Rheumatology

Causes of acute monoarthritis

Common MCQ
1-Gout & Pseudogout 2-Trauma 3- Haemarthrosis
4-Spondyloarthritis 5- Psoriatic arthritis 6- Reactive arthritis
Less common
1- Rheumatoid arthritis 2- Juvenile idiopathic arthritis 3-Foreign body reaction
4- Tuberculosis 5- Leukaemia* 6-Gonococcal infection
7- Osteomyelitis*
Investigations
1- Aspiration of the affected joint is mandatory. The fluid should be sent for:
culture and Gram stain checked for crystals .
2- Blood cultures 3- CRP levels and ESR are raised
4- Serum uric acid 5- Ruling out 1ry PTH is essential if there is pseudogout.
Management
1-If there is any suspicion of sepsis, IV antibiotics should be given pending the results of
cultures .
2-intra-articular glucocorticoid may be considered after 48 hours of negative synovial fluid culture
3- Treat the underlying cause.

Polyarthritis (This term is used to describe pain and swelling affecting five or
more joints)
Non-inflammatory MCQ
1- Generalised osteoarthritis 2- Haemochromatosis 3-Acromegaly
Inflammatory
1-Viral arthritis 2- Rheumatoid arthritis 3- Seronegative spondyloarthritis
4- SLE 5- Chronic gout 6- Juvenile idiopathic arthritis 7-
Chronic sarcoidosis 8- PSS 10- Hypertrophic osteoarthropathy
Investigations
1-CBC, 2- biochemistry ( Ca, Po4, ALP) 3- ESR, CRP ,
4-viral serology 5-Antibody (ANA, RF ( 6-US or MRI may be required
Management
1-NSAIDs
2-Systemic glucocorticoids can be considered if symptoms are very severe
4- Treatment according to cause.

*Classification:
MCQ
Sero (+ve): 1/R.A -2/SLE-3/ Scleroderma-4/Sjogren Syndrome- 5/polymyositis
Sero (-ve): HLA B-27 1/Ankylosing spondylitis. 2/Psoriatic arthritis.
3/ Reactive arthritis 4/Sclerotic Arthritis 5/IBD Arthritis.
 Rheumatoid Arthritis
Def: Chronic relapsing & remitting poly-arthicular erosive synovitis of small joints
mostly ( hand and feet) with multisystem involvement .
Causes: most likely autoimmune b\c : MCQ
1) Female > male 3:1 2 ) (30-50yrs) middle aged.
3) +ve F\H. 4) Genetic predisposition HALA Dr4 & Dr1
5)Abs that can be found
a) Rheumatoid factor, Most sensitive (70-80%), but low specific.
b) CCP antibody, (Cyclic citrullinated Peptide) highly specific & low sensitive 30%
C) ANA
Clinical Picture:
All hand joints affected except Distal
A- Articular manifestations (Most common presentation):: phalangeal  b\c it's not synovial type.
1-Arthritis :
1\ Symmetrical 2\ Non migratory (irreversible ) .
3\ Erosive. 4\poly articular synovitis > 2-3 joints.(10% Mono)
Mainly affected joints of hands:
1) Wrist, MC Site ( may present with carpal tunnel syndrome). MCQ
2)PIP 3)MCP 4)MTP 5) Ankle 6) Knee 7) Elbow 8) Shoulder 9) Hip (last affected
N.B: The only non-synovial joint affected is Atlanto-Axial Joint Their for its C\I to do neck
extension b\c  Generalized paralysis death.
2-Pain: mostly ass’ with tenderness early morning more than 1hr
3-Swelling: indicates active disease, but NO redness,
if redness  2ry complication (Trauma. Septic arthritis. Gout)
NB: Joint swilling with redness, the 1st aid of management is (Arthrocentesis
4-Muscle wasting: due to
1/nerve compression (median nerve which supplies thenar Msc) compartment syndrome (Rx
by Fsciotomy.)
2/myositis, (Arthritis Tendinitis  myositis) MCQ
3/disused of Muscles (active disease)  wasting.
5- Deformity: the best indicator for chronicity & uncontrolled
1) Wrist joint:
*Erosion of radio styloid process  radial deviation (decrease space).
*piano key deformity: subluxation of Radial styloid process (wrist drop).
2) Metacarpal phalangeal joint:
*ulnar deviation,
*Pop up deformity, Subluxation of metacarpal phalangeal joint.
*Z-deformity of the thumb (flexion of MCP & extension of IPJ)
3) Proximal interphalangeal joint: *
Swan neck deformity (extension of PIP& Flexion of DIP
*Boutonniere deformity, (extension of DIP & flexion of PIP)
4) Metatarsal phalyngeal joint:  hummer toe deformity

B- Extra Arthicular: Less common presentation. Nodules indicate:

1-Skin Manifestations: most common 1/ active disease.
1) subcutaneous nodule. 25%  Most common sites: 2/ severity by size
1/Extensor surface of elbow (single) & hand(multiple).
. 2/ wrist, sacrum & tendon Achilles.
. 3/ sclera (blurred vision ) Ix, by fundoscopy & slit lamp.
. 4/Heart myocardium = H.F
. 5/ lung Asymptomatic. MCQ
2) Palmer erythema 3) Reynaud’s phenomena
4) pyodermal gangrenosum 5) Dubytrene contracture

2-Neurological manifestation :
1)Carpal Tunnel Syndrome:
2)Tarsal compartment syndrome : complains of tingling & parasthesia in foot
3)Cervical cord compression : Atlanto Axial Subluxation Tingling & parasthesia in UL.
4)Mono neuritis multiplex :one group of nerve affected (motor or sensory)
3-Ocular Manifestation :
Kerato conjunctivitis sicca (Sjogran Syndrome ) it’s most common presentation.
Scleritis: most serious presentation painful and affect the vision & corneal erosion.
Episcleritis: not affect the vision & usually painless.
Scleromalascia perforans :
MCQ
4-Pulmonary manifestation:
*subcutaneous nodule which affect the lung  asymptomatic  (Caplan syndrome), * Abs
attacks interstitium of lung (Cryptogenic fibrosing alveolitis) restrictive PFT
* (Pleurisy)  pleuratic chest pain and pleural effusion (Exudate + low suger).
5-Cardiac Manifestation:
H.F & Arrhythmia & IHD due to Vasculitis . Endo+ Myocarditis
Pericarditis: common in R.A  pericardial effusion or complications =rare
Renal Manifestation: Causes of Nephrotic Syndrome
Nephrotic Syndrome but not common now Direct: Amyloidosis
6- Musculoskeletal Manifestation : Indirect Drugs: D-pencillamine
Muscle wasting, Myositis, tendinitis & Baker’s cyst. & Gold Salts.
7- Lymphatic Manifestations :
Felty Syndrome: female, old age >50yrs, Caucasian, long standing (chronic after 15-20
years) Rh.factor +ve & rheumatoid nodule.
C\P: splenomegally + pancyopenia +R.A MCQ
May be associated with Lyphadenopathy, wt loss, Kerato conjunctivitis sicca- (dry eye) ,
chronic ulcers, skin pigmentation & recurrent infections.
INV: Lab: pancytopenia + LFT abnormality & impaired T &B Cell,( risk Lymphoma)
8-Hematological Manifestation :
Commonly R.A Ass’ with Anemia, which caused by Chronic disorder, Pancytopenia NSAIDS,
Methotrexate, Hypersplenism) X-ray: hand deformity.(US & MRI
MCQ most sensitive)
Investigation: Nerve Conduction study: carpal
CBC: HB, WBC or (Felty Synd). tunnel.
ESR & CRP: C.T: to exclude Atlanto Axial
subluxation.
LAB Slit lamp & fundoscopy  eye
Echo& ECG: IHD, Arrhythmia, H.F
Abd U\S: splenomegally &
Specific hepatomegally.
Urine Analysis: Nephrotic Syn
ABs Imaging
1-RF (IgM AGAINST bodys RH Factor of IgG)
+ve, indicate Severity of the disease not Activity. Radiological Feature of Hand:
2-CCP= Specific 1-Soft tissue Swilling.
MCQ 2-Periosteal osteopenia Ca+.
3-ANA= Not sensitive & not specific.
Specific Criteria: 4/7 confirm the diagnosis. 3-No Arthicular Space.
By H\O, 1) Morning stiffness >1 hr for > 6 wks. 4-Deformity.
By Ex, 2) polyarthritis than 3 joints affected. 5-Ulnar Deviation.
3) Small joints > large joints. 6-Ankylosis (arthicular spaces fusion)
4) Symmetrical. 5) Subcutaneous nodule.
By INV, 6) Rh.F  Sero +ve. 7) Evidence of radiological changes of X-ray.
Management: TEAM WORK TREATMENT.
Medical Therapy: DMARD (Disease Modifying Anti Rheumatoid Drugs)DOC
Need 8-12 wks to be effective, so add NSAIDS to reduce the pain, but avoided in Patient
with GIT erosions (Peptic Ulcer) by history taking.
If not responded to NSAIDS Add High dose of steroids for8-12wks,The all the above
mentioned have no effect on the course of the disease, but to decrease a pain.
DMARD’s:
1\ Methotrexate: the DOC of DMARD’s, the best to decrease a Disability & erosions but
have S\E  [(Anti foliate) megaloplastic anemia & Hepatorenal toxicity] so given with Folic
Acid.
 MCQ
2\ Sulphasalasine: one of first line Drugs, But S\E:
1/Gastric Upset 2/Depression. 3/ Oligospermia reversible infertility.
3\ Anti malarial: Hydroxychloroquine: cheap, but cause a Macular Damage.
So must be follow up regularly / 6mounths  Fundoscopy.
Dapsone:  pyodermal gangrenosum & S\C Nodule (Skin CP).
4/Tissue Necrotizing Factor (TNF) modulator agent :
1/ Inflximab(immunosupprasent):CD20 Inhibitor 2/Anti TNF MCQ
Poor Prognosis:
1/ Age of presentation if than 60s yrs. 2/ Sudden Onset of multi systemic.
3/ symptoms lasting for more than 12 months. 4/ if 1ry presentation is an extra arthicular
5/ early deformity within first 6 months – 2 years. 6/ High Anti CCP & RF titer.
Home work: 2017: Q1 to Q20
1001: Q 879 – 881 – 885 – 895 – 897 – 900 – 923 – 927

2) Systemic Lupus Erythromatosis (SLE)

Def: chronic R&R non erosive polyarthicular disease which lead to multi systemic
involvement, due to circulating immune complex and auto anti bodies.
Causes:
A) Autoimmune disease:
1\ female > male 9:1. 2\ onset: 13-40yrs. (child baring age)
3\ ass’ with genetic predisposition HLA Dr2&3.
4\ ass’ with +ve F\H. 5\ass’ with other autoimmune diseases.
6\ circulating Abs:
1) ANA (anti-nuclear antibody) highly sensitive 90% or more but not specific
2) Double strander DNA Abs 50%of cases  highly specific & Low sensitive
3) Rh.F  low sensitivity & specificity.
Anti-phospholipied syndrome :
4) Anti RO & Anti LA: related with pregnancy
May be associated with SLE but not
 Infertility. Or  Spontaneous Abortion. Or 
mandatory
Intra uterine fetal death. Or  Neonatal Lupus 
CP: 1-Blood cloths (DVT) 2-Miscarriage,
Congenital Heart Defect 3th degree Heart Block.
3-Rash, 4- Chronic Headach ,
B) Environmental: It’s propagated by sunlight
C) Hormonal: Exacerbated by estrogen & progesterone . Dementia &Seizers
***Clinical Picture*** Dx:1-APL anti. 2- Anti cardiolipin
A\ Arthicular: first feature to develop (most common) Abs 3- VDRL +Ve 4- ESR usally N
1-polyarthicular affects large joints than small joints. 2- Asymmetrical.
3- Migratory (flitting) or (fulminate), 4-Non erosion
5-Deformity  Rupture of tendon  (Jaccauds arthropathy)
6-Pain, tenderness, swilling & Redness.
B) Extra Arthicular: 80% mostly with skin manifestation.
1-Skin manifestation: is the most common feature of SLE.
1\ Malar Flush (Butter Fly): Painful, itchy+Affect Nose & Cheeks Sparing Nasolabial fold.
2\ Alopecia: Non scaring Alopecia, (Reversible).
Discoid Lupus :red plagues with crusts, most common in extremities But in scalp
. scarring alopecia by fibrous tissue growing.
3\ photosensitivity: Common in black, Rx: by sun blocking creams.
4\ Mouth Ulcer: Early painless but if exposed to infection lately painful.
5\Nail fold Infarction + Pre angular erythema + Splinter Hge (common).
6\ Reynaud’s phenomena (2ry) :
7\ Levedo Reticularis: Redness + patchy pallor colure of skin (Arms & L.L).
2- Neurological Manifestation:
1\ Psychosis ( affect visual & auditory function)= Cerebral lupus 60%.
2\ Epilepsy. 3\ Peripheral Neuropathy, less common.
3- Lung: Pleursy Plural effusion + ILD
4- Cardiac:
Endo Myo  pericarditis  Pancarditis (Non infective= LIBMAN SACKS SYN)
5- Renal:
Vasculitis  B.V of Bowman’s capsule  Nephritic Syn [Haematuria & Proteinuria] .
6- GIT Manifestations:
Severe Abd pain (epigastric) due to peritonitis. peptic ulcer Acute Pancreatitis
7- Hematology:
Autoimmune hemolytic Anemia. MCC
8- Lymphatic system :
CBC: H.B *Anemia (Auto immune
Lymphadenopathy common 50% + Splenomegaly 20-30%
Hemolytic Anemia). Comb’s test +ve
*Pancytopenia ( low WBC)
Investigations ESR increased & CRP (normal) if high
LAB indicate infection. C3 & C4 =low
RFT & Proteinuria +*Renal biopsy

Specific
Abs Imaging
X-ray of affected joint:
EEG: for neurological manifestation.
1-ANA: 90% +ve, high sensitive & low specific. CXR: lung (ILD). 2-
Ds DNA Ab: highly specific. ECG &ECHO:
Anti RO & LA: Pregnancy. Endoscopy: *Peptic ulcer.
VDRL: Venereal Disease Research Laboratory,
Diagnostic Criteria for SLE: *** Clinically (Mostly) > 4 Dx
1) Mallor Rash. 2) Discoid Lupus. 3) Oral ulcer. 4) Photosensitivity.
5) Arthritis (than 2 joints) 6) Serositis;( Peritonitis, Pleuritis, pericarditis)
7) Renal involvement 8) Hematological Disorder 9) Neurological Disorders
10) By INV: *Immunologically: ANA & Ds.DNA.
Management of SLE:
1-Occupational. 2-Psychotherapy  depression (group therapy).
3-Physiotherapy  rehabilitation. 4-Orthopedics to treat deformities (not mostly)
5- Sunrise  sun blocking creams. 6-pregnancy  screening of Abs.
A-*Coetaneous: DOC is anti-malarial drugs (Hydroxychloroquine & Dapson creams) If not
responded,  Methotrexate cream (strong immunosuppressant).
B-*Joint manifestations: Hydroxycloroquine but if not responded  NSAIDS,
C-*reynauds phenomena: Ca+ channel blocker (Nefidipine)
D-*End Organ Damage :  immediately Start with High Dose Steroids or imunosupression
E-* Hypertension, DOC is ACE inhibitor (captopril). *causes of Death in SLE:
1/Renal Lupus nephritis. (Mostly)
Prognosis:
2/CNS Involvement.
* 90% of them Life span exceeds 5yrs survival rate.
3/Cardiac IHD,
Drugs induced SLE: (Anti histone antibodies +ve)
when they use some drugs give symptoms similar to SLE, except symptoms of CNS & Renal
Involvement, also may find same Abs but impossible to find, Ds.DNA &+ve VDRL. This case
called  pseudo Lupus, Rx by stop the drug.

1/Aspirin high dose 300mg long 2/ Phonation , 3/ methyl dopa 4/ phenobarbitone.

5/ isoniazide 6/procaine amide. 7/ hydralazin. 8/ Minocycline.
Home work: 2017: Q21 to
9/ B-Blocker. Q32
1001: Q 876 – 883 – 889 – 892 – 893 – 896 – 898 – 906 – 907 – 925 – 929
3) Scleroderma (progressive Systemic Sclerosis )
Def: Chronic Multi systemic of unknown etiology, affects micro BV & Skin.
Cause: mostly *Autoimmne:
1-female 4:1. 2– Middle aged group. 3-+ve F\H. 4– ass’ with other autoimmune diseases.
5– Antibodies (Rh.F, ANA, ASD70 & ACM Abs)  skin & micro vascular disorder.

Skin Micro vascular

Onset : initiates later on.
1- mostly deposition of fibers in
C\P: Face  Mask Face, b\c of
thickening .
2- by stretching  tapered Nose.
3- Microstomia (Fish Mouth) .
4- hyper pigmented with hypo
pigmented areas, called Salt &
pepper appearance.
*Initiates firstly before Skin
manifestations.
1-Years with no complains except ,
Reynaud’s phenomena(2ry)
2- sausage like fingers
3- long & tapered fingers Sclerodactyly,
4/Continued Ischemia necrosis 
Amputation (indicates chronosity).

Other Manifestations:
1-Joints: non erosive mild arthritis at beginning, then in severe case  Erosive
2-GIT: *Esophagus: Dysphasia & GERD. *Stomach: Early Satiety.
* Duodenum: pyloric stenosis & Gastric outlet Obs  Projectile vomiting.
*Intestine: Bacterial overgrowth  Malabsorption (Blind Loop Syn)
3-Pulmonary: ass’ with ASD70 Abs : ILD  P HTN  R.t Side H.F (Cor pulmunale)
4-Renal : Glomerulonephritis  Nephritic Syn Hypertension crisis cause (Death).
*Types of Scleroderma:
Limited Scleroderma : Diffuse Scleroderma :
Coetaneous manifestation mainly affects face, Hands Coetaneous manifestation mainly affects large area
& feet distally, with no end organ damage, CRESTSyn of skin with internal organs & presentation of
C: Calcinosis. R:Raynauds Phenomena. CREST Syn .
E: Esophageal Involvement S: Sclerodacytly. *ASD70 Abs.
T: Telangectasia. * Poor prognosis.
*+ AC Abs . & *has good prognosis.

* Investigations of Scleroderma:
LAB CBC: Anemia of chronic illness WBC. ESR High & CRP normal unless in case of
infection mostly gastroenteritis. RFT: Renal
Antibodies  ANA 70% , Anti-topoizomeraze Ab (ASD70) 30% (Diffuse type) & AC Abs
60% (Limited Type), to confirm Dx.
Imaging  Barium Meal: Esophagus & barium Enema: Intestinal Manifestation .
No specific criteria, Skin biopsy in untreated case.

Management: symptomatic therapy.

Skin Manifestation  Methotrexate or Dapson. Blind Loop Syn Abc’s.
Lung  High dose steroids & Pulmonary HTN = Bosentan. Kidney  ACE I  B.P.
GERD  omeprazole (proton pump inhibitor). Arthritis  NSAIDS.
Gastric Outlet Synd  Surgery.
Poor prognostic factor:
5years survival rate.  Up to 70%. 1-Old age. 2-Pulmonary HTN. 3-Proteinuria. 4- ESR
5- Diffuse skin disease.
Home work: 2017: Q33 to Q43
1001: 882 – 890 – 899 – 908 – 909 – 920
5)Sjogrens Syndrome
Def: Autoimmune disorder affects exocrine glands
1- female 9:1. 2- Middle age. 3-+F\H. 4-HLA B8&Dr3 5-
ass’ with autoimmune dis.= *Myasthenia grave’s. *Chronic Hepatitis. *R.A * SLE. *KCS.
*1ry biliary cirrhosis 6-
autoimmune circulating AB: (Rh.F, ANA, Anti RO&LA). MCQ
 Lacrimal glands (salivary glands) Parotied Gland Vaginal glands
CP Xerphtlamia (dry Xerostomia (dry Dyspareunia highly
eye)  F.B mouth) (dental risky to infection.
sensation & redness. caries).
Dx: Schemer test Saxon test buccal mucusa
Anti RO 70%, Anti biopsy
LA 30%. RF(90%)
& ANA(70%)
Rx: artificial tear or pillocarpine. lubrication creams
dark glasses.

Other features *non erosive Arthritis. * Reynaud’s phenomena.

* Fever, myalgia, arthralgia *lymphadenopathy  40 times more risk for lymphoma.

Home work: 2017: Q44 to Q47 Autoimmune:

1001: 878 – 911 – 926 1- female 3:1. 2- Middle age.
MCQ 3-+F\H. 4-HLA Dr3
5- ass’ with other Aut I Dz
6)polymyositis & Dermatomiositis
6- AB: (Rh.F, ANA, Anti JO1).
*Etiology is unknown but mostly, autoimmune 
C\P: symmetrical bilateral Painless weakness of proximal Msc’s ( Distally Proximal )
Lower limb then  Upper limb  Myalgia & Arthralgia Late.
Other Muscle affected:
1\ Diaphragm  Res Failure (Apnea) 2\Esophagus  Dysphgia.
3\ Larynx  Horsens of voice
*Skin Manifestation: Dermatomyositis
1\photosensitivity skin rash.
2\Erythematous Skin Rash over, chest  V sign, over shoulder  Shawl sign.
3\ Heliotrop Rash  over cheeks & eyelids.
4\ Gottron Sign  rough red papules over knuckles of fingers if with purities
5\ Calcinosis cutis thickening of finger tips.
6\Reynaud’s phenomena. MCQ
7\Joint Swelling (large joints) not common.
Investigations :
MCQ
LAB  *CBC, ESR &CRP  High ( not in all cases)
* Msc Enzymes: 1\Creatnine Kinase  severity only, in 70% of cases.
. 2\ LDH the same, both used as screening marker.
. Urine analysis  myoglobinuria +ve  severity & activity
Abs= Rh.F+ve, ANA +ve, & Anti JO1AB  +ve, not sensitive.
Imaging =*Electromyogram (EMG), to distinguish from neurological disease. (G.B.S
&Toxoplasmosis).
Specific: Msc Biopsy  projections of T.Lymphocytes & fibroblasts. May presented as patchy
type  so need (MRI guided biopsy)

Management: TEAM WORK THERAPY.[psycho ,occupational & physiotherapy].

1\ High dose of steroids orally, except in cases with Diaphragm involvement & Laryngeal spasm
given I.V. or IV immunoglobulin's
2\ Dyspnea  Mechanical Ventilator.
Myopathy resulting by Steroied side effect  reduce the dose of steroid and adding of
[methotrexate or azathioprine] to preserve the remission stage.
Prognosis Necrotic tissue may change to malignancy in old >60yrs.
Home work: 2017 Q48 to Q50
1001: 891 – 905 – 910
Sero –ve = 1-Ankylosing Spondylitis male > female 3:1
its chronic slowly progressive arthritis which
Site: lower back pain (sacro-iliac j).
mostly affecting Sacro-iliac joint
MCQ Severity: sever early morning pain.
C\P: SOCRAT Onset: gradually.
H\O: Character: electrical dull pain.
1\loss of lordosis. 2\ range of spine movement. Radiation: to spine & Gluteal region.
3\ decreased chest expansion. 4-artralgia of large J 40% Relived: by movement.
Aggravating: Coldness.
Dx:
Associated:
C.T or x-ray of Spine: loss of normal lordosis (bamboo spine)
1\ 2ry osteoporosis. 2\ spinal #.
Rx: 1-Reassurance 2) swimming to asses back Muscles. 3\peripheral arthritis. 4\ *Ant Uveits.
3) Lower back pain  NSAIDS. 5\Prostatits 80%. 6\ pericarditis.
4) Peripheral arthritis & end organ damage  7\M.R & A.R. 8\ amyloidosis.
DMARDS (Methtrexate& sulfasalasine). 9\ pulmonary fibrosis
Timing: early morning.
Home work: 2017: Q51
1001: 887 – 901

2) Reiter Syndrome : (Reactive Arthritis ) : MCQ

*Male > female 15:1, (20-30 years)
Triggered by infections usually infectious Diarrhea caused by food poising (salmonella
dysentery),
C\P: 1- *patient can’t see (Bilateral Conjunctivitis 30%) cant pee (Urethritis), can’t
climb a tree(Arthritis) asymmetrical .
2-circinate balanitis (ulcers on male organ) 3-*Keratoderma blennorrhagia
4-*Oral ulcer (painless) geographical tongue. 5-*Nail Dystrophy
Investigations < the best is History & proved Examination >
Rx: use Steroids  responded to most of cases, used until CP disappearance
Home work: 2017: Q51 to Q55
Crystal Induced Arthropathy:

Gout Pseudo Gout

Mono articular synovitis due to deposition of mono Mono articular synovitis due to deposition of Calcium
sodium urate mono hydrate crystals (MSUM),. pyrophosphate Di hydrate (CPPD) Crystals.
*Mostly with male Mostly with female.
The uric acid increasing by:
1\ production :
*endogenous:(cell lyses ) as in Tumor lysis
*exogenous: digestion (meat)
2\ excretion (renal tubule defect) most common.
*congenital: isolated RTD. (Pediatric).
* Renal failure. MCQ
*Drugs: - Loop Diuretics & (Thiazide.)
– Pyrazinamide. -Cyclosporine. – lead
– Low dose Aspirin b\c long standing use
Alcohol (lactic acidosis).
*Acute symptomatic Gout: *Acute symptomatic Pseudo Gout :
Podagra = crystals deposited at 1stmetatarsal Arthritis: red hot tender swollen joint  mainly affect
phalngeal joint (big toe)  hot, swollen & tender Knee joint but may also, wrist & Shoulder.
Other joints: Ankle, Knee, wrest & Elbow. Distinguished with gout, by arthrocentesis  type of
crystals.
*Chronic Gout: - *chronic pseudo gout :
1-Arthralgia: very severe painful. 1- Arthritis: chronic joint pain.  b\c 2ry
2-Tophi  skin of extensor surfaces of Wrist, osteoarthritis  arthroplasty.
Elbow, fingers, Achilles tendon , ear auricle .
3-Renal Failure 1-CBC:  WBC. 2-ESR (Severity)
Investigations: 3-CRP (Prognosis)  screening
4- renal function, 5-uric acid,
LAB
Arthrocentesis (aspiration): it’s diagnostic 6-Glucose 7-lipid profile
*Spindle shaped  Na Urate.
* Cuboidal (+ve birefringent crystals) 
Ca pyroph Specific
Abs Immaging

X-ray punch out lesion.

Gout Pseudo Gout

Treatment of Acute attack Treatment of Acute attack
Pain  colchicines tab DOC not responded  Same
NSAIDS (Endomethacine not high does Aspirin) not
responded  steroid cream, if not responded oral
or Intra articular steroid
N.B;but never ever use in acute stage  Allopuranol
Treatment of Chronic attack 1-decrease Weight
Allopuranol: hypo uracemic agent. 2-analgesia (endomethacine & paracetamol)
*used in: 1-recurrent attacks, not in acute attacks. 3-Arthroplasty
2- Tophy  at chronic stage can be used.
3- If there is any evidences of joint damage.
4- If gout  renal disease.
5- If greatly elevated Uric acid than 10
Febuxostat also inhibits xanthine oxidase

Home work: 2017: Q56 to Q61

1001: 886 – 894 – 902 – 904 – 912 – 918 – 919 – 928
Vasculitis
of Artery only:
Large B.V: 1\Giant Cell Arthritis. 2\ Takayasu’s arthritis
Medium B.V: 1\classical poly arthritis nodosa. 2\Kawasaki disease.
Small B.V: 1\wegners granulomatosis. 2\ microscopic polyangitis.
. 3\ churg-straus’s syndrome. 4\ henoch schneil purpura.
Wegners granulomatosis:
[c- ANCA +ve] vasculitis of small blood vessels common in female mostly of (nostrils,
eyes & ears).
CP: 1/ Otitis media 2/proptosis 3/Upper airway involvement: [Epistaxiss , hemoptysis,
mucosal ulceration +Pulmonary nodules 50%]
Rx: Steroids

Giant cell arteritis: Takayasu arteritis Poly arthritis nodosa: Churg–Strauss

(PAN) syndrome
Age >60 years 25-30 years >40 years 30-50 years
Gender Female Female 8:1 Male 2:1 Equal
Temporal + ophthalmic Aorta Skin+renal Small vessel
+systemic+nerve
1-blurred vision, 1-claudication, 1\skin: most common , characterised by:
2-temporal headache fever, arthralgia nodules (pin point 1-allergic rhinitis,
localized and weight loss. bruises & erythema ) 2- nasal polyposis
3-pulstile palpable 2-loss of pulses, & levedo reticularis 3- late-onset asthma
temporal B.V bruits , 2\ 70 % affect vasa that is often difficult
4-blindness is 3-hypertension nervorum = neuropathy to control .
reversible if managed 4-aortic affects (motor & The typical acute
early, Or permanent if incompetence. sensory) mostly presentation is with a
not treated symmetrical. triad of
3\ Hypertension b\c of 1-skin lesions (purpura
local vasculitis. or nodules)
4\ renal involvement 2- asymmetric
 Polymyalgia rheumatic: (glomerulonephritis) mononeuritis multiplex
Characteristically associated with shoulder v.rare. 3-eosinophilia.
pain and wasting and jaw pain + features of Up to 50% of patients
giant cell arteritis have abdominal
symptoms provoked by
mesenteric vasculitis .
Pleural or pericardial
effusions due to
serositis may be
present.
Investigation: 1-CBC 2- Angiography  narrowing in B.V.
3- Biopsy: most confirmatory test granuloma .
Treatment: 1- give high dose of steroid 2- Immunosuppressant .

Prognosis Poor if not treated 5-year survival is 50% relapsing = give

83%. steroid to remission
stage.
–mortality rate < 20%.

Behcets Disease:
*Def: Multi systemic vasculitis of unknown etiology, affecting arteries & veins, common
in male >female, (20yrs -40yrs) .
*it’s not autoimmune but related with HLA B51.
Clinical Picture:
Major Criteria: Recurrent painful oral ulcers > 3times /year in almost all pts.
Minor Criteria: 1\Recurrent Genital Ulcer.
2\ eye Involvement  a) Uveitis +Iritis (mostly Ant). b) Conjunctivitis.
. c) Scleritis & episcleritis. d) Retinal vasculitis.
3\ Skin involvement: a) erythema nodosum b) Pseudo folliculitis.
. c) Papule pustular lesion
4\ + pathergy test has diagnostic value (Pastular skin lesion)
(*Dx, clinically: 2minor criteria +major Behcets disease.
Other manifestations:
1\ Abdominal Pain & diarrhea 2\ Headache  non-infective meningitis (aseptic)
3\ venous system  DVT 4\ Arthritis non destructive
Management:
1-Steroid (topical or orally)  inflammation. 2-Chalichicine  joint involvement.
3-Immunosuppressant. 4-Anti-fungal Rx 2ry infection.
Home work: 2017: Q62 to Q67
1001: 877 – 880 – 884 – 903 – 913 - 914 – 915 – 916 – 917 – 924