sequelae from PAH like Right sided HF
Clinical Cases
Clinical Case
Clinical Case
Notes:
- note that
*PMS = Polymiositis
- PMS = progressive proximal muscle weakness
--> almost ALWAYS involves the bilateral shoulder
--> Polymio = PMS is the differential for PMR exept that PMR has bilateral shoulder PAIN, and not weakness for polymiositis
* DMS = Dermatomyositis
- PMS = progressive proximal muscle weakness
--> almost ALWAYS involves the bilateral shoulder
--> Polymio = PMS is the differential for PMR exept that PMR has bilateral shoulder PAIN, and not weakness for polymiositis - DMS = added skin problems
--> macular rash (BUT differnt from SLE since it includes the nasolabial folds)
--> classic heliotrope rash = perioccular edema and rash - Gottron papules = look very similar to gout tophi
DMS Gottron papules
*PMS and DMS = Paraneoplastic Syndromes Often
- note that both PMS and DMS may be secondary paraneoplastic syndromes
--> need to rule this out
--> "POLy myositis" = pancreas, ovary + Lung cancers
need to be ruled out if PMS / DMS is a paraneoplastic syndrome
HLA - PAIR of HULA BEE 27 BOMBERS - *SORCERER KING ARTHUR
- SORCERER KING ARTHUR = psoriatic arthritis
HLA - PAIR of HULA BEE 27 BOMBERS - *ANCHOR SPINE for KING ARTHUR
- ANCHOR SPINE for KING ARTHUR = Ankylosing Spondylitis
HLA - PAIR of HULA BEE 27 BOMBERS - *WRITER KING ARTHUR
- WRITER KING ARTHUR = Riters Syndrome / Reactiv Arthritis
HLA - PAIR of HULA BEE 27 BOMBERS - *SORCERER KING ARTHUR
- SORCERER KING ARTHUR = psoriatic arthritis
DIP joint fusion
- note the closing of the joint space in OA
Clinical Cases
Clinical Case
Clinical Case
Notes:
- note that
Septic arthritis
Notes:
- note that reactive arthritis always happens few weeks after either UTI or STI or enteritis and immune system persists after this
Clinical features of Reiters syndrome = Reactive arthritis
- Keratoderma Blennorrhagica = psoriatic like pustules on the palms and soles of feet
--> this is EXTREMELY characteristics of Reactive arthritis
*Keratoderma Blennorrhagica
- painless desquamative psoriatic-like papulosquamous eruption and is
--> sometimes referred to as pustulosis palmoplantaris and
--> occurs on the palms and soles of the feet. - rash in the palms and soles of feet with a chlamydia infection and reactive arthritis
Large vessel arteries affected by GCA
- external carotid artery END branches
--> Superficial temporal artery
--> Maxillary artery - internal carotid artery branches
--> opthalamic artery to the eyes
*External Carotid Artery Branches
- external carotid artery terminates when it bifurcates into the 2 main large arteries:
- STA = superficial temporal artery
- MA = maxillary artery
--> MA gives off many important branches
--> including the MMA = middle meningeal artery
-->
MA = maxillary artery BRANCHES
- MA gives off many important branches
- MMA = middle meningeal artery
--> lies behind the pterion
--> breaks in skull fractures and gives subarachnoid hemorrhages
Internal Carotid Artery Branches
*Gout
Clinical Cases
Clinical Case
Clinical Case
Notes:
- note that
Gout
Notes:
- crystal arthropathy is the condition of uric acid crystals accumulating in the synovial fluid of joints (athro-) and causing destruction
- note that Prof Obrien said the most common way people develop gout from high uric acid is not from alcoholism or kidney injury
--> mostly from people who have CCF or HF and are taking diuretics - loop diuretics >> thiazide diuretics > thiazide-like diuretics associated with an increased risk of incident gout
- MSU = monosodium urate crystals
Gout Bifiringement
- parallel = yellow
- perpendicular = blue
Clinical Cases
Clinical Case
Clinical Case
Notes:
- note that
*medications that CAUSE and TREAT Gout
- note the ACUTE vs CHRONIC is very different
*Lichen Planus
- 6 P's of Lichen Polygonal PLANUS
- Wickham Striae = white lines
--> seen in lichen planus, especially mucosal lesions - Hepatitis C virus infection may be present in 16% of lichen planus patients.
*Guttate Psoriasis
- major differential for Lichen Planus
- rash on the trunk and extremities like in Lichen Planus
Tx for Lichen Planus
- 1st line = topical steroids
- 2nd line = oral steroids
Different variations and presentations of Lichen Planus
4 main areas of involvement in Lichen Planus
- oral mucosa
- cutaneous lichen planus PLANAR PAULES or PLAQUES
--> trunk and extremities - genital involvment
- nail findings 10% of patients
- cutaneous lichen planus PLANAR PAULES or PLAQUES
Nail lichen planus
Cutaneous lichen planus
- distal limbs
- flexors of forearms and wrists
- lower back
- Köbner phenomenon = arises at areas of trauma or scars
Oral Mucosal lichen planus
